Myocardial Strain Analysis in Acute Coronary Occlusion: A Tool to Assess Myocardial Viability and Reperfusion

Background— This study proposes 2 new echocardiographic indices with potential application in acute coronary artery occlusion to differentiate between viable and necrotic myocardium and to identify reperfusion. We investigated whether the ratio between systolic lengthening and combined late and postsystolic shortening (L-S ratio) could identify viable myocardium and whether systolic myocardial compliance, calculated as systolic lengthening divided by systolic pressure rise, could identify necrotic myocardium. Methods and Results— In anesthetized dogs, we measured left ventricular (LV) pressure and long-axis strain by Doppler echocardiography (SDE) and sonomicrometry. The left anterior descending coronary artery was occluded for 15 minutes with 3-hour reperfusion (n=6), for 4 hours with 3-hour reperfusion (n=6), or for 4 hours with no reperfusion (n=6). Myocardial work was quantified by pressure–segment length analysis, necrosis by triphenyltetrazolium chloride staining, and edema by water content. L-S ratio and systolic compliance were calculated by SDE. The L-S ratio ranged between 0.00 and 1.00 and was well correlated with regional myocardial work (r=0.77, P<0.0001). In entirely passive myocardium, the L-S ratio approached 1 and was similar in viable (0.88±0.02) and necrotic (0.81±0.03) myocardium. Compliance, however, was reduced in necrotic myocardium owing to edema (0.07±0.01%/mm Hg) but was preserved in viable myocardium (0.15±0.01%/mm Hg, P<0.05). Reperfusion of viable myocardium caused a reduction of the L-S ratio after 15 minutes (0.57±0.06, P<0.05), reflecting recovery of function. Reperfusion of necrotic myocardium caused no change in the L-S ratio, but compliance was further reduced within 15 minutes (0.03±0.01%/mm Hg, P<0.05). Conclusion— Myocardial L-S ratio and compliance by SDE identified active contraction and necrosis, respectively. These indices should be tested clinically for assessment of myocardial viability and reperfusion.

[1]  D. Kraitchman,et al.  Persistent diastolic dysfunction despite complete systolic functional recovery after reperfused acute myocardial infarction demonstrated by tagged magnetic resonance imaging. , 2004, European heart journal.

[2]  Charles J Bruce,et al.  Ultrasound Strain Imaging of Altered Myocardial Stiffness: Stunned Versus Infarcted Reperfused Myocardium , 2004, Circulation.

[3]  H. Ihlen,et al.  Strain rate imaging: why do we need it? , 2003, Journal of the American College of Cardiology.

[4]  H. Ihlen,et al.  Postsystolic Shortening in Ischemic Myocardium: Active Contraction or Passive Recoil? , 2002, Circulation.

[5]  G. Sutherland,et al.  Can changes in systolic longitudinal deformation quantify regional myocardial function after an acute infarction? An ultrasonic strain rate and strain study. , 2002, Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography.

[6]  Mario J. Garcia,et al.  Doppler-Derived Myocardial Systolic Strain Rate Is a Strong Index of Left Ventricular Contractility , 2002, Circulation.

[7]  H. Torp,et al.  Myocardial Strain by Doppler Echocardiography: Validation of a New Method to Quantify Regional Myocardial Function , 2000, Circulation.

[8]  Katherine C. Wu,et al.  Microvascular obstruction and left ventricular remodeling early after acute myocardial infarction. , 2000, Circulation.

[9]  A. Støylen,et al.  Real-time strain rate imaging of the left ventricle by ultrasound. , 1998, Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography.

[10]  R. Judd,et al.  Physiological basis of myocardial contrast enhancement in fast magnetic resonance images of 2-day-old reperfused canine infarcts. , 1995, Circulation.

[11]  E. Kinney.  Primer of Biostatistics , 1987 .

[12]  E. Braunwald,et al.  Studies of experimental coronary artery reperfusion. Effects on infarct size, myocardial function, biochemistry, ultrastructure and microvascular damage. , 1983, Circulation.

[13]  M. Fishbein,et al.  Early phase acute myocardial infarct size quantification: validation of the triphenyl tetrazolium chloride tissue enzyme staining technique. , 1981, American heart journal.

[14]  E. Braunwald,et al.  Ultrastructural Evidence of Microvascular Damage and Myocardial Cell Injury After Coronary Artery Occlusion: Which Comes First? , 1980, Circulation.

[15]  W. Hood,et al.  Experimental myocardial infarction. 14. Accelerated myocardial stiffening related to coronary reperfusion following ischemia. , 1978, Chest.

[16]  D Franklin,et al.  Regional Myocardial Function and Dimensions Early and Late after Myocardial Infarction in the Unanesthetized Dog , 1977, Circulation research.

[17]  J. Tyberg,et al.  An Analysis of Segmental Ischemic Dysfunction Utilizing the Pressure‐Length Loop , 1974, Circulation.

[18]  D A Whalen,et al.  Effect of a transient period of ischemia on myocardial cells. II. Fine structure during the first few minutes of reflow. , 1974, The American journal of pathology.

[19]  G. Diamond,et al.  Effect of Coronary Artery Disease and Acute Myocardial Infarction on Left Ventricular Compliance in Man , 1972, Circulation.

[20]  J I Hoffman,et al.  Some sources of error in measuring regional blood flow with radioactive microspheres. , 1971, Journal of applied physiology.