Beta-blockers for systolic dysfunction.
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Adrenergic beta-Antagonists↗
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Prognostic impact of diabetes mellitus in patients with heart failure according to the etiology of left ventricular systolic dysfunction.
OBJECTIVES: We sought to determine the relative impact of diabetes mellitus on prognosis in ischemic compared with nonischemic cardiomyopathy. BACKGROUND: Ischemic myocardium is characterized by increased reliance on aerobic and anaerobic glycolysis. Because glucose utilization by cardiomyocytes is an insulin-mediated process, we hypothesized that diabetes would have a more adverse impact on mortality and progression of heart failure in ischemic compared with nonischemic cardiomyopathy. METHODS: We performed a retrospective analysis of the Studies Of Left Ventricular Dysfunction (SOLVD) Prevention and Treatment trials. RESULTS: In adjusted analyses, diabetes mellitus was strongly associated with an increased risk for all-cause mortality in patients with ischemic cardiomyopathy, (relative risk [RR] 1.37, 95% confidence interval [CI] 1.21 to 1.55; p < 0.0001), but not in those with nonischemic cardiomyopathy (RR 0.98, 95% CI 0.76 to 1.32; p = 0.98). The increased mortality in patients with ischemic cardiomyopathy compared with nonischemic cardiomyopathy was limited to those with ischemic cardiomyopathy and diabetes mellitus (RR 1.37, 95% CI 1.21 to 1.56; p < 0.0001). When patients with ischemic cardiomyopathy and diabetes mellitus were excluded, there was no significant difference in mortality risk between the ischemic and nonischemic cardiomyopathy groups after adjusted analysis (RR 0.99, 95% CI 0.86 to 1.15; p = 0.99). Previous surgical revascularization identified patients within the cohort with ischemic cardiomyopathy and diabetes mellitus, with improved prognosis. CONCLUSIONS: The differential impact of diabetes on mortality and heart failure progression according to the etiology of heart failure suggests that diabetes and ischemic heart disease interact to accelerate the progression of myocardial dysfunction. Evaluation of the potential for revascularization may be particularly important in patients with ischemic cardiomyopathy and diabetes mellitus.
Cohort Studies↗
Value of left atrial function in predicting exercise capacity in heart failure with moderate to severe left ventricular systolic dysfunction.
Left atrial (LA) function is associated with left ventricular (LV) diastolic filling and cardiac output response to exercise. But the relation between LA function and exercise performance has not been adequately evaluated. The aim of this study was to investigate the relation between LA function and exercise capacity in dilated cardiomyopathy (DCM) with cardiopulmonary exercise testing. Forty-four patients with a left ventricular end-diastolic dimension (LVDd) > or = 60 mm and an ejection fraction (EF) < or = 40%, and in normal sinus rhythm were included in this study. Patients were divided into group 1 and group 2 according to their exercise peak oxygen uptake (VO2) (group 1: peak VO2 >14 mL/kg/min, group 2: peak VO2 < or = 14 mL/ kg/min). LA function indices were defined as follows: LA end-systolic diameter (LASd), end-diastolic diameter (LADd), LA systolic volume (LASV), LA diastolic volume (LADV), LA ejection volume (LAEV), and LA ejection fraction (LAEF). LASd, LADd, LASV, and LADV were significantly increased in group 2 (P < 0.001, P < 0.001, P < 0.05, P < 0.005). Group 1 had significantly higher LAEF (P < 0.001 ) and LVEF (P < 0.05). Group 2 had significantly shorter exercise duration, and decreased anaerobic threshold levels and minute ventilation volumes (P < 0.001, P < 0.001, P < 0.005 ). There was a positive correlation between peak VO2 and LVEF (r = 0.46, P = 0.002), and LAEF (r = 0.61, P < 0.001), peak A wave velocity (r = 0.39, P = 0.009), E wave deceleration time (r = 0.56, P < 0.001), and isovolumic relaxation time (IVRT) (r = 0.35, P = 0.04). There was a negative correlation between peak VO2 and LASd (r = -0.53, P < 0.001) LADd (r = -0.59, P < 0.001), LASVI (r = -0.34, P = 0.027), LADVI (r = -0.37, P = 0.001), and the E/A ratio (r = -0.41, P = 0.006), Decreased LAEF and increased LA sizes were associated with decreased peak VO2. The results clearly demonstrate that LA functions at rest are related to exercise performance in patients with heart failure.
Atrial Function, Left↗
Recurrent spontaneous coronary artery dissection with transient left ventricular systolic dysfunction.
Spontaneous coronary artery dissection (SCAD) is a potentially life-threatening entity with a variety of clinical presentations. We report a patient who presented with chest pain and angiographic evidence of coronary dissection. Due to the rapid resolution of symptoms and benign-appearing nature of the dissection, no intervention was pursued and the patient was maintained on medical therapy. She represented 2 days later with substernal chest pain, dynamic EKG changes, positive cardiac biomarkers and a transient depression of her left ventricular function.
Aortic Dissection↗
Is there a role for digoxin in patients with systolic dysfunction?
In early placebo-controlled trials in patients with heart failure who were in sinus rhythm, digoxin improved hemodynamics, signs and symptoms of heart failure, and exercise capacity, and decreased functional deterioration and the need for pharmacologic cointervention. A more recent trial showed that withdrawing digoxin from patients who were clinically stable while receiving diuretics and angiotensin-converting enzyme (ACE) inhibitors often resulted in clinical deterioration, whereas continuing the agent maintained stability. Which patients should initially be treated with digoxin remains to be determined. The effects of digoxin on mortality in patients who are receiving ACE inhibitors must also be established.
Digoxin↗
N-terminal proatrial natriuretic peptide correlates with systolic dysfunction and left ventricular filling pattern in patients with idiopathic dilated cardiomyopathy.
OBJECTIVE: To investigate the diastolic Doppler filling pattern in patients with idiopathic dilated cardiomyopathy and its relation to N-terminal pro-atrial natriuretic peptide (NT-pro-ANP). METHODS: 32 patients (26 male, six female) with idiopathic dilated cardiomyopathy were investigated. All were in sinus rhythm. Conventional M mode echocardiography and Doppler echocardiography was done in each patient. Pulsed wave Doppler inflow signals were obtained and the following variables were measured: maximum E wave, maximum A wave, E/A ratio, E wave deceleration time, A wave deceleration time. NT-pro-ANP was measured using radioimmunoassay. RESULTS: Mean (SD) left ventricular ejection fraction was 34 (7)% and mean left ventricular end diastolic diameter on M mode echocardiography was 69 (7) mm. Left ventricular filling indices were as follows: maximum E wave velocity, 0.86 (0.22) m/s; maximum A wave velocity, 0.71 (0.24) m/s; E/A ratio, 1.41 (0.65). Mean E wave deceleration time was 140 (50) ms; mean A wave deceleration time was 100 (20) ms. In a stepwise forward regression model, NT-pro-ANP correlated significantly with left atrial diameter (r = 0.603; p < 0. 001), left ventricular ejection fraction (r = -0.758; p < 0.001), and Doppler derived E/A ratio (r = 0.740; p < 0.001). CONCLUSIONS: In patients with idiopathic dilated cardiomyopathy there is a relation between NT-pro-ANP and both systolic and diastolic variables. In a multivariate model NT-pro-ANP correlated with left atrial diameter, left ventricular ejection fraction, and Doppler derived E/A ratio on transmitral inflow.
Aged↗
Guideline for the management of heart failure caused by systolic dysfunction: Part I. Guideline development, etiology and diagnosis.
Over the past decade, the conceptual understanding of heart failure has changed significantly. Several large clinical trials have demonstrated that pharmacologic interventions can dramatically reduce the morbidity and mortality associated with heart failure. These trials have extended the therapeutic paradigm for treating heart failure beyond the goal of limiting congestive symptoms of volume overload. This two-part article presents an evidence-based guideline to assist primary care physicians in evaluating and treating patients with heart failure. Part I describes the new paradigm of heart failure and offers guidance for diagnostic testing. Part II presents a treatment guideline.
Evidence-Based Medicine↗
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.
Adult↗
Effect of kidney transplantation on left ventricular systolic dysfunction and congestive heart failure in patients with end-stage renal disease.
OBJECTIVES: We examined the impact of kidney transplantation on left ventricular ejection fraction (LVEF) in end-stage renal disease (ESRD) patients with congestive heart failure (CHF). BACKGROUND: The ESRD patients with decreased LVEF and a poor New York Heart Association (NYHA) functional class are not usually referred for transplant evaluations, as they are considered to be at increased risk of cardiac and surgical complications. METHODS: Between June 1998 and November 2002, 103 recipients with LVEF < or =40% and CHF underwent kidney transplantation. The LVEF was re-assessed by radionuclide ventriculography gated-blood pool (MUGA) scan at six and 12 months and at the last follow-up during the post-transplant period. RESULTS: Mean pre-transplant LVEF% increased from 31.6 +/- 6.7 (95% confidence interval [CI] 30.3 to 32.9) to 52.2 +/- 12.0 (95% CI 49.9 to 54.6, p = 0.002) at 12 months after transplantation. There was no perioperative death. After transplantation, 69.9% of patients achieved LVEF > or =50% (normal LVEF). A longer duration of dialysis (in months) before transplantation decreased the likelihood of normalization of LVEF in the post-transplant period (odds ratio 0.82, 95% CI 0.74 to 0.91; p < 0.001). The NYHA functional class improved significantly in those with normalization of LVEF (p = 0.003). After transplantation, LVEF >50% was the only significant factor associated with a lower hazard for death or hospitalizations for CHF (relative risk 0.90, 95% CI 0.86 to 0.95; p < 0.0001). CONCLUSIONS: Kidney transplantation in ESRD patients with advanced systolic heart failure results in an increase in LVEF, improves functional status of CHF, and increases survival. To abrogate the adverse effects of prolonged dialysis on myocardial function, ESRD patients should be counseled for kidney transplantation as soon as the diagnosis of systolic heart failure is established.
Female↗
Systolic dysfunction in heart failure with a normal ejection fraction: echo-Doppler measurements.
Heart failure with a normal ejection fraction, also called heart failure with preserved ejection fraction or diastolic heart failure, is thought to be characterized by normal systolic function and disturbed diastolic function only. However, studies using newer Doppler-echocardiographic techniques have shown that ventricular function is not normal particularly in the long axis. Ejection is relatively preserved because of increased radial function. Similar findings are seen with normal ageing and the typical precursors of heart failure with a normal ejection fraction such as hypertension, diabetes, and ischemia. There appears to be a spectrum of abnormalities of systolic function from the truly normal to systolic heart failure with heart failure with a normal ejection fraction occupying an intermediate position. The use of ejection fraction, which has a normal distribution, to dichotomize patients with heart failure is not supported on theoretical or experimental grounds, and any cutoff is arbitrary. Patients with heart failure have a mixture of systolic and diastolic abnormalities and variable degrees of remodeling. It is more important to correctly identify these in the individual patient.
Diastole↗
Defining the role of calcium channel antagonists in heart failure due to systolic dysfunction.
Calcium channel antagonists (CCAs) may either be divided into the dihydropyridines (e.g. amlodipine, felodipine, isradipine, lacidipine, nilvadipine, nifedipine, nicardipine etc.), the phenylalkylamines (e.g. verapamil) and the benzothiazepines (e.g. diltiazem) according to their chemical structure, or into first generation agents (nifedipine, verapamil and diltiazem) and second generation agents (subsequently developed dihydropyridine-derivatives). Second generation CCAs are characterized by greater selectivity for calcium channels in vascular smooth muscle cells than the myocardium, a longer duration of action and a small trough-to-peak variation in plasma concentrations. Heart failure is characterized by decreased cardiac output resulting in inadequate oxygen delivery to peripheral tissues. Although the accompanying neurohormonal activation, leading to vasoconstriction and increased blood pressure, is initially beneficial in increasing tissue perfusion, prolonged activation is detrimental because it increases afterload and further reduces cardiac output. At the level of the myocyte, heart failure is associated with increased intracellular calcium levels which are thought to impair diastolic function. These changes indicate that the CCAs would be beneficial in patients with heart failure. There has been a strong interest and increasing experience in the use of CCAs in patients with heart failure. Despite potential beneficial effects in initial small trials, findings from larger trials suggest that CCA may have detrimental effects upon survival and cardiovascular events. However, this may not necessarily be a 'class b' effect of the CCAs as there is considerable heterogeneity in the chemical structure of individual agents. Clinical experience with different CCAs in patients with heart failure includes trials that evaluated their effects on hemodynamic parameters, exercise tolerance and on symptomatology. However, the most relevant results are those from randomized clinical trials that assessed mortality as the primary endpoint. First generation CCAs have direct negative inotropic effects and even sustained release formulations have not proved any beneficial effect upon survival. With second generation CCAs, some benefit on hemodynamic parameters has been observed but none on survival, alone or in combination with ACE inhibitors. It is noteworthy that although amlodipine had a neutral effect on morbidity and mortality in large, randomized, placebo-controlled trials in patients with heart failure, the drug was well tolerated. There is no specific indication for CCAs (first or second generation) in patients with systolic heart failure, alone or in combination with ACE inhibitors, but amlodipine may be a considered in the management of hypertension or coronary artery disease in patients with heart failure.
Angiotensin-Converting Enzyme Inhibitors↗
Heart Failure Society of America (HFSA) practice guidelines. HFSA guidelines for management of patients with heart failure caused by left ventricular systolic dysfunction--pharmacological approaches.
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Adrenergic beta-Antagonists↗
Correlation of B-type natriuretic peptide level to 6-min walk test performance in patients with left ventricular systolic dysfunction.
BACKGROUND: B-type natriuretic peptide (BNP) is a neurohormone that can be measured in blood and is useful in patients with congestive heart failure (CHF). We compared whole blood BNP concentrations to distance walked during a 6-min walk test in patients with CHF. METHODS: Forty-four patients with CHF underwent a 6-min walk test. The distance walked was compared to the BNP concentration on blood collected prior to the walk test. Patients were followed for 16 +/- 2.8 months after testing. RESULTS: A significant correlation was observed between the BNP concentration and the distance walked (r = -0.47, p < 0.001). One patient without congestion died suddenly. Two patients died of progressive heart failure, and two other patients underwent cardiac transplantation. Each of the latter four patients had high BNP concentrations (median 1080 ng/l) and walked short distances (median 183 m). This study indicates that the BNP concentration in blood correlates inversely with the degree of physical capability of patients with heart failure. CONCLUSIONS: The BNP concentration could be used as an alternative to the 6-min walk test to assess the severity of heart failure. The assay for BNP is non-invasive, inexpensive, and results are available at the bedside or in a heart failure clinic.
Adult↗
Prognostic impact of matrix metalloproteinase gene polymorphisms in patients with heart failure according to the aetiology of left ventricular systolic dysfunction.
AIMS: To assess the possible effect of functional polymorphisms in matrix metalloproteinase (MMP) gene promoters on the clinical outcome of patients with heart failure. METHODS AND RESULTS: We studied 444 consecutive patients who were referred to our centre for evaluation of left ventricular dysfunction. We extracted genomic DNA from white blood cells and determined the -1306 C >T MMP-2, -1171 5A > 6A MMP-3, and -1562 C >T MMP-9 polymorphisms. Clinical follow-up (median 717 days) was obtained for 443 patients. The MMP-3 polymorphism had a different impact on cardiac survival in HF patients with ischaemic and non-ischaemic cardiomyopathy (interaction p <0.03). The MMP-3 5A/5A genotype was an independent predictor of cardiac mortality (HR 2.92 [1.23-6.69]; p = 0.01) in patients with non-ischaemic HF. In contrast, there was no evidence for any effect of the MMP-3 genotype on cardiac events in patients with ischaemic cardiomyopathy. The MMP-9 polymorphism was associated with cardiac survival (p < 0.03) independently of HF aetiology. In multivariate analysis, the MMP-9 T allele was an independent predictor of cardiac mortality (HR 1.81 [1.09-3.02]; p = 0.02). Finally, there was no evidence for any association between MMP-2 polymorphism and cardiac survival. CONCLUSION: MMP-3 and MMP-9 polymorphisms contribute to variability in cardiac survival in HF patients. These data suggest that MMP genotyping could provide important additional information for refining risk stratification in patients with heart failure. MMP genotyping may help to select patients who could benefit from MMP inhibition.
Exercise Test↗
Beta-adrenergic blocking agent use and mortality in patients with asymptomatic and symptomatic left ventricular systolic dysfunction: a post hoc analysis of the Studies of Left Ventricular Dysfunction.
OBJECTIVES: This analysis was performed to assess whether beta-adrenergic blocking agent use is associated with reduced mortality in the Studies of Left Ventricular Dysfunction (SOLVD) and to determine if this relationship is altered by angiotensin-converting enzyme (ACE) inhibitor use. BACKGROUND: The ability of beta-blockers to alter mortality in patients with asymptomatic left ventricular dysfunction is not well defined. Furthermore, the effect of beta-blocker use, in addition to an ACE inhibitor, on these patients has not been fully addressed. METHODS: This retrospective analysis evaluated the association of baseline beta-blocker use with mortality in 4,223 mostly asymptomatic Prevention trial patients, and 2,567 symptomatic Treatment trial patients. RESULTS: The 1,015 (24%) Prevention trial patients and 197 (8%) Treatment trial patients receiving beta-blockers had fewer symptoms, higher ejection fractions and different use of medications than patients not receiving beta-blockers. On univariate analysis, beta-blocker use was associated with significantly lower mortality than nonuse in both trials. Moreover, a synergistic reduction in mortality with use of both a beta-blocker and enalapril was suggested in the Prevention trial. After adjusting for important prognostic variables with Cox multivariate analysis, the association of beta-adrenergic blocking agent use with reduced mortality remained significant for Prevention trial patients receiving enalapril. Lower rates of arrhythmic and pump failure death and risk of death or hospitalization for heart failure were observed. CONCLUSIONS: The combination of a beta-blocker and enalapril was associated with a synergistic reduction in the risk of death in the SOLVD Prevention trial.
Adrenergic beta-Antagonists↗
Systolic dysfunction in heart failure with normal ejection fraction: speckle-tracking echocardiography.
Left ventricular (LV) ejection fraction (EF) and LV end-systolic volumes are important measures of LV global function. However, in many patients with symptoms of heart failure, these measures are within normal limits. This condition is classified as heart failure with normal ejection fraction (HFNEF). Reduced EF and increased end-systolic volume, however, require impaired function in a number of LV segments. Therefore, apparently normal systolic function in HFNEF may reflect limited sensitivity of global EF, and assessment of regional systolic function may provide important diagnostic information. The recently introduced method, speckle-tracking echocardiography (STE), represents a simplified, objective, and angle-independent modality for quantification of regional myocardial deformation. The software uses conventional gray-scale B-mode recordings and tracks myocardial speckles, which serve as natural acoustic markers. Radial and longitudinal myocardial deformation can be measured simultaneously from long-axis recordings, radial and circumferential deformation from short-axis recordings, and LV torsion from assessment of apical and basal short-axis rotation. Experimental and clinical studies have demonstrated that the STE method can assess myocardial function accurately in healthy subjects in the settings of acute and chronic ischemia, dyssynchrony, and cardiomyopathy. So far, no STE studies have been performed regarding HFNEF. The purpose of this article is therefore to illustrate the potential of this novel method.
Diastole↗
Combined assessment of cardiac systolic dysfunction and coronary atherosclerosis used to predict future cardiac deaths after starting hemodialysis.
BACKGROUND/AIMS: Identification of end-stage renal disease (ESRD) patients at high risk for cardiac events is important for clinical dialysis management. The present study determined whether the combination of cardiac function and coronary atherosclerosis could predict future cardiac events after starting renal replacement therapy (RRT). METHODS: We prospectively assessed left ventricle ejection fraction (EF) and Gensini score (GS) using angiographic severity of coronary atherosclerosis in 88 consecutive ESRD patients [mean age 62 years; 69 males (78%); 55 patients (64%) with diabetic nephropathy] at the initiation of RRT. EF was analyzed by echocardiogram, and GS was scored by coronary angiography within 3 months after starting RRT. The study end point was cardiac death. For analysis of the association between cardiac death and EF and GS measures, the univariate and multivariate Cox proportional hazards model was used. Sensitivity, specificity, positive predictive value (PPV) and negative predictive value, and accuracy of event-free prediction were evaluated. RESULTS: Twenty-four patients (27%) had low cardiac function (EF <50%; low EF) and 44 patients (50%) had severe coronary atherosclerosis (GS >15; high GS). During a follow-up period of 3 years, cardiac death occurred in 21 patients (24%). The PPV of low EF and high GS was 42 and 39%, respectively; the highest PPV (53%) was obtained when low EF and high GS were combined. The cumulative survival rate at 5 years in patients with both low EF and high GS was significantly lower than those with high EF and low GS (91 vs. 22%, p < 0.0005). CONCLUSION: The combined assessment of cardiac function and coronary atherosclerosis at the initiation of RRT strongly predicts future cardiac events.
Cause of Death↗
Kidney function and mortality among patients with left ventricular systolic dysfunction.
Kidney disease has emerged as a risk factor for mortality in heart failure populations. The objective of this study was to determine the impact of different stages of kidney dysfunction (defined using the Kidney Disease Outcomes Quality Initiative [K/DOQI] classification system) and changes in kidney function on mortality in a cohort of patients with heart failure. A retrospective analysis was conducted of data from the randomized controlled trials Studies of Left Ventricular Dysfunction. A total of 6640 participants with asymptomatic and symptomatic heart failure were studied. Estimated GFR (eGFR) were calculated and then categorized according to the K/DOQI classification system into the following categories: > or =90, 60 to 89, 30 to 59, and 15 to 29 ml/min per 1.73 m2. Reduction in eGFR from baseline was calculated and subsequently categorized according to rate of decline (<5, 5 to 10, 11 to 15, and >15 ml/min per 1.73 m2 per year). Independent of baseline differences, lower levels of eGFR were associated with a higher total mortality compared with those with eGFR > or =90 ml/min (30 to 59 ml/min per 1.73 m2: hazard ratio [HR] 1.32, 95% confidence interval [CI] 1.10 to 1.59, P = 0.004; 15 to 29 ml/min per 1.73 m2: HR 2.54, 95% CI 1.54 to 4.19, P < 0.001). eGFR deteriorated rapidly (>15 ml/min per 1.73 m2 per year) in 12% of participants. This decline was associated with a significant increase in mortality compared with slower decline (<5 ml/min per 1.73 m2 per year), despite adjustments for baseline kidney function, baseline heart failure, or change in heart failure (HR 5.63; 95% CI 4.90 to 6.46; P < 0.0001). The levels of eGFR from the K/DOQI classification system are associated with mortality in a well-characterized heart failure population. Rate of decline in kidney function is a strong predictor of increased mortality in this population, independent of worsening heart failure and baseline kidney function.
Adult↗