In vitro length-tension relations of human ventricular aneurysms

Parmley, William W.; Chuck, Leonard; Kivowitz, Charles; Matloff, Jack M.; Swan, H. J. C.

doi:10.1016/s0002-9149(73)80153-5

Cited by 120 publications

(31 citation statements)

References 12 publications

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“…However, collagen synthesis was not actually decreased by the persistence of myocytes, since the hydroxyproline content normalized per histological unit of fibrous tissue was similar in both the reperfused and the permanently occluded scar groups (see Table 4). In any case, the 1-hour ocdusionreperfusion protocol resulted in a mixed myocytefibrous scar, and thus provided an experimental model that appears to be similar to the mixed muscle-fibrous scars found in some patients after myocardial infarction (Parmley et al, 1973).…”

mentioning

confidence: 60%

Effects of reperfusion after coronary artery occlusion on post-infarction scar tissue.

Connelly¹,

Vogel²,

Wiegner³

et al. 1985

Circulation Research

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SUMMARY. Early reperfusion after a coronary occlusion may reduce myocardial infarct size, but late reperfusion into necrotic myocardium may alter post-infarction healing. In rabbits, we compared 1-or 3-week-old scars resulting from permanent coronary occlusion to those resulting from a 1-or 3-hour occlusion followed by reperfusion. Reperfusion at 1 hour post-occlusion did not affect scar mechanical properties assessed at 1 week post-infarction, but at 3 weeks postinfarction, these scars had a tensile strength significantly lower than those not reperfused (78 ± 11 vs. 158 ± 15 g/mm 2 , P < 0.001). They also were composed of a mixture of fibrous tissue (58 ± 8%) and myocytes (43 ± 8%) with a hydroxyproline content of 23 ± 2.5 mg/g dry weight. The nonreperfused scars had a higher proportion of fibrous tissue (73 ± 3%) by histological evaluation and a 35% higher hydroxyproline content (31 ± 2 mg/g dry weight, P < 0.001) than the scars reperfused after 1 hour. In contrast, 3-week-old scars resulting from late' reperfusion at 3 hours post-occlusion were similar to nonreperfused scars in fibrous tissue composition and hydroxyproline content. Nonetheless, the tensile strength of these scars reperfused 3 hours post-occlusion was significantly less than that of the nonreperfused scars (72 ± 5 vs. 158 ± 15 g/mm 2 , P < 0.001). The lower tensile strength was associated with a lower collagen cross-link density in this reperfused group of scars. At physiological stress levels (approximately 3 g/mm 2 ), all groups of reperfused and nonreperfused scars had similar mechanical properties in terms of natural strain, stiffness, creep, and stress relaxation. Thus, although the reperfused scars ruptured more easily at high stresses, when assessed at physiological stresses their mechanical properties were not significantly different from those of nonreperfused scars. (Circ Res 57: 562-577, 1985)

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mentioning

confidence: 60%

Effects of reperfusion after coronary artery occlusion on post-infarction scar tissue.

Connelly¹,

Vogel²,

Wiegner³

et al. 1985

Circulation Research

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“…This interaction was envisioned by Tennant and Wiggers (1935) as "a struggle between forces causing shortening and those tending to lengthen the fibers" in the ischemic segments. Several investigators have examined the mechanical consequences of such an interaction between "weak and strong" muscles linked in series, such as with isolated strips of hypoxic and normal myocardium placed in series (Tyberg et al, 1969;Wiegner et al, 1978), ventricular aneurysms (Parmley et al, 1973;Janz and Waldron, 1978), asynchrony of ventricular contraction with pacing (Badke et al, 1980), or theoretical models of regionally ischemic ventricles (Elings et al, 1977;Laird and Vellekoop, 1977;Bogen et al, 1980). The magnitude of the mechanical disadvantage produced by the interaction of ischemic and nonischemic segments is thought to be related directly to the size and inversely related to the stiffness of the ischemic area (Elings et al, 1977;Laird and Vellekoop, 1977;Bogen et al, 1980) or of the aneurysmal tissue (Parmley et al, 1973).…”

Section: Discussionmentioning

confidence: 99%

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

Lew¹,

Chen²,

Guth³

et al. 1985

Circulation Research

121

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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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“…Parmley et al 47 showed that chronic ventricular aneurysms which developed after infarction were much stiffer than normal muscle. Hood et al 29 found that muscle stiffening could be detected in dogs 3-5 days after inducing myocardial infarction by ligating the left anterior descending coronary artery.…”

Section: Wall Elasticitymentioning

confidence: 99%