Effect of diltiazem on cardiac remodeling in rats assessed by Doppler echocardiography and mRNA expression.

The purpose of this study was to examine the effect of diltiazem on cardiac dysfunction and the change in cardiac gene expression after myocardial infarction in rats. On the first day after myocardial infarction, rats were randomly assigned to a diltiazem treatment (Dil, n = 7) or an untreated group (MI, n = 8). We then performed Doppler echocardiographic examinations on the rats and measured their hemodynamics at 4 weeks after myocardial infarction. Following these measurements, their cardiac mRNA was analyzed. Diltiazem decreased the mean aortic pressure and heart rate. Left ventricular end-diastolic pressure (LVEDP) and central venous pressure (CVP) increased to 18 +/- 2 mmHg and 5 +/- 1 mmHg (P < 0.01). Diltiazem reduced LVEDP to 14 +/- 1 mmHg (P < 0.05), but it did not change CVP. The weight of the right ventricle in MI was significantly larger than in the control rats (control, n = 7, 0.46 +/- 0.02 g/kg vs. MI, 0.81 +/- 0.06 g/kg; P < 0.01). The left ventricular end-diastolic dimension (LVDd) in MI increased to 8.8 +/- 0.3 mm (P < 0.01, control, 6.1 +/- 0.3 mm). Diltiazem prevented an increase in the weight of the right ventricle (0.69 +/- 0.03 g/kg, P < 0.05) and LVDd (7.7 +/- 0.2 mm, P < 0.05 to MI). The rats within MI showed systolic dysfunction, defined by a decreased ejection fraction (control, 67 +/- 2% vs. MI, 36 +/- 3%, P < 0.01), and diastolic dysfunction, defined by the E-wave deceleration rate (control, 13.4 +/- 1.6 m/s2 vs. MI, 30.4 +/- 3.4 m/s2; P < 0.01). Diltiazem significantly prevented systolic and diastolic dysfunction. The increases in beta-MHC, ANP, and collagen type I and III mRNAs in the noninfarcted left ventricle and right ventricle were significantly suppressed by treatment with diltiazem. alpha-Skeletal actin increased in MI, and alpha-skeletal actin was more increased with Dil. In conclusion, diltiazem prevents cardiac dysfunction and morphological change due to left ventricular remodeling after experimental myocardial infarction.

[Evaluation of patients with cerebral infarction using transesophageal echocardiography: atherosclerotic changes in the thoracic aorta and the branches of the aortic arch].

Atherosclerotic disease of the aortic arch is thought to be a potential source of cerebral emboli, but this disease in the branch of the aortic arch has not been extensively explored. This study assessed atherosclerotic lesions in the thoracic aorta and the branches of the aortic arch using transesophageal echocardiography in patients with cerebral infarction, and simultaneously searched for potential cardiac sources for emboli. Thrombi were detected in the left atrial appendage in nine of 54 patients with cerebral infarction and these patients were excluded. The remaining 45 patients with cerebral infarction (31 males and 14 females aged 68.5 +/- 7.4 years) and 35 normal subjects (21 males and 14 females aged 69.2 +/- 9.5 years) were evaluated. The thickness of the wall was measured in the branches of the aortic arch (brachiocephalic trunk, left common carotid artery and left subclavian artery) as well as the thoracic aorta (ascending aorta, aortic arch and descending aorta). Atherosclerotic lesions were defined as increased echogenicity of the intima (intimal thickening), calcification, protruded plaque, ulceration or plaque with cystic lesion. The thicknesses of the wall in the aortic arch (3.84 +/- 1.25 vs 2.71 +/- 1.33 mm, p < 0.01), left common carotid artery (2.67 +/- 1.10 vs 2.16 +/- 0.91 mm, p < 0.05) and the left subclavian artery (2.52 +/- 0.67 vs 2.15 +/- 0.88 mm, p < 0.05) were significantly greater in patients than in the normal subjects. The incidence of plaque or ulceration was significantly increased in patients with cerebral infarction compared with the normal subjects in the aortic arch (76% vs 43%, p < 0.05) and left common carotid artery (44% vs 17%, p < 0.05). Transesophageal echocardiography can detect possible sources of emboli in the branches of the aortic arch as well as the thoracic arch in patients with cerebral infarction.