Change in QRS morphology as a marker of spontaneous elimination in verapamil-sensitive idiopathic left ventricular tachycardia.

BACKGROUND: Verapamil-sensitive idiopathic left ventricular tachycardia (verapamil-ILVT) is thought to be due to a reentry within the LV fascicular system. Radiofrequency catheter ablation (RFCA) is effective for elimination of the VT; however, a long-term prognosis of patients with verapamil-ILVT is still unclear. METHODS AND RESULTS: Eighty consecutive verapamil-ILVT patients (62 men, 31 ± 12 years of age, LVEF: 65 ± 4%) were enrolled. Seventy-six (95%) cases of VT involved right bundle branch block and left axis deviation. We retrospectively analyzed changes in the QRS duration (ΔQRS-d) and QRS axis (ΔQRS-axis) during follow-up and compared them with recurrence of VT. During a mean follow-up period of 10 years (2-32 years), no sudden death or heart failure occurred. Fifty-one (64%) patients underwent RFCA, and 46 (90%) of them had no VT without any medication after RFCA. The ΔQRS-d (16 ± 2 vs. 8 ± 1 ms, P = 0.24) and ΔQRS-axis (20 ± 4 vs. 4 ± 3 degrees, P = 0.23) were not different in patients with no VT (VT[-]) and those with recurrence of VT (VT[+]). However, in the remaining 29 patients without RFCA, VT was spontaneously eliminated in 16 patients. The ΔQRS-d (30 ± 6 vs. 6 ± 1 ms, P = 0.002) and ΔQRS-axis (23 ± 4 vs. 5 ± 2 degrees, P = 0.001) were significantly larger in VT(-) patients compared to VT(+) patients during follow-up. CONCLUSIONS: Some verapamil-ILVT patients who show QRS morphology changes over the follow-up period may become free from VT without any invasive or pharmacological treatments, suggesting that further altered LV fascicular conduction might eliminate the reentry of verapamil-ILVT.

Differences in the onset mode of ventricular tachyarrhythmia between patients with J wave in anterior leads and those with J wave in inferolateral leads.

BACKGROUND: The pathophysiological mechanism of J wave in anterior leads (A-leads) and inferolateral leads (L-leads) remains unclear. OBJECTIVE: We investigated the onset mode and circadian distribution of ventricular tachyarrhythmia (VTA) episodes between patients with early repolarization syndrome (ERS) and Brugada syndrome (BrS). METHODS: The study enrolled 35 patients with ERS and 52 patients with type 1 BrS with spontaneous ventricular fibrillation who were divided into 4 groups: ERS(A+L) (n = 15), patients with ERS who had a non-type 1 Brugada pattern electrocardiogram in any A-leads (second to fourth intercostal spaces) in control and/or after drug provocation tests; ERS(L) (n = 20), patients with ERS with J wave only in L-leads; BrS(A) (n = 24), patients with BrS without J wave in L-leads; and BrS(A+L) (n = 28), patients with BrS with J wave in L-leads. The onset mode of 206 VTAs obtained from electrocardiograms or implantable cardioverter-defibrillators and the circadian distribution of 352 VTAs were investigated in the 4 groups. RESULTS: Three groups with J wave in A-leads, ERS(A+L), BrS(A), and BrS(A+L), had higher incidences of nocturnal (63%, 43%, and 47%, respectively) and sudden onset VTAs (67%, 97%, and 86%, respectively) with longer coupling intervals of premature ventricular contractions (388.8, 397.3, and 385.6 ms, respectively) than the ERS(L) group with J wave only in L-leads (25%, P = .0019; 19%, P < .0001; and 330.6 ms, P = .0004, respectively), the last of which mainly displayed VTAs with a short-long-short sequence. CONCLUSION: The onset mode of VTAs was different between patients with J wave in A-leads and patients with J wave in only L-leads. The underlying mechanism of J wave may differ between A-leads and L-leads.

Significance of electrocardiogram recording in high intercostal spaces in patients with early repolarization syndrome.

AIMS: Published reports regarding inferolateral early repolarization (ER) syndrome (ERS) before 2013 possibly included patients with Brugada-pattern electrocardiogram (BrP-ECG) recorded only in the high intercostal spaces (HICS). We investigated the significance of HICS ECG recording in ERS patients. METHODS AND RESULTS: Fifty-six patients showing inferolateral ER in the standard ECG and spontaneous ventricular fibrillation (VF) not linked to structural heart disease underwent drug provocation tests by sodium channel blockade with right precordial ECG (V1-V3) recording in the 2nd-4th intercostal spaces. The prevalence and long-term outcome of ERS patients with and without BrP-ECG in HICS were investigated. After 18 patients showing type 1 BrP-ECG in the standard ECG were excluded, 38 patients (34 males, mean age; 40.4 ± 13.6 years) were classified into four groups [group A (n = 6;16%):patients with ER and type 1 BrP-ECG only in HICS, group B (n = 5;13%):ERS with non-type 1 BrP-ECG only in HICS, group C (n = 8;21%):ERS with non-type 1 BrP-ECG in the standard ECG, and group D (n = 19;50%):ERS only, spontaneously or after drug provocation test]. During follow-up of 110.0 ± 55.4 months, the rate of VF recurrence including electrical storm was significantly higher in groups A (4/6:67%), B (4/5:80%), and C (4/8:50%) compared with D (2/19:11%) (A, B, and C vs. D, P < 0.05). CONCLUSIONS: Approximately 30% of the patients with ERS who had been diagnosed with the previous criteria showed BrP-ECG only in HICS. Ventricular fibrillation mostly recurred in patients showing BrP-ECG in any precordial lead including HICS; these comprised 50% of the ERS cohort.

Larger low voltage zone in endocardial unipolar map compared with that in epicardial bipolar map indicates difficulty in eliminating ventricular tachycardia by catheter ablation.

Patients with ischemic and non-ischemic cardiomyopathy often have substrate for ventricular tachycardia (VT) in the endocardium (ENDO), epicardium (EPI), and/or intramural. Although it has been reported that the ENDO unipolar (UNI) voltage map is useful in detecting EPI substrate, its feasibility to detect intramural scarring and its usefulness in radiofrequency catheter ablation (RFCA) remain unclear. To assess the relationship between the left ventricle (LV) ENDO UNI voltage map and the LV EPI bipolar (BIP) voltage map, and to determine the usefulness of the ENDO UNI voltage map to guide RFCA for VT in patients with cardiomyopathy undergoing combined ENDO- and EPI RFCA. Eleven patients with VT undergoing detailed ENDO and EPI electroanatomical mapping of the LV were included (mean age 59 ± 11 years, 9 men). We assessed the value of the LV ENDO UNI voltage map in identifying EPI and/or intramural substrate in these 11 patients with non-ischemic or ischemic cardiomyopathy. The underlying heart disease was dilated cardiomyopathy in 4 patients, cardiac sarcoidosis in 3, hypertrophic cardiomyopathy in 2, and ischemic heart disease in 2 patients. The mean LV ejection fraction was 24 ± 7 %. The low voltage zone (LVZ) was defined as <1.5 mV for LV ENDO BIP electrograms (EGMs), <8.3 mV for LV ENDO UNI EGMs, and <1.0 mV for LV EPI BIP EGMs. The surface area of each LVZ was measured. We also measured the LVZ of the spatial overlap between ENDO UNI and EPI BIP voltage maps using the transparency mode on CARTO software. We performed RFCA at the ENDO and EPI based on activation and/or substrate maps, targeting the LVZ and/or abnormal EGMs. The LVZ was present in the LV ENDO BIP voltage map in 10 of 11 patients (42 ± 33 cm(2)), and in the LV ENDO UNI voltage map in 10 of 11 patients (72 ± 45 cm(2)). The LVZ was present in the EPI BIP voltage map in 9 of 11 patients (70 ± 61 cm(2)), and the LVZ in the ENDO UNI voltage map was also seen in all 9 patients. The location of the LVZ in the EPI BIP map matched that in 45 ± 28 % of ENDO UNI voltage maps. The LVZ in the ENDO UNI voltage map was larger than that in the EPI BIP voltage map in 6 of 11 patients, and RFCA failed in 5 of these 6 patients. In the remaining 5 patients with a smaller LVZ in the ENDO UNI voltage map compared with the EPI BIP voltage map or no LVZ both at ENDO UNI and EPI BIP voltage map, VT was successfully eliminated in 4 of 5 patients. The LV ENDO UNI voltage map is useful in detecting EPI substrate in patients with cardiomyopathy. A larger LVZ in the ENDO UNI voltage map compared to that in the EPI BIP voltage map may indicate the presence of intramural substrate, which leads to difficulty in eliminating VT, even with combined ENDO- and EPI RFCA.

Relationship between coronary plaque vulnerability and serum n-3/n-6 polyunsaturated fatty acid ratio.

BACKGROUND: A low ratio of serum eicosapentaenoic acid to arachidonic acid (EPA/AA) has been associated with cardiovascular events. Higher-grade yellow color coronary plaques are associated with higher plaque vulnerability and higher thrombogenic potential. Therefore, the association between EPA/AA ratio and yellow color grade of coronary plaques was examined. METHODS AND RESULTS: Consecutive patients (n=54) who underwent percutaneous coronary intervention were enrolled in this study. The serum EPA/AA ratio was examined on admission. All patients underwent an angioscopic examination of the culprit vessel to examine the color grade of yellow plaques (0, white; 1, slight yellow; 2, yellow; and 3, intense yellow) and the presence of thrombus. Excluding 16 patients with acute coronary syndrome (ACS), 38 patients with stable angina were divided into 2 groups according to their EPA/AA ratio: the low EPA/AA group (n=19, EPA/AA ratio <0.37 [median]) and the high EPA/AA group (n=19, EPA/AA ratio ≥0.37). The maximum color grade (2.5 ± 0.5 vs. 1.9 ± 0.9; P=0.01) of yellow plaques was significantly higher and the number of non-culprit yellow plaques with thrombus (1.7 ± 0.8 vs. 1.2 ± 1.1; P=0.06) tended to be higher in low EPA/AA than in high EPA/AA stable angina patients. Multivariate analysis revealed that the serum EPA level (odds ratio=0.98, 95% confidence interval=0.96-0.99, P=0.03) was associated with the presence of grade-3 yellow plaques. CONCLUSIONS: A low serum EPA level and a low EPA/AA ratio was associated with high vulnerability of coronary plaques.