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

SYMPATHETIC NERVOUS SYSTEM AND HYPERTENSION: Biochemical, electrophysiological, pharmacological and haemodynamic findings support the existence of sympathetic nervous system activation in primary human hypertension. Analysis of regional sympathetic nervous system function, using both neurophysiological methods for measuring sympathetic nerve firing rates, and neurochemical techniques for quantifying regional noradrenaline spillover to plasma has demonstrated activation of the sympathetic nervous outflows to the heart, the kidneys, and skeletal muscle vasculature, particularly in younger patients. The initiating cause of this sympathetic nervous stimulation is unknown, but estimation of central nervous system noradrenaline turnover in hypertensive patients, using measurements of the washout of noradrenaline and its lipophilic metabolites into the internal jugular veins, indicates that activation of forebrain pressor noradrenergic nuclei is the probable underlying mechanism. CONSEQUENCES OF INCREASED SYMPATHETIC ACTIVITY: The sympathetic activation present in human hypertension no doubt contributes to the blood pressure elevation, and is a legitimate target for therapeutic intervention with imidazoline receptor-binding agents such as rilmenidine. In addition, the sympathetic nervous activation seems to have adverse consequences in hypertensive patients beyond initiating the blood pressure elevation. There is evidence that neural vasoconstriction has metabolic effects, in skeletal muscle impairing glucose delivery to muscle, causing insulin resistance and hyperinsulinaemia, and in liver retarding postprandial clearing of lipids, contributing to hyperlipidaemia. Cardiac sympathetic activation is demonstrably a cause of sudden death in heart failure patients; a comparable arrhythmogenic effect is probable in hypertension. A trophic effect of sympathetic activation on cardiovascular growth is also likely, contributing to the development of left ventricular hypertrophy. Rilmenidine, through its central nervous system actions, has been demonstrated to powerfully reduce sympathetic nervous activity in essential hypertension patients. INHIBITING THE SYMPATHETIC SYSTEM: As the clinical consequences of sympathetic nervous activation in essential hypertension appear to go beyond that of hypertension pathogenesis, extending to a causal influence in atherosclerosis development, cardiovascular hypertrophy and cardiac arrhythmias, it is possible that, of all antihypertensive drugs, those inhibiting the sympathetic nervous system might best reduce cardiovascular risk. This remains to be tested.
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PMID:High blood pressure management: potential benefits of I1 agents. 974 6

1. There is accumulating evidence for a range of abnormalities in the nitric oxide (NO) signalling cascade in human cardiovascular disorders. 2. In the present review we assess the literature detailing such evidence in early (hyperlipidaemia) and end-stage (heart failure) disease, with emphasis on the mechanisms by which the disturbances are thought to occur. 3. Strategies for the correction of disturbed NO signalling in these states are reviewed and include both prescribed pharmacological interventions, such as lipid-lowering therapy and novel uses of angiotensin-converting enzyme inhibitors, as well as non-pharmacological interventions, such as exercise and dietary supplementation with L-arginine and n-3 polyunsaturated fatty acids. 4. In addition to a decreased production/function of NO, the possible detrimental effects of a chronic elevation in NO production in patients with liver cirrhosis, together with a novel use of antibiotics to correct this perturbation, is outlined.
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PMID:Restoration of nitric oxide function in human hyperlipidaemia, congestive heart failure and liver cirrhosis. 975 Sep 51

Cardiovascular disease is the major killer in ESRD. Cardiovascular death risk is at least an order of magnitude higher in ESRD patients, even after adjusting for age and diabetic status. Cardiac failure is a rapidly lethal condition in ESRD patients which appears to mediate much of the adverse prognostic impact of ischemic heart disease. Left ventricular abnormalities are present at initiation of dialysis in about 80% of dialysis patients. These are very highly predictive of future ischemic heart disease, cardiac failure, and death after 2 years on dialysis therapy. Regression of these abnormalities improves prognosis. The associations between many classical risk factors like hyperlipidemia, smoking and hypertension and cardiac outcomes in ESRD are inconsistent. Many factors unique to ESRD and its therapy may be important. In our prospective 10 year study of 433 patients starting dialysis, the following were major risk factors for cardiac disease: hypertension (concentric LVH, LV dilatation, de novo ischemic heart disease, de novo cardiac failure, inverse relationship with mortality); anemia (LV dilatation, de novo cardiac failure and death); hypoalbuminemia (de novo ischemic heart disease, de novo cardiac failure and death). LV abnormalities tended to worsen on dialysis and improve after transplantation suggesting that a uremic environment is cardiotoxic. Many risk factors act in concert to produce cardiovascular disease in ESRD. Many can be treated, suggesting that the huge burden of disease can be reduced considerably.
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PMID:Cardiovascular disease and mortality in ESRD. 983 Dec 36

This paper is a comprehensive and critical review of the updated information available in Spain for the elderly population on the epidemiology of cardiovascular diseases. Clinical (coronary heart disease, heart failure, and cerebrovascular disease) and subclinical (left ventricular hypertrophy, carotid stenosis) cardiovascular diseases are reviewed. Prevalence and distribution of major classical cardiovascular risk factors such as hypertension, hyperlipidemia, diabetes mellitus and smoking and information on new risk factors such as microalbuminuria or abdominal obesity are also presented. The article is also focused on the high rates of morbidity, mortality and the burden of handicap in this age group in comparison with middle-aged people. Finally we call attention to the few and inconsistent population data available for some of the mentioned topics in our country, particularly the lack of specific figures of incidence and risk rates from cohort studies of elderly people in Spain.
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PMID:[Epidemiology of cardiovascular diseases in the Spanish elderly population]. 985 8

Adriamycin (doxorubicin) is one of the most effective chemotherapeutic agents against a variety of cancers, but its usefulness is seriously curtailed by the risk of developing heart failure. Available laboratory evidence suggests that an increase in oxidative stress, brought about by increased free radical production and decreased myocardial endogenous antioxidants, plays an important role in the pathogenesis of heart failure. Adriamycin-induced apoptosis and hyperlipidemia may also be involved in the process. Probucol, a lipid-lowering drug and an antioxidant, completely prevents the occurrence of heart failure by reducing oxidative stress as well as by the modulation of apoptosis and high lipid concentrations. Thus, combined therapy with adriamycin and probucol has a high potential for optimizing the treatment of cancer patients.
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PMID:Adriamycin-induced heart failure: mechanism and modulation. 1088 30

Left ventricular hypertrophy LVH is supposed to be a useful marker of cardiovascular complications during the course of hypertension. Occurrence of other risk factors of atherosclerosis in these hypertensive patients such as hyperlipidemia and smoking deteriorate the prognosis too. The authors compared clinical findings in hypertensive patients with and without left ventricular hypertrophy defined by echocardiography. Hospital records of 185 hypertensive patients treated at our medical department during years 1996-1999 were analysed. Left ventricular hypertrophy was defined by echocardiography (Penn convention) as left ventricular mass index > 134 g/m2 in men and > 110 g/m2 in women. Presence of LVH was found in 109 patients (mean age 66.7 years), absence of LVH in 76 patients (mean age 64.7 years). Both groups of hypertensive patients were matched by demographic parameters by the presence of hyperlipidemia and by smoking habits. Hypertensive patients with diabetes mellitus and obesity were excluded. They were statistically significant in the incidence of heart failure, myocardial infarction, renal failure and mitral regurgitation, and non-significant in the incidence of left ventricular diastolic dysfunction. There were more cardiovascular complications in LVH-positive patients than in those with LVH-negative findings. The incidence of stroke was slightly higher in LVH-negative patients. Left ventricular hypertrophy in patients with hypertension brings usually a complicated course of the disease. The authors recommend to examine the patients with arterial hypertension for the presence of left ventricular hypertrophy as it complicates the course of the disease significantly. (Tab. 3, Fig. 2, Ref. 26.)
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PMID:[Left ventricular hypertrophy in hypertension]. 1115 71

Regional sympathetic activity can be studied in humans using electrophysiological methods measuring sympathetic nerve firing rates and neurochemical techniques providing quantification of noradrenaline spillover to plasma from sympathetic nerves in individual organs. Essential hypertension: Such measurements in patients with essential hypertension disclose activation of the sympathetic outflows to skeletal muscle blood vessels, the heart and kidneys, particularly in younger patients. This sympathetic activation, in addition to underpinning the blood pressure elevation, most likely also contributes to left ventricular hypertrophy, and to the commonly associated metabolic abnormalities of insulin resistance and hyperlipidaemia. Antihypertensive drugs, such as moxonidine, which act primarily by inhibiting the sympathetic nervous system, should have additional clinical benefits beyond those attributable to blood pressure reduction, in protecting against hypertensive complications. Obesity-related hypertension: Understanding the neural pathophysiology of hypertension in the obese has been difficult. In normotensive obesity, renal sympathetic tone is doubled, but cardiac noradrenaline spillover (a measure of sympathetic activity in the heart) is only 50% of normal. In obesity-related hypertension, there is a comparable elevation of renal noradrenaline spillover, but without suppression of cardiac sympathetics (cardiac sympathetic activity being more than double that of normotensive obese and 25% higher than in healthy volunteers). Increased renal sympathetic activity in obesity may be a 'necessary' cause for the development of hypertension (and predisposes to hypertension development), but apparently is not a 'sufficient' cause. The discriminating feature of the obese who develop hypertension is the absence of the adaptive suppression of cardiac sympathetic tone seen in the normotensive obese. Heart failure: In cardiac failure, the sympathetic nerves of the heart are preferentially stimulated. Noradrenaline release from the failing heart at rest in untreated patients is increased as much as 50-fold, similar to the level seen in the healthy heart during near-maximal exercise. Activation of the cardiac sympathetic outflow provides adrenergic support to the failing myocardium, but at a cost of arrhythmia development and progressive myocardial deterioration. Psychosomatic heart disease: No more than 50% of clinical coronary heart disease is explicable in terms of classical cardiac risk factors. There is gathering evidence that psychological abnormalities, particularly depressive illness, anxiety states, including panic disorder and mental stress, are involved here, 'triggering' clinical cardiovascular events, and possibly also contributing to atherosclerosis development. The mechanisms of increased cardiac risk attributable to mental stress and psychiatric illness are not entirely clear, but activation of the sympathetic nervous system seems to be of prime importance.
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PMID:Sympathetic nervous system activation in essential hypertension, cardiac failure and psychosomatic heart disease. 1134 14

Smoking, hypertension, and hyperlipidemia are the three most important modifiable risk factors contributing to the development of cardiovascular disease in older adults. Although the magnitude of risk associated with smoking and hyperlipidemia declines with age, the absolute number of cases attributable to these risk factors increases due to the increasing prevalence of cardiovascular disease. Smoking increases the risk of both coronary events and stroke in the elderly, and there is evidence that smoking cessation is associated with a rapid reduction in risk. Therefore, an aggressive effort to promote smoking cessation is strongly recommended in patients of all ages. Systolic and diastolic hypertension are powerful risk factors for cardiovascular disease in the elderly. Moreover, multiple clinical trials have demonstrated that blood pressure reduction reduces the risk of stroke, coronary events, heart failure, and cardiovascular death in individuals at least up to the age of 90. Accordingly, treatment of both systolic and diastolic hypertension are strongly recommended regardless of patient age. The importance of total serum cholesterol as a coronary risk factor declines with age, but the ratio of low density lipoprotein cholesterol (LDL-C) to high density lipoprotein cholesterol (HDL-C) remains an independent predictor of coronary events in older men and women. In addition, clinical trials have shown that cholesterol reduction is associated with improved clinical outcomes in individuals at or above 75 years of age. At the present time, the value of treating hyperlipidemia in patients greater than 80 years of age is unknown, and therapy in this age group must be individualized. (c)1999 by CVRR, Inc.
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PMID:Aggressive Risk Factor Management in the Elderly: Are You Ever Too Old? 1141 93

Statins are competitive inhibitors of hydroxy-methyl-glutaryl coenzyme A (HMG-CoA) reductase and are the most commonly used drugs to treat hyperlipidaemia. Muscle toxicity is an adverse effect reported with a low incidence and rarely associated with acute renal failure due to rhabdomyolysis. We describe two patients with chronic renal failure treated with pravastatin and simvastatin who suffered rhabdomyolysis and acute renal failure. One patient started pravastatin several days after cessation of bezafibrate and developed acute renal failure without needing dialysis. The other was treated with simvastatin three years ago and suffered rhabdomyolysis when renal function was impaired after indomethacin was prescribed for backache. He needed hemodialysis because of acute cardiac failure and died from a respiratory infection while on mechanical ventilation. Myopathy was reversible in both patients. We recommend starting statins with the lower doses in chronic renal failure and monitoring muscle enzymes when renal function changes or when new drugs with potential interactions are prescribed.
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PMID:[Rhabdomyolysis and acute renal failure secondary to statins]. 1198 93

Left ventricular hypertrophy (LVH) is supposed to be a useful marker of cardiovascular complications during the course of hypertension. Authors compared the presence of heart failure, left ventricular diastolic dysfunction and chronic atrial fibrillation in hypertensive patients with and without left ventricular hypertrophy defined by echocardiography. Hospital records of 192 hypertensives treated in our medical department during years 1996-1999 were analysed. Left ventricular hypertrophy was defined by echocardiography (Penn convention) as left ventricular mass index > 134 g/m2 in men and > 110 g/m2 in women. Presence of LVH was found in 128 patients (mean age 65.9 years), absence of LVH in 64 patients (mean age 64.8 years). Both groups of hypertensives were matched by demographic parameters, by the presence of hyperlipidemia, by smoking habits. Hypertensive patients with left ventricular hypertrophy were more often treated by ACE inhibitors. There were statistically significant more patients with heart failure, left ventricular diastolic dysfunction and chronic atrial fibrillation in LVH-positive patients than in LVH-negative once. There was also statistically significant lower ejection fraction (50.3 +/- 11.4% vs 56.5 +/- 7.4%) in LVH-positive patients than in LVH-negative once. Left ventricular hypertrophy in patients with hypertension brings usually a complicated course of the disease with a high contribution to the development of chronic heart failure.
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PMID:[Heart failure in hypertensive patients with left ventricular hypertrophy]. 1149 79


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