Echocardiographic Changes in Eosinophilic Endocarditis Induced by Churg-Strauss Syndrome.

Eosinophilic myocarditis may be accompanied by Churg-Strauss syndrome (CSS). We report a case of CSS that was accompanied by myocardial changes in the early stage. A 71-year-old woman complained of mild chest pain at rest, but routine echocardiography did not reveal any endocardial abnormalities. Four months later, the patient was hospitalized due to congestive heart failure with neuropathy of both upper extremities. A diagnosis of eosinophilic myocarditis was made based on the patient's laboratory results and the presence of mural thrombus. This case illustrates that, although early eosinophilic myocarditis is an important differential diagnosis in patients with chest pain, it may be difficult to identify in without an apparent mural thrombus.

Eicosapentaenoic Acid combined with optimal statin therapy improves endothelial dysfunction in patients with coronary artery disease.

PURPOSE: Eicosapentaenoic acid (EPA) has been reported to augment endothelial function and improve clinical outcomes in patients with coronary artery disease (CAD). The purpose of this study was to determine whether EPA could improve residual endothelial dysfunction despite adequate lipid-lowering with statin in CAD patients. METHODS: Eighty patients with established CAD, who had been on statin treatment and had serum low-density lipoprotein cholesterol (LDL-C) levels <100 mg/dl, were randomly assigned to receive either 1,800 mg of EPA daily plus statin (EPA group, n = 40) or statin alone (Control group, n = 40). Lipid profiles and flow-mediated dilation (FMD) were assessed just before and after more than 3 months of treatment in both groups. Only patients who had impaired FMD (<6 %) before randomization were enrolled. RESULTS: After treatment for 5.2 ± 1.7 months, the EPA group showed a significant increase in the serum concentration of EPA and EPA to arachidonic acid (AA) (EPA/AA) ratio (62.5 ± 38.1 to 159.8 ± 53.8 µg/ml, 0.45 ± 0.34 to 1.20 ± 0.55, p < 0.01 for both). In the EPA group, serum triglycerides significantly decreased (150.7 ± 92.9 to 119.3 ± 60.7 mg/dl, p = 0.02), whereas no significant change was seen in the Control group. FMD, the primary study endpoint, showed a significant improvement in the EPA group (2.6 ± 1.6 % to 3.2 ± 1.6%, p = 0.02), whereas no significant change was observed in the Control group (2.7 ± 1.6% to 2.4 ± 1.7 %, p = 0.29). CONCLUSIONS: EPA improved endothelial function and impaired FMD in patients with established CAD who were on optimal statin therapy.

Longitudinal heterogeneity of coronary artery distensibility in plaques related to acute coronary syndrome.

BACKGROUND: How coronary distensibility contributes to stable or unstable clinical manifestations remains obscure. We postulated that the heterogeneous plaque distensibility is associated with unstable clinical presentations in patients with acute coronary syndrome (ACS). METHODS AND RESULTS: Seventeen and 19 ACS-related and -unrelated lesions, respectively, were visualized using intravascular ultrasound imaging with simultaneous intracoronary pressure recording. Systolic and diastolic lumen cross-sectional areas were measured at the lesion site and at five evenly spaced sites between the proximal and distal reference sites. The coronary distensibility index and stiffness index ß were calculated for each site and averaged for each coronary segment. Maximal distensibility index, standard deviation and the difference between maximal and minimal distensibility indices within each segment were significantly higher in the ACS-related than -unrelated plaques (5.6 ± 2.3 vs. 3.7 ± 1.8, p < 0.001, 2.1 ± 0.9 vs. 1.1 ± 0.6, p < 0.001 and 5.3 ± 2.3 vs. 2.8 ± 1.5, p < 0.001, respectively). Moreover, the difference in the distensibility index between the lesion site of ACS-related plaques and the immediate proximal site was significantly larger (2.88 ± 2.35 vs. 1.17 ± 1.44, p = 0.022) than that in ACS-unrelated plaques. CONCLUSIONS: Coronary artery distensibility is longitudinally more heterogeneous in ACS-related than-unrelated plaques, especially between the lesion and the immediate proximal site.

Effect of angiotensin converting enzyme inhibitors and beta-blockers on left ventricular remodeling after coronary artery bypass graft surgery.

Preventing left ventricular (LV) remodeling after coronary artery bypass graft surgery (CABG) is important to avoid long-term congestive heart failure. The present study evaluated the effects of angiotensin converting enzyme inhibitors (ACEIs) and beta-blockers on LV remodeling. Twenty-three patients with angina pectoris and 36 with old myocardial infarction underwent CABG. We assessed end diastolic volume index (EDVI), end systolic volume index (ESVI), and ejection fraction (EF) using left ventriculography before and after CABG. Changes in EDVI, ESVI, and EF were studied in the ACEI, beta-blocker, and control groups. Although EDVI was reduced in the ACEI group, ESVI and EF improved only slightly, whereas in the group given beta-blockers, ESVI was reduced, EF improved, and EDVI was minimally reduced. These results indicate that ACEIs and beta-blockers both protect against LV remodeling, although through different mechanisms.