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)

In the present study: (a) physiopathology, (b) clinics, and (c) therapy of cardiothyreosis are discussed. (a) The hyperkinetic syndrome, the earliest clinical sign in thyrotoxicosis (vasodilatation, increase in inotropism, automatism, etc.), is mediated by a two-fold increase in the number of beta-receptors, and supported by an adequate synthesis of ATP and creatinphosphate (CP) in the young and, to a lesser extent, in the elderly. Genetical heart reserves are mobilized, thus significantly increasing the number and the size of mitochondria and also the enzymatic equipment (such as: the alpha-glycerophosphate-dehydrogenase, malic, pentosic cycles, etc.), a.s.o. Due to an excessive adrenergic action (glycogenolysis, an excessive oxygen consumption, up to necrosis, the ATP and CP syntheses dramatically drop; the phosphorus/oxygen ratio decreases to 2 (normal = 4). In this condition, the high functional cardiovascular performances are also impaired (the submaximal effort capacity is attained at a smaller and smaller oxygen consumption; Propranolol 2 mg i.v. decreased the cardiac output by above 30% (vs 10%--normal); electrocardiogram presents aspects of "coronary disease", tachycardia, etc.). An ultrastructural damage occurs: from "mitochondrial disease", partial lysis of myofibrils, to myofibrosis (revealed postmortem), in spite of a reduced degree of coronary atherosclerosis. Ultrastructural and biochemical experimental data support this point of view. (b) The incidence, precocity and severity of the thyrotoxic heart increase with age and the existence of a previous cardiovascular pathology. Cardiothyreosis is not present under 27 years; in 4,353 patients its incidence is of 25% (arrhythmia--21%, heart failure--12%, coronary insufficiency--1-3%). Of a major interest are tachyarrhythmias which may lead to a high mortality by hypodiastolic congestive heart failure, heart failure with secondary hyperaldosteronism, thromboembolic episodes and ventricular fibrillation. Thyrotoxicosis favours the disease of papillary muscles--mitral prolapse and insufficiency, reversible especially in children. (c) The treatment of thyrotoxic heart is an etiologic one (medical, surgical, radioactive--the last two being preferable after the adequate medical therapy). In particular, cardiothyreosis requires a reinforced irradiation (10,000 rads instead of 7,000 rads) in smaller 131I doses. The protection against the increased nocivity of catechols in thyrotoxicosis is very important (which explains the high mortality in the thyrotoxic "storm") and requires propranolol; doses above 2 mg/kilo body/day are recommended. In the elderly, the sensitivity to propranolol decreases: verapamil i.v. is more efficient in paroxysmal tachyarrhythmias (flutter, atrial fibrillation) and in those occurring intra-operatively during halothane narcosis. The anticoagulant therapy is administered in tachyarrhythmias with high ventricular rate, especially in the elderly, to avoid the embolic risk, higher in defibrillation condition.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cardiothyreosis. 182 Oct 70

Left ventricular hypertrophy may be considered the result of an interaction of a myriad of factors, including hemodynamic overload; age, race, and gender of the patient; the stage of hypertensive disease; and other coexisting diseases. This concept is similar to the multifactorial "mosaic of hypertension" described by Page. In addition, the increased left ventricular mass in hypertension may reflect the disposition of collagen tissue and the participation of a myriad of myocytic growth factors, as well as drug therapy. The resultant left ventricular hypertrophy confers increased cardiovascular risk that is independent of the height of arterial pressure. The mechanisms that account for that risk are not yet well understood but include reduced adaptive myocardial reserve, enhanced predisposition to cardiac dysrhythmias and cardiac failure, accelerated atherosclerosis, and reduced (absolute and relative) coronary flow and flow reserve, as well as other possibilities. At present much work is directed to the demonstration of pharmacological reversal of hypertrophy. However, even with that demonstration of reduced cardiac mass with therapy, it will be necessary to show improved risk at the reduced mass that is independent of the reduction of arterial pressure as well as of the effects of those drugs on cardiac rhythm, flow, metabolism, and direct effects on the cardiac myocyte itself.
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PMID:The heart in hypertension: a 1991 overview. 183 56

Advances in regulation by secondary messengers of Ca2+ level in cardiomyocyte and vascular smooth muscle cell cytosols with special reference to the major differences in regulatory effects in cells of the both types are reviewed. The effects of cAMP, cGMP, Ca2+, calmodulin, diacylglycerol and polyphosphoinositides on the Ca(2+)-channel, Ca(2+)-ATPase, plasmalemma, sarcoplasmic reticulum and outer membrane Na+/Ca2+ uniporter function are considered. Compartmentation of secondary messengers and protein kinase in cardiac and vascular smooth muscle cells should be taken into consideration during extrapolation of in vitro data to an in situ situation. The feasible role of impaired phosphorylation of membrane-bound proteins of cardiac and vascular smooth muscle cells in cardiac insufficiency and atherosclerosis is discussed.
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PMID:[Second messengers in heart cells and smooth muscle vessels]. 191 66

Over the last 10 years, our knowledge of immunologically mediated processes involving the myocardium appears to have made quantum leaps. New and important disease entities such as AIDS have appeared and the cardiologist now becomes an important member of the "AIDS team." Our understanding of "older diseases" such as sarcoidosis, Lyme disease, systemic lupus and other connective tissue syndromes has significantly increased. The concept of high-dose steroid therapy for these processes may, in fact, turn out to be futile and more selective, as less dangerous immunosuppression is being introduced. This concept has significantly advanced in the field of cardiac transplantation where immunosuppression has now been usurped by specific immunotherapy aimed at selective aspects of the immune sequence. New and exciting concepts will emerge from the molecular biology laboratory that will have direct bearing on the management of patients with cardiovascular disorders. This information explosion will force the cardiovascular physician to become more in tune with the world of immunology and molecular biology. Many obvious, significant problems remain, such as accelerated atherosclerosis in the transplant patient and the role of myocarditis in the patient with heart failure. However, it will truly be an exciting decade in which to work and watch the unraveling of these mysteries and hopefully, the study of today's problems will give way to solutions and a clearer understanding of the heart as a target of immune injury.
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PMID:The heart as a target organ of immune injury. 191 12

Sixty six patients with atherosclerosis obliterans of the lower limb arteries were found to have severe central hemodynamic disturbances that correlated with the site of impairment. Central hemodynamic changes appeared as increased cardiac output and stroke volume, shortened tension period and prolonged ejection period. Cardiac derangement occurred under unfavorable hemodynamic conditions, which was followed by its hypertension and dilatation. Instrumental signs of preclinical heart failure were revealed in patients with multisegmental lesions, which should be regarded as a risk factor in performing reconstructive plastic operations.
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PMID:[Indicators of central hemodynamics in patients with arteriosclerosis obliterans of the aorta and arteries of the lower extremities]. 192 Nov 30

Advances in cardiovascular research during the past two decades have resulted in an improved understanding of the chain of events that lead to end-stage coronary artery disease. These developments have been paralleled by therapeutic advances that now make it possible to intervene at virtually every stage in the development of advanced cardiac disease, from asymptomatic persons at risk of developing coronary atherosclerosis to patients with end-stage heart failure. By interrupting this chain of events, perhaps at multiple sites, it may be possible to prevent or slow the development of symptomatic heart disease and hopefully prolong life. Many opportunities exist for obtaining further information regarding the underlying pathophysiology, the fundamental mechanisms of action of interventions designed to prevent and/or treat the development of myocardial ischemia and cardiac failure and for effecting favorably the natural history of various forms of heart disease.
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PMID:Resolved and unresolved issues in the prevention and treatment of coronary artery disease: a workshop consensus statement. 200 53

Atherosclerosis frequently develops in SVGs during the first 10 years. This process appears related to coronary risk factors. Several studies have found an association between hyperlipidemia and atherosclerosis documented at pathology. Late changes attributed to atherosclerosis that were observed at angiography were also significantly related to elevated serum levels of total cholesterol and triglycerides. They also were found in association with diabetes, systemic hypertension, and smoking in some studies. Several clinical studies have documented an association of one or several coronary risk factors with postoperative clinical events, including recurrence of angina, myocardial infarction, heart failure, reoperation because of clinical deterioration, and survival. These factors have been shown to act alone or in combination. The most important is an abnormal lipid profile and diabetes. Smoking and hypertension were seldom found to be significant predictors when considered separately, but appear to play an important role in association with the others. Control of coronary risk factors, particularly hyperlipidemia and smoking, seems mandatory in order to prevent SVG atherosclerosis and progression of the disease in the native coronary arteries.
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PMID:Coronary risk factors and the postbypass patient. 204 86

The overall cardiovascular mortality in patients with chronic renal failure is about 30 per cent of which 10 per cent is attributed to myocardial infarction. This prevalence led some workers to propose a hypothesis of "accelerated atherosclerosis" due to the hyperlipidaemia observed in 30 to 70 per cent of patients. However, the concept of accelerated atherosclerosis, which was based essentially on clinical studies, has been questioned. Pericardial effusion is a common complication of chronic renal failure and has been reported in over 62 per cent of patients in echocardiographic studies. There are many causes and symptoms are often mild; systematic echocardiographic examination of patients with renal failure undergoing haemodialysis has shown 32 per cent of pericardial effusions to be asymptomatic. There are two potential complications: cardiac tamponade and, lesser frequently, constrictive pericarditis. Cardiac failure is a common cause of death in patients undergoing long-term dialysis. The myocardial histological appearances are those of fibrosis, the etiology of which is not fully understood although the dialysis membranes and hypotensive episodes occurring during haemodialysis have been thought to play a role. Left ventricular hypertrophy and fibrosis may give rise to ventricular arrhythmias which could explain some of the cases of sudden death observed in patients with renal failure and often wrongly attributed to ischemic heart disease. Another form of myocardial disease which is observed later is characterised by an alteration of systolic function with left ventricular dilatation and hypokinesia and increased end diastolic pressures without an increase in left ventricular wall thickness. Valvular heart disease may also result from renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[So-called uremic heart diseases]. 210 35

The purpose of this article was to review the clinical and experimental features of diabetic cardiomyopathy, with particular relevance to the Black population. One hundred thirty-seven studies were identified, of which 57 were selected as references for this article. Diabetes is associated with the development of cardiomyopathy, independent of coronary atherosclerosis. Pathological studies show myocardial hypertrophy and fibrosis; microvascular pathology is also present, but all of these pathological findings have an uncertain relationship to myocardial failure. Hemodynamic findings of both congestive and restrictive cardiomyopathy have been described. Noninvasive studies revealed abnormal systolic and diastolic function in many diabetic subjects, particularly in the presence of diabetic complications and/or hypertension. Experimental studies have focused on the mildly diabetic dog and the severely diabetic rat. One year of diabetes in dogs resulted in decreased left ventricular compliance and increased interstitial connective tissue. Studies in the diabetic rat showed a marked slowing of contraction and relaxation. Chronic insulin therapy reversed the changes in the rat model. Combining hypertension with diabetes in the rat resulted in increased myocardial and coronary microvascular pathology and greater changes in isolated muscle function, electrophysiology, and contractile protein biochemistry. Many hypertensive diabetic rats died spontaneously, showing signs of congestive heart failure. Diabetic cardiomyopathy is a significant cause of heart failure in diabetic subjects and occurs more frequently in those with microvascular complications and/or hypertension. Clinical studies are needed to clarify the natural history of this disorder, focusing on the benefits of tight control of hyperglycemia and treatment of associated hypertension. Experimental studies will clarify the pathophysiology and contribute to improved therapy. The high prevalence of diabetes and hypertension in Blacks makes these considerations especially relevant to this population.
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PMID:Diabetic cardiomyopathy. 226 38

To elucidate the nature of lipid defects in patients with diabetes mellitus (DM) concurrent with acute myocardial infarction (MI), the study was undertaken to examine the serum concentrations of total cholesterol, triglycerides, alpha- and beta-lipoproteins with DM in the presence of acute MI. 40 non-diabetic patients with acute MI, 23 diabetics with postinfarct cardiosclerosis, and 17 non-insulin-dependent diabetics without signs of coronary atherosclerosis. Urinary epinephrine and norepinephrine excretion was additionally determined in the acute period and 3-4 weeks after therapy. Homogeneous lipid metabolic parameters were found in CHD patients with and without DM and when transient hyperglycemia developed. The patients with acute MI exhibited some increase in lipid consumption to satisfy the energy need for the cardiovascular system, this being true for triglycerides in DM patients. The DM patients who showed low triglyceride levels had more frequently transmural MI and MI complicated with heart failure. Obesity and familial histories of DM and CHD in DM patients with acute MI were ascertained to be accompanied by reduced serum alpha-lipoprotein concentrations.
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PMID:[The nature of changes in lipid metabolism in patients with diabetes mellitus associated with ischemic heart disease]. 227 41


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