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We conducted a retrospective analysis of the Studies Of Left Ventricular Dysfunction (SOLVD) trials to assess the predictive value of the baseline white blood cell (WBC) count on mortality. Mortality was higher in participants with a baseline WBC count >7,000 compared to those with a baseline WBC < or =7,000 (27% vs 21%, p <0.0001). After controlling for important covariates, each increase in WBC count of 1,000/mm3 was significantly associated with an increased risk of all-cause mortality (relative risk [RR] 1.05, p <0.001). Overall, compared with a baseline WBC count < or =7,000, a baseline WBC count >7,000 was significantly associated with an increased risk of all-cause mortality (RR 1.22, p = 0.001). In participants with ischemic left ventricular (LV) dysfunction, a WBC count >7,000 remained significantly associated with an increased risk of all-cause mortality (RR 1.26, p <0.001), whereas in participants with nonischemic LV dysfunction there was no relation between WBC count and mortality (RR 1.08, p = 0.5). Thus, baseline WBC is an independent predictor of mortality in patients with LV dysfunction, specifically in those with ischemic cardiomyopathy.
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Five percent of all hospital medical admissions are patients with heart failure. The incidence is about one new case per 1000 of the general population per year, increasing to >10 per 1000 in those aged >or=85 years. Although the evidence that beta-blockers reduce mortality by about 36% when added to angiotensin-converting enzyme inhibitors is overwhelming, clinicians are still reluctant to use beta-blockers in heart failure, especially in older patients. Here, we examine the evidence for the use of beta-blockers in heart failure in older people and explore the practicalities of their use.
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AIMS: The most widely accepted marker for stratifying the risk of sudden cardiac death (SCD) in post myocardial infarction patients is a depressed left ventricular function. Left ventricular ejection fractions (EF) of 35% or less increase the risk of sudden death but values between 35 and 40% raise concern. The underlying pathophysiological mechanism is sustained ventricular tachycardia or fibrillation, both associated with increased cardiac repolarization variability. We assessed whether the indices of QT variability from a short-term electrocardiographic (ECG) recording predict sudden death. METHODS AND RESULTS: A total of 396 subjects with chronic heart failure (CHF) due to post-ischaemic cardiomyopathy, with an EF between 35 and 40% and in NYHA class I, underwent a 5 min ECG recording to calculate the following variables: QT variance (QT(v)), QT normalized for the square of the mean QT (QTVN), and QT variability index (QTVI). Corrected QT (QT(c)) was calculated from a 12-lead ECG recording. All participants were followed for 5 years. A multivariable survival model indicated that a QTVI greater than or equal to the 80th percentile indicated a high risk of SCD [hazards ratio (HR) 4.6, 95% confidence interval (CI) 1.5-13.4, P = 0.006] and, though to a lesser extent, a high risk of total mortality (HR 2.4, 95% CI 1.2-4.9, P = 0.017). The model including QTVI as a continuous variable confirmed a similar high risk for SCD (HR 2.9, 95% CI 1.3-6.5, P = 0.01) and for total mortality (HR 2.6, 95% CI 1.3-5.2, P = 0.008). CONCLUSION: Although asymptomatic patients with CHF who have a slightly depressed EF are at low risk of sudden death, the category is extraordinarily numerous. The QTVI could be helpful in stratifying the risk of sudden death in this otherwise undertreated population.
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Heart failure is a devastating chronic and progressive cardiac disorder affecting millions of Americans annually. Identifying the cause and initiating treatment early is the key to attempting to slow the progression of the condition. Recommended therapy is treatment with angiotensin-converting enzyme (ACE) inhibitors, diuretics, digoxin, beta blockers, and in patients with symptomatic class III and IV heart failure, the addition of aldactone.
Reducing the exercise intolerance and symptoms experienced by patients with chronic heart failure remains an important focus in their clinical care. A clear shortcoming exists; however, with respect to an appreciation that in addition to standard medical therapy, selected patients with stable heart failure also can benefit from a moderate exercise training program. Improvements in central transport, regional blood flow, and skeletal muscle histology and biochemistry all likely account for the increase in exercise capacity and delay in fatigue that these patients experience. Additionally, the autonomic imbalance that is characteristic of these patients is improved. Although the number of patients with heart failure participating in an exercise program is increasing, much work still exists relative to incorporating this treatment method into the care plans established by physicians and physician extenders.
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