Cases reported "Myocardial Infarction"

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1/410. myocardial infarction complicating neonatal enterovirus myocarditis.

    A 10-week-old, 31-week gestation preterm boy re-presented with heart failure after an initial episode of neonatal aseptic meningitis with positive CSF enterovirus polymerase chain reaction. Investigation demonstrated global myocardial dysfunction with left ventricle posterolateral myocardial infarction. The boy's heart failure was controlled with medical treatment but his myocardial dysfunction persisted 9 months after presentation.
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2/410. Pseudoaneurysm of the left ventricle progressing from a subepicardial aneurysm.

    A 56-year-old man presented with an inferior myocardial infarction and a huge pseudoaneurysm below the inferior surface of the left ventricle, which had progressed from a small subepicardial aneurysm over a 6-month period. Transthoracic echocardiography, doppler color flow images, radionuclide angiocardiography, magnetic resonance imaging and contrast ventriculography all revealed an abrupt disruption of the myocardium at the neck of the pseudoaneurysm, where the diameter of the orifice was smaller than the aneurysm itself, and abnormal blood flows from the left ventricle to the cavity through the orifice with an expansion of the cavity in systole and from the cavity to the left ventricle with the deflation of the cavity in diastole. coronary angiography revealed 99% stenosis at the atrioventricular nodal branch of the right coronary artery. At surgery the pericardium was adherent to the aneurysmal wall and a 1.5-cm orifice between the aneurysm and the left ventricle was seen. Pathological examination revealed no myocardial elements in the aneurysmal wall. The orifice was closed and the postoperative course was uneventful. Over-intense physical activity as a construction worker was considered to be the cause of the large pseudoaneurysm developing from the subepicardial aneurysm. These findings indicate that a subepicardial aneurysm may progress to a larger pseudoaneurysm, which has a propensity to rupture, however, it can be surgically repaired.
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3/410. Transaortic video-assisted removal of a left ventricular thrombus.

    A mobile and pedunculated left ventricular thrombus was developed after acute myocardial infarction in a 59-year-old man, and was successfully removed surgically through the aortic valve using a video-assisted thoracoscope. Transaortic video-assisted thoracoscopy greatly facilitated exposure of the interior of the left ventricle and preserved left ventricular function by avoiding ventriculotomy.
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4/410. Posterior myocardial infarction complicated by rupture of the posteromedial papillary muscle.

    A 61-year-old man was admitted with acute posterior myocardial infarction and, on physical examination, was shown to have a mitral regurgitation (MR) murmur. Transthoracic echocardiography (TTE) showed severe hypokinesis of the posterior wall and severe MR by color flow. Right heart catheterization with a balloon-tipped catheter revealed a pulmonary artery wedge pressure of 30 mmHg. No 'step-up' was seen in blood samples from the right atrium and right ventricle. On angiography, a subtotal occlusion of the mid circumflex artery was found which was angioplastied and stented. As the patient's clinical condition did not improve, he underwent transesophageal echocardiography (TEE) for further evaluation. This showed complete rupture of the posteromedial papillary muscle. The patient underwent urgent surgery with successful mitral valve replacement. The postoperative course was uncomplicated, and clinical improvement seen. This case report underscores the value of TEE in accurate preoperative diagnosis of papillary muscle rupture by providing preoperative anatomic details of the mitral valve apparatus and surrounding structures.
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5/410. Right ventricular infarction with cardiogenic shock treated with percutaneous cardiopulmonary support: a case report.

    A patient with a right ventricular infarction was resuscitated with percutaneous cardiopulmonary support (PCPS), after attempts at reperfusion, high-dose inotropic support and intra-aortic balloon counterpulsation failed to improve the hemodynamic compromise. Emergency PCPS improved the cardiogenic shock and the reduced right ventricular load, allowing the ischemic right ventricle to recover in the setting of unsuccessful reperfusion. This case demonstrates the use of PCPS as a hemodynamic support device for spontaneous recovery of the ischemic right ventricle. PCPS may be a potential therapy for patients with right ventricular infarction.
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6/410. Transcatheter closure of patent foramen ovale for hypoxemia during left ventricular assist device support.

    A patent foramen ovale with right-to-left shunting was responsible, in part, for profound hypoxemia in a patient who required mechanical support with a left ventricular assist device for cardiogenic shock. The patent foramen ovale was detected with contrast transesophageal echocardiography, and the defect was closed successfully with a transcatheter septal defect closure device.
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7/410. Phenoprocoumon, head trauma and delayed intracerebral haemorrhage.

    Delayed traumatic intracerebral haemorrhage (DTICH) constitutes a serious complication of head injury, and several studies have set out to identify predisposing clinical variables and appropriate management strategies. Here we report a distinct and particularly malignant course of DTICH associated with oral anticoagulant therapy.
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8/410. Left coronary artery-left ventricular fistula with acute myocardial infarction, representing the coronary steal phenomenon: a case report.

    A 59-year-old man presented with a left anterior descending coronary artery to left ventricular fistula manifesting as myocardial infarction, representing the coronary steal phenomenon. electrocardiography showed poor R progression in leads V1 through V3. The biochemical markers of myocardial injury were elevated. creatine kinase level was 509 IU/l, creatine kinase MB isoenzyme (CK-MB)47 IU/l, cardiac troponin t 0.62 ng/ml, myosin light chain 6.1 ng/ml, and myoglobin 142 ng/ml. thallium-201 myocardial perfusion imaging with dobutamine stress showed a dobutamine-induced perfusion deficit of the anteroseptal wall of the left ventricle with 0.1 mV ST-segment depression in II, III, aVF, V5, and V6. The mean left anterior descending blood flow measured with the Doppler guidewire was increased from 211 to 378 ml/min. Selective coronary arteriography showed dominant left coronary artery with the contrast medium streaming into the left ventricle via a maze of fine vessels from the distal left anterior descending coronary artery. No critical stenosis of the left anterior descending coronary artery was observed. Administration of acetylcholine 100 micrograms into the left coronary artery did not induce vasoconstriction of that artery. The fistula terminating in the left ventricle was ligated surgically and the patient became free of chest pain. thallium-201 myocardial perfusion imaging with dobutamine stress revealed no perfusion deficit of the anteroseptal wall of the left ventricle. The presence of coronary steal phenomenon was detected by dobutamine stress myocardial imaging.
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9/410. Systolic anterior movement of mitral valve during acute apical myocardial infarction: An unusual mechanism of acute mitral regurgitation.

    We describe a singular case of a 75-year-old woman affected by an anterior acute myocardial infarction in the subset of a very recent orthopaedic surgery. She had had severe mitral regurgitation on coronary angiography. A thorough cardiac echocardiographic examination revealed the particular mechanism of mitral incompetence, consisting of a dynamic anterior mitral leaflet displacement caused by a sustained compensatory left ventricle hypercontractility and favored by postsurgical moderate anemia and mild hypertensive hypertrophy. The use of beta-blockers and the avoidance of pure vasodilators permitted complete reversal of such mechanisms during the clinical course.
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10/410. Sequential changes of hepatocyte growth factor in the serum and enhanced c-Met expression in the myocardium in acute myocardial infarction.

    A 68-year-old male with acute myocardial infarction (AMI) was admitted to the hospital with chest pain that had started 1 day earlier. The serum levels (ng/ml) of hepatocyte growth factor (HGF) were 1.06, 1.22, 1.05, 0.72 and 0.64 on days 2, 3, 4, 5 and 6 postinfarction, respectively. He died suddenly due to cardiopulmonary arrest on day 6. At autopsy, approximately 400 ml of bloody pericardial fluid, caused by rupture of the left ventricle, was detected and the c-Met expression in the myocardium was immunohistochemically found to be most intense in the border zone of the infarcted and non-infarcted region. Although there was no c-Met expression in the infarcted myocardium, it was increased in the myocardial cells surrounding the blood vessels. This is the first report to show sequential changes of HGF in the serum, as well as c-Met expression in the myocardium, in a patient with AMI.
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