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PubMed1989

Diuretics in congestive heart failure.

Congestive heart failure (CHF) is a condition characterized by a number of hormonal and renal adaptations which together conspire to salt and water retention. Diuretic therapy has been, and continues to be, a cornerstone to therapy for CHF. The rational use of diuretics, or diuretic combination such as metolazone-furosemide, can both effectively administer to the congestive symptoms seen in heart failure as well as temper many of the complications of this therapeutic modality.

Diuresis↗

PubMed1988

Neuroendocrine manifestations of congestive heart failure.

Congestive heart failure is a complex clinical syndrome characterized by a number of neuroendocrine responses. These responses are probably an evolutionary vestige of mechanisms designed to defend volume and maintain circulatory homeostasis. Activation of the sympathetic nervous system and renin-angiotensin-aldosterone system and the release of vasopressin have been clearly documented in patients with heart failure. Unlike the normal ventricle, the failing ventricle responds to peripheral vasoconstriction and sodium retention with further hemodynamic embarrassment and circulatory congestion. Certain vasorelaxant natriuretic substances are also released during heart failure, perhaps in an attempt to offset excessive peripheral constriction and sodium retention. Prostaglandin E2, atrial natriuretic peptide (or atrial natriuretic factor) and plasma dopamine are found to be increased in some patients with heart failure. However, peripheral constriction and sodium retention appear to be dominant, particularly in the advanced stages of heart failure. An understanding of these neuroendocrine responses has led to new developments in therapy. Angiotensin-converting enzyme inhibitors have emerged as distinctly useful drugs in the treatment of heart failure. Agents designed to block excessive sympathetic drive and inhibit vasopressin are under investigation. Infusion of atrial natriuretic factors and the use of selective dopamine agonists are also undergoing clinical trials in patients with heart failure. Increased knowledge of the neuroendocrine responses will likely result in even newer and more imaginative therapy.

Animals↗

PubMed1985

Pathophysiology of congestive heart failure.

Congestive heart failure is a syndrome that can be caused by a variety of abnormalities, including pressure and volume overload, loss of muscle, primary muscle disease or excessive peripheral demands such as high output failure. In the usual form of heart failure, the heart muscle has reduced contractility. This produces a reduction in cardiac output, which then becomes inadequate to meet the peripheral demands of the body. The 4 primary determinants of left ventricular (LV) performance are generally altered as follows: (1) There is an intrinsic decrease in muscle contractility. (2) Preload or left atrial filling pressure is increased, resulting in pulmonary congestion and dyspnea. (3) Although systemic blood pressure is often reduced, there is an increase in systemic vascular resistance (afterload), which can further reduce cardiac output. (4) Heart rate is generally increased as part of a compensatory mechanism associated with an increase in sympathetic tone and circulating catecholamines. In patients with coronary disease, there is often an imbalance between myocardial oxygen supply and demand. An increase in heart size may be particularly deleterious by increasing wall tension because of the Laplace relation and increasing myocardial oxygen consumption.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Volume↗

PubMed1980

A general radiologist looks at congestive heart failure.

Congestive heart failure may be difficult to detect. Determination of cardiac size is untrustworthy. Changes in the hili (vessels, bronchi) are reliable. Pulmonary edema may be atypical. Vascular redistribution must be interpreted accurately. Congestive changes with chronic obstructive lung disease may be difficult or impossible to detect. Pleural fluid may present atypically. Changes in pleural surfaces other than in bases produce "new" signs.

Bronchography↗

PubMed1992

The effect of treatment on survival in congestive heart failure.

Congestive heart failure (CHF) is a disorder characterized by a variety of clinical, biochemical, electrophysiological, and hemodynamic abnormalities. During the past two decades, numerous drugs have been employed in the treatment of this complex syndrome, and many agents have been shown to improve symptoms and ventricular function in patients with CHF. Because CHF is associated with a high risk of death, treatment should be directed not only toward the relief of symptoms, but also toward a reduction in mortality. Many variables have been shown to be related to survival; taken individually, however, each is limited in its utility in predicting prognosis. In recent years, large-scale studies with large sample sizes have directly assessed the effects of treatment on mortality in CHF. Results from these trials indicate that vasodilators and angiotensin-converting enzyme (ACE) inhibitors may improve mortality in patients with symptoms of heart failure. Additional trials are now in progress to evaluate the effect of treatment on patients with asymptomatic left ventricular dysfunction.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1993

Newer concepts in the medical management of patients with congestive heart failure.

Congestive heart failure (CHF) remains a major cause of morbidity and mortality in the United States, especially among the elderly. Although an underlying disturbance in cardiac function can be identified in most patients, manifestations of the disease are greatly influenced by other factors, particularly neurohumoral and peripheral adaptive responses which occur secondary to impaired cardiac function. The renin-angiotensin system (RAS) is integrally involved in the pathophysiology of CHF. Originally considered a humoral system, the RAS is now known to exist and operate within cardiac and vascular tissues. The importance of tissue-specific renin-angiotensin systems in CHF is presently under investigation. Most patients with symptomatic CHF benefit from the administration of an ACE inhibitor. Certain asymptomatic patients, such as those with severe left ventricular (LV) dysfunction and those who are at high risk for LV remodeling after anterior wall myocardial infarction, may also benefit from ACE inhibitor therapy. Diuretics and nitrates improve symptoms and often cardiac output in many patients with CHF. Although many new inotropic agents have been tested in CHF patients, none appear clinically superior to digitalis glycosides. The efficacy of digitalis glycosides in CHF may in part result from sympathoinhibitory properties such as the activation of baroreceptor mechanisms. Despite the fact that many CHF patients die from arrhythmias, treatment of asymptomatic ventricular arrhythmias in these patients is not recommended. Patients with symptomatic or sustained ventricular arrhythmias are best treated by a physician experienced in cardiac electrophysiology. Therapy with beta-blocking drugs for CHF patients is controversial. Anticoagulants are recommended for selected patients with CHF. Finally, exercise therapy may improve functional capacity in some patients with CHF through its effects on peripheral blood vessels and skeletal muscle tissues.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1996

Pharmacologic treatment of congestive heart failure.

Congestive heart failure is a clinical syndrome producing symptomatic deterioration, functional impairment, and shortened life span. The syndrome is complex in that it includes both peripheral and cardiac effects which contribute to the progression of heart failure. In the periphery, elevations in the sympathetic nervous system and renin-angiotensin system increase afterload and contribute to further salt and water retention. The central cardiac abnormalities include remodeling of the heart and downregulation of beta receptors. Traditional heart failure therapy has included treatment of fluid retention with diuretics, although their effect on mortality has never been addressed. The most proven therapy in heart failure is treatment with vasodilators, particularly angiotensin-converting enzyme (ACE) inhibitors. Improved survival with ACE-inhibitor therapy has been demonstrated in patients with severe heart failure (CONSENSUS), mild to moderate heart failure (SOLVD), and in comparison with vasodilator therapy with hydralazine isosorbide dinitrate (VHeFT II). Improved survival has also been noted in postmyocardial infarction when the ejection fraction is decreased (SAVE). The ACE inhibitors have now become standard therapy for heart failure regardless of severity. Additive vasodilator therapy with calcium-channel antagonists is under investigation. Inotropic therapy is controversial at present because of disappointing mortality results. The clinical mainstay digitalis remains without convincing mortality reduction data. Other inotropic agents, particularly phosphodiesterase inhibitors, have shown uniformly negative survival results. However, the new mixed action agents vesnarinone and pimobenden have shown favorable data, with vesnarinone demonstrating a mortality reduction effect. Beta-blocker therapy in heart failure has also found renewed interest, particularly with the new agents carvedolol and bucindolol which also have vasodilating properties.

Drug Therapy, Combination↗

PubMed1996

Alterations in skeletal muscle gene expression in the rat with chronic congestive heart failure.

Congestive heart failure is often associated with skeletal muscle abnormalities that contribute to early fatigue and acidosis. Up to the present time, however, the mechanisms responsible for these changes are unclear. Myocardial infarctions were produced by coronary ligation in adult Sprague-Dawley rats. At 20 weeks, 10 control rats, and 15 animals with heart failure [defined by elevated LVEDP (26.1 +/- 3.1 v 2.5 +/- 0.5 mmHg) and RV hypertrophy (300 +/- 21 g v 158 +/- 9 mg)] underwent in vivo measurements of total body, and soleus total protein and myosin heavy chain (MHC) synthesis by [3H]leucine constant infusion. Soleus muscle was also analysed for protein content, and MHC isoenzyme content by SDS-PAGE. Northern blotting also was used to determine levels of the mRNA's encoding type I, IIa, IIb, and IIx MHC, alpha-skeletal actin, COX III, SDH and GAPDH. Soleus muscles in heart failure rats were smaller than controls (112 +/- 6 v 126 +/- 5 mg) and the degree of atrophy was significant when corrected for body mass (0.38 +/- 0.02 v 0.46 +/- 0.02 mg/g. P = 0.007). Although there was no significant difference in plasma leucine flux (an index of whole-body protein synthesis), soleus muscle total and MHC synthesis was reduced in heart failure animals. Whereas the Type I MHC isoenzyme (beta MHC) was the only MHC detected in the soleus of control animals, type II MHC isoenzyme comprised 11.8 +/- 3.1% of the MHC in the heart failure group. Furthermore, steady-state mRNA levels encoding beta MHC were significantly depressed in the heart failure rats, where those encoding Types IIb and IIx MHC were increased. Steady-state mRNA levels of alpha-skeletal actin, cytochrome C oxidase (COX III) and succinate dehydrogenase (SDH) were also significantly depressed. This animal model of chronic heart failure is associated with quantitative and qualitative alterations in skeletal muscle gene expression that are similar to those reported in skeletal muscle of patients with chronic heart failure. The altered phenotype and impaired metabolic capacity may contribute to exercise intolerance in CHF.

Animals↗

PubMed1985

Role of isosorbide dinitrate in management of chronic congestive heart failure.

Congestive heart failure is accompanied by a number of compensatory mechanisms that may overshoot the mark. Among these are excessive arteriolar and venous constriction. Nitrates are effective in producing venodilation, redistributing blood from the chest to the periphery, and lowering right and left atrial pressures. Although oral isosorbide dinitrate is effective in producing acute beneficial hemodynamic effects, it usually does not increase exercise tolerance in the short term. Prolonged administration, however, does increase exercise tolerance and improve clinical class. Isosorbide dinitrate can be effectively combined with an arteriolar dilator such as hydralazine, which increases cardiac output. Such vasodilator therapy is symptomatically effective in patients with heart failure, although there is no evidence to date to suggest a prolongation of life.

Administration, Oral↗

PubMed1985

Neurohumoral mechanisms involved in congestive heart failure.

Congestive heart failure (CHF) promotes an array of biologic changes that are largely designed to compensate for reduced flow. These include activation of the sympathetic nervous system and the renin-angiotensin system, as well as the release of arginine vasopressin. The ultimate expression of these compensatory mechanisms is heightened vascular tone, increased sodium and water retention and antidiuresis. The peripheral circulation is normally under the fine control of circulating and neuronally released moieties, which can directly or indirectly alter vascular tone. Angiotensin II appears to be a key element in this regard because of its multiple biologic activities. Direct arteriolar vasoconstriction, facilitation of norepinephrine release and stimulation of aldosterone are some of the activities that are likely to be of major importance in the syndrome of CHF. Therefore, it is not surprising that converting enzyme inhibitors have a growing role as treatment. Other pharmacologic agents that can reduce sympathetic tone by acting on presynaptic receptors are being developed. Selective dilation of certain vascular beds may be possible with agents designed to interact with vascular dopaminergic receptors. The mechanisms whereby circulating epinephrine and norepinephrine modulate norepinephrine release and vascular tone are beginning to be understood and likely involve presynaptic, postsynaptic and nonsynaptic vascular receptors. A better appreciation of the mechanisms involved in the fine control of the peripheral circulation should allow for more selective and more imaginative pharmacologic therapy for CHF.

Angiotensin II↗

PubMed1990

Interaction of the sympathetic nervous system and electrolytes in congestive heart failure.

Congestive heart failure is characterized by both disturbances in electrolyte homeostasis and neuro-hormonal regulation. Total body potassium is reduced, and this reduction bears a modest relation to activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system. Patients with decompensated heart failure show increases in both plasma epinephrine and plasma norepinephrine, whereas patients with chronic stable heart failure usually have an increase only in plasma norepinephrine. High levels of circulating epinephrine may contribute to the development of hypokalemia by activating skeletal muscle and liver membrane beta 2-adrenergic receptors, which in turn stimulate intracellular cyclic adenosine monophosphate to activate the membrane-bound Na+K(+)-adenosine triphosphatase pump. The net result is that potassium flux across the cell membrane from the extracellular to the intracellular space increases, setting the stage for hypokalemia and possibly serious ventricular arrhythmias. Other mechanisms that may contribute to the development of hypokalemia in heart failure include the kaliuresis brought on by excessive levels of aldosterone. Moreover, it is likely that the activity of facilitated by concomitant activation of the renin-angiotensin system. Increased sympathetic nerve activity may then release additional renin from the kidney (by way of a beta 2-adrenergic mechanism). Therefore, both the sympathetic nervous system and the adrenal medulla may interact to cause hypokalemia in patients with heart failure. Because hypokalemia is known to predispose patients to ventricular arrhythmias, it may be prudent to aggressively maintain serum potassium levels in patients with heart failure in the range of 4 to 5 mEq/liter.

Epinephrine↗

PubMed1992

Baroreceptor reflex function in congestive heart failure.

Congestive heart failure is characterized by decreased parasympathetic and increased sympathetic nervous system activity. Impairment of baroreceptor reflex function may be relevant to this altered neural profile. The effect of cardiopulmonary and arterial baroreceptor stimulation on corresponding afferent neural activity is reduced in experimental models of heart failure. In addition, the heart rate and blood pressure responses to perturbations in arterial and carotid sinus pressure are less in animals with heart failure than in control animals. Comparable observations have been made in humans. Unloading cardiopulmonary baroreceptors with lower-body negative pressure causes less forearm vasoconstriction in patients with heart failure than in healthy subjects. The chronotropic response to changes in arterial and carotid sinus pressure induced by drug infusions or by use of a neck chamber is attenuated in heart failure. These data suggest that abnormalities in cardiopulmonary and arterial baroreceptor reflex function contribute importantly to altered autonomic nervous system activity in heart failure.

Animals↗

PubMed1988

Congestive heart failure.

Congestive heart failure (CHF) is not a single entity but a symptom complex that may represent the consequence of mechanical abnormalities, myocardial abnormalities, and/or disturbances of cardiac rhythm. In turn, it affects virtually every organ system in the body. This review focuses on CHF due to systolic dysfunction of the left ventricle, which comprises the majority of cases of this condition. Recent data suggest that CHF may be the most frequent primary diagnosis in patients on medical services in nonmilitary hospitals in this country: it affects approximately 2% of the United States population, or some 4 million people. The mortality rate for CHF is also worse than for many forms of cancer; thus, new therapeutic alternatives are imperative. In order to devise new therapeutic strategies, a detailed understanding of the pathophysiology of this condition is required. The relative advantages and disadvantages of various pharmacologic and nonpharmacologic approaches are considered in detail. Certain medications, such as the angiotensin converting enzyme (ACE) inhibitors, have been shown to improve survival, and heart transplantation is clearly life-saving for those who are eligible for this therapy. However, the real challenge is to devise strategies to prevent the occurrence of heart failure, or interrupt its progress at a very early stage.

Blood Volume↗

PubMed1989

Pathophysiology and current therapy of congestive heart failure.

Congestive heart failure is a common clinical syndrome, with a relatively poor prognosis in its advanced stages. During the development of heart failure, there is a decline in myocardial contractility and activation of neurohormonal systems. An overshoot of some of these compensatory mechanisms sets the stage for therapeutic interventions. Any of the three therapeutic classes of drugs (inotropic drugs, diuretics or vasodilators) can be used as first-line therapy. Other classes can be added to produce additive effects on ventricular function. Because vasodilators have been shown to prolong life, they should be used routinely in patients with heart failure. Arrhythmias and sudden death are relatively common in heart failure, although the value of antiarrhythmic therapy is less certain. Although current therapy is very helpful in patients with heart failure, it is clear that preventive approaches will be more effective in decreasing morbidity and mortality.

Anti-Arrhythmia Agents↗

PubMed2005

[Risk stratification in congestive heart failure].

Congestive heart failure remains a severe condition. Risk stratification is necessary to assess the prognosis and discuss the potential timing of heart transplant. Numerous criteria have been used, which may be combined to define prognostic scores which, however, are rarely used in routine. A few items, however, may be used to stratify the risk of mortality and sudden death.

Coronary Angiography↗

PubMed2005

Markers of bone metabolism in congestive heart failure.

Congestive heart failure (CHF) is a chronic disease, whose incidence is especially growing in the subpopulation of elderly people. CHF is characterized by dyspnea and fatigue at rest or with exertion, ankle swelling and pulmonary edema. Cardiac transplantation is the ultimate therapeutic measure in patients with end-stage CHF. Some risk factors associated with CHF such as low mobility, renal failure, and prescription of specific drugs may predispose patients to develop osteoporosis. This review article gives an overview about markers of bone metabolism in CHF patients as well as in heart transplant recipients. At first, the physiology of bone metabolism is summarized. Then, a short description of different bone formation and resorption markers is presented. They can be used to characterize actual bone metabolism and can be helpful to explain possible mechanisms of bone loss. Regarding pre-transplant CHF patients, available data indicate that the disturbances in bone metabolism are only subtle. Heart transplant recipients, however, are at increased risk for osteoporotic bone loss due to the use of immunosuppressive agents such as corticosteroids and calcineurin inhibitors. Preventive strategies are able to normalize bone metabolism and to attenuate the high bone loss during the first year after heart transplantation.

Biomarkers↗

PubMedDate not supplied

Encouraging exercise in older adults with congestive heart failure.

Congestive heart failure (CHF) is a chronic medical problem commonly found in older adults. Management of CHF ideally should combine lifestyle modifications and medication management. Exercise prescriptions and encouraging patients with CHF to exercise can have a significant impact on management of symptoms as well as exacerbation of further disease. The recommended exercise program should ideally incorporate 10 to 15 minutes of warm-up with exercise durations of 20 to 30 minutes and a cool-down period generally repeating the warm up exercises. Exercise should be done at least 3 to 5 days per week and should include a combination of aerobic and resistance exercise. The HEART approach provides a useful guide to help motivate older adults with CHF to exercise regularly. In so doing, older adults with CHF will be helped to improve and maintain cardiac status, decrease the symptoms of CHF, and improve overall quality of life.

Aged↗

PubMed2001

Perindopril treatment for congestive heart failure.

Congestive heart failure (CHF) is the most common and lethal consequence of atherosclerotic cardiovascular disease, with a prevalence estimated between 1% and 10%, and very high associated mortality. Preventing the continued progression of established heart failure and improving the prognosis for patients with this disease is difficult, but angiotensin-converting enzyme (ACE) inhibitors have been shown to be effective in reducing mortality in patients with CHF. In a review of the worldwide literature of the efficacy and safety of perindopril erbumine for the treatment of patients with CHF, once-daily treatment with this ACE inhibitor was shown to be effective in patients with CHF of all severities. Its use is associated with a low risk of first-dose hypotension and no unwanted effects on blood pressure in normotensive patients. Perindopril also improves arterial compliance and reverses left ventricular hypertrophy in patients with hypertension. It is well tolerated and has no significant effects on heart rate, indexes of renal function, or plasma lipid profile. It also has no clinically significant interactions with other drugs, including digoxin, likely to be taken by patients with CHF.

Adrenergic beta-Antagonists↗