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

The effect on the left ventricle of changes in the state of the arterial vasculature is best identified by utilizing calculations of pulsatile rather than steady flow phenomena. Impedance is the most satisfactory term to describe this effect. The normal ventricle compensates for changes in impedance largely by changes in preload, but the damaged heart loses this compensatory ability and its stroke volume becomes inversely related to outflow resistance. Patients with heart failure behave in a similar fashion and pharmacologic vasodilation may induce marked improvement in left ventricular pump function. Inappropriate vasoconstriction in heart failure may result from stimulation of the sympathetic or renin-angiotensin system. Early experience with converting enzyme inhibitors suggests that blockade of the formation of angiotensin II may be a useful means of treating some patients with heart failure.
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PMID:Role of vasoconstrictor mechanisms in the control of left ventricular performance of the normal and damaged heart. 38 61

In an attempt to diagnose latent heart failure, a transient increase of afterload to left ventricle was produced by angiotensin II, and the ventricular movement was assessed by echocardiography. Angiotensin II was administered in a dose of 0.075 micrograms/kg body weight. Blood pressure was elevated by 40.5 +/- 14.5 mmHg in 38 cases with latent heart failure and by 41.2 +/- 4.5 mmHg in 30 normal subjects. Yet, only in the former group, posterior wall excursion of left ventricle reduced from 11.4 +/- 2.4 mm to 7.3 +/- 2.3 mm and mean posterior wall velocity from 41.4 +/- 10.1mm/sec to 26.5 +/- 8.8 mm/sec. The rates of these reductions were inversely correlated to the rate of elevation of left ventricular endodiastolic pressure as determined in 5 cases by cardiac catheterization. There was no change in 30 subjects. The data indicate the usefulness of angiotensin-induced echocardiographic changes in detecting latent cadiac failure.
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PMID:Ultrasonodiagnosis of subclinical heart failure by increasing afterload with angiotensin II. 47 Jan 39

The renin-aldosterone system was studied in cardiomyopathic hamsters (CMH) before and after the onset of untreated clinical congestive heart failure. Age-matched random-bred hamsters (RB) served as controls. Before heart failure, there were no differences in body weight accretion, sodium balance, plasma renin activity or in vitro aldosterone production. After the onset of heart failure in CMH, body weight increased at a greater rate than in RB and positive sodium balance was nearly twice control levels. Although plasma renin activity was greater (P less than 0.005) in CMH than in RB (23.4+/-4.2 (mean+/-SEM) vs. 3.8+/-1.8 ng/ml/h), aldosterone production (101+/-15 vs. 95+/-16 ng/h) did not differ. Plasma aldosterone was low or undetectable in RB and in CMH in heart failure. In response to angiotensin stimulation, aldosterone production increased in both strains and did not differ. No difference in muscle potassium content, potassium balance or excretion was detected. Thus, in CMH, congestive heart failure is attended by increased plasma renin activity without a significant increase in aldosterone production, a dissociation which does not appear to be due to adrenal unresponsiveness to angiotensin II or to potassium depletion.
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PMID:Renin and aldosterone in the cardiomyopathic hamster in congestive heart failure. 88 11

The effect of an angiotensin-converting enzyme inhibitor on the circulating levels of angiotensin I, angiotensin II, and arginine vasopressin was studied in dogs subjected to hypotensive hemorrhagic shock. In dogs subjected to hemorrhage but not given the inhibitor, angiotensin II rose 20-fold (from 69 to 1,343 pg/ml of plasma), whereas in dogs subjected to hemorrhage but pretreated with the inhibitor, angiotensin II rose only 2-fold (from 92 to 171 pg/ml of plasma). In the pretreated dogs angiotensin I rose 30-fold (from 108 to 3,232 pg/ml of plasma). There was no statistically significant difference between the vasopressin levels found in the untreated dogs and the levels found in dogs given the inhibitor (1,016 and 1,095 pg/ml of plasma). Of the 15 dogs in the untreated group, five died before retransfusion was completed (four of cardiac failure and one of cardiac arrhythmia); none of the 10 dogs in the inhibitor-treated group died. These observations suggest that the very high levels of angiotensin II observed following severe hemorrhage do not contribute significantly to the increased secretion of vasopressin and that the inhibitor protects against death, possibly by suppressing the very high blood levels of angiotensin II observed following this type of experimental hemorrhagic shock.
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PMID:Effect of angiotensin-converting enzyme inhibitor (SQ 20881) on the plasma concentration of angiotensin I, angiotensin II, and arginine vasopressin in the dog during hemorrhagic shock. 89 Aug 86

The renin-angiotensin-aldosterone system and electrolyte levels in 11 patients with heart failure controlled on digoxin and frusemide were investigated after separate periods of Slow K, spironolactone, and amiloride therapy. When spironolactone or amiloride replaced Slow K, distinct parallel increments in the levels of renin, angiotensin II, and aldosterone resulted. Though plasma potassium was generally higher after spironolactone and amiloride than after Slow K, exchangeable potassium was similar with the three regimens. There was no significant relation between plasma potassium and concurrent exchangeable potassium.
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PMID:Effect of potassium-sparing diuretics on the renin-angiotensin-aldosterone system and potassium retention in heart failure. 97 76

Dogs with experimental high-output heart failure (HOF) exhibit marked retention of salt and water secondary to hypersecretion of both renin and aldosterone. The present study was undertaken to evaluate the systemic and intrarenal arteriolar action of angiotensin II (AII) in dogs with HOF and to provide additional information about the role of AII in low-output states. The intravenous infusion of a specific AII antagonist, [Sar1, Ala8]AII (6 mug/kg min-1), into conscious dogs with HOF decreased the mean arterial pressure (AP) from 101 +/- 7 to 83 +/- 7 mmHg (P less than 0.01) after 45 min of infusion. Intrarenal arterial infusion of the AII antagonist (0.2 and 2.0 mug/kg min-1) into anesthetized dogs with HOF also decreased AP and produced a marked increase in renal blood flow (RBF) with no changes in either creatinine clearance or sodium excretion. Similar results were obtained during the intrarenal infusion of the antagonist into sodium-depleted dogs and dogs with thoracic vena caval constriction, but not in normal dogs. The data demonstrate an important role for AII in the regulation of AP and RBF in high- and low-output states.
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PMID:High-output heart failure in the dog: systemic and intrarenal role of angiotensin II. 116 74

Angiotensin-converting enzyme (ACE) inhibitors are widely used for treatment of heart failure after myocardial infarction (MI). The beneficial effects consist of a combination of hemodynamic effects and interference with cardiac structural alterations. These effects are believed to depend on inhibition of angiotensin II (AII) formation and thus diminished angiotensin receptor stimulation. We administered the angiotensin II-1 (AT-1) receptor antagonist losartan during and after completion of the repair phase of an MI to investigate involvement of the AT-1 receptor in the above described effects of captopril. MI reduced cardiac output (CO) (sham 94 +/- 4 ml/min, MI 78 +/- 5 ml/min) and maximal CO (sham 154 +/- 4, MI 107 +/- 5 ml/min, respectively). Losartan (15 mg/kg/day) resulted in a rightward shift of the AII pressor dose-response curve by a factor of 32-40. Neither CO nor COVL,max was affected by losartan treatment in either phase (late treatment CO = 78 +/- 5, COVL,max = 118 +/- 9 ml/min). Although early treatment with losartan reduced cardiac hypertrophy measured as heart weight, DNA synthesis was reduced only slightly. In contrast, collagen deposition was inhibited completely. The results suggest that the effects of captopril in rats after MI are not dependent on AT-1 receptor-mediated mechanisms.
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PMID:Angiotensin II receptor blockade after myocardial infarction in rats: effects on hemodynamics, myocardial DNA synthesis, and interstitial collagen content. 128 Jul 40

Angiotensin-converting enzyme (ACE) inhibitors act by lowering the level of angiotensin II. The therapeutic benefits of these drugs and their potential side-effects therefore result from suppression of the physiological effects of angiotensin II. It is rational to prescribe an ACE inhibitor when the renin-angiotensin system is activated, as in renin-dependent essential hypertension, malignant hypertension and hypertension associated with heart failure. The beneficial effects of ACE inhibitor must be weighed against the special risks of renovascular hypertension: risk of renal artery thrombosis in case of unilateral stenosis and risk of renal failure if the stenosis is bilateral or affects a solitary kidney. In some situations the renin-angiotensin system is not directly involved in hypertension but may play a local haemodynamic role, as in some cases of primary or diabetic nephropathy. In such case the ACE inhibitors are thought to exert a protective effect. ACE inhibitors were reputed to be less effective in the elderly than in younger patients, but we now know that they can be prescribed with equal success in both instances to reduce peripheral resistance and improve regional blood flow as well as arterial compliance. Finally, ACE inhibitors can be prescribed, albeit with limited effectiveness, when the renin-angiotensin system is not activated, as in low renin hypertension and idiopathic hyperaldosteronism due to adrenal hyperplasia. They are ineffective in case of Conn's adenoma and contra-indicated in pregnant women.
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PMID:[For which hypertensive patient should angiotensin-converting enzyme inhibitor be prescribed or forbidden?]. 129 38

As soon as there is evidence of left ventricular dysfunction, even before clinical signs of chronic cardiac failure (CCF) have developed, intrinsic and extrinsic compensatory mechanisms are brought into play by the body. The majority of these mechanisms are under the influence of neurohumoral systems. When neurohormonal responses persist, as in CCF, they take on a beneficial nature since they participate in adaptation of the cardiovascular system as a whole, but they are also harmful since they worsen the working conditions of the myocardium by their cardiac and peripheral effects. Hyperactivity of the noradrenergic sympathetic nervous system is seen in CCF with levels 2 to 3 times higher as compared with subjects with normal left ventricular function. The circadian rhythm of catecholamines is modified. The increase in circulatory catecholamines is all the greater when cardiac failure is advanced. This release of noradrenaline (NA) is under the control of arterial baroreceptors which normally send to the central nervous system inhibitory inflow from the sympathetic nervous system. Inhibitory tone is released in case of a fall in blood pressure. Noradrenaline acts on beta-predominant myocardial receptors (inotropic and tachycardic) and alpha-predominant vascular receptors, resulting in arteriolar vasoconstriction. There is rapid onset of down regulation of myocardial beta-receptors. This fall essentially concerns beta 1, but beta 2 also, since they may be affected according to the etiology of CCF (ischemia). The Renin Angiotensin System (RAS) is also activated by the fall in systemic blood pressure. This consists of a cascade of reactions leading to the synthesis of angiotensin II responsible for powerful vasoconstriction of all arterial areas, including the coronary vessels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Metabolic changes in cardiac failure]. 130 Sep 20

Growth or altered metabolism of nonmyocyte cells (cardiac fibroblasts, vascular smooth muscle and endothelial cells) alters myocardial and vascular structure (remodeling) and function. However, the precise roles of circulating and locally generated factors such as angiotensin II, aldosterone and endothelin that regulate growth and metabolism of nonmyocyte cells have yet to be fully elucidated. Trials of pharmacologic therapy aimed at preventing structural remodeling and repairing altered myocardial structure to or toward normal in the setting of hypertension, heart failure and diabetes are reviewed. It is proposed that these are therapeutic goals that may reduce cardiovascular morbidity and mortality. Although this hypothesis remains unproved the primary goal of therapy should be to preserve or restore tissue structure and function.
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PMID:Remodeling and reparation of the cardiovascular system. 131 86


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