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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 treatment of heart failure ACE inhibitors gained a unique position because of their beneficial effect on prognosis. The most likely explanation is their influence on factors that determine progression of the disease. These are: progressive deterioration of central hemodynamics, impairment of coronary perfusion, further activation of vasopressor systems, imbalance of sodium and water homeostasis and occurrence of malignant arrhythmias. ACE inhibitors have been shown to modulate these factors in a positive manner. In addition, they may also act by modulating factors, which may exert harmful effects on cardiac function in long term. These are: prevention and regression of the hypertrophy of the left ventricle as well as the media of resistance vessels, prevention of restenosis following PTCA, prevention of cyclosporin-induced premature coronary artery sclerosis, and correction of an impaired glucose metabolism. Whereas the positive effects of ACE inhibitors in the treatment of heart failure are well documented, their value for preventing heart failure has not been established, yet.
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PMID:[ACE inhibition: mechanisms of cardioprotection in chronic heart failure]. 186 32

Optimal metabolic control during the first twelve hours after myocardial infarction may be associated with improved survival in diabetic subjects. A comparison of an intravenous insulin infusion regimen aimed at improving blood glucose levels (n = 35), with 'routine control' (n = 34) in the post infarction period has been carried out in diabetic subjects admitted to four Coronary Care Units over a two year period. However, glycaemic control was similar in both groups (intravenous infusion regimen, mean +/- SD capillary blood glucose 10.3 +/- 2.1 mmol/l, 'routine control' glucose 10.7 +/- 3.6 mmol/l). There were no differences in the rates of arrhythmias (31% v 32%), heart failure (46% v 47%) or mortality (17% v 18%). Mortality in diabetic subjects was lower than that quoted in previous studies but was higher than in non-diabetic subjects admitted to the Coronary Care Unit during the same period. Attempts to improve glycaemic control by means of intravenous insulin infusion were unsuccessful.
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PMID:Metabolic control in diabetic subjects following myocardial infarction: difficulties in improving blood glucose levels by intravenous insulin infusion. 192 6

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

Risk of cardiovascular events was determined over 24 years of surveillance in relation to general adiposity reflected by relative weight and by regional obesity estimated by skinfolds and waist girth per inch of height. Upper quintile values of relative weight, subscapular skinfolds and waist girth were each associated with increased risks of cardiovascular disease in both sexes. Risk of total cardiovascular events increased with the degree of regional, central or abdominal obesity. Mortality from cardiovascular disease was also increased. Increased relative weight and central obesity were both associated with increased risk factors including cholesterol, blood pressure, glucose and uric acid. Changes in weight were mirrored by changes in risk factors with linear trends over a 15 lb range of weight fluctuations. Subscapular skinfold and the ratio of subscapular-to-triceps skinfold, measures of central obesity, were in either sex also associated with an increased probability of coronary attacks in particular. The subscapular skinfold contributed to CHD risk independent of body mass index (BMI). Multivariate analyses taking all the risk factors into account indicate an independent effect of abdominal obesity on stroke, cardiac failure and cardiovascular and all-cause mortality in men. In women, only the subscapular-to-triceps skinfold ratio independently contributes to CHD, cardiovascular and all cause mortality. Regional obesity appears to be an independent contributor to cardiovascular disease at a given level of general adiposity, its effect only partially mediated through promotion of other known risk factors. These data suggest that cardiovascular disease is as closely linked to abdominal as to general adiposity.
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PMID:Regional obesity and risk of cardiovascular disease; the Framingham Study. 199 75

The percentage of persons in the United States over age 65--especially over 85--is increasing more rapidly than other age groups. Two thirds of people over age 65 have blood pressure higher than 140 mm Hg systolic or 90 mm Hg diastolic. Isolated systolic hypertension (systolic blood pressure greater than 160 mm Hg with diastolic blood pressure less than 90 mm Hg) is also highly prevalent. In a number of clinical trials, treatment of diastolic hypertension in the elderly has been shown to be beneficial, although the value of treatment of isolated systolic hypertension is not yet established. The benefit of antihypertensive therapy on the incidence of stroke and heart failure has been clearly established, but prevention of the atherosclerotic complications of high blood pressure (sudden death or myocardial infarction, for example) has not been convincingly demonstrated. Since clinical trials designed to investigate this atherosclerotic complication of hypertension have relied on stepped-care regimens (diuretics and beta blockers), the question arises whether the use of different drugs might have a better effect on prevention of myocardial infarction. The basis for this supposition includes the known adverse effects of diuretics and beta blockers on electrolytes, lipid metabolism, glucose metabolism, insulin resistance, and quality of life. Hypertension treatment in the 1990s will focus on the mechanisms by which blood pressure is lowered by various antihypertensive agents, as well as individualization of drug therapy based on coexisting diseases and conditions. Emphasis will be placed on use of monotherapy whenever possible; diuretics in low doses will probably be used more frequently for second-line therapy. In recognition of their lack of adverse lipid effects and their tolerability, first-line therapy with alpha blockers, angiotensin-converting enzyme inhibitors, and calcium antagonists will become increasingly common. The goal of antihypertensive therapy will be to extend the life expectancy of hypertensive patients to that of subjects without high blood pressure; hopefully, these new treatment approaches will bring us closer to that goal.
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PMID:Epidemiology and evaluation: steps toward hypertension treatment in the 1990s. 201 54

More than the character of the blood pressure elevation, the cardiovascular risk profile should be the prognostic guide for antihypertensive therapeutic decision-making. Hypertension tends to occur in association with other risk factors which augment the risk and need to be considered in evaluating the hazard of hypertension, the urgency for treatment, and the choice of treatment. Elevated blood pressure is often accompanied by blood lipid abnormality, obesity, electrocardiograph (ECG) abnormality, glucose intolerance, and elevated fibrinogen and hematocrit, all of which enhance the risk of cardiovascular sequelae of hypertension. Hypertensive patients at particularly increased risk of cardiovascular events are those with an increased total/HDL-cholesterol ratio, ECG abnormality, impaired glucose tolerance, or the cigarette smoking habit. The risk of a cardiovascular event among hypertensive patients varies over more than a 10-fold range depending on the number of these coexistent risk factors. Multivariate risk formulations are available to allow a composite estimate of the joint conditional probability of a cardiovascular outcome in hypertensive patients with multiple risk factors. Since some antihypertensive agents can adversely affect blood lipids, glucose tolerance, or uric acid values, the risk profile must also be taken into account in choosing the optimal antihypertensive therapy. Also, hypertension is commonly associated with angina, myocardial infarction, left ventricular hypertrophy, stroke, or cardiac failure. These too must be taken under consideration in judging the urgency for treatment and the choice of agents. Thus, hypertension is best regarded as a component of a cardiovascular risk profile in implementing optimal therapy and in assessing its efficacy.
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PMID:The clinical heterogeneity of hypertension. 204 9

A prospective study was carried out to investigate the effects of the ACE inhibitor captopril on glucose tolerance in 14 elderly patients, aged 76 to 89 years, who had co-incident cardiac failure and stable Type II diabetes mellitus. Patients were maintained on their diet and diabetic therapy and were given 12.5 mg captopril twice daily. Clinical findings, including signs of cardiac failure, body weight and blood pressure, biochemical profile and chest X-ray appearance were documented at each visit. Blood glucose tolerance testing was carried out immediately before starting captopril and again 28 days later. A reduction in symptoms of heart failure occurred in all patients and 5 of them reduced their New York Heart Association grade of heart failure. Significant improvement in glucose tolerance occurred in all patients. Four were able to reduce hypoglycaemic therapy and 1 was able to stop his hypoglycaemic agents. This potentially valuable additional benefit of captopril in improving glucose tolerance has not yet been shown to occur with other ACE inhibitors.
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PMID:Effects of captopril on glucose tolerance in elderly patients with congestive cardiac failure. 204 97

A small-for-date infant presented at birth with severe non-immune hydrops, cardiac failure, metabolic acidosis and hypoglycaemia. Ultrasonography disclosed a cardiomyopathy. Initial therapy consisting of artificial ventilation, inotropes and diuretics resulted in partial disappearance of oedema without significant improvement in cardiac function. Episodes of hypoglycaemia recurred despite continuous glucose infusions. Total serum carnitine from cord blood was 1.65 nmoles/ml and was undetectable on day 20. Oral DL-carnitine supplements resulted in normoglycaemia, dramatic improvement in cardiac function and restoration of serum carnitine levels to normal values. The infant was thereafter maintained on carnitine therapy. Follow-up over 1 year showed moderate growth retardation and normal developmental milestones. In order to account for such a severe neonatal presentation of carnitine deficiency, a combination of defective pre- and postnatal carnitine supply with an inborn error of carnitine handling is considered. The present case illustrates the need for evaluation of carnitine status in fetuses and neonates presenting with hydrops associated with cardiac failure.
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PMID:Carnitine deficiency with cardiomyopathy presenting as neonatal hydrops: successful response to carnitine therapy. 210 50

In previous studies, a pharmacological dose of human atrial natriuretic peptide (hANP) was found to increase serum insulin without influencing C-peptide levels. To examine whether blood glucose and insulin response to an oral or i.v. glucose load are influenced by raising hANP levels into the pathophysiological range, eight healthy, normal-weighted, male volunteers were studied. According to a randomized, double-blind study design, an oral glucose tolerance test (ogtt, 75 g) or an i.v. glucose tolerance test (ivgtt, 0.5 g/kg b.w.) were carried out. Beginning 30 minutes before glucose administration infusions of hANP 0.3 micrograms/min) or placebo were given for 180 minutes (ogtt) or 120 minutes (ivgtt). During the hANP-infusions maximal hANP levels were 72 +/- 11 pg/ml (normal less than 25 pg/ml). Responses of blood glucose and C-peptide levels to the glucose load remained unaffected by hANP in both studies. However, hANP increased mean insulin responses (given as area under the curve) by 11.5% in ogtt and by 15.9% in ivgtt (both p less than 0.05). Thus, elevated hANP levels within the pathophysiological range, as observed in chronic heart failure or in hypertension, lead to an increase in serum insulin. Unchanged C-peptide levels demonstrate that hANP does not interfere with insulin secretion, but exclusively inhibits insulin degradation in liver and/or kidney. Further studies are required to elucidate whether these findings play a part in the pathomechanisms of insulin resistance in patients with elevated hANP levels, e.g. in chronic heart failure or hypertension.
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PMID:[The effect of atrial natriuretic peptide on glucose tolerance and insulin level]. 213 3

A group of 65 patients with advanced heart failure was examined with the aim to disclose changes in serum glucose, creatinine, potassium, chloride, and acid-base balance under the influence of intensive diuretic therapy. 50 patients were treated with ordinary furosemide and amiloride combination (average observation time 25 days), in 15 cases amiloride was replaced by captopril 75-150 mg/day (average observation 15.5 days). The results are as follows: 1. We found no rise of glycaemia in non-diabetics with either ordinary diuretic therapy or captopril. On the contrary: stress hyperglycaemia in the beginning of the therapy normalized in the course of it. 2. There was a significant rise of serum creatinine during the first two weeks of therapy with furosemide and amiloride. Reversal of this trend followed after captopril. 3. There was no fall in the average serum chloride concentration during ordinary diuretic therapy. Adding captopril to the regime brought about a rise in serum chloride. 4. Serum potassium had no tendency to fall either after furosemide and amiloride or furosemide and captopril. 5. The acid-base balance showed no shift towards metabolic alkalosis during an intensive but rational diuretic regime either with or without captopril. On the contrary: mild initial metabolic alkalosis had a tendency to normalize with proceeding cardiac compensation.
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PMID:[Metabolic and acid-base changes in intensive diuretic therapy in heart failure]. 219 96


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