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1/139. Evolution of left ventricular diseasein the fetus. Case report.

    A fetal case is described that showed a rapid progression from the features of initial left ventricular fibroelastosis at 20 weeks of gestation to a more marked dilation at 22 weeks and finally to a hypoplastic left ventricle with aortic stenosis at 24 weeks of gestation. This case confirms the evolutive character of left ventricular disease during fetal life.
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2/139. Transient left ventricular dysfunction in childhood sickle cell disease.

    For unclear reasons, myocardial infarction is rare in childhood sickle cell disease, whereas lung, bone, and brain infarcts are more common. During vasoocclusive crisis and infection, acute myocardial ischemia and chronic volume overload from anemia may result in myocardial dysfunction. We report a child who had reversible cardiac dysfunction that mimicked myocardial infarction.
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3/139. Right ventricular myocardial bridge in a patient with pulmonary hypertension--a case report.

    Myocardial bridge is a not uncommon finding in routine diagnostic coronary angiography or pathological examination of the heart. It is almost always confined to the left ventricle and the left anterior descending coronary artery. This report describes a patient with chronic lung disease, severe left ventricular dysfunction, and pulmonary hypertension in whom coronary angiography revealed bridging of the right ventricular branch of the right coronary artery.
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4/139. Right-sided pulsus alternans in diastolic left ventricular dysfunction.

    Pulsus alternans is usually found in patients with reduced systolic ventricular function. We describe a patient with shortness of breath, hypertension, and left ventricular hypertrophy, but with normal left and right systolic function. Pulsus alternans was demonstrated in the pulmonary wedge position, pulmonary artery, and right ventricle, but not in the aorta or left ventricle. Cathet. Cardiovasc. Intervent. 47:336-339, 1999.
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5/139. Acute left ventricular dysfunction and subarachnoid hemorrhage.

    OBJECTIVE: Severe left ventricular (LV) dysfunction associated with acute subarachnoid hemorrhage (SAH) due to cerebral aneurysm rupture. SETTING: An adult 12-bed surgical intensive care unit of a university hospital. PATIENT: A female patient presenting with SAH (Hunt & Hess grade III) and severe left ventricular dysfunction. INTERVENTIONS: central venous pressure, arterial blood pressure, extravascular lung water catheter, transesophageal echocardiography, blood gas analysis, electrocardiograms, and chest x-ray for clinical management. MEASUREMENTS AND MAIN RESULTS: On admission to the district hospital, an electrocardiogram (ECG) revealed a sinus rhythm with transient ST elevations. A transesophageal echocardiography showed a left ventricular ejection fraction (LV-EF) of approximately 10%. Severe LV dysfunction required inotropic and vasopressor support to maintain mean arterial pressure above 60 mmHg, while the first measurement of an extravascular lung water catheter revealed a cardiac index of 2.0 L/min/m2 and moderate hypovolemia. Despite stepwise volume loading that increased intrathoracic blood volume--an indicator of cardiac preload--from 719 mL/m2 to 927 mL/m2, cardiac index remained poor. enoximone lead to a marked increase of cardiac index up to 3.9 L/min/m2 and LV-EF to about 30%, but had to be stopped due to thrombopenia. Surgical clipping of an intracranial aneurysm was postponed because of the impaired cardiac function and was performed on day 18 after admission. Interestingly, neurologic outcome was not as poor as might be expected from the literature. CONCLUSION: Severe left ventricular dysfunction may occur in acute SAH and may necessitate delay of aneurysm surgery.
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6/139. 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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7/139. Dynamic outflow obstruction due to the transient extensive left ventricular wall motion abnormalities caused by acute myocarditis in a patient with hypertrophic cardiomyopathy: reduction in ventricular afterload by disopyramide.

    A 65-year-old woman was admitted to the coronary care unit because of acute pulmonary edema. Immediate 2-dimensional and Doppler echocardiograms revealed extensive left ventricular wall motion abnormalities and left ventricular hypertrophy with extreme outflow obstruction. Although an ECG showed ST-segment elevation in the anterolateral leads, a coronary arteriogram revealed normal epicardial arteries. heart failure was relieved after diminishing the dynamic outflow obstruction with disopyramide administration. An endomyocardial biopsy from the right ventricle on the 8th hospital day showed borderline myocarditis. Wall motion abnormalities gradually normalized within 2 weeks. It is speculated that her pulmonary edema would not have been relieved so readily without the immediate reduction in ventricular afterload by disopyramide. These clinical changes over time were observed with serial echo-Doppler examinations.
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8/139. Segmental degradation of left ventricular wall motion after persistent coronary fistula in a posttransplantation patient: a case report and short review of literature.

    A 50-year-old man received an orthotopic heart transplant because of severe coronary heart disease and congestive heart failure. Two years after the transplantation, a continuous murmur occurred at the left sternal edge after repeated endomyocardial biopsies. Echocardiography and coronary angiography revealed a dilated left anterior descending artery with a fistula to the right ventricle. The circumflex was large with an equally postero-lateral branch, and the right coronary artery was rather small with collaterals to the distal part of the left anterior descending branch. The patient had refused any intervention to close the fistula. The left ventricular levogram was normal. Two years later, in a follow-up angiogram, the left ventricular ejection fraction had decreased as a result of hypo- and akinesis of the apex and posterior wall. We suggest that this local wall motion disturbance derives from a steal phenomenon rather than being a sequela of rejection. The decrease in left ventricular ejection fraction was associated with shortness of breath upon moderate exercise. Standard heart failure medication relieved the patient's symptoms. The observation of local wall motion disturbances in this case, as well as conflicting views in the literature, raises the question whether postbiopsy coronary fistulas in transplant patients should be closed.
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9/139. Reversible left ventricular dysfunction associated with raised troponin i after subarachnoid haemorrhage does not preclude successful heart transplantation.

    Transient abnormalities in ECGs, echocardiograms, and cardiac enzymes have been described in the acute setting of subarachnoid haemorrhage. In addition, left ventricular dysfunction has been reported at the time of brain death. A patient with an acute subarachnoid haemorrhage who presented with raised troponin i (TnI) concentrations and diffuse left ventricular dysfunction is described. After declaration of brain death 32 hours later, the heart was felt initially not suitable for transplantation. A normal cardiac catheterisation, however, lead to successful transplantation of the donor heart. Raised catecholamine concentrations and metabolic perturbations have been proposed as the mechanisms leading to the cardiac dysfunction seen with brain death. This may be a biphasic process, allowing time for myocardial recovery and reversal of the left ventricular dysfunction. awareness of this phenomenon in the acutely ill neurologic population needs to be raised in order to prevent the unnecessary rejection of donor hearts.
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10/139. Dilated phase of hypertrophic cardiomyopathy with mid-ventricular obstruction after 20-year follow-up.

    This paper reports a case of dilated phase in hypertrophic cardiomyopathy with mid-ventricular obstruction. Following the first cardiac catheterization and endomyocardial biopsy, the patient was diagnosed as having hypertrophic cardiomyopathy (HCM) with mid-ventricular obstruction. He had been first diagnosed at the age of 38 years and was subsequently followed for 20 years. Echocardiogram revealed gradually progressive dilatation of the left ventricle, associated with disappearance of the mid-ventricular obstruction. The second cardiac catheterization and endomyocardial biopsy performed at the age of 58 disclosed that the patient was in the dilated phase of HCM with a dip-and-plateau pattern diastolic pressure trace.
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