No abstract

Objective-Because fibrin is transparent and almost invisible by any conventional imaging methodologies, clinical examinations of coronary fibrin thrombus have been ignored, and little is known about its role in the genesis of acute coronary syndrome (ACS). The present study was performed to visualize coronary fibrin thrombus and to examine its role in ACS. Methods and Results-Dye-staining coronary angioscopy using Evans blue dye, which selectively stains fibrin blue but does not stain blood corpuscles, was performed for observation of globular coronary thrombi in 111 ACS patients. The thrombi were aspirated for histological examination. The thrombi were classified by visual appearance into 8 transparent, 3 light-red, 2 frosty glass-like and membranous, 32 white, 8 brown, 34 red, and 19 red-and-white in a mosaic pattern. Transparent thrombi that were not visible by conventional angioscopy were visualized as a blue structure by dye-staining angioscopy, and they were observed in patients with unstable angina (UA) and non-ST elevation myocardial infarction (NSTEMI). The thrombi caused total or subtotal coronary occlusion. The aspirated thrombi were composed of fibrin alone by histology. Fibrin-rich thrombi were visualized using dye-staining angioscopy in 60% of 50 patients with UAϩNSTEMI and in 29% of 61 patients with ST-elevation myocardial infarction. By histology of the aspirated thrombi, fibrin-rich thrombi were observed in 71% of 33 patients with UAϩNSTEMI and in 28% of 35 patients with ST-elevation myocardial infarction. Conclusion-Fibrin-rich coronary thrombi were frequently observed by both dye-staining angioscopy and histology in ACS patients. Rarely, fibrin itself formed a globular thrombus and caused coronary occlusion. (Arterioscler Thromb

Background: Takotsubo cardiomyopathy (TCM) is characterized by systolic ballooning of the left ventricular apex. It is triggered by emotional or physical stress, but the exact mechanism through which stress leads to TCM is not known. Hypothesis: Coronary microvessel apoptosis is the missing link between stress and TCM. Methods: In 8 female patients with TCM, plasma catecholamines,Thrombolysis in Myocardial Infarction (TIMI) coronary flow grade and myocardial perfusion grade, and apoptosis of the coronary microvessels in the biopsied myocardial specimen by terminal deoxynucleotidyl transferase-mediated nick end-labeling (TUNEL) were examined. Results: Plasma epinephrine and norepinephrine were increased to 663 ± 445 and 875 ± 812 pg/mL (mean ± SD), respectively. Acetylcholine-induced delayed myocardial perfusion through the ballooning apical segment without flow disturbance in the epicardial coronary arteries (indicating microvessel spasm) and focal myocardial necrosis were observed in all subjects. Apical ballooning disappeared and myocardial perfusion delay was not inducible 1 month later. The number of vessels having apoptotic endothelial cells/10 vessels in arterioles, venules, and capillaries at initial biopsy and repeat biopsy 1 month later were 8.3 ± 1.4 vs 0.4 ± 1.1, P < 0.0001; 6.8 ± 1.8 vs 0.3 ± 0.7, P < 0.0001; and 7.9 ± 1.0 vs 0.5 ± 0.9, P < 0.0001, respectively. Conclusions: Left ventricular apical ballooning in TCM was considered to be caused by coronary microvessel spasm due to catecholamine-induced endothelial cell apoptosis and myocardial stunning after release of microvessel spasm. Endothelial cell apoptosis of coronary microvessel is therefore considered to be the missing link between stress and TCM.

A sensitive immunoassay system using a specific monoclonal antibody against lipoprotein lipase (LPL) recently demonstrated the presence of an LPL mass in preheparin serum. We reported that a preheparin serum LPL mass (pre-LPL mass) reflected the level of functioning LPL activity in the whole body and could be deeply involved in the progression of coronary atherosclerosis of stable organic angina pectoris. We examined the relation between the pre-LPL mass and acute myocardial infarction (AMI). We studied 44 males with AMI (AMI group) and 16 males with a normal coronary artery (NCA group), and measured the pre-LPL mass by enzyme-linked immunosorbent assay. Coronary risk factors including the pre-LPL mass were compared between the two groups and multiple regression analysis was performed for AMI. There were no significant differences in the lipid data, but the pre-LPL mass level was significantly low in the AMI group (52 +/- 16 vs 41 +/- 14 ng/ml, p = 0.01), and a low pre-LPL mass concentration was observed in the small sized LDL group and/or the Midband positive group. Multiple regression analysis revealed that a low pre-LPL mass and hypertriglyceridemia were independent risk factors for AMI (t value = 2.1, 2.4). The result indicates that a low pre-LPL mass may be an important risk factor for AMI and stable organic angina pectoris.

Wereport a case of dilated cardiomyopathy with hyperthyroidism. A 28-year-old man was admitted because of congestive heart failure and atrial fibrillation, and was newly diagnosed as having hyperthyroidism. Despite administration of antithyroid medication, he developed recurrent congestive heart failure. An echocardiogram revealed a moderately dilated left ventricle with diffuse hypokinesis. Though his thyroid function normalized, the patient's cardiac dysfunction did not improve. Beta-blocker therapy was begun with subsequent improvement in clinical symptoms. This suggests that beta-blocker treatment may be effective in patients with atrial fibrillation associated with cardiomyopathy and hyperthyroidism. (Internal Medicine 34: 762-767, 1995)