ECG signs mimicking acute inferior wall myocardial infarction are associated with elevated myocardial enzymes during isolation of pulmonary vein for focal atrial fibrillation.

In this study, we report an intraprocedural incident in patients undergoing ablation for atrial fibrillation. During left atrial manipulation our patients suffered from acute chest pain, showed ECG signs of an acute inferior wall myocardial infarction, and increased levels of cardiac Troponin I (cTnI). We strongly recommend being aware of unexpected reactions during isolating pulmonary veins for focal atrial fibrillation, especially when passing the dorsal part of the left atrium. If pericardial effusion is ruled out and ECG signs as well as symptoms disappear, the ablation procedure should proceed. We think patients undergoing pulmonary vein ablation for atrial fibrillation should be informed of this threatening complication.     

Early atrial fibrillation during evolving myocardial infarction: a consequence of impaired left atrial perfusion

Seven of 214 patients (3%) with acute myocardial infarction (120 inferior and 94 anterior) developed atrial fibrillation within 3 hr of the onset of chest pain. All seven patients had an inferior infarction and in all seven the left circumflex artery was occluded proximal to the origin of its left atrial circumflex branch. In five patients this occlusion was acute and was the cause of inferior infarction and in the remaining two patients the occlusion was old and the inferior infarction was due to an acute occlusion of the right coronary artery that also supplied extensive collaterals to the previously occluded left circumflex artery. All seven patients also had impaired perfusion to the atrioventricular nodal artery, as evidenced by total occlusion proximal to its origin or by stenosis proximal to its origin associated with second- or third-degree atrioventricular block. In contrast, early atrial fibrillation did not occur in any of the 18 patients with inferior myocardial infarction due to acute occlusion of the distal left circumflex artery or in any of the five patients with inferior infarction due to acute occlusion of the proximal left circumflex artery if perfusion to the atrioventricular nodal artery was not impaired. Early atrial fibrillation did not occur in any of the 90 patients with inferior infarction due to acute occlusion of the right coronary artery, including 12 patients with occlusion proximal to the sinus nodal artery, but without coexistent occlusion of the left circumflex artery.(ABSTRACT TRUNCATED AT 250 WORDS)     

Conduction disturbances and paroxysmal atrial fibrillation during acute inferior myocardial infarction

Associated symptoms and conduction disturbances are reported during acute inferior myocardial infarction. Differentiation of right coronary artery from left circumflex artery occlusion may be difficult since both can present an electrocardiographic pattern of inferior myocardial infarction. Paroxysmal atrial fibrillation is considered a frequent complication of acute myocardial infarction and the patients with paroxysmal atrial fibrillation probably should be targeted for earlier and more aggressive treatment. These patients in the thrombolytic era have a better overall outcome than counterparts in the prethrombolytic era. We describe a case of conduction disturbances and paroxysmal atrial fibrillation in a 51-year-old Italian man with acute inferior myocardial infarction and right coronary artery stenosis.     

Effects of atrial fibrillation on prognosis of acute myocardial infarction

Nine hundred and sixty-nine coronary care patients with acute myocardial infarction were followed for one year. Atrial fibrillation was documented in 107 patients. Compared with patients without atrial fibrillation, those with this arrhythmia were older, had clinically more severe infarction, and had a higher frequency of ventricular fibrillation or tachycardia, and right bundle-branch block. They had similar past histories of ischaemic heart disease and coronary risk factors. Patients with atrial fibrillation had a higher total mortality at 3 months and 12 months. The presence of atrial fibrillation was not associated with any significant increase in mortality within any decade of age or within any subgroup of clinical severity of infarction. The frequency of atrial fibrillation was similar in anterior and inferior infarction. Multiple episodes of atrial fibrillation occurred in 52 patients and episodes usually lasted for over 1 hour. In 50% of patients with single episode of atrial fibrillation the initial ventricular rate was greater than 120 beats per minute.     

Effects of atrial fibrillation on prognosis of acute myocardial infarction.

Nine hundred and sixty-nine coronary care patients with acute myocardial infarction were followed for one year. Atrial fibrillation was documented in 107 patients. Compared with patients without atrial fibrillation, those with this arrhythmia were older, had clinically more severe infarction, and had a higher frequency of ventricular fibrillation or tachycardia, and right bundle-branch block. They had similar past histories of ischaemic heart disease and coronary risk factors. Patients with atrial fibrillation had a higher total mortality at 3 months and 12 months. The presence of atrial fibrillation was not associated with any significant increase in mortality within any decade of age or within any subgroup of clinical severity of infarction. The frequency of atrial fibrillation was similar in anterior and inferior infarction. Multiple episodes of atrial fibrillation occurred in 52 patients and episodes usually lasted for over 1 hour. In 50% of patients with single episode of atrial fibrillation the initial ventricular rate was greater than 120 beats per minute.     

前壁及下壁急性心肌梗死并发心律失常比较分析

目的:比较分析前壁及下壁急性心肌梗死(AMI)后并发心律失常的类型。方法:收集了186例急性心肌梗死患者梗塞后出现的各种心律失常的类型,并作统计分析。结果:①前壁心梗后窦速和室内传导阻滞发生率显著高于下壁心梗(P分别<0.05,<0.01),而下壁心梗后窦缓及房室传导阻滞发生率显著高于前壁心梗(P均<0.01)。②下壁心梗并发房性及室性异位节律(未包括室颤)均显著高于前壁心梗(P均<0.05)。结论:前壁心梗及下壁心梗并发心律失常的类型有差别:前者以窦速和室内传导阻滞较常见,后者以窦缓、房室传导阻滞及房室异位心律常见。     

右室心肌梗死对急性下壁心肌梗死临床特征和预后的影响

目的：分析右室心肌梗死(心梗)对急性下壁心梗临床特征和预后的影响。方法：比较急性单纯性下壁心梗(第一组)和急性下壁心梗合并右室心梗(第二组)两组患的临床特征和院内病死率。结果：共176例患符合入选条件，第一组115例，第二组61例。第一组低血压、快速心律失常(包括阵发性室上性心动过速，阵发性心房颤动，领发室性早搏，室性心动过速，心室纤颤等)、缓慢心律失常(包括窦性心动过缓，房室传导阻滞)、心功能不全的发生率和院内病死率显低于第二组(P＜0．05)。静脉溶栓、急诊PTCA和未行再灌注治疗的院内病死率在第一组的分别为3．23％，3．33％和29．17％，在第二组分别为9．25％，13．04％和82．35％。结论：当急性下壁心梗合并右室心梗时，患的临床表现更为严重，院内病死率增高。积极行溶栓或急诊PTCA治疗，可显降低其院内病死率.     

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.     

Lasso环状标测电极导管指导心房颤动持续过程中心脏大静脉电隔离

目的:报道2例心房颤动(房颤)持续过程中Lasso环状标测电极导管(Lasso电极)指导心脏大静脉 (大静脉)电隔离治疗。方法:2例患者临床症状和心电图记录提示分别为阵发性房颤(PAF)和持续性房颤。经股静脉和颈内静脉穿刺置入右心室和冠状静脉窦电极导管,并行房间隔穿刺和选择性大静脉造影。置入10极 Lasso电极进行大静脉标测。应用普通温控消融导管以局部异常电活动相对最早或频率最快、最紊乱处开始消融,在房颤持续过程中电隔离大静脉至左房连接处,以房颤终止和异常电活动消失或后者与心房电活动无关为消融终点。结果:2例患者共消融7条大静脉。1例PAF患者完成上腔静脉(SVC)和右上肺静脉(RSPV)电隔离后,消融左上肺静脉(LSPV)过程中房颤终止。另1例持续性房颤患者完成SVC、RSFV、LSPV及右下肺静脉电隔离,加做左房峡部、三尖瓣-下腔静脉峡部线性消融后,同步电复律使房颤转为窦性心律。随访1年,无房颤复发和相关并发症。结论:Lasso电极指导下应用普通温控消融导管可于心房颤动持续过程中电隔离大静脉而治疗房颤。     

Can short-long-short sequences predict atrial fibrillation in acute inferior myocardial infarction?

Short-long-short sequences (SLSS), related to atrial ectopic beats (AEBs), predict the recurrence of atrial fibrillation (AF) in some clinical situations. We investigated whether SLSS predict the occurrence of AF in acute phase of inferior myocardial infarction (MI). In patients who developed AF AEBs were more frequent. We concluded that the presence of frequent SLSS could be predictors or preceding factors of the occurrence of AF in acute inferior MI.     

Etiology and pathogenesis of thromboembolism.

Thrombus formation in the left atrium and left ventricle is primarily due to stasis of blood which causes activation of the coagulation system. Migration of thrombotic material into the circulation depends on the dynamic forces of the circulation. Atrial fibrillation is the commonest underlying cardiac disorder predisposing to thromboembolism. Rheumatic mitral stenosis, left atrial enlargement, prior myocardial infarction, hypertension, and echocardiographic left ventricular hypertrophy are risk factors for thromboembolic stroke in elderly patients with chronic atrial fibrillation. Non-valvular atrial fibrillation accounts for 45% of cardiac sources of thromboembolic stroke and includes patients with ischemic heart disease, hypertension, thyrotoxic heart disease, hypertrophic cardiomyopathy, chronic sinoatrial disorder, and idiopathic atrial fibrillation. 15% of cardiac sources of thromboembolic stroke are associated with acute myocardial infarction, 10% with left ventricular aneurysm and mural thrombi remote from an acute myocardial infarction, 10% with rheumatic valvular heart disease, and 10% with prosthetic cardiac valves. Mitral valve prolapse, mitral annular calcium, nonischemic cardiomyopathies, infective endocarditis, nonbacterial thrombotic endocarditis, left atrial myxoma, paradoxical embolism associated with congenital heart disease, calcific aortic stenosis, and complex atherosclerotic plaque within the proximal aorta also contribute to thromboembolism.     

Right atrial infarction, atrial arrhythmia and inferior myocardial infarction form a missed triad: a case report and review of the literature

Atrial infarction is rarely diagnosed before death because of its characteristically subtle and nonspecific electrocardiographic findings. These findings may be overshadowed by changes associated with concomitant ventricular infarction. A case of right atrial infarction accompanied by inferior myocardial infarction with rapid decompensated atrial fibrillation is reported. To increase awareness and knowledge of a complicated diagnosis, the present case is described in the context of a review of the relevant literature.     

Right ventricular infarction: unusual electrocardiographic and electrophysiological manifestations

Right ventricular infarction occurs in 19-43% of patients with acute inferior wall infarction (Lorell et al., 1979). Its clinical, hemodynamic, and anatomic features are well known and include associated inferior wall infarction, distended neck veins, clear lung fields, hypotension, and heart block (Cintron et al., 1981; Coma-Canella et al., 1979; Lloyd et al., 1981; Lopez-Sendon et al., 1981; Raabe and Chester, 1978; Rotman et al., 1974). Isolated right ventricular infarction is less frequent and occurs in 2.5-4.6% of autopsy studies of myocardial infarction (Cohn et al., 1974; Erhardt et al., 1976; Wartman and Hellerstein, 1948). This report describes a patient with isolated right ventricular infarction with unusual electrophysiological findings. Her initial electrocardiogram showed atrial escape rhythm with incomplete right bundle-branch block and left posterior hemiblock. Later, she developed atrioventricular (AV) block with supra- and infra-Hisian, "phase 4," conduction defects. The sinus malfunction and high degree AV block persisted over 2 weeks and an atrioventricular sequential pacemaker was implanted. Hymodynamic study showed that her cardiac output was highly dependent on the heart rate and properly timed AV interval, and the pacemaker was programmed accordingly.     

Incidence and significance of pericardial effusion in acute myocardial infarction as determined by two-dimensional echocardiography

To determine the incidence and clinical significance of pericardial effusion after acute myocardial infarction, two-dimensional echocardiography was serially performed in 66 consecutive patients. Pericardial effusion was observed in 17 (26%); the effusion was small in 13 patients, moderate in 3 and large with signs of cardiac tamponade in 1. In this patient, two-dimensional echocardiography strongly suggested myocardial rupture. The observation of pericardial effusion was not associated with age, sex, previous myocardial infarction, atrial fibrillation or treatment with heparin. It was more often a complication of anterior than of inferior acute infarction. Patients with pericardial effusion had higher peak levels of creatine kinase and lactic dehydrogenase and a higher wall motion score index. More patients with pericardial effusion had congestive heart failure or ventricular arrhythmias, developed a ventricular aneurysm or died within 1 year after their infarction. In conclusion, pericardial effusion is frequently visualized by two-dimensional echocardiography after acute myocardial infarction and its presence is associated with an increased occurrence of complications and cardiac death.     

Ventricular and supraventricular arrhythmias in clinically silent right ventricular infarction

To study the relationship between clinically silent right ventricular infarction and the incidence of a-v block, atrial and ventricular arrhythmias, 100 patients with inferior wall myocardial infarction underwent equilibrium gated radioisotopic angiocardiography. Fifty-four of them had radioisotopic evidence of right ventricular involvement and 43 (80%) of them had a-v block and/or supraventricular arrhythmias during the acute phase of the infarct, while only 10 (22%) of the 46 patients without right ventricular involvement did. As regards the incidence of ventricular tachyarrhythmias, 14 (26%) patients with right ventricular involvement had ventricular tachycardia and/or fibrillation, while only one patient without right ventricular involvement had ventricular tachycardia, and no patients had ventricular fibrillation. Moreover, V4R-precordial lead showed a sensitivity in predicting the risk of developing a-v block/supraventricular arrhythmias and ventricular tachyarrhythmias of 0.84 and 0.79, respectively. Therefore, right ventricular involvement should be suspected when atrial arrhythmias, a-v block and ventricular tachyarrhythmias are found in early acute inferior wall myocardial infarction. On the other hand, when right precordial lead V4R in early acute inferior infarction shows ST-elevation and/or a QS pattern, the sudden occurrence of these arrhythmias should be suspected, and possibly prevented.     

Role of the renin-angiotensin-aldosterone system in atrial fibrillation and cardiac remodeling

PURPOSE OF REVIEW: This review summarizes recent clinical trial evidence showing a reduction in the development and recurrence of atrial fibrillation with angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor-blocking agents (ARBs). It then explores the possible mechanisms for this effect based on current animal models and limited human study. RECENT FINDINGS: Post hoc analyses of trials in patients with heart failure, hypertension, or myocardial infarction have observed reductions in atrial fibrillation among patients treated with ACE inhibitors or ARBs. Recent studies of these agents in animal models of atrial fibrillation suggest that they may prevent atrial fibrillation by reversing the cardiac structural and electrical changes, known as cardiac remodeling, that lead to the development of atrial fibrillation. This concept is also supported by two prospective studies showing that ACE inhibitors and ARBs prevent the recurrence of atrial fibrillation after electrical cardioversion. SUMMARY: Inhibition of the renin-angiotensin-aldosterone system is a novel concept for the treatment of atrial fibrillation that may target the underlying substrate of atrial fibrillation. Further human research is required to determine whether ACE inhibitors and ARBs prevent atrial fibrillation, and if so, whether this is a result of blood pressure lowering alone or a specific effect of these agents. Ongoing research will establish whether ACE inhibitors or ARBs have specific benefits in patients with atrial fibrillation.     

Auricular fibrillation in myocardial infarct]

Auricular fibrillation was observed in 17.8% of patients with large-focal myocardial infarction, mainly in females (p 0.01). The localization of myocardial infarction had no impact on the incidence of auricular fibrillation. The precursors of auricular fibrillation included atrial extrasystoli and an elevated electrolyte coefficient of the blood NaeKe. In the group of patients with myocardial infarction and auricular fibrillation mortality was more common among the females. Auricular fibrillation developing beyond the first postinfarction day worsened the prognosis considerably. The outcome of myocardial infarction did not much depend on the duration of auricular fibrillation and on the cardiac contraction frequency.     

Pulmonary vein dimensions and variation of branching pattern in patients with paroxysmal atrial fibrillation using magnetic resonance angiography

Pulmonary veins are the most frequent origin of focal and paroxysmal atrial fibrillation. Although radiofrequency ablation has been attempted for the treatment of focal and paroxysmal atrial fibrillation, the anatomy of the pulmonary vein is still not fully understood. To investigate the dimensions and anatomical variation of the pulmonary vein in patients with paroxysmal atrial fibrillation, we performed breath-hold gadolinium enhanced magnetic resonance (MR) angiography using a 1.5 T cardiac MR imager (GE CV/i) in 32 patients with paroxysmal atrial fibrillation (61 +/- 8 years old), 11 patients with chronic atrial fibrillation (64 +/- 9 years old), and 26 patients with normal sinus rhythm (55 +/- 15 years old). Three dimensional images of the pulmonary veins were thus obtained, and the diameters of the most proximal portion of the left or right superior pulmonary vein and left or right inferior pulmonary vein were measured. Pulmonary vein branching variations were determined by a visual qualitative analysis by two separate readers' agreements, who were blinded to any clinical information. We focused on the existence of a complex-branching pattern draining into the orifice of four pulmonary veins. Patients with either paroxysmal atrial fibrillation or chronic atrial fibrillation showed larger superior pulmonary veins than those with normal sinus rhythm (mean +/- SD; in the left superior pulmonary vein, 20 +/- 3 mm, 23 +/- 3 mm vs 16 +/- 3 mm, P < 0.05; in right superior pulmonary vein, 19 +/- 4 mm, 19 +/- 2 mm vs 16 +/- 2 mm, P < 0.05). Complex-branching pattern was frequently observed in inferior pulmonary veins in patients with either paroxysmal atrial fibrillation or chronic atrial fibrillation; 25/32 patients with paroxysmal atrial fibrillation, 11/11 patients with chronic atrial fibrillation, compared to 7/26 patients with normal sinus rhythm. Complex-branching patterns were not observed in superior pulmonary veins in any patients in this cohort. CONCLUSION: In patients with paroxysmal atrial fibrillation or chronic atrial fibrillation, significant pulmonary vein dilation occurred mainly in the superior pulmonary veins, while a complex-branching pattern was frequently observed in the inferior pulmonary veins. These MR angiographic findings might be useful when performing radiofrequency ablation procedures and catheter manipulation for the treatment of paroxysmal atrial fibrillation.     

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.     

Subclinical atherosclerosis and risk of atrial fibrillation: the rotterdam study

BACKGROUND: Myocardial infarction is an important risk factor for atrial fibrillation, but the role of subclinical atherosclerosis is unknown. This longitudinal study evaluates whether atherosclerosis affects the risk of atrial fibrillation in persons without overt coronary disease. METHODS: This investigation was part of the Rotterdam Study, a population-based cohort study among persons 55 years or older. Participants with atrial fibrillation at baseline, with a history of myocardial infarction, or with angina pectoris and those who had undergone cardiac operative procedures were excluded, leaving 4407 subjects for the analyses. Baseline intima-media thickness of the common carotid artery and the presence of carotid plaques were used as indices of generalized atherosclerosis. During a median follow-up of 7.5 years, 269 cases of incident atrial fibrillation were identified. Relative risks were calculated with 95% confidence intervals, adjusted for age and sex, using the Cox proportional hazards model. Additional adjustments were made for body mass index, hypertension, systolic blood pressure, serum cholesterol level, smoking, diabetes mellitus, left ventricular hypertrophy on the electrocardiogram, and the use of cardiac medication. RESULTS: The risk of atrial fibrillation was associated with carotid intima-media thickness (relative risk, 1.90; 95% confidence interval, 1.20-3.00, highest vs lowest quartile) and severity of carotid plaques (relative risk, 1.49; 95% confidence interval, 1.06-2.10, severe vs absence). Risk estimates were stronger in women than in men. CONCLUSIONS: Atherosclerosis in participants without manifest atherosclerotic disease is an independent risk factor for atrial fibrillation. These results suggest that aggressive treatment of asymptomatic atherosclerosis may help to prevent atrial fibrillation.