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

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

ACE-inhibitors improve symptoms and prognosis in patients with heart failure. The V-Heft II trial has demonstrated that the beneficial effect of these agents is superior to unspecific vasodilators. Besides sustained arterial and venous vasodilation the inhibition of the neurohumoral axis is thought to play an important role. Angiotensin II and catecholamines not only exert vasoconstrictor effects, but might also contribute to vascular and myocardial growth. Thus, it may not be surprising that the beneficial effects of ACE inhibitors in heart failure only emerge during long-term therapy rather than after short-term administration. It has been shown that these agents improve blood flow to skeletal muscle during exercise after chronic therapy (not acutely), and there is some preliminary evidence that improvement of endothelial function might be involved in this effect, i.e., by reducing the degradation of bradykinin, an endothelial vasodilator. ACE inhibitors reduce LV hypertrophy, an important risk factor for cardiovascular disease and prognosis. Moreover, there is experimental evidence that ACE inhibitors can prevent and even reverse interstitial fibrosis in the left ventricle. Although the plasma renin activity may be normal in patients with chronic heart failure, recent data using polymerase chain reaction indicate that the tissue cardiac renin angiotensin system is activated in the failing human heart as assessed by measurements of angiotensin converting enzyme mRNA and angiotensinogen mRNA which may be an important target for ACE-inhibition.
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PMID:[The value of ACE inhibitors in heart failure (mechanism of action)]. 129 Mar 8

The actions of angiotensin II can be described in terms of the three paradigms listed in Table 1. According to the first paradigm (organ physiology), angiotensin II is a pressor, while the second (cell biochemistry) views it as an extracellular messenger that, by promoting Ca2+ release within cells, causes vasoconstriction and a weak positive inotropic response by the heart. However, neither of these paradigms fully explains the remarkable ability of angiotensin converting enzyme inhibitors to improve the prognosis for patients with heart failure. To account for these clinical effects of angiotensin converting enzyme inhibitors, we will probably need to invoke the third paradigm (gene expression), which views angiotensin II as a growth factor that promotes and modifies protein synthesis. Angiotensin II, therefore, should probably not be viewed simply as a vasoconstrictor with a side effect to promote hypertrophy, but instead as a growth factor that, because it utilizes Ca2+ to mediate its effects on gene expression, also increases smooth muscle tone and myocardial contractility. This view of angiotensin II as a growth factor helps us to understand the clinical benefit of angiotensin converting enzyme inhibitors as arising from inhibition of maladaptive changes in the failing heart (gene expression) as well as from the reduced afterload (organ physiology) that results from decreased smooth muscle tone (cell biochemistry).
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PMID:Is angiotensin II a growth factor masquerading as a vasopressor? 134 1

The intrarenal renin-angiotensin system (RAS) may contribute to the pathophysiology of heart failure by the generation of angiotensin II at local sites within the kidneys. Angiotensin II may directly influence renal hemodynamics, glomerular contractility, and tubular sodium reabsorption, thereby promoting sodium and fluid retention in this syndrome. In the present study, we examined components of the circulating RAS as well as the intrarenal expressions of renin and angiotensinogen mRNA in rats with stable compensated heart failure (HF) 12 wk after experimental myocardial infarction. Renal angiotensinogen mRNA level in vehicle-treated HF rats increased 47%, as compared with sham control rats (P = 0.001). The increase in angiotensinogen mRNA levels was more pronounced in animals with medium (46%, P < 0.05) and large (66%, P < 0.05) infarcts than in those with small infarcts (31%, P = NS). There were no differences in liver angiotensinogen mRNA, circulating angiotensinogen, angiotensin II, plasma renin concentration (PRC), kidney renin content (KRC), and renal renin mRNA level between sham and HFv. In addition, in a separate group of rats with heart failure, we demonstrated that renal angiotensin II concentration increased twofold (P < 0.05) as compared with that of age-matched sham operated controls. A parallel group of heart failure rats (HFe, n = 11) was treated with enalapril (25 mg/kg per d) in drinking water for 6 wk before these measurements. Blood pressure decreased significantly during treatment (91 vs. 103 mm Hg, P < 0.05). Enalapril treatment in HF rats increased renin mRNA level (2.5-fold, P < 0.005), KRC (5.6-fold, P = 0.005), and PRC (15.5-fold, P < 0.005). The increase in renal angiotensinogen mRNA level observed in HFv rats was markedly attenuated in enalapril treated HF rats (P < 0.001), suggesting a positive feedback of angiotensin II on renal angiotensinogen synthesis. These findings demonstrate an activation of intrarenal RAS, but no changes in the circulating counterpart in this model of experimental heart failure, and they support the concept that the intrinsic renal RAS may contribute to the pathophysiology in this syndrome.
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PMID:Evidence for tissue-specific activation of renal angiotensinogen mRNA expression in chronic stable experimental heart failure. 140 Oct 84

The prognosis for patients with congestive heart failure (CHF) is poor, with a mortality exceeding 50% within 5 years from diagnosis. This poor prognosis remains despite improved pharmacological therapy. Because the prevalence of sudden death among these patients is high, reported to exceed 40%, the prognostic importance of ventricular tachyarrhythmias has attracted much interest. Long-term electrocardiographic monitoring of patients with CHF reveals a high prevalence of ventricular premature beats, which in many patients occur frequently or are complex according to Lown criteria. Ventricular tachycardia (three or more consecutive beats) has been recorded in 40% or more of the patient population. Whether the occurrence and/or severity of ventricular tachyarrhythmia detected on Holter electrocardiograms relates to the subsequent prognosis is, however, debated. The occurrence of ventricular tachyarrhythmia may just be an expression of severely compromised left ventricular function, which, in turn, decides the subsequent outcome of the disease. Besides myocardial injury, patients with CHF have many factors that may contribute to the high prevalence of ventricular arrhythmias. Among these are elevated levels of plasma norepinephrine. Angiotensin II may increase the sensitivity to sympathetic nervous system arousal but also promotes renal loss of potassium and magnesium. Treatment with digitalis and diuretic drugs may provoke arrhythmias as well. Heart failure therapy may, however, also improve ventricular arrhythmias. Accordingly, it has been demonstrated that captopril therapy significantly reduces ventricular prematurity, compared with digitalis. In contrast, however, enalapril improvement of mortality was due to a reduction of progressive heart failure, with no difference seen in the incidence of sudden cardiac death (the CONSENSUS study).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of congestive heart failure treatment on incidence and prognosis of ventricular tachyarrhythmias. 172 20

The effects of the angiotensin converting enzyme inhibitor captopril, after treatment for 5-6 weeks with 25 mg t.i.d., were studied in 12 patients with stable moderate heart failure. Five patients received placebo treatment, and the two groups were comparable at baseline. Angiotensin II levels decreased in response to captopril therapy. Skeletal muscle potassium, magnesium and chloride levels did not differ from reference values. Calcium was subnormal (P less than 0.0001), but increased to the reference range during captopril treatment. Phosphofructokinase, a rate-limiting glycolytic enzyme, was in the lower reference range and increased (P less than 0.04) in response to captopril therapy. In conclusion, stable moderate heart failure is associated with low levels of skeletal muscle calcium and phosphofructokinase activity, these metabolic changes tending to return to normal levels with captopril treatment.
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PMID:Skeletal muscle depressed calcium and phosphofructokinase in chronic heart failure are upregulated by captopril--a double-blind, placebo-controlled study. 182 3

There is activation of the renin angiotensin system after both complicated and uncomplicated myocardial infarction. Angiotensin II increases myocardial oxygen consumption whilst reducing coronary flow and is also directly toxic to the myocardium. Angiotensin converting enzyme inhibitors produce beneficial haemodynamic and neuroendocrine changes in patients with acute left ventricular failure, and may have a role in selected patients with cardiogenic shock. There is evidence to suggest that they might prevent the development of late cardiac failure by limiting the extent of post infarction ventricular dilation. Further research is necessary to define their role in the treatment of acute myocardial infarction.
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PMID:Importance of RAA system and the treatment of patients with ACE inhibition after myocardial infarction. 201 17

Several changes in neuroendocrine activity follow failure of cardiac function to satisfy peripheral requirements and contribute to the clinical syndromes of heart failure. Afferent pathways are poorly understood and triggers are both central and peripheral, involving attenuation of atrial and arterial baroreceptor activity. Efferent sympathetic activity is generally increased with resulting vasoconstriction, but responses are organ-specific and differ among heart, kidney, lung and skeletal muscle. Changes in cardiac sympathetic activity are inadequately understood. Enhanced cardiac norepinephrine spillover contrasts with reduced tissue concentration and impaired activity of synthetic enzymes and neuronal catecholamine uptake. Beta-receptor down-regulation further complicates overall adrenergic responsiveness and the balance between enhancement of contractile function and reduction in arrhythmia threshold. Activation of the renin-angiotensin system is potentiated by the sympathetic nervous system and may contribute to vasoconstrictor hyporesponsiveness. Angiotensin II may in turn facilitate the central and peripheral effects of sympathetic activation and the release of vasopressin from the pituitary. Our understanding of the role of vasodilator peptides in heart failure remains rudimentary. It is likely that vasoconstrictor neuroendocrine response adversely influences optimal cardiac function in heart failure and may promote arrhythmogenesis. The neuroendocrine response in individual organs, however, requires intensive study.
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PMID:Neuroendocrine activation in congestive heart failure. 202 Nov 17

Cardiac hypertrophy is characterized by marked abnormalities in the contraction/relaxation pattern of the heart. For example, delayed relaxation is a prominent feature, impairing ventricular filling and coronary flow. In intact heart preparations the relative contribution of fibrosis and of the myocardial cell itself to these abnormalities cannot be correctly assessed. Biochemical studies on the mechanisms of impaired contraction and relaxation and hypertensive heart failure are hampered by the fact that 75% of all heart cells are non-myocytes. We therefore established the model of the isolated calcium-tolerant, adult rat cardiomyocyte as a new approach to the investigation of these problems. Contractility was measured using a videomicroscope system with high time resolution (1 ms). Angiotensin II induced a marked relaxation delay in the cardiomyocyte from normotensive rats and showed a moderate positive inotropic effect, whereas isoproterenol had a strong positive inotropic effect but accelerated relaxation. Therefore, angiotensin II is capable of inducing a relaxation delay even in the absence of coronary ischaemia or hypertension. These first results show that the isolated cardiomyocyte model may be a useful approach to investigating the mechanisms of hypertensive heart disease.
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PMID:Isolated myocardial cells: a new tool for the investigation of hypertensive heart disease. 214 54

Stimulation of the renin angiotensin system, catecholamines and antidiuretic hormone causes prominent vasoconstriction in severe heart failure. Angiotensin converting enzyme inhibitors reverse these effects, and thus ameliorate cardiac function and reduce mortality in severe heart failure. Angiotensin II is an important regulator of renal function in diseases with renal hypoperfusion, and treatment with angiotensin converting enzyme inhibitors may cause a serious decrease in glomerular filtration and hyperkalemia. Asymptomatic heart failure, acute heart failure and acute myocardial infarction are areas where angiotensin converting enzyme inhibitors may prove beneficial in the future.
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PMID:[Treatment of heart failure with angiotensin converting enzyme inhibitors]. 221 71


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