No reflow and extent of infarction during maximal vasodilation in the porcine heart.

Johnson, William Ben; Malone, S.; Pantely, George A.; Anselone, C G; Bristow, James

doi:10.1161/01.cir.78.2.462

Cited by 66 publications

(19 citation statements)

References 36 publications

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“…However, a previous study used FPCE and LGE MRI at the mid-ventricular slices, and the authors found a linear relationship between myocardial perfusion and residual viable myocardium in the infarct zone (6). This linear relationship is consistent with the findings obtained from animal models, in which the relationship is valid over the whole LV (25). Given that the perfusion-viability relationship is universally valid, we believe that the linear relationship between the exercise-induced perfusion change and the amount of residual viable myocardium in the infract zone should be equally applicable to other levels of the LV.…”

Section: Discussionsupporting

confidence: 80%

Exercise training increases myocardial perfusion in residual viable myocardium within infarct zone

Lee

et al. 2011

Magnetic Resonance Imaging

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Purpose: To study the effect of exercise training on the myocardial perfusion in the postinfarct myocardium.Materials and Methods: Twenty-nine patients with stable chronic myocardial infarction were randomly assigned to either a training group (N ¼ 17) or a control group (N ¼ 12). The training group received a 3-month exercise program. Cardiovascular MR was first performed before the training to establish a baseline, and subsequently performed once again upon conclusion of the program. Late gadolinium enhancement was used both to define the infarct and remote zones and to quantify the ratio of the residual viable myocardium (VMR) within the infarct zone. The myocardium was divided into subendocardial and subepicardial layers with equal thickness. The interval change of myocardial perfusion reserve (MPR) was computed for each zone and layer. The association between the exercise-induced perfusion change and VMR was analyzed for layers of the infarct zone.Results: In the training group, the remote zone showed significantly increased MPR. The infarct zone showed no perfusion change in the subendocardial layer, but it demonstrated significantly increased MPR in the subepicardial layer. In the infarct zone, the change in MPR was associated with VMR. Conclusion:In chronic myocardial infarction, the exercise-induced perfusion change in the infarct zone is proportional to the amount of residual viable myocardium.

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Section: Discussionsupporting

confidence: 80%

Exercise training increases myocardial perfusion in residual viable myocardium within infarct zone

Lee

et al. 2011

Magnetic Resonance Imaging

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“…Previous studies have demonstrated that infarct-related artery patency and myocardial perfusion are not necessarily concordant in humans (26,27). Even with epicardial coronary reflow, myocardial perfusion may not be achieved (the lowreflow or no-reflow phenomenon) because of microvascular disruption, plugging by debris or myocardial edema (14,28). Thus, the ability to identify the presence or absence of myocardial perfusion by myocardial contrast echocardiography during the post-acute myocardial infarct period may offer important advantages over simple assessment of infarct-related artery patency during catheterization, and predicts left ventricular function and further remodeling (29).…”

Section: Discussionmentioning

confidence: 99%

Evaluation of stunned and infarcted canine myocardium by real time myocardial contrast echocardiography

Dourado

Tsutsui

Mathias

et al. 2003

Braz J Med Biol Res

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Differentiation between stunned and infarcted myocardium in the setting of acute ischemia is challenging. Real time myocardial contrast echocardiography allows the simultaneous assessment of myocardial perfusion and function. In the present study we evaluated infarcted and stunned myocardium in an experimental model using real time myocardial contrast echocardiography. Sixteen dogs underwent 180 min of coronary occlusion followed by reperfusion (infarct model) and seven other dogs were submitted to 20 min of coronary occlusion followed by reperfusion (stunned model). Wall motion abnormality and perfusional myocardial defect areas were measured by planimetry. Risk and infarct areas were determined by tissue staining. In the infarct model, the wall motion abnormality area during coronary occlusion (5.52 ± 1.14 cm 2 ) was larger than the perfusional myocardial defect area (3.71 ± 1.45 cm 2 ; P < 0.001). Reperfusion resulted in maintenance of wall motion abnormality (5.45 ± 1.41 cm 2 ; P = 0.43 versus occlusion) and reduction of perfusional myocardial defect (1.51 ± 1.29 cm 2 ; P = 0.004 versus occlusion). Infarct size determined by contrast echocardiography correlated with tissue staining (r = 0.71; P = 0.002). In the stunned model, the wall motion abnormality area was 5.49 ± 0.68 cm 2 during occlusion and remained 5.1 ± 0.63 cm 2 after reperfusion (P = 0.07). Perfusional defect area was 2.43 ± 0.79 cm 2 during occlusion and was reduced to 0.2 ± 0.53 cm 2 after reperfusion (P = 0.04). 2,3,5-Triphenyl tetrazolium chloride staining confirmed the absence of necrotic myocardium in all dogs in the stunned model. Real time myocardial contrast echocardiography is a noninvasive technique capable of distinguishing between stunned and infarcted myocardium after acute ischemia.

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“…A number of mechanisms have been proposed to explain these observations including mechanical obstruction from capillary damage (1), neutrophil plugging (2) and tissue edema (3) or increased resistance due to enhanced vasomotor tone (4) or ischemic contracture (5). Johnson et al (20) attempted to dissociate maximal vasodilator capacity from the presence of necrosis in a swine model of ischemia and reperfusion. Using the coronary pressure-flow relationship during constant adenosine infusion, they showed that the vasodilator response is unchanged after 20 min of ischemia and reperfusion.…”

Section: Discussionmentioning

confidence: 99%

Impaired endothelium-dependent vasodilation of coronary resistance vessels in severely stunned porcine myocardium

et al. 1995

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The effect of stunning on endothelium-dependent responses of resistance vessels in vivo remains of interest. We utilized the coronary pressure-flow relationship during maximal vasodilation in anesthetized swine to identify subtle changes in flow reserve within stunned myocardium. Prior to and following stunning, the coronary pressure-flow relationship during maximal doses of intracoronary adenosine was compared with that of the endotheliumdependent vasodilator ATE In 11 anesthetized swine, 30 min of partial LAD occlusion and 40 min of reperfusion reduced fractional shortening from 16 + 4 % to 6 + 5 % (p < 0.05). This caused a rigtward shift of the coronary pressure-flow relationships during infusions of either adenosine or ATP, suggestive of increased extra vascular compressive forces. With adenosine, the slope of the linear portion of the relationship (i.e., coronary pressures > 30 mmHg) was 1.31 +_ 0.54 ml/min-mmHg at baseline and 1.30 + 0.55 ml/min-mmHg following stunning (NS). With ATP however, the slope decreased from 1.34 + 0.48 ml/min-mmHg at baseline to 1.08 + 0.47 ml/minmmHg following reperfusion (p < 0.05), indicating an attenuation of endothelium-dependent vasodilator capacity. In five of the animals, the slope of the pressure-flow relationship during intracoronary nitroprusside was unchanged post-stunning, which is similar to the adenosine results. In conclusion, the data support the hypothesis that endothelium-dependent vasodilation of resistance vessels in the intact animal is altered within severely stunned myocardium. The rightward shift of the coronary pressure-flow relationships with both classes of vasodilators suggest that extra vascular factors may also play a role in limiting coronary flow reserve.

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No reflow and extent of infarction during maximal vasodilation in the porcine heart.

Cited by 66 publications

References 36 publications

Exercise training increases myocardial perfusion in residual viable myocardium within infarct zone

Exercise training increases myocardial perfusion in residual viable myocardium within infarct zone

Evaluation of stunned and infarcted canine myocardium by real time myocardial contrast echocardiography

Impaired endothelium-dependent vasodilation of coronary resistance vessels in severely stunned porcine myocardium

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