Yoko Mikami

Cardiac side population cells have a potential to migrate and differentiate into cardiomyocytes in vitro and in vivo

Side population (SP) cells, which can be identified by their ability to exclude Hoechst 33342 dye, are one of the candidates for somatic stem cells. Although bone marrow SP cells are known to be long-term repopulating hematopoietic stem cells, there is little information about the characteristics of cardiac SP cells (CSPs). When cultured CSPs from neonatal rat hearts were treated with oxytocin or trichostatin A, some CSPs expressed cardiac-specific genes and proteins and showed spontaneous beating. When green fluorescent protein–positive CSPs were intravenously infused into adult rats, many more (∼12-fold) CSPs were migrated and homed in injured heart than in normal heart. CSPs in injured heart differentiated into cardiomyocytes, endothelial cells, or smooth muscle cells (4.4%, 6.7%, and 29% of total CSP-derived cells, respectively). These results suggest that CSPs are intrinsic cardiac stem cells and involved in the regeneration of diseased hearts.

Right-Sided Heart Wall Thickening and Delayed Enhancement Caused by Chronic Active Myocarditis Complicated by Sustained Monomorphic Ventricular Tachycardia

An asymptomatic healthy 65-year-old man was referred to a hospital for inverted T waves in the precordial leads (Figure 1) with paroxysmal advanced atrioventricular block in the ECG. Chest x-ray showed mild cardiac enlargement (Figure 2), and an echocardiogram showed right ventricular (RV) wall thickening (arrow in Figure 3). Five months later, the patient was referred to another hospital complaining of chest discomfort. Coronary angiogram was normal, but sustained monomorphic ventricular tachycardia (VT) occurred. Suffering from incessant VT, the patient was transferred to our hospital. The ECG and echocardiogram were …

Relation Between Signal Intensity on T2-Weighted MR Images and Presence of Microvascular Obstruction in Patients With Acute Myocardial Infarction

OBJECTIVE In experimental animal models and human autopsy studies, hemorrhagic infarction caused by microvascular injury has been detected after coronary reperfusion. The purpose of this study was to determine whether detection of myocardial edema with T2-weighted MRI is influenced by the presence of microvascular obstruction. SUBJECTS AND METHODS Thirty-seven patients underwent black-blood fat-suppressed T2-weighted, rest perfusion, and late gadolinium-enhanced MRI 5.4 +/- 3.1 days after the onset of acute myocardial infarction. On T2-weighted MR images, the signal intensity in relation to that of remote myocardium was determined in the late gadolinium-enhanced and periinfarction areas. Segment-based analysis was performed to determine whether the presence of microvascular obstruction influences the detection of myocardial edema. RESULTS The averaged signal intensity in the late gadolinium-enhanced area without microvascular obstruction was significantly higher than the signal intensity in remote normal myocardium (relative signal intensity, 1.83 +/- 0.50; p < 0.001). In contrast, the signal intensity in the microvascular obstruction area on T2-weighted images was not significantly different from the signal intensity in remote myocardium (relative signal intensity, 1.14 +/- 0.26). The percentages of late gadolinium-enhanced segments with high signal intensity on T2-weighted MR images were 95% (73/77) without microvascular obstruction and 30% (22/73) with microvascular obstruction. CONCLUSION With T2-weighted MRI, infarction-associated edema can be reliably detected in infarct lesions without microvascular obstruction. Microvascular obstruction, however, does not necessarily exhibit high signal intensity on T2-weighted MRI. Careful attention is required in interpretation of cardiac MR images of patients who have experienced acute myocardial infarction and undergone percutaneous coronary intervention. The findings on T2-weighted MR images can be substantial underestimates of the extent of acute myocardial infarction.

Left atrial compensatory function in subjects with early stage primary hypertension assessed by using left atrial volumetric emptying fraction acquired by transthoracic echocardiography

PURPOSE To evaluate left atrial (LA) function in subjects with early stage primary hypertension (HT) and without enlargement of LA, we used transthoracic echocardiogram and measured LA volumetric emptying fraction and compared the results with those in healthy volunteers. MATERIALS AND METHODS 42 subjects with early stage primary HT (21 males, aged 61+/-12 years), within 1 year of HT diagnosis and starting initial treatment, were enrolled in the study. An additional inclusion criterion was normal sinus rhythm electrocardiogram without enlargement of LA. As the control group, 31 healthy volunteers with normal sinus rhythm electrocardiogram (13 male, aged 57+/-11 years) were enrolled. Maximum and minimum volume of LA (LAV max and min, respectively) were selected manually and visually in B mode images acquired from a four-chamber view from apex of left ventricle (LV) using a modified Simpson method, and the LA emptying fraction (LAEF) was calculated by the following formula: LAV min/LAV max x 100 (%). RESULTS There were no significant differences in age, male:female ratio, end-diastolic and end-systolic LV diameter, LA maximum volume, LV ejection fraction and E/A in mitral annulus between the two groups. However, we found that end-diastolic inter-ventricular septum thickness and end-diastolic LV posterior wall thickness were significantly larger in the HT group in comparison with the control group (P<0.01), but the HT group did not fit the classical criteria of LV myocardial hypertrophy. The systolic and diastolic blood pressure, the end-diastolic and end-systolic volume of LV, the total weight of LV myocardium and the LAEF were significantly higher in the HT group than in the control group (P<0.05). CONCLUSIONS In subjects with early stage primary HT with normal sinus rhythm, in spite of a normal LAV, the LAEF may increase. This increase of LAEF may be regarded as one of the compensatory reactions against preload to the left side of the heart and precedes the occurrence of LA enlargement.