Abstract
The progression of regional dysfunction during angina pectoris was studied in eight patients with coronary artery disease. Single plane left ventriculograms were obtained using a high fidelity micromanometer-tipped catheter both at rest and immediately after rapid cardiac pacing. Each image of the left ventriculogram was digitized and transferred to a computer. The boundary of the ventricular cavity was automatically determined and sequentially superimposed. Regional shortening was quantified by a radial coordinate system originating at the center of gravity of the end-diastolic silhouette. Thirty-two radial grids were drawn around the center of gravity, and the length of each radial grid was measured to characterize the centripetal motion of a given surface point. Each radial length was then plotted simultaneously and continuously against left ventricular pressure to generate a pressure-length loop. The area of the pressure-length loop provided an index of regional myocardial work. In the ischemic ventricle, the loops exhibited a striking deformity in configuration. Prolonged relaxation of ischemic segments was associated with outward motion of the normal segments. Shortening of the normal segment occurred earlier than that of the ischemic segment associated with its stretch. Thus, the loops of the two areas inclined in opposite directions. Pacing stress increased the magnitude of hypofunction in the potentially ischemic area, the average extent of shortening being reduced by 30% and the segmental work by 25% (p less than 0.005). In the normal area, contrary to the significant increase in segmental shortening (20% above control values [p less than 0.005]), the average segmental work remained at 7% below control values because of an augmented deformation of the loop.(ABSTRACT TRUNCATED AT 250 WORDS)
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