Submitted on January 15, 2004
Accepted on September 5, 2004
Biphasic Temporal Pattern in Exercise Capacity after Myocardial Infarction in the Rat: Relationship to Left Ventricular Remodeling
Nathan A Trueblood1*, Patrick R Inscore1, Daniel Brenner2, Daniel Lugassy1, Carl S Apstein3, Douglas B Sawyer4, and Wilson S Colucci4
1 Myocardial Biology Unit, Boston University School of Medicine, Boston, MA, USA
2 Cardiac Muscle Research Laboratory, Boston University School of Medicine, Boston, MA, USA
3 Cardiac Muscle Research Laboratory, Boston University School of Medicine, Boston, MA, USA; Department of Medicine, Boston University Medical Center, Boston, MA, USA
4 Myocardial Biology Unit, Boston University School of Medicine, Boston, MA, USA; Department of Medicine, Boston University Medical Center, Boston, MA, USA
* To whom correspondence should be addressed. E-mail: truebna{at}earlham.edu.
ABSTRACT
Introduction: Following myocardial infarction (MI), there is progressive left ventricular (LV) remodeling and impaired exercise capacity. We tested the hypothesis that LV remodeling results in structural and functional changes that determine exercise impairment post-MI.
Methods: Rats underwent coronary artery ligation (n = 12) or sham (n = 11) surgery followed by serial exercise tests and echocardiography for 16 weeks post-MI. LV pressure-volume relationships were determined using a blood-perfused Langendorff preparation.
Results: Exercise capacity was 60% of shams immediately post-MI (P < 0.05) followed by a recovery to near normal during weeks 5 - 8. Thereafter, there was a progressive decline in exercise capacity to ~40% of shams (P < 0.01). At both 8 and 16 weeks post-MI, fractional shortening (FS) was reduced and end-diastolic diameter (EDD) was increased (P < 0.01). However, neither FS nor EDD correlated with exercise at 8 or 16 weeks (r2 < 0.12; P > 0.30). LV septal wall thickness was increased at both 8 (P = 0.17 vs. shams) and 16 weeks (P = 0.035 vs. shams) post-MI, and correlated with exercise at both times (r2 > 0.50 and P < 0.02 at 8 and 16 weeks). Neither end-diastolic volume nor LVDPmax at 16 weeks correlated with exercise capacity.
Conclusions: Exercise capacity follows a biphasic time-course post-MI. An immediate decrease is followed by an early recovery phase that is associated with compensatory LV hypertrophy. Subsequently, there is a progressive decrease in exercise capacity that is independent of further changes in LV volume or contractile function.
