Deleterious effects due to hemorrhage after myocardial reperfusion

Bresnahan, Gerald F.; Roberts, Robert; Shell, William E.; Ross, John; Sobel, Burton E.

doi:10.1016/0002-9149(74)90742-5

Cited by 268 publications

(69 citation statements)

References 16 publications

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“…Hemorrhagic myocardium has also been found at necropsy in patients with acute myocardial infarction who underwent thrombolytic reperfusion or surgical revascularization (31). Accordingly, there has been concern that reperfusion can convert a bland infarct into a hemorrhagic one and, more importantly, that hemorrhage due to coronary reperfusion may lead to the extension of myocardial necrosis (32).…”

Section: Reperfusion-induced Hemorrhagementioning

confidence: 99%

Myocardial reperfusion: a double-edged sword?

Braunwald¹,

Kloner²

1985

J. Clin. Invest.

1,231

569

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Section: Reperfusion-induced Hemorrhagementioning

confidence: 99%

Myocardial reperfusion: a double-edged sword?

Braunwald¹,

Kloner²

1985

J. Clin. Invest.

1,231

569

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“…Several experimental9' 10 and clinical studies' [1][2][3][4][5][6][7][8][9][10][11][12][13][14] have shown that the early reflow of blood to ischemic myocardium increases the creatine kinase (CK) recovery rate. Accordingly, the total amount of CK that is released into the plasma may be greater than the amount of CK released from an area of myocardial necrosis of the same size without reperfusion.…”

mentioning

confidence: 99%

Quantitative relationship between left ventricular function and serum cardiac myosin light chain I levels after coronary reperfusion in patients with acute myocardial infarction.

et al. 1987

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To estimate the extent of myocardial infarction after coronary artery reperfusion, serum levels of cardiac myosin light chain (LC) I and creatine kinase (CK) were determined serially in 49 patients with acute myocardial infarction. Intracoronary thrombolysis was successful in 25 patients (reperfusion group), and 24 patients were treated in a conventional manner (control group). The peak level of CK appeared significantly earlier in the reperfusion group (1 1.3 + 3. 1 hr, mean + SD) than in the control group (21.6 ± 7.2 hr). Cumulative release of CK was significantly related to angiographically determined left ventricular ejection fraction 1 month after the attack in both groups (r = -.50; -.45, respectively). However, the amount of cumulative release of CK in the reperfusion group was greater compared with that in those with the same left ventricular ejection fraction in the control group. Peak appearance time of LCI was almost equal in the two groups (3.8 ± 1.4 vs 3.9 ± 1.2 days). Peak levels of LCI were related to the left ventricular ejection fraction in the reperfusion group (r = -.63) and in the control group (r = -.74), and the slopes of their regression lines were similar. The cardiac index obtained on the day of onset in the two groups was related to peak levels of LCI but not to total release of CK. These results suggest that serum levels of LCI reflect the changes in left ventricular function after acute myocardial infarction, regardless of the presence of coronary reperfusion. Thus, serial determinations of LCI in serum facilitate noninvasive assessment of the effects of intracoronary thrombolysis on infarct size. Circulation 76, No. 6, 1251-1261, 1987 IT HAS BEEN SHOWN that the intracoronary infusion of thrombolytic drugs can bring about coronary artery recanalization and this has been proposed as a way of reducing the extent of acute myocardial infarction. 1, 2 Although recent clinical investigations suggest beneficial effects of intracoronary thrombolysis,-5 many laboratory studies have pointed out the deleterious effects of coronary reperfusion, including massive myocardial hemorrhage, refractory arrhythmias, or noreflow phenomenon.68 Therefore, for evaluation of salvage and damage to the myocardium after throm-

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“…1975), verapamil (Karlsberg et al. 1977), cobra venom (Maroko er al.. 1978), and reperfusion (Bresnahan et al, 1974;Vatner et al, 1978). Myocardial CK depletion also correlated with attenuation of ultrasound (Mimbs et al, 1977), myocardial IT-palmitate uptake , electrocardiographic evidence of infarction (Maroko et al, 1971), and reduction in coronary flow by the microsphere technique (Kjekshus and Sobel, 1970).…”

Section: Discussionmentioning

confidence: 96%

“…The interval of 8 h was chosen based on data in our own laboratory (Karlsberg et al, 1977;Bresnahan et al, 1974), and that of others (Hillis et al, 1976;Peter el al.. 1977), suggesting that evolution of infarction, uncomplicated by extension, is complete within 5-8 h. Infarction was produced in conscious animals in part because it would be more analogous to that of the clinical situation and to avoid any potential effects of anesthesia on infarct size, reflex activity, coronary flow, or hemodynamics. Despite the administration of nitroglycerin in doses such that no significant increase in heart rate was observed over that of the controls, we did not observe any beneficial effect on infarct size as determined by enzymatic or morphologic techniques.…”

Section: Discussionmentioning

confidence: 99%

The effect of intravenous nitroglycerin on coronary blood flow and infarct size during myocardial infarction in conscious dogs

Fukuyama

Roberts

1980

Clinical Cardiology

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Summary: Nitroglycerin (TNG), based on electrocardiographic evidence, has been shown to reduce myocardial ischemia, but its effect on morphometrically and enzymatically estimated infarct size has not been defined. Accordingly, coronary occlusion was produced in 50 conscious dogs without LV failure. Twenty-five received TNG (200-300 pg/min i.v. for 8 h) and the results compared with those in 25 untreated dogs. Coronary blood flow was measured with I4'Ce, 85Sr, and 95Nb (9 pm) after occlusion before TNG, 30 min after TNG, and again at 8 h. Mean blood pressure decreased from 103 to 84 mmHg with TNG vs. 99 to 94 mmHg in controls (p<0.02). Average heart rates were similar [ 135f26 vs. 120f33 beats/min (SD)]. TNG Did not increase total transmural coronary flow in any region but increased subendocardial flow in the central ischemic areas by 45% (0.09 ml/min/g vs. 0.13 ml/min/g). Animals were sacrificed after 24 h. Infarct size estimated morphometrically (25f 1.5 vs. 2 6 f 1.5 of LV weight) and from myocardial CK depletion ( 2 3 f 2 vs. 2 3 f 2 ) was similar for the two groups. Thus, despite increased subendocardial flow, prolonged i.v. TNG did not decrease infarct size even though a difference of 15% would have been detected with this sample size. TNG May relieve coronary spasm but does not appear to be beneficial with sustained coronary occlusion.

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Deleterious effects due to hemorrhage after myocardial reperfusion

Cited by 268 publications

References 16 publications

Myocardial reperfusion: a double-edged sword?

Myocardial reperfusion: a double-edged sword?

Quantitative relationship between left ventricular function and serum cardiac myosin light chain I levels after coronary reperfusion in patients with acute myocardial infarction.

The effect of intravenous nitroglycerin on coronary blood flow and infarct size during myocardial infarction in conscious dogs

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