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PubMed1988

Compensatory changes of sympathetic tone, the renin-angiotensin-aldosterone system, vasopressin, and ANF as potential therapeutic targets in congestive heart failure.

Congestive heart failure (CHF) is not only reflected by such mechanical problems as forward- and backward failure, but it is also associated with a complex pattern of compensatory neuro-endocrine mechanisms, e.g., enhanced activity of both the sympathetic nervous system (SNS) and the renin-angiotensin-aldosterone system (RAAS); enhanced release of vasopressin from the pituitary gland; enhanced release of the atrial natriuretic factor (ANF) from the cardiac atria. These neuro-endocrine mechanisms not only operate as such but also display a complex pattern of mutual interactions. These mechanisms, though potentially beneficial short-term, may also be harmful when persisting during progression of the disease. For this reason they offer potential targets in the treatment of CHF besides the classical measures aimed directly at improving cardiac contractility. The following groups of drugs are discussed as therapeutic measures that suppress the aforementioned detrimental compensatory mechanisms: various types of vasodilator drugs; diuretics; beta 1-adrenoceptor blocking agents in low dosage; saralasin; ACE-inhibitors. So far, the enhanced release of vasopressin and ANF have not offered realistic new therapeutic targets in CHF, although their pathophysiologic issue is highly relevant.

Atrial Natriuretic Factor↗
PubMed1988

The pathophysiologic profile of congestive heart failure.

Congestive heart failure (CHF) evolves either from an excessive workload or in response to loss of myocardium, both of which cause cardiac hypertrophy, increased cardiac pressure, and loss of functional reserve. Nearly 60% of patients in heart failure present with ischemic cardiomyopathy, which in its chronic form exhibits biventricular dilatation, elevated left ventricular mass, and extensive large-vessel atherosclerosis. The hypertrophy is proportional to the loss of myocardium, although animal studies suggest this varies with the infarct size. However, recent studies indicate that early afterload reduction may relieve the hypertrophic stimulus and prevent degeneration. Some 30% to 40% of patients in heart failure present with an idiopathic dilated cardiomyopathy, with a patchy but diffuse loss of tissue on microscopy, reactive hypertrophy in the surviving cells, and interstitial fibrosis and replacement scarring. The ultrastructural changes still await clarification. The role of pharmacologic intervention still remains unclear. However, any reduction in mortality will necessitate the identification of those cellular changes that inevitably lead to secondary degeneration of the remaining viable myocardium.

Cardiomyopathy, Dilated↗
PubMed1988

Managing congestive heart failure.

Congestive heart failure, a constellation of signs and symptoms that result from the heart's inability to provide sufficient oxygenated blood to metabolizing tissues, is a major cause for concern in the elderly. The prognosis is ominous, with a 10% per year mortality rate after the initial CHF episode, and a 30 to 60% per year rate for patients who remain symptomatic despite digitalis and diuretic treatment. Common etiologies in CHF are discussed, and a case history illustrating CHF symptomatology is provided. The role of diuretics, digitalis, ACE-inhibitors, and other pharmacologic agents is reviewed and updated, and the value of patient education is discussed.

Aged↗
PubMed1988

Congestive heart failure.

Congestive heart failure (CHF) is a condition that is increasing in incidence and is associated with significant morbidity and mortality rates. The main abnormality that underlies CHF is depressed myocardial function. The resulting decrease in cardiac output activates several peripheral compensatory mechanisms, which may further impair ventricular function and worsen the prognosis. Although systolic dysfunction is the traditional descriptor of CHF, diastolic dysfunction is increasingly recognized as a distinct entity. In prescribing therapy the predominant type of ventricular dysfunction and the peripheral components of the heart failure should be identified. The ultimate aim is to alleviate symptoms, minimize complications and prolong survival. Recent data from two multicentre trials have suggested that vasodilators can achieve these goals. Trials are under way to assess the impact of early vasodilator therapy on CHF.

Calcium Channel Blockers↗
PubMedDate not supplied

Current management of congestive heart failure.

Congestive heart failure is a major public health problem in developed countries. There have been significant advances in the management of this condition over the last few decades. However, many patients are still not receiving adequate therapy. Optimal management requires appropriate investigation, education, counselling, medical treatment and planned follow-up. This review outlines the recommended approach for optimal management of patients with heart failure.

Cardiovascular Diseases↗
PubMed1996

[Pharmacologic treatment of chronic congestive heart failure].

Congestive heart failure (CHF) continues to be a lethal end stage of cardiovascular diseases caused by hypertension, coronary heart disease, valve deformity, diabetes and cardiomyopathy. Current therapy for CHF can maintain function, improve quality of life, and prolong survival. Diuretics, angiotensin-converting enzyme inhibitors (ACE), and digoxin remain in standards of therapy. Diuretics remains an important component of the symptomatic management of patients with CHF, but severely II patients may require additional agents. One option frequently used in patients who exhibit resistance to loop diuretics is infusion of low-dose dopamine. Combination diuretics may effectively increase urine output, with the addition of thiazide or spironolactone. Documentation of the clinical benefit of ACE inhibitors represents the most important advance in therapeutics for CHF in the last decade. ACE inhibitors improves left ventricular function, and survival and unless contraindicated, patients with left ventricular systolic dysfunction should receive high dose ACE inhibitor with diuretic if there is peripheral oedema. For patients who cannot take an ACE inhibitor the combination of hydralazine and nitrates may offer some prognostic benefit. Digoxin has been the traditional first drug of choice for CHF, but with protracted controversy about its efficacy and safety. It is hope that new agents as vesnarione, and ibopamine may improve contractility without having adverse consequences. Acceptance of beta-blockade as a potentially beneficial therapeutic intervention increase in the past year. This year, improved diastolic function and afterload reduction were reported with beta-blockade. Amiodarone unlike other antiarrhythmic drugs does not seem depress left ventricular function, and may be the best drug in patients with CHF and symptomatic arrhythmias. The correct role of anticoagulation in patients with CHF remains controversial. Although the benefits of anticoagulation for the treatment of most patients with atrial fibrillation are increasingly accepted, it has not been shown to improve outcome in patients with CHF in normal sinus rhythm.

Angiotensin-Converting Enzyme Inhibitors↗
PubMedDate not supplied

Pharmacotherapy in congestive heart failure: Hyperkalemia in congestive heart failure.

Hyperkalemia is not an uncommon occurrence in the congestive heart failure patient, particularly when renal failure coexists. Hyperkalemia in CHF is typically medication-related. Its occurrence is inevitably linked to the simultaneous ingestion of angiotensin-converting enzyme inhibitors and beta-blockers, and more recently, aldosterone receptor antagonists, such as spironolactone. The most devastating consequence of hyperkalemia is its cardiotoxicity that can be fairly insidious in its rate of development. The therapy of hyperkalemia in congestive heart failure can involve both acute and semiacute management phases. Acute hyperkalemia management includes measures that block the adverse membrane effects of hyperkalemia, such as intravenous calcium administration, and efforts to shift potassium intracellularly, such as occurs with intravenous bicarbonate and/or inhaled beta-agonists. Semiacute management of hyperkalemia includes measures to increase urinary potassium excretion and administration of binding resins, such as Kayexalate®. Prevention is the cornerstone of hyperkalemia management in the heart failure patient and requires that careful attention be directed to both identifying exogenous sources of potassium and pinpointing the maximum tolerable dose of either an angiotensin-converting enzyme inhibitor or an angiotensin-receptor blocker. (c)2001 by CHF, Inc.

Journal Article↗
PubMed2005

Learning from failure: congestive heart failure in the postgenomic age.

The prognosis of heart failure is worse than that of most cancers, but new therapeutic interventions using stem and other cell-based therapies are succeeding in the fight against it, and old drugs, with new twists, are making a comeback. Genetically engineered animal models are driving insights into the molecular mechanisms that cause hearts to fail, accelerating drug discoveries, and inspiring cell-based therapeutic interventions for both acquired and inheritable cardiac diseases.

Animals↗
PubMed1999

Effect of pacing chamber and atrioventricular delay on acute systolic function of paced patients with congestive heart failure. The Pacing Therapies for Congestive Heart Failure Study Group. The Guidant Congestive Heart Failure Research Group.

BACKGROUND: Previous studies of pacing therapy for dilated congestive heart failure (CHF) have not established the relative importance of pacing site, AV delay, and patient heterogeneity on outcome. These variables were compared by a novel technique that evaluated immediate changes in hemodynamic function during brief periods of atrial-synchronous ventricular pacing. METHODS AND RESULTS: Twenty-seven CHF patients with severe left ventricular (LV) systolic dysfunction and LV conduction disorder were implanted with endocardial pacing leads in the right atrium and right ventricle (RV) and an epicardial lead on the LV and instrumented with micromanometer catheters in the LV, aorta, and RV. Patients in normal sinus rhythm were stimulated in the RV, LV, or both ventricles simultaneously (BV) at preselected AV delays in a repeating 5-paced/15-nonpaced beat sequence. Maximum LV pressure derivative (LV+dP/dt) and aortic pulse pressure (PP) changed immediately at pacing onset, increasing at a patient-specific optimal AV delay in 20 patients with wide surface QRS (180+/-22 ms) and decreasing at short AV delays in 5 patients with narrower QRS (128+/-12 ms) (P<0.0001). Overall, BV and LV pacing increased LV+dP/dt and PP more than RV pacing (P<0.01), whereas LV pacing increased LV+dP/dt more than BV pacing (P<0.01). CONCLUSIONS: In this population, CHF patients with sufficiently wide surface QRS benefit from atrial-synchronous ventricular pacing, LV stimulation is required for maximum acute benefit, and the maximum benefit at any site occurs with a patient-specific AV delay.

Aged↗
PubMedDate not supplied

Pharmacotherapy in congestive heart failure: diuretic resistance and strategies to overcome resistance in patients with congestive heart failure.

Congestive heart failure is a complex clinical hemodynamic disorder characterized by chronic and progressive pump failure and fluid accumulation. Although the overall impact of diuretic therapy on congestive heart failure mortality remains unknown, diuretics remain a vital component of symptomatic congestive heart failure management. Over time, sodium and water excretion are equalized before adequate fluid elimination occurs. This phenomenon is thought to occur in one out of three patients with congestive heart failure on diuretic therapy and is termed diuretic resistance. In congestive heart failure, both pharmacokinetic and pharmacodynamic alterations are thought to be responsible for diuretic resistance. Due to disease chronicity, symptomatic management is vital to improved quality of life and enhancing diuretic response is therefore pivotal.

Diuretics↗
PubMed2004

Catheter ablation for atrial fibrillation in congestive heart failure.

BACKGROUND: Congestive heart failure and atrial fibrillation often coexist, and each adversely affects the other with respect to management and prognosis. We prospectively evaluated the effect of catheter ablation for atrial fibrillation on left ventricular function in patients with heart failure. METHODS: We studied 58 consecutive patients with congestive heart failure and a left ventricular ejection fraction of less than 45 percent who were undergoing catheter ablation for atrial fibrillation. We selected as controls 58 patients without congestive heart failure who were undergoing ablation for atrial fibrillation, matched according to age, sex, and classification of atrial fibrillation. We evaluated the patients' left ventricular function and dimensions, symptom score, exercise capacity, and quality of life at baseline and at months 1, 3, 6, and 12. RESULTS: After a mean (+/-SD) of 12+/-7 months, 78 percent of the patients with congestive heart failure and 84 percent of the controls remained in sinus rhythm (P=0.34) (69 percent and 71 percent, respectively, were in sinus rhythm without the administration of antiarrhythmic drugs). The patients with congestive heart failure had significant improvement in left ventricular function (increases in the ejection fraction and fractional shortening of 21+/-13 percent and 11+/-7 percent, respectively; P<0.001 for both comparisons), left ventricular dimensions (decreases in the diastolic and systolic diameters of 6+/-6 mm and 8+/-7 mm, respectively; P=0.03 and P<0.001, respectively), exercise capacity, symptoms, and quality of life. The ejection fraction improved significantly not only in patients without concurrent structural heart disease (24+/-10 percent, P<0.001) and those with inadequate rate control before ablation (23+/-10 percent, P<0.001), but also in those with coexisting heart disease (16+/-14 percent, P<0.001) and adequate rate control before ablation (17+/-15 percent, P<0.001). CONCLUSIONS: Restoration and maintenance of sinus rhythm by catheter ablation without the use of drugs in patients with congestive heart failure and atrial fibrillation significantly improve cardiac function, symptoms, exercise capacity, and quality of life.

Aged↗
PubMed1994

Congestive heart failure: early recognition of congestive heart failure in the primary care setting.

Approximately 400,000 patients in the United States are newly diagnosed with congestive heart failure each year. The vast majority of these patients will not survive 5 years. Symptoms that indicate a decline in patient status often go unrecognized by providers. Early identification of insidious changes and prompt intervention can improve cardiac function and decrease the incidence of acute episodes and repeated hospitalizations. Nurse practitioners in the primary care setting are often called upon to manage these patients. By understanding the physiological changes as they occur and the underlying etiology, management is enhanced.

Heart Failure↗
PubMed1996

Importance of congestive heart failure and interaction of congestive heart failure and left ventricular systolic function on prognosis in patients with acute myocardial infarction.

Left ventricular (LV) systolic function and congestive heart failure (CHF) are important predictors of long-term mortality after acute myocardial infarction. The importance of transient CHF and the interaction of CHF and LV function on prognosis has not been studied in detail previously. In the TRAndolapril Cardiac Evaluation Study, 6,676 consecutive patients with acute myocardial infarction 1 to 6 days earlier had LV systolic function quantified as wall motion index (echocardiography), which is closely correlated to LV ejection fraction. To study the interaction of CHF and wall motion index on long-term mortality, separate analyses were performed in patients with different levels of LV function. Risk ratio (95% confidence intervals [CI]) were determined from proportional hazard models subgrouped by wall motion index or CHF adjusted for age and gender. Heart failure was separated into transient or persistent. Wall motion index and CHF are correlated. Furthermore, there is an interaction between wall motion index and CHF. The prognostic importance of wall motion index depends on whether patients have CHF or not: the risk ratio associated with decreasing 1 wall motion index unit is 3.0 (2.6 to 3.4) in patients with CHF, and 2.2 (1.7 to 2.9) in patients without CHF when adjusted for age and gender. Similarly, the prognostic importance of CHF depends on the level of wall motion index: the risk ratio associated with CHF is 3.9 (1.8 to 8.3) when the wall motion index is <0.8 and 1.9 (1.5 to 2.3) when the wall motion index is >1.6. Transient CHF is an independent risk factor (risk ratio 1.5, confidence interval [CI] 1.3 to 1.8) although milder than persistent CHF (risk ratio 2.8, CI 2.5 to 3.2).

Aged↗
PubMed2003

Losartan corrects abnormal frequency response of renal vasculature in congestive heart failure.

In congestive heart failure, renal blood flow is decreased and renal vascular resistance is increased in a setting of increased activity of both the sympathetic nervous and renin-angiotensin systems. The renal vasoconstrictor response to renal nerve stimulation is enhanced. This is associated with an abnormality in the low-pass filter function of the renal vasculature wherein higher frequencies (> or =0.01 Hz) within renal sympathetic nerve activity are not normally attenuated and are passed into the renal blood flow signal. This study tested the hypothesis that excess angiotensin II action mediates the abnormal frequency response characteristics of the renal vasculature in congestive heart failure. In anesthetized rats, the renal vasoconstrictor response to graded frequency renal nerve stimulation was significantly greater in congestive heart failure than in control rats. Losartan attenuated the renal vasoconstrictor response to a significantly greater degree in congestive heart failure than in control rats. In control rats, the frequency response of the renal vasculature was that of a first order (-20 dB/frequency decade) low-pass filter with a corner frequency (-3 dB, 30% attenuation) of 0.002 Hz and 97% attenuation (-30 dB) at > or =0.1 Hz. In congestive heart failure rats, attenuation did not exceed 45% (-5 dB) over the frequency range of 0.001-0.6 Hz. The frequency response of the renal vasculature was not affected by losartan treatment in control rats but was completely restored to normal by losartan treatment in congestive heart failure rats. The enhanced renal vasoconstrictor response to renal nerve stimulation and the associated abnormality in the frequency response characteristics of the renal vasculature seen in congestive heart failure are mediated by the action of angiotensin II on renal angiotensin II AT1 receptors.

Angiotensin II↗
PubMed2000

Tei-index in patients with mild-to-moderate congestive heart failure.

BACKGROUND: Congestive heart failure is related to contraction and relaxation abnormalities of the ventricle. Isolated analysis of either mechanism may not be reflective of overall cardiac dysfunction. A combined myocardial performance index (isovolumic contraction time plus isovolumic relaxation time divided by ejection time, 'Tei-Index') has been described which may be more effective for analysis of global cardiac dysfunction than systolic and diastolic measures alone. It was the aim of the present investigation to evaluate the Tei-Index against invasive examination. METHODS AND RESULTS: Eighty-one subjects were included in a consecutive manner, among 125 patients undergoing left heart catheterization for invasive measurement of left ventricular end-diastolic pressure; 43 patients had congestive heart failure (35 male, 8 female, 68+/-6 years) defined by NYHA functional class >/=2 (mean 2.5+/-0.5) and left ventricular end-diastolic pressure >/=16 mmHg (mean 20+/-4) and 38 subjects (32 male, 6 female, 66+/-5 years) without symptoms of heart failure (NYHA functional class I) and with normal left ventricular end-diastolic pressure (mean 12+/-3 mmHg) served as a control group. Using conventional echo-Doppler methods, parameters assessed were: ejection fraction, peak velocities of early (E) and late (A) diastolic filling, the E/A ratio, deceleration time, isovolumic contraction time, isovolumic relaxation time and ejection time. The Tei-Index was obtained by subtracting ejection time from the interval between cessation and onset of the mitral flow. The control group and patients with congestive heart failure did not differ with respect to the E/A ratio (0.86+/-0.27 vs 0.90+/-0.44, P=ns), deceleration time (203+/-42 ms vs 206+/-36 ms, P=ns) and isovolumic relaxation time (97+/-16 ms vs 94+/-26 ms, P=ns). The ejection fraction was slightly reduced in patients with congestive heart failure (46+/-11% vs 55+/-8%, P<0.05). The Tei-Index was easily and reproducibly measured in all subjects. The mean value of the Tei-Index was significantly different between the control group and patients with congestive heart failure (0.39+/-0.10 vs 0.60+/-0.18, P<0.001). Receiver operating characteristic curve analysis for the Tei-Index yielded an area under the curve of 0.88+/-0.038. Using a Tei-Index >/=0.47 as the cutpoint, congestive heart failure was identified with a sensitivity of 86% and a specificity of 82%. No correlation was observed between the Tei-Index and heart rate (r=0.22, P=ns), systolic blood pressure (r=0.16, P=ns) or diastolic blood pressure (r=0.08, P=ns). The Tei-Index was significantly related to left ventricular end-diastolic pressure (r=0.46, P<0.01). CONCLUSION: The Tei-Index is a sensitive indicator of overall cardiac dysfunction in patients with mild-to-moderate congestive heart failure. The Tei-Index is easily obtained and may be used in the work-up of patients with suspected cardiac dysfunction.

Aged↗
PubMed2004

An endoscopic study of upper-GI mucosal changes in patients with congestive heart failure.

BACKGROUND: Congestive heart failure results in an increase in systemic venous pressure that is transmitted to the inferior vena cava and to the hepatic veins. This can cause GI vascular and mucosal congestion. The aim of this study was to define upper-GI mucosal changes in patients with congestive heart failure. METHODS: A total of 57 patients with congestive heart failure presenting with GI symptoms underwent upper endoscopy. Echocardiography was performed in all patients to determine the ejection fraction and the degree of tricuspid regurgitation. Transabdominal US was performed to measure the diameters of the hepatic veins, the inferior vena cava, and the portal vein. The presence and the severity of gastropathy and duodenopathy were compared with the parameters relating to severity of cardiac failure. RESULTS: Of the 57 patients studied, gastric mucosal changes were observed in 50 (88%), duodenal mucosal changes in 31 (54%), and esophageal mucosal changes in none. Gastric mucosal changes were the following: mosaic-like pattern (n = 50), punctate spots (n = 34), thickened folds (n = 5), watermelon stomach (n = 3), and telangiectasia (n = 10). Duodenal mucosal changes were the following: mosaic-like pattern (n = 29), thickened folds (n = 8), and telangiectasia (n = 2). Upper-GI symptoms were associated with gastropathy ( p = 0.027) and duodenopathy ( p = 0.003). The presence and the severity of duodenopathy showed a high degree of positive correlation with the presence and the severity of gastropathy (gamma value 0.690; p value <0.001). Patients with gastropathy and duodenopathy had higher mean inferior vena cava and hepatic vein diameters than those without gastropathy and duodenopathy. The severity of duodenopathy but not that of gastropathy was significantly associated with increasing severity of tricuspid regurgitation ( p = 0.001), larger portal vein diameter ( p = 0.02), and lower ejection fraction ( p = 0.008). CONCLUSIONS: Among patients with congestive cardiac failure with GI symptoms, changes of congestive gastropathy are evident in 88% and duodenopathy in 54%. The presence and the severity of duodenopathy was significantly associated with increasing severity of features of congestive heart failure.

Adolescent↗
PubMedDate not supplied

Pharmacotherapy in congestive heart failure: ACE inhibitors and anemia in congestive heart failure.

The use of angiotensin-converting enzyme inhibitors can be accompanied by a number of adverse events, including cough, angioedema, and hyperkalemia, as well as a peculiar form of functional renal insufficiency. Other, less obvious side effects accompany ACE inhibitor use, such as a reduction in red blood cell production. This feature of ACE inhibitor use may be employed to good effect, as in the management of post-transplant erythrocytosis. Alternatively, the suppressive effect of ACE inhibitors on red blood cell production may intensify the anemia of chronic renal failure and/or congestive heart failure. The untreated congestive heart failure patient typically has an increased red blood cell mass as a consequence of increased erythropoietin levels, with the latter governed by congestive heart failure-related renal hypoxia. This is not expressed as an increase in hemoglobin concentration because of the increase in plasma volume that marks advanced congestive heart failure. ACE inhibitor therapy can be expected to both reduce plasma volume and decrease red blood cell production. As a result, the hemoglobin concentration changes very little in the ACE inhibitor-treated congestive heart failure patient and usually falls in the low normal range. Recently, erythropoietin has been employed to good effect in congestive heart failure patients with borderline anemia. (c)2000 by CHF, Inc.

Journal Article↗