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Background: Tachycardia worsens cardiac performance in acute decompensated heart failure (ADHF). We investigated whether heart rate (HR) optimization by landiolol, an ultra-short-acting β1-selective blocker, in combination with milrinone improved cardiac function in patients with ADHF and rapid atrial fibrillation (AF). Methods and Results: We enrolled9 ADHF patients (New York Heart Association classification IV; HR, 138 ± 18 bpm; left ventricular [LV] ejection fraction, 28 ± 8%; cardiac index [CI], 2.1 ± 0.3 L/min–1/m–2; pulmonary capillary wedge pressure [PCWP], 24 ± 3 mm Hg), whose HRs could not be reduced using standard treatments, including diuretics, vasodilators, and milrinone. Landiolol (1.5–6.0 µg/kg–1/min–1, intravenous) was added to milrinone treatment to study its effect on hemodynamics. The addition of landiolol (1.5 µg/kg–1/min–1) significantly reduced HR by 11% without changing systolic blood pressure (BP) and resulted in a significant decrease in PCWP and a significant increase in stroke volume index (SVI), suggesting that HR reduction restores incomplete LV relaxation. Administration of more than 3.0 µg/kg–1/min–1 of landiolol decreased BP, CI, and SVI. Conclusion: The addition of landiolol at doses of <3.0 µg/kg/min to milrinone improved cardiac function in decompensated chronic heart failure with rapid atrial fibrillation by selectively reducing HR. [ABSTRACT FROM AUTHOR]

Objectives: Patients surviving an acute myocardial infarction (AMI) are different today than when oral β-blockers first were shown to have an incremental effect on mortality. They are now, as opposed to then, offered revascularization procedures and effective secondary prevention. In this pilot-study, we aimed to explore the prescription of β-blockers to these patients stratified by their left ventricular ejection fraction (LVEF). Methods: Consecutive stable patients treated with a percutaneous coronary intervention (PCI) procedure following an AMI were included for measurement of LVEF after 1–5 days. β-Blocker treatment was recorded at inclusion and after 3 months. Results: We included 159 patients, 89% with LVEF ≥40% (56% had a LVEF ≥50% [preserved], 33% LVEF 40–49% [mid-range] and 11% LVEF <40% [reduced]). At discharge the prescription rates of β-blockers according to LVEF stratification were 79% for preserved, 79% for mid-range and 94% for reduced LVEF. After 3 months 72% of all patients continued such treatment. Conclusions: In this prospective study, a large proportion of contemporary managed patients with AMI but without clinical heart failure does not have reduced LVEF shortly after PCI, but the majority is still treated with a β-blocker. [ABSTRACT FROM AUTHOR]

Objectives: With the present therapeutic advances in the era of primary percutaneous coronary intervention (PCI), the role of β-blockers in ST elevation acute myocardial infarction (STEMI) has remained contentious. Methods: We analyzed the data and clinical outcomes of 901 STEMI patients who had undergone primary PCI. We classified the patients into β-blocker (n = 598) and non-β-blocker groups (n = 303). Results: The cumulative incidence of all-cause death was 10.0% in the β-blocker group and 25.4% in the non-β-blocker group (p < 0.001). The incidence of major adverse cardiac events (MACE) was 22.1% in the β-blocker group and 34.3% in the non-β-blocker group (p < 0.001). The relative hazard ratio (HR) of β-blockers for all-cause death and MACE with low left ventricle ejection fraction (LVEF; <50%) was 0.55 [95% confidence interval (CI) 0.35-0.86, p = 0.009] and 0.75 (95% CI 0.51-1.09, p = 0.125), respectively. In patients with normal LVEF (≥50%), the relative HR of β-blockers for death and MACE were 0.50 (95% CI 0.29-0.88, p = 0.016) and 0.75 (95% CI 0.51-1.12, p = 0.162), respectively. After propensity score matching of the difference of the baseline characteristics, the Kaplan-Meier survival curve demonstrated lower mortality in the β-blocker group than in the non-β-blocker group with both low LVEF and normal LVEF (p = 0.02 and p = 0.001, respectively). Conclusions: β-Blockers have beneficial clinical outcomes in the era of primary PCI for STEMI, regardless of the LVEF. © 2015 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Objective: Recently, we reported that low-dose landiolol (1.5 µg·kg-1·min-1), an ultra-short-acting β-blocker, safely decreased the heart rate (HR) in patients with acute decompensated heart failure (ADHF) and sinus tachycardia, thereby improving cardiac function. We investigated whether low-dose landiolol effectively decreased the HR in ADHF patients with rapid atrial fibrillation (AF). Methods: We enrolled 23 ADHF patients with rapid AF (HR ≥120 beats·min-1 and New York Heart Association class III-IV) and systolic heart failure (SHF: n = 12) or diastolic heart failure (DHF: n = 11) who received conventional therapy with diuretics, vasodilators, and/or low-dose inotropes. They were administered continuous intravenous infusion of low-dose landiolol (1.0-2.0 µg·kg-1·min-1), and their electrocardiograms and blood pressures were monitored for 24 h thereafter. Results: Two hours after starting landiolol, the HR was reduced significantly (22%), without a reduction in blood pressure, and remained constant thereafter. The HR reduction 2 h after landiolol administration was significantly greater in the DHF group than in the SHF group. No incidence of hypotension was recorded. Conclusions: Digitalis or amiodarone is currently recommended for HR control in ADHF patients with rapid AF. Our results showed that continuous infusion of low-dose landiolol may also be useful as first-line therapy in these patients. © 2013 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Thebeneficial effects of β-blocker therapy in patients with heart failure have been confirmed. However, the effects of β-blockers on myocardial perfusion defects are unclear. The aim of this study was to evaluate the effect of β-blockers on myocardial perfusion defects estimated by thallium-201 myocardial scintigraphy in patients with dilated cardiomyopathy (DCM) and to investigate the relationships between β-blocker treatment and myocardial damage and cardiac function. Methods:201Tl and echocardiography were performed in 37 patients before and after 6 months of β-blocker therapy. Extent score (ES) by 201Tl was used to quantitate myocardial perfusion defects before and after treatment. Results: ES was significantly decreased by β-blocker therapy. According to the change in ES, DCM patients were classified into three groups, patients who improved, patients showing no change and patients who deteriorated. In the improvement and no-change groups, β-blocker therapy induced a reduction in left ventricular dimensions and an associated increase in ejection fraction. However, in the deterioration group, left ventricular dimensions and ejection fraction were unchanged. There was a significant relationship between the change in left ventricular dimension at end-diastole and the change in ES. Conclusions: β-Blocker therapy could attenuate myocardial perfusion defects in some patients with DCM. The improvement in left ventricular function associated with β-blocker therapy may be related to the attenuation in myocardial perfusion defects. Copyright © 2005 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

In clinical trials β-blockers (BB) are well tolerated in patients with systolic congestive heart failure (CHF). In contrast in daily practice treatment initiation and titration appear to be more difficult and may differ in various BB - but systematic data are lacking. We randomized 87 patients with systolic CHF (mean age 70.1 ± 10.6 years, 24% females, LVEF 0.28 ± 0.10, NYHA III-IV 29%) to treatment with either bisoprolol or carvedilol, in order to assess and compare the maximally achievable number of patients on treatment with these BB and the maximally achieved dosage during a minimum of 2 months attendance at our out patient heart failure clinic. In those randomized to bisoprolol, mean dose at 2 months was 33% of target dose (3.1 ± 2.6 mg ) and 41% at discharge. In those on carvedilol, the mean dose at 2 months was 27% of target dose (13.4 ± 14.0 mg) and 32% at discharge. Thirty-nine and 40% of the bisoprolol and carvedilol treated patients, respectively, had stopped treatment at discharge. None of the figures differed significantly between the two treatment groups and no baseline parameter predicted BB tolerability. Thus, almost twice the number of unselected patients with systolic CHF attending a heart failure clinic focusing on systematic medical titration were intolerant to BB treatment and only a minority reached target dose treatment. The present data reveal no clear difference with respect to tolerability of carvedilol and bisoprolol, and no parameter predicts tolerability. [ABSTRACT FROM AUTHOR]

Background: We have reported that a marked elevation in serum C-reactive protein (CRP) level is a predictor for infarct expansion and cardiac rupture after AMI. Although β-blockers prevent cardiac rupture after AMI, their effect on serum CRP elevation has not been determined. Methods: We studied a total of 154 patients with first Q-wave AMI. Patients complicated by pump failure were excluded from this study. Eighty-two patients received β-blocker treatment within 24 h of the onset of AMI, while 72 patients received no β-blocker treatment. Peak serum creatine kinase (CK) and CRP levels were determined by serial measurements. Results: There was no difference between the groups according to age, sex, coronary risk factors, pre-infarction angina, infarct site, prior use of cardiovascular drugs, use of revascularization therapy, and prevalence of multivessel disease. β-Blocker treatment was associated with a lower peak CRP level (6.9 ± 6.1 vs.10.8 ± 9.3 mg/dl, p = 0.002), a shorter duration from the onset to the peak CRP level (2 ± 1 vs. 3 ± 2 days, p < 0.0001), a lower incidence of cardiac rupture (p = 0.03) and lower in-hospital cardiac mortality (p = 0.02), despite similar peak CK levels. Conclusion: The early use of β-blockers is associated with decreased serum CRP level and a favorable clinical outcome after first Q-wave AMI, suggesting some beneficial effects of β-blockers on infarct healing after AMI.Copyright © 2003 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Historically, postural hypotension has been cited as a consideration which might influence the selection of antihypertensive therapy. The common symptoms (dizziness, blackouts, syncope) give cause for concern but they are not attributed to every class of antihypertensive drug. For example, administration of a β-blocker is not generally associated with symptomatic postural hypotension, whereas the α-blocker prazosin was particularly problematical, with a significant and well-recognized risk of first-dose postural effects. Titration from a low starting dose and careful selection/monitoring of patients have been successfully used to circumvent this problem. However, since there is a relatively high incidence of postural hypotensive symptoms in elderly patients in general, it may be a misconception to attribute such symptoms to any particular type of antihypertensive drug. Furthermore, with the newer α[sub 1] -blockers, such as doxazosin, which have a more gradual onset of action, there is a markedly reduced tendency for postural hypotension to occur. Thus, it is perhaps time to reassess the real significance of iatrogenic postural hypotension in the selection of antihypertensive therapy.Copyright © 2001 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]