Thomas Brüggemann

Extent of Early ST Segment Elevation Resolution: A Simple but Strong Predictor of Outcome in Patients With Acute Myocardial Infarction

OBJECTIVES This study proposed to verify the prognostic power of early ST segment elevation resolution in patients with acute myocardial infarction from the Intravenous Streptokinase in Acute Myocardial Infarction study data base. BACKGROUND Data from a small prospective study suggested that use of two cutoff points for three different levels of ST segment resolution 3 h after the start of thrombolysis may be an efficient way to predict outcome in an individual patient. METHODS The three groups of ST segment resolution were defined as 1) complete resolution (> or = 70% [552 patients]) or only slight ST segment elevation (127 patients); 2) partial resolution (< 70% to 30% [475 patients]); 3) no resolution (< 30% to > 0% [362 patients]). Infarct size was measured from creatine kinase isoenzyme, MB fraction, release and from the number of Q waves. Left ventricular function was assessed in 818 patients 1 month after infarction. RESULTS For complete, partial and no ST segment resolution 3 h after the start of streptokinase or placebo infusion, enzyme release was 1.2, 1.8 and 2.1 IU/ml x h; number of Q waves 1.7, 2.5 and 3.0; and ejection fraction 60%, 53% and 49%, respectively (all adjusted p = 0.0000). Mortality rate at 21 days was 2.2%, 3.4% and 8.6%, respectively. No ST segment resolution was the most powerful independent predictor of early mortality (p = 0.0001). Survival rate curves at 6-year follow-up showed significant mortality differences with increasing divergence (p = 0.0003 anterior infarction; p = 0.005 inferior infarction). In subgroups with an overall higher risk of dying, mortality was strongly determined by the extent of early ST segment resolution. CONCLUSIONS The extent of ST segment elevation resolution conveys useful early information about outcome in an individual patient after acute myocardial infarction.

Intravenous short-term infusion of streptokinase in acute myocardial infarction.

Short-term i.v. infusion of streptokinase was performed in 93 patients within 6 hours after the onset of acute myocardial infarction. Twenty-six patients underwent angiography in the acute phase (group A) and 52 underwent angiography in the fourth week only (group B); 15 patients had no angiography. Seven patients died during the hospital stay and six suffered nonfatal reinfarctions. There were no bleeding complications. In 11 of 21 group A patients, occluded coronary arteries were opened within 1 hour after the streptokinase infusion was started. In 84% of groups A and B, the infarct-related coronary artery was patent in the fourth week. In 75% of the patent arteries, the residual luminal diameter stenosis was less than 70%. According to serial serum CK-MB curves, recanalization was achieved mostly within 1–2 hours. Myocardial salvage was indicated by improvement in local contraction disorders in the recanalized group A patients and by the significant relationship between infarct size and time from symptom onset to treatment in group B. These data suggest that a high-dose, short-term, i.v. infusion of streptokinase is a safe and efficient method of restoring coronary blood flow. Expeditious initiation of i.v. streptokinase infusion is a critical determinant for early recanalization and salvage of myocardium. Patients with thrombotically subtotal occlusion probably receive the most benefit. Evaluation of the true impact on survival and myocardial function will require controlled clinical trials.

Circadian variation of sudden cardiac death reflects age-related variability in ventricular fibrillation.

BackgroundPrevious studies report a morning peak in the occurrence of out-of-hospital sudden cardiac death but lack detailed information on underlying arrhythmias. We used the documentation system of the semiautomated defibrillators used by emergency medical technicians to investigate the circadian pattern of defined arrhythmias and the influence of demographic patient characteristics on this pattern. Methods and ResultsFrom December 1988 to December 1990, 703 consecutive patients (63% men; age, 67±17 years) with sudden cardiac death were registered in the Klinikum Steglitz area of the Berlin emergency care system. Determination of time of day of the event was based on the arrival time of the rescue squad. A marked circadian variation (P<.0001) in the occurrence of sudden cardiac death was observed with a primary morning peak (6 AM to noon) and a secondary afternoon peak (3 to 7 PM). The subgroup of294 patients with ventricular fibrillation as initially documented arrhythmia showed a similar circadian variation (P<.0001). In significant contrast (P<.01), patients with asystole (n=260) or pulseless bradyarrhythmias (n=149) were more evenly distributed during the daytime with a primary night trough. Multivariate logistic regression analysis revealed that the circadian pattern of ventricular fibrillation was similar in both gender groups but tended to differ with regard to age: patients older than 65 years demonstrated a monophasic distribution, whereas patients aged 65 years or less had a biphasic distribution with peaks in the morning and in the afternoon. ConclusionsThe circadian pattern of sudden cardiac death reflects primarily a circadian variation in onset of ventricular fibrillation. The different circadian patterns of ventricular fibrillation, pulseless bradyarrhythmias, and asystole suggest different pathophysiological mechanisms of causation of death. The age dependence of the pattern of ventricular fibrillation may indicate different underlying external or endogenous triggers.

Circadian variation of sustained ventricular tachyarrhythmias terminated by appropriate shocks in patients with an implantable cardioverter defibrillator

To determine the circadian variation of sustained ventricular tachyarrhythmias, 78 consecutive patients with an implanted cardioverter defibrillator were analyzed with regard to the occurrence of spontaneous shock episodes during a mean follow-up period of 18 +/- 12 months. In 39 patients 207 shock episodes that terminated potentially life-threatening ventricular tachyarrhythmias could be related to an exact time of onset. A circadian variation (p < 0.001) of these events was demonstrated, with a primary morning peak between 7 hours and 11 hours and a secondary, much smaller peak between 16 hours and 20 hours. This finding indicates the relevance of endogeneous or exogeneous triggers in the cause of malignant arrhythmias that potentially lead to sudden cardiac death. Subgroup analyses revealed an association of the circadian pattern to the New York Heart Association functional classification, indicating perhaps a different role of triggers in different patient populations.

Follow-up after coronary arterial reperfusion with intravenous streptokinase in relation to residual myocardial infarct artery narrowings

Short- and long-term changes in residual stenosis of the myocardial infarct-related coronary arteries in patients with successful reperfusion by intravenous streptokinase have not been determined until now. In 15 patients the residual diameter stenosis decreased significantly from 62 +/- 9% after 24 hours to 55 +/- 13% in the fourth week (p less than 0.005). Quantitative angiographic analyses in 61 patients with patent infarct-related coronary arteries in the fourth week revealed a mean diameter stenosis of 61 +/- 13%. The patients were followed up 34 +/- 10 months. Sixteen had elective coronary artery bypass surgery or percutaneous transluminal coronary angioplasty (PTCA). Eighteen without coronary artery bypass surgery or PTCA had undergone repeat angiography after 26 +/- 9 months. Twenty-five (41%) have had a residual diameter stenosis greater than 65% in the fourth week. A stenosis greater than 65% was found in: 4 of 5 patients with late reinfarction; 3 of 7 with 1-vessel coronary artery disease and persistent angina, compared with none of 11 with a stenosis less than 65%; 6 of 7, whose silent reocclusion had been found at long-term follow-up compared with 1 of 9 with a residual stenosis less than 65%. In 8 patients with persistent patency of the infarct artery, the stenosis had decreased significantly from 55 +/- 6% to 36 +/- 12% (p less than 0.005). Correspondingly, there was a significant improvement in the infarct-related left ventricular wall motion disorders.(ABSTRACT TRUNCATED AT 250 WORDS)

Impact of late coronary artery reperfusion on left ventricular function one month after acute myocardial infarction (results from the ISAM study)

To evaluate the impact of late reperfusion of an infarct-related coronary artery on left ventricular (LV) function in the month after myocardial infarction, findings from 368 patients in the Intravenous Streptokinase in Myocardial Infarction study are presented. All patients had a late peaking in the creatine kinase-MB serum time-activity curve, suggesting absence of early reperfusion. Contrast angiography was performed 1 month after the acute event. The infarct-related coronary artery was patent in 74 of 116 (64%) streptokinase-treated patients and 141 of 252 (56%) patients treated with anticoagulant therapy (placebo group). In all baseline variables, including the actually developed enzymatic and electrocardiographic infarct sizes, there were no differences between the patent- or occluded-artery groups. A patent infarct artery 1 month after infarction was associated with significantly better LV function regardless of the vessel involved and whether or not patients had been treated with streptokinase. Ejection fraction in patients with patent versus occluded artery was 56 +/- 13 versus 50 +/- 14 (p less than 0.0005). Most benefit was noted in patients in whom the proximal left anterior descending coronary artery was affected: ejection fraction was 52 +/- 14 versus 36 +/- 12% (p less than 0.0005). Our data confirm that restoration of adequate flow through an infarct-related coronary artery beyond the time window for actual salvage of ischemic myocardium has a definite beneficial effect on LV function.

Risk stratification following myocardial infarction in the thrombolytic era: a two-step strategy using noninvasive and invasive methods☆

OBJECTIVES We prospectively performed a two-step risk assessment in patients in the early phase after acute myocardial infarction (MI). BACKGROUND Noninvasive methods like Holter electrocardiographic monitoring (HM) and determination of the left ventricular ejection fraction (EF) as well as the invasive technique of programmed ventricular stimulation (PVS) have been used to identify patients in the late phase after MI as candidates for prophylactic implantation of a cardioverter/defibrillator. However, it is unclear whether these results can be transferred to patients following acute MI. METHODS A series of 657 patients with acute MI (< or = 75 years) underwent HM and EF. If one of the two methods yielded abnormal findings (HM > or = 20 ventricular ectopic beats/h/> or =10 ventricular pairs/day/ventricular tachycardia; EF < or = 40%), PVS was done (abnormal PVS: induction of monomorphic ventricular tachycardia, duration >10 s, cycle length > or = 230 ms). RESULTS Of 657 patients, 304 (46%) had either an abnormal HM or EF. The PVS performed in 146 of 304 patients was abnormal in 22. During a mean follow-up of 37 months, there were 106 (16%) deaths, being sudden in 24 (3.6%), nonsudden cardiac in 45 (6.8%). The incidence of arrhythmic events (sudden cardiac death, symptomatic ventricular tachycardia, cardiac arrest) was 18% (4/22) with an abnormal PVS and only 4% (5/124) with a normal PVS (odds ratio 4.0, p=0.032). CONCLUSIONS The rate of arrhythmic events is low in post-MI patients in the 1990s. Nevertheless, a two-step risk stratification is helpful in selecting candidates for a defibrillator trial aiming at primary prevention of sudden cardiac death after MI.

Early assessment of outcome by ST-segment analysis after thrombolytic therapy in acute myocardial infarction

As an early marker of outcome, the sum of ST-segment elevation resolution between the electrocardiogram before and 3 hours after initiation of thrombolysis was investigated in 77 patients with acute myocardial infarction. Prospectively, three groups were defined according to complete (> or = 70%, n = 34), partial (< 70% to > or = 30%, n = 26), or no (< 30%, n = 17) ST resolution. There were considerable differences in the enzyme-determined infarct size (alpha-hydroxybutyrate dehydrogenase release for complete, partial, and no ST resolution: 529 +/- 397 IU/L, 689 +/- 484 IU/L, and 1293 +/- 742 IU/L, respectively; p = 0.0001) and the angiographic left ventricular function 1 week later (ejection fraction 58% +/- 10%, 53% +/- 13%, and 43% +/- 12%, respectively, p < 0.01; regional dyssynergic area 24 +/- 19, 39 +/- 23, and 50 +/- 21 U2, respectively, p < 0.01). Early reperfusion as assessed by creatine kinase release measured in 15-minute intervals was 90%, 65%, and 18%, respectively (p = 0.0001). Differences in degrees of ST-elevation resolution at 3 hours may help facilitate timely screening of patients for appropriate therapeutic intervention. Patients with complete ST resolution may be considered for early discharge, and patients with no ST resolution may be candidates for an early invasive approach or additional thrombolytic therapy.

Prognostic value of ischemia during Holter monitoring and exercise testing after acute myocardial infarction

Exercise testing is generally accepted for prognostic assessment of patients after infarction, but the prognostic value of transient myocardial ischemia during ambulatory electrocardiographic monitoring remains controversial. Of 281 consecutive postinfarction patients, 173 patients (132 men, 41 women) were prospectively studied with 24-hour Holter monitoring 14 +/- 5 days after acute myocardial infarction, and with submaximal exercise testing after 15 +/- 7 days. Patients with either conduction disturbances or pacemaker rhythm and 71 patients with digitalis medication were excluded. Myocardial ischemia was defined as horizontal or descending ST depressions or transient ST elevations > or = 0.1 mV with or without angina pectoris. The follow-up period was 1 year. Myocardial ischemia was observed in 40 patients (23%) during Holter monitoring, and 96% of the episodes were asymptomatic. Ischemia occurred during exercise testing in 46 patients (27%), two thirds of whom had no symptoms. Ischemia was detected by both methods (group A) in 19 patients (11%), with exercise testing only (group B) in 27 patients (16%), and with Holter monitoring only (group C) in 21 patients (12%). In 106 patients (61%), ischemia could not be ascertained at all. The 4 groups were comparable with regard to sex and age distribution, coronary risk factors, and medication. During follow-up, 50 patients (29%) experienced clinical cardiac events: 6 patients died, 7 had recurrent myocardial infarction, 14 developed unstable angina pectoris and required immediate revascularization, and 23 patients had recurrent but stable angina.(ABSTRACT TRUNCATED AT 250 WORDS)

Transient ST segment depression during holter monitoring: How to avoid false positive findings

To increase the specificity of 24-hour Holter monitoring in detecting transient myocardial ischemia, we separated genuine ST deviations from those dependent on artifacts by adding a detailed shape analysis of real-time printouts to the usual criteria of significant ST segment depression. We screened 116 apparently healthy subjects; 31 had to be excluded, because of pathologic findings in preliminary examinations. The remaining 85 (49 women and 36 men; mean age, 43.1 years) underwent Holter monitoring for assessment of the extent, frequency, and duration of episodes of horizontal and descending ST segment depression of at least 0.1 mV that persisted for at least 60 msec after the J point and that were at least 1 minute apart. On the basis of these criteria, six subjects (7.1%) showed 24 episodes of horizontal or descending ST segment depression with a mean of 0.2 mV (range, 0.15 to 0.25 mV), a frequency of four episodes per 24 hours (one to nine), and a duration of 12.2 minutes (range 3-range 41 minutes). Supplementary criteria--e.g., sudden onset of ST segment depression, identical orientation of PQ and ST segments, or simultaneous increase in R and P wave amplitude--made it possible to identify ST changes caused by artifacts in four volunteers. In only two subjects (2.4%) could true silent ischemia not be differentiated from false positive results. Thus consideration of only the extent, frequency, and duration of episodes does not permit a differentiation between true silent ischemia and false positive results. A supplementary shape analysis increases the specificity of ST segment analysis in detecting transient myocardial ischemia during 24-hour Holter monitoring.