Remote noninfarcted region dysfunction soon after first anterior myocardial infarction. A magnetic resonance tagging study.

BACKGROUND Previous studies have demonstrated hyperkinetic endocardial motion of noninfarcted myocardium early after myocardial infarction (MI). We wished to substantiate the findings of increased function of remote noninfarcted regions using magnetic resonance (MR) myocardial tagging in patients soon after anterior MI. METHODS AND RESULTS Twenty-eight patients (25 male; mean age, 52 years) were studied on day 5 +/- 2 after first anterior MI. All had single-vessel left anterior descending coronary artery (LAD) disease and had received reperfusion therapy but had evidence of regional left ventricular (LV) dysfunction and an ejection fraction (EF) < or = 50%. Breath-hold, segmented k-space, gradient-echo MR tagging was performed with short-axis imaging spanning the LV. Percent circumferential shortening (%S) on a topographic basis, LV mass, and EF were measured. Regional %S was compared with that in 10 normal subjects (7 male; mean age, 43 years). We found reduced intramyocardial %S throughout the LV in the patient group. Percent shortening was lower in patients compared with control subjects at all sites along the long axis of the ventricle (9 +/- 5% versus 23 +/- 3% at the apex, P < .0001; 11 +/- 5% versus 21 +/- 3% at the midventricle, P < .0001; 14 +/- 3% versus 17 +/- 5% at the base, P < .02). The basal lateral and midinferior regions, remote from LAD territory, demonstrated reduced %S and a strong trend toward reduced %S, respectively. CONCLUSIONS Patients on day 5 after first anterior MI with single-vessel disease demonstrate reduced intramyocardial circumferential shortening throughout the LV, including remote noninfarcted regions. Potential mechanisms include altered coronary vasodilatory properties, changes in regional mechanical load, or mechanical tethering to infarcted regions.

[1]  R. Kerber,et al.  Effects of Acute Coronary Occlusion on the Motion and Perfusion of the Normal and Ischemic Interventricular Septum: An Experimental Echocardiographic Study , 1976, Circulation.

[2]  G. Diamond,et al.  Functional abnormalities in nonoccluded regions of myocardium after experimental coronary occlusion. , 1976, The American journal of cardiology.

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

[4]  G. Beller,et al.  Echocardiographic Detection of Infarct-localized Asynergy and Remote Asynergy During Acute Myocardial Infarction: Correlation with the Extent of Angiographic Coronary Disease , 1983, Circulation.

[5]  F. Sheehan,et al.  Coronary anatomy and left ventricular function in the first 12 hours of acute myocardial infarction: the Western Washington Randomized Intracoronary Streptokinase Trial. , 1985, Circulation.

[6]  R. Bache,et al.  Mechanisms of remote myocardial dysfunction during coronary artery occlusion in the presence of multivessel disease. , 1986, Circulation.

[7]  R. Smalling,et al.  Reciprocal functional interaction of adjacent myocardial segments during regional ischemia: an intraventricular loading phenomenon affecting apparent regional contractile function in the intact heart. , 1986, Journal of the American College of Cardiology.

[8]  H W Woo,et al.  Advantages and applications of the centerline method for characterizing regional ventricular function. , 1986, Circulation.

[9]  C. Visser,et al.  Prognostic implications of regional hyperkinesia and remote asynergy of noninfarcted myocardium. , 1986, The American journal of cardiology.

[10]  F. Sheehan,et al.  Intravenous streptokinase for acute myocardial infarction. Effects on global and regional systolic function. , 1988, Circulation.

[11]  E. Zerhouni,et al.  Human heart: tagging with MR imaging--a method for noninvasive assessment of myocardial motion. , 1988, Radiology.

[12]  R. Califf,et al.  Prognostic implications and predictors of enhanced regional wall motion of the noninfarct zone after thrombolysis and angioplasty therapy of acute myocardial infarction. The TAMI Study Groups. , 1989, Circulation.

[13]  L. Axel,et al.  MR imaging of motion with spatial modulation of magnetization. , 1989, Radiology.

[14]  B. Healy,et al.  Coronary reserve is depressed in postmyocardial infarction reactive cardiac hypertrophy. , 1990, Circulation.

[15]  A. Weyman,et al.  Natural history of left ventricular size and function after acute myocardial infarction. Assessment and prediction by echocardiographic endocardial surface mapping. , 1990, Circulation.

[16]  L Axel,et al.  Circumferential Myocardial Shortening in the Normal Human Left Ventricle: Assessment by Magnetic Resonance Imaging Using Spatial Modulation of Magnetization , 1991, Circulation.

[17]  E. McVeigh,et al.  Cardiac Tagging with Breath‐Hold Cine MRI , 1992, Magnetic resonance in medicine.

[18]  G. Lamas,et al.  Left ventricular remodeling in the year after first anterior myocardial infarction: a quantitative analysis of contractile segment lengths and ventricular shape. , 1992, Journal of the American College of Cardiology.

[19]  L Axel,et al.  Regional differences in function within noninfarcted myocardium during left ventricular remodeling. , 1993, Circulation.

[20]  A de Roos,et al.  Left ventricular wall motion analysis in patients with acute myocardial infarction using magnetic resonance imaging. , 1993, Magnetic resonance imaging.

[21]  W. H. Guier,et al.  Accurate systolic wall thickening by nuclear magnetic resonance imaging with tissue tagging: correlation with sonomicrometers in normal and ischemic myocardium. , 1993, Journal of the American College of Cardiology.

[22]  L. Axel,et al.  Regional Heterogeneity of Function in Hypertrophic Cardiomyopathy , 1994, Circulation.

[23]  S. Perlini,et al.  Regional nonischemic performance as assessed by end-systolic measures of shortening and thickening. , 1994, Journal of the American College of Cardiology.

[24]  A. Maseri,et al.  Reduced coronary vasodilator function in infarcted and normal myocardium after myocardial infarction. , 1994, The New England journal of medicine.

[25]  E. Hoffman,et al.  Intramural myocardial shortening in hypertensive left ventricular hypertrophy with normal pump function. , 1994, Circulation.

[26]  G. Aurigemma,et al.  Geometric changes allow normal ejection fraction despite depressed myocardial shortening in hypertensive left ventricular hypertrophy. , 1995, Journal of the American College of Cardiology.

[27]  J. Rumberger,et al.  Serial changes in left and right ventricular systolic and diastolic dynamics during the first year after an index left ventricular Q wave myocardial infarction. , 1995, Journal of the American College of Cardiology.

[28]  L Axel,et al.  Segmental motion and deformation of transmurally infarcted myocardium in acute postinfarct period. , 1995, The American journal of physiology.

[29]  L. Axel,et al.  Angiotensin-converting enzyme inhibition limits dysfunction in adjacent noninfarcted regions during left ventricular remodeling. , 1996, Journal of the American College of Cardiology.