The role of ultrafiltration in patients with decompensated heart failure.

Congestion, due in large part to hypervolemia, is the primary driver of heart failure (HF) admissions. Relief of congestion has been traditionally achieved through the use of loop diuretics, but there is increasing concern that these agents, particularly at high doses, may be deleterious in the inpatient setting. In addition, patients with HF and the cardiorenal syndrome (CRS) have diminished response to loop diuretics, making these agents less effective at relieving congestion. Ultrafiltration, a mechanical volume removal strategy, has demonstrated promise in achieving safe and effective volume removal in patients with cardiorenal syndrome and diuretic refractoriness. This paper outlines the rationale for ultrafiltration in CRS and the available evidence regarding its use in patients with HF. At present, the utility of ultrafiltration is restricted to selected populations, but a greater understanding of how this technology impacts HF and CRS may expand its use.

Correlation of impedance cardiography with invasive hemodynamic measurements in patients with advanced heart failure: the BioImpedance CardioGraphy (BIG) substudy of the Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness (ESCAPE) Trial.

BACKGROUND: Impedance cardiography (ICG) is a noninvasive modality that uses changes in impedance across the thorax to assess hemodynamic parameters, including cardiac output (CO). The utility of ICG in patients hospitalized with heart failure is uncertain. METHODS: The BioImpedance CardioGraphy in Advanced Heart Failure study was a prospective substudy of the Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness. A total of 170 subjects underwent blinded ICG measurements using BioZ (CardioDynamics, San Diego, CA); of these, 82 underwent right heart catheterization. We compared ICG with invasively measured hemodynamics by simple correlation and compared overall ICG hemodynamic profiles ("wet" [thoracic fluid content > or =47/kOhm in men and > or =37/kOhm in women] and "cold" [cardiac index < or =2.2 L min(-1)m(-2)) versus those determined by invasive measurements (wet [pulmonary capillary wedge pressure > or =22 mm Hg] and cold [cardiac index < or =2.2 L min(-1)m(-2)). We also determined whether ICG measurements were associated with subsequent death or hospitalization within 6 months. RESULTS: There was modest correlation between ICG and invasively measured CO (r = 0.4 to 0.6 on serial measurement). Thoracic fluid content measured by ICG was not a reliable measure of pulmonary capillary wedge pressure. There was poor agreement between ICG and invasively measured hemodynamic profiles (kappa < or =0.1). No ICG variable alone or in combination was associated with outcome. CONCLUSIONS: In hospitalized patients with advanced heart failure, ICG provides some information about CO but not left-sided filling pressures. Impedance cardiography did not have prognostic utility in this patient population.

Characteristics and outcomes in African American patients with decompensated heart failure.

BACKGROUND: Outcomes in patients with chronic heart failure vary by race. Racial differences in the characteristics and outcomes of patients with acute decompensated heart failure (ADHF) have not been well characterized. Therefore, we assessed race-related differences in presentation, treatment, in-patient experiences, and short-term mortality due to ADHF before and after accounting for known covariates. METHODS: The Acute Decompensated Heart Failure National Registry database was analyzed to evaluate demographic and mortality differences in African American and white patients with ADHF entered into the database from its initiation in September 2001 to December 31, 2004. Stratified analyses by cause, age, left ventricular function, and history of heart failure subgroups were also conducted. RESULTS: A total of 105,872 episodes of ADHF occurred in white patients and 29,862 occurred in African American patients. African American patients with ADHF were younger than white patients (mean [SD] age, 63.5 [15.4] vs 72.5 [12.5] years) and had lower mean left ventricular ejection fractions. The prevalence of hypertension, diabetes mellitus, and obesity was higher in African American patients. African American race was associated with lower in-hospital mortality after adjustment for known predictors (2.1% vs 4.5%; adjusted odds ratio [OR], 0.79; 95% confidence interval [CI], 0.72-0.87; P < .001). This association persisted for all age cohorts, was independent of the use of intravenous vasoactive drugs, and was especially present in African American patients in the nonischemic subgroup (adjusted OR, 0.74; 95% CI, 0.57-0.96) but not the ischemic subgroup (adjusted OR, 0.91; 95% CI, 0.76-1.09). CONCLUSION: In ADHF, African American race is associated with lower in-hospital mortality compared with white race, despite certain indicators of increased disease severity.

Sex differences in the association between leptin and CRP: results from the Dallas Heart Study.

OBJECTIVE: Higher C-reactive protein (CRP) levels in women compared with men may reflect sex differences in the relationship between obesity and inflammation. We evaluated how the adipokine leptin influenced these relationships. METHODS AND RESULTS: Dual energy X-ray absorptometry measurements of fat mass and plasma levels of leptin and CRP were measured in 1188 women and 1102 men from the Dallas Heart Study. Analyses were stratified by sex and a leptin/percent fat index was created to evaluate the association between leptin and CRP independent of fat mass. Women had higher body mass index, percent fat mass, and plasma levels of CRP and leptin. CRP levels correlated with leptin levels in both women (Spearman rho=0.48, p<0.0001) and in men (rho=0.27, p<0.0001). In multivariable models adjusting for confounders including total fat mass, leptin/percent fat index remained significantly associated with logCRP in women (p=0.005), but not in men (p=0.95). A significant interaction was observed between sex and leptin levels on CRP (p(interaction)=0.03). CONCLUSION: Leptin was associated with CRP independent of other measures of obesity in women, but not in men. These findings suggest that sex differences in CRP may reflect sex-related differences in the inflammatory responses to obesity, and may in part, be mediated by leptin.

Low voltage on the electrocardiogram is a marker of disease severity and a risk factor for adverse outcomes in patients with heart failure due to systolic dysfunction.

BACKGROUND: The prognostic implications of low QRS voltage on the electrocardiogram (ECG) in heart failure (HF) are not well characterized. METHODS: We manually measured and summed the QRS voltage in all 12 leads of the ECG (sumQRS) in two cohorts: (1) 415 patients with a low left ventricular ejection fraction followed up in a HF clinic ("clinic cohort") and (2) 100 subjects with advanced HF who had an ECG within 1 year preceding cardiac transplantation ("pretransplant cohort"). Low voltage was defined as the lowest quartile of the clinic cohort (sumQRS <12 mV) and its prevalence was compared in the two cohorts. The associations of low voltage with 1-year outcomes were assessed in the clinic cohort. RESULTS: In the clinic cohort, the frequency of low voltage was higher in New York Heart Association class 4 versus class 1-3 patients (34% vs 22% respectively, P = .04). The frequency of low voltage in the pretransplant cohort (47%) was twice that of the clinic cohort (24%, P < .001). After 1 year of follow-up in the clinic cohort, low ECG voltage was associated with a higher rate of death (14% vs 5%, P = .008) and the composite end point of death or HF hospitalization (35% vs 20%, P = .004). These associations persisted in multivariable analyses adjusting for important confounders. CONCLUSIONS: Low ECG voltage is a marker of the severity of HF and is a risk factor for adverse outcomes in patients with systolic HF at 1 year.

Treatment of the African-American patient with congestive heart failure.

African Americans have a higher burden of cardiovascular disease than white Americans, including a higher prevalence of heart failure. In addition, heart failure in African Americans conforms to a more malignant natural history. Hypertension is most often cited as the sole etiology of heart failure in African Americans. Most of the major trials of pharmacotherapy for the management of chronic heart failure have failed to include significant numbers of African-American patients. Based on the available evidence, there is no reason to withhold standard evidence-based medical therapy for heart failure. Even though there is much controversy as to the efficacy of angiotensin-converting enzyme (ACE) inhibitors and beta blockers in African Americans, in the absence of definitive data they should be used. Recently, the combination of isosorbide dinitrate and hydralazine has been demonstrated to improve survival in African Americans with New York Heart Association class III and IV heart failure, and represents an adjunctive treatment option when added to standard medical therapy consisting of ACE inhibitors, beta blockers, digoxin, diuretics, and aldosterone antagonists. Emerging evidence suggests that this therapy may be targeting a novel mechanism of heart failure progression (ie, nitric oxide bioavailability) found in African Americans.

Novel therapies for heart failure: vasopressin and selective aldosterone antagonists.

Despite favorable improvements in mortality, heart failure (HF) remains a problematic illness due to the ever-present burden of hospitalization. Clearly, novel treatment strategies are needed. This review focuses on two newer pharmacologic targets: arginine vasopressin and aldosterone. Arginine vasopressin receptor antagonists will most likely serve as an adjunct to or replacement of standard diuretic therapy in selected patients. The safety and efficacy of chronic therapy with oral arginine vasopressin receptor antagonists in large groups of congestive HF patients is currently under investigation. Aldosterone antagonism is emerging as a treatment of severe congestive HF. Recent large-scale clinical trials using aldosterone antagonists have proven that those with HF or left ventricular dysfunction postmyocardial infarction derive a survival benefit from aldosterone antagonism. Whether aldosterone antagonism should be prescribed in all patients with HF is unclear; however, in carefully selected and managed patients, aldosterone antagonism is helpful.

beta-Blocker therapy for congestive heart failure: clinical considerations.

Excessive activation of the sympathetic nervous system and local release of norepinephrine are detrimental to the failing myocardium. Blockade of the beta-adrenergic receptor system is now a potent strategy. Earlier concerns that beta-blockade would thwart compensatory mechanisms that preserve myocardial function are no longer valid in the compensated state. Over the past 2 decades, a large body of evidence has accrued indicating marked benefits in symptoms and survival as well as favorable changes in myocardial architecture with beta-blocker therapy in patients who have compensated heart failure with impaired systolic function. This article outlines the rationale for beta-blocker therapy, examines both the early and the large-scale clinical work with beta-blocker therapy for congestive heart failure, highlights additional novel aspects of beta-blocker therapy for heart failure, and outlines expert recommendations about the use of beta-blockers in patients with systolic dysfunction.