The effect of changes in afterload on systolic bulging.

Abstract

It has been previously shown that after acute coronary occlusion, the extent of systolic bulging is dependent on preload and the function of the remote nonischemic myocardium is influenced by the motion of the ischemic myocardium as well as by the loading conditions. To examine the isolated effects of changing afterload on the movement of acutely ischemic and nonischemic myocardium, seven open-chest, anesthetized dogs were paced from the left atrium at a rate of 100 beats/min after crushing of the sinus node. The pulmonary artery was perfused artificially and the left ventricular end-diastolic pressure (LVEDP) was carefully controlled with a right heart bypass system. Twenty minutes after occlusion of the left anterior descending artery, the peak left ventricular pressure (LVP) was adjusted to three levels (70, 90, and 110 mm Hg) by blood withdrawal or aortic constriction, while the LVEDP was kept constant (8.3 + 2.3 mm Hg). Segment length in the ischemic (IZ) and nonischemic zones (NZ) were measured with sonomicrometers and total, isovolumetric, and ejection systolic shortening (%zXL) were calculated. Changes in left ventricular minor-axis diameter were measured with diameter crystals. Increasing the peak LVP increased the LVP both at aortic valve opening and closing. To keep the LVEDP constant as peak LVP was increased, the cardiac output had to be decreased (p < .0001).In the IZ, increasing the peak LVP increased isovolumetric bulge (-13.6 + 3.4%, -14.4 ± 3.7%, and -15.0 3.7% at LVP 70, 90, and 110 mm Hg, respectively, p < .00005) and decreased ejection %AL (4.8 4.6%, 4.1 ± 4.3%, and 3.3 ± 4.4%, p < .05) so that total %AL was decreased (p < .001). In the NZ, increasing the peak LVP decreased both isovolumetric %AL (8.4 ± 2.7%, 7.1 + 2.9% and 6.3 ± 2.8%, p < .0005) and ejection %zSL (10.8 ± 6.5%, 9.6 + 4.4%, and 8.8 ± 4.2%, p < .05) so total %AL was reduced (p < .0005). We conclude that increasing afterload increases the extent of the bulge in the ischemic zone and hypothesize that these changes are caused directly by an increase in wall tension. Increasing afterload also decreases shortening in nonischemic myocardium. Circulation 77, No. 1, 221-226, 1988

Effects of Changes in Afterload on Regional Wall Motion in Acute Ischemic Canine Heart.

“…Therefore, the change in stroke volume, which was decreased by angiotensin II and increased by nitroprusside, seemed to depend on the change in ejection shortening in the non-ischemic region alone. Thus our results regarding the influence of change in afterload on regional wall motion differ in two major ways from data reported by Noma et al (1988b). First, our data indicate that isovolumetric shortening in the non--ischemic and ischemic regions changed in opposite directions when afterload changed, while they reported that lowering afterload increased isovolumetric shortening in the non-ischemic region and lessened systolic expansion in the ischemic region (Noma et al 1988b).…”

“…Thus our results regarding the influence of change in afterload on regional wall motion differ in two major ways from data reported by Noma et al (1988b). First, our data indicate that isovolumetric shortening in the non--ischemic and ischemic regions changed in opposite directions when afterload changed, while they reported that lowering afterload increased isovolumetric shortening in the non-ischemic region and lessened systolic expansion in the ischemic region (Noma et al 1988b). Second, in the present experiment, ejection shortening in the ischemic region remained unchanged by changes in peak left ventricular pressure while their report showed a decrease in ejection shortening in the ischemic region when peak left ventricular pressure was elevated (Noma et al 1988b).…”

“…First, our data indicate that isovolumetric shortening in the non--ischemic and ischemic regions changed in opposite directions when afterload changed, while they reported that lowering afterload increased isovolumetric shortening in the non-ischemic region and lessened systolic expansion in the ischemic region (Noma et al 1988b). Second, in the present experiment, ejection shortening in the ischemic region remained unchanged by changes in peak left ventricular pressure while their report showed a decrease in ejection shortening in the ischemic region when peak left ventricular pressure was elevated (Noma et al 1988b). These differences might be related to the differences in experimental model, method of changing afterload, and the level of peak left ventricular pressure.…”

“…Changes in afterload also modify wall motion in both regions in acute ischemia (Theroux et al 1974 Noma et al (1988b) reported that increase in the peak left ventricular pressure decreased isovolumetric shortening in the non-ischemic region and increased paradoxical expansion in ischemic region. However, the reason for this was unclear.…”

Effects of Tachycardia on Regional Wall Motion in Acute Ischemic Canine Heart

“…On the other hand, the increase in the bulging in the ischemic region with the increase in heart rate can be partly explained by the reduction of the end-diastolic length (Ishikawa et al 1993). In the isovolumetric contraction phase, the increment of the shortening in the non-ischemic region has been explained by the augmentation of bulging in the ischemic region that is increased when the preload is decreased or the afterload increased (Lew and Ban-Hayashi 1985;Noma et al 1988a;Ishikawa et al 1993;Sakuma et al 1993). But when the heart rate increased, the increase of the bulging in the ischemic region was not accompanied by shortening in the non-ischemic region.…”