bluuebunny/crossref_metadata_2025_split huggingface dataset:
Electroconvulsive therapy‐induced transient T‐wave inversions on ECG
Authors: Cockey George H. , Richard Conti C. 
Published: February 2009

AbstractElectroconvulsive therapy (ECT), regarded as safe, well tolerated, and one of the most effective treatments for depression, is used frequently in patients with underlying coronary artery disease. ECT has been associated with ST depression and arrhythmias probably due to increased myocardial demand in patients with coronary artery disease. This report describes a case of transient new T‐wave inversions in precordial leads V2 and V3 and flattening of T waves in leads III, V3, V4, V5, and a VF after two courses of ECT in a patient with minimal cardiac risk factors, normal echocardiogram, and normal pre‐ECT electrocardiogram (ECG). These T‐wave changes may represent increased sympathetic activity induced by ECT. Previous prospective studies of 26 and 21 patients undergoing serial ECT found only one new T‐wave inversion and no pathologic Q waves on serial ECGs, suggesting that this is a rare finding.
Acute reversal of pheochromocytoma‐induced catecholamine cardiomyopathy
Authors: Nanda Ardaman S. , Feldman Adam , Liang Chang‐Seng 
Published: February 2009

AbstractPheochromocytoma is a rare neuroendocrine tumor. We report a case of pheochromocytoma‐induced cardio‐myopathy in an 18‐year‐old white female. A review of the literature indicated that this is the most dramatic reversal of pheochromocytoma cardiomyopathy reported. With aggressive medical management, there was complete recovery of the hemodynamic, echocardiographic, and electrocardiographic abnormalities within 14 days. This case emphasizes the importance of aggressive and appropriate medical therapy in pheochromocytoma heart disease.
Mitral valve prolapse causing severe mitral regurgitation in a patient with absent right pulmonary artery
Authors: Yip Alex S. B. , Chow Wing Hing , Lee Denise F. M. , Cheung King Loong 
Published: February 2009

AbstractA 33‐year‐old man was investigated for dyspnea on exertion and the presence of a pansystolic murmur. Physical examination revealed dextrocardia confirmed by chest radiograph, which also showed oligemic right lung field. Subsequent cardiac catheterization revealed secundum atrial septal defect, persistent left sided superior vena cava, and severe mitral valve prolapse causing severe mitral regurgitation with pulmonary hypertension. The right pulmonary artery was absent. It is the first report of the association between severe mitral valve prolapse and absent right pulmonary artery.
Preoperative strategies to assess cardiac risk before noncardiac surgery
Authors: Younis Liwa T. , Douglas Miller D. , Chaitman Bernard R. 
Published: February 2009

AbstractThe strategies recommended in the preoperative cardiac risk assessment prior to major vascular and nonvascular surgery are reviewed. The role of clinical evaluation, noninvasive stress testing (exercise test, stress myocardial perfusion imaging, stress echocardiography), and Holter monitoring during the preoperative evaluation are outlined and the value of intervention based on the use of each test is discussed. Recommended strategies to evaluate patients based on their clinical risk markers in addition to the results of the noninvasive risk assessment are presented.
Coronary angioplasty for the control of intractable ventricular arrhythmia
Authors: Bhaskaran Ambika , Seth Ashok , Kumar Anil , Pande Abhay , Kler Tarlochan , Bhandari Suman , Bhatia Madan Lal 
Published: February 2009

AbstractVentricular arrhythmias (VAs) that occur following an acute extensive anterior myocardial infarction (MI) usually respond to conventional antiarrhythmic regimes of treatment. Rarely, the VA may prove intractable to therapy. This report is of three patients who presented at varying time frames (3 h to 10 weeks) following an anterior MI. They exhibited sustained monomorphic ventricular tachycardia and hemodynamic instability despite multiple antiarrhythmic drug therapy, intravenous magnesium, direct‐current cardioversion (DCCV), overdrive pacing (in one case), and intra‐aortic balloon counterpulsation (IABP). Although there was no clinical evidence of continuing ischemia and although coronary angiography that was done in each case showed the infarct‐related artery (IRA) to subtend akinetic areas on left ventricular (LV) angiogram, percutaneous transluminal coronary angioplasty (PTCA) of the IRA was done in all three cases. Reestablishing patency of the IRA helped in controlling the VA dramatically with average therapeutic doses of antiarrhythmic drugs. All three patients showed this control to have been maintained over a follow‐up period of more than 1 year, with partial improvement in LV function and signal‐averaged electrocardiogram negative for late potentials. Thus, in patients with extensive infarction and intractable VA, PTCA of the IRA may provide control of VA even in the absence of clinical signs of active ischemia or viable muscle mass.
Postinfarction ventricular aneurysms
Authors: Friedman Brian M. , Dunn Marvin I. 
Published: February 2009

AbstractVentricular aneurysms are circumscribed, thinwalled fibrous, noncontractile outpouchings of the ventricle. The majority are apically located, true aneurysms of the left ventricle (LV) that occur as a consequence of transmural myocardial infarction (MI). The precursor of aneurysm formation appears to be infarct expansion early after acute MI and occurrence generally relates to infarct size. The presence of underlying hypertension and the use of steroids and nonsteroidal anti‐inflammatory agents may promote aneurysm formation. The clinical sequelae include congestive heart failure (CHF), thromboembolism, angina pectoris, and ventricular tachy‐arrhythmias. Late rupture is a particular complication of false aneurysms in which the pericardium is the aneurysm wall. The diagnosis may be suspected by the clinical finding of a diffuse, pansystolic apical thrust, persistent ST‐segment elevation on the electrocardiogram, and distortion of the cardiac silhouette on chest x‐ray. This can be confirmed using echocardiography, radionuclide ventriculography, and cardiac catheterization. The latter has the additional advantage of being able to delineate the coronary anatomy. Management involves prevention, specific therapy for the various clinical manifestations, and surgery. Therapeutic interventions with thrombolytic agents, aspirin, heparin, and beta blockers that are applied early in the evolution of an MI may limit infarction size, thereby reducing the tendency toward infarct expansion and aneurysm formation. Patients with mild CHF can usually be controlled with the standard combination of angiotensin‐converting enzyme inhibitors, diuretics, and digoxin. Thromboembolism is best prevented by anticoagulation with warfarin for at least 3 months after the acute MI. The choice of pharmacotherapy for ventricular tachyarrhythmias should be guided by electrophysiologic studies. The treatment of patients with angina pectoris utilizes conventional therapeutic modalities. Refractory angina and high‐risk coronary anatomic subsets have replaced CHF as the commonest indications for surgical intervention in recent studies. In these patients, aneurysmectomy is often performed as an aside to the primary revascularization procedure. Although aneurysmectomy may improve the functional status and ejection fraction of some patients with CHF, its effect on prognosis is less certain. The prognostic advantage of surgery appears to be related more to coronary revascularization than to the aneurysm resection per se.
Left atrial size—A risk factor for left atrial thrombi in mitral stenosis
Authors: Conradie C. , Marx J.D. , Schall R. 
Published: February 2009

AbstractIn a follow‐up study, 77 patients with predominant mitral stenosis were examined to investigate the role of left atrial (LA) enlargement in LA thrombi. Fifteen (19.4%) patients had LA thrombi. Of these, 2 (13.3%) were in sinus rhythm and 13 (86.7%) in atrial fibrillation. Fourteen (93.3%) of the patients with LA thrombi had an LA size≥4.8 cm. Only one (6.7%) patient had an LA size of 4.4 cm and was in atrial fibrillation. The median LA size in patients with LA thrombi was 5.2 cm compared with 4.75 cm in patients without LA thrombi (p<0.01). The relative risk for LA thrombi in patients with an LA size≥4.8 cm compared with patients with an LA size<4.8 cm was 10.0 (95% confidence interval 1.4 to 71.4). It was thus confirmed that LA enlargement≥4.8 cm is an in dependent risk factor for LA thrombi in patients with mitral stenosis.
Tilt table evaluation for control pediatric patients: Comparison with symptomatic patients
Authors: Berkowitz Jeffrey B. , Auld Debbie , Hulse J. Edward , Campbell Robert M. 
Published: February 2009

AbstractThis study was designed to evaluate pediatric control patients during head‐up tilt in comparison with symptomatic neurocardiogenic syncope patient head‐up tilt responses. Twenty‐three pediatric control (c) patients (13 females, 10 males; 11.9 ± 3.1 years) were tested with head‐up tilt (HUT) and compared with 66 symptomatic (s) patients. Baseline drug‐free HUT (cHUT‐1), a second drug‐free HUT (cHUT‐2), and a final HUT with isoproterenol infusion (cHUT‐3) were each performed at 80° tilt angle for 30 min or until positive. For comparison, 66 symptomatic patients (41 females, 25 males; 13.6 ± 2.5 years) underwent drug‐free HUT (sHUT‐1); negative responders during sHUT‐1 underwent follow‐up HUT with isoproterenol (sHUT‐2). HUT data were compared for both groups at both 30 and 20 min tilt duration. Twelve control patients (52%) had a symptomatic response during cHUT‐1 at 18±8 min. During cHUT‐2, 5 of 23 patients were positive at 13±5 min; each had previously tested positive during cHUT‐1. Two patients, each positive in cHUT‐1 and cHUT‐2, refused cHUT‐3. The only patient testing positive during cHUT‐3 was test positive in cHUT‐1 but negative for cHUT‐2. In comparison, 43 of 66 (65%) symptomatic patients tested positive during drug‐free sHUT‐1 at 11±6 min. Subsequently, 20 of the 23 negative patients underwent HUT with isoproterenol (sHUT‐2), with 8 of 20 testing positive. Thus, 51 of 66 symptomatic patients (77%) were called “true positives.” Chi‐square analysis for comparison of 30 min cHUT‐1 (12/23 positive patients) versus sHUT‐1 (43/66 positive patients) yielded no statistical difference. However, analysis of data limited to 20 min tilt duration showed 7 of 23 positive cHUT‐1 versus 38 of 66 positive sHUT‐1 patient responses (p = 0.025). It is concluded that (1) pediatric HUT is relatively nonspecific in a control population (52% false positive), (2) concordance for consecutive positive control tilts is low, (3) isoproterenol does not increase overall predisposition to positive pediatric control patient response, and (4) an 80° tilt protocol limited to 20 min duration may help differentiate between false and true positive responses.
Intracardiac thrombi: Frequency, location, etiology, and complications: A morphologic review—Part II
Authors: Waller Bruce F. , Rohr Todd M. , Mclaughlin Todd , Grider Larry , Taliercio Charles P. , Fetters Julie 
Published: February 2009

AbstractIntracardiac thrombus is a frequent finding at necropsy. Various cardiac disorders have been associated with its presence. Part II of this 5‐part article focuses on atherosclerotic coronary heart disease (myocardial infarction) as an etiology for intracardiac thrombus.
Myocardial infarction with an initially normal electrocardiogram—Angiographic findings
Authors: Caceres Luis , Cooke David , Zalenski Robert , Rydman Robert , Lakier Jeffrey B. 
Published: February 2009

AbstractTo analyze the paradox of acute myocardial infarction (AMI) with an initially normal electrocardiogram (ECG), we reviewed the records of 732 patients discharged with a final diagnosis of AMI over a 2‐year period. Twenty‐one patient were identified whose initial ECG was normal and who underwent coronary arteriography during the index hospitalization. According to the ECG evolution, three distinct groups were identified: Group 1: those who subsequently developed ST elevation or Q waves (n = 7), Group 2: those who developed ST depression or T‐wave inversion (n = 8), and Group 3: those whose ECG remained normal (n = 6). Peak creatine kinase (CK), timing of the first ECG change, life‐threatening complications, and location of the infarct‐related coronary lesion were recorded. Infarct‐related coronary lesions were also classified into those in a major coronary trunk versus those in secondary branches. The incidence of AMI with a normal ECG was 3.7%. There was no difference in the frequency of coronary artery involvement in the groups studied: left anterior descending (33%), right coronary artery (38%), and circumflex (28%). All ECG changes developed within the first 48 h of hospitalization; 17 ± 15 in Group 1, and 24 ± 12 h in Group 2. All six patients who had a persistently normal ECG (Group 3) had lesions in branch vessels (p < 0.05 when compared with Group 1 plus Group 2). Patients who developed ST elevation or Q waves (Group 1) always had a major artery trunk involved (p < 0.05 when compared with Group 2 plus Group 3). Patients in Group 3 had less myocardial damage and fewer complications compared with the other two groups. Myocardial infarction with an initial normal ECG is uncommon and may result from involvement of any of the three coronary arteries. Electrocardiographic evolution usually occurs within the first 48 h of hospitalization. Patients whose ECGs remain normal appear to have culprit lesions in coronary branches, smaller infarctions, and fewer in‐hospital complications.
Is the time domain signal‐averaged electrocardiogram helpful in patients with ventricular tachycardia without apparent structural heart disease?
Authors: Orlov Yelena S. K. , Brodsky Michael A. , Orlov Michael V. , Allen Byron J. , Winters Rex J. 
Published: February 2009

AbstractThe signal‐averaged electrocardiogram (SAECG) has been a screening method for identifying patients at risk for ventricular tachycardia (VT) in the setting of coronary artery disease (CAD). Its significance in patients with VT unrelated to CAD or left ventricular dysfunction is undetermined. In order to define the value of SAECG in this patient population further, we compared the time domain SAECG at 25,40, and 80 Hz filters in 35 patients with clinically symptomatic VT in the absence of structural heart disease was compared with 10 normal controls and 10 patients with CAD and inducible VT. SAECG data in patients without structural heart disease were intermediate between normal controls and patients with CAD. No single or combined SAECG criterion helped to differentiate between patients with inducible and noninducible VT. There was no concordance to other arrhythmia testing. It was concluded that signal‐averaged electrocardiography may have little screening value in VT unrelated to CAD or left ventricular dysfunction.
Silent cortical strokes associated with atrial fibrillation
Authors: Hara Masahide , Ooie Tatsuhiko , Yufu Kunio , Tsunematsu Yoshihiro , Kusakabe Takanori , Ooga Masatoshi , Saikawa Tetsunori , Sakata Toshiie 
Published: February 2009

AbstractTo clarify whether silent cortical strokes (SCS) could be a predictor of symptomatic stroke in patients with atrial fibrillation (AF), 72 patients with AF (50 with chronic AF, 22 with paroxysmal AF) were studied. Patients with mitral stenosis, history of myocardial infarction, or dilated cardiomyopathy were excluded from this study. Using cranial magnetic resonance imaging (MRI), the patients were divided into those with SCS (23 patients, Group 1) and those without SCS (49 patients, Group 2). The incidence of symptomatic stroke was then compared between the two groups. Three patients (13%) in Group 1 developed symptomatic brain infarction; this is statistically significant (p < 0.05), compared with the patients in Group 2, none of whom experienced symptomatic stroke. We suggest that SCS is a predictor of symptomatic cerebral infarct in patients with AF. Therefore, it is thought to be important to diagnose SCS using cranial MRI or computed tomography and to keep patients with SCS under close surveillance.
Effectiveness of intravenous propafenone for conversion of recent‐onset atrial fibrillation: A placebo‐controlled study
Authors: Bellandi Francesco , Cantini Fabrizio , Pedone Tiziana , Palchetti Roberto , Bamoshmoosh Mohamed , Dabizzi Roberto Piero 
Published: February 2009

AbstractTo evaluate the efficacy of propafenone in converting recent‐onset atrial fibrillation (AF) lasting <7 days, 182 patients were treated intravenously with propafenone (Group 1, n = 98) and with placebo 0.9% saline solution (Group 2, n = 84) in a double blind study. The treatment was continued until sinus rhythm (SR) was restored, but for no more than 24 h. Eighty‐nine patients treated with propafenone (90.8%) and 27 patients treated with placebo (32.1%) responded to the treatment and SR was restored (p < 0.0005). The mean time for SR restoration was 2.51± 2.77 h in Group 1, and 17.15± 7.8 h in Group 2 (p < 0.0005). In both groups the patients in whom SR was not restored (nonresponders) had larger left atrial size and longer duration of AF than responders at the onset of the arrhythmia. Nonresponders in Group 1 showed a decrease in mean ventricular rate (MVR) from 143± 16 to 101± 18 (p < 0.0005), while in the nonresponders in Group 2 no reduction of MVR was observed. Two patients whose SR was restored with propafenone had sinus standstill lasting 3.4 and 3.8 s, respectively. Propafenone used intravenously is an effective, quick, and safe drug for treating AF. Moreover, it significantly reduces MVR in nonresponders.
Functional explanation for increased atrial natriuretic peptide in systemic sclerosis
Authors: Kazzam Elsadig , Caidahl Kenneth , Hedner Thomas , Waldenström Anders 
Published: February 2009

AbstractWe related atrial natriuretic peptide (ANP) among 30 consecutive patients with systemic sclerosis (SScl) and 48 gender‐ and age‐matched controls to the measurements of left ventricular (LV) function as evaluated by echocardiography and external pulse curves to determine possible causative factors for an increased level of plasma ANP. The patients had a markedly elevated plasma ANP level (239.4± 59 vs. 178.2± 36 pmol/1, p < 0.0005), which was not related to LV systolic function, heart rate, or blood pressure. Patients had LV hypertrophy and plasma ANP correlated directly to interventricular septal thickness (r = 0.41, p < 0.005), LV posterior wall thickness (r = 0.32, p < 0.01), and wall thickness to cavity dimension (r = 0.44, p < 0.0005), LV mass index (r = 0.40, p < 0.005). LV early filling properties were impaired, with reduction of atrial emptying index (p < 0.0005) and increased contribution of atrial contraction to LV filling. Plasma ANP correlated to atrial emptying index (r = 0.41, p < 0.0005) and to apex‐car‐diographic a wave (r = 0.28, p <0.05). Plasma ANP was also related to left atrial dimension index (r = 0.27, p < 0.05), and was still related to atrial emptying index, but not to left atrial dimension, when considering the degree of LV hypertrophy in multivariate analysis. We conclude that ANP is elevated in patients with SScl. Reduced LV compliance, probably due to increased fibrosis, may cause changes in atrial pressure sufficient to stimulate ANP production without systolic dysfunction as a prerequisite.
Familial endocrine myxolentiginosis
Authors: Panossian David H. , Marais Gary E. , John Marais H. 
Published: February 2009

AbstractWe present an unusual case of a left atrial myxoma as a feature of a familial mesoectodermal disorder and review the literature. The new term ‘familial endocrine myxolentiginosis’ is proposed, which is descriptive of the major clinical components of the syndrome. Myriad features of this disorder include (1) cardiac myxomas; (2) cutaneous myxomas; (3) multiple lentigines or blue nevi, particularly of the head and neck; (4) bilateral primary pigmented nodular adrenocortical hyperplasia; (5) unusual testicular tumors; (6) pituitary tumors; (7) myxoid fibroadenomas of the breast; (8) myxomatous disorder of the stroma of the breast; (9) ductal adenoma of the breast; and (10) psammomatous melanotic schwannoma. A tentative diagnosis is suggested by identifying two features and a definitive diagnosis is made by three or more features. The clinical and pathologic features of cardiac myxoma in familial endocrine myxolentiginosis are identical to those of familial cardiac myxoma: age < 40 years, atypical locations, multicentric origins, and recurrent presentations. A Venn diagram classification for cardiac myxomas is proposed. We include photographic, echocardiographic, biopsy, and adrenal computerized tomography documentation in our patient. Recognition of this disorder is important because of its clinical, surgical, and genetic implications. The availability of transesophageal echocardiographic technology should allow early diagnosis of this underdiagnosed entity. Clinicians should consider this entity in the differential diagnosis of their patients with any one of these manifestations.
Restenosis following coronary angioplasty: Clinical presentations and therapeutic options
Authors: Levine Glenn N. , Chodos Andrew P. , Loscalzo Joseph 
Published: February 2009

AbstractRestenosis following angioplasty is an iatrogenic disease of increasing frequency. Restenosis may be defined in terms of either angiographic or clinical criteria. Definitions of angiographic restenosis have varied in different studies, accounting in part for the differences in reported restenosis rates. Most studies now define angiographic restenosis as either a >50% loss of initial gain or an absolute lesion stenosis of ≥50% at follow‐up angiogram. Common clinical end points used in defining restenosis include recurrent angina, need for repeat revascularization, or myocardial infarction. Despite technical advances and multiple pharmacologic interventions, most studies have found that the incidence of angiographic restenosis remains in the range of 40%; in none of these studies, however, was complete angiographic follow‐up obtained, and thus actual restenosis rates may be somewhat higher. In several studies, clinical restenosis has been found to occur in approximately 36–40% of patients. Thus, a minority of patients with angiographic restenosis have no clinical manifestations. Most patients who develop symptoms of restenosis develop these symptoms within the first 3 months after angioplasty. The presenting symptom in the majority of these patients is progressive exertional angina. Patients occasionally will present with unstable angina and only rarely with acute myocardial infarction. In patients who present with recurrent chest pain, several features have been found to be helpful in predicting whether they will have angiographic restenosis at follow‐up angiography. Patients who present 1–6 months after angioplasty with typical anginal symptoms have a high likelihood of having angiographic restenosis. By contrast, patients who present more than 6 months after percutaneous transluminal coronary angioplasty with recurrent chest pain are more likely to have new, significant coronary lesions to account for their symptoms. Noninvasive testing in patients with clinical presentations suggestive of restenosis can, in general, add only modest information in predicting whether restenosis is indeed present. A negative exercise thallium test appears to have a high specificity in ruling out restenosis and may be helpful in patients who present with more atypical symptoms. Repeat angioplasty is the therapy most frequently utilized to treat restenosis, although coronary artery bypass surgery or medical therapy may be reasonable alternative therapies. Clinical success rates with repeat angioplasty are >90%, and major complications are rare; however, restenosis will recur in a significant percentage of these patients. Some patients who develop such recurrent restenoses will ultimately benefit from a strategy of repeat angioplasties, although many will require surgical revascularization.