Serial magnetic resonance imaging of microvascular remodeling in the infarcted rat heart

Citation
C. Waller et al., Serial magnetic resonance imaging of microvascular remodeling in the infarcted rat heart, CIRCULATION, 103(11), 2001, pp. 1564-1569
Citations number
32
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CIRCULATION
ISSN journal
00097322 → ACNP
Volume
103
Issue
11
Year of publication
2001
Pages
1564 - 1569
Database
ISI
SICI code
0009-7322(20010320)103:11<1564:SMRIOM>2.0.ZU;2-9
Abstract
Background-Alterations in the coronary circulation are important determinan ts of myocardial function, Few data are available, however, about microvasc ular changes in reactive hypertrophy. With MRI, serial determination of myo cardial microcirculation after myocardial infarction (MI) is feasible. Methods and Results-We quantitatively determined myocardial perfusion and r elative intracapillary blood volume using an MRI technique. Infarct size, m yocardial 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 i nfarcted group, maximum perfusion decreased significantly from 8 to 16 week s (5.6 +/-0.3 versus 3.5 +/-0.2 mL.g(-1).min(-1), P<0.01) compared with sha m animals (5.5<plus/minus>0.3 versus 5.0 +/-0.2 mL.g(-1).min(-1) P=0.17). M yocardial 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<plus/minus>41.7 versus 549.2 +/- 32.3 mg). Basal relative intracapi llary blood volume increased significantly to 15.7 +/-0.5 vol% at 8 weeks a fter 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 occ ur 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 m ay therefore contribute to the development of heart failure.