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Ann Thorac Surg 2007;83:47-54
© 2007 The Society of Thoracic Surgeons

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Original Articles: Cardiovascular

Altered Myocardial Shear Strains Are Associated With Chronic Ischemic Mitral Regurgitation

^a Department of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford
^b Department of Radiology, Stanford University School of Medicine, Stanford
^c Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford
^d Research Institute of Palo Alto Medical Foundation, Palo Alto, California

Accepted for publication August 22, 2006.

^_* Address correspondence to Dr Miller, Department of Cardiothoracic Surgery, Falk Cardiovascular Research Center, Stanford University School of Medicine, Stanford, CA 94305-5247 (Email: dcm{at}stanford.edu).

Presented at the Poster Session of the Forty-second Annual Meeting of The Society of Thoracic Surgeons, Chicago, IL, Jan 30–Feb 1, 2006.

BACKGROUND: Ischemic mitral regurgitation (IMR) limits life expectancy and can lead to postinfarction global left ventricular (LV) dilatation and remodeling, the pathogenesis of which is not completely known. We tested the hypothesis that IMR perturbs adjacent myocardial LV systolic strains.

METHODS: Thirteen sheep had three columns of miniature beads inserted across the lateral LV wall, with additional epicardial markers silhouetting the ventricle. One week later posterolateral infarction was created. Seven weeks thereafter, the animals were divided into two groups according to severity of IMR ( 1+, n = 7, IMR[–] vs 2+, n = 6, IMR[+]). Four dimensional marker coordinates and quantitative histology were used to calculate ventricular volumes, transmural myocardial systolic strains, and systolic fiber shortening.

RESULTS: Seven weeks after infarction, end-diastolic (ED) volume increased similarly in both groups, end-systolic (ES) E₁₃ (circumferential-radial) shear increased in both groups, but more so in IMR(+) than IMR(–) (+0.12 vs 0.04, p < 0.005), and E₁₂ (circumferential-longitudinal) shear increased in IMR(–) but not IMR(+) (+0.04 vs –0.01, p < 0.005). There were no significant differences in ED or ES remodeling strains or systolic fiber shortening between IMR(–) and IMR(+).

CONCLUSIONS: An equivalent increase in LV end-diastolic (ED) volume in both groups, coupled with unchanged ED and end-systolic remodeling strains as well as systolic circumferential, longitudinal, and radial strains, argue against a global LV or regional myocardial geometric basis for the cardiomyopathy associated with IMR. Further, similar systolic fiber shortening in both groups militates against an intracellular (cardiomyocyte) mechanism. The differences in subepicardial E₁₂ and E₁₃ shears, however, suggest a causal role of altered interfiber (cytoskeleton and extracellular-matrix) interactions.