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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Right ventricular hemodynamics were evaluated in 179 patients with coronary artery disease to determine the effects of chronic ischemia on right ventricular diastolic pressure. Abnormal right ventricular filling pressures occurred only in patients with an abnormal right ventricular systolic pressure or an abnormal left ventricular end-diastolic pressure. Of the 63 patients whose right ventricle was stressed by an increased systolic load secondary to passive pulmonary hypertension, 44 (72 percent) had an abnormal right ventricular end-diastolic pressure. In this group obstruction of vessels serving the right ventricular free wall or septum, or both, was almost universal (43 of 44, 98 percent) and a significantly increased incidence of inferior infarction (P less than 0.05) was noted. Such obstruction was significantly less frequent in patients with normal filling pressures (10 of 17, 59 percent; P less than 0.001). Compared with patients with coronary artery disease, patients with passive pulmonary hypertension due to aortic stenosis or mitral stenosis had significantly greater degrees of pulmonary hypertension (P less than 0.05) yet slightly lesser elevations of right ventricular end-diastolic pressure. These data suggest that in patients with ischemic heart disease the right ventricle exhibits diastolic dysfunction at lower levels of afterload stress than it would with normal coronary blood flow.
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PMID:Right ventricular diastolic pressure in coronary artery disease. 50 30

In 13 patients with acute coronary insufficiency (intermediate syndrome, postinfarction angina, and progressive angina), samples of the ischemic area of the myocardium were studied with the electron microscope and by morphometric methods in order to describe quantitatively the mitochondrial population. Three indices were measured: the fractional volume of the mitochondrial compartment of the cytoplasm, the number of mitochondria per unit volume of heart tissue, and the average individual mitochondrial volume. As a control, the same study was performed on samples obtained from patients with chronic coronary insufficiency and mitral stenosis. In all the ischemic hearts the most conspicuous ultrastructural modification of the muscle cells consisted in an irregular distribution of the mitochondriranules. Generally, odd shaped mitochondria were found. The modifications were not diffuse, and almost normal heart muscle cells were seen alongside deeply altered ones. In addition a definite decrease in the fractional volume of the mitochondrial compartment was found, which was apparently due to a decrease in the number of mitochondria per unit volume of cytoplasm. The average individual mitochondrial volume was similar in acute coronary insufficiency and in the control cases. On the basis of this evidence it is postulated that in sublethal ischemia definite ultrastructural modifications of the heart muscle cells are associated with a decrease in the number of mitochondria per unit volume of cytoplasm.
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PMID:Ultrastructural and morphometric study of the human heart muscle cell in acute coronary insufficiency. 52 66

In 53 patients with mitral- or aortic-mitral valve disease, the content of ATP and lactate of the papillary muscles resected at the time of valve replacement was investigated at the beginning of ischemic arrest and at the time of reperfusion. Profound body hypothermia (25 degrees C) and injection cardioplegia using magnesium-aspartate-procaine were applied for myocardial protection. In hypertrophic papillary muscles the myocardial ATP content decreased at a slower rate (ATP decay 12% of the initial value after 60 minutes of ischemia) than in normal papillary muscles obtained from patients with isolated mitral stenosis (ATP decay 33% of the initial value after 40 minutes of ischemia). 20% of the patients required temporary inotropic circulatory support postoperatively for 12 to 88 hours. The ATP content of the papillary muscles of these patients differed only little from those, in who no myocardial failure occurred. However the myocardial lactate levels were higher in patients in whom a low cardiac output state evolved.
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PMID:[Behaviour of ATP and lactate in human papillary muscle during profound hypothermia and injection cardioplegia with magnesium-asparatate-procaine (author's transl)]. 75 Dec 88

Left atrial ball thrombus is an infrequent clinical syndrome, which can have a catastrophic outcome but can be readily treated when recognized. It is usually a complication of long-standing rheumatic mitral stenosis. Symptomatic presentation is variable: fragmentation of the thrombus followed by peripheral embolization will produce ischemia or infarction of myocardium, brain, viscera, or extremities; random, intermittent, partial, or total occlusion of the mitral valve orifice may cause syncope, pulmonary congestion, and occasionally sudden death in other patients. Embolic and obstructive phenomena may also occur together. Cardiac physical findings usually suggest mitral stenosis; variability in the intensity of the diastolic rumble is common. Two-dimensional echocardiography is the gold standard for identifying ball thrombus. Cardiac catheterization provides assessment of coronary artery status when needed. The outcome of untreated ball thrombus is unlikely to be favorable. The results of anticoagulation and thrombolysis are unpredictable and potentially as harmful as no treatment at all. Current evidence although scant suggests that prompt surgical removal of the free thrombus, often in conjunction with mitral valve repair or replacement, is the appropriate therapeutic course in most patients.
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PMID:Left atrial ball thrombus: review of clinical and echocardiographic manifestations with suggestions for management. 203 92

Diastolic heart failure is characterized by increased resistance to diastolic filling of one or both cardiac ventricles. Although some degree of diastolic failure exists in most patients presenting clinically with heart failure, a substantial subset of patients have relatively pure diastolic heart failure with normal systolic function. Diastolic heart failure can be due to structural abnormalities that increase resistance to ventricular inflow, and these structural abnormalities can be extramyocardial (e.g., constrictive pericarditis and mitral stenosis) or intramyocardial (e.g., fibrosis and amyloidosis). In addition to structural abnormalities, physiological derangement of myocardial inactivation and relaxation can contribute importantly to diastolic dysfunction in patients with heart failure. There is mounting evidence that advanced myocardial hypertrophy is associated with increased resistance to ventricular diastolic inflow due to both structural alteration (increased wall thickness and altered collagen matrix) and impaired diastolic relaxation of the hypertrophied myocardium. Physiological mechanisms for impaired relaxation in advanced hypertrophy remain controversial but can include disordered function of myocardial sarcoplasmic reticulum, subendocardial ischemia, and altered adenylate cyclase function. Diastolic dysfunction can play an important role in the genesis of flash pulmonary edema seen in patients with ischemic heart disease because myocardial ischemia is associated with a decline in relaxation rate, increased resistance to early diastolic filling, and in some cases, a striking upward shift in the left ventricular diastolic pressure-volume relation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diastolic dysfunction and congestive heart failure. 213 51

This report tests the hypothesis that, in early diastole, motion of the anterior left atrial wall corresponds to the motion that can be observed in the contiguous posterior wall of the aortic root. To test this hypothesis, we examined the effects of mitral stenosis, exercise in normals, exercise induced left ventricular ischemia, left ventricular hypertrophy and left ventricular dysfunction on this slope. Each altered early diastolic atrioventricular interaction as predicted and therefore, the early diastolic motion of the anterior left atrial wall does appear to be mirrored by the early diastolic slope of the posterior wall of the aortic root. Consequently, if interpreted in the clinical context, measurement of early diastolic slope of the posterior wall of the aortic root may serve as a useful guide to separate patients with severe from those with mild mitral stenosis.
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PMID:Early diastolic posterior aortic root slope, a clinical guide to the severity of mitral stenosis. 403 Oct 2

To clarify the types and frequency of myocardial fibrosis and vascular lesions caused by different types of the rheumatic valvular disease, 41 autopsied hearts with rheumatic valvular lesions were examined and the following results were obtained. As to myocardial fibrosis, 1) perivascular fibrosis, caused mainly by perivascular inflammation and partly by myocardial strain, varied in grade according to the types of the valvular disease, i.e., most severe in mitral regurgitation (MR) and combined valvular disease (CVD) and least in mitral stenosis (MS); 2) Aschoff's nodes: 3 typical and 8 atypical cases were found; 3) perimycial fibrosis due to myocardial strain: most severe in MR and CVD and least in MS; and 4) irregular patchy fibrosis, caused mainly by myocarditis and partly by ischemia, was noticed in all types of the valvular disease. As to vascular lesion, 1) angitis was found in 7 cases and most frequently in MR; and 2) thickening of the intima and media was found in all types of valvular disease. Thus, myocardial fibrosis and vascular lesion varied according to the types of valvular disease, and not only hemodynamic changes but also myocardial fibrosis and vascular lesions might determine the prognosis of the valvular disease.
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PMID:Histopathological studies on the myocardial fibrosis and vascular lesion of rheumatic valvular disease. 732 Nov 53

The ability to perform bedside examinations in acutely ill patients, the sensitivity of the technique and the accuracy of serial examinations have led to increasing use of echocardiography in the intensive care setting. In addition to diagnostic information, the procedure provides the clinician with objective reproducible data for noninvasive evaluation of follow-up and therapeutic action. It provides an important approach to the patient with cardiac enlargement and congestive heart failure. In the patient with chest pain it may detect a cause of ischemia other than coronary artery obstruction and in the presence of unquestionable coronary artery disease it provides information towards early recognition and follow-up of complications. In acute left-sided heart failure it helps in the delineation of conditions amenable to specific therapeutic interventions. Echocardiograpy may point to the origin of systemic emboli by detecting mitral and valvular vegetations in infectious endocarditis, mitral stenosis and in rare cases of atrial myxoma. It may accelerate decisions for invasive procedures.
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PMID:[Significance of echocardiography in monitoring blood circulation]. 739 7

A neonate is reported in whom, during Norwood stage I correction for hypoplastic left heart syndrome with mitral stenosis, an organized thrombus was found to protrude from the left coronary ostium into the aortic root. With ventricular assist device support the patient survived despite severe left ventricular ischemia. The presumed origin of the thrombus is from left ventriculocoronary arterial connections that serve to decompress the blind left ventricular cavity.
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PMID:Organized thrombus in left main coronary artery in hypoplastic left heart syndrome. 764 24

We recently encountered a patient with mitral insufficiency, accompanied by PN (polyarteritis nodosa), who developed a cardiac rupture immediately after a mitral valve replacement. The patient was a 60-year-old woman. After she was diagnosed as having mitral stenosis and insufficiency in 1968, the patient developed congestive heart failure and underwent repeated hospital admissions and discharges. In 1989, she was diagnosed as having PN and began to receive a high-dose steroid therapy (prednisolone; total dose 5245 mg). Because of transient brain ischemia and exacerbation of the symptoms of heart failure, the patient underwent mitral valve replacement on December 19, 1991. For anesthesia, oxygen, fentanyl, midazolam and vecuronium were administered. During surgery, catecholamine, nitroglycerin and prostaglandin E1 were continuously infused intravenously. The patient was weaned smoothly from the cardiopulmonary bypass. The operation was completed in about 6 hours. Her postoperative course was satisfactory until she suddenly developed left ventricular rupture and died 6 hours after surgery. The rupture seemed to be attributable to a weakening of the myocardial wall following long-term, high-dose steroid therapy, and to myocardial degeneration caused by PN-associated necrotizing vasculitis of myocardial arterioles.
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PMID:[Anesthetic management of a patient with polyarteritis nodosa who suddenly developed cardiac rupture after valve replacement]. 790 39


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