Electrocardiographic antecedents of primary ventricular fibrillation. Value of the R-on-T phenomenon in myocardial infarction.

Primary ventricular fibrillation was seen in 20 of 450 consecutive patients (4-4%) admitted within 24 hours after the onset of acute myocardial infarction. Compared with patients without primary ventricular fibrillation they showed a lower mean age group and a higher incidence of anterior infarction. Warning ventricular arrhythmias preceded primary ventricular fibrillation in 58% of cases. However, warning arrhythmias were also present in 55% of patients without primary ventricular fibrillation. The following mechanisms of initiation of primary ventricular fibrillation were seen. 1) In one patient, it was initiated by supraventricular premature beats showing aberrant intraventricular conduction. 2) In 2 patients, ventricular tachycardia degenerated into primary ventricular fibrillation. 3) In 17 patients, it was initiated by a ventricular premature beat; in 10 of these, the premature beat showed early coupling (RR/QT less than 1--the R-on-T phenomenon). However, ventricular premature beats showing the R-on-T phenomenon were also observed in 49% of patients without primary ventricular fibrillation. In 7, primary ventricular fibrillation was initiated by a late-coupled ventricular premature beat (RR/QT greater than 1); in 2, the very late coupling resulted in a ventricular fusion beat. The study suggests that warning arrhythmias and the R-on-T phenomenon are poor predictors of primary ventricular fibrillation in acute myocardial infarction. The observation that 41% of primary ventricular fibrillation was initiated by a late-coupled ventricular premature beat suggests that ventricular vulnerability during acute myocardial infarction may extend throughout most of the cardiac cycle and is not necessarily confined to the QT interval.     

Prognostic significance of arrhythmias in acute myocardial infarction (author's transl)]

Ventricular arrhythmias represent a common precursor of ventricular fibrillation in acute myocardial infarction in man. Frequent ventricular ectopic beats (greater than 5/min), multifocal ectopic beats, ventricular bigeminy, ventricular salvoes, ventricular tachycardia, and the R-on-T phenomenon have been considered as warning arrhythmias. However, recent studies have given rise to some doubt concerning the value of warning arrhythmias as predictors of ventricular fibrillation. In many a case there is no warning arrhythmia prior to ventricular fibrillation or these arrhythmias do not fulfill the criteria of warning arrhythmias. In other cases the warning arrhythmias develop so briefly before ventricular fibrillation that no prophylactic measure can be instituted. Warning arrhythmias may occur at equal frequency in patients with and without consecutive ventricular fibrillation. This also applies to the R-on-T phenomenon as a warning arrhythmia and as the initiating mechanism of ventricular fibrillation. In nearly half the cases ventricular fibrillation is initiated by a late ventricular ectopic beat. In view of these data of the literature, the so-called warning arrhythmias seem to have lost their predictive value. They represent a common phenomenon in acute myocardial infarction in man. However, ventricular fibrillation may also occur without any prior ventricular arrhythmias, above all during the first day of acute myocardial infarction. The frequency of ventricular fibrillation decreases in the course of infarction. Therefore the time during acute myocardial infarction may be a better guide whether to institute prophylactic antiarrhythmic therapy than the occurrence of ventricular arrhythmias. To date, the beneficial effect of prophylactic administration of lidocaine has remained controversial though a recent double-blind study has strongly suggested that lidocaine is able to prevent ventricular fibrillation. If these results should be confirmed by others, this would ask for routine administration of lidocaine in each case with acute myocardial infarction during the first day.     

The "R-on-T" phenomenon: an update and critical review.

The "R-on-T phenomenon" is the superimposition of an ectopic beat on the T wave of a preceding beat. Early observations suggested that R-on-T was likely to initiate sustained ventricular tachyarrhythmias. More recent experimental and clinical observations suggest that R-on-T is not a critical determinant of primary ventricular fibrillation in acute myocardial infarction; represents few of the initiating beats of paroxysmal ventricular tachycardia; and represents at worst only a small risk in terms of sudden death. Apparently when the capacity for sustained repetitive beating has not been clinically obvious, R-on-T is quite unlikely to result in ventricular tachyarrhythmias, even in the presence of coronary heart disease. However, in the setting of acute myocardial infarction, inability to always identify the precursors of tachyarrhythmias strengthens the argument for prophylactic treatment of patients.     

Primary ventricular fibrillation complicating acute myocardial infarction

A controversy exists about whether or not primary ventricular fibrillation in patients with acute myocardial infarction is always preceded by premonitory cardiac arrhythmias. The monitoring system in the Toronto General Hospital Coronary Unit yields a permanent record of every heartbeat and provides a unique opportunity to answer this question. Of 851 patients with proved myocardial infarction, primary ventricular fibrillation developed in 20; 12 of these had frequent ventricular arrhythmias before ventricular fibrillation. In 5 patients, ventricular fibrillation occurred without any warning arrhythmia and the remaining 3 patients had only rare ventricular premature beats.     

Initiation of ventricular fibrillation by supraventricular beats in patients with acute myocardial infarction.

The role of supraventricular extrasystoles in the initiation of ventricular arrhythmia was studied in 72 consecutive patients who developed primary ventricular fibrillation during the acute phase of myocardial infarction. In six patients (8%), a total of 12 episodes of ventricular fibrillation and 16 episodes of ventricular tachycardia were initiated by supraventricular extrasystoles. Ventricular fibrillation and tachycardia were initiated by single supraventricular extrasystoles in 16 and by salvos greater than or equal to two beats in 12 episodes. The RR coupling interval of the supraventricular impulse immediately preceding ventricular tachycardia ranged from 240 to 420 ms (mean 356 (62)) and was characteristic of R-on-T (prematurity index less than 1) in 63% of episodes. Average peak serum creatine kinase activity in the six patients in whom ventricular tachycardia was initiated by a supraventricular extrasystole was 1275 units compared with 720 units in the remaining 66 patients. Five of these six patients later showed evidence of pump failure. Lignocaine or procainamide or both suppressed the ventricular arrhythmia in five of the six patients. The initiation of ventricular fibrillation or tachycardia by supraventricular extrasystoles in acute myocardial infarction is not uncommon and may reflect the increased vulnerability of the heart after a large infarct. These arrhythmias may respond to drugs that suppress ventricular irritability.     

Initiation of ventricular fibrillation by supraventricular beats in patients with acute myocardial infarction

The role of supraventricular extrasystoles in the initiation of ventricular arrhythmia was studied in 72 consecutive patients who developed primary ventricular fibrillation during the acute phase of myocardial infarction. In six patients (8%), a total of 12 episodes of ventricular fibrillation and 16 episodes of ventricular tachycardia were initiated by supraventricular extrasystoles. Ventricular fibrillation and tachycardia were initiated by single supraventricular extrasystoles in 16 and by salvos greater than or equal to two beats in 12 episodes. The RR coupling interval of the supraventricular impulse immediately preceding ventricular tachycardia ranged from 240 to 420 ms (mean 356 (62)) and was characteristic of R-on-T (prematurity index less than 1) in 63% of episodes. Average peak serum creatine kinase activity in the six patients in whom ventricular tachycardia was initiated by a supraventricular extrasystole was 1275 units compared with 720 units in the remaining 66 patients. Five of these six patients later showed evidence of pump failure. Lignocaine or procainamide or both suppressed the ventricular arrhythmia in five of the six patients. The initiation of ventricular fibrillation or tachycardia by supraventricular extrasystoles in acute myocardial infarction is not uncommon and may reflect the increased vulnerability of the heart after a large infarct. These arrhythmias may respond to drugs that suppress ventricular irritability.     

The value of warning arrhythmias in the prediction of ventricular fibrillation within one hour of coronary occlusion. Experimental studies in the baboon

Factors associated with the development of ventricular fibrillation after coronary artery ligation were studied in a subhuman primate (Cape Chacma baboon). In 25 or 66 per cent of 38 baboons, primary ventricular fibrillation occurred within the first hour after the onset of acute myocardial infarction. Increasing age, total heart weight, and the size of the infarct were directly related to the incidence of primary ventricular fibrillation. Anterolateral infarcts had the highest risk of ventricular fibrillation. Anteroseptal and posterior infarcts had the best survival rate for the first hour. Male baboons were more prone to develop ventricular fibrillation than were females. There was no definite progression from ventricular ectopic beats to ventricular fibrillation. In the presence of ventricular tachycardia (even when brief in duration), ventricular bigeminy, or R-on-T beats, ventricular fibrillation has to be expected from the time of onset of the arrhythmia till 30, 20, or 10 minutes have elapsed, respectively. Beyond these times, ventricular fibrillation did not develop during the experimental period. Conversely, the absence of these signs could predict survival for 1 hour. The over-all efficiency of the warning signs in predicting ventricular fibrillation or survival was 85 per cent. Ventricular fibrillation occurred without any of these 3 warning signs in only 1 baboon (5 per cent of all cases). It is suggested that these warning arrhythmias could have a practical value in the management of patients with acute myocardial infarction of recent onset by anticipating the time of impending ventricular fibrillation.     

Significance of R-on-T phenomenon in early ventricular tachyarrhythmia susceptibility after acute myocardial infarction in the thrombolytic era

We investigated the clinical significance and mechanism of the R-on-T phenomenon in the current thrombolytic era as potential precipitant of R-on-T-induced early ventricular tachyarrhythmias in patients with a thrombolysed acute myocardial infarction. We also examined the role of QT dispersion on ventricular vulnerability and its association with R-on-T-initiated ventricular tachyarrhythmias. A total of 93 patients underwent 24-hour Holter monitoring starting at hospital admission before thrombolysis. Patients were classified into 2 groups: those with (n = 76) and those without (n = 17) reperfusion according to electrocardiographic criteria. All R-on-T ventricular premature complexes (VPCs) and R-on-T-initiated arrhythmic events (ventricular tachycardia [VT], ventricular fibrillation) were counted to estimate arrhythmia density and severity in 2 time periods during and after completion of thrombolysis. Measurements of QT and QTc intervals and dispersion parameters were obtained on the 12-lead electrocardiogram before thrombolysis and at 24 hours in patients with and without R-on-T VTs. Overall, R-on-T VPCs were rarely observed (1.8% of total VPCs over 24 hours), occurring more frequently during than after thrombolysis (at a rate of 8 vs 0.6 VPCs/hour, p = NS) and at a higher rate during thrombolysis in nonreperfused than in perfused patients (15 vs 8/hour, p = NS). Three VF episodes were observed in 1 reperfused patient, and all were R-on-T initiated. Episodes of nonsustained R-on-T VTs (3.3% of total VTs over 24 hours) appeared more frequent during than after thrombolysis (at a rate of 0.8 vs 0.05 VPCs/ hour, p = NS), and compared with non-R-on-T VTs they were significantly faster (374 +/- 56 ms vs 411 +/- 69 ms; p < 0.05), with a trend toward longer duration. Our findings indicate that R-on-T VPCs and R-on-T VTs are early rare features in acute myocardial infarction, and do not serve as triggers of severe ventricular tachyarrhythmia. The study of ventricular repolarization did not elicit an identifiable risk factor of R-on-T VT susceptibility.     

Primary heart arrest during dynamic ECG in the myocardial infarct patient during convalescence. Contribution of 4 cases

Four cases of cardiac arrest occurred during Holter monitoring are described. All patients had sustained an acute myocardial infarction thirteen-fourteen days prior to recording and were fully mobilized. In all of them the fatal arrhythmic event was ventricular fibrillation (VF). ECG analysis revealed an increase in heart rate before initiation of VF in one patient only. Warning ventricular arrhythmias were present in two patients. Transient ST segment changes during monitoring were noted in all patients. In three cases the arrhythmia was initiated by an ectopic ventricular beat (EVB) with R-on-T phenomenon; in two of them the EVB occurred after a sinus beat following a long post-ectopic pause. The different electrical events able to induce VF showed a variable and unpredictable pattern of occurrence and association in different patients and at different times in the same patient. Therefore, no specific "trigger" of the fatal arrhythmia could be identified.     

Analysis of the pattern of initiation of sustained ventricular arrhythmias in patients with implantable defibrillators

INTRODUCTION: The purpose of this study was to analyze the pattern of initiation of sustained ventricular arrhythmias in patients with varying types of underlying structural heart disease. METHODS AND RESULTS: The study group consisted of 90 patients with an implantable cardioverter defibrillator. Cardiovascular diagnoses included coronary artery disease in 64 patients (71%). The patients were divided into four groups based on the type and severity of structural heart disease. Two hundred sixty episodes of sustained ventricular arrhythmias were analyzed. The mean coupling interval of the initiating beat of all ventricular arrhythmias was 523 +/- 171 msec. The coupling interval of the initiating beat was longer in patients with impaired ventricular function, particularly those with nonischemic dilated cardiomyopathy. The prematurity index was similar regardless of the type of underlying structural heart disease. However, the prematurity index was shorter in patients with polymorphic ventricular tachycardia (VT) compared to those with monomorphic VT. A pause was observed more commonly before the onset of polymorphic VT/ventricular fibrillation than sustained monomorphic VT. Two hundred twenty-two (85%) of the arrhythmia episodes were initiated by a late-coupled premature beat, 33 (13%) were initiated by an early-coupled premature beat, and 5 episodes (2%) were initiated with a short-long-short sequence. The pattern of initiation of the ventricular arrhythmias was similar in all patient groups and for both monomorphic and polymorphic tachycardias. CONCLUSION: These findings demonstrate that sustained ventricular arrhythmias typically are initiated by late-coupled ventricular premature depolarizations, regardless of the type or severity of underlying structural heart disease or resultant arrhythmia.     

Ventricular arrhythmias prior to discharge after acute myocardial infarction.

One hundred consecutive patients in sinus rhythm and without routinely prescribed antiarrhythmic therapy were investigated for ventricular ectopic beats (VEB) prior to discharge after an acute myocardial infarction. The registration was performed for three hours during the day, including light exercise, and three hours at night. The overall VEB frequency was 70%. 34% had uniform VEBs, 22% multiform VEB'S, ANd 11% paired VEB'S 2% HAD THE R-on-T phenomenon and 1% ventricular tachycardia (VT). Ventricular irritability was more common in patients discharged after reinfarction, an estimated large infarct, if they had shown VT or ventricular fibrillation in the acute phase or when treated with diuretics only because of heart failure. There was no lowering of the VEB incidence at night, 17 patients having had ventricular arrhythmias at night only. In 5 cases the VEB'S were of a higher degree during exercise than at rest.     

Decreases by magnesium of QT dispersion and ventricular arrhythmias in patients with acute myocardial infarction.

AIMS: Magnesium treatment suppresses ventricular arrhythmias in acute myocardial infarction and possibly mortality after infarction, but the underlying mechanisms are inadequately understood. We tested whether the effect of magnesium could be attributed to an influence on the autonomic control of the heart, changes in disturbed repolarization, relief of ischaemia or limitation of myocardial injury. METHODS AND RESULTS: Fifty-nine consecutive patients with acute myocardial infarction were randomized to receive 70 mmol of magnesium (n = 31) infused over 24 h or placebo (n = 26). Occurrence of ventricular arrhythmias and heart rate variability (SD of 5-min mean sinus beat intervals over a 24 h period, SDANN; low frequency/high frequency amplitude ratio, LF/HF ratio), and the number of ischaemic episodes on vectorcardiography were measured from the first day of treatment. QT dispersion corrected for heart rate was measured from the 12-lead ECG. Magnesium decreased the number of hourly ventricular premature beats (P < 0.001) and the number of ventricular tachycardias (P < 0.05). QT dispersion corrected for heart rate was decreased in both measurements at 24 h and 1 week (P < 0.001). SDANN and LF/HF ratio were unchanged. The number of ischaemic episodes on vectorcardiography were equal, and peak creatine kinase MB release did not differ between the groups. In testing the pathophysiological mechanisms, serum magnesium levels after infusion correlated with hourly ventricular premature beats (rs = -0.47; P < 0.01), ventricular tachycardias (rs = -0.26; P < 0.05), and QT dispersion corrected for heart rate (rs = -0.75; P < 0.001), but not with SDANN, LF/HF ratio or peak creatine kinase MB. QT dispersion corrected for heart rate correlated with hourly ventricular premature beats (rs = 0.48; P < 0.001) and ventricular tachycardias (rs = 0.27; P < 0.05). CONCLUSIONS: Magnesium suppresses early ventricular arrhythmias in acute myocardial infarction. The decreased arrhythmicity is related to enhancement of homogeneity in repolarization, but not to attenuation of prevailing ischaemia, improvement of autonomic nervous derangements or myocardial salvage.     

Role of early cycle ventricular extrasystoles in initiation of ventricular tachycardia and fibrillation: Evaluation of the R on T phenomenon during acute ischemia in a canine model

Eighteen open chest dogs anesthetized with pentobarbital sodium were studied to determine the role of early cycle premature ventricular beats in the initiation of ventricular tachycardia and fibrillation during the initial 30 minutes of acute myocardial ischemia. The coupling interval and prematurity index (R-R′/R-R) of every premature beat after a sinus beat were determined during both the “immediate” (2 to 12 minutes) and “delayed” (13 to 30 minutes) phases of ventricular arrhythmias that follow acute coronary ligatlon. During the immediate phase, characterized by marked fractionation of local electrograms and delayed intramyocardial conduction, early cycle beats were infrequent (8 percent of extrasystoles) and initiated only 3 (4 percent) of 75 episodes of ventricular tachycardia and fibrillation. However, during the delayed phase, characterized by less fractionation and more uniform conduction, early cycle beats were both more frequent (24 percent of extrasystoles, p < 0.001) and more successful (20 [34 percent] of 59 episodes, p < 0.001) in initiating ventricular tachycardia and fibrillation. Thus, the underlying electrophysiologic derangements appeared to be of primary importance in determining both the frequency and relative malignancy of early cycle beats during acute myocardial ischemia.     

Sudden death during ambulatory Holter monitoring

Four cases of sudden cardiac death during ambulatory Holter monitoring are described. All had coronary arterial disease. Two patients were on antiarrhythmic drug therapy and both had a prolonged QTc-interval on their resting electrocardiogram. The predominant rhythm was sinus rhythm in all. In one patient, severe bradycardia terminated in asystole. In the remaining 3 patients, ventricular flutter (which was initiated in 2 instances by a short run of polymorphous ventricular tachycardia) degenerated into ventricular fibrillation. The lethal event was triggered once by an early cycle ventricular premature beat and twice by late cycle ventricular premature beats. There was no specific pattern of warning arrhythmias preceding sudden cardiac death. Signs of ischemia/sympathetic overactivity preceding sudden cardiac death were found in 3 patients. Autopsy studies were performed in 2 patients and revealed acute ischemic myocardial damage.     

Lidocaine in the early phase of acute myocardial infarction: the controversy over prophylactic or selective use

In acute myocardial infarction, lidocaine is considered the drug of choice for the treatment of malignant ventricular arrhythmias. While initially a so-called "selective" treatment strategy prevailed, in which lidocaine was administered only after the onset of certain "warning arrhythmias," the prophylactic use of lidocaine in acute myocardial infarction has been gaining wider usage in intravenous and intramuscular application in recent years. Both therapeutic applications have been found to be problematic of late, which has led to increasingly restrictive use of lidocaine. While in selective treatment forms, the definition and prompt recognition of the so-called warning arrhythmias created especially acute problems, the prophylactic therapeutic use is problematic due to the occurrence of sometimes serious side effects, which is to be expected as the size of the collective being treated increases. Both treatment forms also appear limited by the narrow preventive efficacy of lidocaine against malignant ventricular arrhythmias, especially against ventricular fibrillation. The current therapeutic recommendation for lidocaine in acute myocardial infarction should be limited to patients presenting with very frequent and complex ventricular arrhythmias, especially when these are elicited by an R-on-T phenomenon. Side effects and other therapeutic problems encountered when the therapeutic modality is switched or adjusted can be greatly reduced by careful dosing and selection of the optimal combination substances.     

Malignant premature ventricular beats in ambulatory patients.

The characteristics of premature ventricular beats predisposing to ventricular tachycardia or fibrillation were assessed by 24-h ambulatory monitoring and maximal treadmill exercise testing in 339 cardiac patients with premature ventricular beats. Premature ventricular beats were divided into early (Q-premature ventricular beat less than QT), late (within the last 20% of the cardiac cycle), and midcycle. Ventricular tachycardia was recorded in 45 patients and ventricular fibrillation, in three. The frequency of ventricular tachycardia or fibrillation was 32% in patients with late, 16% in patients with early, and 7% in patients with midcycle premature ventricular beats (P less than 0.05). Patients with frequent (less than 10/min) multiformed premature ventricular beats had a frequency of ventricular tachycardia or fibrillation of 44%, while only 13% of patients with frequent uniformed premature ventricular beats had ventricular tachycardia (P less than 0.05). Ambulatory patients with ventricular tachycardia or fibrillation have frequent multiformed premature ventricular beats, and the ventricular tachycardia or fibrillation is usually triggered by late premature ventricular beats.     

QT dispersion and early arrhythmic risk in acute myocardial infarction

BACKGROUND: This study sought to find out QT dispersion in healthy individuals and patients of acute myocardial infarction and to find correlation, if any, between QT dispersion and the incidence of ventricular arrhythmias in acute myocardial infarction. METHODS AND RESULTS: QT dispersion was calculated from a 12-lead electrocardiogram in 100 patients of acute myocardial infarction admitted in intensive coronary care unit and 100 age- and sex-matched healthy individuals. In patients of acute myocardial infarction, QT dispersion was calculated on admission, 24 hours after admission and at the time of discharge from intensive coronary care unit. Average QT dispersion in acute myocardial infarction was found to be significantly higher on admission (76.4 +/- 18.3 ms), 24 hours after admission (62.88 +/- 17.52 ms) and at the time of discharge from intensive coronary care unit (51.79 +/- 16.79 ms) than in healthy individuals (29.76 +/- 6.06 ms; p<0.05). QT dispersion was found to be significantly increased in patients of acute myocardial infarction with ventricular arrhythmias (82.06 +/- 16.86 ms) than in those without (66.75 +/- 16.28 ms; p<0.01). Patients of acute myocardial infarction with ventricular tachycardia or ventricular fibrillation had significantly increased QT dispersion (96.25 +/- 15.97 ms) than those who had only ventricular premature beats (80 +/- 15.04 ms; p<0.01). QT dispersion was found to be significantly greater in patients with anterior wall acute myocardial infarction (79.80 +/- 18.19 ms) than in those with inferior wall acute myocardial infarction (71.9 +/- 17.48 ms; p<0.05). At the time of discharge from intensive coronary care unit no statistically significant difference was found in QT dispersion in those who received thrombolysis (51.58 +/- 16.05 ms) and those who did not (48.18 +/- 14.68 ms; p>0.05). QT dispersion was found to be significantly higher in those who died (88.66 +/- 15.97 ms) than in those who survived (74.23 +/- 17.91 ms; p<0.05). QT dispersion was significantly higher in ventricular arrhythmic deaths (97.14 +/- 17.04 ms) than those who had non-arrhythmiac deaths (81.25 +/- 11.25 ms; p<0.05). CONCLUSIONS: Interlead QT variation and its measure as QT dispersion challenges our current approach to the electrocardiographic assessment of arrhythmic risk. QT dispersion may provide a potentially simple, cheap, non-invasive method of measuring underlying dispersion of ventricular excitability.     

Cardiac arrest caused by undersensing of a temporary epicardial pacemaker

The R-on-T phenomenon is a well-known entity that predisposes to dangerous arrhythmias. Typically, a premature ventricular complex occurring at the critical time during the T wave of the preceding beat precipitates ventricular tachycardia and fibrillation. This phenomenon can occur not only in asynchronous ventricular pacemakers, but also in synchronous pacemakers, if loss of sensing of the intrinsic rhythm becomes evident. A patient who was fitted with a temporary epicardial wire, following cardiac surgery and experienced repeated episodes of polymorphic ventricular tachycardia caused by the R-on-T phenomenon, is described.     

Twenty-four-hour electrocardiographic study in the active very elderly

Cardiac rhythm was studied by means of 24-hour ambulatory ECG in 18 active outpatients, mean age 92.3 +/- 2.3 years. The main characteristics observed were the following: a broad dynamic heart rate range; relatively rare atrial fibrillation (5.5%); incidence of simple atrial and ventricular premature beats, complex atrial premature beats or supraventricular tachycardia in all subjects, while ventricular tachycardia and R-on-T phenomenon were present in only one subject. The 'arrhythmic normality' parameters in the very elderly probably need to be revised, and only severe ventricular arrhythmias appear to be an abnormal phenomenon.     

Dynamics of QT dispersion in acute myocardial infarction

BACKGROUND: We studied the dynamics of QT dispersion in patients with acute myocardial infarction, and compared them with those in controls. METHODS AND RESULTS: Serial electrocardiograms of patients admitted to our institute with acute myocardial infarction were analyzed for QT dispersion, and compared with those of healthy age- and sex-matched controls. QT dispersion from 12 leads was measured as maximum QT minus minimum QT interval in ms. The mean QT dispersion of 114 +/- 29.6 ms was significantly higher in patients with acute myocardial infarction on admission as compared to 51.45 +/- 5.56 ms in controls (p < 0.001). QT dispersion showed a dynamic change in patients with acute myocardial infarction who were thrombolyzed, being 109.11 +/- 5.77 ms, 87.59 +/- 5.88 ms, 75.89 +/- 18.33 ms, and 68.20 +/- 12.66 ms on admission, post-thrombolysis, and on days 3 and 7, respectively. During a similar time period, nonthrombolyzed patients showed a QT dispersion of 132.38 +/- 36.04 ms, 130.47 +/- 34.42 ms, 111.11 +/- 24.94 ms, and 106.25 +/- 27.64 ms, respectively: the difference between the 2 groups at all periods was significant (p < 0.01). Mean QT dispersion values in patients who developed ventricular tachycardia or ventricular fibrillation were significantly higher than in patients who did not develop ventricular tachycardia or ventricular fibrillation (p < 0.01). CONCLUSIONS: Mean QT dispersion is significantly increased after acute myocardial infarction, and shows a dynamic decrease with time, the difference being more marked in thrombolyzed patients. Mean QT dispersion levels are higher in patients with ventricular tachycardia and ventricular fibrillation compared to patients with acute myocardial infarction without these arrhythmias. The changes in QT dispersion are dynamic, and it may serve as a non-invasive marker of susceptibility to malignant ventricular arrhythmias.