Return of left ventricular function after reperfusion in patients with myocardial infarction: importance of subtotal stenoses or intact collaterals.

Rogers, W. Todd; Hood, William P.; Mantle, John A.; Baxley, William A.; Kirklin, James K.; Zorn, Gerlinde; Nath, Hrudaya

doi:10.1161/01.cir.69.2.338

Cited by 167 publications

(29 citation statements)

References 38 publications

(9 reference statements)

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“…However. this reperfusion syndrome, consisting of relief of chest pain, resolution of ST segment elevation, and CK washout, has a sound physiologic basis and its validity is supported by (1) experimental studies,479 (2) the complete concordance between the occurrence of this syndrome and the finding of patency of the artery of infarction in our study, and (3) the excellent concordance between these signs and angiographically recognized reperfusion in several intracoronary streptokinase studies.29 5 In the intracoronary studies of Lee, Rentrop, Mathey, and Ganz and their colleagues,9 50 > the clinical signs of reperfusion usually occurred within minutes of the angiographic demonstration of arterial patency and in some studies, these clinical signs were used to indicate when to check the patency of the artery of infarction by angiography.9°08-5' Furthermore, these clinical signs of reperfusion have also been adopted by several other investigators using intravenous streptokinase. '6 19.…”

supporting

confidence: 71%

The effects of the rate of intravenous infusion of streptokinase and the duration of symptoms on the time interval to reperfusion in patients with acute myocardial infarction.

Lew¹,

Laramee²,

Cercek³

et al. 1985

Circulation

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We studied the influence of the following variables on the time interval from initiation of an intravenous infusion of 750,000 U of streptokinase until reperfusion (reperfusion time) in 140 consecutive patients with an evolving acute myocardial infarction: (1) the rate of infusion of streptokinase, (2) the duration of chest pain before initiation of treatment, (3) patient age, (4) patient sex, (5) location of infarction, (6) history of previous myocardial infarction, and (7) pretreatment pathologic Q waves. The time of reperfusion was recognized by clinical criteria that were completely concordant with the anatomic findings in all 1 19 patients in whom patency or occlusion of the artery of infarction was established at delayed angiography (n = 116) or at postmortem examination (n = 3). The mean reperfusion time for the 129 patients for whom data were available was 49 36 min. The reperfusion time was inversely related to the rate of infusion of streptokinase (r = .41, p < .001), but this effect of infusion rate appeared to plateau at rates of greater than 500 U/kg/min. In the 64 patients receiving infusions at rates of 500 U/kg/min or less, the mean reperfusion time was 60 + 40 min, whereas in the 58 patients receiving the drug at rates greater than 500 U/kg/min it was 35 + 22 min (p < .001). The duration of chest pain before treatment was the only other studied variable found to influence the reperfusion time, but only at infusion rates of less than 250 U/kg/min (r= .6, p < .01). Our findings indicate that in patients with acute myocardial infarction who receive high-dose intravenous streptokinase, the time interval to reperfusion can be minimized by increasing the infusion rate up to at least 500 U/kg/min and by shortening the delay from onset of symptoms to treatment.Circulation 72, No. 5, 1053No. 5, -1058No. 5, , 1985 EARLY REPERFUSION of the artery of infarction may limit the extent of myocardial necrosis in patients with an evolving acute myocardial infarction' and improve ventricular function"5 and survival.i' 9 Both experimental' 02 and clinical"3-"' studies indicate that the critical determinant of the extent of myocardial necrosis and salvage is the duration of myocardial ischemia before reperfusion. In clinical practice, this ischemic period comprises (1) the time interval from the onset of infarction to the commencement of treatment, which is predominantly a logistical problem, 1620 and (2)-the time interval from commencement of treatment until reperfusion, which is predominantly a biological variable. In this study, we investigate the potential effect of the following factors on the time interval from treatment until reperfusion by intravenous streptokinase: (1) the rate of infusion of streptokinase, (2) the duration of chest pain before initiation of treatment, (3) patient age, (4) patient sex, (5) the location of infarction, (6) the presence of eletrocardiographic and/or historical evidence of a previous infarction, and (7)

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supporting

confidence: 71%

The effects of the rate of intravenous infusion of streptokinase and the duration of symptoms on the time interval to reperfusion in patients with acute myocardial infarction.

Lew¹,

Laramee²,

Cercek³

et al. 1985

Circulation

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“…In patients surviving after successful recanalization, 45% showed a degree of stenosis of 90% or less in the infarct-related coronary artery after thrombolysis26 and 29% had good collateral circulation. 27 In animal preparations, the duration of occlusion after which reperfusion can salvage the myocardium in the risk area is within 60 to 120 min in the pig heart without collateral circulation 10, 28 and within 6 hr in the dog heart with rich collaterals.29 Our group I exhibited recanalization 2 to 6 hr after the onset ofAMI without good collaterals. Therefore the discrepancy between patients who survived and those who died may be explained by the degree of collateral circulation and the degree of recanalization.…”

Section: Discussionmentioning

confidence: 80%

Quantitative analysis of infarct size, contraction band necrosis, and coagulation necrosis in human autopsied hearts with acute myocardial infarction after treatment with selective intracoronary thrombolysis.

et al. 1987

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To assess the importance of contraction band necrosis (CBN) in patients with acute myocardial infarction (AMI) treated with selective intracoronary thrombolysis, CBN, coagulation necrosis, and infarct size (expressed as CBN + coagulation necrosis) were analyzed quantitatively in 16 autopsied hearts. Intracoronary thrombolysis was performed from 2 to 6 hr after the onset of AMI, and the time from the onset of AMI to death was 7 to 168 hr. Cineangiography revealed no evidence of good collateral circulation in any of the patients. The 16 patients were classified into three groups: six patients with successful thrombolysis (100% to 99% stenosis, group I), five patients with unsuccessful thrombolysis (100% to 100%, group II), and five patients with 99% stenosis before thrombolysis (group III). Among the three groups, there were no significant differences in the time from the onset of AMI to thrombolysis, the time from the onset of AMI to death, the cause of death, or the degree of collateral circulation. The percentage of the risk area involved by the infarct in group 1 (82 6%) was similar to that in group 11 (80 + 1 1 %). Infarct size was not reduced in group I because collateral circulation was not good and because the degree of recanalization after thrombolysis was 1%. However, the percentage of the infarct area with CBN was significantly higher in group 1 (20 + 9%) then in group 11 (3 + 3%). This finding shows that diffuse CBN occurred after reperfusion in patients with AMI treated with thrombolysis. In group III, three hearts had a smaller infarct area than that in group I or II and a larger area-of CBN than that in group II. In the other two hearts, the infarct area was similar to that in groups I and II and the CBN area was as small as in group II. We believe that in the former three cases, spontaneous recanalization occurred before thrombolysis and a considerable portion of the risk area was salvaged. In all three groups, the distribution of CBN was mainly in the peripheral zone of the infarct area. Most of the noninfarct tissue areas in the risk area were in the outer third of the left ventricular wall. These findings reflect the transmural gradient of ischemic cellular damage in human AMI. The degree of ischemia immediately before reperfusion is milder in the areas of CBN than in the areas of coagulation necrosis in human AMI. In conclusion, a method should be developed to protect the heart against CBN to reduce infarct size. Circulation 76, No. 5, 981-989, 1987. SINCE Rentrop et al.' first described selective intracoronary thrombolysis in patients with acute myocardial infarction (AMI) in 1979, the technique has been used more and more widely. An

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“…The importance of anterograde flow or collateral circulation to the infarct region for recovery of left ventricular function after late reperfusion has been documented in several studies (15,16). In the current study, we included only patients with total occlusion of the proximal left anterior descending artery.…”

Section: Mechanismsmentioning

confidence: 99%

Clinical Implication of Persistent Ischemic Chest Pain on Admission in Patients with Late Reperfused Acute Myocardial Infarction.

et al. 2002

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Object Although previous studies reported that late reperfusion might prevent left ventricular dilation after acute myocardial infarction (AMI), implication of persistent ischemic chest pain on admission remains to be investigated. This study was undertaken to assess the implication of persistent ischemic chest pain on in-hospital outcomeand left ventricular function after late reperfused AMI. Methods and Patients Westudied 63 patients with a firstanterior AMIwhounderwent percutaneous coronary intervention 6 to 24 hours (ll.2±4.5 hours) after the onset.Of 63 patients, 48 (76%) had persistent ischemic chest pain on admission.Results Incidence of in-hospital death, reinfarction or congestive heart failure was similar between the 2 groups. Pretreatment left ventricular ejection fraction and end-diastolic volume were similar between the 2 groups. Predischarge angiography was performed at 17±5 days after the onset. Late reperfusion prevented the dilation of left ventricular end-diastolic volume in patients with chest pain (78±12 to 75±17 ml/m2, p=0.15), but did not in those without (75±20 to 93±28 ml/m2, p=0.03). A multivariate analysis revealed that absence of persistent ischemic chest pain was an independent predictor of predischarge left ventricular end-diastolic volume >100 ml/m2 (odds ratio 0.10, p=0.04).Conclusions Our data demonstrated that absence of persistent ischemic chest pain appears to be a simple and reliable marker which predicts left ventricular dilation after late reperfused AMI. (Internal Medicine 41: 920-924, 2002)

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Return of left ventricular function after reperfusion in patients with myocardial infarction: importance of subtotal stenoses or intact collaterals.

Cited by 167 publications

References 38 publications

The effects of the rate of intravenous infusion of streptokinase and the duration of symptoms on the time interval to reperfusion in patients with acute myocardial infarction.

The effects of the rate of intravenous infusion of streptokinase and the duration of symptoms on the time interval to reperfusion in patients with acute myocardial infarction.

Quantitative analysis of infarct size, contraction band necrosis, and coagulation necrosis in human autopsied hearts with acute myocardial infarction after treatment with selective intracoronary thrombolysis.

Clinical Implication of Persistent Ischemic Chest Pain on Admission in Patients with Late Reperfused Acute Myocardial Infarction.

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