Background and Objectives：Platelet activation and aggregation, with resultant arterial thrombus formation, play pivotal roles in the pathophysiology of acute coronary syndrome (ACS). The efficacy of tirofiban, a specific inhibitor of the platelet glycoprotein IIb/IIIa receptor, combined with heparin, or low molecular heparin (LMWH), in the management of ACS were evaluated. Subjects and Methods：One hundred seventeen patients (60.8± 10.9 years, 76 male), with unstable angina or non-ST elevation myocardial infarction, who had ST-T changes and elevated troponin, were divided into 4 groups：Group

We describe the case of a 17-year-old boy with Becker's muscular dystrophy (BMD) presenting with rapid progression from hypertrophic cardiomyopathy to heart failure within 2 years. Initial echocardiogram showed severe hypertrophy of left ventricle (LV) and right ventricle (RV) with normal chamber size, and preserved LV systolic function. Microscopic study of cardiac muscle obtained by endomyocardial biopsy of the interventricular septum showed severe hypertrophy of the muscle fibers and interstitial fibrosis. Follow-up echocardiogram 2 years after the first examination exhibited marked dilated LV and RV with severe LV global hypokinesia. Follow-up endomyocardial biopsy demonstrated increased interstitial cellular matrix. Immunohistochemical staining for dystrophin revealed significant loss of dystrophin along the sarcoplasmic membrane of the right biceps brachii muscle, compatible with BMD.

We report the case of a 35-yr-old patient who presented with high fever and chills. He had undergone a patch closure of the ventricular septal defect 18 yr before. One year later, a VVI pacemaker was implanted via the right subclavian vein because of complete heart block. Nine years after that, a new VVI pacemaker with another right ventricular electrode was inserted controlaterally and the old pacing lead was abandoned. Trans-thoracic and trans-esophageal echocardiogram identified the pacemaker lead in the right ventricle (RV) attaching hyperechoic materials and also a fluttering round hyperechoic mass with a stalk in the RV outflow tract. Cultures in blood and pus from pacemaker lead grew Achromobacter xylosoxidans. A diagnosis of pacemaker lead endocarditis due to Achromobacter xylosoxidans was made. In this regards, the best treatment is an immediate removal of the entire pacing system and antimicrobial therapy.

Many evidences suggest that atherosclerosis is an inflammatory disease and inflammatory markers can be an important prognostic factors in acute coronary syndrome. Hydroxymethylglutaryl (HMG-CoA) reductase inhibitors (statins) have been shown anti-inflammatory property that are independent of lipid-lowering effects. We evaluated the effects of 2-month treatment with simvastatin (40 mg/d, n=20) on plasma levels of circulating high-sensitivity C-reactive protein (hsCRP), inflammatory cytokines [tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6], and adhesion molecules [p-selectin and monocyte chemotactic peptide (MCP)-1] with placebo group (n=20) in 40 normocholesterolemic patients (LDL＜130 mg/dl) with acute coronary syndrome. Simvastatin therapy significantly reduced plasma levels of total cholesterol and LDL-cholesterol (p=0.05, p=0.02, respectively) compared with placebo group. Simvastatin therapy also significantly reduced plasma levels of hsCRP and IL-6 (p=0.03, p=0.03, respectively) compared with placebo group. But, the reduction of hsCRP and IL-6 levels with simvastatin was unrelated to the degree of LDL-cholesterol's reduction. The effect of simvastatin on the reduction of hsCRP and IL-6, but not on the other inflammatory cytokines and adhesion molecules, have potential implications in the management of acute coronary syndrome with normocholesterolemia.

In Western countries, sudden cardiac death (SCD) is closely related to coronary artery disease, but in Korea the clinical characteristics of SCD are not well determined. Over a 4-year period (June 1995 to May 1999), 186 cases of SCD, ranging in age from 16 to 75 years, were admitted to the Chonnam National University Hospital. In 82 (44.1%) of these, neither symptoms nor evidence of structural heart disease was found and so their clinical characteristics were investigated. There were 66 (80.5%) men and 16 (19.5%) women (male/female ratio = 4.1 : 1). The mean age was 50±14 years: 19 (23.2%) were in their 40s, 21 (25.6%) in their 50s, and 17 (20.7%) in their 60s. The time of circulatory collapse witnessed in 68 cases of SCD showed 2 peaks: between midnight and 03.00 h (n=16, 23.5%) and between 09.00 h and midday (n=15, 22.1%). Unexplained SCD occurred at home in 48 (64.9%) cases and on the street in 12 (16.2%); it occurred during normal daily routine activity in 23 (39.6%) and during sleep in 15 (25.9%). Thirty-three patients (40.2%) experienced various prodromal symptoms, including chest discomfort (n=13, 15.9%) and dyspnea (n=8, 9.8%). The electrocardiogram taken on arrival recorded asystole in 65 (79.3%) and ventricular fibrillation in 17 (20.7%). Idiopathic ventricular fibrillation was diagnosed in 14 (10 men, 4 women; 45±11 years) of 21 patients who recovered spontaneous circulation. Five (6.1%) patients were discharged alive, and an implantable cardioverter-defibrillator was implanted in 2. Unexplained SCD is common in Korea and develops predominantly in middle-aged males around midnight or in the late morning usually with no prodromal symptoms (59.8%). Idiopathic ventricular fibrillation is thought to be one of the important causes. (Jpn Circ J 2001; 65: 18 -22)