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

Congestive heart failure causes substantial patient morbidity and mortality in the United States. Symptoms and physical findings can be helpful in diagnosis but have limited sensitivity and specificity. Objective measurement of ventricular function is essential in virtually all patients in whom a diagnosis of heart failure is suspected. Reversible causes of heart failure must be sought. Outpatient management includes education and counseling, emphasis on and assessment of compliance with diet, and pharmacologic treatment. Angiotensin-converting enzyme inhibitors are the mainstay of treatment but are underused, and maximal doses are not given apparently because of concern about side effects. Diuretic therapy should be administered only as needed to manage fluid overload. Calcium channel blockers are relatively contraindicated in patients with impaired ventricular function. Patient follow-up should be guided by the results of the medical history and physical examination. Routine serial testing of ventricular function and exercise performance is discouraged.
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PMID:Diagnosis and outpatient management of congestive heart failure. 747 38

Recent clinical investigations have provided new insights into physiologic alterations taking place as heart failure progresses. As a result, new end points may be more relevant to monitor in patients, rather than the classical assessment of severity based on subjective evaluation of functional capacity. Structural changes of the myocardium, referred to as remodeling, have profound effects on the performance of the left ventricle and on long-term prognosis. Left ventricular ejection fraction may serve as a clinical marker for remodeling changes. Remodeling changes involve hypertrophy of the muscle mass, dilation of the left ventricle, and a change in the shape of the ventricle. Histologically, these changes are produced by myocyte lengthening, interstitial growth, and myocyte slippage. The consequences of remodeling include an abnormal bio-energetic state because of the augmented wall stress and accentuated myocardial oxygen consumption. The elevated wall stress promotes further hypertrophy. Superimposed on the remodeling changes is neurohormonal activation. Both remodeling and neurohormonal activation are directly related to mortality. An experimental canine model has been used successfully to investigate the potential impact of pharmacologic intervention on remodeling. Angiotensin-converting enzyme inhibitors and the combination of hydralazine and isosorbide dinitrate have been shown in clinical trials to reduce long-term mortality and increase ejection fraction. The effects of these drugs appear to be mediated in part by alterations in remodeling and neurohormonal activation. Thus, left ventricular ejection fraction can be used as a clinical marker for remodeling processes, and plasma norepinephrine levels can be used as a marker for neurohormonal activation.
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PMID:Critical review of heart failure: the role of left ventricular remodeling in the therapeutic response. 748 20

Angiotensin-converting enzyme inhibitors have been extensively studied and established in the treatment of hypertension, heart failure, and ventricular dysfunction. They have various cardiac and vascular protective effects, but the relevant mechanisms of action in these areas remain to be fully understood. Possible effects of converting-enzyme inhibition related to maintenance of normal endothelial function and inhibition of atherosclerosis should be distinguished from effects on myointimal proliferation related to vascular injury and regression of vascular hypertrophy from blood pressure reduction. Experimental animal studies have showed benefit from converting-enzyme inhibition in preventing myointimal proliferation after vascular injury in some species, but no such effect has been shown in clinical studies of restenosis following coronary angioplasty. Laboratory studies have demonstrated a protective effect of converting-enzyme inhibition on endothelial vasomotor function. Further studies have demonstrated prevention of atherosclerosis in hyperlipidemic rabbits and cholesterol-fed cynomolgus monkeys. Possible mechanisms of action apart from blood pressure lowering include inhibition of angiotensin II and other tissue growth factors and accumulation of kinins. These data, among others, provide sufficient rationale for clinical studies to determine whether converting-enzyme inhibitors can reduce atherosclerotic disease and thus widen their application as cardiac and vascular protective agents.
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PMID:The effects of ACE inhibition on progression of atherosclerosis. 751 40

The purpose of this study was to determine the effects of bradykinin (BK), substance P (SP) and histamine on plasma exudation in the skin of conscious dogs with and without pacing-induced heart failure. We also determined the role tissue angiotensin I-converting enzyme (ACE) and neutral endopeptidase (NEP) play in modulating these responses. We found that intradermal injection of BK, SP and histamine induced a significant, concentration-dependent Evans blue exudation in normal dogs (p < 0.05). Bradykinin-induced responses were significantly potentiated by captopril (p < 0.05). In contrast, phosphoramidon potentiated BK-induced responses only at low concentrations of BK. Both captopril and phosphoramidon had no significant effects on SP- and histamine-induced Evans blue exudation. BK- and SP-induced responses were significantly attenuated, whereas histamine-induced Evans blue exudation was significantly potentiated in dogs with heart failure. We conclude that heart failure is associated with attenuation of BK- and SP-, but not histamine-induced plasma exudation in the peripheral microcirculation and that these responses are not modulated by tissue ACE and NEP.
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PMID:Plasma exudation in conscious dogs with experimental heart failure. 753 20

The renin-angiotensin system is critical for regulating extracellular fluid volume and blood pressure. Angiotensin II, the active peptide hormone produced by the renin enzymatic cascade, sustains vascular volume and blood pressure by constricting vessels, stimulating adrenal aldosterone secretion, increasing renal tubular sodium absorption, activating the sympathetic nervous system, and increasing cardiac contractility. These actions are a disability in the pathophysiologic states of hypertension and congestive heart failure (CHF), however, since reactive increases in renal renin and angiotensin II stimulate sympathetic activity and renal sodium retention, leading consequently to circulatory volume over-load. The actions of angiotensin II are mediated by its interactions with specific cell-surface angiotensin II receptors, namely, AT1 and AT2; most cardiovascular actions of angiotensin II come from its interaction with the AT1 receptor. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin-II-receptor blockers antagonize the actions of the renin-angiotensin axis, neutralizing its effects on hypertension and heart failure. Losartan is the first oral, nonpeptide, selective AT1-receptor blocker to be approved. Clinical trials show it to be effective and well tolerated as therapy for hypertension and CHF. Data obtained thus far suggest ACE inhibitors and AT1-receptor blockers have similar efficacy for treating these conditions, but the receptor blockers appear to produce fewer adverse effects. Whether the sustained increase in angiotensin II concentrations after AT1-receptor antagonism produces deleterious effects is not known. The concern is that these high levels may stimulate unblocked AT2 receptor; the effect of that stimulation may not be important, however.
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PMID:Angiotensin receptors: physiology and pharmacology. 763 61

A systolic blood pressure greater than 160 mm Hg is a more significant risk factor for cardiovascular disease than a diastolic blood pressure greater than 95 mm Hg, regardless of a patient's age. Treatment of isolated systolic hypertension significantly reduces the incidence of both fatal and nonfatal cardiovascular events, even in patients who are over 80 years of age. Non-pharmacologic measures and behavior modification should be tried for three to six months in a patient with mildly elevated blood pressure (140 to 160 mm Hg/90 to 100 mm Hg). If these measures fail or the patient has target-organ disease or multiple cardiac risk factors, medication may be prescribed earlier. Half the usual recommended dose should be initially prescribed in the frail elderly. Long-acting diuretics or beta blockers are recommended first-line agents. Angiotensin-converting enzyme inhibitors, calcium channel blockers and alpha blockers have not been shown to reduce mortality in hypertensive patients who do not have comorbid disease. Angiotensin-converting enzyme inhibitors may benefit hypertensive patients with heart failure, and calcium channel blockers may help those with angina, especially vasospastic angina.
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PMID:Hypertension in the elderly. 863

The left ventricle can change its size and shape as a result of external load and/or loss of viable myocytes. This process, defined as remodeling, can be adaptive, as in compensatory hypertrophy and dilation secondary to myocardial infarction, or maladaptive in response to long-standing systemic hypertension. In addition to ventricular enlargement and cellular hypertrophy, extensive interstitial collagen deposition also occurs during this remodeling process. The increased fibrous tissue and hypertrophied myocytes can also lead to inappropriate energy production and utilization. Angiotensin-converting enzyme (ACE) inhibitors have the ability to modulate both cellular hypertrophy and collagen deposition. These effects represent, in part, the mechanism by which ACE inhibitors modify ventricular remodeling, the subsequent development and clinical expression of heart failure, and finally, the improvement in the mortality of patients with heart failure.
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PMID:Ventricular remodeling and angiotensin-converting enzyme inhibitors. 770 61

When initiated a few days after myocardial infarction, angiotensin-converting enzyme inhibition exerts beneficial effects on survival and morbidity in patients with asymptomatic left ventricular systolic dysfunction or symptomatic heart failure. During the acute phase of a myocardial infarction, angiotensin-converting enzyme inhibition appears to be well tolerated, to prevent the development of heart failure in patients with asymptomatic left ventricular systolic dysfunction and to improve the hemodynamic and clinical variables of heart failure when present. Accordingly, early angiotensin-converting enzyme inhibition is clearly indicated in patients with acute myocardial infarction associated with asymptomatic left ventricular dysfunction or clinical evidence of heart failure. Angiotensin-converting enzyme inhibition may also be beneficial when thrombolytic agents fail to restore coronary patency in patients with acute myocardial infarction.
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PMID:Indications for immediate angiotensin-converting enzyme inhibition in patients with acute myocardial infarction. 777 15

Angiotensin-converting enzyme (ACE) inhibition therapy has now become firmly ensconced in the modern therapeutic approach to all stages of congestive heart failure (CHF), including the early presymptomatic phase. Although its benefit is abundantly proven as add-on therapy in established CHF, after digitalis and diuretics, smaller and shorter studies have shown that, as second-line therapy and combined with diuretics, it may be preferable to digoxin with an undoubted benefit in postinfarction failure. As first-line therapy in early presymptomatic CHF, the evidence is also good, based on the prevention arm of the Studies of Left Ventricular Dysfunction (SOLVD), albeit in predominantly postinfarction patients, and on the Survival and Ventricular Enlargement (SAVE) study on postinfarction patients. ACE inhibitors given prophylactically or therapeutically helped to prevent clinical heart failure in the SOLVD and SAVE studies. These data suggest a role for ACE inhibitors as effective first-line monotherapy in early heart failure, acting on left ventricular function to avoid or lessen unfavorable remodeling. There are some contraindications or cautions for the use of ACE inhibitors in CHF, such as preexisting hypotension, high-renin states such as bilateral renal artery stenosis with hypertensive heart failure, aortic stenosis combined with CHF, overdiuresis with excess sodium depletion, and significant preexisting renal failure. ACE inhibition therapy may have deleterious effects on renal function in heart failure, for example, by decreasing the glomerular filtration rate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fundamental role of angiotensin-converting enzyme inhibitors in the management of congestive heart failure. 777 32

The treatment of heart failure has advanced greatly over the past two decades. Angiotensin-converting enzyme inhibitors have become standard therapy, not only in symptomatic patients but also in those with asymptomatic left ventricular dysfunction. Diuretic regimens have become increasingly potent and sophisticated. Much of the controversy over the efficacy of digoxin has been resolved, although its effect on survival is still uncertain. Most symptomatic patients, therefore, should be treated with what has become "standard" triple therapy, but practices vary as to when and at what dose to use these medications. More problematic is how to treat the patient who remains symptomatic on a three-drug regimen, and how to manage ancillary but important issues such as arrhythmias and thromboembolic risk. This article reflects the author's personal approach to managing the patient with left ventricular systolic dysfunction in 1994.
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PMID:A personal perspective on the treatment of heart failure in 1994. 804 83


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