BACKGROUND:Regional differences in recovery of tachycardia-induced changes of atrial electrophysiological properties have not been well studied.METHODS AND RESULTS:In the control group (5 dogs), atrial effective refractory period (AERP) and inducibility of atrial fibrillation (AF) were assessed before and every 4 hours for 48 hours after complete atrioventricular junction (AVJ) ablation with 8-week VVI pacing. In experimental group 1 (15 dogs), AERP and inducibility of AF were assessed before and after complete AVJ ablation with 8-week rapid right atrial (RA) pacing (780 bpm) and VVI pacing. In experimental group 2 (7 dogs), AERP and inducibility of AF were assessed before and after 8-week rapid left atrial (LA) pacing and VVI pacing. AERP and inducibility and duration of AF were obtained from 7 epicardial sites. In the control group, atrial electrophysiological properties obtained immediately and during 48-hour measurements after pacing did not show any change. In the 2 experimental groups, recovery of atrial electrophysiological properties included a progressive recovery of AERP shortening, recovery of AERP maladaptation, and decrease of duration and episodes of reinduced AF. However, recovery of shortening and maladaptation of AERP and inducibility of AF was slower at the LA than at the RA and Bachmann's bundle.CONCLUSIONS:The LA had a slower recovery of tachycardia-induced changes of atrial electrophysiological properties, and this might play a critical role in initiation of AF.

BACKGROUNDThe effect of verapamil on long-term tachycardia-induced atrial electrical remodeling has not been reported.METHODS AND RESULTSForty-eight dogs were randomly divided into verapamil and control groups. The dogs in the verapamil group received verapamil 120 mg every day, those in the control group did not receive verapamil. Atrial effective refractory period (AERP), inducibility of atrial fibrillation (AF), and duration of AF were assessed before and after complete atrioventricular junction ablation with 1-day, 1-week, or 6-week rapid atrial pacing (780 bpm). AERP shortening, AERP dispersion, AERP maladaptation, and inducibility of AF after 1-day pacing was significantly attenuated by verapamil. However, verapamil did not have any significant effect on these parameters in the dogs with 1-week or 6-week pacing. Verapamil did not have any significant effect on the conduction velocity in the dogs with 1-day, 1-week, or 6-week pacing. Before rapid atrial pacing, verapamil significantly prolonged the duration of AF. In the dogs with 1-day pacing, the duration of AF measured immediately after termination of pacing was similar between the control and verapamil groups. However, in the dogs with 1-week or 6-week pacing, the duration of AF after pacing was significantly longer in the verapamil group.CONCLUSIONSVerapamil cannot prevent long-term (1 and 6 weeks, respectively) tachycardia-induced changes of atrial electrophysiological properties. Furthermore, verapamil increases the duration of AF in the dogs either before or after long-term rapid atrial pacing.

Atrial fibrillation (AF) is a common arrhythmia after coronary artery bypass surgery (CABG). The purpose of this study was to determine the role of P wave duration, amplitude and dispersion in the prediction of AF after CABG. This study included 120 patients undergoing elective CABG. Clinical characteristics, 12-lead electrocardiogram (ECG), echocardiogram and coronary angiogram were obtained in all patients. We measured P wave duration, amplitude and dispersion from 12-lead ECG in each patient. After CABG, all patients were continuously monitored for AF attacks in the intensive care unit and ordinary ward. Our results showed that age greater than 60 years was the strongest predictor of postoperative AF (p<0.01), with a 3.7-fold greater likelihood of developing postoperative AF compared to ages less than 60 years. Gender was another independent predictor of postoperative AF, with men being 3.0 times more likely to develop postoperative AF compared to women (p=0.03). The presence of prolonged P wave duration (≥100 ms in lead II) was also an independent predictor (p=0.04), with 2.9-fold greater risk of developing postoperative AF compared to a P wave duration of less than 100 ms. The P wave dispersion was similar between patients with and without postoperative AF (29±15 vs. 33±15 mm, p=NS). In conclusion, old age, male gender and prolonged P wave duration were independent predictors of AF after CABG. However, P wave dispersion and amplitude did not provide significant information in the prediction of postoperative AF.

A 72-year-old woman who presented with transient electrocardiographic ST segment elevation and left ventricular asynergy in an acute phase of subarachnoid hemorrhage was found to have normal coronary angiogram and normal Tc-99m PYP myocardial infarct scan. These findings suggested that noninvasive Tc-99m PYP myocardial infarct scan could substitute coronary angiogram for differentiating wall motion and electrocardiographic abnormalities secondary to subarachnoid hemorrhage from those caused by coronary artery disease in patients with subarachnoid hemorrhage.

Recent genotype-phenotype correlation studies in familial hypertrophic cardiomyopathy (FHC) have revealed that some mutations in the beta- myosin heavy chain (BMHC) gene may be associated with a high incidence of sudden death and a poor prognosis. Coexistence of sudden death and end-stage heart failure in several families with FHC has recently being reported; however, the genetic basis of such families has not been clearly demonstrated. A three-generation Chinese familial hypertrophic cardiomyopathy (FHC) family (family HLI) with two cases of end-stage heart failure and three cases of sudden death was analyzed. The average age of death in the affected members in this family was 34 years old. Genetic linkage analysis using polymorphisms in the (alpha- and beta-myosin heavy chain genes revealed that FHC in this family is significantly linked to the BMHC gene without recombinations. Single-strand conformation polymorphism analysis of exons 8, 9 and 13 to 23 in the BMHC gene showed a polymorphic band on exon 14 that is in complete linkage with the disease status in this family. DNA sequencing analysis in the affected members revealed an 453Arg-->Cys mutation in the BMHC gene. To our knowledge this is the first reported mutation of FHC in Chinese. Our data suggest that the 453Arg-->Cys mutation is associated with a malignant clinical course in FHC due not only to sudden death but also to end-stage heart failure.

The association between left atrial spontaneous echo contrast (SEC) and a history of systemic arterial embolization was evaluated in 359 consecutive patients with rheumatic mitral valve disease during a 3-year period. All patients underwent transesophageal echocardiographic (TEE) and cardiac catheterization studies. Of these, 207 patients had predominant mitral stenosis, 55 had significant mitral regurgitation, and the remaining 97 with xenograft mitral valve replacement developed valvular dysfunction (32 resulted in predominant mitral stenosis and 65 in significant mitral regurgitation). Left atrial SEC was detected in 108 patients (group A) and was absent in 251 (group B). Group A patients showed a higher frequency of left atrial thrombi or history of previous embolization than those in group B (59.3% vs 7.2%; p < 0.001). Group A patients also had a higher frequency of recent (≤1 week before TEE study) and remote (>1 week before TEE study) embolization than did group B patients (recent: 19.4% vs 2.8% [p < 0.001]; remote: 13.0% vs 4.0% [p < 0.001]). Multivariate analysis showed that left atrial SEC (p = 0.01) was the only independent predictor of systemic arterial embolization. It is concluded that patients with left atrial SEC had a significantly higher risk for thromboembolism, and TEE is a useful modality to identify this subset of patients with rheumatic mitral valve disease.

To compare transthoracic and transesophageal echocardiography in the diagnosis of intracardiac tumors, 17 patients (8 men and 9 women, aged 19 years to 67 years) whose intracardiac tumors were detected by echocardiography were studied in a 4‐year period. Of these, 14 patients underwent cardiac surgery and 13 were proved to have tumors. There were 4 false‐positive and 2 false‐negative diagnoses by transthoracic echocardiography, but only one false‐positive and no false‐negative diagnosis by transesophageal echocardiography. The stalk of a myxoma was detected clearly in 5 of 11 patients by transthoracic echocardiography, whereas in 10 of 11 it was detected by transesophageal echocardiography. The detailed morphologic characteristics of the tumor, such as contour of the tumor, and the presence of cysts and calcification in the tumor, were seen more clearly with transesophageal echocardiography than with transthoracic echocardiography. © 1994 John Wiley & Sons, Inc.

Spontaneous echo contrast is uncommon in pericardial effusion. We report the case of a patient with massive malignant pericardial effusion causing cardiac tamponade in which the intense spontaneous echo contrast was found in the effusion by echocardiography. It was suggested that both the heavy blood content and a large amount of pericardial effusion were needed to create the phenomenon of spontaneous echo contrast in the pericardial cavity.

Systemic arterial embolization imparts a significant risk of serious complications throughout the lives of patients with rheumatic heart disease. Left atrial (LA) thrombi have been thought to be the major source of emboli. A transesophageal echocardiography (TEE) study of 260 consecutive patients with rheumatic mitral valve disease was performed during a period of 24 months, with particular reference to understanding the association between LA thrombi and embolic complications. Of these patients, 155 had predominant mitral stenosis, 24 had significant mitral regurgitation, and the remaining 81 with xenograft mitral valve replacement developed valvular dysfunction (25 resulted in predominant mitral stenosis and 56 in significant mitral regurgitation). LA thrombi were detected in 38 patients (group A) and absent in 222 (group B). Group A patients had a higher frequency of recent (≤1 week before TEE study) and remote (>1 week before) embolization than did group B patients (recent: 26.3 vs 5.4% [p < 0.001]; remote: 18.4 vs 5.0% [p < 0.01]). The frequency of atrial fibrillation was also greater in group A patients (100 vs 74.3%; p < 0.001). The exclusion of patients with significant mitral regurgitation and sinus rhythm had no effect on the association between LA thrombi and evidence of previous embolization. It is concluded that TEE is a convenient diagnostic modality that can be used to identify a subset of patients with rheumatic mitral valve disease at high risk for systemic embolization. Consequently, preventive anticoagulation for possible embolic complications should be more vigorously adhered to in patients with rheumatic mitral valve disease and LA thrombi.