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QT interval lengthening in cardiac disease relates more to left ventricular systolic dysfunction than to autonomic function.

BACKGROUND: There are multiple influences on the QTc interval, including the autonomic nervous system. Which influence is the principal determinant of the variation in QTc interval between different cardiac diseases is not yet clear, though some studies have suggested that the QTc interval primarily reflects sympatho-vagal balance. This study investigated this claim further. AIM: To determine if autonomic tone was the prime determinant of variation in the QTc interval between subjects with different cardiac diseases. METHODS: Subjects with different cardiac diseases were studied, QTc interval determined and correlated with three different measures of the autonomic nervous system, that of baroreflex sensitivity, catecholamine levels (epinephrine and norepinephrine) and sympatho-vagal balance as determined by power spectrum analysis. RESULTS: 47 subjects were studied, comprising 17 subjects with heart failure, 14 subjects with left ventricular hypertrophy and 16 control subjects. For the group as a whole there was no relationship between QTc interval and any measure of the autonomic nervous system function, but there was a reasonable relationship between fractional shortening and QTc interval (r=0.47, P<0.003). For subjects with an echocardiographic fractional shortenings less than 0.35 (which correlates with an ejection fraction of <50%), a strong relationship between fractional shortening and QTc interval remained (r=0.57, P<0.002), but in addition a relationship between QTc interval and catecholamine levels developed (for epinephrine: r=0.67, P<0.002; and for norepinephrine: r=0.62, P<0.005). Multiple regression analysis showed that fractional shortening and epinephrine levels were independently related to QTc interval. CONCLUSION: In subjects with a variety of cardiac diseases, the prime determinant of QTc interval is left ventricular systolic performance rather than the autonomic nervous system, though in subjects with low normal and less fractional shortenings catecholamine levels are independently related to QTc interval.

Autonomic Nervous System↗

Drug therapy of heart failure caused by systolic dysfunction in the elderly.

The presence of multiple medical illnesses often distinguishes elderly patients with heart failure and can make pharmacologic management of symptomatic heart failure challenging in this population. Physiologic changes that occur with normal aging may complicate clinical assessment. Limited data from large clinical trials of heart failure therapy are applicable to aged patients. Available data suggest that elderly patients should be treated with the same regimen as younger patients but that more careful attention should be paid to dosing, especially when initiating a new drug. History and physical examination techniques can be used to uncover evidence of congestion and inadequate perfusion and are critical adjuncts when making therapeutic decisions. The objectives of therapy for elderly patients with heart failure must be individualized within the larger context of patients' goals and stage of life.

Adrenergic Antagonists↗

Is left ventricular systolic dysfunction in hypertensive patients with heart failure normalized by long-term antihypertensive therapy?

The critical left ventricular (LV) mass when hypertensive heart failure appears, and whether LV dysfunction in hypertensives with heart failure is normalized by long-term antihypertensive therapy were investigated. LV dimension, LV mass, LV mass index, LV ejection time (LVET) and pre-ejection period (PEP) were measured in 27 normal subjects and 56 essential hypertensives, the latter divided into three groups: group I, without LV hypertrophy; group II, with LV hypertrophy; and group III, with hypertensive heart failure. LV mass and LV mass index were 135.0 +/- 23.8 g and 85.8 +/- 11.7 g/m2, respectively, in normal controls, 133.0 +/- 30.8 g and 82.0 +/- 18.4 g/m2 in group I, 222.3 +/- 38.0 g and 136.1 +/- 19.9 g/m2 in group II, and 422.0 +/- 30.3 g and 235.7 +/- 19.6 g/m2 in group III of essential hypertensives. The upper limits of LV mass and LV mass index in group II (mean + 2SD) were about 300 g and 180 g/m2, respectively. Significant shortening of LVET was observed only in group III, but PEP was prolonged with an increase in LV mass. LV diastolic dimension and PEP were not normalized by long-term antihypertensive therapy (mean: 16 months). These results indicate that the critical LV mass marking the transition from non-failing hypertrophied left ventricle to failing ventricle associated with essential hypertension is about 300 g, or LV mass index of 180 g/m2, and that LV dilatation and depressed myocardial contractility in essential hypertensives with a past history of congestive heart failure were not normalized by chronic antihypertensive therapy.

Adult↗

Management of heart failure. IV. Anticoagulation for patients with heart failure due to left ventricular systolic dysfunction.

OBJECTIVE: This article reviews the incidence of arterial thromboembolism in patients with heart failure who are not receiving anticoagulants. We also examine whether more severe ventricular dysfunction increases this incidence and the efficacy and risks of anticoagulation for patients in sinus rhythm. DATA SOURCES: English-language studies referenced in MEDLINE or EMBASE (January 1966 to September 1993) were reviewed. We used the search terms heart failure, congestive; congestive heart failure; heart failure; cardiac failure; and dilated cardiomyopathy in conjunction with the terms anticoagulation, cerebrovascular disorders, stroke, and thromboembolism. STUDY SELECTION: All studies with separate data for patients with chronic heart failure not receiving anticoagulants were included. Articles addressing valvular heart disease or heart failure secondary to acute myocardial infarction or Chagas' disease were excluded. Studies of the occurrence of left ventricular mural thrombi were also reviewed. DATA EXTRACTION AND SYNTHESIS: Inclusion and exclusion criteria, prevalence of atrial fibrillation, mean follow-up, and the occurrence of arterial thromboembolic events were extracted. If the incidence was not given, this was estimated using the proportion of patients with events divided by the mean follow-up. CONCLUSION: The incidence of arterial thromboembolism ranged from 0.9 to 5.5 events per 100 patient-years, with the largest studies reporting incidence of 2.0% and 2.4%. Findings regarding the relationship between ventricular function and thromboembolic events are contradictory. No controlled trial has assessed the efficacy or risks of anticoagulation for patients with heart failure and sinus rhythm, and reported efficacy in case series ranged from 0% to 100%. Until adequate studies are performed, anticoagulation should be discouraged for patients with heart failure who are in sinus rhythm.

Anticoagulants↗

Apolipoprotein E epsilon4 allele is associated with left ventricular systolic dysfunction.

BACKGROUND: Apolipoprotein (APOE) epsilon4 allele has been associated with cardiac dysfunction in Alzheimer's disease and beta-thalassemia. We investigated the association between APOE genotypes and left ventricular dysfunction in a population of community-dwelling elderly subjects. METHODS: This study was performed in the Rotterdam Study, a population-based prospective cohort study among elderly subjects. For 2206 participants, a baseline echocardiogram and blood specimens for APOE typing were available. Cardiac dysfunction was considered present when fractional shortening was or=65 years. CONCLUSION: The APOE epsilon4 allele is an independent risk factor for cardiac dysfunction in elderly people. Besides well-known effects on atherosclerosis and cholesterol levels, there may be other mechanisms, such as apoptosis, through which this allele exerts negative effects on myocardial performance.

Age Factors↗

Systolic dysfunction is a predictor of long term mortality in men but not in women with heart failure.

AIMS: To evaluate possible gender differences in clinical profile and outcome of patients hospitalised with heart failure. METHODS AND RESULTS: During 1996 a total of 1065 hospital in-patients had confirmed heart failure, with follow-up data through 2002. Women (58%) were significantly older, had higher prevalence of hypertension and diabetes, and lower prevalence of ischaemic heart disease, chronic pulmonary disease and alcoholism. The proportion of patients with normal left ventricular ejection fraction (LVEF) increased with age, but in all age groups women had normal LVEF more frequently than men. Echocardiography was performed less frequently in females: 62% vs. 71% in men, P<0.01, and this finding was consistent in all age groups. During follow-up (median 19 months) 507 patients died (216 men [48.8%] and 291 women [46.8%]). Gender was not a predictor of survival when LVEF was included in the model (RH Male Gender 0.8, 95% CI 0.6 to 1.1, P=0.2). There was a significant interaction gender-LVEF (P=0.048): survival was similar in both genders with LVEF >0.3 but women with LVEF </=0.3 had a better prognosis than their male counterparts. CONCLUSIONS: Survival is similar in women irrespective of LVEF and in men with LVEF >0.3 while men with severely depressed LVEF have a worse prognosis.

Adolescent↗

Alcohol consumption and prognosis in patients with left ventricular systolic dysfunction after a myocardial infarction.

OBJECTIVES: We assessed the influence of alcohol intake on the development of symptomatic heart failure (HF) in patients with left ventricular (LV) dysfunction after a myocardial infarction (MI). BACKGROUND: In contrast to protection from coronary heart disease, alcohol consumption has been linked to cardiodepressant effects and has been considered contraindicated in patients with HF. METHODS: The Survival And Ventricular Enlargement (SAVE) trial randomized 2231 patients with a LV ejection fraction (EF) <40% following MI to an angiotensin-converting enzyme inhibitor or placebo. Patients were classified as nondrinkers, light-to-moderate drinkers (1 to 10 drinks/week), or heavy drinkers (>10 drinks/week) based on alcohol consumption reported at baseline. The primary outcome was hospitalization for HF or need for an open-label angiotensin-converting enzyme inhibitor. Analyses were repeated using alcohol consumption reported three months after MI. RESULTS: Nondrinkers were older and had more comorbidities than light-to-moderate and heavy drinkers. In univariate analyses, baseline light-to-moderate alcohol intake was associated with a lower incidence of HF compared with nondrinkers (hazard ratio [HR] 0.71; 95% confidence interval [CI] 0.57 to 0.87), whereas heavy drinking was not (HR 0.91; 95% CI 0.67 to 1.23). After adjustment for baseline differences, light-to-moderate baseline alcohol consumption no longer significantly influenced the development of HF (light-to-moderate drinkers HR 0.93; 95% CI 0.75 to 1.17; heavy drinkers HR 1.25; 95% CI 0.91 to 1.72). Alcohol consumption reported three months after the MI similarly did not modify the risk of adverse outcome. CONCLUSIONS: In patients with LV dysfunction after an MI, light-to-moderate alcohol intake either at baseline or following MI did not alter the risk for the development of HF requiring hospitalization or an open-label angiotensin-converting enzyme inhibitor.

Alcohol Drinking↗

White blood cell count and mortality in patients with ischemic and nonischemic left ventricular systolic dysfunction (an analysis of the Studies Of Left Ventricular Dysfunction [SOLVD])

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.

Aged↗