n the process of cardiac remodeling after myocardial infarction (MI), infarct expansion occurs as an acute dilatation and thinning of the infarcted region, and is followed by ventricular dilatation and myocardial hypertrophy in the non-infarcted regions. This cardiac remodeling is associated with progressive systolic and diastolic dysfunction, and an increased incidence of congestive heart failure and sudden death. [1][2][3][4] The changes in the myocardial tissue are related to structural rearrangement in the infarcted and non-infarcted regions, characterized by myocardial cell damage, hypertrophy and expression of extracellular matrix components. It is well known that the angiotensin blockade can prevent cardiac remodeling and has prolonged survival in both experimental models of MI and in patients after MI. 5-9 Beta-adrenergic blockers are also used in the treatment of MI and have been shown to reduce morbidity and mortality, presumably by preventing myocardial ischemia and arrhythmia. [10][11][12] However, the effects of -adrenergic blockers on left ventricular (LV) remodeling after MI are still unclear. Previous experimental studies have suggested that propranolol promotes LV dilation following MI, which would adversely affect LV function 13,14 and we have reported that 100 mg·kg -1 ·day -1 of atenolol facilitated LV remodeling after MI. 15 However, other -adrenergic block- Circulation Journal Vol.66, March 2002ers, which have a vasodilating action, do not have clear beneficial effects on ventricular remodeling after MI. Nipradilol (3,4-dihydro-8-(2-hydroxy-3-isopropylamino) propoxy-3-nitroxy-2H-1-benzopyran) is a non-selectiveadrenergic blocker that has a vasodilating action partly mediated by a nitrate moiety of its chemical structure. 16,17 Experimentally, nipradilol prevents the increase in heart weight, LV end-diastolic pressure (LVEDP) and LV enddiastolic volume index after MI, 18,19 but it is still unclear whether nipradilol prevents the progressive systolic and diastolic dysfunction that accompanies the change in the non-infarcted myocardial tissue during cardiac remodeling after MI. To elucidate the effects of nipradilol on cardiac remodeling in a rat model of MI, LV geometry and cardiac function were assessed by Doppler echocardiography and the cardiac gene expression of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), which are markers of the hypertrophic response of cardiomyocytes, and collagen I and III, which are markers of fibrosis, in non-infarcted areas of the left and right ventricles were investigated by northern blot analysis. Methods Experimental ProtocolMI was produced, as described previously, 20 in male Wistar rats, weight 290-310 g (Clea Japan, Osaka, Japan). Briefly, the rats were anesthetized by injection of pentobarbital sodium (35 mg/kg ip) and a left thoracotomy was performed under volume-controlled mechanical ventilation (tidal volume, 3.0 ml; respiration rate, 60 cycles/min). A ligature of 6-0 prolene was placed around the proximal left anterior descending c...
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.
Anomalous origin of the left coronary artery from the pulmonary artery is rare but causes myocardial ischemia and sudden death. A few patients with this anomaly can survive to adulthood without sufficient collateral coronary flow or surgical intervention. We present here a case of acute inferior myocardial infarction, which may occur due to thrombotic occlusion of the right coronary artery, in a 63-year-old woman with anomalous origin of the left coronary artery from the pulmonary artery, providing specific coronary angiographic findings.
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