Regional left ventricular wall motion in pacing induced angina.

Left ventricular cineangiograms (30 degrees right anterior oblique projection) and high fidelity left ventricular pressure were recorded at rest in 10 individuals with normal hearts and at rest and during an episode of angina provoked by rapid atrial pacing in 14 patients with obstructive coronary artery disease. Angiograms were digitised frame by frame. The ventricular perimeter was divided into 40 segments and regional ventricular function was examined by means of isometric and contour plots and by the construction of segmental pressure-wall displacement loops. In 10 patients 12 abnormal resting regions were identified. The commonest (11 regions) was delayed onset of inward endocardial motion during systole which was manifest by diagonal contour lines on the contour plot. Six regions (five with associated delay in onset of inward motion) showed resting hypokinesis. Angina was associated with the development of 19 new regions of abnormal wall motion in 12 patients. Fourteen of these regions of abnormality were thought to be primary events occurring as a consequence of ischaemia and five to be secondary events occurring in normally perfused regions of myocardium. Hypokinesis occurred in 12 regions, developing in a region with normal amplitude at rest in seven and as an extension of resting hypokinesis in five. In 10 out of 12 cases the region of hypokinesis developed in a region showing diagonal contour lines at rest. Asynchrony with delay in the timing of peak inward displacement relative to minimum volume occurred with angina in eight regions (in six cases concomitant with hypokinesis and in two cases in isolation). In contrast with hypokinesis the pattern of wall motion at rest did not permit regions developing asynchrony with angina to be identified. Pressure-displacement loops show that regional hypokinesis is associated with reduced segmental work and that regional asynchrony (delayed or premature timing of peak inward endocardial displacement) is associated with a loss of efficiency of energy transfer between the myocardium and the circulation. These observations illustrate the complex nature of wall motion abnormalities occurring with angina.