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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The results of the catamnestic study of case reports and records of postmortem examination of 102 patients with bronchial asthma (BA) aged 47 to 88 years who died at a general hospital during 1976-1988 indicate that in the overwhelming majority of cases, there took place death "with asthma" rather than death "from asthma". At the same time the dominant pathology was coronary heart disease (acute coronary failure, myocardial infarction, progressive heart failure associated with atherosclerotic and postinfarction cardiosclerosis). Emphasis is laid on the fact that according to the autopsy data, the rate of the recognized stenosing atherosclerosis of the coronary arteries considerably exceeded the number of cases of coronary heart disease documented clinically (typical angina pectoris of effort, significant macrofocal myocardial infarction). The characteristic features of the group under observation included an unexpectedly frequent combination of BA and malignant neoplasms (24 cases), including lung cancer in 13 of these cases.
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PMID:[An analysis of the causes of death in bronchial asthma patients (based on the data from a 13-year prospective observation)]. 236 7

Calcium channel blocking drugs, or "calcium antagonists", have been increasingly used in the last decade, both as valuable cardiovascular drugs, and as tools to investigate the pharmacology of the calcium channels which play a vital role in the excitation-activation coupling of many excitable cells. Three important developments, "patch clamping" to investigate single calcium channels, ligand binding studies to investigate the calcium antagonist "receptor sites", and the introduction of novel calcium channel activators, or "calcium agonists", have recently led to greater understanding of the mechanism of action of drugs on the calcium channel. We show here how the calcium channel modulators interact with the binding sites to increase or decrease calcium flux, and hence to modulate the activity of many excitable tissues. We predict that these new developments will soon result in the isolation of purified calcium channels, and investigation of their subtypes and drug sensitivities. This information could lead to the introduction of novel, more selective calcium antagonists for a variety of indications such as atherosclerosis or neurological disorders. Of particular interest is the potential of tissue-selective calcium agonistic drugs to combat cardiac failure or endocrinological disorders.
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PMID:Modulation of calcium channel function by drugs. 241 32

1 The responses to substance P, isoprenaline and noradrenaline were observed on human isolated coronary arteries removed from 30 human hearts, and were classified according to the age of the hearts, the presence or absence of cardiac failure and the degree of atherosclerosis. 2 The endothelium-dependent vasodilator, substance P (0.1 microM), relaxed rings precontracted with prostaglandin F2 alpha, (PGF2 alpha, 1 microM) when they were devoid of atherosclerosis. The presence of moderate or severe lesions of atherosclerosis abolished this response. There was no difference in the response, related to either the age of the hearts or to the presence or absence of cardiac failure. 3 The dose-response curves to isoprenaline (an endothelium-independent vasodilator) were also markedly altered by the presence of atherosclerotic lesions, while aging and the presence of cardiac failure did not alter the maximal relaxation. These last 2 factors induced only a rightward shift of the dose-response curves. 4 On severely atherosclerotic rings, beta-adrenoceptor-mediated responses were so altered that the effect of noradrenaline was wholly vasoconstrictor (via alpha-adrenoceptors). This response was not modified after pretreatment with atenolol (10 microM). 5 It is concluded that atherosclerosis in human coronary arteries, induces alterations in the responses to substance P and to beta-adrenoceptor agonists. The beta-adrenoceptor-mediated relaxations seem more influenced by the presence of atherosclerosis than they are by aging or by the down-regulation induced by cardiac failure. Conversely, the alpha-adrenoceptor responses appear to be well preserved.
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PMID:The influence of atherosclerosis on the mechanical responses of human isolated coronary arteries to substance P, isoprenaline and noradrenaline. 244 99

Hypertension increases cardiovascular morbidity and mortality two- to fourfold. The chief hazards are now atherosclerosis and coronary disease. Risk is proportional to the degree of systolic or diastolic blood pressure elevation at any age, in either sex. More than the character of blood pressure elevation, commonly associated risk factors markedly influence the hazard. The risk of coronary heart disease is concentrated in hypertensive patients with a high total/high-density lipoprotein (HDL)-cholesterol ratio, impaired glucose tolerance, high fibrinogen, electrocardiographic (ECG) abnormalities, and who are cigarette smokers. Evidence of organ involvement such as left ventricular function are hallmarks of impending cardiovascular sequelae. Electrocardiogram-left ventricular hypertrophy (ECG-LVH) behaves like myocardial infarction in its clinical course, predisposing at the same rate to sudden death, infarction, cardiac failure, and stroke. Consideration of cardiovascular risk factors is required to evaluate properly the need for treatment, select the best treatment, set goals, and determine the efficacy of treatment. Awaiting evidence of organ involvement is dangerous since the first such evidence is often a sudden death, stroke, or myocardial infarction. Optimal treatment must improve the composite risk profile as well as lower the blood pressure.
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PMID:Risk factors in hypertension. 246 76

High blood pressure (BP) is associated with increased risk of vascular disease, including myocardial infarction and stroke. Since drugs that lower BP will reduce the risk of those complications of hypertension that are due to high pressure (strokes due to small-vessel disease, including lacunar infarction and intracerebral hemorrhage due to rupture of microaneurysms, heart failure, and renal failure), it has been assumed that such drugs would also reduce the risk of myocardial infarction due to atherosclerosis. However, in addition to hypertension, many other factors are involved in the atherosclerotic process including blood lipids such as cholesterol, blood platelets, and arterial flow disturbances such as turbulence and vortex formation. Some drugs that lower BP have unwanted effects on blood lipids and arterial flow patterns, which are thought to offset the benefit of BP reduction, whereas other drugs have beneficial effects on such factors. Ames has calculated that the adverse effects of antihypertensive drugs on lipids are enough to completely offset the benefit of treating mild hypertension. We have shown that antihypertensive drugs have different effects on blood velocity, and that these effects are associated with differences in the effects of drugs on arterial flow disturbances at the site of carotid stenosis in man, such that propranolol reduced, and hydralazine increased, the occurrence of abnormal high-velocity flow patterns associated with turbulence and vortex formation. In cholesterol-fed hypertensive rabbits (one-kidney Goldblatt), propranolol was more effective than hydralazine in preventing the occurrence of aortic atherosclerosis, even though hydralazine lowered blood pressure more effectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypertension and atherosclerosis: effects of antihypertensive drugs on arterial flow patterns. 248 Nov 60

In canine and porcine coronary arteries, experimental atherosclerosis (induced by endothelial denudation followed by a high-cholesterol diet) potentiates the vasoconstrictor effects of histamine, serotonin, and ergonovine. In isolated human atherosclerotic coronary arteries, only hypersensitivity to histamine has been demonstrated. This discrepancy could be due to several factors. First, the atherosclerotic lesions in human vessels are different from those observed in the animal, since experimental atherosclerosis often corresponds only to the early stage of the disease in humans. Second, the human atherosclerotic coronary arteries were isolated mainly from patients with cardiac failure, a condition that alters the responses of coronary smooth muscle to vasoactive amines. With regard to endothelium-dependent vasodilators, marked attenuations of the relaxations to substance P, bradykinin, and the Ca2+ ionophore A23187 have been described in isolated human atherosclerotic arteries. Acetylcholine elicits variable responses in these preparations and even if the arteries are devoid of atherosclerotic lesions, it often fails to relax them. In addition to this endothelial dysfunction, severely atherosclerotic human coronary vessels exhibit a slightly decreased responsiveness to nitroglycerin and SIN-1 but not to forskolin. Another abnormality of the smooth muscle is a marked attenuated beta-adrenergic relaxation. Thus, atherosclerosis of human coronary vessels induces not only marked alterations in endothelium-dependent responses but also modifies the sensitivity to several endothelium-independent vasodilators.
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PMID:Atherosclerosis and responses of human isolated coronary arteries to endothelium-dependent and -independent vasodilators. 248 97

Hypertension increases cardiovascular morbidity and mortality two to four-fold. The chief hazards are now atherosclerosis and coronary disease. The risk is proportional to the degree of systolic or diastolic blood pressure elevation at any age, in either sex. More than the character of the blood pressure elevation, commonly associated risk factors markedly influence the hazard. The risk of coronary heart disease is concentrated in hypertensives with a high total/high density lipoprotein (HDL) cholesterol ratio, impaired glucose tolerance, high fibrinogen, those with ECG abnormalities and cigarette smokers. Evidence of organ involvement such as left ventricular hypertrophy, proteinuria or impaired left ventricular function are hallmarks of impending cardiovascular sequelae. The presence of ECG-LVH behaves like myocardial infarction in its clinical course, predisposing at the same rate to sudden death, myocardial infarction, cardiac failure and stroke. Consideration of all cardiovascular risk factors is required to evaluate properly the need for treatment, select the best treatment, and set goals and determine the efficacy of treatment. Waiting until there is evidence of organ involvement is dangerous since the first such evidence is often sudden death, a stroke or a myocardial infarction. Optimal treatment must improve the composite risk profile as well as lower the blood pressure. This can be achieved by hygienic (dietary) measures or pharmacological therapy in those who do not respond to diet alteration, weight control and exercise.
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PMID:An integrated view of hypertension. 260 26

The recent discovery of endothelium-derived relaxation factor (EDRF) has altered the traditional classification of vasodilators used in angina pectoris and heart failure. If a vasodilator induces release of EDRF from the epithelium it is classified as endothelium-dependent, if not it is independent. Sodium nitroprusside and SIN-1 (active metabolite of molsidomine) are the main independent vasodilators since the endothelium relaxation factor appears to be principally a nitric oxide radical in these synthetic vasodilators. In contrast, calcium-channel blockers and a good number of endogenous chemical mediators (acetylcholine, bradykinin, serotonin, etc.) are endothelium-dependent. Furthermore, simple increase in blood flow through the large vessels can result in endothelium-dependent vasodilation (flow rate-dependence) the extent of which depends on the drug examined. The fact that the pharmacologic response of a vasodilator can be altered under certain pathologic conditions (atherosclerosis, hypertension, diabetes, etc.) further increases the importance of the role of the vascular endothelium in the action of vasodilators since endothelial modulation may then be completely diverted to secretion of endothelium-derived contracting factors (EDCFS).
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PMID:[Vasodilator agents and the vascular endothelium]. 262 13

Since our initial orthotopic heart transplant (OHT) in 1968, the first in Europe, 1130 patients with ages ranging from 1 month to 66 years have been referred to us. The cause of irreversible myocardial damage was idiopathic cardiomyopathy in 74%, ischemic heart disease in 19% and left ventricular failure after valvular replacement in 7%. A total of 540 transplantations, 463 orthotopic, 40 heterotopic and 37 heart-lungs were carried out. Features of the early post-operative course include temporary (first week) cardiac instability treated by isoproterenol. Later complications included rejection (95%) and side-effects of immunosuppressive therapy; infection (83%), osteoporosis, malignancy, graft atherosclerosis (2%). Cyclosporine (Cy) was responsible for diastolic hypertension, renal dysfunction, hirsutism, hyperplasia of the gingiva, hepatic dysfunction, and seizures. The survival rate of the Cy-treated patients was 68% at 7 years. All survivors have virtually normal social and professional lives, included the longest survivor 14 years after the operation. Recently in 34 patients in acute irreversible cardiac failure and who cannot have a transplant in time, we implant a total artificial heart (TAH) type JARVIK 7 during a period from 1-150 days. There has been no mechanical failure, hemolysis or thrombo-embolism and only one right ventricular device malposition; 20 patients died before transplantation, 13 were successfully transplanted, 1 is still on the artificial heart. Heart transplantation, and TAH used as a bridge to transplantation are now an accepted therapeutic means for irreversibly cardiac failure in selected patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Current problems in cardiac transplantation. 266 Sep 20

Coronary vascular disease in the cardiac transplant recipient has become the third most frequent cause of death or retransplantation after infection and acute rejection. A unique pattern of concentric fibrointimal thickening develops within 1 year of cardiac transplantation; however, it is relatively inapparent on routine arteriography. The disease progresses primarily in distal vasculature, leading to progressive occlusion. Angiographically discrete lesions associated microscopically with advanced atherosclerotic plaques frequently occur in the more proximal vessels often associated with thrombus. The number of rejection episodes is somewhat predictive of the development of transplant coronary disease. Annual arteriograms performed in cardiac transplant recipients have revealed several distinctive angiographic features that include clockwise rotation of the heart, presence of coronary arterial-cameral fistulae, presumably resulting from right ventricular endomyocardial biopsy specimens and collateralization of the brachial anastomosis from coronary atrial branches. It is concluded that serial angiography in cardiac transplant recipients is important in the early detection of progressive graft atherosclerosis, a process that is clinically silent until such time as overt heart failure or cardiogenic shock occurs.
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PMID:Angiographic implications of cardiac transplantation. 267 63


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