BACKGROUND: Alterations in the coronary circulation are important determinants of myocardial function. Few data are available, however, about microvascular changes in reactive hypertrophy. With MRI, serial determination of myocardial microcirculation after myocardial infarction (MI) is feasible. METHODS AND RESULTS: We quantitatively determined myocardial perfusion and relative intracapillary blood volume using an MRI technique. Infarct size, myocardial mass, and left ventricular volumes were determined with cine MRI. Rats were investigated at 8, 12, and 16 weeks after MI (mean MI size 24.1+/-2.0%) or sham operation. Vasodilation was induced by adenosine. In the infarcted group, maximum perfusion decreased significantly from 8 to 16 weeks (5.6+/-0.3 versus 3.5+/-0.2 mL. g(-1). min(-1), P<0.01) compared with sham animals (5.5+/-0.3 versus 5.0+/-0.2 mL. g(-1). min(-1), P=0.17). Myocardial mass increased significantly (559.1+/-20.8 mg at 8 weeks versus 690.9+/-42.7 mg at 16 weeks, P<0.05) compared with sham-operated animals (516.3+/-41.7 versus 549.2+/-32.3 mg). Basal relative intracapillary blood volume increased significantly to 15.7+/-0.5 vol% at 8 weeks after MI and remained elevated (16.8+/-0.6 vol%) at 16 weeks compared with 12.1+/-0.3 vol% (P<0.01) in sham-operated rats. CONCLUSIONS: Our results indicate that significant microvascular changes occur during cardiac remodeling. Hypoperfusion in the hypertrophied myocardium is related to an increase in vascular capacity, suggesting a compensatory vasodilatory response at the capillary level. These microvascular changes may therefore contribute to the development of heart failure.
BACKGROUND: Alterations in the coronary circulation are important determinants of myocardial function. Few data are available, however, about microvascular changes in reactive hypertrophy. With MRI, serial determination of myocardial microcirculation after myocardial infarction (MI) is feasible. METHODS AND RESULTS: We quantitatively determined myocardial perfusion and relative intracapillary blood volume using an MRI technique. Infarct size, myocardial mass, and left ventricular volumes were determined with cine MRI. Rats were investigated at 8, 12, and 16 weeks after MI (mean MI size 24.1+/-2.0%) or sham operation. Vasodilation was induced by adenosine. In the infarcted group, maximum perfusion decreased significantly from 8 to 16 weeks (5.6+/-0.3 versus 3.5+/-0.2 mL. g(-1). min(-1), P<0.01) compared with sham animals (5.5+/-0.3 versus 5.0+/-0.2 mL. g(-1). min(-1), P=0.17). Myocardial mass increased significantly (559.1+/-20.8 mg at 8 weeks versus 690.9+/-42.7 mg at 16 weeks, P<0.05) compared with sham-operated animals (516.3+/-41.7 versus 549.2+/-32.3 mg). Basal relative intracapillary blood volume increased significantly to 15.7+/-0.5 vol% at 8 weeks after MI and remained elevated (16.8+/-0.6 vol%) at 16 weeks compared with 12.1+/-0.3 vol% (P<0.01) in sham-operated rats. CONCLUSIONS: Our results indicate that significant microvascular changes occur during cardiac remodeling. Hypoperfusion in the hypertrophied myocardium is related to an increase in vascular capacity, suggesting a compensatory vasodilatory response at the capillary level. These microvascular changes may therefore contribute to the development of heart failure.
Authors: Danny J J Wang; Xiaoming Bi; Brian B Avants; Tongbai Meng; Sven Zuehlsdorff; John A Detre Journal: Magn Reson Med Date: 2010-11 Impact factor: 4.668
Authors: Moriel H Vandsburger; Robert L Janiczek; Yaqin Xu; Brent A French; Craig H Meyer; Christopher M Kramer; Frederick H Epstein Journal: Magn Reson Med Date: 2010-03 Impact factor: 4.668
Authors: Benjamin E Northrup; Kyle S McCommis; Haosen Zhang; Shuddhadeb Ray; Pamela K Woodard; Robert J Gropler; Jie Zheng Journal: J Cardiovasc Magn Reson Date: 2008-11-17 Impact factor: 5.364