[Acute myocardial infarction in patients with angiographically normal coronary arteries: clinical features and medium term follow-up]. / Akuter Myokardinfarkt bei Patienten mit angiographisch unauffälligen Koronararterien: Klinische Charakterisierung und Verlaufsbeobachtung.

BACKGROUND: Acute myocardial infarction (MI) in patients with normal coronary arteries has been recognized for several years. In most cases its etiology is unknown. The objective of the present study was to describe clinical features and medium term follow-up of those patients. PATIENTS AND METHODS: Between April 1991 and December 1996, 9860 coronary angiographies were performed in our hospital. During this period 17 patients with documented myocardial infarction and completely normal coronary arteries were identified. Acute myocardial infarction was defined as the clinical event with acute angina pectoris, ST-elevation typical for myocardial infarction, and an increase in serum creatinine phosphokinase (CPK) above 125 U/l. RESULTS: The mean peak CPK was 675 U/l (range: 129-1760 U/l). All 17 patients revealed significant ST-segment elevation. According to the ECG criteria there was no predilection for a specific location of MI (9 anterior MIs and 8 inferior MIs). Thrombolytic therapy was performed in 9 patients. In 12 patients areas of localized hypo- or akinesia were shown on left ventricular cineangiography. The mean ejection fraction was 61.5+/-10.3%. The age and sex distribution revealed a bimodel character: there was a younger age group of 9 patients, all men with a mean age of 35.9 years (31-43) and all strong cigarette smokers (mean 28 cigarettes/day) and there was an older group of 7 patients (1 man, 6 women) with a mean age of 56,4 years (47-68) and no significant association with cigarette smoking. During a mean follow-up period of 48.6 months (31-85 months) no patient died and no patient suffered from recurrent chest pain and used nitroglycerin occasionally. CONCLUSION: Patients with acute MI and angiographically normal coronary arteries show a bimodal sex and age distribution: a younger age group, all men and uniformly strong cigarette smokers and an older group predominantly women with no significant association with cigarette smoking. Both groups seem to have a favorable prognosis.

[Enzymatic markers of reperfusion in acute myocardial infarct. With data from the ISAM study]. / Enzymatische Marker der Reperfusion bei akutem Myokardinfarkt. Mit Daten aus der I.S.A.M.-Studie.

Despite advances in therapy acute myocardial infarction is associated with a mortality rate of up to 30%. Early and complete reperfusion of the infarct related artery (defined as TIMI flow 3 at 90 minutes following therapy) as obtained with thrombolytic therapy in 50 to 80% of patients improves survival and enhances ventricular function. Failure to achieve recanalization should prompt further intervention (second attempt of thrombolysis or rescue-PTCA). Various cardiac markers known from diagnosing acute myocardial infarction or risk stratification in unstable angina pectoris have been assessed in their ability to predict successful reperfusion/failure of therapy. Following reperfusion creatinkinase (CK) and its isoform CK-MB, troponin and myoglobin show an early and rapid rise to a high maximum value with rapid normalization. For creatinkinase time to peak values of less than 9 hours or rates of increase of > 50 U/h (> or = 10 U/h for CK-MB activity) within the first 2.5 hours following thrombolysis have been suggested as useful indicators of successful reperfusion. The same applies for a troponin (T)slope > 0.5 ng/ml/h within the first hour (Table 5). The major limitation in applying either creatinkinase, troponin or even lactatdehydrogenase (LDH) is their comparatively late release (4 to 6 hours) following myocardial infarction. In that respect myoglobin (though not specific for cardiac injury) seems ideal for guidance of intervention after failed thrombolysis. The I.S.A.M. study included 1,741 patients with acute myocardial infarction of less than 6 hours duration being given either streptokinase or placebo. Serial blood samples for measurement of cardiac enzymes were drawn within the first 50 hours. In the streptokinase group the time to peak concentration of CK-MB activity was significantly lower (mean 10.9 hours vs 16.1 hours following initiation of treatment) as was the area under the CK-MB curve indicating reduction of infarct size (Table 2). A substudy investigating the myoglobin release in 120 patients having received streptokinase or placebo demonstrated higher maximum values in the streptokinase group (mean 3008 vs 2097 ng/ml), a shorter time to peak interval following treatment (3.4 vs 6.5 hours) and a reduction in infarct size as suggested by a smaller area under the myoglobin curve (17,377 vs 23,240 ng/ml x h) (Table 3). For LDH/alpha-HBDH the reduction in time to peak intervals was less impressive (Table 4). In angiographic studies with TIMI flow 3 at 90 minutes in the infarct related artery in 22 patients (Figure 5) the maximum myoglobin value was reached in less than 4.2 hours (mean value plus SEM) following treatment (9.5 hours for CK-MB activity). Therefore, myoglobin seems to be the preferred marker in reperfusion assessment.