Background. Basal posterior left ventricle (LV) hyperkinesis following catecholamine infusion in anteroseptal acute myocardial infarction (AMI) can potentially reduce mitral annular size, leading to excessive leaflets beyond coaptation and left ventricular outflow tract (LVOT) obstruction.
Methods. Dobutamine was infused (40μg/kg/min) in 24 anesthetized open-chest dogs with anteroseptal AMI by the direct ligation of the proximal left anterior descending artery. Systolic thickening of the basal posterior wall, antero-posterior mitral annular dimension, and LVOT pressure gradient were measured by Doppler and 2-dimensional echocardiography.
Results. 1) LVOT obstruction [pressure gradient (PG)30 mmHg] was produced in 13 of 24 dogs. 2) LVOT PG was significantly correlated with increased posterior wall thickening (r2 = 0.45, p<0.05) and decreased annular dimension (r2 = 0.75, p<0.001).
Conclusion. LVOT obstruction following catecholamine infusion in anteroseptal AMI is related to basal posterior LV hyperkinesis, leading to reduced mitral annular dimension with potential excessive leaflets beyond coaptation.

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Background. C-reactive protein (CRP) level and monocytosis are associated with left ventricular (LV) remodeling in patients with AMI.
Methods. One hundred twenty-nine consecutive patients with the first acute myocardial infarction (AMI) underwent myocardial contrast echocardiography (MCE) 2 weeks after successful reperfusion.
Results. LV end-diastolic volume index (LVEDVI) at pre-discharge was significantly higher in the no-reflow group than the reflow group (64±17 vs. 58±11 mL/m2, p< 0.01). The no-reflow group had a higher CRP level and peak monocyte counts than the reflow group (9.5±5.2 vs. 5.8±3.5 mg/dl, p<0.0001; and 1026±400 vs. 824±278/μl, p<0.001, respectively). Peak CRP (relative risk [RR] 1.21, 95% confidence interval [CI] 1.01-1.45, p<0.05) and peak monocyte counts (RR 1.003, 95% CI 1.001-1.006, p<0.01) were independent determinants of the no-reflow phenomenon.
Conclusion. Microvascular dysfunction following tissue inflammation may play an important role in the LV remodeling after AMI.

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A giant ball-thrombus was found in the left atrium in 78 year-old female with non-valvular lone atrial fibrillation. Intraoperative echocardiography revealed the thrombus was floating freely inside the left atrium. The thrombus was sometimes scarcely entrapped into the mitral annulus and bounded back toward the left atrium. The removed thrombus was 45×35×20mm in size.

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