Patients Receiving Beta Blockers Research Articles

Impact of metformin, statins, and beta blockers on survival in patients with primary ovarian cancer: combined analysis of four prospective trials of AGO-OVAR and ENGOT/GCIG collaborators

ObjectiveThe aim of this study was to investigate the association of co-medication with metformin, a statin, or beta blocker with survival in patients with primary ovarian cancer.MethodsIndividual data from three...

Beta blockers in traumatic brain injury: a systematic review and meta-analysis

BackgroundTraumatic brain injury (TBI) is a major cause of death and disability worldwide. Beta blockers have shown promise in improving mortality and functional outcomes after TBI. The aim of this...

Abstract 10068: Guideline Directed Medical Therapy in Newly Diagnosed Heart Failure with Reduced Ejection Fraction in the Community: Impact of Heart Failure Clinic

Introduction: Guideline-directed medical therapy (GDMT) dramatically improves outcomes in heart failure with reduced ejection fraction (HFrEF). Our goal was to examine GDMT use in community patients with newly diagnosed HFrEF. Methods: We performed a population-based, retrospective cohort study of all Olmsted County, Minnesota residents with newly diagnosed HFrEF (EF≤40%) 2007-2017. We excluded patients with contraindications to medication initiation (allergy, intolerance, heart rate<50 for beta blockers, SBP <80mm Hg for beta blockers, ACEi/ARB/ARNI; high creatinine (>3 mg/dL ACEi/ARB/ARNI, >2.5 men or >2.0 mg/dL women for mineralocorticoid receptor antagonists, MRAs) or hyperkalemia (potassium >5 meQ/L for ACEi/ARB/ARNI, MRA). We examined use and peak dose achieved for beta blockers, HF beta blockers (metoprolol succinate, carvedilol, bisoprolol), ACEi/ARB/ARNI, and MRA in the first year after HFrEF diagnosis. We used logistic regression to evaluate predictors of GDMT use. Results: From 2007-2017, 1160 patients were diagnosed with HFrEF (mean age 69.7 years, 65.6% men). Most eligible patients received beta blockers (92.1%) and ACEi/ARB/ARNI (86.5%) in the first year after HFrEF. However, only 63.6% of patients were treated with a HF beta blocker, and most did not receive MRAs (82.6%). The percentage of treated patients reaching medication target doses was 20.5% for HF beta blockers, 25.3% for ACEi/ARB/ARNI, and 11.2% for MRA. Compared to patients not seen in an HF clinic, patients seen in an HF clinic (n=380, 32.8%) were at greater odds of receiving beta blockers (OR 3.85, 95% CI 1.79-8.33); HF beta blockers (OR 3.85, 95% CI 2.63-5.26); ACEi/ARB/ARNIs (OR 3.85, 95% CI 2.17-6.67); and MRAs (OR 3.03, 95% CI 2.08-4.35). Other independent predictors of GDMT use included younger age (beta blockers, ACEi/ARB/ARNI), male gender (MRAs), higher SBP (beta blockers, ACEi/ARB/ARNI), lower EF (HF beta blockers), higher BMI (MRAs), and diabetes (ACEi/ARB/ARNI, p<0.05 for each). Conclusions: In this population-based study, most patients with newly diagnosed HFrEF received beta blockers and ACEi/ARB/ARNIs, but goal doses were usually not achieved. GDMT use was much higher in patients referred to an HF clinic.

Clinical characteristics, management, and outcomes of patients with electrical storm: single centre experience

Abstract Background Electrical storm (ES) is a life-threatening condition caused by recurrent malignant ventricular arrhythmia (≥3 episodes of ventricular tachycardia (VT) or ventricular fibrillation within 24 hours). ES patient management is challenging and can involve antiarrhythmic medication, sedation, and invasive procedures such as catheter ablation. Purpose The aim of this study is to report the clinical profile and management of ES patients who attended an arrhythmia reference centre. Methods Patients who presented with ES at our centre over a five-year period were consecutively enrolled. Patient data were retrospectively collected from hospital records. Patients with in-hospital death were excluded form data analysis. Results Seventy-six patients were included (84% male, mean age 73±10 years). 55% of patients had ischemic heart disease. The mean left ventricle ejection fraction (LVEF) was 33±4%, with 22% of patients having a severe reduction in systolic ventricular function (EF <35%). Baseline characteristics are reported in Table 1. During hospitalisation, 30% of patients underwent coronary angiography and 30% of these had percutaneous coronary revascularization. Patients were managed with pharmacological treatment, including continuous infusion of antiarrhythmic drugs (45% of patients received at least one antiarrhythmic), sedation (12%), and electrolytic solutions (38%). More details on ES management are reported in Table 2. All patients were evaluated for transcatheter ablation. After a mean of 6 days, 25% underwent transcatheter VT ablation during hospitalisation. In 7 patients (9%), catheter ablation was planned and performed during a subsequent hospitalisation. At discharge, 93% of patients received beta blockers and 68% received amiodarone. Overall, 65% were discharged with at least two antiarrhythmic drugs. The mean length of hospitalisation was 10±9 days, with 6±4 days spent in the intensive care unit. Eighteen patients (23%) had at least one subsequent hospitalisation for ES. After a mean follow-up of 20 months, the cumulative mortality rate was 27%, without a significant difference in mortality rates between ablated and non-ablated patients (27% and 28%, respectively). Baseline mean creatinine levels were higher (1.73±1.1 vs. 1.27±0.1 mg/dl, p<0.05), and LVEF was lower (27±3% vs. 35±17%, p<0.05) in patients who died during follow-up as compared to survivors. A trend toward a longer QTc interval duration (482±47 vs. 467±28 ms) and longer QRS duration (139±36 vs. 131±7 ms) was also found among patients who died during follow-up. Conclusion In our centre, ischemic heart disease was the most common heart disease in patients presenting with ES. In more than one third of patients, VT transcatheter ablation was performed as a therapeutic strategy in addition to drug therapy. Among patients who died during the follow-up, baseline creatinine levels were higher and LVEF was lower compared with survivors. Funding Acknowledgement Type of funding sources: None. Table 1Table 2

Clinical presentation of Long QT Syndrome in a case series study in Iraq

Background: Long QT syndrome is an important cause of arrhythmic death, and it is characterized by electrocardiographic changes and a prolonged QT interval. Patients may present with sudden cardiac death, recurrent syncope, and palpitation.Objective: Clinical orientation for the Long QT syndrome and minimizing its misdiagnosis to achieve high diagnostic index.Patients and Methods: Patients presenting with ventricular arrhythmias, syncope, dizzy spells, and prolonged, non-drug-induced QT interval from 2004 uptil 2019 at Al Nasirya Heart Center , Al Sulaimanya Heart Hospital, and Al Nahrain Teaching Hospital were enrolled in this study. All aptients studied clinically and followed up. Management included beta blocker drug therapy and ICD implantation.Results: Forty-two patients were included within 15 years, comprising 22 pediatric and 20 adult patients (26 males, 16 females). Ventricular fibrillation reported in 18 patients and ventricular tachycardia in five patients. Thirty-eight patients received beta blockers, and 85% showed marked reduction in ventricular arrhythmia events. Implantable cardioverter-defibrillator (ICD) was implanted in 34 patients.The diagnosis of Long QT syndrome was missed in 85% of cases during the provisional medical contacts .Conclusion: In this case series study patients with LQTS presented with syncope, recurrent dizzy spells or palpitation. The diagnosis requires high index of diagnostic suspicion.This case study is intended to orient physicians to diagnosis this fatal problem.

Cardioprotection in patients with cancer undergoing chemotherapy: A network meta-analysis.

e12008 Background: Introduction of anthracycline or trastuzumab based regimen for various types of cancer during the past two decades led to substantial improvement in life expectancy, yet resulting in increased prevalence of unintended side effects. Left ventricular systolic dysfunction is a known complication of the currently employed chemotherapy regimens with anthracycline or trastuzumab which not only affects patient’s cardiac outcome but also limits their therapeutic opportunities, especially continuation or reintroduction of chemotherapy treatment. We aimed to perform comprehensive network meta analysis to synthesize data from randomized clinical trials (RCT) comparing all modern regimens to prevent cardiotoxicity in such patients. Methods: We performed a comprehensive search of pubmed, embase, google scholar and TRIP database for all RCT comparing cardioprotective effects of medication in patients with various types of cancer on chemotherapy with either an anthracycline or trastuzumab based regimen from 1997 to 2019. Left ventricular ejection fraction (LVEF) was measured by transthoracic echocardiogram or cardiac magnetic resonance imaging. Patients treated with either Angiotensin Converting Enzyme-Inhibitor(ACE) or Angiotensin receptor blocker(ARB) were combined into one group. Primary outcome was change in LVEF between start and end of the chemotherapy. Network meta-analyses were conducted using consistency and inconsistency models. Results: A total of 16 studies with 1459 patients were included in the analysis where either an Anthracycline or Trastuzumab based chemotherapy regimen was administered. 369 patients received beta blockers(BB), 351 received either an ACE or ARB, 61 received a combination of BB and either an ACE or ARB, 20 received a statin and 657 were given a placebo. The primary cancer was breast cancer in 8 studies, one each of lymphoma, blood cancers and remaining 6 being mixed. Mean age was 48.81 years. Compared to patients on placebo there was a significant cardioprotective effect (smaller reduction in LVEF) noted with ACE/ARB (beta coef 5.2 (1.5-8.9), p<0.01), BB(beta coef 4.62 (0.8-7.8), p<0.02), and spironolactone beta coef 12.9 (1.9-23.4), p<0.03) There was an evidence of inconsistency with all p>0.3, other than in spironolactone arm as there were suggestion of inconsistency with p<0.01 likely due to the presence of single study. Conclusions: BB and ACE/ARB are associated with reduction in cardiotoxicity in patients with cancer undergoing cancer chemotherapy with an anthracycline or trastuzumab based regimen.

INFLUENCE OF BETA BLOCKERS ON THE HEMODYNAMIC RESPONSE TO INTRAVENOUS INOTROPES IN ACUTE DECOMPENSATED HEART FAILURE

Previous studies have demonstrated altered hemodynamic response to intravenous inotrope in chronic, stable heart failure patients receiving beta blocker (BB). The purpose of this study is to assess the effect of BB on hemodynamic response to intravenous inotrope in patients with acute decompensated

Beta blockers in critically ill patients with traumatic brain injury: Results from a multicenter, prospective, observational American Association for the Surgery of Trauma study.

Beta blockers, a class of medications that inhibit endogenous catecholamines interaction with beta adrenergic receptors, are often administered to patients hospitalized after traumatic brain injury (TBI). We tested the hypothesis that beta blocker use after TBI is associated with lower mortality, and secondarily compared propranolol to other beta blockers. The American Association for the Surgery of Trauma Clinical Trial Group conducted a multi-institutional, prospective, observational trial in which adult TBI patients who required intensive care unit admission were compared based on beta blocker administration. From January 2015 to January 2017, 2,252 patients were analyzed from 15 trauma centers in the United States and Canada with 49.7% receiving beta blockers. Most patients (56.3%) received the first beta blocker dose by hospital day 1. Those patients who received beta blockers were older (56.7 years vs. 48.6 years, p < 0.001) and had higher head Abbreviated Injury Scale scores (3.6 vs. 3.4, p < 0.001). Similarities were noted when comparing sex, admission hypotension, mean Injury Severity Score, and mean Glasgow Coma Scale. Unadjusted mortality was lower for patients receiving beta blockers (13.8% vs. 17.7%, p = 0.013). Multivariable regression determined that beta blockers were associated with lower mortality (adjusted odds ratio, 0.35; p < 0.001), and propranolol was superior to other beta blockers (adjusted odds ratio, 0.51, p = 0.010). A Cox-regression model using a time-dependent variable demonstrated a survival benefit for patients receiving beta blockers (adjusted hazard ratio, 0.42, p < 0.001) and propranolol was superior to other beta blockers (adjusted hazard ratio, 0.50, p = 0.003). Administration of beta blockers after TBI was associated with improved survival, before and after adjusting for the more severe injuries observed in the treatment cohort. This study provides a robust evaluation of the effects of beta blockers on TBI outcomes that supports the initiation of a multi-institutional randomized control trial. Therapeutic/care management, level III.

Predictors of cross-clamp-induced intraoperative monitoring changes during carotid endarterectomy using both electroencephalography and somatosensory evoked potentials

ObjectiveThe efficacy of selective shunting during carotid endarterectomy (CEA) using intraoperative monitoring (IOM) for detection of cerebral ischemia is well established. There is mounting evidence that monitoring of both electroencephalography (EEG) and somatosensory evoked potentials (SSEPs) increases the sensitivity of cerebral ischemia detection. Predictors of cerebral ischemia requiring selective shunt placement using IOM of both EEG and SSEPs have not been previously identified. MethodsConsecutive patients who underwent CEA between January 1, 2000, and December 31, 2010, were retrospectively analyzed. Primary end points were IOM changes at any time during the operation or IOM changes with carotid cross-clamping. Risk factors assessed included demographics; baseline comorbidities; severity of ipsilateral and contralateral disease; symptomatic status; and use of statin, antiplatelet, and beta-blocker medications. Univariate and multivariate logistic regression was used for analysis. ResultsDuring the 11-year study period, a total of 758 patients underwent 804 CEAs (mean age, 70.6 ± 9.5 years; 59.8% male; 39.2% symptomatic) using IOM of both SSEPs and EEG for selective shunting guidance. Postoperative stroke rate was 1.37%; 27.1% of patients had significant SSEP or EEG changes, and 49.1% of these were clamp induced (within 5 minutes of cross-clamping). Of these patients, 83.2% received a shunt (11.4% overall). The most common reason that a shunt was not placed after cross-clamp-induced changes was that the changes resolved with further blood pressure elevation (8 of 17 patients). Clamp-induced IOM changes were predictive of postoperative stroke (odds ratio [OR], 5.5; P = .005). Risk factors for clamp-induced IOM changes were contralateral carotid occlusion (OR, 2.5; P = .01), symptomatic stenosis (OR, 1.8; P = .006), and diabetes (OR, 1.6; P = .03), whereas there was a trend toward increased risk with female sex (OR, 1.5; P = .08). Risk factors for any IOM change (clamp and nonclamp induced) were symptomatic carotid stenosis (OR, 1.8; P < .001), use of beta blockers (OR, 1.5; P = .03), and female sex (OR, 1.5; P = .02). ConclusionsWhereas some patients can be expected to experience IOM changes by monitoring of SSEPs and EEG, a much smaller percentage will receive a shunt. Contralateral carotid occlusion, symptomatic stenosis, diabetes, and female sex increase the risk of clamp-induced IOM changes and should be anticipated to need a shunt. Patients receiving beta blockers are likely to experience IOM changes during the operation that are not associated with clamping.

Abstract 4662: Beta blockers abrogate EGFR TKI resistance induced by adrenergic receptor-mediated upregulation of IL-6 and modulation of the LKB1/AMPK/mTOR axis

Abstract Therapeutic strategies to target EGFR tyrosine kinase inhibitor (TKI) resistance mediated by mechanisms other than T790M are a major clinical challenge. Studies have implicated IL-6 as a mediator of EGFR TKI resistance, and IL-6 is known to be regulated by adrenergic receptors (AR) in some cancers. We investigated whether adrenergic pathways can promote T790M-independent EGFR TKI resistance in preclinical models and in clinical studies. We found that β2-AR was highly expressed in our panel of 119 cell lines and in NSCLC clinical specimens. Activation of β-ARs by stress hormones such as norepinephrine (NE) induced a dramatic rise in IL-6, and this occurred through β2-ARs. β-AR inhibitors (i.e. propranolol), but not α-AR inhibitors, blocked IL-6 induction. Analysis of downstream signaling pathways revealed that β2-ARs induced IL-6 expression through activation of adenylyl cyclase, p90RSK and CREB. To identify novel signaling pathways modulated by ARs, we stimulated NSCLC cell lines with NE and analyzed protein lysates by RPPA to detect expression and activation of &amp;gt;100 proteins. β-AR signaling inactivated the tumor suppressor LKB1 through phosphorylation of S428 and subsequently increased mTOR activity. LKB1 inactivation was critical for IL-6 induction. This finding is important as LKB1 loss is known to be a driver of NSCLC resistance and metastasis. Moreover, we found that β2-AR activation promoted EGFR TKI resistance in cell lines and in mouse models of EGFR mutant NSCLC. The effect of β-AR on EGFR TKI resistance was blocked by the addition of the beta blocker propranolol or IL-6 antibodies, in vitro and in vivo. Consistent with our preclinical studies, in the phase III ZEST clinical study testing erlotinib vs vandetanib, we found that high plasma levels of IL-6 was associated with a worse PFS and OS in the erlotinib arm. In addition, we found that circulating levels of IL-6 were significantly lower in NSCLC patients incidentally receiving beta blockers in the BATTLE trial. Finally, we analyzed the influence of incidental beta blocker use in the LUX-Lung3 study testing afatinib vs chemotherapy in EGFR mutant NSCLC patients. In patients not receiving beta blockers, the median PFS was 11.1 and 6.9 months for afatinib and chemotherapy, respectively, and afatinib improved PFS with a hazard ratio (HR) of 0.60. In patients receiving beta blockers, the median PFS was 13.6 and 2.5 for afatinib and chemotherapy, respectively, and afatinib improved PFS with a HR of 0.25. In conclusion, our preclinical and clinical data provide evidence that β2-AR activation can upregulate IL-6 in EGFR mutant+ NSCLC, modulate the LKB1/AMPK/mTOR axis, and promote EGFR TKI resistance. Moreover, EGFR mutant+ patients using beta blockers had greater relative PFS benefit from afatinib vs chemotherapy compared with those not using beta blockers, supporting future clinical testing of EGFR TKIs in combination with beta blockers. Citation Format: Monique B. Nilsson, Huiying Sun, Lixia Diao, Pan Tong, Youhong Fan, Hai Tran, Diane Liu, Guillermo Armaiz Pena, Jing Wang, Phil Rowe, Alan Webster, Jack Lee, Daniel Gomez, Waun Ki Hong, Ignacio Wistuba, Anil Sood, John Heymach. Beta blockers abrogate EGFR TKI resistance induced by adrenergic receptor-mediated upregulation of IL-6 and modulation of the LKB1/AMPK/mTOR axis. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 4662.

Leitliniengerechte Behandlung bei chronischer Herzinsuffizienz im Rahmen der Hausarztzentrierten Versorgung. Ergebnisse einer Evaluationsstudie

Family doctor centred health care (German abbreviation: HzV) agreements in Baden-Wuerttemberg provides that every year the strategies and results of at least two high-quality guidelines shall be discussed and worked on in quality circles. In this regard, the 'heart failure' guideline by the German Society of General Practice and Family Medicine (DEGAM) is especially important due to the high treatment costs and the continuously increasing prevalence of this medical condition. Another specified objective of the HzV agreements is to increase the DMP participation rate. The study addressed two questions: Is the medical care provided to patients with chronic heart failure who are being treated under HzV more compliant with guidelines than routine care? Does further improvement result from working on the guidelines in quality circles?Routine data were provided by the AOK Baden-Wuerttemberg statutory health insurance company. Patients with heart failure receiving treatment under an HzV agreement (HzV group) were compared with patients receiving routine care (control group) with regard to quality of care eight months before and eight months after working on the guideline on heart failure in quality circles. Primary endpoints were the prescription of ACE inhibitors, AT1 antagonists and beta blockers in accordance with guidelines. Adjustment for various covariates was done by means of multivariate multilevel regression.Data were available for 3,667 practices [1,295 HzV practices; 2,158 non-HzV practices]. After applying validated diagnosis criteria, 16,584 patients were included in the intervention group and 28,992 in the control group. The HzV group received significantly better care in terms of the primary endpoint "prescription of ACE inhibitors or AT1 antagonists" (73.1 % vs. 69.3 % of the patients received ACE inhibitors or AT1 antagonists at T0 (OR 1.40; 95% CI [1,25; 1,57]; p < .001). 54.2 % vs. 52.3 % of the patients received beta blockers at T0 (not significant after adjustment, p = .260). No further improvement could be demonstrated to result from working on guidelines in quality circles.The treatment of HzV patients with chronic heart failure is more compliant with guidelines than that of patients receiving routine care. Quality of care was already high at the beginning, and working on guidelines in quality circles had no noticeable effect. The increased DMP participation rate, which is one of the specified objectives of the HzV agreements, appears to have a mediation effect.

The effects of dexmedetomidine on attenuation of stress response to endotracheal intubation in patients undergoing elective off-pump coronary artery bypass grafting

This study was designed to study the efficacy of intravenous dexmedetomidine for attenuation of cardiovascular responses to laryngoscopy and endotracheal intubation in patients with coronary artery disease. Sixty adult patients scheduled for elective off-pump coronary artery bypass surgery were randomly allocated to receive dexmedetomidine (0.5 mcg/kg) or normal saline 15 min before intubation. Patients were compared for hemodynamic changes (heart rate, arterial blood pressure and pulmonary artery pressure) at baseline, 5 min after drug infusion, before intubation and 1, 3 and 5 min after intubation. The dexmedetomidine group had a better control of hemodynamics during laryngoscopy and endotracheal intubation. Dexmedetomidine at a dose of 0.5 mcg/kg as 10-min infusion was administered prior to induction of general anaesthesia attenuates the sympathetic response to laryngoscopy and intubation in patients undergoing myocardial revascularization. The authors suggest its administration even in patients receiving beta blockers.

Frequency and management of troponin I elevation in patients treated with molecular targeted therapies in phase I trials

Cardiotoxicity of molecular targeted therapies (MTT) is poorly understood and is being investigated among patients with metastatic solid tumours. The frequency of cardiac events among patients receiving MTT has been evaluated in various ways, particularly troponin elevations. We prospectively evaluated cardiotoxicity among patients included in Phase 1 trials receiving molecular targeted therapies (MTT) for a metastatic solid tumour. At baseline, all patients were examined before the first cycle and monitored including a clinical examination, ECG and troponin I measurement. A trans-thoracic echocardiography was performed at baseline and before each cycle. Patients were enrolled in different trials investigating : an anti-VEGF monoclonal antibody, anti-VEGFR tyrosine kinase inhibitors, and a kinesin inhibitor. Among the 90 patients evaluated, 10 (11%) experienced chest pain and troponin I elevation (n = 2,20%) or asymptomatic troponin I elevation (n = 8, 80%) during follow-up. All patients were re-evaluated at the time of symptoms or troponin I elevation with trans-thoracic echocardiography, cardiac magnetic resonance and coronary angiography. All except one patient, had a normal LVEF during their re-evaluation. One patient exhibited ECG changes (T wave inversion). No QTc interval prolongation was found. On cardiac magnetic resonance, no late gadolinium myocardial enhancement was observed. All coronary angiographies were normal (no occlusion, or coronary stenosis >50%). All patients received beta blockers and aspirin. All Patients were re-challenged with the study drug and no cardiotoxicity was observed during follow up. Troponin elevations are frequent among patients receiving molecular targeted therapies. Re-challenging these patients after a careful evaluation and under medical treatment seems to be possible. The mechanism underlying troponin elevations does not seem to be associated with coronary occlusion nor with toxic myocarditis.

Comparison of Late Mortality in Hospitalized Patients >70 Years of Age With Systolic Heart Failure Receiving Beta Blockers Versus Those Not Receiving Beta Blockers

Beta blockers are underprescribed to elderly patients with systolic heart failure (HF). We studied whether the prescription of a beta blocker is associated with a survival benefit in a nonselected population of patients >70 years of age hospitalized with acute HF and systolic dysfunction. We studied 272 consecutive patients >70 years (median 77.0, interquartile range 73.4 to 81.1) hospitalized with acute HF (left ventricular ejection fraction 34 +/- 8%) during a 2-year period. At discharge, beta-blocker therapy was prescribed in 139 patients (51.1%). A propensity score for the likelihood of receiving beta-blocker therapy was developed and showed a good performance (c-statistic = 0.825 and Hosmer-Lemeshow p = 0.820). After discharge, 120 patients (44.1%) died during the follow-up (median 31 months, interquartile range 12 to 46). Cox regression analysis showed a lower risk of death associated with beta-blocker prescription (p <0.001, hazard ratio [HR] 0.450, 95% confidence interval [CI] 0.310 to 0.655), which persisted after risk adjusting for the propensity score (HR 0.521, 95% CI 0.325 to 0.836, p = 0.007). In a propensity-matched cohort of 130 patients, there was a significantly lower mortality in patients receiving beta blockers (log rank 0.009, HR 0.415, 95% CI 0.234 to 0.734, p = 0.003). Risk reduction associated with beta blockade was observed with both high doses (HR 0.472, 95% CI 0.300 to 0.742, p = 0.001) and low doses (HR 0.425, 95% CI 0.254 to 0.711, p = 0.001). In conclusion, beta-blocker prescription at discharge in a nonselected population >70 years of age hospitalized with systolic HF is associated with a significantly lower risk of death even at low doses. This benefit remains consistent after adjustment for potential confounders.

Risk of Cardiac Events in Patients With Asthma and Long-QT Syndrome Treated With Beta2 Agonists

The clinical course and risk factors associated with beta(2)-agonist therapy for asthma have not been investigated previously in patients with the long-QT syndrome (LQTS). The risk of a first LQTS-related cardiac event due to beta(2)-agonist therapy was examined in 3,287 patients enrolled in the International LQTS Registry with QTc > or = 450 ms. The Cox proportional hazards model was used to assess the independent contribution of clinical factors for first cardiac events (syncope, aborted cardiac arrest, or sudden death) from birth through age 40. Time-dependent beta(2)-agonist therapy for asthma was associated with an increased risk for cardiac events (hazard ratio [HR] = 2.00, 95% confidence interval 1.26 to 3.15, p = 0.003) after adjustment for relevant covariates including time-dependent beta-blocker use, gender, QTc, and history of asthma. This risk was augmented within the first year after the initiation of beta(2)-agonist therapy (HR = 3.53, p = 0.006). The combined use of beta(2)-agonist therapy and anti-inflammatory steroids was associated with an elevated risk for cardiac events (HR = 3.66, p <0.01); beta-blocker therapy was associated with a reduction in cardiac events in those using beta(2) agonists (HR = 0.14, p = 0.05). In conclusion, beta(2)-agonist therapy was associated with an increased risk for cardiac events in patients with asthma with LQTS, and this risk was diminished in patients receiving beta blockers.

Levosimendan may provide a better neurohormonal response in heart failure patients receiving beta blocker therapy — Reply

The hemodynamic effects of levosimendan have been shown to be maintained or even enhanced by beta blockers. Furthermore, levosimendan has recently been reported to represent mortality benefit in patients receiving beta blockers. However, it is not clear whether these favorable effects of levosimendan under beta blockade are also suggested by a better neurohormonal response. We evaluated neurohormonal response to levosimendan in patients receiving beta blocker in our study population on the basis of the comments of Giamouzis and colleagues on previously published article, in which both levosimendan and dobutamine were found to be very effective inotropic agents in achieving favorable neurohormonal response but levosimendan had a better and prolonged effect. The findings of recent subgroup analysis suggested that levosimendan treatment trended toward a greater reduction in NT-proBNP levels and therefore may provide a better neurohormonal response in patients receiving beta blockers as compared with those patients not receiving beta blocker.

Does Beta Blocker Therapy Affect the Diagnostic Accuracy of Adenosine Single-Photon-Emission Computed Tomographic Myocardial Perfusion Imaging?

We retrospectively evaluated perfusion defect presence, extent, and severity in 158 consecutive patients receiving beta blockers, who underwent adenosine single-photon-emission computed tomography (SPECT) myocardial perfusion imaging (MPI) and coronary angiography. Seventy-six patients (group 1) had their beta blockers withdrawn 48 hours prior to testing, and 82 patients (group 2) remained on the beta blocker regimen. Groups 1 and 2 were similar in gender, age, pretest symptoms, and history of coronary artery disease (CAD). Group 1 patients had higher resting heart rates (79 +/- 19/min versus 68 +/- 13/min; P < 0.001), peak heart rates (91 +/- 21/min versus 80 +/- 15/min; P < 0.001), resting diastolic blood pressures (82 +/- 14 mm Hg versus 74 +/- 13 mm Hg; P < 0.001), peak systolic blood pressures (139 +/- 23 mm Hg versus 124 +/- 23 mm Hg; P < 0.001), and peak diastolic blood pressures (72 +/- 12 mm Hg versus 68 +/- 11 mm Hg; P = 0.04) than group 2 patients. Group 1 also had a higher incidence of angina during the 48 hours off beta blockers than group 2 (10% versus 2%; P < 0.001). There was no significant difference between the two groups in symptoms and side effects during adenosine infusion, quantitated lung/heart ratio, visually assessed lung uptake, transient ischemic dilation, post-stress ejection fraction, summed stress score, summed rest score, and summed difference score. In conclusion, in patients with CAD, beta blocker therapy does not affect the extent, severity, and reversibility of perfusion defects on adenosine SPECT MPI.

Levosimendan Reduces Mortality When Compared with Dobutamine in Patients Receiving Beta Blockers: The SURVIVE Study

Levosimendan Reduces Mortality When Compared with Dobutamine in Patients Receiving Beta Blockers: The SURVIVE Study

449 Levosimendan reduces mortality when compared with dobutamine in patients receiving beta blockers

449 Levosimendan reduces mortality when compared with dobutamine in patients receiving beta blockers

To band or to block for primary prophylaxis against variceal bleeding?

To band or to block for primary prophylaxis against variceal bleeding?