BACKGROUND: The early diagnosis of myocardial ischemia is still challenging. The aim of the present study was to determine whether subendocardial hypokinesis and post-systolic contraction could be early markers of myocardial ischemia. METHODS AND RESULTS: Thirty-one consecutive patients with flow-limiting severe coronary stenosis but without visually abnormal left ventricular wall motion underwent quantitative echocardiography. Myocardial strain was measured using layer-by-layer analysis in severely hypoperfused segments. Radial strain (RS) was measured in the subendocardial, subepicardial, and total wall (innerRS, outerRS, and totalRS, respectively). Circumferential strain (CS) was also measured as 3 separate layers: subendocardial, mid-layer, and subepicardial layers (innerCS, midCS, and outerCS, respectively). Post-systolic shortening (PSS) was defined as the peak strain after end systole, and post-systolic strain index (PSI) was calculated as PSS divided by end-systolic strain. TotalRS was similar between ischemic and normally perfused segments, but innerRS and inner/outer RS ratio were significantly smaller in the ischemic segments than in corresponding segments in healthy subjects. Receiver operating characteristic analysis identified an optimum cut-off for PSI of 0.6. The combined criteria of inner/outer RS ratio <1.0 and PSI >0.6 achieved 95% specificity for the presence of flow-limiting stenosis. CONCLUSIONS: Combined assessment of both subendocardial contractile impairment and PSS is very useful in identifying a severely hypoperfused left ventricular wall even without visual wall motion abnormality.
BACKGROUND: The early diagnosis of myocardial ischemia is still challenging. The aim of the present study was to determine whether subendocardial hypokinesis and post-systolic contraction could be early markers of myocardial ischemia. METHODS AND RESULTS: Thirty-one consecutive patients with flow-limiting severe coronary stenosis but without visually abnormal left ventricular wall motion underwent quantitative echocardiography. Myocardial strain was measured using layer-by-layer analysis in severely hypoperfused segments. Radial strain (RS) was measured in the subendocardial, subepicardial, and total wall (innerRS, outerRS, and totalRS, respectively). Circumferential strain (CS) was also measured as 3 separate layers: subendocardial, mid-layer, and subepicardial layers (innerCS, midCS, and outerCS, respectively). Post-systolic shortening (PSS) was defined as the peak strain after end systole, and post-systolic strain index (PSI) was calculated as PSS divided by end-systolic strain. TotalRS was similar between ischemic and normally perfused segments, but innerRS and inner/outer RS ratio were significantly smaller in the ischemic segments than in corresponding segments in healthy subjects. Receiver operating characteristic analysis identified an optimum cut-off for PSI of 0.6. The combined criteria of inner/outer RS ratio <1.0 and PSI >0.6 achieved 95% specificity for the presence of flow-limiting stenosis. CONCLUSIONS: Combined assessment of both subendocardial contractile impairment and PSS is very useful in identifying a severely hypoperfused left ventricular wall even without visual wall motion abnormality.
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