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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A review summarizing recent findings on the causes of the development, pathogenesis, diagnosis and treatment of acute cardiac failure. It is a condition when the heart is unable to pump blood in amounts needed for the metabolic activity of tissues. It may be the first manifestation of disease or acute deterioration of chronic heart failure. The most frequent causes of acute left-sided failure include acute myocardial infarction, arterial hypertension, valvular defects, myocarditis, toxic damage or metabolic myocardial disorders. In right-sided failure pulmonary embolism, extensive affections of the lungs and pleura, right ventricular infarction and affection of the pericardium predominate. The clinical picture of cardiac failure is due to a combination fo the basic disease, evoking causes, signs of an inadequate minute volume, transudation of fluids into the interstitium and the presence of compensating mechanisms. The diagnosis of cardiac failure is based on an analysis of subjective and objective clinical symptoms and other auxiliary examinations such as X-ray examination of the chest, electrocardiogram, echocardiography, examination of blood gases and other laboratory examinations. In right-sided insufficiency the examination is supplemented by pulmonary scintigraphy, possibly by catheterization of the right heart and pulmonary angiography. As to the differential diagnosis, we must differentiate from acute cardiac failure, asthma bronchiale, spontaneous pneumothorax, dyspnoea in neuroasthenic patients, non-cardiac pulmonary oedema. Treatment of cardiac failure involves lifestyle and dietary provisions, medicamentous treatment which has undergone great changes in recent years. Cardiac failure is controlled by reduction of the cardiac filling pressure and support of the efficiency of the cardiac pump (Inotropy) and control of excessive fluid and salt retention. Decisive for the subsequent development of the disease is diagnosis of the basic cardiac or non-cardiac disease and its aimed treatment. In uncontrolled cardiac failure mechanical support of cardiac activity and transplantation of the heart are options.
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PMID:[Clinical aspects of acute heart failure]. 892 24

The management of unexplained syncope begins with the patient's history and physical examination, which are oriented to help separate benign from serious causes. Malignant etiologies are more likely to occur with exertional syncope. Cardiac causes should be considered, particularly cardiomyopathy, postoperative congenital heart disease, right ventricular dysplasia, anomalous coronary artery, pulmonary artery hypertension, myocarditis, long QT syndrome, and Wolff-Parkinson-White syndrome. Neurological and metabolic disorders may underlie a syncope episode. After malignant causes of syncope have been excluded and the diagnosis of neurocardiac syncope has been established, treatment strategies include behavior modification, salt and increased fluids, and pharmacological agents. Efficacious agents include beta-blockers, dysopyramide, fludrocortisones, and alpha agents. Yet, behavior modification alone may be as effective as salt or pharmacological therapy. Because the natural history of neurocardiac syncope in children is spontaneous resolution, it is appropriate to try the simple measures before introducing drug therapy.
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PMID:Unexplained syncope: clinical management. 927 5

Angiotensin II (Ang II), the effector peptide of the renin-angiotensin system (RAS), regulates volume and electrolyte homeostasis and is involved in cardiac and vascular cellular growth in humans and other species. This system, which has been conserved throughout evolution, plays an important role in cardiac and vascular pathology associated with hypertension, coronary heart disease, myocarditis and congestive heart failure. The traditional RAS is viewed as a system in which circulating Ang II is delivered to target organs and cells. However, in the past decade, a local RAS has been described in cardiac cells, providing evidence for autocrine and paracrine pathways by which biological actions of Ang II could be mediated. The critical actions of Ang II are mediated primarily through the AT1, G-protein (guanylyl nucleotide binding protein) coupled receptor. In addition to coupling to conventional G-protein signal transduction pathways, the AT1 receptor was recently shown to increase the tyrosine phosphorylation of several intracellular substrates, including the STAT (Signal Transducers and Activators of Transcription) family of novel transcription factors, in rat cardiac fibroblasts, myocytes and vascular smooth muscle cells, and AT1 receptor transfected CHO cells. It has been shown that Ang II stimulates the tyrosine phosphorylation and nuclear translocation of Stat1 (Stat 91) and Stat3 (Stat 92). Angiotensin II acting directly through the AT1 receptor, induces the formation of a complex of STAT proteins termed SIF (sis-inducing factor) which binds the DNA sequence, SIE (sis-inducing element) present in the promotor element of many genes. This provides evidence for a direct role of Ang II in mediating inflammatory and remodeling responses through the JAK-STAT pathway. Thus, it is likely that the JAK-STAT pathway has an important role in Ang II-mediated effects on gene transcription, cardiac and vascular cellular growth/development, and inflammatory responses.
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PMID:Molecular mechanisms of angiotensin II in modulating cardiac function: intracardiac effects and signal transduction pathways. 940 64

Sudden cardiac death is the leading cause of death in industrialized countries. It is most frequently due to ventricular tachyarrhythmias occurring in the presence of coronary heart disease, but mechanisms linking sudden death to coronary atherosclerosis are still unclear. In autopsy studies of sudden death patients, the incidence of acute thrombotic coronary occlusions has varied between 4 and 74%. In over 600 consecutive patients with implantable cardioverter-defibrillators, we observed that appropriate shocks for electrogram-verified ventricular tachyarrhythmias was only very rarely followed by signs of acute myocardial infarction (< 3% of cases), not supporting the coronary occlusion theory of fatal arrhythmias. Cellular hypertrophy compensating for cell loss due to ischemia, intraventricular hypertension, cardiomyopathy, and myocarditis might play a role in arrhythmogenesis as evidenced by the fact that experimental induction and regression of hypertrophy are paralleled by changes in the inducibility of ventricular tachyarrhythmias. Atherogenic hyperlipidemias are associated with a systemic inflammatory response manifested by leukocytosis (lymphocytosis) and complex upregulations of proinflammatory-prothrombotic mediators, such as platelet-activating factor, cytokines, and hemostasis factors. The diurnal regulation of these mediators parallels circadian rhythms of coronary morbidity and mortality. Some upregulated mediators have been shown to exert direct arrhythmogenic effects. The potential contribution of hyperlipidemia-associated inflammatory factors to arrhythmogenesis is important, because it opens new molecular targets for antiarrhythmic drug design.
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PMID:Sudden cardiac death: still more questions than answers. 947 68

Numerous analyses are used in the differential diagnosis between primary and secondary dilated cardiomyopathy (PDC, SDC). The aim of this study was to assess the dimensions of heart cavities in patients with dilated cardiomyopathy (DC) by 1-D and 2-D echocardiography. Thirty-six consecutive patients who satisfied the PDC criteria, and 103 patients with criteria of SDC, were followed-up clinically, radiographically, electrocardiographically and by 1-D and 2-D echocardiography, in the period from December 1991 to April 1994, at the Department of Internal Medicine of the Clinical Hospital Split. The patients with PDC were significantly younger than those with SDC (44.4 +/- 10.4: 64.4 +/- 8.4 year). There were significantly more males than females in both DC subgroups. NYHA classification, sinus rhythm and atrial fibrillation did not differ considerably in both DC subcategories. The etiologic factor was ischaemic DC in 85.4% (88/103), systemic arterial hypertension in 11.6% (12/103), and thyrotoxicosis in 2.9% (3/103) of patients with SDC. Alcoholic DC in one patient, peripartal DC in two female patients and viral myocarditis in six patients with PDC were suspected. In the total of 75% (27/36) patients with PDC, a clear etiological factor in case histories was not defined. Left ventricular ejection fraction, diameter and myocardial thickness, as well as left atrium diameter, did not differ significantly in patients with PDC, at variance with SDC patients. Right ventricular enddiastolic diameter (31.55 +/- 4.8 mm: 26.62 +/- 8.6 mm, p < 0.05) and the ratio between enddiastolic diameters of the right and left ventricle were significantly larger in patients with PDC than in those with SDC (0.45 +/- 0.03: 0.37 +/- 0.05, p < 0.05). We conclude that right ventricle is significantly wider in PDC than in SDC patients. Compared with other noninvasive methods, 1-D and 2-D echocardiography is probably the method of choice (particularly in our environment) in the differentiation of primary and secondary DC.
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PMID:[Significance of right ventricular dimensions in the differential diagnosis of primary and secondary dilated cardiomyopathy]. 949 Mar 76

The mechanisms by which increased mortality and morbidity occur in individuals with preexistent cardiopulmonary disease following acute episodes of air pollution are unknown. Studies involving air pollution effects on animal models of human cardiopulmonary diseases are both infrequent and difficult to interpret. Such models are, however, extensively used in studies of disease pathogenesis. Primarily they comprise those developed by genetic, pharmacologic, or surgical manipulations of the cardiopulmonary system. This review attempts a comprehensive description of rodent cardiopulmonary disease models in the context of their potential application to susceptibility studies of air pollutants regardless of whether the models have been previously used for such studies. The pulmonary disease models include bronchitis, emphysema, asthma/allergy, chronic obstructive pulmonary disease, interstitial fibrosis, and infection. The models of systemic hypertension and congestive heart failure include: those derived by genetics (spontaneously hypertensive, Dahl S. renin transgenic, and other rodent models); congestive heart failure models derived by surgical manipulations; viral myocarditis; and cardiomyopathy induced by adriamycin. The characteristic pathogenic features critical to understanding the susceptibility to inhaled toxicants are described. It is anticipated that this review will provide a ready reference for the selection of appropriate rodent models of cardiopulmonary diseases and identify not only their pathobiologic similarities and/or differences to humans but also their potential usefulness in susceptibility studies.
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PMID:Rodent models of cardiopulmonary disease: their potential applicability in studies of air pollutant susceptibility. 953 9

Angiotensin converting enzyme inhibitors (ACE) have become an important part in the pharmacotherapy of hypertension, in this indication they were used for the first time in the eighties. Later the indication was extended to heart failure (where they evidently reduce the mortality), acute myocardial infarction (there they prevent cardiac remodelling), and in myocarditis (vasodilatation, effect on spasms and on free oxygen radicals). As to non-cardiological indications the most important indications are nephrological-diabetic and non-diabetic nephropathies. Nowadays already different types of ACE inhibitors are available. They differ as to their chemical structure (they contain a sulphydryl or carboxyl group in the molecule, they are proline derivatives etc.) as well as by other properties (lipophilia, specificity, absorption rate, period of action). The authors gives a list of preparations encountered most frequently on our market and they discuss non obvious indications.
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PMID:[Angiotensin-converting enzyme inhibitors. Familiar drugs--new indications]. 958 98

A 25-year-old woman was admitted to our center for left heart failure. The clinical, electrocardiographic and bioptic findings suggested an acute lymphocytic myocarditis. One month later, paroxysmal hypertension and high urinary excretion of noradrenaline revealed the presence of a pheochromocytoma.
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PMID:An unusual case of myocarditis. 974 Apr 90

Autopsy findings of 10 patients with Takayasu arteritis (TA) are presented. These patients include six females and four males with a mean age of 22.6+/-10.2 years. Hypertension was the commonest mode of presentation. On autopsy, the vascular lesions in the aorta comprised of stenosis (eight), dilatation (six), aneurysm (two) and dissection of aorta involving its arch, thoracic and abdominal aorta (one). Abdominal aorta was the commonest site of involvement (nine patients) and renal artery was involved in six patients. Histologically, the three types of lesions were identified--active, fibrotic and combination of active and fibrotic lesions. Active inflammatory lesions in the arterial circuit were present despite a clinically chronic (silent) phase of the disease. Cardiac involvement included left ventricular hypertrophy (nine), right ventricular hypertrophy (four), biventricular hypertrophy (three), myocarditis (two) (rheumatic and Takayasu's myocarditis--one patient each) and involvement of coronary artery (one). The pulmonary artery was involved in two patients. Kidneys showed changes of malignant hypertension and benign nephrosclerosis in one patient each. Associated tuberculosis was present in four patients. The causes of mortality were congestive heart failure (four), chronic renal failure (two), intracranial bleed, aneurysmal rupture and pulmonary thromboembolism in one patient each. Thus, the major causes of morbidity and mortality in Indian patients with TA is due to severe uncontrolled hypertension and its effect on heart, kidney and brain. The disease appears to have a persistent activity for a prolonged period even when it appears to be clinically silent.
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PMID:An autopsy study of Takayasu arteritis in India. 995 7

Abnormalities of the microvasculature are centrally involved in the pathogenesis of some forms of heart disease, but in others are consequences of it. Microvascular abnormalities may contribute to the progression of viral myocarditis and Chagas' disease. Focal abnormalities may occur early in some cardiomyopathies and do occur later in most types of myocarditis. The thickening of arteriolar walls in chronic hypertension is likely to contribute significantly to the impairment of coronary haemodynamics associated with adaptive ventricular hypertrophy and the consequent diminution of coronary reserve, increasing diffusion distances and failure of angiogenesis to compensate. However, the resulting myocyte necrosis stimulates inflammatory angiogenesis. When ischemic myocyte injury becomes irreversible there is a concomitant loss of capacity for reperfusion, the no-reflow phenomenon. Less severe temporary ischemia reduces the proportion of functional capillaries. Multiple mechanisms are involved in this microvascular stunning, including: reperfusion injury; leukocyte activation; adhesion and accumulation; and impaired endothelium-dependent vasodilation. Many of the microvascular changes are those of the inflammatory response to cell death and form part of a final common pathway in myocarditis, cardiomyopathy, cardiac hypertrophy and failure, and ischemic heart disease. Stimulation of angiogenesis prior to myocyte necrosis in hypertrophy and control of leukocyte activity in ischemic heart disease could minimize myocyte loss.
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PMID:Microvascular involvement in cardiac pathology. 999 May 24


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