[Pathological features and diagnostic significance of lung biopsy in occupational lung diseases].

Objective: To investigate the clinicopathological characteristics of occupational lung diseases, to reduce the missed diagnoses and misdiagnoses of the diseases and to help standardize the diagnosis and treatment of these patients. Methods: A total of 4 813 lung biopsy specimens (including 1 935 consultation cases) collected at the Department of Pathology, Nanjing Drum Tower Hospital, Nanjing, China from January 1st, 2017 to December 31th, 2019 were retrospectively analyzed. Among them, 126 cases of occupational lung diseases were confirmed with clinical-radiological-pathological diagnosis. Special staining, PCR and scanning electron microscopy were also used to rule out the major differential diagnoses. Results: The 126 patients with occupational lung diseases included 102 males and 24 females. All of them had a history of exposure to occupational risk factor(s). Morphologically, 68.3% (86/126) of the cases mainly showed pulmonary fibrotic nodules, dust plaque formation or carbon end deposition in pulmonary parenchyma. 16.7% (21/126) of the cases mainly showed welding smoke particle deposition in the alveolar cavity and lung interstitium while 15.1% (19/126) of the cases showed granulomas with fibrous tissue hyperplasia, alveolar protein deposition or giant cell interstitial pneumonia. The qualitative and semi-quantitative analyses of residual dust components in the lung under scanning electron microscope were helpful for the diagnosis of welder's pneumoconiosis and hard metal lung disease. Conclusions: The morphological characteristics of lung biopsy tissue are important reference basis for the clinicopathological diagnosis and differential diagnosis of occupational lung diseases. Recognizing the characteristic morphology and proper use of auxiliary examination are the key to an accurate diagnosis of occupational lung diseases on biopsy specimens.

[Effects of anterolateral thigh free flap with fascia lata in repairing dura mater defect after resection of head squamous cell carcinoma].

Objective: To evaluate the clinical effects of anterolateral thigh free flap with fascia lata in the repair of dura mater defect after resection of head squamous cell carcinoma. Methods: From June 2016 to June 2018, Xijing Hospital of Air Force Medical University applied the free transplantation of anterolateral thigh flap with fascia lata to repair the dura mater defect of 12 patients with head squamous cell carcinoma, including 9 males and 3 females, aged from 35 to 74 years. The size of scalp soft tissue defects in patients after carcinoma resection ranged from 12 cm×10 cm to 24 cm×21 cm, and the size of dura mater defect of patients ranged from 7 cm×6 cm to 16 cm×14 cm. The size of flap of patients ranged from 14 cm×12 cm to 27 cm×24 cm, and the size of fascia lata ranged from 8 cm×7 cm to 17 cm×15 cm. The superficial temporal artery and middle temporal vein were connected by end to end anastomosis with the first musculocutaneous perforating branch of the descending branch of lateral femoral artery and its accompanying vein. The flap donor area was transplanted with autologous split-thickness skin graft from trunk and fixed with packing. Postoperative survival of flaps and skin grafts was observed. The patients were followed up regularly. The cranial magnetic resonance imaging was performed to observe the recurrence of intracranial tumors and dural integrity, shape of the flap and whether the donor site region was left with significant dysfunction were observed. Results: All the flaps and skin grafts survived well in 12 patients after surgery. Ten patients had primary healing at the edge of the flap suture; 2 patients had local sinus tract formation at the suture site of flap, with a small amount of cerebrospinal fluid leakage, and were recovered after outpatient dressing change. The patients were followed up for 10 to 36 months, and 3 patients with tumors involving in the dura mater sagittal sinus region had postoperative intracranial tumor recurrence. The tumor was resected again. All the patients had good dural integrity. The flaps of all patients were in good shape, and no obvious dysfunction remained in the flap donor site. Conclusions: Free transplantation of anterolateral thigh flap with fascia lata is an effective and reliable method to repair the dura mater defect following head squamous cell carcinoma resection. It can repair the scalp and dura mater defects caused by the invasion of squamous cell carcinoma and provide possibilities for skull reconstruction.

[Expression of E-cadherin, N-cadherin, ß-catenin and their clinical significance in laryngeal carcinoma].

OBJECTIVE: To investigate the expression of E-cadherin(E-cad), N-cadherin(N-cad), ß-catenin(ß-cat), which are the markers of Epithelial-mesenchymal transition and analyze their relationships with the clinicopathological features and the prognosis of the laryngeal squamous cell carcinoma. METHODS: The expression levels of E-cad, N-cad, ß-cat in 76 tumor tissues and their corresponding adjacent normal laryngeal tissues were determined by immunohistochemistry method. Relationships between the proteins' expression and clinicopathological features were analyzed. Survival curves were calculated using the Kaplan-Meier method. Differences in the survival rates were analyzed by the log-rank test among different expression groups. Cox's regression model was used to examine the independent predictor of the prognosis of the laryngeal cancer. RESULTS: The expression levels of E-cad, N-cad, ß-cat in tumor tissues and adjacent normal tissues were statistically significant(P<0.001). The expression level of E-cad and ß-cat in the laryngeal carcinoma was related to lymph node metastasis, clinical pathological stage and differentiation degree (P<0.05), while N-cad expression level was associated with clinical stage and differentiation degree (P<0.05). The expression of E-cad was correlated with the expression of ß-cat (P=0.001), and the expression of N-cad was correlated with ß-cat (P=0.02), but the expression of E-cad was not correlated with N-cad. There were four subgroups of patterns of E-cad and N-cad expression: E-cad (+ )/N-cad (-), E-cad (+ ) /N-cad (+ ), E-cad (-) /N-cad (-), E-cad (-) /N-cad (+ ). The expression level of each group was related to the clinical pathological stage and differentiation degree (P<0.05). The expression level of E-cad/ß-cat was associated with lymph node metastasis, clinical pathological stage and differentiation degree (P<0.01). Log-rank analysis showed that the prognosis of negative and positive groups was statistically different (P<0.05), and the combined analysis showed that the prognosis of E-cad/N-cad or E-cad/ß-cat group was significantly different (P<0.01). Cox's regression model analysis showed that the clinical stage and ß-cat were independent predictors of the prognosis of laryngeal carcinoma. CONCLUSIONS: The low expression of E-cad, high abnormal expression of N-cad and ß-cat played an important role in the occurrence and development of laryngeal carcinoma. It can provide a reference for evaluating clinical prognosis. The clinical pathological stage and ß-cat can be used as independent predictors for the prognosis of laryngeal carcinoma.

Long-term follow-up of arrhythmia characteristics and clinical outcomes in heart transplant patients.

INTRODUCTION: Arrhythmias occur frequently after heart transplantation (HT), but knowledge of their impact on long-term outcomes is limited. This study sought to investigate the characteristics of the arrhythmias among biatrial orthotopic HT patients during long-term follow-up. METHODS: This study included 217 patients who received biatrial orthotopic HT. Patients were classified into 5 groups according to the arrhythmia episodes that occurred >1 month after HT: no arrhythmias (group 1; n = 149); atrial tachyarrhythmias only (group 2; n = 34); ventricular tachyarrhythmias only (group 3; n = 9); bradyarrhythmias only (group 4; n = 7); or double/triple arrhythmias (group 5; n = 18). We analyzed their long-term outcomes respectively. RESULTS: During 83 ± 51 months of follow-up, all-cause mortality rates were higher in groups 3 (88.9%) and 5 (72.2%) compared with the other groups (groups 1, 2, and 4: 21.5%, 41.2%, and 57.1%, respectively; P < .001). Cardiovascular mortality rates were higher in groups 4 (42.9%) and 5 (61.1%) compared with the other groups (groups 1, 2, and 3: 8.1%, 20.6%, and 0% respectively; P < .001). Noncardiovascular mortality rate was greater in group 3 (88.9%) compared with the other groups (groups 1, 2, 4, and 5: 13.4%, 20.6%, 14.3%, and 11.1%, respectively; P < .001). Sudden death rates were higher in groups 4 (42.9%) and 5 (44.4%) compared with the other groups (groups 1, 2, and 3: 7.4%, 8.8%, and 0%, respectively; P < .001). CONCLUSION: Patients with posttransplantation arrhythmias experienced significantly worse clinical outcomes.

Impact of transisthmus linear ablation of typical atrial flutter on coronary sinus activation time.

Complete or incomplete bidirectional isthmus conduction block after linear ablation of atrial flutter is difficult to interpret without detailed multiple electrodes mapping along the tricuspid annulus and the low right atrial isthmus area. The influence of isthmus block on the intraatrial septal and coronary sinus activation has not been assessed by endocardial mapping. This study was designed to analyze the intraartial and interatrial activation times in a retrospective fashion to investigate (1) whether isthmus conduction block can change the coronary sinus activation sequence during low lateral right atrial pacing, and (2) the correlation between change of coronary sinus activation time and isthmus conduction block. Sixty-five consecutive patients (mean age, 57 +/- 18 years) with clinically documented typical atrial flutter were studied. A 20-pole "Halo" catheter was placed around the tricuspid annulus including the entire low right atrial isthmus to verify complete bidirectional isthmus block. Activation time from ostium to distal coronary sinus (OCS-->DCS), and interatrial septum and isthmus activation times during right atrial pacing were analyzed and compared before and after incomplete or complete isthmus block. Complete bidirectional isthmus block was achieved in 50 (77%) patients. During low lateral right atrial pacing, linear ablation at low right atrial isthmus results in a significant delay of activation in all coronary sinus recording sites with greater extent at the ostium area without influence on interatrial septum activation in complete and incomplete isthmus conduction block. The difference of the OCS-->DCS interval before and after ablation, delta (OCS-->DCS), was well correlated with results of isthmus conduction block and significantly longer in patients with complete than those with incomplete isthmus block (34 +/- 11 vs 11 +/- 8 ms, P < 0.001), thereby allowing a value of 20 ms as a discriminative parameter to differentiate incomplete (< 20 ms) from complete (> or = 20 ms) isthmus counterclockwise conduction block with a sensitivity of 96% and a specificity of 88%. In conclusion, creation of a line of block at the inferior vena cava-tricuspid annulus isthmus could change coronary sinus activation sequence during low lateral right atrial pacing in sinus rhythm. The change of coronary sinus activation time after linear ablation, delta (OCS-->DCS), was well correlated with isthmus conduction block by using a value > or = 20 ms to discern complete counterclockwise isthmus block.

Red wine inhibits monocyte chemotactic protein-1 expression and modestly reduces neointimal hyperplasia after balloon injury in cholesterol-Fed rabbits.

BACKGROUND: Wine consumption decreases the risk of myocardial infarction. Intimal hyperplasia contributes to restenosis after angioplasty. Local ethanol delivery inhibits intimal hyperplasia after balloon injury in rabbit iliac and pig coronary arteries. The effects of wine consumption on intimal response and monocyte chemotactic protein-1 (MCP-1) expression were studied in cholesterol-fed rabbits. METHODS AND RESULTS: Male rabbits were fed a 2% cholesterol diet together with red wine (12.5% vol, 5 mL/kg body wt per day; n=7), white wine (13.3% vol, 5 mL/kg body wt per day; n=7), or no wine as a control (n=8) for 6 weeks. A balloon injury of the abdominal aorta was performed at the end of the third week. Abdominal aortas were harvested at the end of 6 weeks. Neointimal hyperplasia was measured morphometrically. MCP-1 expression was determined by Northern blot, in situ hybridization, and immunohistochemistry. Rabbits fed red wine had significantly less neointimal hyperplasia than did control rabbits (intima/media area ratio 0.59+/-0.05 [red wine group] versus 0.79+/-0.07 [control group], P<0.05). However, rabbits fed white wine showed a trend (but not significant) toward less intimal response compared with control rabbits (intima/media area ratio 0.65+/-0.04 [white wine group] versus 0.79+/-0.07 [control group], P=0.165). Both red wine and white wine significantly reduced MCP-1 mRNA and protein expression in the aorta. CONCLUSIONS: Long-term consumption of red wine and white wine inhibits MCP-1 expression, and in the small number of animals studied, red wine modestly reduces neointimal hyperplasia. Since red wine exhibits higher antioxidant capacity than does white wine, the decreased intimal response might be partly attributed to its antioxidant effects.

Persistent atrial flutter in patients treated for atrial fibrillation with amiodarone and propafenone: electrophysiologic characteristics, radiofrequency catheter ablation, and risk prediction.

INTRODUCTION: Antiarrhythmic drugs have been reported to promote the conversion of atrial fibrillation to atrial flutter in patients with paroxysmal atrial fibrillation. However, information about the electrophysiologic mechanism and response to radiofrequency ablation of these drug-induced atrial flutters is limited. Furthermore, the determinants of the development of persistent atrial flutter in patients treated for atrial fibrillation with antiarrhythmic drugs are still unknown. METHODS AND RESULTS: Among the 136 patients treated for atrial fibrillation with amiodarone (n = 96) or propafenone (n = 40), 15 (11%, mean age 65.5 +/- 12.3 years) were identified to have subsequent development of persistent atrial flutter based on surface ECG characteristics during antiarrhythmic drug treatment. The mean interval between the beginning of drug treatment and the onset of atrial flutter was 5.0 +/- 5.5 months. Intracardiac mapping and entrainment studies revealed that 11 patients had counterclockwise typical atrial flutter, and 4 had clockwise typical atrial flutter. All 15 patients underwent successful ablation with creation of complete bidirectional isthmus conduction block. After a mean follow-up of 12.3 +/- 4.2 months, 14 (93%) of 15 patients who underwent successful ablation and continued taking antiarrhythmic drugs have remained in sinus rhythm. Univariate analysis of clinical variables demonstrated that only atrial enlargement was significantly related to the occurrence of persistent atrial flutter. CONCLUSION: In patients with atrial fibrillation, persistent typical atrial flutter might occur during antiarrhythmic drug treatment, and atrial enlargement was a risk factor for the development of such an arrhythmia. Radiofrequency ablation and continuation of pharmacologic therapy offered a safe and effective means of achieving and maintaining sinus rhythm.

Electrophysiologic characteristics of a dilated atrium in patients with paroxysmal atrial fibrillation and atrial flutter.

This study investigated the difference of atrial electrophysiologic characteristics between a normal and dilated atrium and compared them among patients with paroxysmal atrial fibrillation and flutter. Twenty-seven patients with paroxysmal atrial fibrillation and 28 patients with paroxysmal atrial flutter were divided into four subgroups, according to the presence of a normal atrium or bilateral atrial enlargement. Thirty patients without atrial arrhythmia (20 patients with normal atrium and 10 patients with bilateral atrial enlargement) were included in control group. The atrial refractoriness in patients with a dilated atrium was longer than those with normal atrial size. In patients with paroxysmal atrial fibrillation and patients of control group, the P-wave duration and interatrial conduction velocity with or without atrial enlargement were similar. However, in patients with paroxysmal atrial flutter, P-APCS (86 +/- 10 ms vs. 73 +/- 9 ms, p < 0.05) and P-ADCS (109 +/- 9 ms vs. 95 +/- 9 ms, p < 0.05) in patients with a dilated atrium were longer than in patients with a normal atrium. The patients with paroxysmal atrial fibrillation or atrial flutter all demonstrated longer P-wave duration and interatrial conduction time than control group. Among the groups with a normal atrium or a dilated atrium, atrial refractoriness in patients with paroxysmal atrial flutter was shorter than that in control group. Moreover, in the patients with a normal atrium, the potential minimal wavelength in control group (6.6 +/- 1.7) was longer than that of paroxysmal atrial fibrillation (5.3 +/- 1.1), or atrial flutter (5.0 +/- 1.2). These findings suggest that atrial electrophysiologic characteristics of a dilated atrium were different from those of normal atrium, and these changes were different between paroxysmal atrial fibrillation and flutter. Multiple factors are considered to be related to the genesis of atrial tachyarrhythmias.

Effects of procainamide and dl-sotalol on the changes of atrial electrophysiology induced by high current stimulation.

The relation between high current atrial stimulation and antiarrhythmic drugs was not clear. We evaluated the effects of procainamide and dl-sotalol on the electrophysiological changes induced by high current stimulation. Effects of high current atrial stimulation on effective refractory period, dispersion of refractoriness, conduction velocity, and wavelength of the earliest atrial premature beat were evaluated at baseline and after infusion of procainamide (10 patients) and dl-sotalol (10 patients). High current atrial stimulation shortened effective refractory period locally (-12% +/- 4.0%, -7.0% +/- 3.0%, -5.1 +/- 3.3%, and -3.0 +/- 2.0%, at 0, 7, 14, and 21 mm from the S1 stimulation site, respectively; P < 0.001); increased the dispersion of refractoriness (from 17.8 +/- 8.5 to 27.4 +/- 12.5 ms, P < 0.001); decreased conduction velocity of the earliest premature beat (from 0.58 +/- 0.10 to 0.52 +/- 0.09 ms, P = 0.01); and decreased wavelength of the earliest atrial premature beat (from 10.9 +/- 2.4 to 8.8 +/- 2.1 cm, P < 0.001). These effects of high current stimulation persisted after procainamide infusion. However, after dl-sotalol infusion, high current atrial stimuli did not change the dispersion of refractoriness (23.1 +/- 10 ms vs 26.4 +/- 10.4 ms; P > 0.05, twice diastolic threshold vs 10 mA); conduction velocity of the earliest premature beat (0.54 +/- 0.06 ms vs 0.50 +/- 0.06 ms, P > 0.05); or wavelength of the earliest premature atrial beat (11.5 +/- 1.6 m/s vs 10.1 +/- 1.7 cm; P > 0.05). Although high current atrial stimulation shortened effective refractory period locally, increased dispersion of refractoriness, and decreased the wavelength of the earliest premature atrial impulse, these effects were abolished by dl-sotalol but not procainamide.

Role of atrial electrophysiology and autonomic nervous system in patients with supraventricular tachycardia and paroxysmal atrial fibrillation.

OBJECTIVES: The purposes of this study were to evaluate the atrial electrophysiology and autonomic nervous system in patients who had paroxysmal supraventricular tachycardia (PSVT) associated with paroxysmal atrial fibrillation (PAF). BACKGROUND: PAF frequently appeared in patients with PSVT. However, the critical determinants for the occurrence of PAF were not clear. METHODS: This study population consisted of 50 patients who had PSVT with (n=23) and without (n=27) PAF. Atrial pressure, atrial size, atrial effective refractory periods (AERPs), and AERP dispersion were evaluated during baseline and PSVT, respectively. Twenty-four hour heart rate variability and baroreflex sensitivity (BRS) were also examined. RESULTS: There was greater baseline AERP dispersion in patients with PAF than in those without PAF. The atrial pressure, atrial size, AERPs in the right posterolateral atrium and distal coronary sinus, and AERP dispersion were increased during PSVT as compared with those during baseline. Patients with PAF had greater AERP dispersion than those without PAF during PSVT. The differences of atrial size, right posterolateral AERP, and AERP dispersion between baseline and PSVT were greater in patients with PAF than in those without PAF. BRS, but not heart rate variability, was higher in patients with PAF than in those without PAF. Univariate analysis showed that higher BRS (>4.5 ms/mm Hg, p=0.0002, odds ratio=16.1), AERP dispersion during PSVT (>40 ms, p=0.0008, odds ratio=9.7), and increase of right atrial area during PSVT (>2 cm2, p=0.016, odds ratio=10.7) were significantly correlated with the occurrence of PAF in patients with PSVT. CONCLUSIONS: Disturbed atrial electrophysiology and higher vagal reflex could play important roles in the genesis of PAF in patients with PSVT.

Radiofrequency ablation of idiopathic left ventricular tachycardia with changing ECG morphology.

Idiopathic left ventricular tachycardia is a distinct clinical entity with a typical ECG of right bundle branch block and left axis deviation. We presented a 39-year-old man with idiopathic left ventricular tachycardia, which demonstrated change in the configuration of QRS complex during successive radiofrequency catheter ablation. We proposed that this idiopathic left ventricular tachycardia may have alternative pathways within the reentrant circuit leading to different exits.

Tachycardia-induced change of atrial refractory period in humans: rate dependency and effects of antiarrhythmic drugs.

BACKGROUND: Atrial fibrillation (AF) has been shown to shorten the atrial effective refractory period (ERP) and make the atrium more vulnerable to AF. This study investigated the effect of atrial rate and antiarrhythmic drugs on ERP shortening induced by tachycardia. METHODS AND RESULTS: Seventy adult patients without structural heart disease were included. For the first part of the study, right atrial ERP was measured with a drive cycle length of 500 ms before and after 10 minutes of rapid atrial pacing using five pacing cycle lengths (450, 400, 350, 300, and 250 ms) in 10 patients. For the second part of the study, the remaining 60 patients were included to study the effects of antiarrhythmic drugs on changes in atrial ERP induced by AF. Atrial ERP was measured with a drive cycle of 500 ms before and after an episode of pacing-induced AF. After the patients were randomized to receive one of six antiarrhythmic drugs (procainamide, propafenone, propranolol, dl-sotalol, amiodarone, and verapamil), atrial ERP was measured before and after another episode of pacing-induced AF. In the first part of the study, atrial ERP shortened significantly after 10 minutes of rapid atrial pacing, and the degree of shortening was correlated with pacing cycle length. The second part of the study showed that atrial ERP shortened after conversion of AF (172+/-15 versus 202+/-14 ms, P<0.0001) and that ERP shortening was attenuated after verapamil infusion (-4.6+/-1.2% versus -15.1+/-3.4%, P<0.001) but was unchanged after infusion of the other antiarrhythmic drugs. Furthermore, all of these antiarrhythmic drugs could decrease the incidence and duration of secondary AF. CONCLUSIONS: The atrial ERP shortening induced by tachycardia was a rate-dependent response. Verapamil, but not other antiarrhythmic drugs, could markedly attenuate this effect. However, verapamil and the other drugs could decrease the incidence and duration of secondary AF.

Electropharmacologic effects of class I and class III antiarrhythmia drugs on typical atrial flutter: insights into the mechanism of termination.

BACKGROUND: Acute effects of class I and class III antiarrhythmia drugs on the reentrant circuit of typical atrial flutter are not fully studied. Furthermore, the critical electrophysiologic determinants of flutter termination by antiarrhythmia drugs are not clear. METHODS AND RESULTS: The study population consisted of 36 patients (mean age, 53+/-17 years) with clinically documented typical atrial flutter. A 20-pole "halo" catheter was positioned around the tricuspid annulus. Incremental pacing was performed to measure the conduction velocity along the isthmus and lateral wall, and extrastimulation was performed to evaluate atrial refractory period in the baseline state and after intravenous infusion of ibutilide, propafenone, and amiodarone. Efficacy of these drugs in conversion of typical atrial flutter and patterns of termination were also determined. Ibutilide significantly increased the atrial refractory period and decreased conduction velocity in the isthmus at short pacing cycle length. It terminated atrial flutter in 8 (67%) of 12 patients after prolongation of flutter cycle length due to increase (86+/-19%) of conduction time in the isthmus. Propafenone predominantly decreased conduction velocity with use dependency and significantly increased atrial refractory period, but it only converted atrial flutter in 4 (33%) of 12 patients. Amiodarone had fewer effects on atrial refractory period and conduction velocity than did ibutilide and propafenone, and it terminated atrial flutter in only 4 (33%) of 12 patients. Termination of typical atrial flutter was due to failure of wave front propagation through the isthmus, which occurred with cycle length oscillation, abruptly without variability of cycle length, or after premature activation of the reentrant circuit. CONCLUSIONS: Ibutilide, with a unique increase in atrial refractoriness, was more effective in conversion of atrial flutter than were propafenone and amiodarone.

Long-term outcome of radiofrequency catheter ablation for typical atrial flutter: risk prediction of recurrent arrhythmias.

INTRODUCTION: Little is known about the predictors of recurrent atrial flutter or fibrillation after successful radiofrequency ablation of typical atrial flutter. In addition, there is only limited evidence suggesting that elimination of atrial flutter would modify the natural history of atrial fibrillation in patients who experienced both of these arrhythmias. The aims of the present study were to investigate the long-term results of radiofrequency catheter ablation and to examine the predictors for late occurrence of atrial fibrillation in a large population with typical atrial flutter. METHODS AND RESULTS: The study population consisted of 144 patients (mean age 56 +/- 18 years) with successful ablation of clinically documented typical atrial flutter. In the first 50 patients, successful ablation was defined as termination and noninducibility of atrial flutter; for the subsequent 94 patients, successful ablation was defined as achievement of bidirectional isthmus conduction block and no induction of atrial flutter. The clinical and echocardiographic variables were analyzed in relation to the late occurrence of atrial flutter or fibrillation. Over the follow-up period of 17 +/- 13 months, 14 (9.7%) patients had recurrence of typical atrial flutter. In the first 50 patients, 8 (16%) had recurrence of atrial flutter, compared with only 6 (6%) of the following 94 patients. Patients with incomplete isthmus block had a significantly higher incidence of recurrent atrial flutter than those with complete isthmus block (6/16 vs 0/78, P < 0.0001) in the following 94 patients. There was no predictor for recurrence of atrial flutter after successful ablation as determined by univariate and multivariate analysis. Although successful ablation of atrial flutter eliminated atrial fibrillation in 45% of patients with a prior history of atrial fibrillation, 31 (21.5%) of 144 patients undergoing this procedure developed atrial fibrillation during the follow-up period. Univariate analysis revealed that three clinical variables were related to the occurrence of atrial fibrillation: (1) the presence of structural heart disease; (2) a history of atrial fibrillation before ablation; and (3) inducible sustained atrial fibrillation after ablation. By multivariate analysis, only a history of atrial fibrillation and inducible sustained atrial fibrillation could predict the late development of atrial fibrillation after atrial flutter ablation. CONCLUSION: Radiofrequency catheter ablation of typical atrial flutter is highly effective and associated with a low recurrence rate of atrial flutter, but atrial fibrillation continues to be a long-term risk for patients undergoing this procedure. The presence of structural heart disease and prior spontaneous or inducible sustained atrial fibrillation increases the risk of developing atrial fibrillation.

Effects of different atrial pacing modes on atrial electrophysiology: implicating the mechanism of biatrial pacing in prevention of atrial fibrillation.

BACKGROUND: Multiple-site atrial pacing has been shown to prevent recurrence of atrial fibrillation. However, information about the mechanisms of different atrial pacing modes in prevention of atrial fibrillation was not clear. METHODS AND RESULTS: Forty-two patients without structural heart disease were classified into group 1 and group 2 according to absence or presence of clinical atrial fibrillation, respectively. Atrial conduction time and electrogram width of the right posterior interatrial septum (RPS) were measured during drive-train stimulation (S1) and early extrastimulation (S2). The locations of S1 were the high right atrium (HRA), distal coronary sinus (DCS), or both sites simultaneously. Effective refractory periods (ERPs) of the HRA and DCS were also determined during S1 stimulation at each site and during biatrial pacing. The ERPs were not different between single-site atrial pacing and biatrial pacing. In contrast, early S2 stimulation at the HRA caused greater atrial conduction delay and greater increment of electrogram width of the RPS in patients with a history of atrial fibrillation. Biatrial pacing significantly reduced the conduction delay and electrogram width of the RPS caused by HRA extrastimulation. In addition, in 17 group 2 patients, atrial fibrillation was induced by an early HRA S2 coupled to HRA pacing. However, with the same coupling interval of S2 at HRA, only 6 of them had the arrhythmia induced during biatrial pacing. Furthermore, conduction delay and increase of electrogram width caused by early S2 at the HRA were reduced by biatrial pacing only in patients whose arrhythmia induction was successfully prevented by biatrial pacing. CONCLUSIONS: Biatrial pacing reduced both the atrial conduction delay and increase of electrogram width at the RPS caused by early S2 at HRA, and these effects could prevent induction of atrial fibrillation.

Characterization of low right atrial isthmus as the slow conduction zone and pharmacological target in typical atrial flutter.

BACKGROUND: Previous electrophysiological studies in patients with typical atrial flutter suggested that the slow conduction zone might be located in the low right atrial isthmus, which is a path formed by orifice of inferior vena cava, eustachian valve/ridge, coronary sinus ostium, and tricuspid annulus. The conduction characteristics during atrial pacing and responses to antiarrhythmic drugs of this anatomic isthmus were unknown. METHODS AND RESULTS: Forty-four patients, 20 patients with paroxysmal supraventricular tachycardia (group 1) and 24 patients with clinically documented paroxysmal typical atrial flutter (group 2), were studied. A 20-pole halo catheter was situated around the tricuspid annulus. Incremental pacing from the low right atrium and coronary sinus ostium was performed to measure the conduction time and velocity along the isthmus and lateral wall in the baseline state and after intravenous infusion of procainamide or sotalol. In both groups, conduction velocity in the isthmus during incremental pacing was significantly lower than that in the lateral wall before and after infusion of antiarrhythmic drugs. Furthermore, gradual conduction delay with unidirectional block in the isthmus was relevant to initiation of typical atrial flutter. Compared with group 1, group 2 had a lower conduction velocity in the isthmus and shorter right atrial refractory period. Procainamide significantly decreased the conduction velocity, but sotalol did not change it. In contrast, sotalol significantly prolonged the atrial refractory period with a higher extent than procainamide. After infusion of procainamide, the increase of conduction time in the isthmus accounted for 52+/-19% of the increase in flutter cycle length, and 5 of 12 patients (42%) had spontaneous termination of typical flutter. After infusion of sotalol, typical flutter was induced in only 6 of 12 patients (50%) without significant prolongation of flutter cycle length. CONCLUSIONS: The low right atrial isthmus with rate-dependent slow conduction properties is critical to initiation of typical human atrial flutter. It may be the potentially pharmacological target of antiarrhythmic drugs in the future.