Effects Of Beta-blocker Therapy Research Articles

Effect of beta-blocker therapy on weight loss outcomes after sleeve gastrectomy & Roux-en-Y gastric bypass

BackgroundPatients taking beta-blockers (BBs) commonly experience weight gain. There is limited research exploring how BBs impact weight loss after bariatric surgery. ObjectivesWe examined how BBs impact 12-month weight loss in patients undergoing sleeve gastrectomy (SG) or Roux-en-Y gastric bypass (RYGB). SettingLarge midwest health system. MethodsWe reviewed health records of SG and RYGB patients (2011-2022) and categorized them by BB usage (none, pre-, post-, or pre- and postoperative). Multivariable linear regression models examined the relation between BB use, percent total body weight loss (%TBWL), and percent excess body mass index lost (%EBMIL). ResultsA total of 889 individuals (SG, n = 485; RYGB, n = 404) had complete data. RYGB led to greater %TBWL compared to SG (31% versus 26%, P < .01) and greater %EBMIL (79% versus 64%, P < .01). BB status did not significantly affect 12-month %TBWL or %EBMIL. ConclusionsBB use may not significantly affect weight loss 12 months after bariatric surgery. This finding could enable physicians to prescribe BBs for improved blood pressure control in bariatric surgery patients with less concern of blunting weight loss. Longer term follow-up with a larger sample size would be an important next step to better characterize the relationship between BB usage and bariatric surgery.

Investigating the effects of beta-blockers on circadian heart rhythm using heart rate variability in ischemic heart disease with preserved ejection fraction

Heart failure is characterized by sympathetic activation and parasympathetic withdrawal leading to an abnormal autonomic modulation. Beta-blockers (BB) inhibit overstimulation of the sympathetic system and are indicated in heart failure patients with reduced ejection fraction. However, the effect of beta-blocker therapy on heart failure with preserved ejection fraction (HFpEF) is unclear. ECGs of 73 patients with HFpEF > 55% were recruited. There were 56 patients in the BB group and 17 patients in the without BB (NBB) group. The HRV analysis was performed for the 24-h period using a window size of 1,4 and 8-h. HRV measures between day and night for both the groups were also compared. Percentage change in the BB group relative to the NBB group was used as a measure of difference. RMSSD (13.27%), pNN50 (2.44%), HF power (44.25%) and LF power (13.53%) showed an increase in the BB group relative to the NBB group during the day and were statistically significant between the two groups for periods associated with high cardiac risk during the morning hours. LF:HF ratio showed a decrease of 3.59% during the day. The relative increase in vagal modulated RMSSD, pNN50 and HF power with a decrease in LF:HF ratio show an improvement in the parasympathetic tone and an overall decreased risk of a cardiac event especially during the morning hours that is characterized by a sympathetic surge.

Effect of beta-blocker therapy on the response to mavacamten in patients with symptomatic obstructive hypertrophic cardiomyopathy.

In the EXPLORER-HCM trial, mavacamten improved exercise capacity and symptoms in patients with obstructive hypertrophic cardiomyopathy (oHCM). Mavacamten effects on the primary endpoint, a composite of peak oxygen consumption (VO2 ) and New York Heart Association (NYHA) class, were greater in patients not receiving background beta-blockers than in those receiving beta-blockers. We sought to determine if the effect of background treatment was consistent across other clinically meaningful parameters. Subgroup analyses by beta-blocker use were performed in patients with oHCM from the EXPLORER-HCM and mavacamten long-term extension (MAVA-LTE) studies. In EXPLORER-HCM, 189 patients (75.3%) were receiving beta-blockers, and 62 (24.7%) were receiving non-dihydropyridine calcium channel blockers or no background HCM medication; 170 patients (90.4%) receiving beta-blockers had chronotropic incompetence. Improvements in peak VO2 at week 30 with mavacamten versus placebo were lower with beta-blockers (mean difference [95% confidence interval (CI)]: 1.04 [0.12, 1.95] ml/kg/min) than without beta-blockers (mean difference [95% CI]: 2.69 [1.29, 4.09] ml/kg/min); improvements in non-heart rate-dependent parameters (VE /VCO2 slope) appeared unaffected by beta-blockers. Improvements in functional capacity parameters at week 30 with mavacamten versus placebo were independent of beta-blockade for post-exercise left ventricular outflow tract gradient (mean difference [95% CI]: -37.9 [-48.0, -27.9] mmHg with beta-blockers; -33.5 [-53.6, -13.3] mmHg without beta-blockers), proportion of patients with reduction of ≥1 NYHA class, Kansas City Cardiomyopathy Questionnaire clinical summary scores and N-terminal pro-B-type natriuretic peptide. Mavacamten benefits were reproduced and maintained in MAVA-LTE regardless of beta-blockade. Mavacamten improved measures of functional capacity, left ventricular outflow tract obstruction, symptom burden and biomarkers in patients with HCM regardless of beta-blocker use. Beta-blocker use was often associated with chronotropic incompetence, affecting peak VO2 and other heart rate-dependent measures, but had minimal impact on heart rate-independent measures.

Sympathetic and Vagal Nerve Activity in COPD: Pathophysiology, Presumed Determinants and Underappreciated Therapeutic Potential.

This article explains the comprehensive state of the art assessment of sympathetic (SNA) and vagal nerve activity recordings in humans and highlights the precise mechanisms mediating increased SNA and its corresponding presumed clinical determinants and therapeutic potential in the context of chronic obstructive pulmonary disease (COPD). It is known that patients with COPD exhibit increased muscle sympathetic nerve activity (MSNA), as measured directly using intraneural microelectrodes-the gold standard for evaluation of sympathetic outflow. However, the underlying physiological mechanisms responsible for the sympathoexcitation in COPD and its clinical relevance are less well understood. This may be related to the absence of a systematic approach to measure the increase in sympathetic activity and the lack of a comprehensive approach to assess the underlying mechanisms by which MSNA increases. The nature of sympathoexcitation can be dissected by distinguishing the heart rate increasing properties (heart rate and blood pressure variability) from the vasoconstrictive drive to the peripheral vasculature (measurement of catecholamines and MSNA) (Graphical Abstract Figure 1). Invasive assessment of MSNA to the point of single unit recordings with analysis of single postganglionic sympathetic firing, and hence SNA drive to the peripheral vasculature, is the gold standard for quantification of SNA in humans but is only available in a few centres worldwide because it is costly, time consuming and requires a high level of training. A broad picture of the underlying pathophysiological determinants of the increase in sympathetic outflow in COPD can only be determined if a combination of these tools are used. Various factors potentially determine SNA in COPD (Graphical Abstract Figure 1): Obstructive sleep apnoea (OSA) is highly prevalent in COPD, and leads to repeated bouts of upper airway obstructions with hypoxemia, causing repetitive arousals. This probably produces ongoing sympathoexcitation in the awake state, likely in the "blue bloater" phenotype, resulting in persistent vasoconstriction. Other variables likely describe a subset of COPD patients with increase of sympathetic drive to the heart, clinically likely in the "pink puffer" phenotype. Pharmacological treatment options of increased SNA in COPD could comprise beta blocker therapy. However, as opposed to systolic heart failure a similar beneficial effect of beta blocker therapy in COPD patients has not been shown. The point is made that although MSNA is undoubtedly increased in COPD (probably independently from concomitant cardiovascular disease), studies designed to determine clinical improvements during specific treatment will only be successful if they include adequate patient selection and translational state of the art assessment of SNA. This would ideally include intraneural recordings of MSNA and-as a future perspective-vagal nerve activity all of which should ideally be assessed both in the upright and in the supine position to also determine baroreflex function.

PO-641-07 PATIENTS WITH LONG QT SYNDROME HAVE A PRIMARY SINOATRIAL NODE PHENOTYPE OF INTRINSIC CHRONOTROPIC INSUFFICIENCY

Long QT syndrome (LQTS) is a cardiac channelopathy characterized by QT prolongation and the potential for ventricular torsadogenic-mediated syncope, sudden cardiac arrest, and sudden cardiac death. Whether patients with LQTS have a primary sinoatrial node (SAN) phenotype of chronotropic insufficiency has been speculated but not demonstrated because of the confounding effects of beta blocker therapy.

Effect of beta blocker therapy following myocardial infarction in optimally treated patients in the reperfusion era – a Danish, nationwide, and registry-based cohort study

Abstract Background and purpose European and American cardiovascular treatment guidelines advocate for two and three years of beta-blocker (BB) treatment, respectively, following myocardial infarction (MI). Contemporary continued efficacy of longer-term use of BB in stable coronary artery disease has been debated in the era of reperfusion. We aim to investigate the cardio-protective effect associated with BB treatment in patients following MI. Methods Using nationwide databases, we included optimally treated patients with first-time MI undergoing coronary angiography (CAG) or percutaneous coronary intervention (PCI) during admission and treated with both acetyl-salicylic acid and statins post-discharge between 2003 and 2017. Patients with prior history of MI, BB use or any other possible indication or contraindication for BB treatment (heart failure, cardiac arrhythmias or procedures, asthma, chronic obstructive pulmonary disease) were excluded. Continued BB exposure was defined as two redeemed prescriptions within the first 180 days following discharge, one of them within 90 days. Follow-up began 180 days following discharge in patients alive and with no further cardiovascular events or procedures prior. Patients were followed for a maximum of three years. Primary outcomes were cardiovascular death and recurrent MI in patients stratified by BB treatment using adjusted Cox regression models. Results A total of 27,068 patients optimally treated for MI were included (57% acute PCI, 26% sub-acute PCI, 17% CAG without intervention). At study start 180 days following MI, 79% of the patients were on BB treatment (median age 61 years, 75% male) and 21% were not (median age 62 years, 69% male). Cumulative incidence of cardiovascular death and recurrent MI did not differ significantly comparing patients on BB treatment with patients not on BB treatment (Figure). In multivariable analyses, BB treatment was associated with a similar risk of cardiovascular death and recurrent MI compared to the patients not receiving BB treatment (hazard ratios with [95% confidence intervals] correspondingly; 0.89 [0.68–1.17] and 1.02 [0.89–1.18]) (Figure 1). When stratifying the cohort according to calendar year and type of procedure during admission, we found similar results as the main analysis. No interaction for sex was found. Conclusions In this nationwide cohort study of optimally treated patients following MI at 180 days in the reperfusion era, we found a very good prognosis with only 1.2% suffering cardiovascular death and 4.7% suffering a recurrent MI within three years. In total 79% of patients were receiving BB treatment, but we found no difference suggesting BB to be associated with an improved cardiovascular prognosis. These findings challenge current clinical practice and guideline recommendation, suggesting that the role of long-term BB use may be obsolete among optimally treated MI patients. Further investigations, preferably a randomized trial, are warranted. Figure 1 Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): Ib Mogens Kristiansens Almene Fond, Snedkermester Sophus Jacobsen og Hustru Astrid Jacobsens Fond

QT correction using Bazett's formula remains preferable in long QT syndrome type 1 and 2.

BackgroundThe heart rate (HR) corrected QT interval (QTc) is crucial for diagnosis and risk stratification in the long QT syndrome (LQTS). Although its use has been questioned in some contexts, Bazett's formula has been applied in most diagnostic and prognostic studies in LQTS patients. However, studies on which formula eliminates the inverse relation between QT and HR are lacking in LQTS patients.We therefore determined which QT correction formula is most appropriate in LQTS patients including the effect of beta blocker therapy and an evaluation of the agreement of the formulae when applying specific QTc limits for diagnostic and prognostic purposes.MethodsAutomated measurements from routine 12‐lead ECGs from 200 genetically confirmed LQTS patients from two Swedish regions were included (167 LQT1, 33 LQT2). QT correction was performed using the Bazett, Framingham, Fridericia, and Hodges formulae. Linear regression was used to compare the formulae in all patients, and before and after the initiation of beta blocking therapy in a subgroup (n = 44). Concordance analysis was performed for QTc ≥ 480 ms (diagnosis) and ≥500 ms (prognosis).ResultsThe median age was 32 years (range 0.1–78), 123 (62%) were female and 52 (26%) were children ≤16 years. Bazett's formula was the only method resulting in a QTc without relation with HR. Initiation of beta blocking therapy did not alter the result. Concordance analyses showed clinically significant differences (Cohen's kappa 0.629–0.469) for diagnosis and prognosis in individual patients.ConclusionBazett's formula remains preferable for diagnosis and prognosis in LQT1 and 2 patients.

Effects of beta-blocker therapy on mortality after elective colon cancer surgery: a Swedish nationwide cohort study

ObjectiveColon cancer surgery remains associated with substantial postoperative morbidity and mortality despite advances in surgical techniques and care. The trauma of surgery triggers adrenergic hyperactivation which drives adverse stress responses....

Effect of beta-blocker therapy in patients with or without left ventricular systolic dysfunction after acute myocardial infarction.

This observational study aimed to investigate the association between beta-blocker therapy and clinical outcomes in patients with acute myocardial infarction (AMI), especially with mid-range or preserved left ventricular systolic function. Among 13 624 patients enrolled in the Korea Acute Myocardial Infarction Registry-National Institute of Health (KAMIR-NIH), 12 200 in-hospital survivors were selected. Patients with beta-blockers showed significantly lower 1-year major adverse cardiac events (MACE), which was a composite of cardiac death, MI, revascularization, and readmission due to heart failure [9.7 vs. 14.3/100 patient-year; hazard ratio (HR) 0.84, 95% confidence interval (CI) 0.72-0.97; P = 0.022). However, this association had a significant interaction with left ventricular ejection fraction (LVEF). Beta-blocker therapy at discharge was associated with lower 1-year MACE in patients with LVEF ≤40% (HR 0.63, 95% CI 0.48-0.81; P < 0.001), and 40% <LVEF < 50% (HR 0.69, 95% CI 0.51-0.94; P = 0.020), but not in patients with LVEF ≥50% (HR 1.16, 95% CI 0.91-1.48; P = 0.234). Beta-blocker therapy at discharge was associated with better 1-year clinical outcomes in patients with reduced or mid-range LVEF after AMI, but not in patients with preserved LVEF. These data suggested that the long-term beta-blocker therapy may be guided by LVEF.

Bisoprolol therapy does not reduce right ventricular sympathetic activity in pulmonary arterial hypertension patients.

Right ventricular (RV) function and autonomic dysfunction are important determinants of morbidity and mortality in patients with pulmonary arterial hypertension (PAH). Although successful in animal studies, effects of beta-blocker therapy on RV function in clinical trials were disappointing. To understand this discrepancy, we studied whether beta-blocker therapy changes RV sympathetic activity. Idiopathic PAH (IPAH) patients received beta-blocker therapy (uptitrated to a maximal tolerated dose) and underwent cardiac magnetic resonance imaging, right heart catheterization, and a [11C]-hydroxyephedrine positron emission tomography ([11C]HED PET) scan at baseline to determine, respectively, RV ejection fraction (RVEF), RV pressures, and sympathetic activity. [11C]HED, a norepinephrine analogue, allows determination of sympathetic innervation of the RV. [11C]HED retention index reflects norepinephrine transporter activity. As a consequence of excessive catecholamine levels in the synaptic cleft, this transporter may be downregulated. Therefore, low [11C]HED retention index indicates high sympathetic activity. 13 IPAH patients underwent [11C]HED PET scans at baseline and after bisoprolol treatment. Although heart rate was reduced, systemic modulation of autonomic activity by bisoprolol did not affect local RV sympathetic nerve activity, RV function, or RV wall tension. In PAH patients, RV [11C]HED retention index was lower compared to LV tracer uptake (p<0.01) and was related to systolic wall tension (R2 = 0.4731, p<0.01) and RV function (R2 = 0.44, p = 0.01). In RV failure, the tolerated dosage of bisoprolol did not result in an improvement of RV function nor in a reduction in RV sympathetic activity.

Effects of beta-blocker therapy on mortality after elective colon cancer surgery

Effects of beta-blocker therapy on mortality after elective colon cancer surgery

Effect of beta-blocker therapy on clinical outcomes, safety, health-related quality of life and functional capacity in patients with chronic obstructive pulmonary disease (COPD): a protocol for a systematic literature review and meta-analysis with multiple treatment comparison

IntroductionPatients with chronic obstructive pulmonary disease (COPD) who have a clinical indication for beta-blocker therapy, are often not prescribed such medication, despite evidence suggesting that beta-blockers are not associated with...

Effect of beta-blocker therapy on early mortality after emergency colonic cancer surgery.

Emergency colorectal cancer surgery is associated with significant mortality. Induced adrenergic hyperactivity is thought to be an important contributor. Downregulating the effects of circulating catecholamines may reduce the risk of adverse outcomes. This study assessed whether regular preoperative beta-blockade reduced mortality after emergency colonic cancer surgery. This cohort study used the prospectively collected Swedish Colorectal Cancer Registry to recruit all adult patients requiring emergency colonic cancer surgery between 2011 and 2016. Patients were subdivided into those receiving regular beta-blocker therapy before surgery and those who were not (control). Demographics and clinical outcomes were compared. Risk factors for 30-day mortality were evaluated using Poisson regression analysis. A total of 3187 patients were included, of whom 685 (21·5 per cent) used regular beta-blocker therapy before surgery. The overall 30-day mortality rate was significantly reduced in the beta-blocker group compared with controls: 3·1 (95 per cent c.i. 1·9 to 4·7) versus 8·6 (7·6 to 9·8) per cent respectively (P < 0·001). Beta-blocker therapy was the only modifiable protective factor identified in multivariable analysis of 30-day all-cause mortality (incidence rate ratio 0·31, 95 per cent c.i. 0·20 to 0·47; P < 0·001) and was associated with a significant reduction in death of cardiovascular, respiratory, sepsis and multiple organ failure origin. Preoperative beta-blocker therapy may be associated with a reduction in 30-day mortality following emergency colonic cancer surgery.

The effects of beta-blocker therapy on early mortality following emergency colon cancer surgery

The effects of beta-blocker therapy on early mortality following emergency colon cancer surgery

Influence of beta-blocker therapy on the risk of infections and death in patients at high risk for stroke induced immunodepression.

BackgroundStroke-induced immunodepression is a well characterized complication of acute ischemic stroke. In experimental studies beta-blocker therapy reversed stroke-induced immunodepression, reduced infection rates and mortality. Recent, heterogeneous studies in stroke patients could not provide evidence of a protective effect of beta-blocker therapy. Aim of this study is to investigate the potential preventive effect of beta-blockers in subgroups of patients at high risk for stroke-induced immunodepression.MethodsData from a prospectively derived registry of major stroke patients receiving endovascular therapy between 2011–2017 in a tertiary stroke center (University Medical Center Göttingen. Germany) was used. The effect of beta-blocker therapy on pneumonia, urinary tract infection, sepsis and mortality was assessed using multivariate logistic regression analysis.ResultsThree hundred six patients with a mean age of 72 ± 13 years and a median NIHSS of 16 (IQR 10.75–20) were included. 158 patients (51.6%) had pre-stroke- and continued beta-blocker therapy. Beta-blocker therapy did not reduce the incidence of pneumonia (OR 0.78, 95% CI 0.31–1.92, p = 0.584), urinary tract infections (OR 1.51, 0.88–2.60, p = 0.135), sepsis (OR 0.57, 0.18–1.80, p = 0.334) or mortality (OR 0.59, 0.16–2.17, p = 0.429). Strokes involving the insula and anterio-medial cortex increased the risk for pneumonia (OR 4.55, 2.41–8.56, p<0.001) and sepsis (OR 4.13, 1.81–9.43, p = 0.001), while right hemispheric strokes increased the risk for pneumonia (OR 1.60, 0.92–2.77, p = 0.096). There was a non-significantly increased risk for urinary tract infections in patients with beta-blocker therapy and insula/anterio-medial cortex strokes (OR 3.12, 95% CI 0.88–11.05, p = 0.077) with no effect of beta-blocker therapy on pneumonia, sepsis or mortality in both subgroups.ConclusionsIn major ischemic stroke patients, beta-blocker therapy did not lower post-stroke infection rates and was associated with urinary tract infections in a subgroup with insula/anterio-medial strokes.

161 - Effect of Beta-Blocker Therapy on Hospital Readmission and Mortality in Heart Failure Patients with Ongoing Cocaine Use

Background: Beta blockers are first line agents for reduction of symptoms, hospitalization and mortality in heart failure patients with reduced ejection fraction (HFrEF). However, the safety and efficacy of continuous beta-blocker therapy (BBT) in patients who actively use cocaine remain controversial and available literature is limited. We aimed to evaluate the effect of BBT on hospital readmission and mortality in HFrEF patients with ongoing cocaine use. Methods: We conducted a retrospective chart review of patients with a new diagnosis of HFrEF between 2011 and 2014 based on ICD9-CM codes. We included patients aged 18 and older who tested positive for cocaine on a urine toxicology test obtained at the time of index admission. Patients were followed for 1 year. We assessed for Beta-blocker prescription rate at the time of discharge from the index admission. A multivariate logistic regression was used to assess the effect of BBT on the 30-day all-cause and heart failure related readmissions. The 1-year mortality rate was also reported. Results: In our study population N = 268 and mean age [in yrs] = 54 (std = 6.9), the beta-blocker prescription rate is 86.2%. The 30-day readmission rate for BBT vs no BBT groups were 20% vs 41% (OR 0.17, 95% CI = 0.05–0.56, P = .004) for heart-failure related readmissions and 25% vs 46% (OR 0.19, 95% CI = 0.06–0.64, P = .007) for all-cause readmissions. The 1-year mortality rates for BBT vs no BBT groups were 5% vs 8% (OR 0.88, 95% CI = 0.17–7.19, P = .91). Conclusion: Physicians continue to prescribe outpatient Beta-blocker for most HFrEF patients regardless of cocaine-use status. BBT reduces 30-day all-cause and heart failure related readmission rate but not 1-year mortality in HFrEF patients with ongoing cocaine use. Large observational studies are needed to further elucidate the efficacy and safety of continuous BBT in this population.

Effect of Beta-Blocker Therapy, Maximal Heart Rate, and Exercise Capacity During Stress Testing on Long-Term Survival (from The Henry Ford Exercise Testing Project)

Whether lower heart rate thresholds (defined as the percentage of age-predicted maximal heart rate achieved, or ppMHR) should be used to determine chronotropic incompetence in patients on beta-blocker therapy (BBT) remains unclear. In this retrospective cohort study, we analyzed 64,549 adults without congestive heart failure or atrial fibrillation (54 ± 13years old, 46% women, 29% black) who underwent clinician-referred exercise stress testing at a single health care system in Detroit, Michigan from 1991 to 2009, with median follow-up of 10.6years for all-cause mortality (interquartile range 7.7 to 14.7years). Using Cox regression models, we assessed the effect of BBT, ppMHR, and estimated exercise capacity on mortality, with adjustment for demographic data, medical history, pertinent medications, and propensity to be on BBT. There were 9,259 deaths during follow-up. BBT was associated with an 8% lower adjusted achieved ppMHR (91% in no BBT vs 83% in BBT). ppMHR was inversely associated with all-cause mortality but with significant attenuation by BBT (per 10% ppMHR HR: no BBT: 0.80 [0.78 to 0.82] vs BBT: 0.89 [0.87 to 0.92]). Patients on BBT who achieved 65% ppMHR had a similar adjusted mortality rate as those not on BBT who achieved 85% ppMHR (p >0.05). Estimated exercise capacity further attenuated the prognostic value of ppMHR (per-10%-ppMHR HR: no BBT: 0.88 [0.86 to 0.90] vs BBT: 0.95 [0.93 to 0.98]). In conclusion, the prognostic value of ppMHR was significantly attenuated by BBT. For patients on BBT, a lower threshold of 65% ppMHR may be considered for determining worsened prognosis. Estimated exercise capacity further diminished the prognostic value of ppMHR particularly in patients on BBT.

Effect of beta-blocker therapy on heart rate response in patients with hypertension and newly diagnosed untreated obstructive sleep apnea syndrome

BackgroundBeta1-receptor antagonists (BBs) are commonly administered in the treatment of cardiovascular disease (CVD). The reported benefits of BB use in CVD patients with concomitant obstructive sleep apnea (OSA) may be limited by their impact on apnea-induced bradycardias. Therefore the aim of the study was to test the influence of BBs on periapneic heart rate (HR) fluctuations in hypertensive patients with newly-detected and untreated OSA. MethodsWe studied 88 hypertensive patients (56 on BBs and 32 BB naive) with newly-diagnosed moderate-to-severe OSA who were free of major pulmonary comorbidities and did not require antiarrhythmic therapy. ECGs recorded during sleep were investigated for heart rate (HR) responses to apneas allowing to compare extreme HR accelerations and decelerations between the groups. ResultsAverage sleep-time HR was comparable in BB-naive (BB−) and BB-treated (BB+) patients. Direct comparisons showed that HR decelerations were also similar in the two subgroups (53.8±9.6 vs. 54.4±7.8bpm; P=0.78, for BB− and BB+, respectively) however, BBs blunted the OSA-induced HR accelerations (82.3±12.2 vs. 74.3±10.0; P=0.003). After adjusting for baseline HR and magnitude of desaturations, HR decelerations were more evident in BB-naive group whereas tachycardic responses remained blunted in the BB+ group. The incidence of ectopies and conduction abnormalities were comparable across two groups. ConclusionsBeta-blockers do not potentiate apnea-induced HR decelerations, attenuate apnea-induced increases in heart rate and do not influence incidence of ectopies and conduction abnormalities in patients with hypertension and moderate-to-severe, untreated OSA.

TCTAP A-094 Effect of Beta-blocker Therapy on Mortality Rates in Stable Coronary Artery Disease Patients with Normal Left Ventricular Function After Percutaneous Coronary Intervention.

Beta-blocker therapy has been shown to benefit patients presenting with acute myocardial infarction (AMI) or left ventricular (LV) dysfunction. However, whether Beta-blockers provide a similar benefit in stable coronary artery disease (SCAD) patients with normal LV function is unknown. A population

Abstract MP78: Effect of Beta-Blocker Therapy, Maximal Heart Rate and Exercise Capacity During Stress Testing on Long-Term Survival

Background: Whether beta-blocker therapy (BBT) attenuates the prognostic value of percentage-predicted maximal heart rate (ppMHR) achieved during stress testing remains unclear. The combined effect of ppMHR and exercise capacity on long-term mortality is unknown. Methods: We analyzed 67,772 adults (54 ± 13 years old, 54% men (36,639 of 67,772), 29% black (19,834 of 67,772)) from The FIT Project, a retrospective cohort study of patients who underwent physician-referred exercise stress testing at a single healthcare system between 1991 and 2009. Patients were categorized by baseline use of BBT. Maximal age-predicted heart rate was defined as 220-age. We derived adjusted mortality rates over the range of ppMHR using margins of response logistic regression models. Our primary model included adjustment for demographic data, resting blood pressures, medical history, pertinent medications, and indication for stress testing. Our secondary model included further adjustment for exercise capacity. Results: There were 10,594 deaths over 11 ± 5 years of follow-up. Patients on BBT tended to have more comorbidities and other medication use (P&lt;.001). After accounting for differences between BBT groups, BBT was associated with an 8% lower ppMHR (83% in BBT vs. 91% in no BBT) in both men and women. ppMHR was inversely associated with all-cause mortality in both analyses performed (P≤.001), though the association was significantly attenuated by BBT (P=.03) [Panel A]. Exercise capacity further attenuated the prognostic value of ppMHR in all patients, particularly in those on BBT, and reduced the difference in risk between those on BBT and not on BBT (P=.08) [Panel B]. Conclusion: BBT attenuated the association between ppMHR achieved during stress testing and long-term mortality. Exercise capacity further attenuated the prognostic significance of ppMHR, particularly in patients on BBT.