Interatrial septal thickness as a marker of structural and functional remodeling of the left atrium in patients with atrial fibrillation

BACKGROUND/AIMS: There have been reports that interatrial septal (IAS) thickness is increased in patients with atrial fibrillation (AF). This study was performed to investigate whether IAS thickness determined by transthoracic echocardiography (TTE) represents the amount of left atrium (LA) structural and functional remodeling. METHODS: The study population consisted of 104 consecutive patients who underwent catheter ablation (CA) for AF (paroxysmal atrial fibrillation [PAF], 82; persistent atrial fibrillation [PeAF], 22). IAS thickness and left atrium volume (LAV) using TTE, and LA voltage (LAVOL) using 3-dimensional electroanatomical mapping system were assessed during sinus rhythm. RESULTS: IAS thickness was significantly correlated with maximal LAV (LAVmax) (r = 0.288, p = 0.003), mean LAVOL (r = -0.537, p or = 2) compared to other groups according to CHA2DS2-VASc score (p = 0.019). During a follow-up of 19.6 months, 23 subjects (22.1%; PAF, 17; PeAF, 6) had recurrence of arrhythmia. Univariate analysis showed that LAVmax, minimal LAV, mean LAVOL, LVEFtotal, LVEFactive, and IAS thickness were associated with recurrence of arrhythmia. However, on multivariate analysis, only mean LAVOL and LAEFactive were independent risk factors for recurrence. CONCLUSIONS: Although IAS thickness showed significant correlations with parameters for LA structural and functional remodeling, this parameter alone could not independently predict recurrence of arrhythmia after CA for AF.

Inadvertently Developed Ventricular Fibrillation during Electrophysiologic Study and Catheter Ablation: Incidence, Cause, and Prognosis

BACKGROUND AND OBJECTIVES: Ventricular fibrillation (VF) can inadvertently occur during electrophysiologic study (EPS) or catheter ablation. We investigated the incidence, cause, and progress of inadvertently developed VF during EPS and catheter ablation. SUBJECTS AND METHODS: We reviewed patients who had developed inadvertent VF during EPS or catheter ablation. Patients who developed VF during programmed ventricular stimulation to induce ventricular tachycardia or VF were excluded. RESULTS: Inadvertent VF developed in 11 patients (46.7+/-9.3 years old) among 2624 patients (0.42%); during catheter ablation for atrial fibrillation (AF) in nine patients, frequent ventricular premature beats (VPBs) in one, and Wolff-Parkinson-White (WPW) syndrome were observed in one. VF was induced after internal cardioversion in six AF patients due to incorrect R-wave synchronization of a direct current shock. Two AF patients showed spontaneous VF induction during isoproterenol infusion while looking for AF triggering foci. The remaining AF patient developed VF after rapid atrial pacing to induce AF, but the catheter was accidentally moved to the right ventricular (RV) apex. A patient with VPB ablation spontaneously developed VF during isoproterenol infusion. The focus of VPB was in the RV outflow tract and successfully ablated. A patient with WPW syndrome developed VF after rapid RV pacing with a cycle length of 240 ms. Single high energy (biphasic 150-200 J) external defibrillation was successful in all patients, except in two, who spontaneously terminated VF. The procedure was uneventfully completed in all patients. At a mean follow-up period of 17.4+/-15.5 months, no patient presented with ventricular arrhythmia. CONCLUSION: Although rare, inadvertent VF can develop during EPS or catheter ablation. Special caution is required to avoid incidental VF during internal cardioversion, especially under isoproterenol infusion.

Time-Related Alterations of Endogenous Ouabain in DOCA-Salt Hypertensive Rats

BACKGROUND AND OBJECTIVES: Controversy exists regarding the role of endogenous ouabain in the pathogenesis of DOCA-salt induced hypertension. The purpose of this study was to investigate the role of endogenous ouabain in the development of hypertension in DOCA-salt rats. MATERIALS AND METHODS: The mean blood pressure and heart rate were recorded in 1, 2 and 4 week old control and DOCA-salt treated rats. The endogenous levels of ouabain in the plasma, hypothalamus, pituitary and adrenal glands of the 1, 2 and 4 week old control and DOCA-salt treated rats were also measured using a radioimmunoassay. RESULTS: The mean blood pressures in the 2 and 4 week old DOCA-salt treated rats were significantly higher than those of the controls. There was no significant change in the heart rate between the DOCA-salt treated and control groups. In the 4 week old DOCA-salt treated rats, the endogenous level of ouabain in the adrenal glands was higher than that in the control rats, but this was only weakly significant. The endogenous level of ouabain in the hypothalamus was significantly higher in the 1 week old DOCA-salt treated rats than in the control, but this significance disappeared in the 2 and 4 week old DOCA-salt treated rats. CONCLUSION: These results suggest that the endogenous level of ouabain contributes to the development and maintenance of high blood pressure in DOCA-salt rats. Further studies will be required to elucidate the relationship between the endogenous level of ouabain and DOCA-salt hypertension.

The Relationship between Serum Adiponectin, Essential Hypertension, LV Mass Index, and LV Diastolic Function

BACKGROUND AND OBJECTIVES: Adiponectin is known for its anti-inflammatory and anti-atherogenic effects. The purpose of this study is to characterize the relationships among serum adiponectin, essential hypertension (EH), left ventricular mass index (LVMI), and LV diastolic function. SUBJECTS AND METHODS: Serum adiponectin by RIA and body mass index were measured in 275 patients (M: F=137: 138). We calculated LVMI, E/A ratio, deceleration time (DT), and isovolumetric relaxation time (IVRT) by using echocardiograms. RESULTS: The serum adiponectin level of the hypertensive group was significantly lower than that of the non-hypertensive group (9.9+/-9.8 ug/mL vs. 12.9+/-9.5 ug/mL, p<0.05). Plasma adiponectin was negatively correlated with LVMI (r=-0.329, p<0.001), BMI (r=-0.290, p<0.001), and IVRT (r=-0.485, p<0.05), but was positively correlated with E/A (r=+0.359, p<0.001). CONCLUSION: These results suggest that a decrease in serum adiponectin is associated with an increase in blood pressure and BMI, progress of LVH, and decrease in LV diastolic function.

Relations Among Coronary Flow Reserve, Left Ventricular Mass and Diastolic Function in Patients with Chest Pain and Normal Coronary Angiograms

BACKGROUND AND PURPOSE: Left ventricular hypertrophy (LVH) is a well known cardiovascular risk factor, independent of hypertension, even in the absence of epicardial coronary artery disease. Possible mechanisms have been proposed, including increased LV mass, reduced coronary flow reserve (CFR) and diastolic filling abnormalities. However, the relations among LV hypertrophy, diastolic function, hypertension and coronary flow reserve (CFR) in patients with chest pain and normal coronary angiograms have not been well defined. SUBJECTS AND METHOD: Twenty-six patients with chest pain and normal coronary angiograms were included. LV mass, isovolumic relaxation time (IVRT), deceleration time (DT) and E/A ratio were assessed by 2-D echo-cardiography. Coronary blood flow velocity before and after intracoronary adenosine were measured using intracoronary Doppler wire (FIoWire). CFR was defined as ratio of peak flow velocity after adenosine to baseline flow velocity. Subjects were devided into 4 groups according to presence of LVH and hypertension and the parameters were compared among groups. RESULTS: FR was lower (p<0.01) in the groups with either hypertension or LVH or both than in the groups without them. The decrement in CFR was not linearly related to the degree of LVH (r=0.31, p=0.135). Although there were modest increment in IVRT and DT and decrement in E/A ratio in the groups with hypertension or LVH or both, there was no statistical significance. CONCLUSION: These findings suggest that the underlying mechanism of impaired CFR in patients with LVH or hypertension may be the consequence of primary coronary microvascular lesion rather than the process of left ventricular hypertrophy.