Infarct size estimated from serial serum creatine phosphokinase in relation to left ventricular hemodynamics.

Bleifeld, W.; Mathey, D.; Hanrath, Peter; Buss, H; Effert, S

doi:10.1161/01.cir.55.2.303

Cited by 176 publications

(29 citation statements)

References 11 publications

(4 reference statements)

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“…Multiple strategies have been used to evaluate myocardial infarct size, and each has its advantages and limitations. Infarct size measured by serial CK-MB assessment correlates with left ventricular failure, 23,24 presence of Q waves, 25 and mortality, 24 -26 although these findings are debated. Nevertheless, cardiac-enzyme release has been used to show a reduction in infarct size by streptokinase treatment versus placebo, 27 alteplase versus streptokinase, 28 and angioplasty versus streptokinase.…”

Section: Discussionmentioning

confidence: 99%

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Effect of Pexelizumab, an Anti-C5 Complement Antibody, as Adjunctive Therapy to Fibrinolysis in Acute Myocardial Infarction

et al. 2003

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for the COMPLY InvestigatorsBackground-Complement activation mediates myocardial damage that occurs during ischemia and reperfusion through multiple pathways. We performed 2 separate, parallel, double-blind, placebo-controlled trials to determine the effects of pexelizumab (a novel C5 complement monoclonal antibody fragment) on infarct size in patients receiving reperfusion therapy: COMPlement inhibition in myocardial infarction treated with thromboLYtics (COMPLY) and COMplement inhibition in Myocardial infarction treated with Angioplasty (COMMA). The COMPLY trial is reported here. Methods and Results-Overall, 943 patients with acute ST-segment elevation myocardial infarction (MI) (20% with isolated inferior MI) receiving fibrinolysis were randomly assigned Ͻ6 hours after symptom onset to placebo, pexelizumab 2.0-mg/kg bolus, or pexelizumab 2.0-mg/kg bolus plus 0.05 mg/kg per h for 20 hours. Infarct size determined by creatine kinase-MB area under the curve was the primary analysis, which included patients who received at least some study drug and fibrinolysis (nϭ920). The median infarct size did not differ by treatment (placebo, 5230; bolus, 4952; bolus plus infusion, 5557 [ng/mL] · h; bolus versus placebo, Pϭ0.85; bolus plus infusion versus placebo, Pϭ0.81), nor did the 90-day composite incidence of death, new or worsening congestive heart failure, shock, or stroke (placebo, 18.6%; bolus, 18.4%; bolus plus infusion, 19.7%). Pexelizumab inhibited complement for 4 hours with bolus-only dosing and for 20 to 24 hours with bolus-plus-infusion dosing, with no increase in infections. Conclusions-When used adjunctively with fibrinolysis, pexelizumab blocked complement activity but reduced neither infarct size by creatine kinase-MB assessment nor adverse clinical outcomes.

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Section: Discussionmentioning

confidence: 99%

“…CK and CK-MB were measured at enrollment (baseline) and 4,8,12,16,24,36,48, and 72 hours after enrollment. All samples were analyzed at a core laboratory.…”

Section: Infarct Size Assessmentmentioning

confidence: 99%

Effect of Pexelizumab, an Anti-C5 Complement Antibody, as Adjunctive Therapy to Fibrinolysis in Acute Myocardial Infarction

et al. 2003

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“…28 In contrast, clinical studies have suggested that this cut-off may be much later. 29 Reasons for the longer time to the onset of irreversibility in man might include incomplete occlusion of the artery responsible for the infarct, the presence of collateral flow sufficient to maintain viability until therapy can be initiated, and/or differences in the nature of the infarction process in man compared with animals. In the present study the cut-off appeared to be approximately 14 hr, since all patients demonstrating significant improvement in their scintigraphic studies with TNG had been treated within 13.5 hr of the onset of their chest pain.…”

Section: Discussionmentioning

confidence: 99%

A randomized prospective trial of intravenous nitroglycerin in patients with acute myocardial infarction.

et al. 1983

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A prospective randomized study of intravenous nitroglycerin (TNG) administered for 48 hr after acute infarction was undertaken to determine whether clinical improvement and/or evidence of preservation of ischemic myocardium could be demonstrated. One hundred four patients were randomly assigned to TNG (n = 56) and placebo groups (n = 48). TNG was infused at a rate sufficient to lower mean arterial pressure 10%, monitored noninvasively. When all TNG-and placebo-treated patients were compared, no significant differences in clinical or laboratory outcomes could be demonstrated. TNG-and placebo-treated patients were retrospectively subdivided into early and late treatment groups (treatment begun <10 hr vs 3 10 hr after onset of symptoms). Early TNG treatment was associated with a lower incidence of infarct complications within the first 10 days, defined by new congestive heart failure, infarct extension, or cardiac death (15% in early TNG compared with a mean of 39% in the other three subgroups; p = .003). Mortality at 3 months was lower in the group treated early with TNG (15%) compared with a mean of 25% in the other three subgroups (p = NS). No significant differences were found in peak creatine kinase (CK) blood levels, creatine kinase infarct size, or preservation of precordial R waves by serial electrocardiographic mapping. Among 49 patients with pretreatment and day 7 to 14 posttreatment left ventricular ejection fraction measurements, improvement of 3 10% occurred in 35% of TNG patients treated early compared with 6% of those treated late with TNG, 11% of those treated early with placebo, and 0% of those treated late with placebo (p = .004). Similarly, in 68 patients in whom paired thallium scintigrams were taken, a decrease of B75% in the computer-determined thallium defect score was seen in 48% of TNG patients treated early, compared with 14% of TNG patients treated late, 33% of placebo patients treated early and 0% of placebo patients treated late (p = .039). Patients demonstrating significant scintigraphic improvement were treated earlier, tended to have less severe initial scintigraphic abnormalities, inferior rather than anterior infarctions, a longer history of angina, and no prior history of heart failure. Thus intravenous TNG could not be shown to result in significant improvement in clinical or scintigraphic outcomes when the patient population was analyzed as a whole. After retrospective subgroup analysis, intravenous TNG could be shown to protect ischemic myocardium in the subset of patients with smallto-moderate sized myocardial infarctions when treatment was begun within 10 hr of the onset of symptoms. The results of this trial also suggest that future clinical trials designed to show a reduction in infarct size might limit patient entry to those admitted early after symptom onset and those with significant abnormalities in their admission scintigraphic studies. Larger-scale studies are needed to determine whether TNG therapy can significantly reduce mortality and to further define the...

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“…Patients randomized for treatment with propranolol were given 0.1 mg/kg propranolol intravenously over 10 min followed by 320 mg of propranolol orally over the next 27 hours. This was given in divided doses of 40 mg, at 1, 3,7,11,15,19,23, and 27 hours after entry to the trial. Treatment Using the measured levels and the individually determined KD, the total cumulative CPK appearance (large closed circles) is plotted.…”

Section: Methodsmentioning

confidence: 99%

Reduction of enzyme levels by propranolol after acute myocardial infarction.

Peter¹,

Norris²,

Clarke³

et al. 1978

Circulation

200

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SUMMARY The effect of propranolol (0.1 mg/kg intravenously followed by 320 mg given over 27 hour orally) on serum levels of creatine kinase enzyme was studied in a randomized trial involving 95 patients seen within 12 hours of onset of symptoms of uncomplicated myocardial infarction. In 15 patients who were treated with propranolol within 4 hours of onset, and who eventually developed pathological Q waves, peak measured enzyme levels were 27% (P < 0.0125) lower than in 19 control patients who were also seen THE WELL-KNOWN EFFICACY of beta-adrenergic blocking drugs for the treatment of angina pectoris53 suggests that these drugs should also be effective for the acute imbalance between oxygen supply and demand which occurs during the early stages of myocardial infarction. Apart from an encouraging report by Snow in 1965,4 however, a number of carefully randomized early clinical trials of beta blockers5-9 showed no effect on hospital mortality from infarction nor on the incidence of arrhythmias in treated patients compared with controls.A number of recent developments suggest, however, that the use of beta-adrenergic blocking drugs in the acute stage of myocardial infarction should be re-investigated. First, there is the evidence that long-term beta blockade prolongs life after myocardial infarction'0 11 and that this may be due in part to the prevention of new ischemic events.'2 Second, there is evidence that propranolol given prophylactically to experimental animals reduces myocardial infarct size;3-5 this suggests that measurements of infarct size should be used as an end-point for therapeutic trials in man. Third, doses of propranolol used in previous trials (40-80 mg per day) were comparatively low and were administered orally and comparatively late after the onset. Patients given this low dose do not develop blood levels within the therapeutic range for 24-48 hours after first administration of the drug. 16The present trial proposed to investigate the effect of highloading doses of propranolol given within 12 hours of onset of symptoms of infarction on serum creatine phosphokinase (CPK) levels.'7', Results show that CPK levels were reduced by propranolol if the drug was given within four hours of onset of the most severe chest pain.Patients and MethodsWe included in this study those infarctions which were of moderate severity since we postulated they would ultimately within 4 hours of the onset but had no specific treatment. Total calculated enzyme appearance was also lower in the treated patients (reduced 25%, P < 0.05) as was the calculated rate of appearance (33%, P < 0.005). No significant difference was found for treated compared with control patients entering the trial more than 4 hours after the onset of chest pain. This evidence suggests that propranolol may reduce the size of uncomplicated infarctiops if it is given intravenously within 4 hours of the onset.cause a moderately high enzyme release for which a reduction would be both easily measurable and clinically meaningful. At the same time it was r...

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Infarct size estimated from serial serum creatine phosphokinase in relation to left ventricular hemodynamics.

Cited by 176 publications

References 11 publications

Effect of Pexelizumab, an Anti-C5 Complement Antibody, as Adjunctive Therapy to Fibrinolysis in Acute Myocardial Infarction

Effect of Pexelizumab, an Anti-C5 Complement Antibody, as Adjunctive Therapy to Fibrinolysis in Acute Myocardial Infarction

A randomized prospective trial of intravenous nitroglycerin in patients with acute myocardial infarction.

Reduction of enzyme levels by propranolol after acute myocardial infarction.

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