Biochemical markers of myocardial ischemia and necrosis

The biochemical markers of myocardial ischaemia have to be interpreted according to their kinetics; their interests depend on the clinical presentation. They are helpful to orient to a myocardial ischaemia in front of undefined chest pain, to stratify the outcome of acute coronary syndrome without ST segment elevation, to evaluate the amount of myocardial damage following infarction, to detect the failure of thrombolysis therapy and probably to stratify the post percutaneous coronary intervention outcome.     

Repeat thrombolysis in acute myocardial infarction

The author describes a case-history of streptokinase intolerance during treatment of acute myocardial infarction (IM) where it was impossible to ensure rescue percutaneous coronary angioplasty (PTCA) and to resolve this condition by subsequent alteplase treatment. The author discusses whether it is justified and indicated to use this procedure rarely mentioned in the literature.     

Emergency thrombolysis in acute myocardial infarction

The goal of thrombolytic treatment in acute myocardial infarction is to reestablish permanent blood flow, salvage ischemic myocardium, and reduce mortality. If patency is achieved sufficiently early and is maintained, left ventricular function is preserved and mortality decreases. The recent experience with tissue plasminogen activator and streptokinase in the TIMI I trial is reviewed with specific attention to reperfusion, reocclusion, and bleeding. Other studies concerning left ventricular preservation and mortality are also discussed. Current guidelines for antithrombotic therapy and thrombolysis are discussed. It is extremely important to adequately select patients to avoid side effects. Thorough lysis of the thrombus must be achieved to reduce the risk of rethrombosis. Simultaneous heparin should be administered to treat ongoing thrombosis. Additional antithrombotic therapy with aspirin and acute vasodilation to reduce vasoconstriction probably also decrease the likelihood of reocclusion. Because this treatment predisposes to bleeding, extreme care should be taken to avoid vascular punctures and invasive procedures in these patients. The association of immediate percutaneous transluminal coronary angioplasty has not been beneficial in preventing further events; on the contrary, adverse effects have been associated with this acute intervention.     

Prehospital thrombolysis in acute myocardial infarction

The benefit and risk of prehospital thrombolysis for acute myocardial infarction (AMI) were evaluated in a double-blind randomized trial. Patients presenting less than 4 hours after symptom onset received 2 million units of urokinase as an intravenous bolus either before (group A, n = 40) or after (group B, n = 38) hospital admission. The mean time interval from onset of symptoms to thrombolytic therapy was 85 +/- 51 minutes in group A and 137 +/- 50 minutes in group B (p less than 0.0005). In 91% of the patients, thrombolytic therapy was administered less than 3 hours after symptom onset. Complication rates during the pre- and in-hospital period were low and did not differ between groups. Three patients died (1 in group A, 2 in group B) from reinfarction 7 to 14 days after admission. Left-sided cardiac catheterization before discharge revealed a patency rate in the infarct-related artery of 61% in group A and 67% in group B (difference not significant). Global left ventricular function and regional wall motion at the infarct site did not differ significantly between group A and B (ejection fraction 51 +/- 10%, n = 28 vs 53 +/- 14%, n = 28; wall motion -2.3 +/- 1.3 vs -2.2 +/- 1.1 standard deviation, respectively). Also, peak creatine kinase did not differ significantly (838 +/- 634 U/liter in group A vs 924 +/- 595 U/liter in group B). Prehospital thrombolysis using a bolus injection of urokinase has a low risk when performed by a trained physician with a mobile care unit. The saving of 45 minutes in the early stage of an acute infarction through prehospital thrombolysis did not appear to be important for salvage of myocardial function.     

Intracoronary thrombolysis in acute myocardial infarction

Forty-seven patients with acute myocardial infarction (MI) underwent intracoronary infusion of Thrombolysin or streptokinase. In 41, a completely reoccluded artery was reopened. Patency was associated with appearance of arrhythmias, relief of pain, gradual return of the ST-segment to the baseline and appearance of abnormal Q waves. Creatine kinase (CK) and MB-CK enzyme levels peaked earlier. Serial thallium scintigrams showed reduction in defect size after reperfusion, and the ejection fraction was higher compared with control. Eighteen patients were recommended for coronary bypass surgery for recurrent pain or severe multivessel disease.     

Bleeding after thrombolysis in acute myocardial infarction

232 consecutive patients with acute myocardial infarction weretreated either with 2 x 10⁶ IU urokinase as an intravenous bolusinjection, or 250000 IU streptokinase intracoronary, or 60 mgrecombinant tissue-type plasminogen activator (rt-PA) over 90min. All patients enrolled had chest pain for more than 30 minand less than 3 h before admission and a typical electrocardiogram.Contra-indications to thrombolytic treatment were absent. Allbleeding complications occurring within 24 h after admissionwere assumed to be due to thrombolytic therapy. Bleeding complicationsoccurred in 14 patients (6.5%). Only seven patients receiveda blood transfusion (3%). No correlation was evident betweenprevious hypertension, diabetes mellitus, smoking, sex, age,fibrinogen level before and 24 h after thrombolytic therapyand bleeding complications. The risk of bleeding was not significantlydifferent between the different thrombolytic regimens despitemarked differences in the fall of the fibrinogen level. Thedecrease of fibrinogen following thrombolytic therapy did notinfluence the patency rate of the infarct vessel. Thrombolytictherapy in acute myocardial infarction is a safe treatment evenamong patients advanced in years and with medically controlledhypertension and diabetes mellitus, irrespective of the kindof thrombolytic treatment.     

Repeat thrombolysis for acute myocardial infarction

BACKGROUND: Thrombolysis is still the first line of treatment for acute myocardial infarction in the United Kingdom. In a significant proportion of these patients thrombolytic therapy fails to restore patency of the occluded artery or is followed by early re-infarction. The best management of this group of patients is not clear although repeat doses of thrombolysis are commonly administered especially in the district general hospitals that do not have access to invasive facilities. We performed a retrospective clinical study to determine the outcome of repeat thrombolysis for acute myocardial infarction in patients with failed initial thrombolysis or early re-infarction. METHODS: Ninety-two patients who received two or more doses of thrombolysis for acute myocardial infarction were compared with 98 contemporary similar patients who received only one dose of thrombolysis. Case notes of all patients were examined for retrospective analysis. Main outcome measures were death, heart failure and need for in-hospital revascularization. RESULTS: Compared to the group thrombolysed once, in the rethrombolysed group there were significantly more deaths at 30 days (p=0.0016), more heart failure (with lower mean ejection fraction), more cardiac arrests as well as more frequent coronary angiography and percutaneous coronary interventions (PCIs). The incidence of haemorrhage in the two groups did not differ. CONCLUSIONS: The need for repeat thrombolysis identifies a group of patients with a high risk of early complications. Although repeat thrombolysis is safe, these patients then need close monitoring with a view to early intervention. For such patients admitted to district general hospitals without interventional facilities early referral to a tertiary center should be considered.     

Coronary artery thrombolysis in acute myocardial infarction

Coronary thrombolysis with streptokinase infusion can be achieved if performed during the first 4 hours of the onset of myocardial infarction. It has been a consistent finding that lysis of the thrombus can reestablish angiographically documented, antegrade coronary flow. Restoration of blood flow and preservation of ischemic myocardium can be achieved after coronary thrombolysis. Coronary artery bypass surgery or percutaneous transluminal coronary angioplasty may be necessary when significant obstructive coronary artery lesions due to atherosclerotic plaques remain after successful thrombolysis.     

Biochemical markers in the diagnosis of myocardial infarction

The diagnosis of myocardial necrosis due to acute myocardial infarction (AMI) and other causes has long been based on the plasma levels of cardiac troponins. Other markers of myocardial injury such as myoglobin, heart-type fatty acid binding protein, glycogen phosphorylase isoenzyme BB, or the early and sensitive total stress marker copeptin remain to be just attractive options used primarily to early rule out AMI and in risk stratification. Recent years have seen the introduction of a routine practice of the high-sensitivity cardiac troponin assays capable of detecting diagnostic elevations in plasma troponin levels as early as the first hours of myocardial injury. However, this assay tends to identify very often low plasma troponin levels in primarily noncardiac conditions and also in healthy or apparently healthy individuals. Hence, this novel technology warrants further study.     

Changing paradigms in thrombolysis in acute myocardial infarction

Acute myocardial infarction occurs when a ruptured coronary artery plaque causes sudden thrombotic occlusion of a coronary artery and cessation of coronary artery blood flow. This paper reviews the underlying coronary pathology in progressive coronary atherosclerosis, mechanisms of plaque rupture and arterial occlusion and the time relationship between coronary occlusion and myocardial necrosis. Reperfusion can be achieved by chemical thrombolysis with different thrombolytic agents. Early lysis is achieved best by prehospital administration, a transtelephonic monitor, a mobile intensive care unit, active general practitioner treatment or by warning the emergency room of impending arrival of a patient. Thrombolytic therapy may be unsuccessful and not achieve Grade III TIMI flow in less than 4 h (or even 2 h) due to inadequate or intermittent perfusion or reocclusion. Adjuvant therapy includes aspirin and platelet receptor antagonists. Bleeding is a constant danger. Direct percutaneous transluminal coronary angioplasty (PTCA) may be as effective or better than chemical thrombolysis. Reperfusion protects the myocardium and salvages viable tissue. It also improves mechanical remodelling of the ventricle. Long-term follow-up has shown that quantum leaps of fresh coronary occlusion causes step-wise progression in patient disability and that further early, prompt reperfusion can salvage myocardium and prevent this inexorable progress of the disease.     

Successful intracoronary thrombolysis in cocaine-associated acute myocardial infarction

We describe a case of cocaine-associated acute myocardial infarction managed by cardiac catheterization and intracoronary thrombolysis. Based on this and other reported cases, it appears that an invasive approach to the management of cocaine-associated acute myocardial infarction is advantageous over intravenous thrombolysis. Such a strategy would define the pathophysiology of acute myocardial infarction in the setting of cocaine use and allow mechanical intervention should pharmacologic therapy be unsuccessful. Cathet. Cardiovasc. Diagn. 42:294–297, 1997. © 1997 Wiley-Liss, Inc.