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

The impact of nonrheumatic atrial fibrillation, hypertension, coronary heart disease, and cardiac failure on stroke incidence was examined in 5,070 participants in the Framingham Study after 34 years of follow-up. Compared with subjects free of these conditions, the age-adjusted incidence of stroke was more than doubled in the presence of coronary heart disease (p less than 0.001) and more than trebled in the presence of hypertension (p less than 0.001). There was a more than fourfold excess of stroke in subjects with cardiac failure (p less than 0.001) and a near fivefold excess when atrial fibrillation was present (p less than 0.001). In persons with coronary heart disease or cardiac failure, atrial fibrillation doubled the stroke risk in men and trebled the risk in women. With increasing age the effects of hypertension, coronary heart disease, and cardiac failure on the risk of stroke became progressively weaker (p less than 0.05). Advancing age, however, did not reduce the significant impact of atrial fibrillation. For persons aged 80-89 years, atrial fibrillation was the sole cardiovascular condition to exert an independent effect on stroke incidence (p less than 0.001). The attributable risk of stroke for all cardiovascular contributors decreased with age except for atrial fibrillation, for which the attributable risk increased significantly (p less than 0.01), rising from 1.5% for those aged 50-59 years to 23.5% for those aged 80-89 years. While these findings highlight the impact of each cardiovascular condition on the risk of stroke, the data suggest that the elderly are particularly vulnerable to stroke when atrial fibrillation is present.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial fibrillation as an independent risk factor for stroke: the Framingham Study. 186 65

A total of 85 patients (68 with coronary heart disease in the presence of effort angina of various functional classes (a major group) and 17 with neurocirculatory++ dystonia and cardialgic syndrome (a control group)) were examined. Heart failure severity and blood flow distribution in the functioning myocardial areas were evaluated in transient ischemia induced by atrial pacing. Three levels of coronary venous blood flow were defined in patients with coronary heart disease. A relationship between the coronary blood flow, disease history duration, and coronary blood flow changes was examined in cardioselective exercise.
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PMID:[Status of coronary venous blood flow in patients with ischemic heart disease in myocardial ischemia induced by the atrial stimulation test]. 189 38

Since 1980 cardiac manifestations of Lyme borreliosis have been described as selflimited conduction and transient left ventricular disorders or even cardiomegaly. An etiologic role of Borrelia burgdorferi in long-standing chronic heart disturbances is suggested by the cultivation of a strain of Borrelia burgdorferi which we were able to isolate from an endomyocardial biopsy of a patient with long-standing dilated cardiomyopathy. The aim of this study was to acquire information about the prevalence of serum antibodies to Borrelia burgdorferi in patients with dilated cardiomyopathy. By ELISA, we studied the sera of 72 consecutive patients with chronic heart failure due to dilated cardiomyopathy, of 55 patients with coronary heart disease, and of 61 healthy blood donors; positive ELISA values were determined in 26.4%, 12.7%, and 8.2% of serum samples, respectively. These findings further suggest an association or even an etiologic role for Borrelia burgdorferi in dilated cardiomyopathy.
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PMID:Borrelia burgdorferi as an etiologic agent in chronic heart failure? 194 16

Cardiac insufficiency, coronary heart disease, and arrhythmia are not only more frequent in elderly patients, they are very often combined. By reason of cardiac morbidity and general morbidity as well as changed physiological and pathophysiological conditions, diagnosis of cardiac disease in elderly patients is more difficult. These conditions also apply to modifications in the therapy of cardiac diseases in advanced age. Especially pharmacodynamic and pharmacokinetic effects in advanced age combined with multimorbidity also account for the risk of interactions because of the simultaneous application of different pharmacological groups.
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PMID:[Characteristics of therapy of heart diseases in old age]. 195 82

More and more patients with coronary heart disease (CAD) are admitted to intensive care units. The drugs used to treat these patients have various effects on the myocardium which must be known in order to avoid worsening the CAD. This review examines the metabolic effects on the myocardium of the most commonly used drugs in intensive care. The physiology of myocardial oxygen supply is first recalled with regard to the coronary circulation, myocardial oxygen extraction and consumption. Digitalis glycosides do not affect the coronary circulation, but the decrease myocardial oxygen consumption in patients with heart failure, mainly by lowering heart rate. Dihydropyridine calcium blockers (nifedipine, nicardipine) increase coronary blood flow, despite a decrease in arterial blood pressure. Their effects on myocardial oxygen consumption are mediated by a sympathetic reflex. Verapamil decreases the heart rate and myocardial inotropism, and is responsible for coronary vasodilation. The result is a decrease in myocardial oxygen consumption. Diltiazem and bepridil have almost similar effects: they decrease myocardial oxygen consumption and increase blood supply to the heart. It has been recently shown that verapamil was the most depressant calcium channel blocking agent, and that it resulted in the most important decrease in myocardial metabolism. Beta-blocking agents decrease myocardial metabolism, except those with an important intrinsic sympathomimetic activity, such as pindolol. Amiodarone can be considered as an alpha and beta blocking drug: its main effect is to counteract the effects of endogenous catecholamines on myocardial metabolism. The sympathomimetic amines (noradrenaline, adrenaline, isoprenaline, dopamine, dobutamine) increase, to different extents, myocardial oxygen consumption. Vasodilators, such as the nitrates or sodium nitroprusside, decrease cardiac filling pressures, and increase myocardial blood flow, thus lowering myocardial oxygen consumption. Phosphodiesterase inhibitors (amrinone, enoximone) have both an inotropic and a vasodilating effect. They decrease cardiac afterload, and increase blood supply to the myocardium; this compensates for the increase in myocardial oxygen consumption due to the increase in myocardial contractility. Because all the drugs used in intensive care have different effects on myocardial metabolism, their reasoned use should avoid an inappropriate increase in oxygen demand.
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PMID:[Changes in myocardial metabolism induced by drugs used during intensive care]. 197 Apr 63

A study was made of the effect of ethacizine administered in a single dose and continuously on myocardial contractility and hemodynamics in 78 patients with coronary heart disease, neurocirculatory dystonia and myocardiodystrophy suffering from impaired cardiac rhythm. In 28 patients, ethacizine was administered in combination with glutamic acid and in 23 with digoxin. In patients with coronary heart disease, particularly in those with heart failure, ethacizine produced a negative inotropic effect. Introduction into the treatment of digoxin or glutamic acid smoothed over the cardiodepressive action of the drug. When administered continuously in a dose of 150-300 mg/day, ethacizine is an effective antiarrhythmic drug.
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PMID:[The characteristics of the action of ethacizine and its combination with digoxin and glutamic acid on the hemodynamic indices and myocardial contractile capacity in patients with a heart rhythm disorder]. 198 Jul 53

The bulk of the mortality (60%) in hypertension occurs in those with mild to moderate elevations of blood pressure, and the chief hazard is coronary disease. Although progression in the severity of hypertension has been slowed with drug therapy, the benefits for coronary outcome and all-cause mortality have been equivocal. Only a 10% reduction in coronary heart disease morbidity and mortality has been shown, an improvement that is not only small, but is statistically insignificant. Only vascular events such as renal failure, stroke, aortic dissection and cardiac failure have been reduced by antihypertensive therapy. Recent trials comparing beta-blockers with other antihypertensive drugs have failed to show the expected promise based on their effectiveness following a myocardial infarction. However, two large trials suggest that they may be effective against coronary heart disease in male non-smokers. A number of possible reasons for this therapeutic failure to reduce coronary heart disease have been postulated. The trials may have been too short to significantly affect the atherosclerotic progression. Also, sample sizes were too small to detect a sizeable reduction in coronary heart disease events. Furthermore, no attention was paid to improvements in the coronary heart disease risk profile, since drugs currently in use are known to have adverse effects on blood lipids, glucose tolerance and uric acid. It is even possible that a predisposition to sudden death is associated with antihypertensive therapy. The trials suggest that in attempts to prevent coronary heart disease, control of smoking and of serum lipids are particularly important in hypertensive persons and may be more effective than controlling the blood pressure alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Implications of the primary prevention trials against coronary heart disease. 198 70

Combinations of beta-adrenoreceptor blocking agents and vasodilators have been widely used because of their favorable hemodynamic actions and their high efficacy. In comparison with the free combination of the two active principles, substances that combine vasodilation and beta-blockade in a single molecule may lead to a simplification of therapy and thus to an improvement in compliance. Substances that show clear beta-blocking and vasodilating actions at therapeutic doses have already been introduced to therapy or are in an advanced stage of clinical development. The vasodilating action of amosulalol, carvedilol and labetalol is achieved by blockade of the alpha 1-receptors. In contrast, partial agonistic action on beta 2-receptors is responsible for the vasodilatation with dilevalol. This mechanism probably also plays an important role in the vasodilatation induced by celiprolol. While classical beta-blocker lead to a rise in peripheral resistance and to a marked fall in cardiac output, peripheral resistance falls during treatment with vasodilating beta-blockers. The cardiac output is either only slightly reduced or virtually unchanged. Surprisingly, three months' treatment with the vasodilating beta-blocker bucindolol in patients with severe heart failure led to a rise in cardiac output and in ejection fraction and to a reduction of the heart rate and pulmonary wedge pressure. An improvement of left-ventricular function was also obtained on administration of carvedilol in patients with coronary heart disease. Theoretically, it is conceivable that substances with additional alpha 1-blocking actions, such as labetalol, carvediolol or amosulalol, or with partial agonistic activity such as celiprolol or dilevalol, would have a clearly more favourable effect on the blood lipid profile than the classical beta-blocking agents. Initial results appear to confirm this, but final conclusions will only be possible when the results of prospective comparative studies are available.
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PMID:Experimental and clinical pharmacology of carvedilol and other drugs combining vasodilation and beta-adrenoceptor antagonism in a single molecule. 198 54

Analysis of 34 years of follow-up of Framingham Study data provides clinically relevant insights into the prevalence, incidence, secular trends, prognosis, and modifiable risk factors for the occurrence of heart failure in a general population sample. Heart failure was found to be highly prevalent, affecting about 1% of persons in their 50s and rising progressively with age to afflict 10% of persons in their 80s. The annual incidence also increased with age, from about 0.2% in persons 45 to 54 years, to 4.0% in men 85 to 94 years, with the incidence approximately doubling with each decade of age. Women lagged slightly behind men in incidence at all ages. Male predominance was because of a higher rate of coronary heart disease, which confers a fourfold increased risk of heart failure. Heart failure, once manifest, was highly lethal, with 37% of men and 33% of women dying within 2 years of diagnosis. The 6-year mortality rate was 82% for men and 67% for women, which corresponded to a death rate fourfold to eightfold greater than that of the general population of the same age. Sudden death was a common mode of exitus and accounted for 28% of the cardiovascular deaths in men and 14% in women with heart failure. Hypertension and coronary disease were the predominant causes for heart failure and accounted for more than 80% of all clinical events. Factors reflecting deteriorating cardiac function were associated with a substantial increase in risk of overt heart failure. These include low vital capacity, sinus tachycardia, and ECG evidence of left ventricular hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Epidemiology of heart failure. 200 Jul 73

A health risk appraisal function has been developed for the prediction of stroke using the Framingham Study cohort. The stroke risk factors included in the profile are age, systolic blood pressure, the use of antihypertensive therapy, diabetes mellitus, cigarette smoking, prior cardiovascular disease (coronary heart disease, cardiac failure, or intermittent claudication), atrial fibrillation, and left ventricular hypertrophy by electrocardiogram. Based on 472 stroke events occurring during 10 years' follow-up from biennial examinations 9 and 14, stroke probabilities were computed using the Cox proportional hazards model for each sex based on a point system. On the basis of the risk factors in the profile, which can be readily determined on routine physical examination in a physician's office, stroke risk can be estimated. An individual's risk can be related to the average risk of stroke for persons of the same age and sex. The information that one's risk of stroke is several times higher than average may provide the impetus for risk factor modification. It may also help to identify persons at substantially increased stroke risk resulting from borderline levels of multiple risk factors such as those with mild or borderline hypertension and facilitate multifactorial risk factor modification.
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PMID:Probability of stroke: a risk profile from the Framingham Study. 200 1


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