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

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

Chronic infusion of atrial natriuretic factor (ANF) decreased blood pressure in two-kidney, one clip (2-K, 1C), spontaneously hypertensive rat (SHR) and one-kidney, one clip (1-K, 1C) models of experimental hypertension in the rat, but produced increased sodium excretion only in the 1-K, 1C model. In ANF-infused 2-K, 1C animals plasma renin activity did not differ from normotensive controls. Atrial content of immunoreactive (ir) ANF was significantly lower in SHR and 1-K, 1C animals. At 40-50 days old, cardiomyopathic hamsters had a higher concentration of plasma irANF and a lower ANF content in the left but not in the right atrium, although the difference in plasma ANF was more obvious once heart failure was well established. At 110-130 and 200-300 days old, the hamster atrial ANF content was not only lower in the left but also in the right atrium. No differences were observed in plasma irANF between normal subjects and either untreated or treated essential hypertensive patients. However, a significantly higher plasma ANF was observed in two groups with secondary hypertension, primary hyperaldosteronism and renovascular hypertension. Bolus injection of ANF into healthy subjects produced a dose-related decrease in blood pressure and an increase in the heart rate and natriuresis.
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PMID:Some physiopathological aspects of atrial natriuretic factor. 294 34

Operation for tumors responsible for a Conn's syndrome was performed in 16 patients, 11 women and 5 men, over a period of 13 years, the average time before diagnosis being 5 1/2 years. All patients presented hypertension, permanent in 14 and paroxysmal in 2 cases while blood potassium levels were below 3 mmol/l in all patients. Diagnosis was confirmed by elevation of plasma aldosterone and of urine tetrahydroaldosterone, associated with low plasma renin activity not responding to a stimulus. The tumor was demonstrated by imaging in 15 cases before operation and its mean size was 1.7 cm. Investigatory methods for diagnosis and localization are discussed. One patient died during the immediate post-operative period from decompensated cardiac failure. Long-term review showed persistent hypertension in 5 patients but electrolyte disturbances were corrected in all cases. Lack of consistency of results of surgical reduction in case of hyperplasia suggests that only patients with hyperaldosteronism related to an adrenal cortex tumor should be operated upon.
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PMID:[Surgery of Conn's syndrome. Apropos of 16 cases]. 370 May

Spironolactone, a competitive aldosterone receptor antagonist (ARA), has traditionally been the treatment of first choice in idiopathic hyperaldosteronism (IHA) and for preoperative management of aldosterone producing adenoma (APA). Spironolactone is partially absorbed, is extensively metabolized mainly by the liver and its therapeutic properties are attributable to active metabolite canrenone. At therapeutic doses of 25 to 400 mg per day, spironolactone effectively controls blood pressure and hypokalemia in the majority of cases. Endocrine side effect are often associated and mainly consist of gynecomastia, decreased libido and impotence in man and menstrual irregularities in women. Canrenone and the K+ salt of canrenoate are also in clinical use: they avoid the formation of intermediate products with anti-androgenic and progestational actions, resulting in a decreased incidence of side effects. Furthermore, a relatively new selective ARA compound (eplerenone) with reduced affinity for androgen and progesterone receptors, is currently undergoing clinical trials. In essential hypertension aldosterone can contribute to hypertension and increases the incidence of myocardial hypertrophy and cardiovascular events. On the other hand, inhibition of Renin-Angiotensin-Aldosterone System (RAAS) is associated with a decrease in blood pressure, with a regression of left ventricular hypertrophy and a reduction of target organ damage. Thus, ARA have been proposed as complementary treatment associated to ACE inhibitors and angiotensin receptor antagonists. Aldosterone is also known to play an important role in pathophysiolgy of congestive heart failure (CHF). In vitro and in vivo evidences suggest that aldosterone promotes myocardial fibrosis. This effect reflects direct, extra-epithelial actions of aldosterone via cardiac MR which are counteracted by ARAs in animal models. The RAAS is chronically activated in CHF. Non potassium-sparing diuretics further stimulate the RAAS and cause hypokalemia. Thus, use of ARAs in CHF was first proposed to correct potassium and magnesium depletion. At present ARAs are indicated in the management of primary hyperaldosteronism, in oedematous conditions in patients with CHF, in cirrhosis of the liver accompanied by oedema and ascites, in essential hypertension and in hypokalemic states. Its indication as adjunctive therapy of heart failure is currently under investigation. In fact, it is well known that even high doses of ACE inhibitors may not completely suppress the RAAS; aldosterone 'escape' may occur through non angiotensin II dependent mechanisms. Addition of spironolactone to an ACE inhibitor causes marked diuresis and symptomatic improvement. During the last few years, the RALES study (Randomized Aldactone Evaluation Study) was organized to explore the efficacy of combination therapy with spironolactone and ACE inhibitor in patients with CHF, class III or IV NYHA. The study was stopped 18 months early because the results were so statistically and clinically significant that it would be unethical to continue the trial. It is reported a 30 percent decrease in mortality and hospitalisation for cardiac causes in spironolactone-treated group vs placebo group.
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PMID:Aldosterone antagonists in hypertension and heart failure. 1079 May 93

As patients age, congestive heart failure becomes an increasingly important problem and accounts for up to 20% of hospital admissions for patients over 65 years. With technological improvements in the treatment of coronary artery disease, improved survival after myocardial infarction, and better hypertension therapy, patients are living longer, thus the need for successful management of older patients with chronic heart failure. The elderly, especially minorities, tend to be under-represented in congestive heart failure trials. This article will focus on the care of the geriatric patient with congestive heart failure.
Conn Med 2003 Sep
PMID:Congestive heart failure and the elderly. 1458 31

Animal studies have shown that during high sodium intake aldosterone induces cardiac fibrosis and renal nephrosclerosis through activation of mineralocorticoid receptors. In the human heart mineralocorticoid receptors and activity of the enzyme 11beta-hydroxysteroid-dehydrogenase type 2, which is required for the activation of mineralocorticoid receptors by aldosterone, are both present. In clinical medicine the profibrotic effect of aldosterone has been related to diastolic dysfunction, arrhythmia and progression of cardiac and renal failure. The addition of an aldosterone receptor antagonist to optimal treatment in patients with heart failure causes a decrease in serum markers of collagen turnover and a decline in cardiac morbidity and mortality. These findings are a strong indication of a profibrotic effect of aldosterone in cardiac failure. Studies concerning the profibrotic effect of aldosterone in patients with primary hyperaldosteronism are contradictory and at the moment no data are available about a potential antifibrotic effect of aldosterone receptor antagonists in patients with impaired renal function.
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PMID:[Profibrotic effects of aldosterone]. 1536 22

Aldosterone is increasingly considered to have a fundamental role in the pathophysiology of cardiovascular disease. Primary aldosteronism is a much more common cause of secondary hypertension than once suspected, accounting for approximately 10% of cases. Screening for primary aldosteronism should be considered even in the presence of normokalaemia. The non-classical effects of aldosterone, some of which are transcription-independent, may be of similar or greater importance than its traditional effects on the kidney. Treatment of primary aldosteronism should be specific and aim to ameliorate all hormone-related effects of aldosterone, not just the most obvious manifestation of hypertension. Mineralocorticoid antagonism, shown to lead to significant additional survival advantage in heart failure, offers the best prospect for achieving therapeutic goals. For the increasing proportion of patients with primary aldosteronism suitable for long-term medical treatment, mineralocorticoid receptor blockade (better tolerated with eplerenone) should be considered the most appropriate choice of treatment, pending the development of better alternatives.
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PMID:The pharmacological treatment of primary aldosteronism. 1655 72

The roles of aldosterone and mineralocorticoid receptors in cardiovascular disease have been expanded, refined, and distinguished over the past decade. Primary aldosteronism has been shown to represent 8-13% (rather than <1%) of unselected hypertensive patients, and patients with primary aldosteronism to have higher indices of cardiovascular damage than controls of the same age, sex, and BP status. While this represents a clearly expanded role for aldosterone, it is improbable that the hormone (as opposed to the mineralocorticoid receptor) plays a major role in other instances of essential hypertension, in cardiac failure, or in atherosclerosis. Evidence from studies in these conditions supports a substantial role for mineralocorticoid receptor activation; low baseline aldosterone levels, and evidence from experimental in vivo studies, support a role for normal levels of physiologic glucocorticoids in activating mineralocorticoid receptors (MR) in the context of tissue damage and reactive oxygen species generation. These relatively recent insights suggest the potential therapeutic role for MR antagonists across a spectrum of cardiovascular disease, as vascular protectants even when circulating levels of aldosterone are low.
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PMID:The role of aldosterone and mineralocorticoid receptors in cardiovascular disease. 1761 Mar 42

Aldosterone is an adrenal hormone that regulates sodium, fluid, and potassium balance. Jerome Conn first described the syndrome of autonomous and excessive aldosterone secretion or "primary aldosteronism." Contrary to the historical belief, recent studies indicate that primary aldosteronism is a common cause of hypertension with a prevalence of 5-10% among general hypertensive patients. Various animal models have demonstrated that aldosterone in association with a high salt diet results in target-organ inflammation and fibrosis. Similarly, cross-sectional and observational human studies have demonstrated the association of aldosterone with development and severity of hypertension, congestive heart failure, coronary artery disease, chronic kidney disease, and metabolic syndrome. Several interventional studies have also demonstrated the beneficial effects of mineralocorticoid receptor antagonists in these disease processes, particularly hypertension, heart failure, and post myocardial infarction, further supporting the role of aldosterone in their pathogenesis. We review the role of aldosterone in these various cardiovascular disease processes along with potential mechanisms and treatment.
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PMID:Aldosterone and cardiovascular disease. 1913 16

A 48 year-old obese male with hypertension was admitted to our department because of severe right-dominant heart failure. His heart rhythm was 2:1 atrial flutter and the left ventricle was diffusely hypertrophic and hypokinetic. Primary aldosteronism was diagnosed based on severe hypokalemia (2.6 mEq/L) and a low renin-high aldosterone state with hypertension despite the use of an angiotensin-II receptor blocker, but its etiology could not be clarified with computed tomography, adrenal scintigraphy, and adrenal vein sampling. Ascites and edema rapidly worsened. Ascites aspiration was performed daily, until serum potassium was normalized by a full dose of an aldosterone receptor blocker (spironolactone 100 mg/day). A diuretic (furosemide) was then added. Rate control of atrial flutter was obtained with a beta-adrenergic blocker, and anticoagulation therapy was started. His heart failure was successfully controlled. Coronary arteries were normal on coronary arteriograms, and an endomyocardial biopsy sample obtained from the left ventricle did not show any specific pathological findings. Blood pressure was well controlled with the full dose of the aldosterone receptor blocker, but he died one year later due to intracerebral hemorrhage. As his heart failure was right dominant, we believe that its etiology may have been hyperaldosteronism-induced cardiomyopathy, and not advanced hypertensive heart disease.
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PMID:Primary aldosteronism with right-dominant heart failure. 2071 49


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