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Ann Thorac Surg 2007;84:51-60
© 2007 The Society of Thoracic Surgeons

Original Articles: Cardiovascular

Alterations in Lateral Left Ventricular Wall Transmural Strains During Acute Circumflex and Anterior Descending Coronary Occlusion

Frank Langer, MDa, Filiberto Rodriguez, MDa, Allen Cheng, MDa, Saskia Ortiz, MDa, Katherine B. Harringtona, Mary K. Zasioa, George T. Daughters, MSa,b, John C. Criscione, MD, PhDc, Neil B. Ingels, PhDa,b, D. Craig Miller, MDa,*

a Department of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, California
b Laboratory of Cardiovascular Physiology and Biophysics, Palo Alto Medical Foundation Research Institute, Palo Alto, California
c Department of Biomedical Engineering, Texas A&M University, College Station, Texas

Accepted for publication March 8, 2007.

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

Presented at the Poster Session of the Forty-first Annual Meeting of The Society of Thoracic Surgeons, Tampa, FL, Jan 24–26, 2005.

Background: Increased circumferential-radial shear in the midlateral left ventricle adjacent to ischemic myocardium has been observed during acute midcircumflex ischemia in open-chest animals. Extending this work, we studied transmural strains in closed-chest animals during acute proximal–circumflex (pCX) and proximal–left anterior descending (pLAD) occlusions.

Methods: Six sheep had radiopaque markers implanted to silhouette the left ventricle and measure regional systolic fractional area shortening; three transmural bead columns were inserted into the midlateral wall for transmural myocardial strain analysis. After 8 weeks, three-dimensional marker coordinates were obtained using biplane videofluoroscopy, both before and during separate 1-minute pLAD and pCX balloon occlusions. Systolic strains were assessed along circumferential, longitudinal, and radial axes, and then transformed into fiber strains using quantitative microstructural measurements.

Results: Acute pLAD occlusion and pCX occlusion caused similar hemodynamic insults. Systolic fractional area shortening revealed that the beads were in the ischemic territory during pCX occlusion, but adjacent to the ischemic myocardium during pLAD occlusion. Transmural circumferential strain and fiber shortening fell in the ischemic region during pCX occlusion, but remained normal when adjacent to the ischemic myocardium during pLAD occlusion. Circumferential-radial shear strain increased in the lateral left ventricle during pCX occlusion, but reversed in this same region during pLAD occlusion. Longitudinal-radial shear also decreased during pLAD occlusion.

Conclusions: Reversal of lateral wall circumferential-radial shear and decreased longitudinal-radial shear during acute pLAD occlusion reflects altered mechanical interaction between ischemic and nonischemic myocardium. Increased circumferential-radial shear during pCX occlusion also reflects mechanical interaction. The direction of circumferential-radial shear deformation depends on the location of the adjacent ischemic territory.






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