Multiple neurohumoral modulating agents in systolic dysfunction heart failure: are we lowering blood pressure too much?

BACKGROUND: Disease-modifying drug treatment in heart failure (HF) reduces blood pressure. Titration of these agents is guided by clinic blood pressure readings; however, the impact of such treatment on blood pressure is unknown because diurnal blood pressure patterns remain poorly described. The aim of this study was to examine the impact of additional neurohumoral modulating agents on ambulatory blood pressure monitoring (ABPM) control in patients with systolic HF and examine the relationship between the burden of hypotension and clinical outcomes. METHODS AND RESULTS: In a prospective analysis on 45 patients undergoing initiation and optimization of additional medications (angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, or beta-blockers), mean daytime systolic (P = .035) and mean daytime and nocturnal diastolic hypotensive episodes (both P < .001) increased significantly posttitration. There was no change in clinic blood pressure before and after titration. In a cross-sectional analysis on 144 patients, those with the most diastolic hypotensive episodes had higher rates of HF readmissions (P = .01) and the composite end point of all-cause mortality and all-cause readmissions (P = .03). CONCLUSIONS: Additional neurohumoral modulating agents could produce significant increases in 24-hour hypotension burden despite reassuring clinic blood pressure readings. The burden of diastolic hypotension is independently predictive of HF readmissions and the composite end point of all-cause mortality and emergency readmissions.

Need and evolution of need for device therapy in a community heart failure population.

BACKGROUND: New guidelines for implantable cardiac defibrillators (ICD) and cardiac resynchronisation therapy (CRT) have expanded the potential use for device therapy. The implications of this on a community heart failure (HF) population are unknown. AIM: To assess the need for device therapy and the change in need over time. METHODS: We reviewed device need in a community HF population using ESC guidelines. Change in need was assessed by comparing data between an annual visit called TP2 and an earlier visit called TP1. Patients' need and change in need between TP1 and TP2 was determined. RESULTS: 210 patients were included; mean age 70+/-12 years, 67% male and 54% ischaemic. At TP1, 34% of patients were suitable for ICD and 3% for CRT. At TP2, 22% and 1% were suitable respectively. Of those suitable for ICD at TP1, 19% lost the need at TP2; in addition 9% of patients unsuitable for ICD at TP1 had acquired the need by TP2. Fifty five percent of patients were unsuitable for ICD at either time point, and 16% were suitable at both time points. CRT need was negligible but also noted to change. CONCLUSION: ICD need is substantial in a community HF population, but CRT need is limited. ICD need changes significantly. Identifying those likely to change their need may optimise ICD use.

Outpatient intravenous diuretic therapy; potential for marked reduction in hospitalisations for acute decompensated heart failure.

BACKGROUND: Heart failure patients have frequent readmissions for acute decompensated heart failure (ADHF). AIMS: To examine the feasibility, safety and outcomes of outpatient intravenous (IV) diuretic therapy in treating ADHF. METHODS: A retrospective analysis was performed of all patients included in a hospital-based heart failure disease management programme, who received outpatient IV diuretic therapy for the management of ADHF between 2002 and 2006. Changes in clinical and biochemical parameters from time of therapy to stability were measured. RESULTS: One hundred and seven patients (mean age 71+/-11 years) received outpatient IV diuretic therapy for ADHF IV diuretic administration reduced weight (p<0.001), blood pressure (p<0.01) and BNP (p=0.01). It increased urea (p=0.01) and creatinine (p=0.07). Seventy-two percent of patients stabilised following IV diuretics and did not require admission. No patients were hospitalised for hypotension or hypokalaemia. One patient was hospitalised for renal failure. Two patients died post admission. CONCLUSION: Outpatient IV diuretic administration for ADHF is safe, cost effective and reduces hospitalisations. This service may expand the potential of a disease management programme to manage ADHF out of hospital and thereby reduce the hospital dependency of this condition.

Improvement but no cure of left ventricular systolic dysfunction in treated heart failure patients.

BACKGROUND: Recent advances in pharmacological and pacemaker-based treatments for heart failure (HF) have brought about significant improvements in left ventricular function. AIMS: To identify the proportion of treated systolic HF patients in whom left ventricular systolic function improves and/or returns to normal. METHODS: This was a retrospective analysis of 221 HF patients. Improvement in left ventricular function was defined as an improvement in ejection fraction (LVEF) of > or =10% on echocardiography. Return to normal was defined as an improvement of LVEF to > or =50% and a reduction in left ventricular end diastolic diameter to < or =55 mm. Changes in BNP were also recorded. RESULTS: Improvement in LVEF was observed in 44.3% of patients and return to normal systolic function in 10.9%, only 2.3% had both a return to normal echocardiographic parameters and a BNP<100 pg/ml. A higher percentage of the improved group were on target doses of beta-blockers (p=0.004). Baseline BNP was not a predictor of improvement. There was a trend towards a reduction in HF readmissions in the improved group (p=0.07) but no difference in the risk of death or all-cause readmission. CONCLUSION: While a substantial proportion of treated HF patients have an improvement in left ventricular function over time, only a small proportion return to normal dimensions and LVEF, underlining the permanent nature of ventricular damage in the vast majority of patients.

Tolerability of carvedilol in patients with heart failure and concomitant chronic obstructive pulmonary disease or asthma.

BACKGROUND: A substantial proportion of the population with congestive heart failure (CHF) has concomitant airway disease. Little information exists on the tolerability of carvedilol in patients with chronic obstructive pulmonary disease (COPD). In this study, we assessed the tolerability and efficacy of carvedilol in patients with CHF and concomitant COPD or asthma. METHODS: Between 1996 and 2000, a total of 487 patients began receiving open-label carvedilol. Forty-three (9%) had COPD (n = 31) or asthma (n = 12). Spirometry supported clinical diagnosis in all, and full pulmonary function testing supported diagnosis in 71%. Sixty percent began carvedilol therapy in the hospital and underwent measurement of peak expiratory flow rates (PEFR) before and after dosing. RESULTS: In patients with COPD, mean forced expiratory volume in one second (FEV(1)) was 62% +/- 13% predicted, reversibility was 4% +/- 4% with bronchodilators, and FEV(1)/FVC was 62% +/- 8%. Mean PEFR was 325 +/- 115 liter/min before the dose and increased by 17% 2 hours after the carvedilol dose (p = 0.04). In patients with asthma, mean FEV(1) was 80% +/- 17% predicted, reversibility was 13% +/- 7%, and FEV(1)/FVC was 74% +/- 11%. Mean PEFR was 407 +/- 161 liter/min before the dose with no significant change 2 hours after the dose. Carvedilol was introduced safely in 84% of patients with COPD, with only 1 patient withdrawn from therapy for wheezing. In contrast, only 50% of patients with asthma tolerated carvedilol. Survival at 2.5 years was 72%. In survivors, left ventricular end-diastolic diameter decreased from 76 +/- 11 mm to 72 +/- 14 mm (p = 0.01), left ventricular end-systolic diameter decreased from 65 +/- 13 mm to 60 +/- 15 mm (p = 0.01), and fractional shortening increased from 14% +/- 7% to 17% +/- 7% (p = 0.05) at 12 months. CONCLUSIONS: Patients with CHF and COPD tolerated carvedilol well with no significant reversible airflow limitation, but patients with CHF and asthma tolerated carvedilol poorly. The effect of carvedilol on left ventricular dimensions and function in patients with concomitant airway diseases was similar to that seen in our general group of patients. Asthma remains a contraindication to beta-blockade.