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

Left ventricular hypertrophy is an important complication of essential hypertension. Some antihypertensive drugs have been shown to allow regression of cardiac hypertrophy, both in spontaneously hypertensive rats and in hypertensive patients. Recent results show that the agents which interfere with the functions of the sympathetic nervous system, converting enzyme inhibitors and calcium antagonists are effective in reducing arterial blood pressure and regression of left ventricular hypertrophy. The use of vasodilators and diuretics may under certain circumstances, however, even exacerbate cardiac hypertrophy. Regression of left ventricular hypertrophy in hypertension does not appear to depend solely on reduction of arterial blood pressure. Other factors seem to modulate the myocardial response to antihypertensive treatment. Included among these mechanisms are neural, humoral, haemodynamic and biochemical factors. The available experimental data further suggest that some functional derangements and biochemical changes associated with hypertrophy may be reversed by antihypertensive treatment. There is, however, insufficient experience with human subjects to determine whether a reduction in left ventricular mass is associated with lower incidences of heart failure or mortality than may be achieved by adequate blood pressure control alone.
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PMID:Regression of cardiac hypertrophy with drug treatment in spontaneously hypertensive rats. 615 98

Labetalol is a combined alpha- and beta-adrenoceptor blocking agent for oral and intravenous use in the treatment of hypertension. It is a nonselective antagonist at beta-adrenoceptors and a competitive antagonist of postsynaptic alpha 1-adrenoceptors. Labetalol is more potent at beta that at alpha 1 adrenoceptors in man; the ratio of beta-alpha antagonism is 3:1 after oral and 6.9:1 after intravenous administration. Labetalol is readily absorbed in man after oral administration, but the drug, which is lipid soluble, undergoes considerable hepatic first-pass metabolism and has an absolute bioavailability of approximately 25%. There are no active metabolites, and the elimination half-life of the drug is approximately 6 hours. Unlike conventional beta-adrenoceptor blocking drugs without intrinsic sympathomimetic activity, labetalol, when given acutely, produces a decrease in peripheral vascular resistance and blood pressure with little alteration in heart rate or cardiac output. However, like conventional beta-blockers, labetalol may influence the renin-angiotensin-aldosterone system and respiratory function. Clinical studies have shown that the antihypertensive efficacy of labetalol is superior to placebo and to diuretic therapy and is at least comparable to that of conventional beta-blockers, methyldopa, clonidine and various adrenergic neuronal blockers. Labetalol administered alone or with a diuretic is often effective when other antihypertensive regimens have failed. Studies have shown that labetalol is effective in the treatment of essential hypertension, renal hypertension, pheochromocytoma, pregnancy hypertension and hypertensive emergencies. In addition, preliminary studies indicate that labetalol may be of value in the management of ischemic heart disease. The most troublesome side effect of labetalol therapy is posture-related dizziness. Other reported side effects of the drug include gastrointestinal disturbances, tiredness, headache, scalp tingling, skin rashes, urinary retention and impotence. Side effects related to the beta-adrenoceptor blocking effect of labetalol, including asthma, heart failure and Raynaud's phenomenon, have been reported in rare instances.
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PMID:Labetalol: a review of its pharmacology, pharmacokinetics, clinical uses and adverse effects. 631 May 29

In hypertension, irrespective of its underlying etiology, the baseline pretreatment renin-sodium profile predicts the antihypertensive action or the lack of it for five major types of antihypertensive drugs: 1) diuretic agents; 2) beta-receptor blockers; 3) converting-enzyme inhibitors; 4) the alpha 1 postsynaptic blocker, prazosin; and 5) the calcium channel blockers, verapamil and nifedipine. Moreover, vigorous compensatory activation of the renin-angiotensin system in response to therapy often explains initial drug ineffectiveness or resistance to treatment by diuretics and nonspecific vasodilators. This correlation between renin system behavior and antihypertensive drug efficacy likely reflect basic pharmacologic-physiologic interactions. This correlation is also observed in congestive heart failure without hypertension, where operant renin-aldosterone profiles may help to explain both drug efficacy and drug resistance to commonly administered therapeutic agents. Accordingly, a control system analysis of the renin axis has broad applications in therapy. The analysis is also conceptually significant since it exposes the operation of fundamentally different mechanisms of increased vascular resistance to flow occurring in different patients with hypertension or heart failure. One form is renin-angiotensin-mediated whereas the other, in the absence of renin, is associated with sodium-volume excess and/or abnormal alpha-adrenergic and calcium channel activity. Further definition of these two mechanisms of increased peripheral resistance could lead to a better understanding of the pathogenesis of some forms of essential hypertension and congestive heart failure.
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PMID:Renin system activity as a determinant of response to treatment in hypertension and heart failure. 635 36

Using the fluorimetric method, the activity of dipeptidyl-carboxypeptidase (DCP) was studied in 85 patients suffering from essential hypertension. It was ascertained that the DCP activity in the blood serum of such patients was significantly higher than in normal subjects. The highest activity of the enzyme was observed in cases where essential hypertension was aggravated by chronic heart failure or an acute impairment of the cerebral circulation. Inflammatory processes in hypertensive patients were associated with a considerable fall in the serum enzyme activity.
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PMID:[Changes in dipeptidyl carboxypeptidase activity during hypertension and its complications]. 636 55

The distribution of myocardial blood flow (MBF) was evaluated in pressure-induced LV hypertrophy of foxhounds. At the early stage of developing hypertrophy, i.e., 3 months after aortic banding (+ 53% LV weight) resting MBF and flow reserve were not significantly different from control hearts. One year after banding (+94% LV weight) myocardial flow reserve had clearly decreased. Acute coronary stenosis of 60 and 70% cross-sectional area resulted in a moderate fall of flow reserve in controls and hearts with early hypertrophy. In hearts with extensive hypertrophy the drop of poststenotic MBF was considerably greater affecting preferentially the subendocardium. The data suggest that myocardial blood flow was impaired before any signs of heart failure were observed. Furthermore a decrease of MBF may not be confined to forms of hypertrophy induced by renal and idiopathic hypertension.
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PMID:Myocardial flow reserve in experimental cardiac hypertrophy. 644 91

Hypertension and obesity are two disorders that have been closely related, each occurring in greater frequency with the other than in an otherwise normal population. Although a causal relationship has not been established between the two, their coincidence carries increased risk of cardiovascular morbidity and mortality. This report summarizes the pathophysiological studies from our laboratory concerning their interrelationship and offers a rational hypothesis for the mechanisms underlying this enhanced risk. Patients with hypertension demonstrate an increased total peripheral resistance that explains hemodynamically the rising arterial pressure with advancing vascular disease. In response to this increased afterload imposed upon the heart, the left ventricle adapts itself structurally through a process of concentric hypertrophy. In addition, in most patients with essential hypertension, plasma volume progressively contracts and renal vascular resistance increases in proportion to the rise in arterial pressure and total peripheral resistance. In contrast, in obesity-hypertension there is a superimposed factor of volume overload upon the hemodynamic abnormality. The result is an additional cardiac stimulus for eccentric hypertrophy due to the increased ventricular preload. This factor enhances left ventricular stroke work and its attendant myocardial oxygen demands, thereby providing a dual overload on cardiac function that can explain the increased risk of heart failure related to these associated conditions. In contrast to the compounding adverse hemodynamic effects on the heart, there does not seem to be an additive hemodynamic effect of obesity on hypertensive renal vascular disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The problem of obesity and hypertension. 662 65

Chronic glomerulonephritis (CGN) is responsible for 105 (1.16%) of all 9015 necropcies in a multi-specialized hospital but it occupies the third place after chronic pyelonephritis and diabetic glomerulosclerosis 9.20 per cent. In 91.4 per cent of the deceased of CGN arterial hypertension (AH) had been concomitant, with an average duration, according to anamnestic data, 6.28 years with a mainly light and moderate hypertrophy of left ventricle. Those that died of CGN without AH lived 9.20 years, on the average, wore than those with hypertension. In about 30 per cent of CGN with AH, the hypertension contributed to the lethal end prior to the terminal uremia--from cardiac insufficiency--25 per cent and cerebrovascular stroke 4.16 per cent. The significantly poorer atherogenesis in aorta and coronary and cerebral arteries is worth mentioning in case of CGN with hypertension as compared with the essential hypertension. (The deceased examined were not dialyzed). That atherogenesis is even poorer than hypertension of chronic pyelonephritis.
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PMID:[Incidence of chronic glomerulonephritis and its hypertonic terminal-stage syndrome and the severity of the cardiovascular changes among 9015 autopsied patients over 14]. 663 5

Hypertension is the most common chronic disease in the West Indies, and is a major health problem today being among the 10 most common causes of death in the English-speaking territories of the region. Most patients have essential hypertension. Renal failure, stroke, and cardiac failure are the most common complications, myocardial infarction being relatively uncommon in black patients. While an earlier report from the Caribbean suggested that beta-blockers were not effective for treating black hypertensives, recent experience with these drugs show that they are useful particularly when administered along with a diuretic. Beta-blockers may be required in higher doses than those commonly recommended for patients in Europe and North America, but even small doses of thiazide diuretics are effective in lowering the blood pressure of West Indian hypertensives. West Indians show a combination of personalistic, naturalistic, and modern medical beliefs, which need to be understood in order to mount effective programmes for the management of hypertension in the community.
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PMID:Hypertension in the West Indies. 664 70

The influence of various disease states, other than hypertension, on the pharmacokinetic behaviour of hydralazine is not completely known. In the present study the pharmacokinetics of oral hydralazine has been evaluated in 7 patients with severe, chronic heart failure, using 8 compensated hypertensives as controls. The pharmacokinetics was evaluated by measuring the plasma concentrations of hydralazine ("apparent" and "real" hydralazine) and hydralazine pyruvate hydrazone, and by assessing acetylator phenotype after a small dose of dapsone. The AUC (area under the plasma concentration curve) following a single, oral 50 mg dose was significantly larger in patients with chronic heart failure NYHA Class III-IV than in patients with essential hypertension without cardiac decompensation. A decreased rate of hepatic elimination of hydralazine is suggested as a major contributory factor to this finding.
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PMID:Pharmacokinetics of oral hydralazine in chronic heart failure. 665 41

We have developed radiotracer techniques, based on measurement of the rate of spillover of noradrenaline to plasma, to simultaneously estimate total, and organ-specific, sympathetic nervous activity in humans. In 27 unmedicated subjects without renal or liver disease, or cardiac failure, regional noradrenaline spillover rates were as follows: lungs 33% of total noradrenaline release to plasma, kidneys 22%, skeletal muscle 20%, hepatomesenteric 9%, skin 5%, and heart 3%. These findings have relevance to numerous previous studies on the importance of the sympathetic nervous system in the pathogenesis of human essential hypertension. The indices of overall sympathetic nervous tone which have been used, such as measurements of plasma noradrenaline concentration or total NA release to plasma, are seen to be not sufficiently specific, since the organs and regions thought to be central to hypertension pathogenesis (kidney, heart, splanchnic circulation) are responsible for no more than 35% of all noradrenaline released to plasma. Organ-specific noradrenaline spillover measurements are better suited to the elucidation of any sympathetic nervous system pathophysiology in human hypertension. Early results point to an increase in renal sympathetic tone in young patients with essential hypertension.
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PMID:Total, and organ-specific, noradrenaline plasma kinetics in essential hypertension. 669 62


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