Acute myocardial infarction promptly complicated by atrial fibrillation during Holter recording]

We observed, during Holter recording, a case of inferior acute myocardial infarction complicated by paroxystic hyperkinetic atrial fibrillation, which occurred 12 min after the onset of acute irreversible myocardial ischemia. The atrial fibrillation was preceded by a complex pattern of hyperkinetic supraventricular arrhythmias characterized by single premature supraventricular beats, paired premature supraventricular beats and many runs of paroxystic supraventricular tachycardia. The most plausible hypothesis is that atrial fibrillation and the preceding arrhythmic pattern have been due to an extension of ischemia from ventricular to atrial myocardium.     

The incidence and timing of major arrhythmias following successful primary angioplasty for acute myocardial infarction.

BACKGROUND: The potential benefits of direct percutaneous transluminal coronary angioplasty (PTCA) on malignant arrhythmias in the hospital phase of acute myocardial infarction have not yet been established. METHODS: We prospectively investigated the incidence and timing of major arrhythmias occurring during direct PTCA and within 24 hours of mechanical reperfusion in 90 consecutive patients with acute myocardial infarction undergoing successful direct PTCA within 12 hours of symptom onset. RESULTS: Ventricular fibrillation and complete atrioventricular block occurred exclusively during direct PTCA and both resolved in the catheterization laboratory. Holter monitoring showed that ventricular tachyarrhythmias, such as runs of more than 3 extrasystoles, were detectable only during the first 8 hours after direct PTCA. CONCLUSIONS: In our group of patients undergoing successful direct PTCA, no in-hospital life-threatening arrhythmias occurred after this procedure.     

Electrophysiologic actions and antifibrillatory efficacy of subacute left stellectomy in a conscious, post-infarction canine model of ischemic ventricular fibrillation

The autonomic nervous system appears to modulate ventricular arrhythmias associated with acute myocardial ischemia. This study investigated the electrophysiologic effects and antifibrillatory actions of subacute left stellectomy in a conscious, post-infarction canine model of sudden cardiac death. Twenty-two dogs with a previous anterior wall myocardial infarction and inducible ventricular arrhythmias were randomized to undergo either left stellectomy (n = 12) or remain as sham-denervated controls (n = 10). Five to 7 days post left stellectomy, there were no significant changes in heart rate, electrocardiographic intervals or ventricular refractoriness compared to sham-denervated controls. Acute posterolateral ischemia was produced in left stellectomy and sham-denervated dogs by anodal current-induced thrombosis via a previously positioned electrode in the left circumflex coronary artery. Ventricular fibrillation developed within 1 hour of the onset of ischemia (early ventricular fibrillation) in 3/12 (25%) left stellectomy dogs versus 8/10 (80%) sham-denervated controls (P less than 0.05). However, 24-hour mortality rate was 5/12 (42%) after left stellectomy versus 8/10 (80%) after sham denervation (P = 0.072). Small differences in regional myocardial norepinephrine content, which is a marker for neuronal integrity, occurred in the mid-posterolateral and mid-anteroseptal regions of the left ventricle after left stellectomy. Overall norepinephrine concentration after left stellectomy was 409.70 +/- 9.90 ng/g vs 428.07 +/- 10.84 ng/g in sham controls (P = NS). In summary, subacute left stellectomy significantly reduces the incidence of ventricular fibrillation occurring within 1 hour of the onset of acute posterolateral ischemia at a distance to a previous myocardial infarction in conscious dogs, and tends to reduce the ischemic post-infarction mortality at 24 hours after the onset of ischemia. This protective effect of left stellectomy is not due to any alteration in cardiac electrophysiologic parameters measured prior to the development of acute posterolateral ischemia, nor is it related to regional denervation as determined by myocardial tissue concentration of residual norepinephrine.     

Carbon monoxide and lethal arrhythmias in conscious dogs with a healed myocardial infarction

Environmental studies suggested that exposure to carbon monoxide (CO) increases cardiovascular mortality among patients with coronary artery disease. We investigated whether, in dogs with a healed anterior myocardial infarction at low and high risk for ventricular fibrillation, acute exposure to CO has adverse effects during acute myocardial ischemia combined with exercise. One month after myocardial infarction, 17 dogs had ventricular fibrillation and 16 survived during the combined exercise and ischemia test. These tests were then repeated in all dogs with different concentrations of carboxyhemoglobin (COHb) (from 5% to 15%). With 15% COHb, heart rate (HR) at rest and during exercise was higher (p less than 0.05) than in the control tests. Surprisingly, the reflex HR response to acute ischemia was also altered; namely, the HR reduction characteristic of the low-risk animals was anticipated and accentuated (-31 +/- 25 versus 2 +/- 30 beats/min, p less than 0.05). Conversely, the HR increase characteristic of the high-risk group was reduced by CO (44 +/- 52 versus 72 +/- 43 beats/min, p less than 0.05). With 15% COHb, malignant arrhythmias occurred in two of the low-risk dogs and in none of the high-risk dogs. In the latter, CO was tested with a combination of exercise work load and myocardial ischemia duration not associated with ventricular fibrillation (VF) in the control condition. This study demonstrated that brief exposure to CO (1) profoundly alters the reflex HR response to exercise and to acute myocardial ischemia and (2) does not enhance the occurrence of malignant arrhythmias in conscious dogs with a healed myocardial infarction.     

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.     

Evolution of late potential activity in the first six weeks after acute myocardial infarction

The evolution of surface ventricular late potential activity was studied in 50 patients during the 6 weeks after first acute myocardial infarction (AMI). In 15 of 47 patients (32%) late potential activity appeared within 6 hours of the onset of major symptoms. Its prevalence overall remained approximately 30% at each recording time but with marked individual variability in appearance. Late potential activity was associated with late ventricular arrhythmias (greater than 24 hours after AMI) but not with early ventricular arrhythmias (less than 24 hours after AMI). Late ventricular arrhythmias or sudden death occurred only in the 6 patients with late potential activity (p less than 0.05). Early ventricular fibrillation (15 patients) occurred equally in the patients with and without late potential activity. Thus, late potential activity occurs at some stage in the first 6 weeks after AMI in 50% of patients, but its timing is variable. It is a sensitive but not specific predictor of late ventricular arrhythmias and sudden death, but not of early ventricular fibrillation.     

Holter monitoring of ventricular arrhythmias in a randomised, controlled study of intravenous streptokinase in acute myocardial infarction

The occurrence of ventricular arrhythmias attributed to streptokinase treatment in acute myocardial infarction is not well defined. Holter monitoring was performed for 24 hours in 81 patients with suspected acute myocardial infarction randomised in a ratio of 2:1 to intravenous streptokinase 1.5 x 10(6) IU (n = 55) or placebo infusion (n = 26) 6.7 hours (mean) after the onset of symptoms. No episodes of ventricular fibrillation were recorded. For the whole 24 hour period and during the first three hours after the start of treatment the incidence and frequency of ventricular arrhythmias were similar in the patients randomised to streptokinase and to placebo. But when the results in patients randomised "early" after the onset of symptoms of suspected acute myocardial infarction were analysed separately the frequency of abnormal complexes, pairs, runs, and repetitive arrhythmias seemed to be higher in patients allocated to streptokinase. This may reflect arrhythmias associated with reperfusion.     

Holter monitoring of ventricular arrhythmias in a randomised, controlled study of intravenous streptokinase in acute myocardial infarction.

The occurrence of ventricular arrhythmias attributed to streptokinase treatment in acute myocardial infarction is not well defined. Holter monitoring was performed for 24 hours in 81 patients with suspected acute myocardial infarction randomised in a ratio of 2:1 to intravenous streptokinase 1.5 x 10(6) IU (n = 55) or placebo infusion (n = 26) 6.7 hours (mean) after the onset of symptoms. No episodes of ventricular fibrillation were recorded. For the whole 24 hour period and during the first three hours after the start of treatment the incidence and frequency of ventricular arrhythmias were similar in the patients randomised to streptokinase and to placebo. But when the results in patients randomised "early" after the onset of symptoms of suspected acute myocardial infarction were analysed separately the frequency of abnormal complexes, pairs, runs, and repetitive arrhythmias seemed to be higher in patients allocated to streptokinase. This may reflect arrhythmias associated with reperfusion.     

The effects of practolol on the dysrhythmias complicating acute ischemic heart disease

The cardioselective beta-adrenoceptor blocking agent practolol was used in the management of ventricular and supraventricular dysrhythmias associated with acute myocardial Infarction in 134 patients, and in the management of these dysrhythmias in 19 patients with acute myocardial ischemia. Practolol was frequently effective in controlling ventricular dysrhythmias which occurred within the first 24 hours after the onset of symptoms of acute myocardial infarction. It was also effective in controlling the ventricular dysrhythmias which occurred after resuscitation from ventricular fibrillation. It was of particular value when therapeutic doses of lidocaine had been ineffective. Practolol was much less effective in controlling ventricular dysrhythmias which occurred more than 24 hours after acute infarction. Atrial fibrillation and atrial flutter were infrequently abolished by practolol in undigitalized patients after acute myocardial infarction. There was no correlation between the effectiveness of practolol and the blood concentration of the drug. One adverse effect of practolol was the occurrence of sinus bradycardia with or without an increase in the frequency of ventricular ectopic beats. Bradycardia was sometimes accompanied by hypotension. Severe hypotension occasionally occurred in the absence of bradycardia.     

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.     

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.     

Spontaneous and electrically induced ventricular arrhythmias during acute ischemia superimposed on 2 week old canine myocardial infarction

The arrhythmogenic effect of acute reversible myocardial ischemia before and 2 weeks after experimental myocardial infarction was investigated in 37 dogs that underwent reversible 10 min occlusion of the first major marginal branch of the left circumflex coronary artery. Subsequently, 24 of the dogs underwent experimental myocardial infarction with permanent left anterior descending coronary ligation, and 13 dogs served as sham-operated controls. Two weeks later, an open chest programmed electrical stimulation was performed in the 13 sham-operated and 24 postinfarction dogs to determine its accuracy in predicting the ventricular arrhythmias that develop during a subsequent episode of acute reversible ischemia. After programmed electrical stimulation, the left circumflex marginal branch was reversibly occluded for 10 min at the same site. The incidence of spontaneous ventricular fibrillation during reversible left circumflex marginal coronary occlusion did not differ from the first to the second study in sham-operated dogs, whereas in the postinfarction dogs, it increased from 13% before infarction to 54% after infarction (p = 0.005). The outcome of programmed electrical stimulation predicted spontaneous ventricular arrhythmias during coronary occlusion in only 21% of the postinfarction dogs. The accuracy of programmed electrical stimulation was 42% and its predictive value was 47% in detecting the dogs with spontaneous ventricular fibrillation. Regional myocardial blood flow measurements by microsphere technique identified the severity of reversible ischemia in the infarct border and periinfarction zones as a correlate of spontaneous ventricular fibrillation during coronary occlusion. In contrast, total infarct size correlated with electrically induced but not with spontaneous ventricular arrhythmias.     

Late clinical outcome in patients with early ventricular fibrillation after myocardial infarction

Whether ventricular fibrillation occurring within 48 h after acute myocardial infarction is associated with particular clinical features and poor prognosis, especially in patients with anterior myocardial infarction, is still debated. Therefore, clinical variables and in-hospital and 1 year mortality rates were analyzed in 2,088 patients, aged 18 to 95 years (mean +/- SD 64 +/- 12), admitted to the hospital with acute myocardial infarction between 1979 and mid 1984. One hundred forty-seven patients (7%) had at least one episode of ventricular fibrillation occurring within 48 h of hospital admission. Of these, 25% died during their initial hospitalization compared with 13% of patients without early ventricular fibrillation (p less than 0.001). In greater than 50% of patients with early ventricular fibrillation, the immediate cause of death was left ventricular failure or cardiogenic shock. In contrast, the 1 year mortality rate after hospital discharge was not significantly greater in patients with than in those without early ventricular fibrillation (15 versus 11%, respectively), particularly in the subgroup of patients with anterior myocardial infarction in which the mortality rate tended to be lower in patients with early ventricular fibrillation (8 versus 14%, respectively). Similar mortality results were found when only primary (not associated with left ventricular failure) ventricular fibrillation was analyzed. The left ventricular ejection fraction and the incidence of complex ventricular arrhythmias from 24 h ambulatory electrocardiographic monitoring obtained at hospital discharge were not different in survivors with or without early ventricular fibrillation (0.45 +/- 0.13 versus 0.49 +/- 0.14 and 41 versus 41%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

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.     

Effects of verapamil on ventricular rhythm during acute coronary occlusion

The effects of verapamil on electrophysiologic parameters of the ventricle were studied during acute coronary occlusion in anesthetized open-chest dogs. Those parameters measured in the study were idioventricular automaticity, ventricular conduction, and fibrillation threshold. The incidence of rapidly repetitive beats and fibrillation induced by two successive premature beats was also studied. Verapamil significantly decreased idioventricular automaticity (in five dogs), improved conduction through the ischemic area (in six dogs), and increased fibrillation threshold of the ischemic ventricular (in eight dogs). The drug was effective in abolishing rapidly repetitive beats and fibrillation induced by closely coupled premature beats during acute coronary occlusion. Rapidly repetitive beats occurred in nine out of 15 dogs and these repetitive beats were degenerated into fibrillation in seven dogs before verapamil. Following pretreatment with the drug, rapidly repetitive beats and fibrillation occurred in none of the 15 dogs. The results indicate that verapamil can be very effective against ventricular arrhythmias occurring in association with myocardial infarction.     

急性心肌梗死直接冠状动脉成形术后再灌注心律失常分析

目的 分析急性心肌梗死直接冠脉成形术后严重再灌注心律失常发生的状况，探讨其预防和紧急治疗方法。方法 行直接经皮冠状动脉成形术的急性心肌梗死患者245例，根据梗死相关动脉分成三组，LAD组：126例；RCA组：97例；LCX组：22例。统计各组经皮冠状动脉成形术后再灌注心律失常发生的状况。结果 共151例患者发生严重的再灌注心律失常，发生率为61．6％；加速性室性自主心律发生率最高(22．0％)，与梗死相关动脉无关；其次是室性早搏(19．2％)，以LAD组最高(27．8％)。RCA组缓慢性心律失常(窦缓、窦性停搏、高度房室传导阻滞)发生率(35．1％)显著高于LAD组(3．9％)和ICX组(22．7％)：LCX组各种再灌注心律失常发生率界于LAD组和RCA组之间。结论 急性心肌梗死直接冠脉成形术后严重心律失常总的发生率较高，心律失常的类型与梗死相关动脉有明确的相关性。     

The incidence, significance and prognosis of arrhythmias in acute myocardial infarction.

Concepts of the incidence, significance and prognosis of almost all cardiac arrhythmias during acute myocardial infarction have changed greatly in the last 15 years. In some cities facilities are available to reach patients in the very earliest phases of ischaemia or infarction. As previously suspected but now confirmed, ventricular fibrillation occurs commonly at this time and depending on whether ischaemia or infarction is the basis of its occurrence, has a variable long-term prognosis. In the coronary care unit ventricular arrhythmias are more frequent than was originally believed and current research suggests that they have little if any predictive value in defining individuals who would develop ventricular fibrillation. Such events, however, appear related to the severity of myocardial or coronary artery disease. Similarly, asystole and heart block in acute myocardial infarction are important causes of mortality through their association with severe underlying disease. Other cardiac arrhythmias are not infrequent in acute myocardial infarction. They may carry an immediate prognostic implication for the patient but rarely have long-term implications. Autonomic nervous system disturbances may underlie many arrhythmias occurring particularly in the earliest phases of infarction.     

Coronary artery revascularization in patients with sustained ventricular arrhythmias in the chronic phase of a myocardial infarction: effects on the electrophysiologic substrate and outcome

OBJECTIVES: The objective of this study was to analyze the influence of coronary artery revascularization in patients with ventricular arrhythmias. BACKGROUND: Coronary artery revascularization is an effective treatment for myocardial ischemia; however, its effect on ventricular arrhythmias not related to an acute ischemic event has not been carefully studied. METHODS: Sixty-four patients (58 men, mean age 65 +/- 8 years old) with prior myocardial infarction, spontaneous ventricular arrhythmias not related to an acute ischemic event (55 ventricular tachycardia, 9 ventricular fibrillation) and coronary lesions requiring revascularization were studied prospectively. Electrophysiological study was performed before and after revascularization, and events during follow-up were analyzed. RESULTS: At initial study 61 patients were inducible into sustained ventricular arrhythmias. After revascularization, in 62 survivors, 52 out of 59 patients previously inducible were still inducible (group A), and 10 patients were noninducible (group B). No differences were found in clinical, hemodynamic, therapeutic and electrophysiological characteristics between both groups. During 32 +/- 26 months follow-up, 28/52 patients in group A (54%) and 4/10 patients in group B (40%) had arrhythmic events (p = 0.46). An ejection fraction <30% predicted recurrent arrhythmic events (p = 0.02), but not the presence of demonstrable ischemia before revascularization (p = 0.42), amiodarone (p = 0.69) or beta-adrenergic blocking agent therapy (p = 0.53). Total mortality was 10% in both groups. CONCLUSIONS: In patients with ventricular arrhythmias in the chronic phase of myocardial infarction, probability of recurrence is high despite coronary artery revascularization, but mortality is low if combined with appropriate antiarrhythmic therapy. Recurrences are related to the presence of a low ejection fraction but not to demonstrable ischemia before revascularization, amiodarone or beta-blocker therapy nor are they the results of electrophysiological testing after revascularization.     

Myocardial infarction related atrial fibrillation: role of endogenous adenosine.

Exogenous administration of adenosine induces atrial fibrillation in up to 7.0% of patients. Animal studies affirm endogenous adenosine released in response to tissue hypoxia may play a mechanistic role in arrhythmias associated with myocardial ischaemia or hypoxia. Therefore, atrial fibrillation occurring early after the acute phase of myocardial infarction involving atrial tissue may be secondary to an excessive accumulation of adenosine that leads to a shortening of atrial refractory period. Early in the course of acute inferior myocardial infarction, two patients (males aged 45 and 68) suffered new onset sustained atrial fibrillation that was abrupt in onset and complicated their clinical management. They were administered 250 mg theophylline as a slow intravenous injection at a rate of 100 mg/min or until conversion to normal sinus rhythm occurred. Both patients converted to normal sinus rhythm within five minutes of the administration of theophylline. In up to 52 hours of continuous ECG monitoring after the theophylline administration the atrial fibrillation did not recur. Neither patient experienced any adverse outcome from theophylline administration. These observations are the first reported in humans or laboratory animals to suggest that atrial fibrillation, presumably due to elevated interstitial atrial concentration of adenosine caused by myocardial ischaemia, can be terminated with an adenosine receptor antagonist. However, the hypothesis that excessive accumulation of endogenous adenosine in atrial tissue may induce atrial fibrillation is well substantiated by other investigators. Thus, A1 adenosine receptor antagonists may prove to be valuable in the management of ischaemia related atrial fibrillation.