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Background Action potential alternans can induce ventricular tachyarrhythmias and manifest on the surface ECG as T-wave alternans (TWA) and QRS alternans (QRSA). We sought to evaluate microvolt QRSA in cardiomyopathy patients in relation to TWA and ventricular tachyarrhythmia outcomes. Methods and Results Prospectively enrolled cardiomyopathy patients (n=100) with prophylactic defibrillators had 12-lead ECGs recorded during ventricular pacing from 100 to 120 beats/min. QRSA and TWA were quantified in moving 128-beat segments using the spectral method. Segments were categorized as QRSA positive (QRSA+) and/or TWA positive (TWA+) based on ≥2 precordial leads having alternans magnitude >0 and signal:noise >3. Patients were similarly categorized based on having ≥3 consecutive segments with alternans. TWA+ and QRSA+ occurred together in 31% of patients and alone in 18% and 14% of patients, respectively. Although TWA magnitude (1.4±0.4 versus 4.7±1.0 µV, P <0.01) and proportion of TWA+ studies (16% versus 46%, P <0.01) increased with rate, QRSA did not change. QRS duration was longer in QRSA+ than QRSA-negative patients (138±23 versus 113±26 ms, P <0.01). At 3.5 years follow-up, appropriate defibrillator therapy or sustained ventricular tachyarrhythmia was greater in QRSA+ than QRSA-negative patients (30% versus 8%, P =0.02) but similar in TWA+ and TWA-negative patients. Among QRSA+ patients, the event rate was greater in those without TWA (62% versus 21%, P =0.02). Multivariable Cox analysis revealed QRSA+ (hazard ratio [HR], 4.6; 95% CI, 1.5-14; P =0.009) and QRS duration >120 ms (HR, 4.1; 95% CI, 1.3-12; P =0.014) to predict events. Conclusions Microvolt QRSA is novel phenomenon in cardiomyopathy patients that can exist without TWA and is associated with QRS prolongation. QRSA increases the risk of ventricular tachyarrhythmia 4-fold, which merits further study as a risk stratifier.

Background: Although QRS duration (QRSd) is an important determinant of cardiac resynchronization therapy (CRT) response, non-responder rates remain high. QRS fragmentation can also reflect electrical dyssynchrony. We hypothesized that quantification of abnormal QRS peaks (QRSp) would predict CRT response., Methods: Forty-seven CRT patients (left ventricular ejection fraction = 23±7%) were prospectively studied. Digital 12-lead ECGs were recorded during native rhythm at baseline and 6 months post-CRT. For each precordial lead, QRSp was defined as the total number of peaks detected on the unfiltered QRS minus those detected on a smoothed moving average template QRS. CRT response was defined as >5% increase in left ventricular ejection fraction post-CRT., Results: Sixty-percent of patients responded to CRT. Baseline QRSd was similar in CRT responders and non-responders, and did not change post-CRT regardless of response. Baseline QRSp was greater in responders than non-responders (9.1±3.5 vs. 5.9±2.2, p = 0.001) and decreased in responders (9.2±3.6 vs. 7.9±2.8, p = 0.03) but increased in non-responders (5.5±2.3 vs. 7.5±2.8, p = 0.049) post-CRT. In multivariable analysis, QRSp was the only independent predictor of CRT response (Odds Ratio [95% Confidence Interval]: 1.5 [1.1-2.1], p = 0.01). ROC analysis revealed QRSp (area under curve = 0.80) to better discriminate response than QRSd (area under curve = 0.67). Compared to QRSd ≥150ms, QRSp ≥7 identified response with similar sensitivity but greater specificity (74 vs. 32%, p<0.05). Amongst patients with QRSd <150ms, more patients with QRSp ≥7 responded than those with QRSp <7 (75 vs. 0%, p<0.05)., Conclusions: Our novel automated QRSp metric independently predicts CRT response and decreases in responders. Electrical dyssynchrony assessed by QRSp may improve CRT selection and track structural remodeling, especially in those with QRSd <150ms., Competing Interests: The authors have declared that no competing interests exist.

Background: QRS abnormalities may not be apparent in sinus rhythm in electrically stable cardiomyopathy patients who can have quiescent but highly arrhythmogenic substrate. Here, we test the hypothesis that differential changes in QRS construction during right-ventricular apex pacing (RVP) as opposed to atrial pacing (AP) will identify latent substrate for ventricular arrhythmias (VA) and death., Methods: Forty patients with cardiomyopathy free of VA underwent baseline 114-electrode body-surface electrocardiogram during AP (100 beats per minute [bpm]) and RVP (100 and 120 bpm). The filtered-averaged QRS at each electrode was deconstructed into individual intra-QRS and post-QRS ventricular myopotentials (V MP ). The primary outcome was VA or death. Prognostic accuracy of V MP was validated using V1 to V6 leads in another prospective cohort of 44-cardiomyopathy patients., Results: Twenty-six patients were eligible for initial analysis. After 5 ± 2 years of follow-up, eight (31%) patients had VA (VA Pos ) while rest were uneventful (VA Neg ). During AP 100 , VA Pos patients expressed more V MP than VA Neg patients (16 ± 1 vs 12 ± 1, P = 0.02). RVP 100 and RVP 120 in VA Pos patients introduced an additional 5.5 ± 0.5 and 6.0 ± 0.5 V MP (P < 0.0001 vs AP 100 ). The relative change with RVP 120 versus AP 100 in VA Neg patients exceeded VA Pos patients by 1.2 ± 0.5 V MP (P = 0.03). Increment in V MP count of <8 in lead-V5 with RVP 120 compared to AP 100 best predicted VA (area under curve 0.81, P = 0.01). In the validation cohort, primary outcome occurred in 13 (33%) patients. Native QRS features and AP 100 alone failed to predict primary outcome. Patients with increment in V MP count of <8 in lead-V5 with RVP 120 versus AP 100 had 7.9-fold increased risk of primary outcome (95% confidence interval 1.01, 61.61; P = 0.049)., Conclusion: Cardiomyopathy patients at risk of VA or death perturb the QRS less than low-risk patients with differential pacing. This functional response may be useful to identify arrhythmogenic substrate., (© 2018 Wiley Periodicals, Inc.)

Background: T-wave alternans (TWA), a marker of electrical instability, can be modulated by cardiac resynchronization therapy (CRT). The relationship between TWA and heart failure response to CRT has not been clearly defined., Methods and Results: In 40-patients (age 65±11 years, left ventricular ejection-fraction [LVEF] 23±7%), TWA was evaluated prospectively at median of 2 months (baseline) and 8 months (follow-up) post-CRT implant. TWA-magnitude (Valt >0μV, k≥3), its duration (d), and burden (Valt ·d) were quantified in moving 128-beat segments during incremental atrial (AAI, native-TWA) and atrio-biventricular (DDD-CRT) pacing. The immediate and long-term effect of CRT on TWA was examined. Clinical response to CRT was defined as an increase in LVEF of ≥5%. Native-TWA was clinically significant (Valt ≥1.9μV, k≥3) in 68% of subjects at baseline. Compared to native-TWA at baseline, DDD-CRT pacing at baseline and follow-up reduced the number of positive TWA segments, peak-magnitude, longest-duration and peak-burden of TWA (44±5 to 33±5 to 28±4%, p = 0.02 and 0.002; 5.9±0.8 to 4.1±0.7 to 3.8±0.7μV, p = 0.01 and 0.01; 97±9 to 76±8 to 67±8sec, p = 0.004 and <0.001; and 334±65 to 178±58 to 146±54μV.sec, p = 0.01 and 0.004). In addition, the number of positive segments and longest-duration of native-TWA diminished during follow-up (44±5 to 35±6%, p = 0.044; and 97±9 to 81±9sec, p = 0.02). Clinical response to CRT was observed in 71% of patients; the reduction in DDD-CRT paced TWA both at baseline and follow-up was present only in responders (interaction p-values <0.1)., Conclusion: Long-term CRT reduces the prevalence and magnitude of TWA. This CRT induced beneficial electrical remodeling is a marker of clinical response after CRT., Competing Interests: The authors have declared that no competing interests exist.

An ECG recorded from a patient with an implanted cardiac pacemaker showed a striking high frequency pulsing on the ST-T segments linked with each QRS complex. In this report we present an approach to the clatter on the ECG and discuss various potential diagnoses that can have closely similar pattern., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Brugada pattern electrocardiogram (ECG) unmasking can occur due to various drugs. There are old reports of the acute infarction pattern in aluminum phosphide (rodenticide)-related toxic myocarditis. The given case illustrates the Brugada pattern and various other ECG abnormalities in a patient with this poisoning. The old reported cases of the acute infarction pattern are also likely the Brugada pattern.