Rupture of the interventricular septum. Mechanical complications are typical in infarctions in elderly women. Likewise, a murmur that was not present indicates abnormal blood flow: the most frequent complications are mitral insufficiency, which would present with a musical or piante murmur, and VSD, which presents with a murmur radiating to the right border (think of the direction of blood flow).

An 87-year-old woman with a history of hypertension was admitted 48 hours ago to the coronary unit for acute myocardial infarction with ST-segment elevation of anterior location. She reported dyspnea. Examination revealed a systolic murmur with fremitus, radiating to the right sternal border, which was not present on admission. What complication do you suspect?

Heart failure due to extensive necrosis.

[Mid-systolic ejection murmur with thrill caused by right ventricular outflow tract obstruction secondary to septal aneurysm following myocardial infarction: a case report].

A 71-year-old woman with a history of previous myocardial infarction was transferred to our hospital for evaluation of chest pain and ventricular tachycardia. On admission, a loud mid-systolic ejection murmur accompanied by a thrill was found at the left sternal border in the third intercostal space, and it was significantly accentuated in the post-extrasystolic beat. Abnormal Q waves and ST elevations were noted in leads I, aVL and V5,6 on electrocardiograms. Echocardiograms, confirmed a septal-to-apical aneurysm, and a thin interventricular septum (IVS) with paradoxical motion. Right ventricular (RV) catheterization showed a pressure gradient of 21 mmHg between the outflow tract (RVOT) and the apex, and a mid-systolic ejection murmur was recorded in the RVOT on an intracardiac phonocardiogram. Coronary arteriograms revealed total occlusion of the left anterior descending artery in its proximal portion, and a 90% stenosis of the circumflex artery. A left ventriculogram demonstrated a septal-to-apical aneurysm with a markedly reduced ejection fraction of 0.16. A right ventriculogram showed obstruction to RVOT caused by systolic ballooning of the IVS. In this patient, the mid-systolic ejection murmur was probably caused by the obstruction of the outflow tract secondary to septal aneurysm following old myocardial infarction.

Left ventricular free wall rupture associated with a combination of acute myocardial infarction and stress-provoked cardiomyopathy: An autopsy case.

A 74-year-old female was admitted to our hospital due to prolonged chest pain that had lasted about 2 h. An electrocardiogram revealed ST-elevation in leads I, aVL, and V3-6, with an increase in myocardial necrosis markers. Emergency coronary angiography was performed, and left ventriculography showed the typical features of apical ballooning, and so a diagnosis of Takotsubo cardiomyopathy (TC) was made. On the 10th day after admission, the patient suddenly went into cardiopulmonary arrest because of a blow-out type left ventricular (LV) free wall rupture. Despite extensive cardiopulmonary resuscitation, the patient died. The autopsy revealed hemopericardium and a perforating wound located in the anterior wall of the LV. It was revealed that the diagonal branch of the coronary artery was occluded, and so a diagnosis of TC coexisting with acute myocardial infarction (AMI) was made. No previous case of TC accompanied by AMI has been reported. We present its clinical course during hospitalization and the result of a histopathologic examination.

Delayed ventricular septal rupture complicating anterior wall myocardial infarction.

A 59-year-old woman was admitted to our hospital with acute pulmonary oedema and cardiogenic shock 35 days after anterior ST elevation myocardial infarction. She developed a new loud pan systolic murmur. Echocardiography revealed a ventricular septal rupture with a significant left to right shunt. She was immediately transferred to the local cardiothoracic unit where she underwent a successful ventricular septal defect (VSD) repair. Ventricular septal rupture often presents within the first 24 hours of acute myocardial infarction and is rare thereafter. It carries a poor mortality (41-80%) even when recognised. Timely recognition of this life-threatening complication can help reduce the resultant morbidity and mortality. Doctors should be aware that this well-recognised complication may present unusually late as in this case.

Exertional dyspnea after myocardial infarction: thinking beyond the diagnosis of heart failure.

We herein present an unusual case of a pseudoaneurysm of the left ventricular myocardium, which is a rare and fatal complication of myocardial infarction. A 64-year-old man with a history of bipolar disorder and arterial hypertension was hospitalized for delayed presentation ST-elevation myocardial infarction. He was admitted to our hospital 24 hours after symptom onset. Diagnostic coronary angiography revealed 95% stenosis at the distal third of the right coronary artery, and he underwent a primary percutaneous coronary intervention to the culprit lesion. Despite administration of a diuretic and optimization of other pharmaceutical treatment, his heart failure deteriorated. Electrocardiography showed a sinus rhythm with Q-wave formation in the inferior wall leads (II, III, aVF), T-wave inversion in the same leads, and borderline QT prolongation (QTc of 490 ms). No ST elevation suggestive of left ventricular aneurysm formation was noticed. Forty days later, cardiac ultrasound revealed a dyskinetic cavity (pseudoaneurysm) in continuity with the posterior-inferior wall of the myocardium, resulting in severe mitral valve regurgitation. Unfortunately, the patient died while awaiting surgical treatment. Although most patients with left ventricular pseudoaneurysm have a relatively benign outcome, those with symptoms of heart failure must be urgently diagnosed and treated.

[Clinical and anatomical features of acute myocardial infarction associated with double rupture of the interventricular septum and ventricular free wall].

Four patients with acute myocardial infarction (MI) complicating double rupture; interventricular septum and ventricular free wall ruptures, were studied. All patients had histories of hypertension, and pre-infarction angina pectoris of short duration less than 8 days without previous MI. The sites of infarction were anteroseptal in 2 patients and inferoposterior in the other 2. Only one case was complicated with mild pump failure (Killip class II). Blood pressure was adequately controlled after the onset of MI in all patients. Interventricular septal rupture occurred between 2 and 10 days after the onset of MI. Free wall rupture occurred between 2 and 22 days after MI. Types of free wall ruptures were oozing in 2 patients and blow-out in the other 2. Surgical repair was performed in 2 patients with the oozing type rupture, who however died soon after surgery. The autopsy findings were as follows: 3 patients had left ventricular free wall ruptures and one had right ventricular free wall rupture. One of the patients with left ventricular free wall rupture showed a secondary rupture of a pseudo-ventricular aneurysm. Postmortem coronary angiograms revealed 3 patients with single-vessel disease and one patient with double-vessel disease, indicating that coronary arterial lesions and complicated heart failure were not severe in these 4 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

[A successful surgical repair of ventricular septal perforation following acute myocardial infarction in a 83-year-old man].

A 83-year-old man, who experienced a sudden severe malacia 13 days before, was admitted, complaining of dyspnea since 8 hours before. A loud systolic murmur of Levine IV/VI was audible on the left sternal border of the 4th intercostal space. The chest X-ray film demonstrated severe pulmonary congestion. The ECG showed abnormal Q waves in II, III, a VF and V1-5. The right heart catheterization revealed an intraventricular shunt from left to right and thus ventricular septal perforation (VSP) 13 days after acute anteroseptal-inferior myocardial infarction was diagnosed. Continuing an aggressive medical treatment with the intraaortic balloon pumping, an emergency operation for VSP was performed 2 days after the onset. A single Teflon patch was sutured on the left side of the septum around VSP (2.5 x 2.5 cm) and the ventricular free wall was closed including the patch with two felt strips. The patient survived through the operation and is doing well at the 11 months of follow-up. Twenty patients above 70 years old have been surgically treated with success for VSP after acute myocardial infarction in Japan. Our patient was the oldest.

Acute Dyspnea After Inferior-Wall Myocardial Infarction.

A 57-year-old woman presented with acute-onset dyspea with a duration of more than 2 days. Four days earlier, she had been thrombolyzed with streptokinase for inferior wall myocardial infarction in a nearby hospital. On examination, we found that the patient had elevated jugular venous pressure and systolic murmur in left lower parasternal region. In addition, there was a ventricular septal rupture in the posterobasal interventricular septum, with at least 2 exit points into the right ventricle. Timely identification of ventricular septal rupture before PCI is of paramount importance, as it has major implications in management of the patient.

[Echocardiographic manifestations of postinfarction perforation with extensive dissection of the interventricular septum: report of an autopsied case].

This is a report of the echocardiographic features of postinfarction perforation associated with dissection of the interventricular septum (IVS) in a 61-year-old woman. She had acute myocardial infarction and was admitted to a nearby hospital, and later admitted to our CCU because hemodynamic deterioration. On admission, she was somnolent and hypotensive (90/64 mmHg), with sinus tachycardia, marked cyanosis, and peripheral edema. On auscultation there were a harsh holosystolic murmur over the LLSB and moist rales in both lung fields. An ECG revealed extensive anterior and inferior infarctions. Catheterization data confirmed O2 step-up in the right ventricle. Two-dimensional echocardiograms demonstrated extensive dissection of the IVS characterized by an echo-free lumen extending from the apex to the cardiac base in the long-axis and partly reaching the left ventricular free wall in the short-axis with the concomitant paradoxical movement of the IVS. Autopsy disclosed marked hemorrhagic infarction and extensive dissection of the IVS forming a lumen (5 X 5.5 X 2 cm3) corresponding exactly to the echocardiographic free space. In addition, a shunt between the right and left ventricles was confirmed by the presence of two perforations near the apex on the right and left sides of the IVS, whose diameters were 6 and 10 mm, respectively.

Ventricular septal rupture after early successful thrombolytic therapy in acute myocardial infarction: a case report.

Ventricular septal defect (VSD) is a severe complication of acute myocardial infarction and has a high mortality rate. This complication appears to have declined in the reperfusion era. It has mostly been reported in elderly or female patients who suffer from anterior wall infarction, patients with multivessel coronary artery disease (CAD) or occluded infarct-related artery (IRA) without collateral circulation, or patients who have had delayed reperfusion therapy. Here, we report the case of a 60-year-old male patient who presented with persistent chest pain and Killip I ST-segment-elevation myocardial infarction. Thrombolytic therapy was started 3 hours after the onset of chest pain. Based on the subsidence of chest pain, resolution of the elevated ST segment, and early peak of cardiac enzymes, reperfusion was thought to be successful. However, on the third day of admission, the patient complained of dyspnea after defecation and was found to have new-onset grade 3 pansystolic murmur over the left sternal border. Cardiac echography showed an apical VSD. A Swan-Ganz catheter was inserted into the right side of the heart; analysis of blood oxygen saturation revealed a 6% step-up of oxygen in the right ventricle. Coronary angiography showed only one-vessel CAD and TIMI 3 flow in the IRA. The patient received intensive medical management and underwent VSD repair and internal mammary artery bypass grafting to the left anterior descending artery. His recovery was uneventful. This case illustrates that VSD can be found in patients receiving early successful reperfusion therapy, with one-vessel CAD, and TIMI 3 flow in the IRA.

Serious takotsubo cardiomyopathy: an autopsy case presenting severe irreversible myocardial damage after frequent episodes of recurrence.

Takotsubo cardiomyopathy is characterized by transient dysfunction of the medial to apical segment of the left ventricle. Recurrence within a few months or years has been reported and serious complications, including arrhythmia, acute cardiac shock and cardiac rupture, can arise; however, recurrence is rare and takotsubo cardiomyopathy is typically a reversible functional disorder. A 91-year-old Japanese woman with a past medical history of angina pectoris, hypertension and uterine carcinoma noted bilateral axillary pain and presented herself to an emergency room. Although the pain improved and she went home, there were several subsequent episodes of recurrent chest pain. At approximately 1 week after the onset, she was hospitalized as her symptom worsened. Electrocardiography showed low voltage in limb and chest leads, and ST-segment elevation in leads II, III, aVF and V3 to V6. Echocardiography revealed medial to apical dyskinesia and basal hypercontractility of the left ventricle, and cardiac tamponade. Pericardiocentesis improved the symptom, but not her cardiac dysfunction. At 3 days after her admission, cardiopulmonary resuscitation was performed due to ventricular fibrillation. She died on the 5th day of admission (2 weeks after the onset). At autopsy, the left ventricle was dilatated and the apical ventricular wall was thin. On microscopy, remarkable wavy change and thinning of myocardium were diffusely observed, especially at the apex and the anterior to lateral wall of the left ventricle, interventricular septum and right ventricle, intermingled with interstitial fibrosis, hemorrhage and neutrophil infiltration. Contraction band necrosis was mainly observed on the posterior to inferior wall of the left ventricle. Our case showed severe morphological myocardial change after several chest pain episodes that were considered to be takotsubo cardiomyopathy. This notable case suggests that the frequent recurrence of serious takotsubo cardiomyopathy is life threatening and can lead to irreversible serious myocardial degeneration.

Peculiar mechanical complication of myocardial infarction.

A 58-year-old man presented to the chest pain unit with crescendo angina over 24 hours and worsening dyspnoea of 10 hours duration. He was a known diabetic and hypertensive on regular treatment for 10 years and a habitual smoker with over 15 pack-years smoking duration. Examination revealed a profusely diaphoretic and dyspnoeic (respiratory rate of 45/min) individual with a blood pressure of 100/60 mm Hg and heart rate of 124 beats/min. He was hypoxic and his oxygen saturation in the ambient air was 64%. His jugular venous pressure was elevated with a prominent V wave. Cardiovascular examination revealed a harsh grade IV/VI systolic murmur over the lower left parasternal border. There were bilateral extensive crepitations heard over the lung fields. ECG on admission revealed presence of Q wave and ST elevation in leads II and III, aVF with ST depression in I and aVL. X-ray chest showed normal cardiac shadow and features of grade III pulmonary venous hypertension. Transthoracic echocardiography is shown in figure 1.Figure 1Transthoracic echocardiogram short axis view at mid cavity level, 2D (A) and colour Doppler (B) image. <bWhat is the most likely diagnosis</b?A. Left ventricular (LV) true aneurysmB. LV pseudoaneurysmC. LV pseudo-pseudoaneurysmD. Ventricular septal rupture (VSR)E. LV free wall rupture.

[Myocardial dissection in infarction of the right ventricle. Clinical echocardiographic and pathological aspects].

Dissection of the inferior wall of the right ventricle during the acute phase of myocardial infarction with right ventricular involvement is a mechanical complication which has been recently identified, the diagnosis being almost exclusively post-mortem. The authors report the clinical, echocardiographic and pathological features of myocardial dissection in four patients. Between 1985 and 1988, the diagnosis of myocardial dissection was made by echocardiography in 4 patients aged 77 to 80 years, admitted to hospital for an acute inferior wall myocardial infarction. All 4 patients had signs of acute right ventricular failure indicating right ventricular necrosis and a loud systolic murmur at the left sternal border; 2 patients were in shock. The ECG showed signs of inferior wall infarction with, in 2 patients, electrical changes suggestive of right ventricular involvement. Echocardiography showed dissection of the inferior wall of the right ventricle as a pulsatile, echo-free space in the diaphragmatic wall of the right ventricle which appeared to obstruct right ventricular ejection in end systole to a variable degree. The outcome was fatal in all cases with death resulting from refractory myocardial failure. Pathological analysis confirmed biventricular inferior wall infarction also involving the posterior part of the interventricular system, the site of a small tear on the left side which communicated with a neo-cavity dissecting the RV posterior wall. The right coronary artery was totally occluded in all cases. The anatomical lesions were fully concordant with the echocardiographic data: the dissection filled with blood from the left ventricle at each systole creating a pulsatile space in the diaphragmatic wall of the ventricle obstructing ejection.

Complete Dissection of the Interventricular Septum Following Myocardial Infarction.

In this report, we present a case of interventricular septal dissection (IVSD) following inferior wall myocardial infarction (MI) in a 64-year-old patient; the patient ultimately recovered after prompt resuscitation and intervention, despite the high mortality associated with these cases. A 64-year-old male with a history of hypertension and obesity was brought to the hospital following an episode of syncope at home. He had been experiencing chest tightness over the past few days prior to the admission. On physical exam, he had a heart rate of 72 beats per minute and blood pressure of 73/52 mmHg. His electrocardiogram revealed ST-segment elevations in leads II, III, and aVF. Emergent coronary angiography revealed 100% occlusion of the right coronary artery (RCA) with no collateral supply and 95% stenosis of the left anterior descending (LAD) artery. Aspiration thrombectomy and balloon angioplasty and subsequent stenting of the RCA were performed. Transthoracic echocardiogram with color Doppler was performed, which confirmed the presence of a defect in the septum. Color Doppler demonstrated a clear jet entering the ventricular septum from the left ventricle (LV), with the jet traversing the entire length of the septum through a dissection and entering into the right ventricle (RV), consistent with complete IVSD. The patient subsequently underwent a successful bovine pericardial patch repair of the ventricular septum. IVSD is a rare anomaly of the IVS. An echocardiogram is a useful tool to establish the diagnosis. The mortality rate after ventricular septal rupture remains high. Fortunately, our patient had interventricular dissection without rupture. Prompt surgical repair remains the choice of treatment for this condition.

Concurrent true inferoposterior left ventricular aneurysm and ventricular septal rupture secondary to inferior myocardial infarction: a case report.

Although left ventricular aneurysm (LVA) is the most common mechanical complication of myocardial infarction (MI), it rarely involves the inferior or posterior left ventricular wall. Ventricular septal rupture (VSR) may be a fatal mechanical complication of MI but rarely occurs in the posterior or inferior portion of the interventricular septum. Thus, LVA and VSR as two mechanical complications of MI in the same patient are extremely rare. A 65-year-old woman, who had inferior ST-segment elevation myocardial infarction 2 months before without reperfusion therapy, was admitted with exertional dyspnoea for 1 month. Echocardiography and computed tomography revealed true inferoposterior LVA and VSR as concurrent complications of MI. These imaging findings were confirmed during cardiac surgery. After successful coronary bypass grafting and ventriculoplasty, the patient recovered quickly and was discharged from the hospital. A rare case of post-infarction inferoposterior LVA with concurrent interventricular septal rupture was reported. Transthoracic and transoesophageal echocardiography and cardiac computed tomography were valuable tools for the diagnosis of this rare condition. Combined coronary bypass grafting and ventriculoplasty were effective in treating this often fatal complication of inferior MI.

[A successful repair of left ventricular rupture after surgical treatment of ventricular septal perforation complicated due to acute myocardial infarction].

A 75-year-old woman was admitted complaining of anterior chest pains, and peripheral coldness. The 6th day after admission, a loud systolic murmur of Levine IV/VI was audible at the apex. The chest X-ray film demonstrated a cardiomegaly and ST elevation in the V1-V5 leads. UCG and right-heart catheterization revealed an intraventricular shunt from left to right, and the diagnosis of ventricular septal perforation after acute antero-septal myocardial infarction was confirmed. Although, we were continuing and aggressive medical treatment with the intraaortic balloon pumping, an emergency operation for ventricular septal perforation was performed, 15 days after onset. The direct closure of the septal perforation and the plication of the left ventricular free wall with two felt strips were performed. The postoperative course seemed well. But in the 3rd postoperative day, massive bleeding was recognized through the drainage tube. The left ventricular rupture was suggested, and a massive blood transfusion was done. An emergency operation was performed. Another left ventricular free wall was lacerated about 6 mm at the apex. The laceration was closed with teflon felt strips. The patient survived through the operation, and is doing well after 7 years since the operation.

[Giant left ventricular false aneurysme revealing a silent myocardial infarction].

Left ventricular false aneurysms are rare. They are secondary to a myocardial rupture which is contained by adherent pericardium and scar tissue. LV pseudoaneurysm contains no endocardium or myocardium unlike left ventricular true aneurysm. Most cases of LV pseudoaneurysm are related to acute myocardial infarction in inferior or posterior wall. We report a case of a 56-year-old man with a medical history of chronic cigarette smoking, dyslipidemia, and obesity. The patient had no myocardial infarction before. He was admitted for evaluation of important shortness of breath at effort without chest pain for 5 months. Physical exam find an enlarged left ventricular. The electrocardiogram revealed Q waves and ST segment elevation in leads V1 to V6. Transthoracic echocardiogram showed a large thrombosed apical left ventricular false aneurysm, severe left ventricular dysfunction, which were confirmed by cardiac magnetic resonance imaging, this exam also showed no viability in the mid left anterior descending coronary artery territory. The coronary angiography showed an occlusion of the mid left anterior descending coronary artery and a stenosis of the first diagonal artery. The patient was offered a surgical aneurysectomy with coronary artery bypass. The surgery was successful with amelioration of symptoms. We present a rare case of a giant false left ventricular aneurysm complicating a silent myocardial infarction in the anterior wall. The diagnosis is made by cardiac echocardiogram and cardiac magnetic resonance imaging. Because of the important risk of rupture, the surgical treatment is required.

[Rupture of the ventricular septum following acute myocardial infarction].

Septal rupture (SR) during acute myocardial infarction (AMI) was found in 23 patients of 4 300 consecutive cases of AMI. In 55% the SR was diagnosed clinically by the appearance of a murmur, in 23% by shock and in 22% by heart failure. Eventually every patient developed a pan-systolic murmur. In 82% of the cases the murmur was best heard at the lower left sternal border. In half of the patients the location of the murmur suggested the possibility of papilary muscle rupture or dysfunction. In 68% of cases the rupture occurred during the first week after the onset of AMI. Cardiac catheterization was performed in 17 patients, pulmonary hypertension was found in all of them. Pulmonary blood flow was twice the systemic blood flow (P less than 0.005). Coronary angiograms performed in 6 patients showed three vessel disease in 5 cases. Five patients underwent surgery. Three of them survived. All of the 17 patients who had medical treatment died. Ten within the first week after AMI, 5 within the first month and 2 late deaths. Autopsy was performed in 15 cases. Eighty percent had coronary narrowing in several vessels. SR measured between 5 and 20 millimeters in 78% and was found in the anterior septum in 61%. In the cases who were in shock, the ventricular myocardium was extensively damaged. We conclude that once the diagnosis of SR is established, the patient should undergo surgical closure of the SR and coronary revascularization if necessary. Early surgical indication is particularly important in patients at risk of developing shock.

A case of recent myocardial infarction with cardiac failure.

A 50-year-old hypertensive smoker presented with a typical angina of 2 days duration. An urgent ECG revealed extensive anterior wall myocardial infarction. In view of the delayed presentation, the patient was conservatively managed with heparin. In-hospital echocardiogram showed akinesia of entire left anterior descending artery (LAD) territory with severe left ventricular (LV) dysfunction. He was discharged with a plan for early coronary intervention. However, he presented a fortnight later with acute pulmonary oedema. General appraisal revealed a restless individual who was dyspnoeic and diaphoretic at rest. On clinical examination, the patient was in hypotension with features of biventricular failure. A 12-lead ECG showed QS pattern with persistent ST segment elevation in precordial leads. The chest radiograph demonstrated features of pulmonary oedema, cardiomegaly and bilateral pleural effusion. Creatine Phosphokinase-MB (CPK-MB) was negative. A preliminary transthoracic echocardiography was done (figure 1 and see online supplementary video 1). What is the most likely diagnosis based on the echocardiogram? LV pseudo-aneurysm with contained ruptureDissecting intramural haematoma of LV apexVentricular apical aneurysm with thrombusLV non-compaction with prominent ventricular trabaculations.

[Papillary muscle rupture complicating with acute myocardial infarction: a case report].

Cardiogenic shock caused by papillary muscle rupture in acute myocardial infarction is potentially reversible by surgical treatment. A case of posterior myocardial infarction in a 79-year-old woman is reported. She was admitted to the hospital in cardiogenic shock. She had been suffered from chest pain for three days before admission. On physical examination diffuse rales and a grade 4/6 holosystolic apical murmur were present. The diagnosis of an acute posterior myocardial infarction was based on the electrocardiographic findings and serum creatine kinase level. Coronary angiography visualized subtotal occlusion of the left circumflex coronary artery. Transesophageal echocardiography demonstrated severe mitral regurgitation and the ruptured anterior papillary muscle connected to normal chordae tendineae and posterior mitral leaflet. In systole, the head of the ruptured papillary muscle moved like a whip in the left atrium. At operation, the ruptured papillary muscle was confirmed. Mitral valve replacement with a 27 mm St. Jude Medical prosthesis and coronary artery bypass grafting to the left circumflex coronary artery was performed. Postoperatively she was weaned intraaortic balloon pumping after 4 days and recovered uneventfully.

[Acute rupture of the interventricular septum in posterior wall infarction (author's transl)].

A rupture of the interventricular septum, as described in a case report, is found in 2% of myocardial infarctions. Clinical symptom loud systolic murmur audible at the left sternal border associated with a thrill and with signs of cardiogenic shock. The diagnosis is made by right heart catheterisation which shows a typical oxygen stepup between right atrium and right ventricle, by which the rupture of the interventricular septum can be differentiated from acute papillary muscle rupture. The therapy should be at first hemodynamic stabilisation by drugs and intraaortic balloon pump for 4 to 6 weeks and then closure of the ventricular septal defect by operation.

Delayed ventricular septal rupture complicating acute inferior wall myocardial infarction.

Ventricular septal rupture is a potentially fatal complication of acute myocardial infarction. Its incidence has declined with modern reperfusion therapy. In the era of percutaneous coronary interventions, it occurs a median of 18-24 hours after myocardial infarction and is most commonly associated with anterior myocardial infarction. We present a case of delayed ventricular septal rupture complicating acute inferior wall myocardial infarction. A 53-year-old Caucasian male presented with epigastric pain for three days and electrocardiographic evidence for an acute inferior wall myocardial infarction. Coronary angiography revealed a total occlusion of the proximal right coronary artery. Reperfusion was achieved by balloon angioplasty followed by placement of a bare metal stent. On hospital day six, the patient developed acute respiratory distress, a new loud pansystolic murmur, and hemodynamic instability. Echocardiography revealed the presence of a large defect in the inferobasal interventricular septum with significant left-to-right shunt consistent with ventricular septal rupture. The patient underwent emergent surgical repair with a bovine pericardial patch. Ventricular septal rupture after myocardial infarction should be suspected in the presence of new physical findings and hemodynamic compromise regardless of revascularization therapy.

Takostubo syndrome combined with ventricular septal perforation: a case report.

The precise clinical features and etiologic basis of Takotsubo syndrome remain unclear, although an association with emotional or stressful triggers has been recognized. Ventricular septal perforation is a very rare life-threatening complication. A 77-year-old female patient presented to the hospital with unrelieved chest tightness and shortness of breath. Three months ago, the patient's electrocardiogram revealed ischemic T wave inversion of the anterior wall, along with an increase in myocardial injury markers. There was no evidence of a ventricular septal defect on echocardiography. The patient was admitted to the respiratory department to treat lung lesions. The electrocardiogram demonstrated dynamic changes following admission, and the myocardial markers returned to normal, but the echocardiography revealed a ventricular septal defect. The initial diagnosis was ventricular septal perforation because of myocardial infarction with acute anterior ST-segment elevation. Coronary angiography revealed no abnormalities, but left ventricular angiography revealed an enlarged apex and VSD, with a right ventricular shunt bundle. Later, cardiac MRI revealed an apical ventricular septal defect. Further inquiry of the patient's medical history revealed that her husband died unexpectedly three months ago, and her daughter was seriously injured in a car accident, causing the patient severe emotional distress. Takotsubo syndrome was then determined in conjunction with the patient's medical history, symptoms, signs, and pertinent examinations. Without using a catheter or a surgical procedure, we managed the patient's medical condition. Two weeks later, the patient was discharged with symptoms improved. Takotsubo syndrome is comparable to an acute myocardial infarction on clinical and electrocardiographic examination in the absence of significant coronary disease. Although ventricular septal perforation is most commonly associated with acute myocardial infarction, it can also happen following Takotsubo syndrome. Takotsubo syndrome complicated by ventricular septal perforation is easily misdiagnosed. The early recognition and management of this condition can avoid or reduce morbidity and mortality.

List of cardiology mnemonics

Renal failure Embolism: pulmonary Complications of Myocardial Infarction Darth Vader Death Arrythmia Rupture(free ventricular wall/ ventricular septum/ papillary muscles) Tamponade Heart failure (acute or chronic) Valve disease Aneurysm of Ventricles Dressler's Syndrome thromboEmbolism (mural thrombus) Recurrence/ mitral Regurgitation Coronary artery bypass graft: indications DUST:p. 31 Depressed ventricular function Unstable angina Stenosis of the left main stem Triple vessel disease ECG: left vs. right bundle block WiLLiaM MaRRoW:p. 31 W pattern in V1-V2 and M pattern in V3-V6 is Left bundle block. M pattern in V1-V2 and W in V3-V6 is Right bundle block. Exercise ramp ECG: contraindications RAMP:p. 31 Recent MI Aortic stenosis MI in the last 7 days Pulmonary hypertension Endocarditis FROM JANE: Fever Roth's spots Osler's nodes Murmur of heart Janeway lesions Anemia Nail hemorrhage Emboli Heart valve sequence Try Puling My Aorta:p. 3 Tricuspid

InternalMed_Harrison

Palpation may reveal cardiac enlargement and abnormal contraction of the cardiac impulse (left ventricular dyskinesia). Auscultation can uncover arterial bruits, a third and/or fourth heart sound, and, if acute ischemia or previous infarction has impaired papillary muscle function, an apical systolic murmur due to mitral regurgitation. These auscultatory signs are best appreciated with the patient in the left lateral decubitus position. Aortic stenosis, aortic regurgitation (Chap. 283), pulmonary hypertension (Chap. 304), and hypertrophic cardiomyopathy (Chap. 287) must be excluded, since these disorders may cause angina in the absence of coronary atherosclerosis. Examination during an anginal attack is useful, since ischemia can cause transient left ventricular failure with the appearance of a third 1582 and/or fourth heart sound, a dyskinetic cardiac apex, mitral regurgitation, and even pulmonary edema. Tenderness of the chest wall, localization of the discomfort with a single

Myocardial rupture

Classification Myocardial ruptures can be classified as one of three types. Type I myocardial rupture is an abrupt slit-like tear that generally occurs within 24 hours of an acute myocardial infarction. Type II is an erosion of the infarcted myocardium, which is suggestive of a slow tear of the dead myocardium. Type II ruptures typically occur more than 24 hours after the infarction occurred. Type III ruptures are characterized by early aneurysm formation and subsequent rupture of the aneurysm. Another method for classifying myocardial ruptures is by the anatomical portion of the heart that has ruptured. By far the most dramatic is rupture of the free wall of the left or right ventricles, as this is associated with immediate hemodynamic collapse and death secondary to acute pericardial tamponade. Rupture of the interventricular septum will cause a ventricular septal defect. Rupture of a papillary muscle will cause acute mitral regurgitation.

InternalMed_Harrison

Diagnosis Due to the unstable condition of these patients, supportive therapy must be initiated simultaneously with diagnostic evaluation (Fig. 326-2). A focused history and physical examination should be performed, blood specimens sent to the laboratory, and an electrocardiogram (ECG) and chest x-ray obtained. Etiologies of Cardiogenic Shock or Pulmonary Edema Acute myocardial infarction/ischemia LV failure Ventricular septal rupture Papillary muscle/chordal rupture–severe MR Ventricular free wall rupture with subacute tamponade Other conditions complicating large MIs Post-cardiac arrest Post-cardiotomy Refractory sustained tachyarrhythmias Acute fulminant myocarditis End-stage cardiomyopathy LV apical ballooning Takotsubo’s cardiomyopathy Hypertrophic cardiomyopathy with severe outflow obstruction Aortic dissection with aortic insufficiency or tamponade Severe valvular heart disease Other Etiologies of Cardiogenic Shockb RV failure due to:

Ventricular Septal Rupture Following Acute Myocardial Infarction.

ST-segment elevation myocardial infarction (STEMI) is a known medical exigency that has seen considerable advances in medical treatment, dramatically boosting survival rates. Post myocardial infarction ventricular rupture is a major serious mechanical complication following myocardial infarction. We present a case of a 68-year-old male admitted to the emergency department with heaviness in the chest, for which electrocardiography was done and it was suggestive of anterior and lateral wall myocardial infarction. After six hours he experienced breathlessness, jugular venous pressure (JVP) was raised, and auscultation revealed early systolic murmur at apex suggestive of ventricular septal rupture. An urgent echocardiogram was done and it confirmed the diagnosis of ventricular septal rupture (VSR). To enhance the prognosis, early identification and appropriate care are required, which necessitate a thorough clinical evaluation that raises the possibility of mechanical problem, as late presentation is one of the major risk factors for developing VSR. VSR can manifest itself in numerous ways, based on the patient's condition. Right clinical judgement and ECG are required to establish a quick diagnosis, as a result, to determine the most appropriate treatment at the appropriate time.

InternalMed_Harrison

The precordium is usually quiet, and the apical impulse may be difficult to palpate. In patients with anterior wall infarction, an abnormal systolic pulsation caused by dyskinetic bulging of infarcted myocardium may develop in the periapical area within the first days of the illness and then may resolve. Other physical signs of ventricular dysfunction include fourth and third heart sounds, decreased intensity of the first heart sound, and paradoxical splitting of the second heart sound (Chap. 267). A transient midsystolic or late systolic apical systolic murmur due to dysfunction of the mitral valve apparatus may be present. A pericardial friction rub may be heard in patients with transmural STEMI at some time in the course of the disease, if they are examined frequently. The carotid pulse is often decreased in volume, reflecting reduced stroke volume. Temperature elevations up to 38°C may be observed during the first week after STEMI. The arterial pressure is variable; in most

[Myocardial infarct caused by dissection of the anterior interventricular ramus after blunt thoracic trauma--a case report].

A 23 year old man, having experienced sudden retrosternal pain, radiating to both hemithoraces, with dyspnea at rest was admitted to another hospital. The physical examination of heart and lung was unremarkable, but the patient showed discrete signs of a respiratory infection. Because of the young age and the history of a respiratory infection, the differential diagnosis perimyocarditis was favored and an appropriate treatment was begun. Five days later the patient was transferred to our center for cardiac catheterization and further treatment. After admission the patient was reported to be hit by a football shortly before the onset of symptoms. The electrocardiogram and chemical values showed the signs of myocardial damage with extensive myocardial necrosis. In the coronary arteriography a dissection of the proximal left anterior descending artery of a length of about 2 cm was seen; in the levocardiogram anterior akinesis was verified. Because of the already completed myocardial infarction, the short distance of the lesion to the left main coronary artery, and the restored flow in the left anterior descending, a non-invasive treatment was preferred. A control coronary arteriography five days later showed solely an irregularity of the vessel wall, the coronary dissection was not further demonstrable.

Acute myocardial infarction with papillary muscle rupture.

The subject of this report is a 57-year-old obese, hypertensive woman who had been well until the onset of severe chest pain and hypotension. She had to be defibrillated four times on her way to the hospital. The diagnosis of acute inferior-posterior infarction was made by electrocardiogram (ECG) and there was a markedly elevated serum creatine kinase (CK) (including the MB fraction). The patient had a very low cardiac output and ejection fraction. A lung scan revealed possible pulmonary embolism for which she was anticoagulated. She remained hypotensive and hypoxemic and, on Day 17 of her hospital stay, she had a bout of severe dyspnea. A new systolic murmur was heard and the clinical diagnosis of ruptured papillary muscle was made and confirmed by echocardiography, and later at autopsy. All three coronary arteries were severely atherosclerotic and, in addition, the right coronary artery was completely closed by a thrombus. This case clearly illustrates the major pathological changes in the heart that correlate with the clinical findings in patients with a myocardial infarct that is complicated by left ventricular papillary muscle rupture. The pathophysiological effects of this condition, as illustrated in this case report, include the following:1. The posterior papillary muscle wa s almost completely separated from its base, with only a thin strip of muscle intact. The mistral valve thus was insufficient (a "flail valve''); this markedly reduced the ejection fraction of the left ventricle, increased its end-diastolic volume and pressure, produced a damming of blood in the pulmonary circulation, and this resulted in the pulmonary edema seen on the chest x-ray.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute myocardial infarction with ventricular septal rupture.

The interventricular septum is one of the three main sites at which the myocardium can rupture. The features of the interventricular septal rupture that occurred in a 72-year-old woman are characteristic of interventricular septal ruptures in general: (1) they occur most commonly in elderly women; (2) the most common site is the mid-portion of an acute, transmural anteroseptal apical infarct; (3) they are also most common during the patient's first heart attack; (4) the clinical diagnosis of acute myocardial infarct is confirmed by both ECG and by serum enzyme levels; (5) the usual time of the rupture is 3-10 days after the onset of the infarction (it occurred after 3 days in our patient); (6) a new cardiac murmur usually is heard and the patient frequently goes into shock; (7) the diagnosis can be confirmed by a step-up in pO2 levels from right atrium to right ventricle; (8) the usual cause is severe old coronary atherosclerosis with a recent thrombotic occlusion as the final precipitating event.

Peripartum myocardial infarction associated with coronary spasm and acquired protein S deficiency: A case report.

Coronary angiography (CAG) findings of acute myocardial infarction (AMI) in pregnant women are characterized by a high incidence of normal coronary arteries. This is the first report of AMI with normal coronary arteries during pregnancy, showing coronary spasm and pregnancy-related acquired protein S (PS) deficiency. A 30-year-old Japanese woman was admitted to an emergency department. One hour before admission, she developed sudden onset of precordial discomfort, back pain, and dyspnea. She was a primigravida at 39 weeks' gestation and had no abnormality in the pregnancy thus far. She had no history of heart disease, diabetes, hypertension, dyslipidemia, deep vein thrombosis (DVT), smoking, or oral contraceptive use and no family history of ischemic heart disease, hemostasis disorder, or DVT. She did not take any medication. Electrocardiography showed ST-segment elevations in leads II, III, aVF, and V2-V6. Heart-type fatty acid-binding protein was positive. Echocardiography showed hypokinesis of the anterior interventricular septum and inferior wall. Continuous intravenous infusion of isosorbide dinitrate was initiated. Coronary computed tomography angiography revealed diffuse narrowing of the apical segment of the left anterior descending coronary artery. Three hours after admission, troponin T became positive, and the following enzymes reached their peak levels: creatine kinase (CK), 1,886 U/L; CK-muscle/brain, 130 U/L. She was diagnosed with transmural AMI due to severe coronary spasm and administered benidipine hydrochloride. Five hours after admission, premature membrane rupture occurred. Emergency cesarean section was performed. There were no anesthetic or obstetrical complications during the operation. On postpartum day 1, the free PS antigen level was low (29%). On postpartum day 18, she was discharged with no reduction in physical performance. Four months after the infarction, CAG showed normal coronary arteries. Acetylcholine provocation test showed diffuse vasospasm in the coronary artery. She was advised that her next pregnancy should be carefully planned. Two years after delivery, free PS antigen level was within normal range, at 86%. She had not experienced recurrence of angina during the 2-year period. Her child was also developing normally. In addition to coronary spasm, pregnancy-related acquired PS deficiency may be involved in AMI etiology.