Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

All calcium antagonists have the ability to decrease the symptoms and signs in some patients with ischemic heart disease and help lower the blood pressure in hypertensive persons, but in clinical doses nifedipine does not exhibit antiarrhythmic properties, although these are an important part of the action of verapamil, diltiazem and some substances with a similar chemical structure. In certain disorders beta-adrenergic blocking drugs are useful adjuncts, and under some circumstances, particularly variant angina and supraventricular arrhythmias, specific calcium antagonists are the drugs of choice. More data are needed to define the role of calcium antagonists during cardiopulmonary bypass, in the protection of the ischemic myocardium, in the management of hypertrophic cardiomyopathy and in specific cases of primary pulmonary hypertension. When used with an appropriate sense of perspective and careful observation, calcium antagonists provide useful additional means of helping selected patients suffering from particular cardiovascular diseases.
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PMID:Clinical value of calcium antagonists in treatment of cardiovascular disorders. 613 Oct 86

All calcium antagonists have the ability to decrease the symptoms and signs in some patients with ischemic heart disease and help lower the blood pressure in hypertensive persons, but in clinical doses nifedipine does not exhibit antiarrhythmic properties, although these are an important part of the action of verapamil, diltiazem and some substances with a similar chemical structure. In certain disorders beta-adrenergic blocking drugs are useful adjuncts, and under some circumstances, particularly variant angina and supraventricular arrhythmias, specific calcium antagonists are the drugs of choice. More data are needed to define the role of calcium antagonists during cardiopulmonary bypass, in the protection of the ischemic myocardium, in the management of hypertrophic cardiomyopathy and in specific cases of primary pulmonary hypertension. When used with an appropriate sense of perspective and careful observation, calcium antagonists provide useful additional means of helping selected patients suffering from particular cardiovascular diseases.
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PMID:Calcium antagonists and cardiovascular disorders. 624 45

Clinical experience with calcium antagonists in congestive heart failure has, to date, been mainly restricted to the use of nifedipine but there is either no or only a limited extent of information available on diltiazem and verapamil. In patients with acute and chronic congestive heart failure, single-dose administration of nifedipine was seen to lead to a decrease in systemic vascular resistance, left ventricular filling pressure and ventricular volumes as well as to an increase in stroke volume, ejection fraction and mean velocity of circumferential fiber shortening. These favorable effects could not be detected in eight patients during a three-week treatment phase with 80 mg nifedipine daily: resting blood pressure, cardiac volumes, echocardiographically-dimensions and exercise tolerance were unchanged as compared with placebo. In patients with ischemic heart disease and impaired ventricular function, in addition to an improvement in systolic function, single-dose nifedipine administration led to favorable effects on diastolic function with a shift of the diastolic pressure-volume relationship downward and to the diastolic pressure-volume relationship downward and to the left. In patients with severe aortic regurgitation, the observed increase in effective cardiac output affected by nifedipine was primarily attributable to an increase in heart rate. In the presence of an initially-elevated systemic vascular resistance, the regurgitation fraction decreased. In pulmonary hypertension, favorable hemodynamic effects have been reported after acute administration of verapamil as well as diltiazem and nifedipine. In individual cases, promising results in patients with primary pulmonary hypertension have been reported during long-term therapy with nifedipine provided that a favorable initial response could be documented.
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PMID:Calcium antagonists in heart failure. 685 66

The echocardiographic and clinical study was performed in six patients (three acute pulmonary embolism, one for each hypertensive cardiomyopathy, ischemic heart disease and primary pulmonary hypertension) who had a diastolic monophasic triangular pattern of the tricuspid valve echogram. Left-sided and right-sided IRT / square root R-R, ICT / square root R-R, PEP, Q-Mc and Q-Tc, and PEP / ET (IRT; isovolumic relaxation time, ICT; isovolumic contraction time, PEP; preejection time, Q-Mc or Q-Tc; interval of the Q wave of the ECG to the closing point of the mitral or tricuspid valve, and ET; ejection time) were measured from echocardiograms, and the comparisons of these parameters were made between two kinds of echogram with or without triangular pattern of the tricuspid valve. There were no significant differences in the left-sided parameters between the two kinds of echocardiograms. The mitral valve echogram showed a persistent M-shaped pattern irrespective of the pattern of the tricuspid valve. Right-sided IRT / square root R-R and ICT / square root R-R were significantly prolonged and Q-Tc was significantly shortened in the echogram with a triangular pattern of the tricuspid valve. Right ventricular (RV) catheterization was performed using a Swan-Ganz catheter in four patients with the triangular pattern of the tricuspid valve echogram. The mean pulmonary artery pressure ranged from 24 to 96 mmHg (40 mmHg on an average) and RV end-diastolic pressure from 8 to 17 mmHg (12 mmHg on An average). The possible explanation for the production of the triangular tricuspid valve echogram was an impaired early diastolic relaxation and increased stiffness of the RV due to the acute pressure overloading, resulting in a delayed opening and an early closing of the tricuspid valve. We conclude that a diastolic monophasic triangular pattern of the tricuspid valve echogram is a reflection of an impaired early diastolic relaxation and an increased end-diastolic stiffness of the RV.
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PMID:[Echocardiograms of a monophasic triangular wave of the tricuspid valve]. 718 4

Recent studies have shown that intracellular Ca2+ handling is abnormal in the myocardium of patients with end-stage heart failure. Muscles from the failing hearts showed a prolonged Ca2+ transient and a diminished capacity to restore a low resting Ca2+ level during diastole. Accordingly, we examined whether this defect in Ca2+ transport function is due to alterations in sarcoplasmic reticulum gene expression. We determined the messenger RNA (mRNA) levels of sarcoplasmic reticulum Ca2+ transport proteins in failing human hearts from 17 cardiac transplant recipients with a diagnosis of dilated cardiomyopathy, primary pulmonary hypertension, or ischemic heart disease. The expression levels of each mRNA were compared with each other and then correlated with that of atrial natriuretic factor (ANF) mRNA in the failing ventricle. The mRNA levels for the calcium release channel (ryanodine receptor, RYR2), Ca2+ uptake pump (Ca(2+)-ATPase, SERCA2 isoform), and phospholamban differed significantly between heart samples but showed an inverse relation with that of ventricular ANF mRNA. In contrast, calsequestrin mRNA levels remained unchanged in these failing hearts. In addition, beta-myosin and alpha-cardiac actin mRNA levels also showed an inverse relation with ANF mRNA levels. These changes were observed in both right and left ventricles of hearts with congestive heart failure due to dilated cardiomyopathy, primary pulmonary hypertension, or ischemic heart disease. The results are consistent with the hypothesis that abnormal calcium handling in the sarcoplasmic reticulum of failing hearts is due to the altered expression of the genes encoding sarcoplasmic reticulum proteins.
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PMID:Alterations in sarcoplasmic reticulum gene expression in human heart failure. A possible mechanism for alterations in systolic and diastolic properties of the failing myocardium. 841 95

Primary pulmonary hypertension (PPH) is often associated with angina-like chest pain, the mechanism of which is controversial. A 37-year-old woman with severe PPH and angina had transient ischemic ECG changes and reversible anterior perfusion defect on 201thallium scintigraphy. Coronary angiography revealed severe stenosis of the left main coronary artery (LMCA) and otherwise normal vessels. After heart-lung transplantation, examination of the explanted heart showed normal coronary arteries. Compression of the LMCA by the dilated pulmonary artery trunk was responsible for myocardial ischemia. This mechanism should be considered in patients with PPH and angina and might contribute to the high sudden death rate.
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PMID:Left main coronary artery compression during primary pulmonary hypertension. 931 24

Hoarseness of voice due to paralysis of the left recurrent laryngeal nerve caused by a dilated left atrium in mitral stenosis as discussed by Ortner, is a subject of controversy. Different authors have cited different mechanisms as explanation. A variety of cardiac problems such as primary pulmonary hypertension, ischaemic heart disease, various congenital heart disorders can all lead to paralysis of the left recurrent laryngeal nerve. Most authors believe that pressure in the pulmonary artery causes the nerve compression. In Papua New Guinea cor pulmonale and rheumatic heart disease are the commonest cardiac disorders seen. Ortner's syndrome is a rarity and has never been reported from here before. Here three different case reports are presented with mitral stenosis, primary pulmonary hypertension and combined mitral stenosis and regurgitation and the pathogenesis of hoarseness is discussed.
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PMID:Ortner's syndrome revisited. 965 3

Based on the clinical observation that patients with right or left heart failure often present with hyperuricaemia, the relation between serum urate values and haemodynamic variables was studied in patients with primary pulmonary hypertension (PPH) as well as in patients with advanced ischaemic heart disease or dilated cardiomyopathy. The study was a retrospective analysis of 39 patients with PPH and 36 patients with left heart disease, examining serum urate levels in association with haemodynamic variables. Elevated urate concentrations were found in 79% of the PPH patients. There was no association between serum urate levels and mean pulmonary artery pressures, but a significant correlation was found between urate levels and the cardiac index (r=0.48; p=0.0021) and an even stronger correlation between serum urate levels and mean right atrial pressures (r=0.83; p<0.0001). A similar association was found in a subgroup of 21 PPH patients not receiving diuretics. In 36 patients with ischaemic heart disease or dilated cardiomyopathy, hyperuricaemia was present in 78% and was significantly associated with elevated right atrial pressures (r=0.40; p=0.031) and even more so with elevated left atrial pressures (r=0.55; p=0.0005) but not with the cardiac index (r=0.034; p=0.86). The data show that hyperuricaemia in patients with cardiac dysfunction is closely related to elevated right or left atrial filling pressures.
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PMID:Hyperuricaemia in patients with right or left heart failure. 1023 47

Cardiac abnormalities in birth asphyxia were first recognised in the 1970s. These include (i) transient tricuspid regurgitation which is the commonest cause of a systolic murmur in a newborn and tends to disappear without any treatment unless it is associated with transient myocardial ischemia or primary pulmonary hypertension of the newborn (ii) transient mitral regurgitation which is much less common and is often a part of transient myocardial ischemia, at times with reduced left ventricular function and, therefore, requires treatment in the form of inotropic and ventilatory support (iii) transient myocardial ischemia (TMI) of the newborn. This should be suspected in any baby with asphyxia, respiratory distress and poor pulses, especially if a murmur is audible. It is of five types (A to E) according to Rowe's classification. Type B is the most severe with respiratory distress, congestive heart failure and shock. Echocardiography helps to rule out critical left ventricular obstructive lesions like hypoplastic left heart syndrome or critical aortic stenosis. ECG is very important for diagnosis of TMI, and may show changes ranging from T wave inversion in one lead to a classical segmental infarction pattern with abnormal q waves. CPK-MB may rise and echocardiogram shows impaired left ventricular function, mitral and/or tricuspid regurgitation, and at times, wall motion abnormalities of left ventricle. Ejection fraction is often depressed and is a useful marker of severity and prognosis. Treatment includes fluid restriction, inotropic support, diuretics and ventilatory resistance if required (v) persistent pulmonary hypertension of the newborn (PPHN). Persistent hypoxia sometimes results in persistence of constricted fetal pulmonary vascular bed causing pulmonary arterial hypertension with consequent right to left shunt across patent ductus arteriosus and foramen ovale. This causes respiratory tension and right ventricular failure with systolic murmur of tricuspid, and at times, mitral regurgitation. Treatment consists of oxygen and general care for mild cases, ventilatory support, ECMO and nitric oxide for severe cases. Cardiac abnormalities in asphyxiated neonates are often underdiagnosed and require a high index of suspicion. ECG and Echo help in early recognition and hence better management of these cases.
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PMID:Cardiac abnormalities in birth asphyxia. 1095 39

Circulating levels of endothelin-1 (ET-1) are elevated in a number of pathophysiological conditions. Our aim was to determine the effect of overexpression of the peptide on ET receptors in human blood vessels. Aorta and pulmonary arteries were removed from patients with dilated cardiomyopathy (CDM), ischaemic heart disease (IHD), and primary pulmonary hypertension (PPH) and compared with controls. Sections of the medial (smooth muscle) layer were incubated with [125I]ET-1 and increasing concentrations of FR139317, an endothelin-A- (ET(A)) selective antagonist. FR139317 competed for the binding of iodinated ET-1 monophasically, indicating that all vessels examined expressed ET(A)-receptors in the media. ET(B)-receptors could not be detected, either in the control vessels or in those from patients with disease. There was no change in affinity (K(D)) but there was a significant (*p < 0.05) reduction in ET(A)-receptor density (Bmax) by 20-50% in diseased tissues, compared with controls. These results suggest that ET(A)-receptors are downregulated as an adaptive response to increased levels of ET-1.
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PMID:Endothelin-A-receptors in human aorta and pulmonary arteries are downregulated in patients with cardiovascular disease: an adaptive response to increased levels of endothelin-1? 1107 25


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