To evaluate the hypothesis that increasing the potential for glycolytic metabolism would benefit the functioning of infarcted myocardium, we investigated whether mild exercise training would increase the activities of oxidative enzymes, expression of carbohydrate-related transport proteins (monocarboxylate transporter MCT1 and glucose transporter GLUT4), and myosin heavy chain (MHC) isoforms. Myocardial infarction (MI) was produced by occluding the proximal left coronary artery in rat hearts for 30 min. After the rats performed 6 wk of run training on a treadmill, the wall of the left ventricle was dissected and divided into the anterior wall (AW; infarcted region) and posterior wall (PW; noninfarcted region). MI impaired citrate synthase and 3-hydroxyacyl-CoA dehydrogenase activities in the AW (P < 0.01) but not in the noninfarcted PW. No differences in the expression of MCT1 were found in either tissues of AW and PW after MI, whereas exercise training significantly increased the MCT1 expression in all conditions, except AW in the MI rats. Exercise training resulted in an increased expression of GLUT4 protein in the AW in the sham rats and in the PW in the MI rats. The relative amount of MHC-beta was significantly increased in the AW and PW in MI rats compared with sham rats. However, exercise training resulted in a significant increase of MHC-alpha expression in both AW and PW in both sham and MI rats (P < 0.01). These findings suggest that mild exercise training enhanced the potential for glycolytic metabolism and ATPase activity of the myocardium, even in the MI rats, ensuring a beneficial role in the remodeling of the heart.
yocardial flow reserve (MFR) is defined as the ratio of maximal to basal myocardial blood flow (MBF), and it is related to the severity of coronary artery stenosis. [1][2][3][4][5][6][7][8] Therefore, the MFR value is clinically useful for decision-making and the strategy of coronary intervention. Recent studies have shown that MFR is impaired by age 9 and coronary risk factors, such as smoking, 10 hyperlipidemia (HPL), 11,12 diabetes mellitus (DM), 13 and hypertension (HTN), 14 even in the absence of coronary stenosis. The MFR can be accurately measured invasively and noninvasively. Clinical evaluation of MFR using positron emission tomography (PET) is a safe and repeatable method to use for patients without coronary artery disease, 15-17 compared with invasive methods such as Doppler flow-wire. 18 Several studies have reported that MFR is impaired, together with the poor prognosis, in both patients with dilated cardiomyopathy (DCM) [19][20][21][22][23][24] and those with hypertrophic cardiomyopathy (HCM). [25][26][27][28][29][30] In particular, the prognosis is poorer for patients with the dilated phase of HCM (DHCM), who have systolic dysfunction and left ventricular (LV) remodeling, than in those with DCM. However, the pathophysiological differences between these 2 types of cardiomyopathies remain unclear. The purpose of this study was to compare MBF, MFR and coronary vascular resistance (CVR) between patients with DCM and those with DHCM, using 15 O-labeled water PET,8,[31][32][33] which is similar to 13 N ammonia PET. 34 Methods Study PopulationWe studied 30 patients with cardiomyopathies (23 men, 7 women; mean age 60.9±12.3 years) who were admitted to the Department of Cardiovascular Medicine, Kyoto University Hospital because of worsening heart failure. The group included 23 patients with DCM (Group A) and 7 patients with DHCM (Group B). After admission, the patients were treated with conventional medical therapy, and Circ J 2007; 71: 884 -890 (Received October 10, 2006; revised manuscript received January 24, 2007; accepted February 26, 2007 (MFR) is impaired in patients with nonischemic cardiomyopathy, and the reduced MFR may be related to poor prognosis. Several studies report that the mortality rate for patients with DHCM is higher than for DCM, but the difference between these 2 cardiomyopathies is still unclear. The purpose of this study was to assess the MFR of these 2 cardiomyopathies, using 15 O-water positron emission tomography (PET) to elucidate their differences. Methods and ResultsIn total 30 patients were investigated: 23 with DCM (Group A) and 7 with DHCM (Group B). All those who were in a stable condition underwent cardiac catheterization. Myocardial blood flow (MBF) at rest and under ATP infusion was measured by 15 O-water PET, and the MFR was calculated. There were no significant differences in the hemodynamics of the 2 groups. The mean MFR in DHCM was significantly lower than that in DCM (1.49±0.31 vs 2.62±1.08; p=0.042), whereas MBF at rest did not differ (DCM vs DHCM: 0.66±0.20 ...
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These results indicate that increased uptake of BMIPP in stunned myocardium is mainly due to decreased beta-oxidation in tissue and increased shunt retention of BMIPP in the triglyceride pool, and thereby provide further insight into the pathophysiology of stunned myocardium.
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