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The dataset generation failed because of a cast error
Error code: DatasetGenerationCastError
Exception: DatasetGenerationCastError
Message: An error occurred while generating the dataset
All the data files must have the same columns, but at some point there are 2 new columns ({'source', 'index'}) and 4 missing columns ({'title', 'id', 'content', 'contents'}).
This happened while the json dataset builder was generating data using
hf://datasets/roxyroxygod/statpearls/statpearls/index/ncbi/MedCPT-Article-Encoder/metadatas.jsonl (at revision 3a33ed28a822cac56efc098cd43c1dedae743c17)
Please either edit the data files to have matching columns, or separate them into different configurations (see docs at https://hf.co/docs/hub/datasets-manual-configuration#multiple-configurations)
Traceback: Traceback (most recent call last):
File "/src/services/worker/.venv/lib/python3.9/site-packages/datasets/builder.py", line 1870, in _prepare_split_single
writer.write_table(table)
File "/src/services/worker/.venv/lib/python3.9/site-packages/datasets/arrow_writer.py", line 622, in write_table
pa_table = table_cast(pa_table, self._schema)
File "/src/services/worker/.venv/lib/python3.9/site-packages/datasets/table.py", line 2292, in table_cast
return cast_table_to_schema(table, schema)
File "/src/services/worker/.venv/lib/python3.9/site-packages/datasets/table.py", line 2240, in cast_table_to_schema
raise CastError(
datasets.table.CastError: Couldn't cast
index: int64
source: string
to
{'id': Value(dtype='string', id=None), 'title': Value(dtype='string', id=None), 'content': Value(dtype='string', id=None), 'contents': Value(dtype='string', id=None)}
because column names don't match
During handling of the above exception, another exception occurred:
Traceback (most recent call last):
File "/src/services/worker/src/worker/job_runners/config/parquet_and_info.py", line 1417, in compute_config_parquet_and_info_response
parquet_operations = convert_to_parquet(builder)
File "/src/services/worker/src/worker/job_runners/config/parquet_and_info.py", line 1049, in convert_to_parquet
builder.download_and_prepare(
File "/src/services/worker/.venv/lib/python3.9/site-packages/datasets/builder.py", line 924, in download_and_prepare
self._download_and_prepare(
File "/src/services/worker/.venv/lib/python3.9/site-packages/datasets/builder.py", line 1000, in _download_and_prepare
self._prepare_split(split_generator, **prepare_split_kwargs)
File "/src/services/worker/.venv/lib/python3.9/site-packages/datasets/builder.py", line 1741, in _prepare_split
for job_id, done, content in self._prepare_split_single(
File "/src/services/worker/.venv/lib/python3.9/site-packages/datasets/builder.py", line 1872, in _prepare_split_single
raise DatasetGenerationCastError.from_cast_error(
datasets.exceptions.DatasetGenerationCastError: An error occurred while generating the dataset
All the data files must have the same columns, but at some point there are 2 new columns ({'source', 'index'}) and 4 missing columns ({'title', 'id', 'content', 'contents'}).
This happened while the json dataset builder was generating data using
hf://datasets/roxyroxygod/statpearls/statpearls/index/ncbi/MedCPT-Article-Encoder/metadatas.jsonl (at revision 3a33ed28a822cac56efc098cd43c1dedae743c17)
Please either edit the data files to have matching columns, or separate them into different configurations (see docs at https://hf.co/docs/hub/datasets-manual-configuration#multiple-configurations)Need help to make the dataset viewer work? Make sure to review how to configure the dataset viewer, and open a discussion for direct support.
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string | title
string | content
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article-100024_0 | Chronic Total Occlusion of the Coronary Artery -- Continuing Education Activity | Chronic total occlusion (CTO) lesions are diagnosed in patients who are undergoing coronary angiography as part of the evaluation of ischemic heart disease, cardiomyopathy, or valvular heart disease. CTO revascularization has not shown benefit in rates of all-cause mortality, myocardial infarction, stroke, and repeat revascularization and is commonly performed to improve a patient's quality of life by reducing their angina symptoms. This activity reviews the evaluation and treatment of chronic total occlusion of the coronary artery and highlights the role of the interprofessional team in evaluating and treating this condition. | Chronic Total Occlusion of the Coronary Artery -- Continuing Education Activity. Chronic total occlusion (CTO) lesions are diagnosed in patients who are undergoing coronary angiography as part of the evaluation of ischemic heart disease, cardiomyopathy, or valvular heart disease. CTO revascularization has not shown benefit in rates of all-cause mortality, myocardial infarction, stroke, and repeat revascularization and is commonly performed to improve a patient's quality of life by reducing their angina symptoms. This activity reviews the evaluation and treatment of chronic total occlusion of the coronary artery and highlights the role of the interprofessional team in evaluating and treating this condition. |
article-100024_1 | Chronic Total Occlusion of the Coronary Artery -- Continuing Education Activity | Objectives: Describe the histopathology of a chronic total occlusion (CTO) lesion. Review the risk factors for developing chronic total occlusion (CTO) lesions. Outline the typical presentation of a patient with chronic total occlusion (CTO) lesions. Explain the importance of improving care coordination amongst the interprofessional team( primary care physician, cardiologist, and interventionist) to enhance the delivery of care for patients with chronic total occlusion (CTO). Access free multiple choice questions on this topic. | Chronic Total Occlusion of the Coronary Artery -- Continuing Education Activity. Objectives: Describe the histopathology of a chronic total occlusion (CTO) lesion. Review the risk factors for developing chronic total occlusion (CTO) lesions. Outline the typical presentation of a patient with chronic total occlusion (CTO) lesions. Explain the importance of improving care coordination amongst the interprofessional team( primary care physician, cardiologist, and interventionist) to enhance the delivery of care for patients with chronic total occlusion (CTO). Access free multiple choice questions on this topic. |
article-100024_2 | Chronic Total Occlusion of the Coronary Artery -- Introduction | A coronary chronic total occlusion (CTO) is defined as 100% occlusion of a coronary artery for a duration of greater than or equal to 3 months based on angiographic evidence. The TIMI (thrombolysis in myocardial infarction) flow grading system is a scoring classification from 0-3 referring to the levels of coronary blood flow assessed during coronary angiography. The TIMI flow grading system is as below [1] : TIMI 0 flow (no perfusion-complete occlusion) - the absence of any forward flow beyond a coronary occlusion. TIMI 1 flow (penetration without perfusion) - faint forward flow beyond the occlusion, associated with an incomplete filling of the distal coronary bed. TIMI 2 flow (partial reperfusion) - delayed forward flow with complete filling of the distal coronary bed. TIMI 3 flow (full perfusion) - normal flow, which fills the distal coronary bed. | Chronic Total Occlusion of the Coronary Artery -- Introduction. A coronary chronic total occlusion (CTO) is defined as 100% occlusion of a coronary artery for a duration of greater than or equal to 3 months based on angiographic evidence. The TIMI (thrombolysis in myocardial infarction) flow grading system is a scoring classification from 0-3 referring to the levels of coronary blood flow assessed during coronary angiography. The TIMI flow grading system is as below [1] : TIMI 0 flow (no perfusion-complete occlusion) - the absence of any forward flow beyond a coronary occlusion. TIMI 1 flow (penetration without perfusion) - faint forward flow beyond the occlusion, associated with an incomplete filling of the distal coronary bed. TIMI 2 flow (partial reperfusion) - delayed forward flow with complete filling of the distal coronary bed. TIMI 3 flow (full perfusion) - normal flow, which fills the distal coronary bed. |
article-100024_3 | Chronic Total Occlusion of the Coronary Artery -- Introduction | A "true" CTO is defined as 100% occlusion of a coronary artery with TIMI 0 flow; whereas a "functional" CTO is defined as severely stenotic, yet, less than a 100% occlusion of the coronary artery with TIMI 1 flow for a duration of greater than or equal to 3 months based on angiographic evidence. [2] Moreover, it is difficult to identify the exact period over which a CTO lesion is present in the absence of serial angiograms. Therefore, it is mostly estimated based on available clinical information related to the timing of the event that caused the occlusion, for example, prior myocardial infarction or sudden change in anginal symptoms with electrocardiogram changes consistent with the location of the occlusion. However, in many patients, the age of the CTO cannot be determined with confidence. | Chronic Total Occlusion of the Coronary Artery -- Introduction. A "true" CTO is defined as 100% occlusion of a coronary artery with TIMI 0 flow; whereas a "functional" CTO is defined as severely stenotic, yet, less than a 100% occlusion of the coronary artery with TIMI 1 flow for a duration of greater than or equal to 3 months based on angiographic evidence. [2] Moreover, it is difficult to identify the exact period over which a CTO lesion is present in the absence of serial angiograms. Therefore, it is mostly estimated based on available clinical information related to the timing of the event that caused the occlusion, for example, prior myocardial infarction or sudden change in anginal symptoms with electrocardiogram changes consistent with the location of the occlusion. However, in many patients, the age of the CTO cannot be determined with confidence. |
article-100024_4 | Chronic Total Occlusion of the Coronary Artery -- Etiology | Risk factors for CTO lesion in patients are as below [3] : Known coronary artery disease or history of myocardial infarction Excessive tobacco use High LDL cholesterol, low HDL cholesterol Diabetes Sedentary lifestyle Hypertension Family history of premature disease End-stage kidney disease Obesity Postmenopausal women | Chronic Total Occlusion of the Coronary Artery -- Etiology. Risk factors for CTO lesion in patients are as below [3] : Known coronary artery disease or history of myocardial infarction Excessive tobacco use High LDL cholesterol, low HDL cholesterol Diabetes Sedentary lifestyle Hypertension Family history of premature disease End-stage kidney disease Obesity Postmenopausal women |
article-100024_5 | Chronic Total Occlusion of the Coronary Artery -- Epidemiology | CTO lesions are found in approximately one-quarter to one-third of patients undergoing diagnostic coronary angiography. The true prevalence, however, in the general population is unknown due to a subset of patients with CTO lesions being asymptomatic or minimally symptomatic and never undergoing diagnostic coronary angiography. Patients with a history of coronary artery bypass graft surgery are found to have CTOs of their native vessels more frequently (50% to 55%). In comparison, patients presenting with ST-elevation myocardial infarction (STEMI) are less likely to have a CTO (9% to 11%). [4] [5] | Chronic Total Occlusion of the Coronary Artery -- Epidemiology. CTO lesions are found in approximately one-quarter to one-third of patients undergoing diagnostic coronary angiography. The true prevalence, however, in the general population is unknown due to a subset of patients with CTO lesions being asymptomatic or minimally symptomatic and never undergoing diagnostic coronary angiography. Patients with a history of coronary artery bypass graft surgery are found to have CTOs of their native vessels more frequently (50% to 55%). In comparison, patients presenting with ST-elevation myocardial infarction (STEMI) are less likely to have a CTO (9% to 11%). [4] [5] |
article-100024_6 | Chronic Total Occlusion of the Coronary Artery -- Epidemiology | Data from the National Heart, Lung, and Blood Institute (1997–1999) Dynamic Registry showed that CTO lesions are most common in the right coronary artery and least common in the left circumflex artery. Older patients are more likely to have at least one CTO lesion with 37% prevalence in patients under the age of 65 years, 40% in patients between the ages of 65 to 79 years, and 41% in those patients who are older than 85 years. [6] | Chronic Total Occlusion of the Coronary Artery -- Epidemiology. Data from the National Heart, Lung, and Blood Institute (1997–1999) Dynamic Registry showed that CTO lesions are most common in the right coronary artery and least common in the left circumflex artery. Older patients are more likely to have at least one CTO lesion with 37% prevalence in patients under the age of 65 years, 40% in patients between the ages of 65 to 79 years, and 41% in those patients who are older than 85 years. [6] |
article-100024_7 | Chronic Total Occlusion of the Coronary Artery -- Pathophysiology | Pathogenesis of coronary artery disease, which can progress to CTO lesions, has multiple contributing factors, which include upregulation of the immunologic and inflammatory markers (cytokines, leukocytes, high sensitivity C-reactive protein), endothelial dysfunction, and cholesterol accumulation. Most commonly, it starts with the collection of smooth muscle cells within the intima, and this progresses to macrophages accumulating in the intima leading to pathologic intimal thickening and progression of lesions. [7] [8] | Chronic Total Occlusion of the Coronary Artery -- Pathophysiology. Pathogenesis of coronary artery disease, which can progress to CTO lesions, has multiple contributing factors, which include upregulation of the immunologic and inflammatory markers (cytokines, leukocytes, high sensitivity C-reactive protein), endothelial dysfunction, and cholesterol accumulation. Most commonly, it starts with the collection of smooth muscle cells within the intima, and this progresses to macrophages accumulating in the intima leading to pathologic intimal thickening and progression of lesions. [7] [8] |
article-100024_8 | Chronic Total Occlusion of the Coronary Artery -- Histopathology | Histopathological attributes of a CTO lesion commonly consist of calcium, lipids (both intracellular and extracellular), smooth muscle cells, an extracellular matrix, and neovascularization. Occlusions typically have a dense concentration of collagen-rich fibrous tissue at the proximal and distal ends contributing to a columnar lesion of calcified, resistant fibrous tissue surrounding a softer core of organized thrombus and lipids. Lesion classification is as soft, hard, or a mixture of both. Soft plaques are more frequent in occlusions less than 12 months of age and consist of cholesterol-laden cells and foam cells. Hard plaques are more prevalent in occlusions that are older than 12 months of age and are characterized by dense fibrous tissue with fibrocalcific regions without neovascular channels. [9] | Chronic Total Occlusion of the Coronary Artery -- Histopathology. Histopathological attributes of a CTO lesion commonly consist of calcium, lipids (both intracellular and extracellular), smooth muscle cells, an extracellular matrix, and neovascularization. Occlusions typically have a dense concentration of collagen-rich fibrous tissue at the proximal and distal ends contributing to a columnar lesion of calcified, resistant fibrous tissue surrounding a softer core of organized thrombus and lipids. Lesion classification is as soft, hard, or a mixture of both. Soft plaques are more frequent in occlusions less than 12 months of age and consist of cholesterol-laden cells and foam cells. Hard plaques are more prevalent in occlusions that are older than 12 months of age and are characterized by dense fibrous tissue with fibrocalcific regions without neovascular channels. [9] |
article-100024_9 | Chronic Total Occlusion of the Coronary Artery -- History and Physical | CTO lesions are diagnosed in patients who are undergoing coronary angiography as part of the evaluation of ischemic heart disease, cardiomyopathy, or valvular heart disease. Patients with ischemic heart disease generally present with typical chest pain symptoms (stable or unstable angina), atypical chest pain, NSTEMI, or STEMI. In contrast, patients with different types of cardiomyopathies or valvular heart disease may present with a variety of symptoms, including decompensated congestive heart failure. Therefore, during history taking in patients suspected of having ischemic heart disease, it is essential to have them describe and subjectively quantify their symptoms. | Chronic Total Occlusion of the Coronary Artery -- History and Physical. CTO lesions are diagnosed in patients who are undergoing coronary angiography as part of the evaluation of ischemic heart disease, cardiomyopathy, or valvular heart disease. Patients with ischemic heart disease generally present with typical chest pain symptoms (stable or unstable angina), atypical chest pain, NSTEMI, or STEMI. In contrast, patients with different types of cardiomyopathies or valvular heart disease may present with a variety of symptoms, including decompensated congestive heart failure. Therefore, during history taking in patients suspected of having ischemic heart disease, it is essential to have them describe and subjectively quantify their symptoms. |
article-100024_10 | Chronic Total Occlusion of the Coronary Artery -- History and Physical | The history should also include risk factors for cardiovascular disease (diabetes, tobacco abuse, hypertension, hyperlipidemia) and non-cardiac causes of the patient's symptoms, including pulmonary embolism, aortic dissection, pneumothorax, esophageal rupture or perforating peptic ulcer. Physical examination in these patients should include complete auscultation of the heart and lung sounds together with assessment for heart failure signs including jugular venous distention, Kussmaul sign, hepatojugular reflex, ascites, and peripheral edema. | Chronic Total Occlusion of the Coronary Artery -- History and Physical. The history should also include risk factors for cardiovascular disease (diabetes, tobacco abuse, hypertension, hyperlipidemia) and non-cardiac causes of the patient's symptoms, including pulmonary embolism, aortic dissection, pneumothorax, esophageal rupture or perforating peptic ulcer. Physical examination in these patients should include complete auscultation of the heart and lung sounds together with assessment for heart failure signs including jugular venous distention, Kussmaul sign, hepatojugular reflex, ascites, and peripheral edema. |
article-100024_11 | Chronic Total Occlusion of the Coronary Artery -- Evaluation | A significant component of an assessment for a patient who presents with signs and symptoms of ischemic heart disease is history and physical exam. These should include vital signs (respiratory rate, blood pressure, temperature, and heart rate), review of the patient's medication list, and an electrocardiogram. During their evaluation, the patient should have an assessment for any underlying or comorbid valvular heart disease or heart failure. | Chronic Total Occlusion of the Coronary Artery -- Evaluation. A significant component of an assessment for a patient who presents with signs and symptoms of ischemic heart disease is history and physical exam. These should include vital signs (respiratory rate, blood pressure, temperature, and heart rate), review of the patient's medication list, and an electrocardiogram. During their evaluation, the patient should have an assessment for any underlying or comorbid valvular heart disease or heart failure. |
article-100024_12 | Chronic Total Occlusion of the Coronary Artery -- Evaluation | A healthcare provider should consider thyroid function testing, pulmonary function testing, routine blood work, including cardiac enzymes, chest X-ray, and echocardiography as part of their initial evaluation. If the initial assessment and evaluation are performed on an urgent basis, intravenous access should be obtained and, if no contraindication exists, the patient should be administered aspirin (162 to 325 mg) and nitrates. If available, patients should be placed on a cardiac monitor and should be assessed with pulse oximetry for the need for supplemental oxygen. | Chronic Total Occlusion of the Coronary Artery -- Evaluation. A healthcare provider should consider thyroid function testing, pulmonary function testing, routine blood work, including cardiac enzymes, chest X-ray, and echocardiography as part of their initial evaluation. If the initial assessment and evaluation are performed on an urgent basis, intravenous access should be obtained and, if no contraindication exists, the patient should be administered aspirin (162 to 325 mg) and nitrates. If available, patients should be placed on a cardiac monitor and should be assessed with pulse oximetry for the need for supplemental oxygen. |
article-100024_13 | Chronic Total Occlusion of the Coronary Artery -- Treatment / Management | CTO revascularization has not shown to benefit rates of all-cause mortality, myocardial infarction, stroke, or repeat revascularization; however, it has shown to significantly improve patients' quality of life and reduce symptoms of angina. [10] [11] [12] Nuclear medicine stress test or myocardial viability studies are also used in conjunction with symptoms to objectively demonstrate areas of ischemia or viability supplied by the CTO vessel. Based on current guidelines, patients with single-vessel CTO lesions should undergo coronary artery bypass surgery if they have left main artery disease, proximal LAD disease which supplies a viable anterior wall, or three-vessel disease in a patient with insulin-dependent diabetes, severe left ventricular dysfunction, or chronic kidney disease. [13] | Chronic Total Occlusion of the Coronary Artery -- Treatment / Management. CTO revascularization has not shown to benefit rates of all-cause mortality, myocardial infarction, stroke, or repeat revascularization; however, it has shown to significantly improve patients' quality of life and reduce symptoms of angina. [10] [11] [12] Nuclear medicine stress test or myocardial viability studies are also used in conjunction with symptoms to objectively demonstrate areas of ischemia or viability supplied by the CTO vessel. Based on current guidelines, patients with single-vessel CTO lesions should undergo coronary artery bypass surgery if they have left main artery disease, proximal LAD disease which supplies a viable anterior wall, or three-vessel disease in a patient with insulin-dependent diabetes, severe left ventricular dysfunction, or chronic kidney disease. [13] |
article-100024_14 | Chronic Total Occlusion of the Coronary Artery -- Treatment / Management | In patients who meet the indication for a CTO PCI, informed consent is necessary before the procedure after an extensive discussion about the risks and benefits of CTO PCI for the patient. Due to the challenging nature of the CTO lesions, a successful outcome for PCI in these lesions is when the procedure obtains TIMI-3 flow, and there is less than 50% of residual stenosis in the vessel. | Chronic Total Occlusion of the Coronary Artery -- Treatment / Management. In patients who meet the indication for a CTO PCI, informed consent is necessary before the procedure after an extensive discussion about the risks and benefits of CTO PCI for the patient. Due to the challenging nature of the CTO lesions, a successful outcome for PCI in these lesions is when the procedure obtains TIMI-3 flow, and there is less than 50% of residual stenosis in the vessel. |
article-100024_15 | Chronic Total Occlusion of the Coronary Artery -- Treatment / Management | Multiple scoring systems are available to operators to predict technical success in CTO lesions. One of the most commonly used scoring systems is the J-CTO score, developed using the Chronic Total Occlusion Registry in Japan. A J-CTO score is used to predict the probability of crossing the CTO lesion within 30 minutes, and is inclusive of five independent factors; blunt stump appearance of the proximal cap of the occlusion, occlusion length greater than or equal to 20 mm, calcification detected within the CTO segment, the presence of a greater than 45-degree bend within the CTO segment, and prior failed PCI attempt of the CTO lesion. Each of these independent factors carries 1 point in the J-CTO score; zero is considered easy, a score of one is deemed to be intermediate, two rates as difficult, and greater than or equal to three is considered very difficult, with the probability of crossing within 30 minutes found to be 88%, 67%, 42%, and 10% respectively. [14] | Chronic Total Occlusion of the Coronary Artery -- Treatment / Management. Multiple scoring systems are available to operators to predict technical success in CTO lesions. One of the most commonly used scoring systems is the J-CTO score, developed using the Chronic Total Occlusion Registry in Japan. A J-CTO score is used to predict the probability of crossing the CTO lesion within 30 minutes, and is inclusive of five independent factors; blunt stump appearance of the proximal cap of the occlusion, occlusion length greater than or equal to 20 mm, calcification detected within the CTO segment, the presence of a greater than 45-degree bend within the CTO segment, and prior failed PCI attempt of the CTO lesion. Each of these independent factors carries 1 point in the J-CTO score; zero is considered easy, a score of one is deemed to be intermediate, two rates as difficult, and greater than or equal to three is considered very difficult, with the probability of crossing within 30 minutes found to be 88%, 67%, 42%, and 10% respectively. [14] |
article-100024_16 | Chronic Total Occlusion of the Coronary Artery -- Treatment / Management | Another commonly used score to predict the technical success of CTO PCI is the Prospective Global Registry for the Study of Chronic Total Occlusion Intervention (PROGRESS-CTO) score. This predictor uses four independent factors to assess the CTO lesion, which includes CTO lesion proximal cap ambiguity, moderate/severe tortuosity of the CTO vessel, Circumflex artery CTO, and the absence of interventional collaterals. Each of these factors carries one point and correlates with technical success. A PROGRESS-CTO score of 0 is associated with 91% technical success, a score of 1 correlates with 74%, a score of 2 is 57% percent, and a score of ≥3 is less than 4.3%. [15] | Chronic Total Occlusion of the Coronary Artery -- Treatment / Management. Another commonly used score to predict the technical success of CTO PCI is the Prospective Global Registry for the Study of Chronic Total Occlusion Intervention (PROGRESS-CTO) score. This predictor uses four independent factors to assess the CTO lesion, which includes CTO lesion proximal cap ambiguity, moderate/severe tortuosity of the CTO vessel, Circumflex artery CTO, and the absence of interventional collaterals. Each of these factors carries one point and correlates with technical success. A PROGRESS-CTO score of 0 is associated with 91% technical success, a score of 1 correlates with 74%, a score of 2 is 57% percent, and a score of ≥3 is less than 4.3%. [15] |
article-100024_17 | Chronic Total Occlusion of the Coronary Artery -- Differential Diagnosis | STEMI NSTEMI Pulmonary embolism Aortic dissection Pneumothorax Esophageal rupture Perforating peptic ulcer disease | Chronic Total Occlusion of the Coronary Artery -- Differential Diagnosis. STEMI NSTEMI Pulmonary embolism Aortic dissection Pneumothorax Esophageal rupture Perforating peptic ulcer disease |
article-100024_18 | Chronic Total Occlusion of the Coronary Artery -- Prognosis | In addition to causing symptoms, CTOs have correlations with a worse overall prognosis, with higher rates of death and non-fatal adverse cardiovascular events in several populations. Patients with CTOs tend to be older and have more comorbidities and more significant impairment of left ventricular function. Furthermore, patients with non-revascularized CTOs have higher mortality and a higher risk of major adverse cardiovascular events in comparison to patients with multivessel coronary artery disease who are completely revascularized. [16] [17] | Chronic Total Occlusion of the Coronary Artery -- Prognosis. In addition to causing symptoms, CTOs have correlations with a worse overall prognosis, with higher rates of death and non-fatal adverse cardiovascular events in several populations. Patients with CTOs tend to be older and have more comorbidities and more significant impairment of left ventricular function. Furthermore, patients with non-revascularized CTOs have higher mortality and a higher risk of major adverse cardiovascular events in comparison to patients with multivessel coronary artery disease who are completely revascularized. [16] [17] |
article-100024_19 | Chronic Total Occlusion of the Coronary Artery -- Complications | Percutaneous coronary intervention (PCI) of a CTO lesion on average requires more fluoroscopy time, higher contrast volume, and carries a lower success rate compared to non-CTO PCI’s. CTO PCIs also have a higher complication rate than non-CTO PCIs with major complications, including myocardial infarction, stroke, vessel perforation, and death. However, vascular access site complications during CTO PCI occur at a similar frequency as routine PCI; these include poorly controlled bleeding, hematoma, acute thrombosis, distal embolization, retroperitoneal hemorrhage, dissection of the access artery, arteriovenous fistula, and pseudoaneurysm. Other potentially serious complications include ventricular tachyarrhythmias, bradycardia, allergic reactions, atheroembolism, and contrast nephropathy. [18] [19] [20] [21] [22] [23] | Chronic Total Occlusion of the Coronary Artery -- Complications. Percutaneous coronary intervention (PCI) of a CTO lesion on average requires more fluoroscopy time, higher contrast volume, and carries a lower success rate compared to non-CTO PCI’s. CTO PCIs also have a higher complication rate than non-CTO PCIs with major complications, including myocardial infarction, stroke, vessel perforation, and death. However, vascular access site complications during CTO PCI occur at a similar frequency as routine PCI; these include poorly controlled bleeding, hematoma, acute thrombosis, distal embolization, retroperitoneal hemorrhage, dissection of the access artery, arteriovenous fistula, and pseudoaneurysm. Other potentially serious complications include ventricular tachyarrhythmias, bradycardia, allergic reactions, atheroembolism, and contrast nephropathy. [18] [19] [20] [21] [22] [23] |
article-100024_20 | Chronic Total Occlusion of the Coronary Artery -- Complications | Data analysis of the National Cardiovascular Data Registry-Cath PCI Registry in the United States showed higher in-hospital major adverse cardiovascular event frequency (1.6 versus 0.8 percent; p<0.001) which included mortality (0.4 % versus 0.3%; p<0.001), stroke (0.1% versus 0.1 %; p = 0.045), tamponade (0.3% versus 0.1%; p<0.001), MI (2.7% versus 1.9 %; p<0.001), and urgent CABG surgery (0.8% versus 0.4%; p<0.001) in 22,365 patients who underwent CTO PCI compared with 572,145 patients who underwent non-CTO PCI. CTO PCIs also had lower procedural success rate (59% vs. 96%, p < 0.001) in this registry. [24] | Chronic Total Occlusion of the Coronary Artery -- Complications. Data analysis of the National Cardiovascular Data Registry-Cath PCI Registry in the United States showed higher in-hospital major adverse cardiovascular event frequency (1.6 versus 0.8 percent; p<0.001) which included mortality (0.4 % versus 0.3%; p<0.001), stroke (0.1% versus 0.1 %; p = 0.045), tamponade (0.3% versus 0.1%; p<0.001), MI (2.7% versus 1.9 %; p<0.001), and urgent CABG surgery (0.8% versus 0.4%; p<0.001) in 22,365 patients who underwent CTO PCI compared with 572,145 patients who underwent non-CTO PCI. CTO PCIs also had lower procedural success rate (59% vs. 96%, p < 0.001) in this registry. [24] |
article-100024_21 | Chronic Total Occlusion of the Coronary Artery -- Complications | Another multicenter registry (OPEN-CTO) from 12 CTO-PCI centers of 1,000 consecutive patients undergoing CTO PCI evaluated success rates, complication rates, and health status benefits at one month. CTO PCIs showed a success rate of 86%, with an in-hospital mortality of 0.9%, 1-month mortality of 1.3%. 4.8% of the patients had coronary perforations requiring treatment. Additionally, major adverse cardiovascular events were 7%, myocardial infarction 2.6%, acute kidney injury 0.7%, and stroke 0%. [12] | Chronic Total Occlusion of the Coronary Artery -- Complications. Another multicenter registry (OPEN-CTO) from 12 CTO-PCI centers of 1,000 consecutive patients undergoing CTO PCI evaluated success rates, complication rates, and health status benefits at one month. CTO PCIs showed a success rate of 86%, with an in-hospital mortality of 0.9%, 1-month mortality of 1.3%. 4.8% of the patients had coronary perforations requiring treatment. Additionally, major adverse cardiovascular events were 7%, myocardial infarction 2.6%, acute kidney injury 0.7%, and stroke 0%. [12] |
article-100024_22 | Chronic Total Occlusion of the Coronary Artery -- Deterrence and Patient Education | Patient education should include resources such as videos and pamphlets. Teaching should focus on risk factor reduction and lifestyle modification such as smoking cessation, blood pressure management based on guidelines, screening for new-onset diabetes, and exercise as tolerated. | Chronic Total Occlusion of the Coronary Artery -- Deterrence and Patient Education. Patient education should include resources such as videos and pamphlets. Teaching should focus on risk factor reduction and lifestyle modification such as smoking cessation, blood pressure management based on guidelines, screening for new-onset diabetes, and exercise as tolerated. |
article-100024_23 | Chronic Total Occlusion of the Coronary Artery -- Enhancing Healthcare Team Outcomes | Educating patients at risk for coronary artery disease and making a closed-loop communication between them and their cardiologist for primary and secondary prevention can further improve the management of patients at risk of these CTO lesions. Collaboration with shared decision making (between primary care physician, cardiologist, and interventionist) and communication are vital elements for good outcomes in patients with coronary artery disease and CTO lesions. | Chronic Total Occlusion of the Coronary Artery -- Enhancing Healthcare Team Outcomes. Educating patients at risk for coronary artery disease and making a closed-loop communication between them and their cardiologist for primary and secondary prevention can further improve the management of patients at risk of these CTO lesions. Collaboration with shared decision making (between primary care physician, cardiologist, and interventionist) and communication are vital elements for good outcomes in patients with coronary artery disease and CTO lesions. |
article-100024_24 | Chronic Total Occlusion of the Coronary Artery -- Enhancing Healthcare Team Outcomes | The interprofessional team care provided to the patient must use an integrated care pathway combined with an evidence-based approach to evaluating CTO lesions. The earlier angiographic and demographic predictors of failure to revascularize are identified in CTO lesions; the better is the prognosis and outcome. | Chronic Total Occlusion of the Coronary Artery -- Enhancing Healthcare Team Outcomes. The interprofessional team care provided to the patient must use an integrated care pathway combined with an evidence-based approach to evaluating CTO lesions. The earlier angiographic and demographic predictors of failure to revascularize are identified in CTO lesions; the better is the prognosis and outcome. |
article-100024_25 | Chronic Total Occlusion of the Coronary Artery -- Review Questions | Access free multiple choice questions on this topic. Comment on this article. | Chronic Total Occlusion of the Coronary Artery -- Review Questions. Access free multiple choice questions on this topic. Comment on this article. |
article-100131_0 | Cardiopulmonary Arrest in Adults -- Continuing Education Activity | Cardiopulmonary arrest is the cessation of adequate heart function and respiration and results in death without reversal. Often this condition is found in patients with coronary artery disease. This activity reviews the management and prevention of cardiopulmonary arrest and highlights the role of the interprofessional team in treating patients with this condition. | Cardiopulmonary Arrest in Adults -- Continuing Education Activity. Cardiopulmonary arrest is the cessation of adequate heart function and respiration and results in death without reversal. Often this condition is found in patients with coronary artery disease. This activity reviews the management and prevention of cardiopulmonary arrest and highlights the role of the interprofessional team in treating patients with this condition. |
article-100131_1 | Cardiopulmonary Arrest in Adults -- Continuing Education Activity | Objectives: Outline the typical presentation of a patient who suffers from cardiopulmonary arrest. Summarize the epidemiology of cardiac arrest in the U.S. Summarize the causes of cardiopulmonary arrest. Access free multiple choice questions on this topic. | Cardiopulmonary Arrest in Adults -- Continuing Education Activity. Objectives: Outline the typical presentation of a patient who suffers from cardiopulmonary arrest. Summarize the epidemiology of cardiac arrest in the U.S. Summarize the causes of cardiopulmonary arrest. Access free multiple choice questions on this topic. |
article-100131_2 | Cardiopulmonary Arrest in Adults -- Introduction | Cardiopulmonary arrest (CPA) is the cessation of effective ventilation and circulation. It is also known as cardiac arrest or circulatory arrest. In adults, it is most likely to be caused by a primary cardiac event. The most common electrical mechanism which is responsible for 50 to 80% of cardiopulmonary arrest is ventricular fibrillation (VF). While, 20^% to 30% which represents the less common causes of dysrhythmias involve Pulseless electrical activity (PEA), and asystole. Pulseless sustained ventricular tachycardia (VT) is a less common mechanism. This condition could progress to sudden death if it not treated promptly. Nevertheless, a cardiopulmonary arrest (CPA) could be reversed by cardiopulmonary resuscitation and/or cardioversion or defibrillation, or cardiac pacing. [1] | Cardiopulmonary Arrest in Adults -- Introduction. Cardiopulmonary arrest (CPA) is the cessation of effective ventilation and circulation. It is also known as cardiac arrest or circulatory arrest. In adults, it is most likely to be caused by a primary cardiac event. The most common electrical mechanism which is responsible for 50 to 80% of cardiopulmonary arrest is ventricular fibrillation (VF). While, 20^% to 30% which represents the less common causes of dysrhythmias involve Pulseless electrical activity (PEA), and asystole. Pulseless sustained ventricular tachycardia (VT) is a less common mechanism. This condition could progress to sudden death if it not treated promptly. Nevertheless, a cardiopulmonary arrest (CPA) could be reversed by cardiopulmonary resuscitation and/or cardioversion or defibrillation, or cardiac pacing. [1] |
article-100131_3 | Cardiopulmonary Arrest in Adults -- Introduction | The American Heart Association's AHA periodically releases updates and recommendations for adult basic life support (BLS) and the quality of cardiopulmonary resuscitation (CPR) on adults. Despite the causes, early induction of cardiopulmonary resuscitation (CPR) along with cardiac monitoring will determine which pulseless arrest pathway one has to follow. Evidence suggests that more than 400000 people die of cardiopulmonary arrest in the U.S every year. [2] They may or may not have been diagnosed with cardiopulmonary disease. | Cardiopulmonary Arrest in Adults -- Introduction. The American Heart Association's AHA periodically releases updates and recommendations for adult basic life support (BLS) and the quality of cardiopulmonary resuscitation (CPR) on adults. Despite the causes, early induction of cardiopulmonary resuscitation (CPR) along with cardiac monitoring will determine which pulseless arrest pathway one has to follow. Evidence suggests that more than 400000 people die of cardiopulmonary arrest in the U.S every year. [2] They may or may not have been diagnosed with cardiopulmonary disease. |
article-100131_4 | Cardiopulmonary Arrest in Adults -- Etiology | There are various causes for cardiopulmonary arrest in adults which varies by age and population. However, patients diagnosed with cardiac disease are more susceptible to having a cardiac arrest. Furthermore, it can be classified into different categories, which include cardiac, respiratory, and traumatic causes. But 75% of cardiac arrest incidents are believed to be due to coronary artery diseases. [2] | Cardiopulmonary Arrest in Adults -- Etiology. There are various causes for cardiopulmonary arrest in adults which varies by age and population. However, patients diagnosed with cardiac disease are more susceptible to having a cardiac arrest. Furthermore, it can be classified into different categories, which include cardiac, respiratory, and traumatic causes. But 75% of cardiac arrest incidents are believed to be due to coronary artery diseases. [2] |
article-100131_5 | Cardiopulmonary Arrest in Adults -- Etiology -- Coronary Artery Disease | Coronary artery abnormalities: Anomalous coronary artery anatomy. Acute lesions (platelet aggregation, plaque fissuring, acute thrombosis). Chronic atherosclerosis. coronary artery spasm Myocardial Infarction: Acute Healed | Cardiopulmonary Arrest in Adults -- Etiology -- Coronary Artery Disease. Coronary artery abnormalities: Anomalous coronary artery anatomy. Acute lesions (platelet aggregation, plaque fissuring, acute thrombosis). Chronic atherosclerosis. coronary artery spasm Myocardial Infarction: Acute Healed |
article-100131_6 | Cardiopulmonary Arrest in Adults -- Etiology -- Myocardial Hypertrophy | Secondary Hypertrophic cardiomyopathy Nonobstructive Obstructive | Cardiopulmonary Arrest in Adults -- Etiology -- Myocardial Hypertrophy. Secondary Hypertrophic cardiomyopathy Nonobstructive Obstructive |
article-100131_7 | Cardiopulmonary Arrest in Adults -- Etiology -- Infiltrative and Inflammatory Disorders | Infiltrative diseases Noninfectious inflammatory diseases Myocarditis | Cardiopulmonary Arrest in Adults -- Etiology -- Infiltrative and Inflammatory Disorders. Infiltrative diseases Noninfectious inflammatory diseases Myocarditis |
article-100131_8 | Cardiopulmonary Arrest in Adults -- Etiology -- Inherited Disorders | Early repolarization syndrome. Brugada syndrome Short QT syndrome. Long QT syndrome. Catecholaminergic polymorphic ventricular tachycardia | Cardiopulmonary Arrest in Adults -- Etiology -- Inherited Disorders. Early repolarization syndrome. Brugada syndrome Short QT syndrome. Long QT syndrome. Catecholaminergic polymorphic ventricular tachycardia |
article-100131_9 | Cardiopulmonary Arrest in Adults -- Etiology -- Heart Failure | Ejection fraction less than 35% [3] | Cardiopulmonary Arrest in Adults -- Etiology -- Heart Failure. Ejection fraction less than 35% [3] |
article-100131_10 | Cardiopulmonary Arrest in Adults -- Etiology -- Congenital disease | Tetralogy of Fallot | Cardiopulmonary Arrest in Adults -- Etiology -- Congenital disease. Tetralogy of Fallot |
article-100131_11 | Cardiopulmonary Arrest in Adults -- Etiology -- Respiratory Causes | Airway obstruction: Bronchospasm due to (pulmonary edema, pulmonary hemorrhage, and pneumonia) Severe asthma or Chronic Obstructive Pulmonary Disease (COPD). Pulmonary Embolism Respiratory Muscle Weakness: due to spinal cord injury. | Cardiopulmonary Arrest in Adults -- Etiology -- Respiratory Causes. Airway obstruction: Bronchospasm due to (pulmonary edema, pulmonary hemorrhage, and pneumonia) Severe asthma or Chronic Obstructive Pulmonary Disease (COPD). Pulmonary Embolism Respiratory Muscle Weakness: due to spinal cord injury. |
article-100131_12 | Cardiopulmonary Arrest in Adults -- Etiology -- Traumatic Causes | Overall, the prevalence of cardiac causes is around 50% to 60%. Whilst, the second most common cause that is respiratory insufficiency is around 15% to 40%. [4] | Cardiopulmonary Arrest in Adults -- Etiology -- Traumatic Causes. Overall, the prevalence of cardiac causes is around 50% to 60%. Whilst, the second most common cause that is respiratory insufficiency is around 15% to 40%. [4] |
article-100131_13 | Cardiopulmonary Arrest in Adults -- Epidemiology | Cardiac arrest is divided into out-hospital cardiac arrest (OHCA) and in-hospital cardiac arrest (IHCA). However, the incidence of cardiopulmonary arrest worldwide is not well described. In the U.S, more than 290,000 IHCA occur in adults annually, whilst 326,000 cases of OHCA among adults occur yearly. Half of these are unwitnessed. [4] [5] | Cardiopulmonary Arrest in Adults -- Epidemiology. Cardiac arrest is divided into out-hospital cardiac arrest (OHCA) and in-hospital cardiac arrest (IHCA). However, the incidence of cardiopulmonary arrest worldwide is not well described. In the U.S, more than 290,000 IHCA occur in adults annually, whilst 326,000 cases of OHCA among adults occur yearly. Half of these are unwitnessed. [4] [5] |
article-100131_14 | Cardiopulmonary Arrest in Adults -- Epidemiology | Men and women in middle-age have different susceptibilities to cardiopulmonary arrest; however, the sex differences decrease with increasing age. The difference in risk for cardiopulmonary arrest collateral the variations in age-related risks for other features of coronary heart disease (CHD) between males and females. As the gender gap for signs of coronary heart disease closes in the 6th to 8th decades, the excess risk of arrest in males progressively narrows. In spite of the lower incidence among younger women, CHD risk factors such as diabetes (DM), cigarette smoking, hyperlipidemia, and hypertension (HTN) are very highly influential. | Cardiopulmonary Arrest in Adults -- Epidemiology. Men and women in middle-age have different susceptibilities to cardiopulmonary arrest; however, the sex differences decrease with increasing age. The difference in risk for cardiopulmonary arrest collateral the variations in age-related risks for other features of coronary heart disease (CHD) between males and females. As the gender gap for signs of coronary heart disease closes in the 6th to 8th decades, the excess risk of arrest in males progressively narrows. In spite of the lower incidence among younger women, CHD risk factors such as diabetes (DM), cigarette smoking, hyperlipidemia, and hypertension (HTN) are very highly influential. |
article-100131_15 | Cardiopulmonary Arrest in Adults -- Pathophysiology | Data from postmortem examinations of cardiopulmonary arrest and sudden cardiac death (SCD) victims correlate with the clinical observations on the prevalence of coronary artery disease as the major structural etiologic factor. Higher than 80% of victims have pathologic findings of coronary artery disease. The pathologic description often involves a combination of extensive atherosclerosis of the coronary arteries along with unstable coronary artery lesions, which include various permutations of fissured, eroded, or ruptured plaques; and/or thrombosis. As many as seventy percent of men who die suddenly have preexisting healed myocardial infarctions, whereas only twenty percent have recent acute MIs, in spite of the prevalence of thrombi and unstable plaques. [6] | Cardiopulmonary Arrest in Adults -- Pathophysiology. Data from postmortem examinations of cardiopulmonary arrest and sudden cardiac death (SCD) victims correlate with the clinical observations on the prevalence of coronary artery disease as the major structural etiologic factor. Higher than 80% of victims have pathologic findings of coronary artery disease. The pathologic description often involves a combination of extensive atherosclerosis of the coronary arteries along with unstable coronary artery lesions, which include various permutations of fissured, eroded, or ruptured plaques; and/or thrombosis. As many as seventy percent of men who die suddenly have preexisting healed myocardial infarctions, whereas only twenty percent have recent acute MIs, in spite of the prevalence of thrombi and unstable plaques. [6] |
article-100131_16 | Cardiopulmonary Arrest in Adults -- History and Physical | In numerous patients, warning signs and symptoms may precede a cardiac arrest. Nevertheless, these features are ignored and unrecognized several times because those who survive after experiencing cardiopulmonary arrest, many of them suffer from amnesia while those patients who suffered cardiopulmonary arrest but survived and remember the event reveals that the most common sign was palpitations, shortness of breath, nausea, and chest pain. | Cardiopulmonary Arrest in Adults -- History and Physical. In numerous patients, warning signs and symptoms may precede a cardiac arrest. Nevertheless, these features are ignored and unrecognized several times because those who survive after experiencing cardiopulmonary arrest, many of them suffer from amnesia while those patients who suffered cardiopulmonary arrest but survived and remember the event reveals that the most common sign was palpitations, shortness of breath, nausea, and chest pain. |
article-100131_17 | Cardiopulmonary Arrest in Adults -- History and Physical | Clinicians examing cardiopulmonary arrest should start head-to-toe assessment immediately which will help to formulate the plan of management. The physical examination will help to diagnose the cardiopulmonary arrest as well as provide the most important information regarding the possible cause and the prognosis. While, the history will help to delineate at what time the event took place, what the victim was doing, and the involvement of drugs. In many cases, the gold standard for diagnosing the cardiopulmonary arrest is the loss of carotid pulse, But, many studies have shown that the rescuers often make a mistake while checking the carotid pulse, whether they are laypersons or the healthcare professionals. [7] | Cardiopulmonary Arrest in Adults -- History and Physical. Clinicians examing cardiopulmonary arrest should start head-to-toe assessment immediately which will help to formulate the plan of management. The physical examination will help to diagnose the cardiopulmonary arrest as well as provide the most important information regarding the possible cause and the prognosis. While, the history will help to delineate at what time the event took place, what the victim was doing, and the involvement of drugs. In many cases, the gold standard for diagnosing the cardiopulmonary arrest is the loss of carotid pulse, But, many studies have shown that the rescuers often make a mistake while checking the carotid pulse, whether they are laypersons or the healthcare professionals. [7] |
article-100131_18 | Cardiopulmonary Arrest in Adults -- Evaluation | Cardiopulmonary resuscitation should not be interrupted for doing blood or radiological investigation. However, point of care testing, like blood glucose or serum potassium may be done if it doesn't interfere with cardiopulmonary resuscitation efforts. Point of care ultrasound can also be used to evaluate the activity of the heart during cardiopulmonary resuscitation which has proved beneficial in many studies. [8] | Cardiopulmonary Arrest in Adults -- Evaluation. Cardiopulmonary resuscitation should not be interrupted for doing blood or radiological investigation. However, point of care testing, like blood glucose or serum potassium may be done if it doesn't interfere with cardiopulmonary resuscitation efforts. Point of care ultrasound can also be used to evaluate the activity of the heart during cardiopulmonary resuscitation which has proved beneficial in many studies. [8] |
article-100131_19 | Cardiopulmonary Arrest in Adults -- Treatment / Management | Five stages in the management of the patient with confirmed cardiopulmonary arrest are: Initial evaluation plus Basic Life Support Defibrillation Advanced Life Support Post-resuscitation care Long-term management | Cardiopulmonary Arrest in Adults -- Treatment / Management. Five stages in the management of the patient with confirmed cardiopulmonary arrest are: Initial evaluation plus Basic Life Support Defibrillation Advanced Life Support Post-resuscitation care Long-term management |
article-100131_20 | Cardiopulmonary Arrest in Adults -- Treatment / Management | Once the diagnosis of cardiopulmonary arrest is confirmed, then basic life support (BLS) and defibrillation can be carried out by the public, physicians, paramedical personnel, trained laypersons, and nurses. There is an increasing demand for specialized skills such as Advanced Life Support (ALS), post-resuscitation care, and long-term management of post cardiopulmonary arrest patients. The cardiopulmonary arrest could be reversed by two main interventions, i.e., early CPR and early Automated external defibrillation (AED). The first step involves recognition of the cardiopulmonary arrest and the BLS measures. If defibrillation is available for public use, then it should be activated and used if needed. Next, advanced life support (ALS) measures are used, involving IV/IO medication administration. If spontaneous circulation returns, then the case will undergo post-resuscitation care along with subsequent long-term management. The identification of a cardiopulmonary arrest victim includes ensuring that the patient is unresponsive, pulseless, and having abnormal breathing. Once the patient is identified, immediate CPR and activation of the Emergency Medical Services (EMS) should be done promptly. Nowadays, public access to defibrillation has been adding another layer of response. | Cardiopulmonary Arrest in Adults -- Treatment / Management. Once the diagnosis of cardiopulmonary arrest is confirmed, then basic life support (BLS) and defibrillation can be carried out by the public, physicians, paramedical personnel, trained laypersons, and nurses. There is an increasing demand for specialized skills such as Advanced Life Support (ALS), post-resuscitation care, and long-term management of post cardiopulmonary arrest patients. The cardiopulmonary arrest could be reversed by two main interventions, i.e., early CPR and early Automated external defibrillation (AED). The first step involves recognition of the cardiopulmonary arrest and the BLS measures. If defibrillation is available for public use, then it should be activated and used if needed. Next, advanced life support (ALS) measures are used, involving IV/IO medication administration. If spontaneous circulation returns, then the case will undergo post-resuscitation care along with subsequent long-term management. The identification of a cardiopulmonary arrest victim includes ensuring that the patient is unresponsive, pulseless, and having abnormal breathing. Once the patient is identified, immediate CPR and activation of the Emergency Medical Services (EMS) should be done promptly. Nowadays, public access to defibrillation has been adding another layer of response. |
article-100131_21 | Cardiopulmonary Arrest in Adults -- Treatment / Management -- Initial Evaluation and BLS | Confirming cardiopulmonary arrest need careful examination of the patient's level of consciousness, skin color, breathing movement, and arterial pulse either in the carotid or femoral artery. Just after confirming the arrest, the immediate responsibility of the rescuer is to call Emergency Medical Services and start CPR. | Cardiopulmonary Arrest in Adults -- Treatment / Management -- Initial Evaluation and BLS. Confirming cardiopulmonary arrest need careful examination of the patient's level of consciousness, skin color, breathing movement, and arterial pulse either in the carotid or femoral artery. Just after confirming the arrest, the immediate responsibility of the rescuer is to call Emergency Medical Services and start CPR. |
article-100131_22 | Cardiopulmonary Arrest in Adults -- Treatment / Management -- Initial Evaluation and BLS | It is essential to diagnose the signs of aspirations of a foreign body in the respiratory tract, which includes severe stridor, dyspnea, suprasternal and intercostal retractions. It is recommended to do the Heimlich maneuver if we are suspecting aspiration. | Cardiopulmonary Arrest in Adults -- Treatment / Management -- Initial Evaluation and BLS. It is essential to diagnose the signs of aspirations of a foreign body in the respiratory tract, which includes severe stridor, dyspnea, suprasternal and intercostal retractions. It is recommended to do the Heimlich maneuver if we are suspecting aspiration. |
article-100131_23 | Cardiopulmonary Arrest in Adults -- Treatment / Management -- Initial Evaluation and BLS | Maintaining a patent airway is necessary for successful cardiopulmonary resuscitation. Maneuvers like chin lift, head tilt, and jaw thrust can be used to keep the airway patent. Any visible foreign bodies like displaced dentures should be removed from the oropharynx. Ventilatory aids like oropharyngeal airway (OPA) and the nasopharyngeal airway (NPA) may be used if the rescuer is experiencing difficulty in ventilating the patient. [9] [10] The AHA guideline suggested certain recommendation for doing high-quality CPR: [11] Compression should start within 10 seconds of diagnosing cardiopulmonary arrest. Two breaths to be given after 30 compressions. Excessive ventilation should be avoided. Every effort should be made to reduce the interruption while changing the rescuer or while checking the rhythm. The rate of compression should be between 100 to 120 per minute The depth of compression should be between 2 to 2.4 inches for adults. Adequate time should be given for chest recoil | Cardiopulmonary Arrest in Adults -- Treatment / Management -- Initial Evaluation and BLS. Maintaining a patent airway is necessary for successful cardiopulmonary resuscitation. Maneuvers like chin lift, head tilt, and jaw thrust can be used to keep the airway patent. Any visible foreign bodies like displaced dentures should be removed from the oropharynx. Ventilatory aids like oropharyngeal airway (OPA) and the nasopharyngeal airway (NPA) may be used if the rescuer is experiencing difficulty in ventilating the patient. [9] [10] The AHA guideline suggested certain recommendation for doing high-quality CPR: [11] Compression should start within 10 seconds of diagnosing cardiopulmonary arrest. Two breaths to be given after 30 compressions. Excessive ventilation should be avoided. Every effort should be made to reduce the interruption while changing the rescuer or while checking the rhythm. The rate of compression should be between 100 to 120 per minute The depth of compression should be between 2 to 2.4 inches for adults. Adequate time should be given for chest recoil |
article-100131_24 | Cardiopulmonary Arrest in Adults -- Treatment / Management -- Automated External Defibrillation | The AEDs are easily handled via nonconventional responders, for instance: ambulance drivers, police officers, firefighters, security guards, and laypersons. Recent studies have suggested that AED use via nonconventional responders could improve the survival rates of cardiopulmonary arrest as the arrival of the ALS team takes time, and early defibrillation by non-conventional responders will not only reduce the time for defibrillation but will also improve patient outcome. | Cardiopulmonary Arrest in Adults -- Treatment / Management -- Automated External Defibrillation. The AEDs are easily handled via nonconventional responders, for instance: ambulance drivers, police officers, firefighters, security guards, and laypersons. Recent studies have suggested that AED use via nonconventional responders could improve the survival rates of cardiopulmonary arrest as the arrival of the ALS team takes time, and early defibrillation by non-conventional responders will not only reduce the time for defibrillation but will also improve patient outcome. |
article-100131_25 | Cardiopulmonary Arrest in Adults -- Treatment / Management -- Advanced Cardiac Life Support | Providers can use basic life support along with advanced airway aid and medication like epinephrine and amiodarone for CPR. The advanced airway may include supraglottic airway devices and endotracheal tubes. ACLS team has the further advantage of cardiac rhythm interpretation and using defibrillation when indicated. | Cardiopulmonary Arrest in Adults -- Treatment / Management -- Advanced Cardiac Life Support. Providers can use basic life support along with advanced airway aid and medication like epinephrine and amiodarone for CPR. The advanced airway may include supraglottic airway devices and endotracheal tubes. ACLS team has the further advantage of cardiac rhythm interpretation and using defibrillation when indicated. |
article-100131_26 | Cardiopulmonary Arrest in Adults -- Treatment / Management -- Advanced Cardiac Life Support | ADVANCED CARDIAC LIFE SUPPORT (ACLS) is designed to deliver adequate ventilation, stabilize the blood pressure along with the cardiac output, control cardiac arrhythmias, and restore organ perfusion. Maneuvers needed to accomplish these goals include- Defibrillation and pacing. Endotracheal tube intubation and mechanical ventilation Intravenous line insertion. The rapidity by which defibrillation is performed is an essential element for improving patient outcomes. The AHA guideline suggested certain recommendation for defibrillation- | Cardiopulmonary Arrest in Adults -- Treatment / Management -- Advanced Cardiac Life Support. ADVANCED CARDIAC LIFE SUPPORT (ACLS) is designed to deliver adequate ventilation, stabilize the blood pressure along with the cardiac output, control cardiac arrhythmias, and restore organ perfusion. Maneuvers needed to accomplish these goals include- Defibrillation and pacing. Endotracheal tube intubation and mechanical ventilation Intravenous line insertion. The rapidity by which defibrillation is performed is an essential element for improving patient outcomes. The AHA guideline suggested certain recommendation for defibrillation- |
article-100131_27 | Cardiopulmonary Arrest in Adults -- Treatment / Management -- Advanced Cardiac Life Support | Cardiopulmonary resuscitation should be carried out whilst the AED is being charged Immediate early defibrillation should be given preference over intubation and intravenous line insertion A defibrillator with a biphasic waveform is preferred over monophasic. Manufacturers recommended energy dose should be used for the first shock. If this is not mentioned, then the maximum dose should be used for defibrillation. Fixed versus escalating energy for subsequent shock should depend on manufacturers' recommendations. If the machine has the capability to escalate the energy, then higher energy should be used for a subsequent shock. A single shock strategy should be preferred to stacked shock. | Cardiopulmonary Arrest in Adults -- Treatment / Management -- Advanced Cardiac Life Support. Cardiopulmonary resuscitation should be carried out whilst the AED is being charged Immediate early defibrillation should be given preference over intubation and intravenous line insertion A defibrillator with a biphasic waveform is preferred over monophasic. Manufacturers recommended energy dose should be used for the first shock. If this is not mentioned, then the maximum dose should be used for defibrillation. Fixed versus escalating energy for subsequent shock should depend on manufacturers' recommendations. If the machine has the capability to escalate the energy, then higher energy should be used for a subsequent shock. A single shock strategy should be preferred to stacked shock. |
article-100131_28 | Cardiopulmonary Arrest in Adults -- Treatment / Management -- Advanced Cardiac Life Support | After failed defibrillation, epinephrine, 1mg I/V, should be given. Furthermore, the dose of this drug may be repeated after periods of three to five minutes. Additionally, vasopressin has been recommended as an alternative. [12] | Cardiopulmonary Arrest in Adults -- Treatment / Management -- Advanced Cardiac Life Support. After failed defibrillation, epinephrine, 1mg I/V, should be given. Furthermore, the dose of this drug may be repeated after periods of three to five minutes. Additionally, vasopressin has been recommended as an alternative. [12] |
article-100131_29 | Cardiopulmonary Arrest in Adults -- Treatment / Management -- Advanced Cardiac Life Support | After 2 or 3 failed attempts, immediate intubation and arterial blood gas analysis should be carried out. Those patients who still remain acidotic even after intubation and successful defibrillation should be given 1 new/ kg of NaHCO3 initially, and further 50 percent of the dose may be repeated after 10 minutes. | Cardiopulmonary Arrest in Adults -- Treatment / Management -- Advanced Cardiac Life Support. After 2 or 3 failed attempts, immediate intubation and arterial blood gas analysis should be carried out. Those patients who still remain acidotic even after intubation and successful defibrillation should be given 1 new/ kg of NaHCO3 initially, and further 50 percent of the dose may be repeated after 10 minutes. |
article-100131_30 | Cardiopulmonary Arrest in Adults -- Treatment / Management -- Advanced Cardiac Life Support | Antiarrhythmic therapy with amiodarone may be started after recurrent electrical instability and failed defibrillation. 150 mg amiodarone should be given over 10 minutes, followed by 1 mg/ hr for 6 hours and 0.5 mg/ hour for the next 18 hours. Procainamide is rarely used nowadays. Calcium gluconate is not considered safe, and its use is only reserved for patients having hyperkalemia or have taken a lethal dose of calcium channel blocker. [13] | Cardiopulmonary Arrest in Adults -- Treatment / Management -- Advanced Cardiac Life Support. Antiarrhythmic therapy with amiodarone may be started after recurrent electrical instability and failed defibrillation. 150 mg amiodarone should be given over 10 minutes, followed by 1 mg/ hr for 6 hours and 0.5 mg/ hour for the next 18 hours. Procainamide is rarely used nowadays. Calcium gluconate is not considered safe, and its use is only reserved for patients having hyperkalemia or have taken a lethal dose of calcium channel blocker. [13] |
article-100131_31 | Cardiopulmonary Arrest in Adults -- Treatment / Management -- Postresucitation Care | This phase starts with the successful return of spontaneous circulation. Generally, the Primary ventricular fibrillation after acute myocardial infarction( AMI) are highly responsive to treatment and are readily controlled while in secondary ventricular fibrillation after AMI, resuscitative efforts are usually less successful, and those patients who are resuscitated successfully, the rate of recurrence of VF is very high. Patient outcome is determined by hemodynamic stability. Asystole, bradyarrhythmias, and PEA are commonly seen in hemodynamically unstable patients. [14] | Cardiopulmonary Arrest in Adults -- Treatment / Management -- Postresucitation Care. This phase starts with the successful return of spontaneous circulation. Generally, the Primary ventricular fibrillation after acute myocardial infarction( AMI) are highly responsive to treatment and are readily controlled while in secondary ventricular fibrillation after AMI, resuscitative efforts are usually less successful, and those patients who are resuscitated successfully, the rate of recurrence of VF is very high. Patient outcome is determined by hemodynamic stability. Asystole, bradyarrhythmias, and PEA are commonly seen in hemodynamically unstable patients. [14] |
article-100131_32 | Cardiopulmonary Arrest in Adults -- Treatment / Management -- Postresucitation Care | The outcomes and the clinical picture after In-hospital cardiopulmonary arrest (IHCA) associated with the noncardiac diseases are very poor, and in some successfully resuscitated cases, the post-resuscitation course is controlled by the nature of the underlying illness. Patients with cancer, central nervous system disease, renal failure have a survival rate of less than ten percent after IHCA. | Cardiopulmonary Arrest in Adults -- Treatment / Management -- Postresucitation Care. The outcomes and the clinical picture after In-hospital cardiopulmonary arrest (IHCA) associated with the noncardiac diseases are very poor, and in some successfully resuscitated cases, the post-resuscitation course is controlled by the nature of the underlying illness. Patients with cancer, central nervous system disease, renal failure have a survival rate of less than ten percent after IHCA. |
article-100131_33 | Cardiopulmonary Arrest in Adults -- Treatment / Management -- Long-Term Management After The Survival Of OHCA | Patients who survive cardiopulmonary arrest without irreversible damage to the brain must undergo proper investigation in order to know the etiology and definite intervention so that such episodes can be prevented in the future. | Cardiopulmonary Arrest in Adults -- Treatment / Management -- Long-Term Management After The Survival Of OHCA. Patients who survive cardiopulmonary arrest without irreversible damage to the brain must undergo proper investigation in order to know the etiology and definite intervention so that such episodes can be prevented in the future. |
article-100131_34 | Cardiopulmonary Arrest in Adults -- Treatment / Management -- Long-Term Management After The Survival Of OHCA | Patients with cardiopulmonary arrest due to myocardial ischemia should be managed by surgical, pharmacological ( anti ischemia therapy), and radiological intervention so that long term survival can be improved. | Cardiopulmonary Arrest in Adults -- Treatment / Management -- Long-Term Management After The Survival Of OHCA. Patients with cardiopulmonary arrest due to myocardial ischemia should be managed by surgical, pharmacological ( anti ischemia therapy), and radiological intervention so that long term survival can be improved. |
article-100131_35 | Cardiopulmonary Arrest in Adults -- Treatment / Management -- Long-Term Management After The Survival Of OHCA | Survivors of cardiopulmonary arrest due to diseases, like hypertrophic cardiomyopathies, rare inherited disorders, right ventricular dysplasia, catecholaminergic polymorphic VT, Brugada syndrome, and long QT syndrome, are the candidates for Implantable cardioverter-defibrillator (ICD). | Cardiopulmonary Arrest in Adults -- Treatment / Management -- Long-Term Management After The Survival Of OHCA. Survivors of cardiopulmonary arrest due to diseases, like hypertrophic cardiomyopathies, rare inherited disorders, right ventricular dysplasia, catecholaminergic polymorphic VT, Brugada syndrome, and long QT syndrome, are the candidates for Implantable cardioverter-defibrillator (ICD). |
article-100131_36 | Cardiopulmonary Arrest in Adults -- Differential Diagnosis | Patients with cardiopulmonary arrest will be pulseless and unresponsive. But there are certain conditions having clinical manifestations similar to cardiopulmonary arrest. It includes syncope, seizure, and overdose of certain medications like opioids. [1] We should try to recognize and treat reversible causes of cardiopulmonary arrest commonly referred to as Hs and Ts. It includes- Hypovolemia Hypoxia Hypothermia Hypo/hyperkalemia Acidosis Tension pneumothorax Toxic overdose of drugs Thromboembolism/pulmonary embolism Thrombus/acute myocardial infarction Cardiac tamponade | Cardiopulmonary Arrest in Adults -- Differential Diagnosis. Patients with cardiopulmonary arrest will be pulseless and unresponsive. But there are certain conditions having clinical manifestations similar to cardiopulmonary arrest. It includes syncope, seizure, and overdose of certain medications like opioids. [1] We should try to recognize and treat reversible causes of cardiopulmonary arrest commonly referred to as Hs and Ts. It includes- Hypovolemia Hypoxia Hypothermia Hypo/hyperkalemia Acidosis Tension pneumothorax Toxic overdose of drugs Thromboembolism/pulmonary embolism Thrombus/acute myocardial infarction Cardiac tamponade |
article-100131_37 | Cardiopulmonary Arrest in Adults -- Prognosis | Witnessed cardiopulmonary arrest along with immediate CPR and defibrillation have better patient survival and outcome. [15] Healthy and young patients are more likely to obtain the return of spontaneous circulation as compared to elderly patients with known co-morbidities such as IHD. | Cardiopulmonary Arrest in Adults -- Prognosis. Witnessed cardiopulmonary arrest along with immediate CPR and defibrillation have better patient survival and outcome. [15] Healthy and young patients are more likely to obtain the return of spontaneous circulation as compared to elderly patients with known co-morbidities such as IHD. |
article-100131_38 | Cardiopulmonary Arrest in Adults -- Complications | Various complications can occur during cardiopulmonary resuscitation. AED failure is the most common complication. Other complications include the inability to obtain venous access, rib fracture, pneumothorax, pneumomediastinum, hemothorax, lung laceration, pulmonary hemorrhage, injury to the major vessel, and cardiac tamponade. | Cardiopulmonary Arrest in Adults -- Complications. Various complications can occur during cardiopulmonary resuscitation. AED failure is the most common complication. Other complications include the inability to obtain venous access, rib fracture, pneumothorax, pneumomediastinum, hemothorax, lung laceration, pulmonary hemorrhage, injury to the major vessel, and cardiac tamponade. |
article-100131_39 | Cardiopulmonary Arrest in Adults -- Deterrence and Patient Education | Most of the cardiopulmonary arrest occur outside hospitals. Immediate cardiopulmonary resuscitation and defibrillation are the two main intervention which has shown to improve patient outcomes. [16] [17] Hence, even laypersons with adequate CPR skills and training can save lives. But, sometimes even the trained person hesitate to start CPR because of a lack of confidence and cardiac arrest recognition. [18] This points to the need for improving their skills and confidence by organizing regular training sessions and workshops. | Cardiopulmonary Arrest in Adults -- Deterrence and Patient Education. Most of the cardiopulmonary arrest occur outside hospitals. Immediate cardiopulmonary resuscitation and defibrillation are the two main intervention which has shown to improve patient outcomes. [16] [17] Hence, even laypersons with adequate CPR skills and training can save lives. But, sometimes even the trained person hesitate to start CPR because of a lack of confidence and cardiac arrest recognition. [18] This points to the need for improving their skills and confidence by organizing regular training sessions and workshops. |
article-100131_40 | Cardiopulmonary Arrest in Adults -- Enhancing Healthcare Team Outcomes | The vast majority of patients who experience cardiopulmonary arrest are known cases of coronary artery disease. Cardiopulmonary arrest in such patients can be prevented by reducing the progression of the disease by altering modifiable risk factors and regular medication. In addition, healthcare professionals should educate the patient about the advantages of a healthy diet, regular exercise, effective treatment of dyslipidemia, hypertension (HTN), diabetes (DM), and smoking cessation. Finally, it is the responsibility of healthcare professionals to be well versed with the basic principles and clinical skills needed for effective cardiopulmonary resuscitation. [19] | Cardiopulmonary Arrest in Adults -- Enhancing Healthcare Team Outcomes. The vast majority of patients who experience cardiopulmonary arrest are known cases of coronary artery disease. Cardiopulmonary arrest in such patients can be prevented by reducing the progression of the disease by altering modifiable risk factors and regular medication. In addition, healthcare professionals should educate the patient about the advantages of a healthy diet, regular exercise, effective treatment of dyslipidemia, hypertension (HTN), diabetes (DM), and smoking cessation. Finally, it is the responsibility of healthcare professionals to be well versed with the basic principles and clinical skills needed for effective cardiopulmonary resuscitation. [19] |
article-100131_41 | Cardiopulmonary Arrest in Adults -- Review Questions | Access free multiple choice questions on this topic. Click here for a simplified version. Comment on this article. | Cardiopulmonary Arrest in Adults -- Review Questions. Access free multiple choice questions on this topic. Click here for a simplified version. Comment on this article. |
article-100318_0 | Amantadine Keratopathy -- Continuing Education Activity | Amantadine keratopathy is a rare dose-dependent disease process in which the drug amantadine causes damage to corneal endothelial cells through unknown mechanisms. Damage to the endothelium can ultimately lead to severe corneal edema with decreased visual acuity. Edema is typically reversible with discontinuation of the drug, but irreversible cases requiring corneal transplants have been reported. This activity describes the evaluation and management of amantadine keratopathy and highlights the role of the interprofessional team in improving care for patients with this condition. | Amantadine Keratopathy -- Continuing Education Activity. Amantadine keratopathy is a rare dose-dependent disease process in which the drug amantadine causes damage to corneal endothelial cells through unknown mechanisms. Damage to the endothelium can ultimately lead to severe corneal edema with decreased visual acuity. Edema is typically reversible with discontinuation of the drug, but irreversible cases requiring corneal transplants have been reported. This activity describes the evaluation and management of amantadine keratopathy and highlights the role of the interprofessional team in improving care for patients with this condition. |
article-100318_1 | Amantadine Keratopathy -- Continuing Education Activity | Objectives: Review the pathophysiology of amantadine keratopathy. Explain the risk factors for developing amantadine keratopathy. Identify the treatment options available for amantadine keratopathy. Describe the importance of collaboration and communication among the interprofessional team to advance the care of amantadine keratopathy and to improve outcomes for patients with this condition. Access free multiple choice questions on this topic. | Amantadine Keratopathy -- Continuing Education Activity. Objectives: Review the pathophysiology of amantadine keratopathy. Explain the risk factors for developing amantadine keratopathy. Identify the treatment options available for amantadine keratopathy. Describe the importance of collaboration and communication among the interprofessional team to advance the care of amantadine keratopathy and to improve outcomes for patients with this condition. Access free multiple choice questions on this topic. |
article-100318_2 | Amantadine Keratopathy -- Introduction | Amantadine was originally discovered as an anti-viral to treat influenza in the 1950s. In the late 1960s, it was discovered to be useful in treating tremors and dyskinesia associated with Parkinson's disease and began to be widely used for this purpose. Today amantadine is prescribed for some chronic neurodegenerative and neurocognitive diseases. The mechanism of action of amantadine is largely unknown. Amantadine keratopathy is a term used to describe corneal edema and subsequent decrease in visual acuity that is assumed to be caused by the drug. Corneal edema typically resolves with discontinuation of the drug, although cases requiring corneal transplants have been reported. | Amantadine Keratopathy -- Introduction. Amantadine was originally discovered as an anti-viral to treat influenza in the 1950s. In the late 1960s, it was discovered to be useful in treating tremors and dyskinesia associated with Parkinson's disease and began to be widely used for this purpose. Today amantadine is prescribed for some chronic neurodegenerative and neurocognitive diseases. The mechanism of action of amantadine is largely unknown. Amantadine keratopathy is a term used to describe corneal edema and subsequent decrease in visual acuity that is assumed to be caused by the drug. Corneal edema typically resolves with discontinuation of the drug, although cases requiring corneal transplants have been reported. |
article-100318_3 | Amantadine Keratopathy -- Etiology | The acute onset of corneal edema with amantadine treatment and the resolution with discontinuation of the drug shows a causal relationship. [1] [2] [3] [4] Studies show that amantadine keratopathy occurs in a cumulative and dose-dependent manner. [5] [6] There is a negative correlation between the duration of treatment and endothelial cell density (ECD). [1] The greatest relative risk of corneal edema is seen in patients who are given a high dose for a short period (2000 mg within 30 days RR=2.38). [6] A 4000 mg cumulative dose prescribed within 30 days led to a 3-fold increased risk in corneal edema. [6] Amantadine could act synergistically with other medications that are toxic to the cornea, increasing the risk for corneal edema and permanent damage in these patients. [2] [7] | Amantadine Keratopathy -- Etiology. The acute onset of corneal edema with amantadine treatment and the resolution with discontinuation of the drug shows a causal relationship. [1] [2] [3] [4] Studies show that amantadine keratopathy occurs in a cumulative and dose-dependent manner. [5] [6] There is a negative correlation between the duration of treatment and endothelial cell density (ECD). [1] The greatest relative risk of corneal edema is seen in patients who are given a high dose for a short period (2000 mg within 30 days RR=2.38). [6] A 4000 mg cumulative dose prescribed within 30 days led to a 3-fold increased risk in corneal edema. [6] Amantadine could act synergistically with other medications that are toxic to the cornea, increasing the risk for corneal edema and permanent damage in these patients. [2] [7] |
article-100318_4 | Amantadine Keratopathy -- Etiology | Although ECD is not a highly reliable marker of clinical outcomes, patients with decreased baseline ECD may be at increased risk of amantadine keratopathy. ECD decreases linearly throughout one's lifetime, and the standard deviation of ECD increases in later decades of life. [8] [9] A study of corneas from a large cornea donor database showed that prevalence of ECD <2000 was substantially increased in the eyes of patients >75 years old (odds ratio (OR)=24.6), eyes 65-74 years old (OR=17.8), and eyes with a previous history of cataract surgery (OR=4.8). [9] | Amantadine Keratopathy -- Etiology. Although ECD is not a highly reliable marker of clinical outcomes, patients with decreased baseline ECD may be at increased risk of amantadine keratopathy. ECD decreases linearly throughout one's lifetime, and the standard deviation of ECD increases in later decades of life. [8] [9] A study of corneas from a large cornea donor database showed that prevalence of ECD <2000 was substantially increased in the eyes of patients >75 years old (odds ratio (OR)=24.6), eyes 65-74 years old (OR=17.8), and eyes with a previous history of cataract surgery (OR=4.8). [9] |
article-100318_5 | Amantadine Keratopathy -- Epidemiology | The incidence and prevalence of amantadine keratopathy in the general population are not known as the majority of studies exclude patients with ocular comorbidities (e.g., glaucoma, prior history of corneal edema) where amantadine keratopathy may have an increased prevalence. Amantadine keratopathy has an equal preponderance in males and females. [6] [10] In a phase IV post-marketing surveillance study, the 2-year relative risk (RR) of developing corneal edema or Fuchs dystrophy in patients prescribed amantadine is 1.79 when compared to the general population. Over this period, 36 (0.27%) of the 13,137 patients receiving amantadine (99% of whom received a prescription of 100 mg BID) were diagnosed with Fuchs dystrophy or corneal edema. [10] | Amantadine Keratopathy -- Epidemiology. The incidence and prevalence of amantadine keratopathy in the general population are not known as the majority of studies exclude patients with ocular comorbidities (e.g., glaucoma, prior history of corneal edema) where amantadine keratopathy may have an increased prevalence. Amantadine keratopathy has an equal preponderance in males and females. [6] [10] In a phase IV post-marketing surveillance study, the 2-year relative risk (RR) of developing corneal edema or Fuchs dystrophy in patients prescribed amantadine is 1.79 when compared to the general population. Over this period, 36 (0.27%) of the 13,137 patients receiving amantadine (99% of whom received a prescription of 100 mg BID) were diagnosed with Fuchs dystrophy or corneal edema. [10] |
article-100318_6 | Amantadine Keratopathy -- Epidemiology | There is an increased incidence of amantadine keratopathy within months of treatment initiation, but cases have been reported as late as 6 years after starting therapy, so the relative risk is likely greater than this. [6] [10] [11] The largest retrospective cohort study conducted on amantadine keratopathy showed that patients prescribed amantadine for Parkinson's disease specifically have an increased risk of developing amantadine keratopathy when compared to individuals taking amantadine for other reasons (RR=1.97). [6] This increased risk is likely due to long term treatment. The same study calculates a RR of 1.97 over a 15-year period for Parkinson's patients on amantadine when compared to healthy controls not taking amantadine. [6] | Amantadine Keratopathy -- Epidemiology. There is an increased incidence of amantadine keratopathy within months of treatment initiation, but cases have been reported as late as 6 years after starting therapy, so the relative risk is likely greater than this. [6] [10] [11] The largest retrospective cohort study conducted on amantadine keratopathy showed that patients prescribed amantadine for Parkinson's disease specifically have an increased risk of developing amantadine keratopathy when compared to individuals taking amantadine for other reasons (RR=1.97). [6] This increased risk is likely due to long term treatment. The same study calculates a RR of 1.97 over a 15-year period for Parkinson's patients on amantadine when compared to healthy controls not taking amantadine. [6] |
article-100318_7 | Amantadine Keratopathy -- Pathophysiology | Amantadine causes permanent damage to the corneal endothelium and a decrease in corneal endothelial cell density by unknown mechanisms. [4] [11] [12] Bovine cornea cell cultures showed no signs of corneal endothelial cell apoptosis, although the duration of incubation may not have been sufficient to induce such a change. [13] Corneal endothelial cells are located in a monolayer posterior to Descemet's membrane and the stroma. These cells function to dehydrate and thus maintain the clarity of the cornea via sodium-potassium adenosine triphosphatase (Na/K ATPase) pumps. Loss of corneal endothelium led to edema and blurred vision at a cell density of about 500 cells/mm. Corneal edema in amantadine keratopathy frequently causes loss of visual acuity to 20/200 or hand motion. [2] [3] [4] [11] [12] | Amantadine Keratopathy -- Pathophysiology. Amantadine causes permanent damage to the corneal endothelium and a decrease in corneal endothelial cell density by unknown mechanisms. [4] [11] [12] Bovine cornea cell cultures showed no signs of corneal endothelial cell apoptosis, although the duration of incubation may not have been sufficient to induce such a change. [13] Corneal endothelial cells are located in a monolayer posterior to Descemet's membrane and the stroma. These cells function to dehydrate and thus maintain the clarity of the cornea via sodium-potassium adenosine triphosphatase (Na/K ATPase) pumps. Loss of corneal endothelium led to edema and blurred vision at a cell density of about 500 cells/mm. Corneal edema in amantadine keratopathy frequently causes loss of visual acuity to 20/200 or hand motion. [2] [3] [4] [11] [12] |
article-100318_8 | Amantadine Keratopathy -- Pathophysiology | Because damage to the corneal endothelium is permanent, edema may persist even after discontinuation of the drug, and a corneal transplant may be necessary to restore vision. [12] The primary action of amantadine as a neurologic drug is through an indirect increase in extracellular dopamine by non-competitive inhibition of NMDA receptors. Recent case reports of corneal edema with a similar clinical picture have been attributed to memantine, a drug with similar structure and mechanism of action. [14] Amantadine also has several off-target effects that may contribute to corneal edema. [13] [15] In a study on bovine cornea cultures, amantadine was shown to inhibit K channels similar to the effect of the K channel blocker clotrimazole. Cells in cultures showed an increase in area and cell volume consistent with edema, and gap junctions between cells were disrupted. [13] | Amantadine Keratopathy -- Pathophysiology. Because damage to the corneal endothelium is permanent, edema may persist even after discontinuation of the drug, and a corneal transplant may be necessary to restore vision. [12] The primary action of amantadine as a neurologic drug is through an indirect increase in extracellular dopamine by non-competitive inhibition of NMDA receptors. Recent case reports of corneal edema with a similar clinical picture have been attributed to memantine, a drug with similar structure and mechanism of action. [14] Amantadine also has several off-target effects that may contribute to corneal edema. [13] [15] In a study on bovine cornea cultures, amantadine was shown to inhibit K channels similar to the effect of the K channel blocker clotrimazole. Cells in cultures showed an increase in area and cell volume consistent with edema, and gap junctions between cells were disrupted. [13] |
article-100318_9 | Amantadine Keratopathy -- Pathophysiology | Another recent case study showed that the dopaminergic agonists ropinirole, methylphenidate, and resiniferatoxin induced corneal edema with a similar clinical presentation to amantadine keratopathy. [15] Dopamine D1 receptors (DRD1) have been found on corneal endothelial cells, and dopamine sensitivity has been linked to decreased corneal transparency. Based on these studies, it is likely that acute corneal edema in amantadine keratopathy occurs secondary to interactions with multiple corneal endothelial cell receptors that ultimately disrupt intracellular fluid osmolarity and corneal endothelial cell organization. Damage to the endothelium has been measured by different parameters, including a decrease in endothelial cell density (ECD), a decrease in cell hexagonality (CH), and an increase in the coefficient of variation (CoV). [1] [4] [5] | Amantadine Keratopathy -- Pathophysiology. Another recent case study showed that the dopaminergic agonists ropinirole, methylphenidate, and resiniferatoxin induced corneal edema with a similar clinical presentation to amantadine keratopathy. [15] Dopamine D1 receptors (DRD1) have been found on corneal endothelial cells, and dopamine sensitivity has been linked to decreased corneal transparency. Based on these studies, it is likely that acute corneal edema in amantadine keratopathy occurs secondary to interactions with multiple corneal endothelial cell receptors that ultimately disrupt intracellular fluid osmolarity and corneal endothelial cell organization. Damage to the endothelium has been measured by different parameters, including a decrease in endothelial cell density (ECD), a decrease in cell hexagonality (CH), and an increase in the coefficient of variation (CoV). [1] [4] [5] |
article-100318_10 | Amantadine Keratopathy -- Pathophysiology | Endothelial cell size variation (CoV) demonstrates that some endothelial cells are enlarging to fill gaps and compensate for the loss of surrounding endothelial cells. The percentage of hexagonal cells decreases in response to chemical, mechanical, or hypoxic stress. These parameters are frequently used as markers of endothelial cell viability and pre-operative risk in patients with intrinsic disease of corneal endothelium such as Fuchs endothelial corneal dystrophy (FECD). Corneal endothelium damage may be present in eyes without corneal edema or decreased visual acuity in patients on amantadine therapy. [1] [5] Regardless of whether or not keratopathy develops, endothelial cells do not regenerate after amantadine toxicity occurs. [4] [5] [11] It is likely that amantadine keratopathy occurs in a dose-dependent fashion, with significant variation among individuals in the concentration of amantadine that is ultimately present in the aqueous, even when the prescribed dose of amantadine is the same. [4] [6] | Amantadine Keratopathy -- Pathophysiology. Endothelial cell size variation (CoV) demonstrates that some endothelial cells are enlarging to fill gaps and compensate for the loss of surrounding endothelial cells. The percentage of hexagonal cells decreases in response to chemical, mechanical, or hypoxic stress. These parameters are frequently used as markers of endothelial cell viability and pre-operative risk in patients with intrinsic disease of corneal endothelium such as Fuchs endothelial corneal dystrophy (FECD). Corneal endothelium damage may be present in eyes without corneal edema or decreased visual acuity in patients on amantadine therapy. [1] [5] Regardless of whether or not keratopathy develops, endothelial cells do not regenerate after amantadine toxicity occurs. [4] [5] [11] It is likely that amantadine keratopathy occurs in a dose-dependent fashion, with significant variation among individuals in the concentration of amantadine that is ultimately present in the aqueous, even when the prescribed dose of amantadine is the same. [4] [6] |
article-100318_11 | Amantadine Keratopathy -- History and Physical | In almost all case reports of amantadine keratopathy, the patient describes a sudden onset of painless, bilateral blurring of vision with progressive worsening in the following months. Many patients have a visual acuity of 20/200 or worse at the time of presentation to an ophthalmologist. This history in patients with no past ocular disease, and negative family history of ocular disease, should prompt an extensive workup of medical history and medication exposure. If a patient is taking amantadine, the duration and dosage of treatment should be determined to stratify the patient's risk of amantadine keratopathy. It is important to consider undiagnosed ocular pathologies that may be contributing to visual loss, as amantadine keratopathy is a very rare diagnosis with a nonspecific presentation. | Amantadine Keratopathy -- History and Physical. In almost all case reports of amantadine keratopathy, the patient describes a sudden onset of painless, bilateral blurring of vision with progressive worsening in the following months. Many patients have a visual acuity of 20/200 or worse at the time of presentation to an ophthalmologist. This history in patients with no past ocular disease, and negative family history of ocular disease, should prompt an extensive workup of medical history and medication exposure. If a patient is taking amantadine, the duration and dosage of treatment should be determined to stratify the patient's risk of amantadine keratopathy. It is important to consider undiagnosed ocular pathologies that may be contributing to visual loss, as amantadine keratopathy is a very rare diagnosis with a nonspecific presentation. |
article-100318_12 | Amantadine Keratopathy -- History and Physical | In a patient with vision loss taking amantadine, possible comorbid ocular pathologies should be ruled out by extensive slit lamp examination of the anterior segment, retina, and optic nerve. Slit-lamp examination of the cornea shows diffuse stromal edema with Descemet's folds and absent guttae. Microcystic epithelial edema and loosened epithelia have also been described. | Amantadine Keratopathy -- History and Physical. In a patient with vision loss taking amantadine, possible comorbid ocular pathologies should be ruled out by extensive slit lamp examination of the anterior segment, retina, and optic nerve. Slit-lamp examination of the cornea shows diffuse stromal edema with Descemet's folds and absent guttae. Microcystic epithelial edema and loosened epithelia have also been described. |
article-100318_13 | Amantadine Keratopathy -- Evaluation | Further studies, such as pachymetry, can be used to confirm the presence of corneal edema, monitor disease progression and resolution with discontinuation of amantadine. Specular microscopy studies can be performed to assess the extent of endothelial damage and ECD. | Amantadine Keratopathy -- Evaluation. Further studies, such as pachymetry, can be used to confirm the presence of corneal edema, monitor disease progression and resolution with discontinuation of amantadine. Specular microscopy studies can be performed to assess the extent of endothelial damage and ECD. |
article-100318_14 | Amantadine Keratopathy -- Treatment / Management | The majority of reported cases of amantadine keratopathy have shown complete resolution of corneal edema and visual acuity with discontinuation of amantadine. [2] [3] [4] [11] There have been a few reported cases where corneal edema did not resolve after discontinuation of amantadine. [7] [12] In these cases, visual acuity returned to normal following corneal transplant surgery. It is also possible that comorbid corneal pathologies may have caused further damage to the cornea, preventing the resolution of the disease even with discontinuation of therapy. [16] A more recent case report showed that a patient with a history of amantadine keratopathy was able to continue using the drug with topical steroids without recurrence of edema or a decrease in endothelial cell density. [17] Although topical steroids have not been shown to decrease corneal edema, they could be useful as a prophylactic measure in susceptible individuals. | Amantadine Keratopathy -- Treatment / Management. The majority of reported cases of amantadine keratopathy have shown complete resolution of corneal edema and visual acuity with discontinuation of amantadine. [2] [3] [4] [11] There have been a few reported cases where corneal edema did not resolve after discontinuation of amantadine. [7] [12] In these cases, visual acuity returned to normal following corneal transplant surgery. It is also possible that comorbid corneal pathologies may have caused further damage to the cornea, preventing the resolution of the disease even with discontinuation of therapy. [16] A more recent case report showed that a patient with a history of amantadine keratopathy was able to continue using the drug with topical steroids without recurrence of edema or a decrease in endothelial cell density. [17] Although topical steroids have not been shown to decrease corneal edema, they could be useful as a prophylactic measure in susceptible individuals. |
article-100318_15 | Amantadine Keratopathy -- Treatment / Management | Currently, there is little to no evidence to stratify a patient’s risk of developing amantadine keratopathy. Decreased vision following initiation of treatment should undoubtedly prompt a referral to an ophthalmologist by the prescribing neurologist. Patients with a history of ocular trauma, ocular surgery, corneal or anterior segment disease, and possibly those of a certain age may necessitate a consultation by a corneal specialist prior to initiation of amantadine therapy. However, further research is needed to elucidate guidelines for such practice. Increased corneal backscatter on slit-lamp examination and CCT have been shown to have weak predictive value in the prognosis of FECD. [18] [19] It is unlikely that these data points would be helpful for ophthalmologists in evaluating patients before initiating amantadine therapy. Newer forms of analysis of the cornea, including Scheimpflug tomography, show significant promise in predicting the need for future interventions in FECD prior to the loss of visual acuity. [18] Scheimpflug tomography could be an effective screening method for amantadine keratopathy, although no research has been conducted on this topic. | Amantadine Keratopathy -- Treatment / Management. Currently, there is little to no evidence to stratify a patient’s risk of developing amantadine keratopathy. Decreased vision following initiation of treatment should undoubtedly prompt a referral to an ophthalmologist by the prescribing neurologist. Patients with a history of ocular trauma, ocular surgery, corneal or anterior segment disease, and possibly those of a certain age may necessitate a consultation by a corneal specialist prior to initiation of amantadine therapy. However, further research is needed to elucidate guidelines for such practice. Increased corneal backscatter on slit-lamp examination and CCT have been shown to have weak predictive value in the prognosis of FECD. [18] [19] It is unlikely that these data points would be helpful for ophthalmologists in evaluating patients before initiating amantadine therapy. Newer forms of analysis of the cornea, including Scheimpflug tomography, show significant promise in predicting the need for future interventions in FECD prior to the loss of visual acuity. [18] Scheimpflug tomography could be an effective screening method for amantadine keratopathy, although no research has been conducted on this topic. |
article-100318_16 | Amantadine Keratopathy -- Differential Diagnosis | Fuchs endothelial dystrophy (FECD): Fuchs endothelial dystrophy has the most similar pathophysiology and presentation to amantadine keratopathy. Differentiating features include the presence of guttata on slit-lamp examination and persistence following discontinuation of amantadine. | Amantadine Keratopathy -- Differential Diagnosis. Fuchs endothelial dystrophy (FECD): Fuchs endothelial dystrophy has the most similar pathophysiology and presentation to amantadine keratopathy. Differentiating features include the presence of guttata on slit-lamp examination and persistence following discontinuation of amantadine. |
article-100318_17 | Amantadine Keratopathy -- Differential Diagnosis | Band keratopathy: Calcium deposition in the anterior stroma can look similar to the stomal edema associated with amantadine keratopathy, and the epidemiology is similar due to the age-related progression and association with chronic disease. Patients will generally have a sub-acute or chronic progression of corneal opacification as opposed to that in amantadine keratopathy, and there is an increased association with ocular comorbidities. Like FECD, band keratopathy will not resolve with discontinuation of amantadine. | Amantadine Keratopathy -- Differential Diagnosis. Band keratopathy: Calcium deposition in the anterior stroma can look similar to the stomal edema associated with amantadine keratopathy, and the epidemiology is similar due to the age-related progression and association with chronic disease. Patients will generally have a sub-acute or chronic progression of corneal opacification as opposed to that in amantadine keratopathy, and there is an increased association with ocular comorbidities. Like FECD, band keratopathy will not resolve with discontinuation of amantadine. |
article-100318_18 | Amantadine Keratopathy -- Prognosis | The majority of reported cases have shown a complete resolution of corneal edema and return of visual acuity to baseline upon discontinuation of amantadine, especially in those with no prior ocular history. In patients with an already decreased endothelial cell density, corneal transplant or Descemet membrane endothelial keratoplasty may be indicated. | Amantadine Keratopathy -- Prognosis. The majority of reported cases have shown a complete resolution of corneal edema and return of visual acuity to baseline upon discontinuation of amantadine, especially in those with no prior ocular history. In patients with an already decreased endothelial cell density, corneal transplant or Descemet membrane endothelial keratoplasty may be indicated. |
article-100318_19 | Amantadine Keratopathy -- Complications | Misdiagnosis could lead to unnecessary surgeries and medical interventions as well as significant distress for patients who fail to improve. Because amantadine keratopathy causes permanent damage to the corneal endothelium, failure to recognize this disease or individuals who are susceptible could lead to permanent loss of vision. | Amantadine Keratopathy -- Complications. Misdiagnosis could lead to unnecessary surgeries and medical interventions as well as significant distress for patients who fail to improve. Because amantadine keratopathy causes permanent damage to the corneal endothelium, failure to recognize this disease or individuals who are susceptible could lead to permanent loss of vision. |
article-100318_20 | Amantadine Keratopathy -- Deterrence and Patient Education | Amantadine keratopathy is swelling of the cornea secondary to damage of cells responsible for keeping the cornea deturgescent and transparent. Although the damage is irreversible, the swelling usually resolves with discontinuation of the drug. If symptoms that were previously controlled with amantadine therapy worsen with discontinuation, the neurologist and ophthalmologist need to discuss how to optimize the patient's therapy. | Amantadine Keratopathy -- Deterrence and Patient Education. Amantadine keratopathy is swelling of the cornea secondary to damage of cells responsible for keeping the cornea deturgescent and transparent. Although the damage is irreversible, the swelling usually resolves with discontinuation of the drug. If symptoms that were previously controlled with amantadine therapy worsen with discontinuation, the neurologist and ophthalmologist need to discuss how to optimize the patient's therapy. |
article-100318_21 | Amantadine Keratopathy -- Enhancing Healthcare Team Outcomes | Greater awareness of keratopathy as an adverse effect of amantadine therapy is needed by the interprofessional team that cares for patients with neurodegenerative or neurocognitive disorders. This team includes neurologists, ophthalmologists, and primary care clinicians. Ophthalmologists should understand the pathophysiology of amantadine keratopathy and the irreversible damage to corneal endothelium associated with it. Because medications prescribed by neurodegenerative and neurocognitive disease specialists have an extensive profile of adverse reactions, increased diligence in the review of medications may be necessary for these patients. Nurses and pharmacists can help in identifying this disease by extensively screening patients' past medical history and medications list. The prevalence, risk factors, and complications of amantadine keratopathy remain largely unknown and serve as a possible topic of future research. | Amantadine Keratopathy -- Enhancing Healthcare Team Outcomes. Greater awareness of keratopathy as an adverse effect of amantadine therapy is needed by the interprofessional team that cares for patients with neurodegenerative or neurocognitive disorders. This team includes neurologists, ophthalmologists, and primary care clinicians. Ophthalmologists should understand the pathophysiology of amantadine keratopathy and the irreversible damage to corneal endothelium associated with it. Because medications prescribed by neurodegenerative and neurocognitive disease specialists have an extensive profile of adverse reactions, increased diligence in the review of medications may be necessary for these patients. Nurses and pharmacists can help in identifying this disease by extensively screening patients' past medical history and medications list. The prevalence, risk factors, and complications of amantadine keratopathy remain largely unknown and serve as a possible topic of future research. |
article-100318_22 | Amantadine Keratopathy -- Review Questions | Access free multiple choice questions on this topic. Click here for a simplified version. Comment on this article. | Amantadine Keratopathy -- Review Questions. Access free multiple choice questions on this topic. Click here for a simplified version. Comment on this article. |
article-100323_0 | Stable Angina -- Continuing Education Activity | Angina affects 10 million people in the United States. Providers must be able to differentiate between stable angina and other causes of chest pain to care for their patients appropriately. The recognition and appropriate management of stable angina is critical in reducing the risks of future myocardial infarction. This activity highlights an interprofessional team's diagnosis, evaluation, and management of stable angina. | Stable Angina -- Continuing Education Activity. Angina affects 10 million people in the United States. Providers must be able to differentiate between stable angina and other causes of chest pain to care for their patients appropriately. The recognition and appropriate management of stable angina is critical in reducing the risks of future myocardial infarction. This activity highlights an interprofessional team's diagnosis, evaluation, and management of stable angina. |
article-100323_1 | Stable Angina -- Continuing Education Activity | Objectives: Identify and appropriately diagnose stable angina. Determine the pathophysiology behind myocardial ischemia to assist in treatment options. Identify and manage risk factors to decrease mortality risk with coronary heart disease. Communicate the importance of utilizing an interdisciplinary approach with individuals who have stable angina and multiple comorbidities in order to optimize outcomes. Access free multiple choice questions on this topic. | Stable Angina -- Continuing Education Activity. Objectives: Identify and appropriately diagnose stable angina. Determine the pathophysiology behind myocardial ischemia to assist in treatment options. Identify and manage risk factors to decrease mortality risk with coronary heart disease. Communicate the importance of utilizing an interdisciplinary approach with individuals who have stable angina and multiple comorbidities in order to optimize outcomes. Access free multiple choice questions on this topic. |
article-100323_2 | Stable Angina -- Introduction | Stable angina, also known as typical angina or angina pectoris, is a symptom of myocardial ischemia. Stable angina is characterized by chest discomfort or anginal equivalent that is provoked with exertion and alleviated at rest or with nitroglycerin. This is often 1 of the first manifestations or warning signs of underlying coronary disease. Angina affects 10 million people in the United States (US); given this, it is important to recognize the signs and symptoms and appropriately risk stratify and manage these individuals. [1] | Stable Angina -- Introduction. Stable angina, also known as typical angina or angina pectoris, is a symptom of myocardial ischemia. Stable angina is characterized by chest discomfort or anginal equivalent that is provoked with exertion and alleviated at rest or with nitroglycerin. This is often 1 of the first manifestations or warning signs of underlying coronary disease. Angina affects 10 million people in the United States (US); given this, it is important to recognize the signs and symptoms and appropriately risk stratify and manage these individuals. [1] |
article-100323_3 | Stable Angina -- Etiology | The mechanism behind stable angina is the result of a supply-demand mismatch. The myocardial oxygen demand transiently exceeds the myocardial oxygen supply, often leading to symptoms. Several factors contribute to stable angina; the most common etiology is coronary artery stenosis. This is further discussed below in the section titled ‘Pathophysiology.’ [2] | Stable Angina -- Etiology. The mechanism behind stable angina is the result of a supply-demand mismatch. The myocardial oxygen demand transiently exceeds the myocardial oxygen supply, often leading to symptoms. Several factors contribute to stable angina; the most common etiology is coronary artery stenosis. This is further discussed below in the section titled ‘Pathophysiology.’ [2] |
article-100323_4 | Stable Angina -- Epidemiology | Coronary heart disease impacts over 17 million adults in the United States. Of the 17 million Americans affected, 55% of those are male. It contributes to over 500,000 deaths each year in the US. At age 40 years, the lifetime risk of developing coronary disease is estimated at 49% for men and 32% for women. The incidence of coronary events increases with age, although the male predominance of these events gradually narrows with advancing age. [3] Coronary heart disease/ischemic heart disease is not unique to the US; it is the leading cause of death in adults from low, middle, and high-income countries. [4] | Stable Angina -- Epidemiology. Coronary heart disease impacts over 17 million adults in the United States. Of the 17 million Americans affected, 55% of those are male. It contributes to over 500,000 deaths each year in the US. At age 40 years, the lifetime risk of developing coronary disease is estimated at 49% for men and 32% for women. The incidence of coronary events increases with age, although the male predominance of these events gradually narrows with advancing age. [3] Coronary heart disease/ischemic heart disease is not unique to the US; it is the leading cause of death in adults from low, middle, and high-income countries. [4] |
article-100323_5 | Stable Angina -- Epidemiology | Coronary heart disease can also cause significant debility. This debility can manifest in several ways, 1 of which is angina. Angina affects over 10 million people in the US, with over 500,000 new cases diagnosed each year. [1] [3] | Stable Angina -- Epidemiology. Coronary heart disease can also cause significant debility. This debility can manifest in several ways, 1 of which is angina. Angina affects over 10 million people in the US, with over 500,000 new cases diagnosed each year. [1] [3] |
article-100323_6 | Stable Angina -- Pathophysiology | Simply put, angina results from an imbalance between the myocardial oxygen supply and the myocardial oxygen demand. Understanding the factors that contribute to each of these measures is important. | Stable Angina -- Pathophysiology. Simply put, angina results from an imbalance between the myocardial oxygen supply and the myocardial oxygen demand. Understanding the factors that contribute to each of these measures is important. |
article-100323_7 | Stable Angina -- Pathophysiology | Endothelial cells line the coronary arteries, regulate vascular tone, and prevent intravascular thrombosis. Any disruption in these 2 functions can lead to coronary heart disease. Multiple mechanisms can result in injury or impairment of the endothelial lining. These mechanisms include, but are not limited to, stress, hypertension, hypercholesterolemia, viruses, bacteria, and immune complexes. Endothelial injury triggers an immune response, leading to fibrous tissue formation. Smooth muscle remodeling/fibrous caps can lead to coronary artery stenosis or even acute coronary syndrome. | Stable Angina -- Pathophysiology. Endothelial cells line the coronary arteries, regulate vascular tone, and prevent intravascular thrombosis. Any disruption in these 2 functions can lead to coronary heart disease. Multiple mechanisms can result in injury or impairment of the endothelial lining. These mechanisms include, but are not limited to, stress, hypertension, hypercholesterolemia, viruses, bacteria, and immune complexes. Endothelial injury triggers an immune response, leading to fibrous tissue formation. Smooth muscle remodeling/fibrous caps can lead to coronary artery stenosis or even acute coronary syndrome. |
article-100323_8 | Stable Angina -- Pathophysiology | Coronary artery stenosis is the most common cause of myocardial ischemia. During increased myocardial oxygen demand, the stenosis prevents adequate myocardial oxygen supply. Four main factors contribute to oxygen demand: heart rate, systolic blood pressure, myocardial wall tension, and myocardial contractility. In states of increased demand such as illness, stress, and exercise – we rely on the body’s ability to up-regulate myocardial oxygen supply appropriately. | Stable Angina -- Pathophysiology. Coronary artery stenosis is the most common cause of myocardial ischemia. During increased myocardial oxygen demand, the stenosis prevents adequate myocardial oxygen supply. Four main factors contribute to oxygen demand: heart rate, systolic blood pressure, myocardial wall tension, and myocardial contractility. In states of increased demand such as illness, stress, and exercise – we rely on the body’s ability to up-regulate myocardial oxygen supply appropriately. |
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