Article

Effects of Prophylactic Antiarrhythmic Drug Therapy in Acute Myocardial Infarction

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Abstract

Objective. —To investigate the effects of prophylactic therapy with antiarrhythmic agents on mortality in patients with myocardial infarction.Data Sources and Study Selection. —Data were obtained from all completed, published or unpublished, randomized, parallel controlled trials of antiarrhythmic agents, regardless of sample size. Investigators were contacted for data on patients excluded after randomization.Data Extraction. —Data on mortality were extracted by one author and confirmed where necessary by the others.Data Synthesis. —Mortality data from 138 trials on 98 000 patients were combined by the Yusuf-Peto adaptation of the Mantel-Haenszel method. There were 660 deaths among 11 712 patients allocated to receive class I agents and 571 deaths among 11 517 corresponding control patients (51 trials: odds ratio [OR], 1.14;95% confidence interval [Cl], 1.01 to 1.28; P=03). Of 26 973 patients allocated to receive β-blockers (class II agents), 1464 died compared with 1727 deaths among 26 295 control patients (55 trials: OR, 0.81; 95% CI, 0.75 to 0.87; P=.00001). Of 778 patients allocated to receive amiodarone (a class III agent), 77 died compared with 101 deaths in 779 control patients (eight trials: OR, 0.71; 95% Cl, 0.51 to 0.97; P=.03). There were 982 deaths in 10 154 patients allocated to receive a class IV agent (calcium channel blockers) and 949 deaths in 10 188 control patients (24 trials: OR, 1.04; 95% CI, 0.95 to 1.14; P=.41).Conclusions. —The routine use of class I antiarrhythmic agents after myocardial infarction is associated with increased mortality. β-Blockers have been conclusively demonstrated to reduce mortality. The limited data on amiodarone appear promising. Data on calcium channel blockers remain unpromising.(JAMA. 1993;270:1589-1595)

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... Beta-blockers decrease the incidence of ventricular arrhythmias and the risk of death during ACS and should be administered to all patients with no contraindications (Freemantle et al. 1999), while the prophylactic use of antiarrhythmic drugs might be harmful and is not recommended (Teo, Yusuf, and Furberg 1993). ...
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Chapter Five deals with strategies for managing vascular injuries during video-assisted thoracoscopic lobectomies.
... Although in our study the device only detected 1 exact paroxysmal atrial fibrillation, a moderate number of nonsustained atrial tachycardia episodes were recorded, indicating the unstable hemodynamic and electrical impulses of the atria after myocardial infarction. β-Blocker therapy after myocardial infarction is necessary for survival [14]. Therefore, guidelines based on randomized controlled and large observational studies recommend β-blocker therapy for all patients after myocardial infarction [15,16]. ...
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Background: Acute myocardial infarction may be associated with new-onset arrhythmias. Patients with myocardial infarction may manifest serious arrhythmias such as ventricular tachyarrhythmias or atrial fibrillation. Frequent, prolonged electrocardiogram (ECG) monitoring can prevent devastating outcomes caused by these arrhythmias. Objective: We aimed to investigate the incidence of arrhythmias in patients following myocardial infarction using a patch-type device-AT-Patch (ATP-C120; ATsens). Methods: This study is a nonrandomized, single-center, prospective cohort study. We evaluated 71 patients who had had a myocardial infarction and had been admitted to our hospital. The ATP-C120 device was attached to the patient for 11 days and analyzed by 2 cardiologists for new-onset arrhythmic events. Results: One participant was concordantly diagnosed with atrial fibrillation. The cardiologists diagnosed atrial premature beats in 65 (92%) and 60 (85%) of 71 participants, and ventricular premature beats in 38 (54%) and 44 (62%) participants, respectively. Interestingly, 40 (56%) patients showed less than 2 minutes of sustained paroxysmal atrial tachycardia confirmed by both cardiologists. Among participants with atrial tachycardia, the use of β-blockers was significantly lower compared with patients without tachycardia (70% vs 90%, P=.04). However, different dosages of β-blockers did not make a significant difference. Conclusions: Wearable ECG monitoring patch devices are easy to apply and can correlate symptoms and ECG rhythm disturbances in patients following myocardial infarction. Further study is necessary regarding clinical implications and appropriate therapies for arrhythmias detected early after myocardial infarction to prevent adverse outcomes.
... There has been no significant research in this area in recent years. An older meta-analysis has confirmed that beta blockers reduce mortality by 19% (24). The guidelines recommend beta blockers in patients after myocardial infarction who have left ventricular systolic dysfunction or heart failure with a reduced ejection fraction ≤ 40% (grade of recommendation I A) (2,7). ...
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... Consistent with other studies, the use of anti-anginal medications, such as betablockers, calcium channel blockers, and disease-modifying medications like anti-platelets, and lipid-lowering medications, are negatively correlated with IHD-related hospital admission rates. These medications are mainly maintenance therapy and have been shown to improve symptoms and prolong survival in many studies [34][35][36][37][38]. In acute myocardial infarction, there is a positive correlation with the prescription of nitrates, beta-blockers, and lipid-lowering medications, which is likely attributed to the increased utilisation of these medications during hospitalisations. ...
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Chapter
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Chapter
Dysrhythmias are common during acute myocardial infarction (AMI); these range from benign premature beats to ventricular fibrillation (VF). Reports from the early coronary-care unit (CCU) era suggested that the majority of patients with AMI have some abnormality of heart rhythm (1). In recent years, the management of arrhythmias associated with AMI has evolved significantly, along with other elements of CCU care. Malignant ventricular arrhythmias remain the cause of most prehospital sudden deaths as a result of AMI.
Chapter
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Chapter
Arrhythmias contribute substantially to morbidity and mortality in patients with symptomatic heart failure. Atrial fibrillation is a frequent cause and effect of heart failure exacerbation (1,2). As discussed below, the onset of atrial fibrillation is an independent negative prognostic sign in advanced heart failure (3,4). Approximately 300,000 people in the United States die suddenly each year, presumably largely a result of ventricular arrhythmias; the majority have pre-existing ventricular dysfunction (5). It has been estimated that 50% of deaths in patients with symptomatic heart failure are sudden, presumably arrhythmic (6,7). Furthermore, the relative contribution of sudden death to total mortality seems to be highest in patients with more preserved functional class. Against this highly emotionally charged back drop, the desire to find effective treatment for all patients with congestive heart failure (CHF) is certainly understandable.
Chapter
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Endorsed by: Research and Practical Council of the Ministry of Health of the Russian Federation.
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Background Despite its recommendation by the current guidelines, the role of long-term oral beta-blocker therapy has never been evaluated by randomized trials in uncomplicated ST-segment elevation myocardial infarction (STEMI) patients without heart failure, left ventricular dysfunction or ventricular arrhythmia who underwent primary percutaneous coronary intervention (PCI). Methods and results In a multi-center, open-label, randomized controlled trial, STEMI patients with successful primary PCI within 24 hours from the onset and with left ventricular ejection fraction (LVEF) ≥40% were randomly assigned in a 1-to-1 fashion either to the carvedilol group or to the no beta-blocker group within 7 days after primary PCI. The primary endpoint is a composite of all-cause death, myocardial infarction, hospitalization for heart failure, and hospitalization for acute coronary syndrome. Between August 2010 and May 2014, 801 patients were randomly assigned to the carvedilol group (N = 399) or the no beta-blocker group (N = 402) at 67 centers in Japan. The carvedilol dose was up-titrated from 3.4±2.1 mg at baseline to 6.3±4.3 mg at 1-year. During median follow-up of 3.9 years with 96.4% follow-up, the cumulative 3-year incidences of both the primary endpoint and any coronary revascularization were not significantly different between the carvedilol and no beta-blocker groups (6.8% and 7.9%, P = 0.20, and 20.3% and 17.7%, P = 0.65, respectively). There also was no significant difference in LVEF at 1-year between the 2 groups (60.9±8.4% and 59.6±8.8%, P = 0.06) Conclusion Long-term carvedilol therapy added on the contemporary evidence-based medications did not seem beneficial in selected STEMI patients treated with primary PCI. Trial registration CAPITAL-RCT (Carvedilol Post-Intervention Long-Term Administration in Large-scale Randomized Controlled Trial) ClinicalTrials.gov.number, NCT 01155635.
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