Correlation of regional myocardial blood flow and function with myocardial infarct size during acute myocardial ischemia in the conscious pig.

Savage, Robertm .; Guth, Brian D.; White, Fred N.; Hagan, Arthur D.; Bloor, C. M.

doi:10.1161/01.cir.64.4.699

Cited by 62 publications

(21 citation statements)

References 29 publications

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“…Theroux et al (1974), using subendocardial ultrasonic segment gauges, demonstrated increased end-diastolic segment length, segment shortening, and work in control (nonischemic) areas during 5-minute coronary artery occlusions. Increases in segment shortening of nonischemic areas has since been shown by others (Heyndrickx et al, 1975;Kerber et al, 1976;Theroux et al, 1976Theroux et al, , 1977Pashkow et al, 1977;Rigaud et al, 1979;Savage et al, 1981;Nakamura et al, 1982;Molaug et al, 1983), and has been thought to represent a compensatory response produced by utilization of the Frank-Starling mechanism or by generalized increased sympathetic stimulation. The goals of the current study were, first, to clarify the mechanisms of this apparent hyperfunction response of nonischemic areas and, second, to determine its effectiveness in compensating for loss of systolic function by the ischemic zone.…”

Section: Discussionmentioning

confidence: 88%

“…Several investigators have demonstrated an increase in nonischemic area segment shortening or wall thickening following occlusion of the left circumflex coronary artery (Heyndrickx et al, 1975;Kerber et al, 1976;Theroux et al, 1976Theroux et al, , 1977Savage et al, 1981;Nakamura et al, 1982). Although these investigators did not distinguish between isovolumic and ejection phase changes, the increase in nonischemic area total segment shortening in the study by Theroux et al (1976, Fig. 3) was due primarily to an increase in isovolumic shortening.…”

Section: Discussionmentioning

confidence: 93%

“…56, No. 3, March 1985oux et al, 1977Roan et al, 1979), and the magnitude of aneurysmal bulging is stable for several hours Vokonas et al, 1976;Savage et al, 1981). Indirect evidence that this interaction between ischemic and nonischemic areas is still present several hours after the acute event is provided by two clinical studies (Stack et al, 1983;Sheehan et al, 1983).…”

Section: Discussionmentioning

confidence: 99%

“…DURING acute ischemia of the left ventricle, an increase in systolic shortening has been measured in nonischemic areas in experimental animals by a variety of techniques, including ultrasonic segment gauges (Theroux et al, 1974(Theroux et al, , 1976(Theroux et al, , 1977Heyndrickx et al, 1975;Molaug et al, 1983), epicardial strain gauges (Nakano, 1966;Pashkow et al, 1977), ultrasonic wall thickness gauges (Savage et al, 1981;Nakamura et al, 1982) and echocardiography (Kerber et al, 1976). Some studies using epicardial strain gauges did not find an apparent hyperfunction of nonischemic areas (Banka and Helfant, 1974;Vokonas et al, 1976;Wyatt et al, 1976), indicating that the effects may not always be reflected transmurally.…”

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confidence: 99%

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

Lew¹,

Chen²,

Guth³

et al. 1985

Circulation Research

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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: Discussionmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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

Lew¹,

Chen²,

Guth³

et al. 1985

Circulation Research

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122

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“…Homogeneous Nonischemic Segments (n - 14) With coronary artery occlusion, end-diastolic length increased slightly, by 3.2 ± 1.1%, from a control of 14.5 + 0.8 mm (p < 0.01). Systolic shortening and velocity of shortening did not change significantly from control values of 2.98 + 0.24 mm and 29 ± 2 mm/sec, respectively.…”

mentioning

confidence: 95%

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

Cox¹,

Vatner²

1982

Circulation

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SUMMARY Regional myocardial function and blood flow in endocardial layers were correlated in myocardial segments subtending severely ischemic and adjacent, normally perfused myocardium in conscious dogs 1-3 weeks after recovery from coronary artery occlusion. With coronary artery occlusion induced by a hydraulic occluder, endocardial blood flow ( Through a thoracotomy in the fifth left intercostal space, miniature pressure gauges (Konigsberg Instruments) were implanted in the left ventricle through a stab wound in the apex. Doppler flow transducers were implanted proximally on the left circumflex coronary artery or the left anterior descending coronary artery (LAD) in seven dogs each, and hydraulic occluders were placed distal to the flow transducers. Heparinfilled Tygon catheters (Norton Co.) were implanted in the left atrium and descending thoracic aorta. Several pairs of miniature ultrasonic transducers were implanted into the endocardial third of the left ventricular free wall 1-2 cm apart. The average depth of implantation of the transducers into the myocardial wall was approximately 25-30% of the wall thickness as measured from the endocardial surface to the epicardial surface and positioned such that the segments were approximately parallel to the myocardial fibers at that depth according to the data of Streeter et al.,6 with appropriate corrections in orientation made for segments closer to the base and for those closer to the apex of the left ventricle. The transducers were implanted in potentially ischemic zones, in nonischemic zones and in myocardium subtending both zones, such that one transducer was in a potentially ischemic zone and the other in a nonischemic zone ( fig.

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Physiological Implications of Myocardial Scar Structure

Richardson

Clarke

Quinn

et al. 2015

Comprehensive Physiology

238

201

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Once myocardium dies during a heart attack, it is replaced by scar tissue over the course of several weeks. The size, location, composition, structure and mechanical properties of the healing scar are all critical determinants of the fate of patients who survive the initial infarction. While the central importance of scar structure in determining pump function and remodeling has long been recognized, it has proven remarkably difficult to design therapies that improve heart function or limit remodeling by modifying scar structure. Many exciting new therapies are under development, but predicting their long-term effects requires a detailed understanding of how infarct scar forms, how its properties impact left ventricular function and remodeling, and how changes in scar structure and properties feed back to affect not only heart mechanics but also electrical conduction, reflex hemodynamic compensations, and the ongoing process of scar formation itself. In this article, we outline the scar formation process following an MI, discuss interpretation of standard measures of heart function in the setting of a healing infarct, then present implications of infarct scar geometry and structure for both mechanical and electrical function of the heart and summarize experiences to date with therapeutic interventions that aim to modify scar geometry and structure. One important conclusion that emerges from the studies reviewed here is that computational modeling is an essential tool for integrating the wealth of information required to understand this complex system and predict the impact of novel therapies on scar healing, heart function, and remodeling following myocardial infarction.

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Correlation of regional myocardial blood flow and function with myocardial infarct size during acute myocardial ischemia in the conscious pig.

Cited by 62 publications

References 29 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.

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

Physiological Implications of Myocardial Scar Structure

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