title: Sudden cardiac death in patients with silent myocardial ischemia after myocardial infarction (from the Swiss Interventional Study on Silent Ischemia Type II [SWISSI II]).
abstract: The occurrence of sudden cardiac death (SCD) in patients with silent ischemia after myocardial infarction (MI) and the factors facilitating SCD are unknown. This study aimed to determine the factors facilitating SCD in patients with silent ischemia after MI. In the Swiss Interventional Study on Silent Ischemia Type II (SWISSI II), 201 patients with silent ischemia after MI were randomized to percutaneous coronary intervention (PCI) or medical management. The main end point of the present analysis was SCD. Multivariable regression models were used to detect potential associations between baseline or follow-up variables and SCD. During a mean follow-up of 10.3 +/- 2.6 years, 12 SCDs occurred, corresponding to an average annual event rate of 0.6%. On multivariate regression analysis, the decline in the left ventricular ejection fraction (LVEF) during follow-up was the only independent predictor of SCD (p = 0.011), other than age; however, the baseline LVEF was not. The decline in LVEF was greater in patients receiving medical management than in those who had received PCI (p <0.001), as well as in patients with residual myocardial ischemia or recurrent MI compared with patients without these findings (p = 0.038 and p <0.001, respectively). Compared with medical management, PCI reduced the rate of residual myocardial ischemia (p <0.001) and recurrent MI (p = 0.001) during follow-up. In conclusion, patients with silent ischemia after MI are at a substantial risk of SCD. The prevention of residual myocardial ischemia and recurrent MI using PCI resulted in better long-term LVEF and a reduced SCD incidence.
authors: Department of Geriatrics and Department of General Internal Medicine, University of Bern Hospital Inselspital Bern, Switzerland.
authors: Andreas Wolfgang
authors: AW
authors: Schoenenberger
authors: Richard
authors: R
authors: Kobza
authors: Peiman
authors: P
authors: Jamshidi
authors: Michel
authors: M
authors: Zuber
authors: Antonio
authors: A
authors: Abbate
authors: Andreas Ernst
authors: AE
authors: Stuck
authors: Matthias
authors: M
authors: Pfisterer
authors: Paul
authors: P
authors: Erne
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000328:Adult; D000368:Aged; D017311:Amlodipine / Q000627:therapeutic use; D015906:Angioplasty, Balloon, Coronary; D000959:Antihypertensive Agents / Q000627:therapeutic use; D017298:Bisoprolol / Q000627:therapeutic use; D016757:Death, Sudden, Cardiac / Q000209:etiology* / Q000473:pathology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D008981:Molsidomine / Q000627:therapeutic use; D015999:Multivariate Analysis; D009203:Myocardial Infarction / Q000150:complications* / Q000503:physiopathology / Q000628:therapy; D017202:Myocardial Ischemia / Q000209:etiology* / Q000401:mortality / Q000503:physiopathology; D012044:Regression Analysis; D012307:Risk Factors; D013557:Switzerland; D014665:Vasodilator Agents / Q000627:therapeutic use
chemical_list: D000319:Adrenergic beta-Antagonists; D000959:Antihypertensive Agents; D014665:Vasodilator Agents; D017311:Amlodipine; D008981:Molsidomine; D017298:Bisoprolol