Myocardial function in areas of heterogeneous perfusion after coronary artery occlusion in conscious dogs.

Cox, David A.; Vatner, Stephen F.

doi:10.1161/01.cir.66.6.1154

Cited by 30 publications

(6 citation statements)

References 22 publications

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“…Of note, the magnitude of these changes in this conscious dog study were less than those found in their previous study in the anesthetized dog (Theroux et al, 1974). Velocity of nonischemic area segment shortening has been shown to increase at 5 and 15 minutes after coronary artery occlusion (Heyndrickx et al, 1975) but not after 1 hour (Cox and Vatner, 1982). Savage et al (1981) found a significant increase in wall thickening in the nonischemic area at 15 minutes, 1, 24, and 48 hours after coronary artery occlusion.…”

Section: Discussioncontrasting

confidence: 72%

Mechanisms of augmented segment shortening in nonischemic areas during acute ischemia of the canine left ventricle.

Lew¹,

Chen²,

Guth³

et al. 1985

Circulation Research

122

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SUMMARY. To examine the interaction between normal and nonischemic areas of the left ventricle during acute ischemia, we implanted midwall ultrasonic segment length gauges in the ischemic zone and in nonischemic areas of the canine left ventricle. During acute ischemia, enddiastolic pressure and segment length in the nonischemic areas increased. There was no change from control in the segment length at the time of aortic valve opening and closure. Thus, in nonischemic areas, total segment shortening, as measured by the percent change in segment length from the time of end-diastole to aortic valve closure, increased. This was due to an increase in isovolumic shortening (end-diastole to aortic valve opening) with no change in ejection shortening (aortic valve opening to closure). The progressive increase in isovolumic shortening in nonischemic areas over time was directly paralleled by the progressive development of the isovolumic lengthening or bulge in the ischemic zone. Nonischemic areas, whether adjacent, on the opposite wall, or distant to the ischemic zone, all behaved similarly. Adrenergic blockade did not qualitatively alter these findings. We conclude that acute ischemia induces a mechanical disadvantage which is greater than just the loss of contractile function by the ischemic segment. Despite the apparent hyperfunction of nonischemic areas, the increased total segment shortening is expended in stretching the ischemic zone during isovolumic systole. As a result, there is no significant "compensatory' increase in ejection shortening in nonischemic areas. The results from the present study indicate that augmented total segment shortening in nonischemic areas is due ' to a combination of the Frank-Starling mechanism and regional intraventricular unloading of the nonischemic into the ischemic areas. (Circ Res 56: 351-358, 1985)

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Section: Discussioncontrasting

confidence: 72%

Mechanisms of augmented segment shortening in nonischemic areas during acute ischemia of the canine left ventricle.

Lew¹,

Chen²,

Guth³

et al. 1985

Circulation Research

122

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“…Heart rate increased from 82 ± 23 (mean + SD) to 123 ± 26 beats/min (p<.01) 10 min after circumflex coronary occlusion and remained elevated significantly 3 hr after occlusion. Left ventricular systolic pressure was not significantly changed but end-diastolic pressure increased from 13.4 + 4.8 to 18.6 ± 6.2(p<.01)and 18.1 + 6.8mmHg(p<.01) 10 Data are mean ± SD. C = control; TCO1 = early coronary occlusion (10 min); TCO2 late coronary occlusion (2.5 to 3.0 hr); HIR = heart rate (n = 14); LVSP = left ventricular systolic pressure (n = 14); LVEDP = left ventricular end-diastolic pressure (n = 1P); ( + )dP/dt = peak positive first derivative of left ventricular pressure (n = 13); ( -)dP/dt = peak negative first derivative of left ventricular pressure (n = 13).…”

Section: Resultsmentioning

confidence: 99%

The functional border zone in conscious dogs.

et al. 1987

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Studies focusing on the functional border zone have been performed largely with anesthetized, open-chest preparations. Therefore, we instrumented 14 dogs at sterile surgery with sonomicrometers arrayed to measure systolic wall thickening across the perfusion boundary produced by circumflex coronary occlusion. We fitted sigmoid curves to the data to model the distribution of wall thickening impairment as a function of distance from the perfusion boundary, which was delineated with myocardial blood flow (15 micron diameter microspheres) maps. Using this approach, we defined the functional border zone as the distance from the perfusion boundary to 97.5% of the sigmoid curve's nonischemic asymptote. The lateral extent of the functional border zone, measured 10 min and 3 hr after occlusion, was 32 and 28 degrees of circumference, respectively. To evaluate the severity of nonischemic dysfunction, we measured average systolic wall thickening within the functional border zone. It was reduced from 3.69 +/- 1.10 (mean +/- SD) mm to 2.98 +/- 1.07 mm (p less than .01) and 2.74 +/- 1.12 mm (p less than .01) early and late after coronary occlusion. Thus, a narrow functional border zone was evident during circumflex coronary occlusion in conscious dogs. Its lateral extent was limited to approximately 30 degrees (similar to findings in open-chest, anesthetized dogs), severe dysfunction was restricted to the immediate vicinity of the perfusion boundary, and the average severity of nonischemic dysfunction within the functional border zone was mild.

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“…Only those ischemic segments demonstrating homogeneous reductions of regional endocardial blood flow at both crystal sites were included in the final analysis. Heterogeneous ischemia was defined as a disparity in blood flow to the myocardium surrounding the two crystal sites ranging from 0.4 to 1.4 ml/min per g. This latter criterion was of critical importance, since segments with heterogeneous ischemia were previously shown to exhibit reductions of function similar to those with homogeneous reduction in regional endocardial blood flow (Cox and Vatner, 1982). Changes from control and differences among groups were analyzed by the method of two-way analysis of variance (Armitage, 1973).…”

Section: Methodsmentioning

confidence: 99%

“…Third, measurements of regional myocardial function were limited to the endocardium where homogeneous areas of ischemia could be monitored and confirmed by regional blood flow measurement. When the myocardium surrounding two ultrasonic crystals differed markedly in terms of level of flow reduction, these segments were excluded from the analysis, since these segments, although not uniformly ischemic, behave functionally as if they were homogeneously ischemic (Cox and Vatner, 1982). In the present investigation, 22 of 134 segments were excluded because of heterogeneous perfusion.…”

Section: Figure 7 Time Course Of Systolic Shortening In the Moderatementioning

confidence: 99%

Salvage of myocardial function by coronary artery reperfusion 1, 2, and 3 hours after occlusion in conscious dogs.

Lavallée¹,

Cox²,

Patrick³

et al. 1983

Circulation Research

Self Cite

192

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SUMMARY. The effects of coronary artery occlusion and reperfusion at 1 hour (1-hr group), 2 hours (2-hr group), and 3 hours (3-hr group) were compared with a permanently occluded group (P group) on measurements of overall left ventricular and regional endocardial function over a 4-week period. The studies were conducted in conscious dogs 1-2 weeks after recovery from instrumentation with solid state left ventricular pressure gauges, aortic, and left atrial catheters, hydraulic occluders, and Doppler flow transducers on the left anterior descending or left circumflex coronary arteries, and multiple pairs of ultrasonic transducers implanted in the endocardial third of the left ventricular free wall to measure endocardial segment shortening. During coronary artery occlusion, similar effects were observed in the four groups. At 1 hour after coronary artery occlusion, three classes of ischemia-induced dysfunction were observed; dyskinetic (systolic shortening completely lost and replaced by paradoxical bulging), severely hypokinetic (systolic shortening depressed by 65-95%), and moderately hypokinetic (systolic shortening depressed by 40-65%). Compared with the P group, significant (P < 0.05) return of systolic shortening and velocity of shortening gradually occurred over the 4-week period following reperfusion in all classes of segments in the 1-hour group. In the 2-hour group, systolic shortening returned in the moderately and severely hypokinetic segments, but was slight and not significant in the dyskinetic segments. In the 3-hour group, significant systolic shortening returned only in the moderately hypokinetic segments. The effects of isoproterenol, 0.04 /ig/kg per min, and exercise were compared on 'salvaged' dyskinetic segments prior to and at 1, 2, 3, and 4 weeks after coronary artery occlusion and reperfusion. The responses to isoproterenol were significantly depressed at 1 week after reperfusion and gradually recovered over the 4-week period. At 3-4 weeks after reperfusion, severe exercise also increased shortening and velocity of shortening in 'salvaged' segments. Thus, in the conscious dog, coronary artery reperfusion at 1 hour after coronary artery occlusion results in substantial return of endocardial function even in the most severely ischemic myocardium. The 'salvaged' myocardium responds adequately to myocardial stress with increases in the extent and velocity of systolic shortening, as long as 3-4 weeks after reperfusion are allowed for recovery. However, after 3 hours of coronary artery occlusion, little salvage of regional myocardial function can be induced by acute reperfusion in this model. (Circ Res 53: 235-247, 1983)

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Myocardial function in areas of heterogeneous perfusion after coronary artery occlusion in conscious dogs.

Cited by 30 publications

References 22 publications

Mechanisms of augmented segment shortening in nonischemic areas during acute ischemia of the canine left ventricle.

Mechanisms of augmented segment shortening in nonischemic areas during acute ischemia of the canine left ventricle.

The functional border zone in conscious dogs.

Salvage of myocardial function by coronary artery reperfusion 1, 2, and 3 hours after occlusion in conscious dogs.

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