Background. A wide therapeutic gap exists between evidence-based guidelines and their practice in the primary care, which is primarily attributed to physician and patient adherence.
Background: Recent studies have shown conflicting results regarding a protective effect of statin therapy on atrial fibrillation (AF).Hypothesis: We sought to determine whether statins are effective in reducing the risk of developing arrhythmia in a cohort of 264 patients (49% women, mean age [± standard deviation] 71 [± 12] years) with permanent pacemakers who are at high risk for AF.Methods: All patients who underwent implantation of a permanent pacemaker over a 3 ‐year period were eligible for inclusion in the study. We excluded patients with AF at implantation, incomplete medication information, or less than a yearly follow‐up visit. Atrial fibrillation was diagnosed by ECG documentation, pacemaker interrogation, and Holter monitoring. Statin treatment was verified through a central pharmacy‐computerized database (for most patients) or by chart review. Of the 264 patients, 36% had coronary artery disease.Results: Atrial fibrillation developed in 70 patients (26%) at a median of 359 days post pacemaker implantation. The incidence rate for the first occurrence of AF post pacemaker implantation among patients treated and not treated with statins was 10.5 versus 9.8 events per 100 patient‐years, respectively (p = 0.81). Even after controlling for baseline differences, the hazard ratio (HR) for developing AF among statin users did notachieve statistical significance (HR = 0.59 [0.31‐1.12]).Conclusions: We could not demonstrate that statin therapy had a protective effect against the risk of AF in patients implanted with a permanent pacemaker. The low prevalence of coronary artery disease in our patients may partly explain our results.
Patients with new-onset of atrial fibrillation (NOAF) during acute myocardial infarction (AMI) currently receive long-term oral anticoagulation. The risk for stroke of “early” versus “late” onset of atrial fibrillation (AF) has not been elucidated. Consecutively, AMI patients admitted to a tertiary medical center were analyzed. We excluded patients with preexisting AF, AMI onset ≥24 hours prior to admission, significant valvular disease, fever >38.5°C, in-hospital death, or coronary artery bypass graft. Atrial fibrillation was verified by electrocardiography and medical records. Overall 7061 patients were included, 1.4% developed “early-paroxysmal AF (PAF)” that resolved within 24 hours of admission and 2.5% had “late-AF” beyond the first 24 hours. Median follow-up was ≈6 years. Primary end points included ischemic stroke and all-cause mortality. Stroke rates were higher only in patients with late-AF versus no-AF but not in the early-PAF: 10.6% versus 4.2%, 5.3%, respectively ( P < .001). Death rates were higher in patients with late-AF and early-PAF versus no-AF: 55.3%, 43.2%, and 29.2%, respectively ( P < .001). Congestive heart failure, hypertension, age ≥75, diabetes mellitus, a stroke or transient ischemic attack, vascular disease, age 65-74, female (CHA 2 DS 2 -VASc) score underestimated stroke risk in the late-AF group. In conclusion, the study generates the hypothesis that patients with early-PAF may not have a high stroke risk questioning the indication for long-term anticoagulation.
Recurrent acute myocardial infarctions (AMI) are common and associated with dismal outcomes. We evaluated the clinical characteristics and the prognosis of AMI survivors according to the number of recurrent AMIs (ReAMI) and the time interval of events (TI). A retrospective analysis of patients who survived following hospitalization with an AMI throughout 2002–2017 was conducted. The number of ReAMIs for each patient during the study period was recorded and classified based on following: 0 (no ReAMIs), 1, 2, ≥3. Primary outcome: all-cause mortality up to 10 years post-discharge from the last AMI. A total of 12,297 patients (15,697 AMI admissions) were analyzed (age: 66.1 ± 14.1 years, 68% males). The mean number of AMIs per patient was 1.28 ± 0.7; the rates of 0, 1, 2, ≥3 ReAMIs were 81%, 13.4%, 3.6% and 1.9%, respectively. The risk of mortality increased in patients with greater number of AMIs, HR = 1.666 (95% CI: 1.603–1.720, p < 0.001) for each additional event (study group), attenuated following adjustment for potential confounders, AdjHR = 1.135 (95% CI: 1.091–1.181, p < 0.001). Increased risk of mortality was found with short TI (<6-months), AdjHR = 2.205 (95% CI: 1.418–3.429, p < 0.001). The risk of mortality following AMI increased as the number of ReAMIs increased, and the TI between the events shortened. These findings should guide improved surveillance and management of this high-risk group of patients (i.e., ReAMI).