Beta-blockade Therapy Research Articles

Ability of the Analgesia Nociception Index variations to identify a response to a volume expansion of 250 mL of crystalloids in the operating room (REVANI): a prospective observational study

BackgroundAnalgesia Nociception Index (ANI) is a device based on analysis of the R-R interval and respiratory sinus arrhythmia to assess the balance between sympathetic and parasympathetic activity. The autonomic system is directly affected by load changes. Therefore, monitoring sympathetic tone and its change could theoretically allow tracking of load changes during volume expansion. The aim of the present study was to determine whether changes in ANI are able to track the increase in stroke volume caused by volume expansion (SV).MethodsThis prospective observational study included mechanically ventilated patients undergoing neurosurgery and benefiting from SV monitoring. Exclusion criteria were cardiac dysfunction, arrhythmias, beta-blockade therapy, and dysautonomia. SV was optimized by fluid administration of 250 ml of crystalloid fluid. A positive fluid increase was defined as a SV increase of 10% or more from baseline. Changes in SV and medium ANI (ANIm) were recorded before and 4 to 5 min after volume expansion.ResultsSixty-nine patients had 104 fluid challenges (36 positive and 68 negative). Volume expansion resulted in a greater ANI increase in responders than in nonresponders. The change in ANIm > 5 predicted fluid responsiveness with a sensitivity of 68.4% (95% CI: 67.4% to 69.5%) and a specificity of 51.2% (95% CI: 50.1% to 52.3%). The area under the receiver operating characteristic curve was 0.546 (95% CI: 0.544 to 0.549) and appeared to be affected by remifentanil dose and baseline ANI.ConclusionChanges in ANIm induced by fluid challenge is not able to predict fluid responsiveness in mechanically ventilated patients undergoing neurosurgery.Trial registrationClinical trial registration: NCT04223414.

Reply to the Editor - Maternal inappropriate sinus tachycardia during pregnancy.

We would like to comment on the Letter to the Editor of Dr Wang on our manuscript, Management of Inappropriate Sinus Tachycardia during pregnancy (1Shah A.N. Ferreira S.W. Padanilam B.J. Prystowsky E.N. Management of inappropriate sinus tachycardia during pregnancy.Heart Rhythm O2. 2023; 4: 65-66https://doi.org/10.1016/j.hroo.2022.11.001Abstract Full Text Full Text PDF PubMed Scopus (0) Google Scholar). He acknowledges that we used the standard accepted definition of inappropriate sinus tachycardia (IST) but raises the issue of whether an alternative definition of IST should be used during pregnancy. Indeed, recent data in pregnant women show that median heart rate was 82 bpm at 12 weeks gestation and rose to 91 bpm at 34.1 weeks (2Green L.J. Mackillop L.H. Salvi M. et al.Gestation-specific vital sign reference ranges in pregnancy.Obstet Gynecol. 2020; 135: 653-664Crossref PubMed Scopus (42) Google Scholar). However, the average heart rates in our patients mostly recorded in the early 2nd trimester were typically more than 100 bpm, and more importantly they were highly symptomatic with the added history of rapid and marked increases in heart rate during exertion, a classic presentation of IST. They were referred for further evaluation because their physicians considered them to have something other than the usual mild increase in heart rate with pregnancy. Dr Wang comments on the use of metoprolol to treat these very symptomatic patients, and suggests that the data on its effectiveness in non-pregnant patients remains questionable. The senior author (ENP) has a different experience and has treated scores of IST patients prior to ivabradine availability with substantial success in many using metoprolol succinate. The limiting factor for success is often the inability to use a high enough dose because some of these patients simply cannot tolerate beta-blockade therapy even at a low dose. Further, it is our experience that volume expansion and use of salt supplementation, while valuable in autonomic syndromes of hypotension, are not effective in pure IST without hypotension. Last, although one would like to avoid the use of any drug during pregnancy, metoprolol is considered safe to use if needed (3Page R.L. Joglar J.A. Caldwell M.A. et al.2015 ACC/AHA/HRS Guideline for the management of adult patients with supraventricular tachycardia: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society.Heart Rhythm. 2016; 13: e136-e221Abstract Full Text Full Text PDF PubMed Scopus (67) Google Scholar), and all our patients were treated beyond the first trimester. Risks and benefits of therapy were discussed during the shared decision making process, and all patients wanted to take metoprolol to suppress their marked symptoms. We agree that more data on IST in pregnancy, and the safety of ivabradine, would be useful and encourage others to investigate this problem. To the Editor – Maternal inappropriate sinus tachycardia during pregnancyHeart Rhythm O2PreviewShah and colleagues presented 11 patients with maternal inappropriate sinus tachycardia (IST) during pregnancy.1 Two major points are worth considering. Full-Text PDF Open Access

PREDICTED MAX HEART RATE SHOULD NOT BE USED FOR PATIENTS IN CARDIAC REHABILITATION

https://youtu.be/o3sLspfpDqs BACKGROUND A maximal exercise test is often not available for patients in cardiac rehabilitation (CR) and many programs determine a target heart rate (THR) using equations to estimate maximum heart rate (HRmax). The purpose of this study was to describe the % of patients in which a THR based on an estimated HRmax would result in a heart rate (HR) that is consistent with guidelines (i.e., 50%–80% HR reserve) in patients with heart disease (HD) on beta-blockade therapy. METHODS This was a secondary analysis of the iATTEND study; a randomized trial of facility-based only CR vs. hybrid CR. Subjects included in the present analysis had a history of myocardial infarction, coronary revascularization procedure, or heart failure; beta-blockade therapy; and sinus rhythm. Exclusion criteria were heart transplant, atrial fibrillation, implanted pacemaker, and exercise-induced ischemia. Measured HR reserve (maximum - rest) was determined from a symptom-limited maximal exercise test with gas exchange performed on a treadmill. Estimated HRmax was determined using (a) 220 age and (b) a published equation based on patients with HD with beta-blockade (HD BB; 164-0.72xage). % measured HR reserve associated with 60% and 85% estimated HRmax using each equation was compared to guideline recommended intensity of 50%–80% measured HR reserve. Paired sample t-tests were used to compare measured HRmax to the 2 estimates of HRmax. RESULTS Among 166 subjects (68% male; age= 59±11 yr [mean±SD]) measured HRmax was 133±21 min 1. Compared to measured, estimated HRmax using 220-age was significantly higher (161±11 min- 1; p<.001) and estimated HRmax using HD-BB was significantly lower (121±8 min-1; p<.001). At 60% of 220-age, 19% of subjects would have been provided a THR that was consistent with guidelines; 72% would have been too low. At 60% of HD-BB, 1% of subjects would have been provided a THR that was consistent with guidelines; 99% would have been too low. At 85% of 220-age, 16% of subjects would have been provided a THR that was consistent with guidelines; 84% would have been too high. At 85% of HD-BB, 36% of subjects would have been provided a THR that was consistent with guidelines; 15% would have been too high. CONCLUSION THR based on % estimated HRmax from 220-age and HD-BB do not provide an exercise training HR target that is consistent with guideline recommendations, thus should not be used to prescribe an exercise intensity in patients with HD on BB therapy.

Impact of beta blockade therapy on heart failure with preserved ejection fraction

Background: Heart failure preserved ejection fraction does not have clear guidelines. Because of past meta-analyses investigations, the Beta-blockade has sparked the most attention. Method & Results: We performed a retrospective observational where 1500 adult patients were studied from the period January 1, 2012 to December 31, 2017. After the review, 625 met the criteria to be included in the study. Cardiac reasons for inpatient admission between patients on beta-blockers vs. not on beta-blockers do not differ. The likelihood of requiring critical care admission was similar, and the likelihood of death due to cardiovascular causes between both groups did not differ. Conclusion: The use of beta-blockade therapy is still a subject of debate, especially in the minority (Hispanic and African American) population.

Primary Hyperaldosteronism From Adrenocortical Adenoma Presenting as Seizures and Stroke

Background: Primary hyperaldosteronism, which is unregulated secretion of aldosterone from the adrenal gland, is a common cause of resistant hypertension. Hyperaldosteronism can lead to life threatening cardiovascular and neurological complications emphasizing the crucial need for timely identification and management. We present a case of a young patient who suffered complications as a result of primary hyperaldosteronism. Clinical Case: A 35 year old female with a past medical history of resistant hypertension on four anti-hypertensive medications, primary hyperaldosteronism with known adenoma, CKD stage III, and hyperlipidemia presented to the hospital due to multiple seizures. She was found to be encephalopathic and required intubation for respiratory failure. Her systolic blood pressure was elevated to 250 mmhg. CT scan of the head showed a small left temporal hemorrhage and an MRI brain was revealing of bilateral thalamic infarcts. No neurosurgical intervention, antiplatelet or anticoagulation was recommended. She was admitted to the ICU and started on nitroprusside infusion. CT scan of the abdomen showed a 17 mm right adrenal nodule unchanged from prior imaging. Due to concern for pheochromocytoma, she was started on alpha blockade and subsequently beta blockade therapy. After stabilization of patient’s blood pressure, extubation, and improvement in mental status, she was discharged on new anti-hypertensive medications including spironolactone given her hypokalemia. Further endocrine evaluation was pursued. Work up included urine and plasma catecholamines which were not indicative of pheochromocytoma. Morning cortisol level was within normal limits. Plasma aldosterone level was 30, plasma renin was 0.90 with an aldosterone/renin ratio of 33 suggestive of primary hyperaldosteronism. Though the patient had known primary hyperaldosteronism with an adenoma, she had poor follow up and did not comply with initial recommendation of surgical removal of adenoma prior to her stroke. After medical stabilization following her stroke, a laparoscopic right adrenalectomy was performed. Pathology showed an adrenal cortical adenoma with no evidence of pheochromocytoma. Post-surgical systolic blood pressures were less than 120 mmhg. She was able to come off of spironolactone with plans to gradually discontinue other antihypertensive medications. Conclusion: This case emphasizes the importance of testing for primary hyperaldosteronism particularly in young patients with resistant hypertension. Furthermore, primary hyperaldosteronism should be considered as an underlying etiology for young patients who suffer from strokes particularly in the setting of hypertension. Given the reversibility of primary aldosteronism from an adrenocortical adenoma with surgery, life threatening complications such as cerebrovascular accidents can be prevented.

Cocaine, cardiomyopathy, and heart failure: a systematic review and meta-analysis

Although the cardiotoxic effects of cocaine are universally recognized, the association between cocaine and cardiomyopathy and/or heart failure is poorly understood. To conduct a comprehensive review and meta-analysis on the association between cocaine, heart failure, and cardiomyopathy, we first conducted a broad-term search in PubMed, Embase, Web of Science, and Scopus for human studies containing primary data on the relationship between cocaine and heart failure or cardiomyopathy. We were interested in studies with data beyond acute coronary syndromes. Retrieved studies were grouped into different categories based on possible hypotheses to test by meta-analysis. A second search with specific terms was then conducted. For grouped studies with sufficient clinical and methodological homogeneity, effect sizes were calculated and combined for meta-analysis by the Random Effects model. There is in general a need for more primary data studies that investigate heart failure and/or cardiomyopathy in cocaine users for mechanisms independent of ischemia. There were, however, enough studies to combine by meta-analyses that showed that chronic cocaine use is associated with anatomical and functional changes more consistent with diastolic heart failure instead of the commonly taught dilated cardiomyopathy pathway. In patients without a history of ACS, chronic cocaine use was not associated with significantly reduced EF. The few studies on acute cocaine had conflicting results on whether single-dose intravascular cocaine results in acute heart failure. Studies identified that included beta-blockade therapy in cocaine users with cardiac disease suggest that beta-blockers are not unsafe and that may be effective in the treatment of cocaine-associated heart failure. Chronic cocaine use is associated with anatomical and physiological changes of the heart muscle that are potentially reversible with beta-blockade therapy.

Incidence, risk factors and clinical significance of postoperative haemodynamic instability after adrenalectomy for phaeochromocytoma.

Due to risk of haemodynamic instability (HDI), it has been recommended that patients undergoing adrenalectomy for phaeochromocytoma should be monitored in an intensive care facility. The aim of this study was to evaluate the incidence, risk factors and outcomes of postoperative HDI in these patients. Retrospective cohort study of 46 consecutive patients who underwent open (OA, N=26) or laparoscopic (LA, N=20) adrenalectomy for phaeochromocytoma at a single centre [2007-2017]. HDI was defined as systolic BP >200 or <90 mmHg, heart rate >120 or <50 bpm or vasopressor therapy within 24 hours. Risk factors for intraoperative and postoperative HDI were evaluated by univariable and multivariable analyses. Intraoperative hypertension occurred in 25/42 patients (60%). Preoperative plasma normetanephrine levels ≥3,500 pmol/L were significantly associated with intraoperative hypertension on multivariable analysis [odds ratio (OR) 42; 95% CI: 4-429; P=0.002). Postoperative hypotension occurred in 21/45 patients (47%), and 13 (29%) required vasopressor therapy. Preoperative beta-blockade therapy was the only independent risk factor for postoperative hypotension on multivariable analysis (OR 4.0; 95% CI: 1.2-13.9, P=0.029). No patients (0/9) with tumours <5 cm treated by LA needed postoperative vasopressor therapy, compared to 39% (7/18) treated by OA (P=0.059). Complications developed in 9 patients (20%), and were less likely in those with intraoperative hypertension (8% vs. 41%; P=0.019). There was one postoperative death. Preoperative beta-blockade therapy is an independent risk factor for postoperative HDI after adrenalectomy for phaeochromocytoma. Patients who undergo laparoscopic adrenalectomy (LA) for phaeochromocytomas <5 cm are unlikely to need postoperative vasopressor therapy, and may not require intensive care monitoring.

Acute Coronary Syndrome Secondary to Aortocaval Fistula

This paper reports the case of an 88-year-old male with a history of chronic abdominal aortic aneurysm admitted to the emergency department with resting chest pain consistent with angina. Beta-blockade therapy triggered a cardiogenic shock, which motivated an urgent computed tomography scan and echocardiogram that confirmed high-output-related heart failure secondary to aortocaval fistula. (Level of Difficulty: Beginner.)

Effect of beta-blockade on quantitative microvolt T-wave alternans in 24-hour continuous 12-lead ECG recordings in patients with long QT syndrome.

The aim of study was to investigate effects of beta-blockade on microvolt T-wave alternans (TWA), a precursor of lethal arrhythmia, in patients with long QT syndrome (LQTS). Eleven consecutive LQTS patients, types 1 (n=6), 3 (n=2), and "non-1, non-2, non-3" (n=3) were enrolled. All patients underwent 24-hr continuous 12-lead ECG monitoring before and after initiation of beta-blockade therapy. TWA was measured using the modified moving average method. Seven (63.6%) of the 11 patients studied were symptomatic, with history of cardiac arrest or documented Torsade de Pointes (TdP) in 4 and syncope in three patients. After a median follow-up of 34months, beta-blockade reduced the number of symptomatic patients to 1 with TdP (p<0.02), in whom TdP frequency decreased from 25 events/60months (0.42 event/month) to seven events/69months (0.1 event/month). In association with this reduction in symptoms, peak TWA decreased by 47% in the cohort after a median of eight months of beta-blockade therapy [from 95 (74-130) to 50 (39.5-64.5) µV, p=0.01]. All patients exhibited TWA ≥42µV before beta-blockade therapy, which eliminated these episodes in four patients. Daily frequency of TWA ≥42µV episodes decreased by 87% [from 15 (6-26) to 2 (0-5) episodes/day, p=0.009]. This study is limited by the small sample size and is mainly hypothesis generating. TWA monitoring deserves further evaluation as a risk marker and a guide to therapy in LQTS patients in future large-scale studies.

Sexual regional dimorphism of post-adolescent and middle age brain maturation

This paper reports the case of an 88-year-old male with a history of chronic abdominal aortic aneurysm admitted to the emergency department with resting chest pain consistent with angina. Beta-blockade therapy triggered a cardiogenic shock, which motivated an urgent computed tomography scan and echocardiogram that confirmed high-output-related heart failure secondary to aortocaval fistula. (Level of Difficulty: Beginner.)

INFLUENCE OF BETA-BLOCKERS ON MORTALITY IN CHRONIC HEART FAILURE PATIENTS WITH ATRIAL FIBRILLATION: FINDINGS FROM THE GULF-SAFE

Background: Beta-blockers are known to decrease long-term mortality in patients with heart failure (HF). However, their role in atrial fibrillation (AF) patients with HF is controversial. We hypothesized that beta-blockade therapy in patients presenting to the emergency room (ER) due to AF, and have

Incidence, time of occurrence and response to heart failure therapy in patients with anthracycline cardiotoxicity.

Anthracyclines are commonly used chemotherapeutic medications. In the current analysis, we evaluated all-cause mortality and incidence, timing and response to medical therapy of anthracycline cardiotoxicity. Left ventricular ejection fraction (LVEF) was serially assessed using gated heart pool scan/echocardiography in patients receiving anthracycline-based chemotherapy from January 2009 to December 2014. A total of 1204 patients was administered anthracyclines during the study period. During a median follow up of 32 (interquartile range: 15-58) months, all-cause mortality was 38% (n = 463), with the incidence of cardiotoxicity 10.2% (n = 123). Only 15.4% (n = 19) patients required heart failure hospitalisation, with 48% (n = 59) of patients commenced on beta blockade therapy and/or angiotensin-converting enzyme inhibitors. The majority of patients (73.2%, n = 90) experienced cardiotoxicity within 1 year of anthracycline initiation. The proportion of patients with complete, partial and no LVEF recovery were 16.3% (n = 20), 29.3% (n = 36) and 54.4% (n = 67) respectively. Mortality was higher in the cardiotoxicity group (49% vs 37%, P < 0.01). History of coronary artery disease, leukaemia, idarubicin use and high cumulative anthracycline dose were predictors of cardiotoxicity. Cardiotoxicity after anthracycline use predictably occurs within the first year of therapy and is dose-related, with variable degrees of recovery. While the need for hospitalisation for heart failure was uncommon, medical therapy appears underutilised, suggesting there may be a role for improved surveillance and early initiation of treatment.

Beta-Blockers are Associated with Decreased In-Hospital Mortality and Stroke in Acute Decompensated Heart Failure: Findings from a Retrospective Analysis of a 22-Year Registry in the Middle East (1991-2013).

Beta-blockers reduce mortality in chronic heart failure. To study intra-hospital mortality and adverse cardiovascular (CV) outcomes in relation to beta-blockade therapy in acute decompensated heart failure. We retrospectively analyzed a 22-year registry of acute decompensated heart failure (ADHF) in the Middle East. Out of the total 8066 patients admitted for ADHF, 1242(15.4%) were on beta-blockers on admission. Among those, beta-blockers were discontinued in 26.5%. Despite the existence of less CV comorbidities in patients not treated by beta-blockers, in-hospital mortality and stroke/transient ischemic attacks rates were higher in those patients compared with patients on beta-blockers on admission (14.4 vs. 3.6%, p=0.001, 0.6 vs. 0.1%, p=0.02; respectively). Additionally, continuation of beta-blockers during acute decompensation was associated with less mortality risk (p=0.001). The use of beta-blockers on admission and discharge increased significantly with time whereas in-hospital mortality decreased (p=0.001). Nevertheless, admission year was not a predictor of reduced mortality in patients treated with beta-blockers on admission (OR 0.93, 95% CI [0.56-1.54], p=0.77). Previous beta-blockade therapy in patients presenting with ADHF decreases intra-hospital mortality and the incidence of CV events and stroke/transient ischemic attacks. Moreover, nonwithdrawal of beta-blockers during hospitalization has a favorable outcome.

An Unusual Case of Acute Muscle Weakness

A previously healthy 35-year old man presented to hospital with acute leg weakness following an alcohol binge. On assessment, tachycardia, urinary retention and bilateral upper and lower limb proximal weakness with preserved peripheral power were noted. Biochemistry revealed marked hypokalaemia, which responded to intravenous replacement, and biochemical thyrotoxicosis, leading to the diagnosis of Thyrotoxic Periodic Paralysis (TPP). Anti-thyroid therapy and beta-blockers were commenced and his neurological symptomatology resolved as he became progressively euthyroid. TPP is a rare acquired subtype of hypokalaemic periodic paralysis, typically causing proximal muscle weakness associated with thyrotoxicosis. It is most common in young Asian males. Acute treatment requires cautious oral potassium supplementation, beta-blockade, and anti-thyroid therapy. TPP is prevented by maintaining euthyroidism; otherwise recurrence is likely.

Beta-blockade in experimental fluid-resuscitated sepsis: acute haemodynamic effects of esmolol differ in predicted survivors and non-survivors

Beta-blockade therapy during sepsis has a sound rationale in view of its cardiac, metabolic, inflammatory and other effects [1]. Whether it is safe and efficacious in both good prognosis and poor prognosis patients is yet to be ascertained. We have developed a 72-h fluid-resuscitated rat model of faecal peritonitis, where prognosis can be accurately predicted as early as 6 h post-insult based on the degree of myocardial depression (low stroke volume, high heart rate)[2]. This model offers a useful means of testing safety and efficacy.

Cardiac vignette: An interesting case of concurrent hypertrophic obstructive cardiomyopathy (HOCM) and takotsubo cardiomyopathy (TCM)

A 73-year-old female presented with a syncopal episode on a background of left ventricular outflow tract obstruction of undifferentiated aetiology. Patient reported that the event was sudden and was preceded by palpitations, dizziness and central non-radiating chest discomfort. Witnesses reported that she slumped to the ground, with spontaneous recovery of consciousness after 3 minutes. The patient was admitted for telemetry monitoring under Cardiology. During her stay, routine ECGs revealed new ST elevation in the anterior leads with significant elevation in cardiac enzymes. Patient subsequently underwent emergent cardiac catheterisation which revealed normal coronary arteries and apical ballooning on left ventriculography. (Image 1) Subsequent transthoracic echocardiography revealed akinesis of the apex and hypokinesis of the anterior wall. Left ventricular function was moderately impaired. There was asymmetric hypertrophy of the mid-septal wall with a septal-to-posterior wall thickness ratio of 1.5. Systolic anterior motion of the mitral valve was also appreciated with associated eccentric mitral regurgitation of moderate severity. (Image 2) There was flow acceleration in the LVOT with a resting gradient of 40mmHg and 110mmHg with Valsalva manoeuvre. (Image 3) A diagnosis of Takotsubo Cardiomyopathy with concurrent HOCM was made. Patient was commenced on an ACE inhibitor and Beta-blockade therapy. Patient was subsequently discharged, with plan for outpatient endomyocardial biopsy and genetic testing. This case brings forth an interesting phenomenon of dual myocardial pathologies, with potential for a pre-existing LVOT gradient providing substrate for development of the typical TCM contracture design in context of a sympathetic surge.

Abstract 13770: DWS as an Index of Myocardial Stiffness and a Predictor of Heart Failure Outcome in Patients with Chronic Beta-blockade Therapy

Background: Diastolic dysfunction determines symptoms and prognosis in patients with left ventricular (LV) dysfunction. Diastolic wall strain (DWS) is associated with poor outcomes in heart failure with preserved ejection fraction. However, the utility of DWS is still unknown in heart failure with reduced ejection fraction (HFrEF). Our aim is to determine whether DWS is predictive of the outcome in HFrEF. Methods: We studied 54 HFrEF patients (LVEF&lt;50%) and followed DWS as an index of myocardial stiffness for 6 months after the induction of beta blockade (Bisoprolol 2.5-10 mg / day). DWS was determined in the LV M-mode echocardiogram using the following equation: DWS = {(LV posterior wall thickness at end-systole - LV posterior wall thickness at end-diastole) / LV posterior wall thickness at end-systole}. We followed for 7years after the induction of beta-blockade. Results: DWS increased after the induction of beta-blockade (0.32±0.11 vs 0.25±0.12,p&lt;0.05). DcT, EF and E’ also increased after the induction of beta-blockade. HR at rest and log BNP decreased following beta blockade. Patients with DWS ≤ median (0.25) before the induction of beta-blockade had higher rate of HF hospitalization than those with DWS &gt;median during 7 years (Log-rank p =0.025). DcT, EF, E’, HR at rest and log BNP before the induction of beta blockade were not significant predictors of HF outcome (Log-rank p=0.263, 0.504, 0.0796, 0.289 and 0.877) respectively. Conclusions: Induction of beta-blockade provided an improvement in DWS. DWS might be useful as an index of myocardial stiffness to predict the outcomes in HFrEF patients with chronic beta-blockade therapy.

An Individualized Exercise Prescription to Attenuate Symptoms Associated With Postural Orthostatic Tachycardia Syndrome

An Individualized Exercise Prescription to Attenuate Symptoms Associated With Postural Orthostatic Tachycardia Syndrome

Impact of Beta Blockade Therapy on Long-Term Mortality After ST-Segment Elevation Acute Myocardial Infarction in the Percutaneous Coronary Intervention Era

Although clinical guidelines recommend long-term β-blocker (BB) therapy to decrease mortality after acute myocardial infarction, these recommendations are based predominantly on evidence from before the reperfusion and thrombolytic eras. To investigate the effects of BB therapy for patients with acute myocardial infarctions on mortality in the percutaneous coronary intervention era, a total of 5,628 consecutive patients who were admitted <24 hours after the onset of ST-segment elevation myocardial infarction, treated with emergent percutaneous coronary intervention, and discharged alive were studied. During a median follow-up period of 1,430 days, mortality rates did not differ between patients with and without BB therapy (5.2% vs 6.2%, p= 0.786). Multivariate analysis revealed that BB treatment was not associated with a reduced risk for mortality (hazard ratio 0.935, 95% confidence interval 0.711 to 1.230, p= 0.534). The results of propensity score matching also indicated that the mortality rates did not differ between the 2 groups. However, subgroup analyses among matched populations revealed that BB treatment was associated with a significantly lower mortality risk for high-risk patients, who were defined as those with Global Registry of Acute Coronary Events (GRACE) risk scores ≥121 (hazard ratio 0.596, 95% confidence interval 0.416 to 0.854, p= 0.005) or those administered diuretics (hazard ratio 0.602, 95% confidence interval 0.398 to 0.910, p= 0.016), but not for lower risk patients. In conclusion, BB treatment was associated with reduced long-term mortality in patients after ST-segment elevation myocardial infarction at higher risk, but not in those at lower risk. Although randomized controlled studies are warranted to confirm these results, the implementation of BB therapy for discharged patients with ST-segment elevation myocardial infarction may need to be assessed on the basis of individual mortality risk in the percutaneous coronary intervention era.

Clinical perspective: the importance of heart rate reduction in heart failure

Clinical perspective: the importance of heart rate reduction in heart failure