Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myocardial contractility was studied in 44 patients with ischaemic heart disease (28 with asynergy) without congestive circulatory insufficiency depending on the degree of coronary atherosclerosis and regional disorder in the movement of the wall of the left ventricle by ventriculography and tensiometry (dp/dt max, Veraguth index, VCE40; t-dp/dt max). No dependence was detected between the growth of the total lesions of cardiac arteries and the increase of the end diastolic and end systolic volumes and the fall of the ejection fraction in patients with normokinesia of the left ventricle. However, a strong inverse relationship has been established between the number of the affected segments of the heart and the ejection fraction (r = -0.90). It was shown that indices of contractility reflecting the pre-ejection phase (dp/dt max, Veraguth index VCE40; t-dp/ max) are less sensitive in determining the cardiac insufficiency than Vcf and must be interpreted simultaneously with the results of the regional contractility according to the ventriculography data.
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PMID:[Myocardial contractile capacity in ischemic heart disease depending on the degree of coronary arteriosclerosis and the presence of parietal asynergy of the left ventricle]. 710 48

During the last 4 years 2040 patients with myocardial infarction were admitted to the C.C.U. of the National Institute of Cardiology. Thirty five patient under 40 years of age were studied. Three had Rheumatic heart disease and in 32 the etiology of the myocardial infarction was probably coronary atherosclerosis. The 32 cases under 40 years of age were compared to a group of patients with myocardial infarction older than 40 years of age. A great predominance of myocardial infarction was found in young males which were heavy smokers. There were no significant differences with the presence of obesity and arterial hypertension. In the younger group, myocardial infarction were more frequent in those with intellectual activity and in taxi drivers. The early hospital course was better in the young group they did not have cardiac failure, cardiogenic shock and none died. However, in the long term follow up the younger group had more P.V.C. and ventricular tachycardia. The cardiography of the younger showed an important predominance of lesions in the left coronary artery. It is concluded that in young people, myocardial infarctions seems to occur primarily in smokers with stress in their Kind of living. These patients seem to have less complications in the early and long term courses. However, more cardiac rhythm disorders are present.
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PMID:[Myocardial infarction in patients below the age of 40 (author's transl)]. 711 66

A rare case of localization of a large nodus of dystopic thyroid gland with a picture of follicular colloid goiter in the upper part of the interventricular septum near the right venous ostium and valve cusps (in combination with papillary cancer of the left lobe and isthmus of the thyroid gland) in a woman of 60 is described. The patient died with a second ischemic insult and progressive cardiac insufficiency which (in the presence of atherosclerosis and hypertension) could have developed in direct connection with nodus of the thyroid gland in the interventricular septum of the right ventricle.
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PMID:[Dystopy of the thyroid into the interventricular septum of the heart]. 712 41

The authors studied the microcirculation changes in ascending aorta and left coronary artery of the heart in 25 deceased with myocardial infarction, aged from 52 to 80, with two control groups: 20 cases with complicated atherosclerosis, aged from 54 to 80, and 4 cases--without atherosclerosis, aged 30-45. Histological and histochemical investigation methods were used. The authors found grave changes in vasa vasorum of aorta and coronary artery with the formation of arteries of "closing" type, hyperplasia of the muscular layer of the arterial and venous vessels anf fibrosis of their wall in the deceased with healed myocardial infarction and chronic coronary and cardiac insufficiency. Acute disturbance of blood microcirculation was observed in recent myocardial infarction, analogical to that in case of shock. Necrosis of the type of anemic infarctions and stratification of the wall with hemorrhages and fresh thrombosis were found in the media of aorta and coronary artery in myocardial infarction and atherosclerosis. Both necrosis and stratification are associated with the manifested endothelial proliferation, recent and organized thrombus in the small vasa vasorum and grave structural changes in the supplying vessels of aorta and coronary arteries.
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PMID:[Microcirculation of the aorta and coronary arteries in patients who died of myocardial infarct and generalized arteriosclerosis]. 733 11

In recent years, endothelial dysfunction and arterial remodelling in various cardiovascular diseases have emerged as two key concepts, with numerous interrelationships. Both endothelial dysfunction and arterial remodelling occur in various pathologies including heart failure, atherosclerosis, restenosis after angioplasty, and pulmonary hypertension, and have modified the therapeutic approach by offering new pharmacological targets: specific receptors not only at the site of the vascular smooth muscle cells but also on the endothelial cells, growth factors that stimulate proliferation of smooth muscle, and receptors and enzymes of the extracellular matrix. Among the various substances under research, the present review will discuss angiotensin II receptor antagonists, endothelin receptor antagonists, nitrates-NO donors, potassium channel activators, and substances interfering with proteoglycans and other components of the extracellular matrix.
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PMID:[Arterial wall: a new pharmacological and therapeutic target?]. 748 94

The use of ACE-inhibitors has increased greatly during the last years. They were first used in treating hypertension, but nowadays cardiac diseases, mainly cardiac failure, are common indications. This means that the drugs are used in the treatment of more elderly patients who often have generalised atherosclerosis. This means that the patients must be controlled more often after initiation of treatment, especially concerning kidney function, since treatment with ACE-inhibitors can cause pronounced changes in renal haemodynamics and kidney function. This review focuses on the effects of ACE-inhibitors on renal haemodynamics and kidney function, which may be positive, with preservation of kidney function in diabetic and other chronic nephropathy, or negative, for example in cases with atherosclerotic stenosis of large or small renal arteries. It is concluded, that in cases of diabetic nephropathy an ACE-inhibitor is the "drug of choice" for treatment of hypertension. Furthermore the ACE-inhibitors seem to reduce the rate of deterioration of renal function and proteinuria in other kidney diseases. It is emphasized, that during treatment with ACE-inhibitors kidney function must be controlled before and following one to two weeks of treatment, if the dose is changed and in all cases following two to three months of treatment. Special attention should be given to patients with atherosclerotic manifestations e.g. angina.
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PMID:[Renal function during treatment with angiotensin converting enzyme inhibitors]. 748 49

The effect on kidney function fo treatment of cardiac failure with ACE-inhibitors was examined retrospectively in a material of 87 consecutive patients. Furthermore, it was evaluated whether concomitant treatment with diuretics or existing generalised atherosclerosis as indicated by ongoing treatment with nitrates could be a risk factor concerning reduction of kidney function. In 11.9% of the patients an increase in S-creatinine of > 30% was observed during the first weeks of treatment. It was only necessary to stop treatment in two of these patients. In the remainder S-creatinine decreased again during ongoing treatment. In another 10.7% of patients an increase of 20-30% in S-creatinine was observed. Seventy-two point six percent of the patients had unchanged kidney function during treatment with an ACE-inhibitor. Ongoing treatment with diuretics did not seem to be a risk factor for developing reduced kidney function, whereas significantly more patients on treatment with nitrates, indicating generalised atherosclerosis, developed reduced kidney function during treatment with ACE-inhibitors. It is recommended to control kidney function before, one to two weeks and two to three months following initiation of treatment with ACE-inhibitors and to pay special attention to patients with generalised atherosclerosis.
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PMID:[Renal function during treatment of chronic renal failure with angiotensin converting enzyme inhibitors]. 748 50

By blocking the inward transmembrane calcium current and opposing the effects of increased intracellular ionised calcium, calcium antagonists exert vascular and myocardial effects which are useful therapeutic tools. Coronary and peripheral vascular relaxation results in an increase in coronary flow and a reduction of the afterload and, therefore, of myocardial oxygen consumption. In some cases, negative myocardial inotropic and chronotropic effects also reduce myocardial oxygen requirements. Spastic angina is the indication of choice of all calcium antagonists whereas, to date, verapamil and diltiazem have been shown to be effective in stable angina and, in the post-infarction situation, diltiazem and verapamil decrease the number of cardiovascular events, and verapamil alone has been shown to reduce mortality. All calcium antagonists have been shown to be effective in hypertension and most have a protective effect on the target organs. The main fields of research concern atherosclerosis, the primary prevention of myocardial infarction and the study of molecules which can be used in heart failure.
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PMID:[Calcium antagonists in cardiovascular diseases]. 750 23

Angiotensin-converting enzyme inhibitors have been extensively studied and established in the treatment of hypertension, heart failure, and ventricular dysfunction. They have various cardiac and vascular protective effects, but the relevant mechanisms of action in these areas remain to be fully understood. Possible effects of converting-enzyme inhibition related to maintenance of normal endothelial function and inhibition of atherosclerosis should be distinguished from effects on myointimal proliferation related to vascular injury and regression of vascular hypertrophy from blood pressure reduction. Experimental animal studies have showed benefit from converting-enzyme inhibition in preventing myointimal proliferation after vascular injury in some species, but no such effect has been shown in clinical studies of restenosis following coronary angioplasty. Laboratory studies have demonstrated a protective effect of converting-enzyme inhibition on endothelial vasomotor function. Further studies have demonstrated prevention of atherosclerosis in hyperlipidemic rabbits and cholesterol-fed cynomolgus monkeys. Possible mechanisms of action apart from blood pressure lowering include inhibition of angiotensin II and other tissue growth factors and accumulation of kinins. These data, among others, provide sufficient rationale for clinical studies to determine whether converting-enzyme inhibitors can reduce atherosclerotic disease and thus widen their application as cardiac and vascular protective agents.
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PMID:The effects of ACE inhibition on progression of atherosclerosis. 751 40

Congestive heart failure is the end product of a progressive series of events resulting from acute myocardial damage. Circulatory neurohormonal systems are activated during the acute phase of left ventricular dysfunction resulting from initial myocardial damage and again in the latter phase of decompensated heart failure. However, these neurohormonal mechanisms return to normal during the compensated stage of heart failure. Recent studies have suggested that autocrine/paracrine modulators of cardiovascular function are activated in the preclinical phase preceding the development of overt heart failure. The renin-angiotensin system in particular has been shown to modulate many of the chronic processes involved in the pathophysiology of cardiovascular disorders. Recent studies suggest that locally generated angiotensin II may contribute to the secondary structural changes seen in cardiovascular disorders, such as cardiac hypertrophy and remodelling, coronary artery disease, and atherosclerosis. Thus, inhibition of angiotensin formation with angiotensin converting enzyme (ACE) inhibitors, particularly at the tissue level, may provide valuable cardioprotective effects. Additional evidence points to the efficacy of ACE inhibitors in preventing the progression of asymptomatic left ventricular dysfunction to overt heart failure.
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PMID:Angiotensin as local modulating factor in ventricular dysfunction and failure due to coronary artery disease. 752 57


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