Right ventricular dysfunction predisposes to inducible ventricular tachycardia at electrophysiology studies in patients with acute ST-segment-elevation myocardial infarction and reduced left ventricular ejection fraction.

BACKGROUND: Inducible ventricular tachycardia (VT) is a strong predictor of spontaneous ventricular tachyarrhythmia following ST-segment-elevation myocardial infarction. Reduced left ventricular ejection fraction (EF) predisposes patients to inducible VT after ST-segment-elevation myocardial infarction. However, the role of right ventricular (RV) dysfunction in predisposing to inducible VT has not been described previously. METHODS AND RESULTS: Consecutive patients with ST-segment-elevation myocardial infarction treated with primary percutaneous coronary intervention underwent predischarge radionuclide gated heart pool scan to assess ventricular EF. The study cohort included patients with reduced left ventricular EF (left ventricular EF ≤40%) who underwent electrophysiology study (n=220) in an attempt to induce VT. We defined RV dysfunction as RVEF ≤35%. The end point was sustained monomorphic VT (cycle length ≥200 ms). This was considered a positive study. No inducible arrhythmia, ventricular fibrillation, or flutter (cycle length <200 ms) was considered a negative study. Infarct region, infarct-related artery, male sex, and RVEF ≤35% were univariable predictors of positive test. After multivariable analysis, RVEF ≤35% had the strongest association as an independent predictor of inducible VT at electrophysiology study (P<0.001; odds ratio, 5.8; 95% confidence interval, 3.005-11.262). CONCLUSIONS: RV dysfunction (RVEF ≤35%) predisposed to inducible VT at electrophysiology study in patients with impaired left ventricular EF (≤40%) after acute ST-segment-elevation myocardial infarction treated with primary percutaneous coronary intervention.

Electrocardiographic predictors of electroanatomic scar size in arrhythmogenic right ventricular cardiomyopathy: implications for arrhythmic risk stratification.

INTRODUCTION: The extent of right ventricular (RV) electroanatomic scar (EAS) detected by endocardial voltage mapping (EVM) is a powerful invasive predictor of arrhythmic outcome in patients with arrhythmogenic right ventricular cardiomyopathy (ARVC). Electrocardiogram (ECG) and signal-averaged ECG are noninvasive tools of established clinical value for the diagnosis of electrical abnormalities in ARVC. This study was designed to assess the role of ECG and SAECG abnormalities for noninvasive estimation of the extent and regional distribution of RV-EAS and prediction of scar-related arrhythmic risk. METHODS AND RESULTS: The study population included 49 consecutive patients (38 males, median age 35 years) with a definite diagnosis of ARVC and an abnormal EVM by CARTO system. At univariate analysis, the presence of epsilon waves, the degree of RV dilation, the severity of RV dysfunction, and the extent of negative T waves correlated with RV-EAS% area. Normal T-waves were associated with a median RV-EAS% area of 4.9% (4.5-6.4), negative T waves in V1-V3 of 22.0% (8.5-30.6), negative T waves in V1-V3 extending to lateral precordial leads (V4-V6) of 26.8% (11.5-35.2), and negative T waves in both precordial (V2-V6) and inferior leads of 30.2% (24.8-33.0) (P < 0.001). At multivariate analysis, the extent of negative T waves remained the only independent predictor of RV-EAS% area (B = 4.4, 95%CI 1.3-7.4, P = 0.006) and correlated with the arrhythmic event-rate during follow-up (P = 0.03). CONCLUSIONS: In patients with ARVC, the extent of negative T-waves across 12-lead ECG allows noninvasive estimation of the amount of RV-EAS and prediction of EAS-related arrhythmic risk.

Acute right ventricular infarction.

This article reviews the pathophysiology, hemodynamics, natural history, and management of patients with inferior myocardial infarction complicated by right ventricular infarction. Five key areas are highlighted in which advances may impact catheterization and laboratory management of these acutely ill patients.

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Speckle-tracking radial strain reveals left ventricular dyssynchrony in patients with permanent right ventricular pacing.

OBJECTIVES: Speckle-tracking strain analysis was used to assess the effects of permanent right ventricular (RV) pacing on the heterogeneity in timing of regional wall strain and left ventricular (LV) dyssynchrony. BACKGROUND: Recent studies have shown detrimental effects of RV pacing, possibly related to the induction of LV dyssynchrony. METHODS: Fifty-eight patients treated with His bundle ablation and pacemaker implantation were studied. To assess the effect of RV pacing on time-to-peak radial strain of different LV segments, we applied speckle-tracking analysis to standard LV short-axis images. In addition, New York Heart Association (NYHA) functional class, LV volumes, and systolic function were assessed at baseline and after long-term RV pacing. RESULTS: At baseline, similar time-to-peak strain for the 6 segments was observed (mean 371 +/- 114 ms). In contrast, after a mean of 3.8 +/- 2.0 years of RV pacing, there was a marked heterogeneity in time-to-peak strain of the 6 segments. In 33 patients (57%), LV dyssynchrony, represented by a time difference > or =130 ms between the time-to-peak strain of the (antero)septal and the posterolateral segments, was present. In these patients, a deterioration of LV systolic function and NYHA functional class was observed. In 11 patients, an "upgrade" of the conventional pacemaker to a biventricular pacemaker resulted in partial reversal of the detrimental effects of RV pacing. CONCLUSIONS: Speckle-tracking analysis revealed that permanent RV pacing induced heterogeneity in time-to-peak strain, resulting in LV dyssynchrony in 57% of patients, associated with deterioration of LV systolic function and NYHA functional class. Biventricular pacing may reverse these adverse effects of RV pacing.

Comparison of conduction delay in the right ventricular outflow tract between Brugada syndrome and right ventricular cardiomyopathy: investigation of signal average ECG in the precordial leads.

BACKGROUND: In both Brugada syndrome (BS) and arrhythmogenic right ventricular cardiomyopathy (ARVC), electrical abnormalities in the right ventricular outflow tract (RVOT) are important for arrhythmogenesis. OBJECTIVES: The aim of this study was to compare conduction delay in the right ventricular in BS with that in ARVC using the signal-averaged electrocardiogram. METHODS: Twenty patients with BS (18 men and 2 women; 55 +/- 12 years old; 9 symptomatic and 11 asymptomatic) and eight patients with ARVC (six men and two women; 53 +/- 16 years old) were included. We assessed the presence of late potentials (LPs) and the filtered QRS duration (fQRSd) in V(2) and V(5) using a high-pass filter of 40 Hz (fQRSd:40) and 100 Hz (fQRSd:100). RESULTS: In ARVC, there was no significant difference in fQRSd:40 between V2 and V5 (158 +/- 19 vs. 145 +/- 17 ms, respectively): however, in BS, fQRSd:40 in V2 was significantly longer than fQRSd:40 in V5 (147 +/- 15 vs. 125 +/- 10 ms, P < 0.001). In ARVC, there was no significant difference between fQRSd:40 and fQRSd:100 in V(2) and V(5) (158 +/- 19 vs. 142 +/- 23 ms and 145 +/- 17 vs. 132 +/- 9 ms, respectively). In contrast, in BS, fQRSd:100 was significantly shorter than fQRSd:40 in V2 (110 +/- 8 ms vs. 147 +/- 15, P < 0.001). The relative decrease in fQRSd:100 compared with fQRSd:40 in V2 was significantly greater in BS than in ARVC. CONCLUSION: The dominant prolongation of the fQRSd in the right precordial lead in BS was different from the characteristics of ARVC, which may be caused by the conduction delay due to fibro-fatty replacement in RV.

Right ventricular cardiomyopathy in beta-thalassaemia major.

AIMS: To evaluate right ventricular function in patients with beta-thalassaemia major and congestive heart failure. Background In patients with beta-thalassaemia major a high incidence of cardiac involvement still exists despite improved prognosis with chelation therapy. Development of severe right heart failure is common and has been attributed to pulmonary hypertension secondary to lung haemochromatosis. However, the possibility of direct right ventricular myocardial involvement in the absence of significant pulmonary hypertension has not been adequately investigated. METHODS: Twenty-nine consecutively screened patients with beta-thalassaemia major and congestive heart failure were investigated by Doppler echocardiography, right ventricular first-pass radionuclide examination and cardiac catheterization. Haemodynamic data were obtained both before and after volume loading. A control group of 39 patients with beta-thalassaemia major, free from cardiac disease, and matched for age, gender, body surface area and heart rate was used for comparison. A subset of the control thalassaemic group (n=15) underwent both radionuclide and haemodynamic assessment. RESULTS: The majority of patients were on non-optimal chelation therapy. Only two of 29 patients were found to have cor pulmonale. One other patient suffered from constrictive pericarditis. A restrictive filling pattern in both ventricles and left ventricular systolic dysfunction were evident in the other 26 patients. Pulmonary artery pressure (systolic, 33+/-8 vs 27+/-5 mmHg, P<0.05) and pulmonary vascular resistance (114+/-56 vs 65+/-29 dynes. s. cm(-5), P<0.01) were only mildly elevated in the heart failure group. After volume challenge, cardiac output remained unchanged although the increments of ventricular filling pressures were significant (Deltaright atrial: 4.8+/-2.2 mmHg, P<0.05; Deltapulmonary capillary wedge: 5.6+/-2.9 mmHg, P<0.05) and correlated with each other (r=0.69;P<0.001) in heart failure patients, suggesting pericardial constraint and ventricular interaction. In these patients compared with the control thalassaemic group, a lower right ventricular ejection fraction (29%+/-9 vs 59%+/-6, P<0.0001) without correlation with pulmonary artery pressures was found. Haemodynamically significant right ventricular dysfunction defined as mean right atrial pressure >10 mmHg and ratio of mean right atrial-to-capillary wedge pressure >0.8 was evident in 15 of the 26 patients (58%), all with severe symptoms, representing three fourths of the patients in functional class III and IV. Simultaneous pressure recordings in six of these 15 patients showed equalization of ventricular end-diastolic pressures within 5 mmHg. CONCLUSION: The majority of patients with beta-thalassaemia major and severe congestive heart failure demonstrated a unique haemodynamic pattern similar to that described in predominant right ventricular infarction, indicating severe right ventricular cardiomyopathy in addition to left ventricular dysfunction. The incidence of cor pulmonale as a cause of right heart failure seems to be much lower than previously hypothesized.