Β-blocker Therapy In Patients Research Articles

Impact of Midodrine on Optimization of β-blocker Therapy in Patients with Heart Failure with Reduced Ejection Fraction

Impact of Midodrine on Optimization of β-blocker Therapy in Patients with Heart Failure with Reduced Ejection Fraction

Effects of Long-Term Carvedilol Therapy in Patients With ST-Segment Elevation Myocardial Infarction and Mildly Reduced Left Ventricular Ejection Fraction

The benefits of long-term oral β-blocker therapy in patients with ST-segment elevation myocardial infarction (STEMI) with mildly reduced left ventricular ejection fraction (LVEF; ≥40%) are still unknown. We sought to evaluate the efficacy of β-blocker therapy in patients with STEMI with mildly reduced LVEF. In the CAPITAL-RCT (Carvedilol Post-Intervention Long-Term Administration in Large-Scale Randomized Controlled Trial), patients with STEMI with successful percutaneous coronary intervention with an LVEF of ≥40% were randomly assigned to carvedilol or no β-blocker therapy. Among 794 patients, 280 patients had an LVEF of <55% at baseline (mildly reduced LVEF stratum), whereas 514 patients had an LVEF of ≥55% at baseline (normal LVEF stratum). The primary end point was a composite of all-cause death, myocardial infarction, hospitalization for acute coronary syndrome, and hospitalization for heart failure, and the secondary end point was a cardiac composite outcome: a composite of cardiac death, myocardial infarction, and hospitalization for heart failure. The median follow-up period was 3.7years. The lower risk of carvedilol therapy relative to no β-blocker therapy was not significant for the primary end point in either the mildly reduced or normal LVEF strata. However, it was significant for the cardiac composite end point in the mildly reduced LVEF stratum (0.82/100 person-years vs 2.59/100 person-years, hazard ratio 0.32 [0.10 to 0.99], p=0.047) but not in the normal LVEF stratum (1.48/100 person-years vs 1.06/100 person-years, hazard ratio 1.39 [0.62 to 3.13], p=0.43, p for interaction=0.04). In conclusion, long-term carvedilol therapy in patients with STEMI with primary percutaneous coronary intervention might be beneficial for preventing cardiac-related events in those with a mildly reduced LVEF.

Effect of β-blocker therapy on the level soluble ST2 protein in the blood serum in patients with heart failure with preserved and mildly reduced ejection fraction

Aim. To study the prognostic value of high serum concentration of soluble ST2 protein (sST2) in the development of cardiovascular events after endovascular myocardial revascularization and the possibility of using this biomarker as a target for β-blocker therapy in patients with chronic heart failure (CHF) with preserved (HFpEF) and mildly reduced (HFmrEF) left ventricular ejection fraction.Materials and methods. The study included 72 patients (aged 57–69 years, 81.94% were men) with class I–III CHF of ischemic etiology with HFpEF and HFmrEF. The patients were admitted to the cardiology department for endovascular myocardial revascularization. Before myocardial revascularization, serum concentrations of sST2 and N-terminal pro-brain natriuretic peptide (NT-proBNP) in all patients were analyzed by enzyme-linked immunosorbent assay (ELISA). Doses of β-blockers used in all patients were recalculated into a total daily dose equivalent to metoprolol succinate. Patients were divided into 2 groups depending on the median equivalent dose of metoprolol succinate (“high” ≥ 100 mg / day and “low” &lt; 100 mg / day).Results. In patients of group 1, the serum concentration of sST2 was 30.7% higher (p &lt; 0.001) than in patients of group 2 (40.26 [34.39; 48.92] ng /ml and 27.9 [23.05; 35.27] ng / ml, respectively), the serum NT-proBNP level in group 1 was 22.8% higher (p = 0.049) than in group 2 (167 [129; 330] ng / ml vs. 129 [125; 147] ng / ml, respectively). In patients receiving an equivalent dose of metoprolol succinate &lt; 100 mg / day, the incidence of cardiovascular events was 34% higher (p = 0.002) than in patients receiving an equivalent dose of metoprolol succinate ≥ 100 mg/day. The ROC analysis showed that serum sST2 level ≥ 34.18 ng / ml (sensitivity 78.0%, specificity 90.0%, area under the curve (AUC) 0.906; p &lt; 0.0001) predicts a high risk of cardiovascular events within one year. However, the serum NT-proBNP level was not an informative predictor of cardiovascular events. Conclusion. It was confirmed that increased sST2 serum concentration has high prognostic value in the development of cardiovascular events within a year after endovascular myocardial revascularization. The possibility of using this biomarker as a target for β-blocker therapy in patients with HFpHF and HFmrEF was substantiated. Aggressive use of β-blockers in the group of patients with HFpEF and HFmrEF and sST2 overexpression is preferable in order to reduce the incidence of cardiovascular events.

Stem Cell–Derived Cardiomyocytes and Beta-Adrenergic Receptor Blockade in Duchenne Muscular Dystrophy Cardiomyopathy

BackgroundAlthough cardiomyopathy has emerged as a leading cause of death in Duchenne muscular dystrophy (DMD), limited studies and therapies have emerged for dystrophic heart failure. ObjectivesThe purpose of this study was to model DMD cardiomyopathy using DMD patient-specific human induced pluripotent stem cell (hiPSC)-derived cardiomyocytes and to identify physiological changes and future drug therapies. MethodsTo explore and define therapies for DMD cardiomyopathy, the authors used DMD patient-specific hiPSC-derived cardiomyocytes to examine the physiological response to adrenergic agonists and β-blocker treatment. The authors further examined these agents in vivo using wild-type and mdx mouse models. ResultsAt baseline and following adrenergic stimulation, DMD hiPSC-derived cardiomyocytes had a significant increase in arrhythmic calcium traces compared to isogenic controls. Furthermore, these arrhythmias were significantly decreased with propranolol treatment. Using telemetry monitoring, the authors observed that mdx mice, which lack dystrophin, had an arrhythmic death when stimulated with isoproterenol; the lethal arrhythmias were rescued, in part, by propranolol pre-treatment. Using single-cell and bulk RNA sequencing (RNA-seq), the authors compared DMD and control hiPSC-derived cardiomyocytes, mdx mice, and control mice (in the presence or absence of propranolol and isoproterenol) and defined pathways that were perturbed under baseline conditions and pathways that were normalized after propranolol treatment in the mdx model. The authors also undertook transcriptome analysis of human DMD left ventricle samples and found that DMD hiPSC-derived cardiomyocytes have dysregulated pathways similar to the human DMD heart. The authors further determined that relatively few patients with DMD see a cardiovascular specialist or receive β-blocker therapy. ConclusionsThe results highlight mechanisms and therapeutic interventions from human to animal and back to human in the dystrophic heart. These results may serve as a prelude for an adequately powered clinical study that examines the impact of β-blocker therapy in patients with dystrophinopathies.

Associations between β-blocker therapy and cardiovascular outcomes in patients with diabetes and established cardiovascular disease

The effects of β-blocker therapy in patients with type 2 diabetes (T2D) and established atherosclerotic cardiovascular disease (ASCVD) are unclear. We sought to evaluate associations between β-blocker use in T2D with ASCVD and cardiovascular (CV) outcomes. In patients with T2D and ASCVD enrolled in the Trial Evaluating Cardiovascular Outcomes with Sitagliptin (TECOS), an inverse probability of treatment-weighted Cox proportional hazards model was used to examine the association between baseline β-blocker therapy (at randomization) and the primary CV composite (defined as CV death, non-fatal myocardial infarction [MI], non-fatal stroke, or hospitalization for unstable angina), including in subgroups with prior MI and heart failure (HF); other outcomes evaluated included individual components of the primary composite, hospitalization for HF, and severe hypoglycemic events. Of the 14,671 patients randomized, 9322 (64%) were on a β-blocker at baseline; these patients were more likely to have prior MI or HF. Over a median 3.0 (25th, 75th percentile: 2.2, 3.6) years, the risk of the primary CV composite was significantly higher with baseline β-blocker use versus no β-blocker use (4.5 vs. 3.4 events/100-patient years, adjusted hazard ratio [HR] 1.17, 95% confidence interval [CI] 1.05-1.29); no significant interaction was noted for patients with versus without prior MI or HF. Baseline β-blocker use was not associated with risks for severe hypoglycemic events (HR 1.14, 95% CI 0.88-1.48). In this observational analysis of T2D and ASCVD, baseline β-blocker use was not associated with risks for severe hypoglycemia yet also was not associated with CV risk reduction over 3 years of follow-up, supporting a randomized examination of chronic β-blocker therapy in this patient population. (TECOS ClinicalTrials.gov number, NCT00790205).

Systemic arterial blood pressure determines the therapeutic window of non-selective beta blockers in decompensated cirrhosis.

The safety of non-selective β-blockers in patients with advanced cirrhosis has been questioned in recent years. It was hypothesised that there is a particular therapeutic window. However, the specific limits still need to be determined. To evaluate potential limits of the therapeutic window of non-selective β-blocker therapy in patients with cirrhosis and ascites METHODS: The impact of non-selective β-blockers on 28-day transplant-free survival was analysed in a cohort of 624 consecutive patients with decompensated cirrhosis and ascites. Three potential limits were investigated: spontaneous bacterial peritonitis, acute-on-chronic liver failure, mean arterial blood pressure≤82 and<65mm Hg. Treatment with non-selective β-blockers was associated with a higher 28-day transplant-free survival in the overall cohort (hazard ratio: 0.621; P=.035) as well as in patients with acute-on-chronic liver failure (hazard ratio: 0.578; P=.031) and those with spontaneous bacterial peritonitis (hazard ratio: 0.594; P=.073). In contrast, survival benefits were markedly attenuated in patients with a mean arterial blood pressure≤82mm Hg and completely lost in those with mean arterial blood pressure<65mm Hg (P=.536). In spontaneous bacterial peritonitis patients with a mean arterial blood pressure<65mm Hg non-selective β-blocker treatment was associated with renal impairment. Of note, among those with a mean arterial blood pressure≥65mm Hg non-selective β-blocker intake was consistently associated with superior transplant-free survival (hazard ratio: 0.582; P=.029) irrespective of the presence of spontaneous bacterial peritonitis (hazard ratio: 0.435; P=.028) or acute-on-chronic liver failure (hazard ratio: 0.480 P=.034). Ascites, acute-on-chronic liver failure and spontaneous bacterial peritonitis do not limit the safe use of non-selective β-blockers in patients with cirrhosis. Mean arterial blood pressure might represent a better indicator to determine the therapeutic window of non-selective β-blocker treatment.

Do Patients need Lifelong β-Blockers after an Uncomplicated Myocardial Infarction?

The lifelong use of β-adrenoceptor antagonists (β-blockers) after a myocardial infarction (MI) has been the standard of care based on trials performed before the era of revascularization, when heart failure was common. Large randomized trials in the mid-1980s demonstrated that β-blockers played a major role in improving the in-hospital and long-term survival of patients admitted for MI. However, the implementation of rapid myocardial reperfusion led to a substantial survival benefit and a reduction of heart failure because of reduced infarct size. Modern large longitudinal registries did not provide sufficient evidence to support long-term β-blocker therapy in patients with uncomplicated acute MI. The long-term prescription of this therapy has become a matter of debate given the lack of contemporary evidence, frequent side effects, and treatment adherence issues. Furthermore, this shift into the reperfusion era led to a downgraded recommendation for the use of β-blockers in post-MI patients (class IIa B recommendation) in the 2017 European Society of Cardiology (ESC) recommendations for the treatment of ST-segment elevation MI (STEMI). Three large ongoing multicenter randomized trials (AβYSS, REDUCE-SWEDEHEART, and REBOOT-CNIC) are evaluating early discontinuation of β-blockers after an uncomplicated acute MI. The tested hypothesis is that β-blocker withdrawal is safe versus major adverse cardiovascular events and improves quality of life by reducing side effects. Thus, the present review summarizes the exhaustive evidence-based data for long-term β-blocker use after uncomplicated MI and the ongoing trials.

Effect of β-blockers on 1-year survival and hospitalizations in patients with heart failure and atrial fibrillation: results from ESC-HF Pilot and ESC-HF Long-Term Registry.

Introduction The positive effect of β-blocker therapy in patients with heart failure (HF) and atrial fibrillation (AF) has been questioned. Objectives We aimed to assess the effect of β-blockers and heart rate (HR) control on 1-year outcomes in patients with HF and AF. Patients and methods Of the 2019 Polish patients enrolled in ESC-HF Pilot and ESC-HF Long-Term Registry, 797 patients with HF and AF were classified into 2 groups depending on β-blocker use. Additionally, patient survival was compared between 3 groups classified according to HR: lower than 80 bpm, between 80 and 109 bpm, and of 110 bpm or higher. The primary endpoint was all-cause death and the secondary endpoint was all-cause death or HF hospitalization. Results In patients treated with β-blockers, the primary and secondary endpoints were less frequent than in patients not using β-blockers (10.9% vs 25.6%, P = 0.001 and 30.6% vs 44.2%, P = 0.02, respectively). Absence of β-blocker treatment was a predictor of both endpoints in a univariate analysis but remained an independent predictor only of the primary endpoint in a multivariate analysis (hazard ratio for β-blocker use, 0.52; 95% CI, 0.31-0.89; P = 0.02). The primary and secondary endpoints were more frequent in patients with a HR of 110 bpm or higher, but the HR itself did not predict the study endpoints in the univariate analysis. Conclusions β-blocker use might decrease mortality in patients with HF and AF, but it seems to have no impact on the risk of HF hospitalization. An HR of 110 bpm or higher may be related to worse survival in these patients.

Outcomes of beta blocker use in cocaine-associated chest pain: a meta-analysis

ObjectivesBeta blockers (β-blockers) remain a standard therapy in the early treatment of acute coronary syndromes. However, β-blocker therapy in patients with cocaine-associated chest pain (CACP) continues to be an area...

β-Blocker-Associated Risks in Patients With Uncomplicated Hypertension Undergoing Noncardiac Surgery.

Perioperative β-blocker strategies are important to reduce risks of adverse events. Effectiveness and safety may differ according to patients' baseline risk. To determine the risk of major adverse cardiovascular events (MACEs) associated with long-term β-blocker therapy in patients with uncomplicated hypertension undergoing noncardiac surgery. Association study based on in-hospital records and out-of-hospital pharmacotherapy use using a Danish nationwide cohort of patients with uncomplicated hypertension treated with at least 2 antihypertensive drugs (β-blockers, thiazides, calcium antagonists, or renin-angiotensin system [RAS] inhibitors) undergoing noncardiac surgery between 2005 and 2011. Various antihypertensive treatment regimens, chosen as part of usual care. Thirty-day risk of MACEs (cardiovascular death, nonfatal ischemic stroke, nonfatal myocardial infarction) and all-cause mortality, assessed using multivariable logistic regression models and adjusted numbers needed to harm (NNH). The baseline characteristics of the 14,644 patients who received β-blockers (65% female, mean [SD] age, 66.1 [12.0] years) were similar to those of the 40,676 patients who received other antihypertensive drugs (57% female, mean [SD] age, 65.9 [11.8] years). Thirty-day MACEs occurred in 1.3% of patients treated with β-blockers compared with 0.8% of patients not treated with β-blockers (P < .001). β-Blocker use was associated with increased risks of MACEs in 2-drug combinations with RAS inhibitors (odds ratio [OR], 2.16 [95% CI, 1.54-3.04]), calcium antagonists (OR, 2.17 [95% CI, 1.48-3.17]), and thiazides (OR, 1.56 [95% CI, 1.10-2.22]), compared with the reference combination of RAS inhibitors and thiazides. Results were similar for all-cause mortality. Risk of MACEs associated with β-blocker use seemed especially pronounced for patients at least 70 years old (number needed to harm [NNH], 140 [95% CI, 86-364]), for men (NNH, 142 [95% CI, 93-195]), and for patients undergoing acute surgery (NNH, 97 [95% CI, 57-331]), compared with patients younger than 70 years, women, and patients undergoing elective surgery, respectively. Antihypertensive treatment with a β-blocker may be associated with increased risks of perioperative MACEs and all-cause mortality in patients with uncomplicated hypertension.

β-Blocker Therapy for Patients with Hypertension.

β-Blocker Therapy for Patients with Hypertension.

National assessment of early β-blocker therapy in patients with acute myocardial infarction in China, 2001-2011: The China Patient-centered Evaluative Assessment of Cardiac Events (PEACE)–Retrospective AMI Study

Since 2007, clinical practice guidelines have recommended β-blocker therapy early in the course of acute myocardial infarction (AMI) for patients who are not at high risk for complications. Our objective was to perform a national quality assessment of early β-blocker use during hospitalization for AMI over the past decade in China. We conducted medical record review of a nationally representative sample of patients admitted to Chinese hospitals with AMI and studied those without absolute contraindications to β-blocker therapy in 2001, 2006, and 2011. We evaluated the use, type, and dose of β-blockers within the first 24 hours of admission over time and identified predictors of not using this treatment both in ideal candidates and in those with risk factors for cardiogenic shock. Among 14,241 patients with AMI (representing 43,165 patients in 2001, 106,167 patients in 2006, and 221,874 patients in 2011 in China, respectively), 45.1% had no contraindications to early β-blocker therapy; 21.1% had risk factors for cardiogenic shock but no absolute contraindication. β-blocker use in ideal patients was 54.3% in 2001, 67.8% in 2006, and 61.8% in 2011 (P = .28 for trend). Predictors of nontreatment were older age, lower systolic blood pressure, lower heart rate, absence of chest discomfort, and admission to a nonteaching hospital. Use in patients with risk factors for cardiogenic shock was 42.6% in 2001, 59.5% in 2006, and 52.9% in 2011 (P = .31 for trend). Metoprolol was used most frequently (91.5%), but dosages were often below those recommended in guidelines. The use of early β-blocker therapy for patients with AMI in China is suboptimal, with underuse in patients who could benefit and substantial use among those who might be harmed. Patterns of use have not changed over time, thus creating an important target of efforts to improve quality of care for AMI.

β-Blocker Therapy for Patients With Hypertension—Reply

β-Blocker Therapy for Patients With Hypertension—Reply

Contraindicated Initiation of β-Blocker Therapy in Patients Hospitalized for Heart Failure

Contraindicated Initiation of β-Blocker Therapy in Patients Hospitalized for Heart Failure

β-Blocker therapy and cardiovascular outcomes in patients who have undergone percutaneous coronary intervention after ST-elevation myocardial infarction

The effect of β-blockers in ST-elevation myocardial infarction (STEMI) patients who have undergone primary percutaneous coronary intervention (PCI) has not been adequately evaluated. Using a large multi-center registry in Japan, we identified 3,692 patients who underwent PCI within 24 h from onset of STEMI and were discharged alive from 2005 to 2007. Three-year cardiovascular outcomes were compared between the 2 groups of patients with (N = 1,614) or without (N = 2,078) β-blocker prescription at discharge. Compared with patients in the no-β group, patients in the β group were younger, more frequently male, more often had hypertension and atrial fibrillation but less often had chronic obstructive pulmonary disease than in the no-β group. Statins and angiotensin-converting enzyme inhibitors/angiotensin receptor blockers were more frequently prescribed in the β group. Crude incidence of cardiac death and/or recurrent myocardial infarction (cardiac death/MI) tended to be higher in the β group (7.6 vs. 6.2%, log-rank p = 0.1). After adjusting for potential confounders, β-blockers were associated with significantly higher risk for cardiac death/MI (hazard ratio 1.43, 95% CI: 1.06-1.94, p = 0.01). β-Blocker prescription at discharge was not associated with better cardiovascular outcomes in patients who underwent PCI after STEMI. Large-scale randomized controlled trials are needed to evaluate the role of β-blocker therapy in these patients.

Clinical Considerations of Heritable Factors in Common Heart Failure

Heart failure is a common condition responsible for at least 290 000 deaths each year in the United States alone.1 A small minority of heart failure cases are attributed to Mendelian or familial cardiomyopathies. The majority of systolic heart failure cases are not familial but represent the end result of 1 or many conditions that primarily injure the myocardium sufficiently to diminish cardiac output in the absence of compensatory mechanisms. Paradoxically, because they also injure the myocardium, it is the chronic actions of the compensatory mechanisms that in many instances contribute to the progression from simple cardiac injury to dilated cardiomyopathy and overt heart failure. Thus, the epidemiology of common heart failure appears to be just as sporadic as its major antecedent conditions (atherosclerosis, diabetes, hypertension, and viral myocarditis). Familial trends in preclinical cardiac remodeling2 and risk of developing heart failure3 reveal an important role for genetic modifiers in addition to clinical and environmental factors. Candidate gene studies performed over the past 10 years have identified a few polymorphic gene variants that modify risk or progression of common heart failure.4 Whole-genome sequencing will lead to the discovery of other genetic modifiers that were not candidates.5 The imminent availability of individual whole-genome sequences at a cost competitive with available genetic tests for familial cardiomyopathy will no doubt further expand the list of putative genetic heart failure modifiers. Heart failure risk alleles along with traditional clinical factors will need to be considered by clinical cardiologists in their design of optimal disease surveillance and prevention programs and in individually tailoring heart failure management. The use of individual genetic make-up is likely to have the earliest and greatest impact on managing patients with heart failure by tailoring available pharmacotherapeutics to optimize patient response and minimize adverse effects (ie, the …

Effect of βblocker therapy in patients with chronic heart failure based on ischemic heart disease- Carvedilol versus Bisoprolol-

Background: Carvedilol and bisoprolol have been reported to improve prognosis in CHF. However, there is little examination, basal disease of CHF compared both drug only for IHD. Purpose: Comparative effects of carvedilol and bisoprolol in patients with CHF based on IHD. Subjects and Methods: Of 1080 consecutive patients admitted for HF worsening, in hospital death and administered carvedilol or bisoprolol before admission were excluded. 469 patients administered carvedilol or bisoprolol on discharge.

Acute ischemic events in HF—should we include sudden death?

Over the past decade, the use of β-blockers has transformed the management and prognosis of patients with heart failure (HF). A post hoc analysis of the SENIORS study now raises questions about the validity of a composite 'ischemic' end point that includes sudden death in trials of β-blocker therapy for patients with HF.

Efficacy and Safety of Carvedilol in Treatment of Heart Failure with Chronic Kidney Disease

Background— The safety and efficacy of different types of β-blocker therapy in patients with non–dialysis-dependent chronic kidney disease (CKD) and systolic heart failure (HF) are not well described. We assessed whether treatment of systolic HF with carvedilol is efficacious and safe in adults with CKD. Methods and Results— We performed a post hoc analysis of pooled individual patient data (n=4217) from 2 multinational, double-blinded, placebo-controlled, randomized trials, CAPRICORN (Carvedilol Postinfarct Survival Control in Left Ventricular Dysfunction Study) and COPERNICUS (Carvedilol Prospective Randomized, Cumulative Survival study). Primary outcome was all-cause mortality. Secondary outcomes included cardiovascular mortality, HF mortality, first HF hospitalization, the composite of cardiovascular mortality or first HF hospitalization, and sudden cardiac death. Non–dialysis-dependent CKD was defined by estimated glomerular filtration rate ≤60 mL/min/1.73 m 2 , using the abbreviated Modification of Diet in Renal Disease equation. CKD was present in 2566 of 4217 (60.8%) of the cohort, 50.4% of whom were randomly assigned to carvedilol therapy. Within the CKD group, treatment with carvedilol decreased the risks of all-cause mortality (hazard ratio [HR], 0.76; 95% confidence interval [CI], 0.63 to 0.93; P =0.007), cardiovascular mortality (HR, 0.76; 95% CI, 0.62 to 0.94; P =0.011), HF mortality (HR, 0.68; 95% CI, 0.52 to 0.88; P =0.003), first hospitalization for HF (HR, 0.74; 95% CI, 0.61 to 0.88; P =0.0009), and the composite of cardiovascular mortality or HF hospitalization (HR, 0.75; 95% CI, 0.65 to 0.87; P &lt;0.001) but was without significant effect on sudden cardiac death (HR, 0.76; 95% CI, 0.56 to 1.05; P =0.098). There was no significant interaction between treatment arm and study type. Carvedilol was generally well tolerated by both groups of patients, with an increased relative incidence in transient increase in serum creatinine without need for dialysis and other electrolyte changes in the CKD patients. However, in a sensitivity analysis among HF subjects with estimated glomerular filtration rate &lt;45 mL/min/1.73 m 2 (CKD stage 3b), the efficacy of carvedilol was not significantly different from placebo. Conclusions— This analysis suggests that the benefits of carvedilol therapy in patients with systolic left ventricular dysfunction with or without symptoms of HF are consistent even in the presence of mild to moderate CKD. Whether carvedilol therapy is similarly efficacious in HF patients with more advanced kidney disease requires further study.

Effect of Beta-Blocker Therapy on Rehospitalization Rates in Women Versus Men With Heart Failure and Preserved Ejection Fraction

Beta blockers are empirically used in many patients with heart failure (HF) and preserved ejection fraction (HFpEF) because they allow more time for diastolic filling and because they improve outcomes in patients with systolic HF. However, recent data suggest that impaired chronotropic and vasodilator responses to exercise, which can worsen with beta blockade, may play a key role in the pathophysiology of HFpEF. We prospectively examined the association between beta-blocker therapy after hospitalization for decompensated HF and HF rehospitalization at 6 months in 66 consecutive patients with HFpEF (71 +/- 13 years old, 68% women, 42% Black). Subjects were stratified based on receiving (BB+; 15 men, 28 women) or not receiving (BB-) beta-blockers at hospital discharge. In men, HF rehospitalization occurred less frequently in the BB+ than in the BB- group, albeit nonsignificantly (20% vs 50%, p = 0.29). In women, HF rehospitalization occurred more frequently in the BB+ than in the BB- group (75% vs 18%, p <0.001). In univariate analyses, discharge beta-blocker was associated with HF rehospitalization in women (odds ratio [OR] 14.00, 95% confidence interval [CI] 3.09 to 63.51, p = 0.001), but not in men (OR 0.25, 95% CI 0.03 to 1.92, p = 0.18). In a forward logistic regression model that offered all univariate predictors of HF rehospitalization, discharge beta blocker remained an independent predictor of HF rehospitalization in women (OR 11.06, 95% CI 1.98 to 61.67, p = 0.006). In conclusion, this small observational study suggests that beta-blocker therapy may be associated with a higher risk of HF rehospitalization in women with HFpEF. The risks and benefits of beta-blocker therapy in patients with HFpEF should be evaluated in randomized, controlled trials.