Independent of the severity of coronary artery disease, diabetic patients have an increased risk of developing heart failure. This clinical entity has been considered to be a distinct disease process referred to as 'diabetic cardiomyopathy'. Experimental studies suggest that extensive metabolic perturbations may underlie both functional and structural alterations of the diabetic myocardium. Translational studies are, however, limited and only partly explain why diabetic patients are at increased risk of cardiomyopathy and heart failure. Although a range of diagnostic methods may help to characterize alterations in cardiac function in general, none are specific for the alterations in diabetes. Treatment paradigms are very much limited to interpretation and translation from the results of interventions in non-diabetic patients with heart failure. This suggests that there is an urgent need to conduct pathogenetic, diagnostic and therapeutic studies specifically in diabetic patients with cardiomyopathy to better understand the factors which initiate and progress diabetic cardiomyopathy and to develop more effective treatments.
word count: 149None of the authors have any conflicts of interest.
BackgroundLocalizing the origin of outflow tract ventricular tachycardias (OTVT) is hindered by lack of accuracy of electrocardiographic (ECG) algorithms and infrequent spontaneous premature ventricular complexes (PVCs) during electrophysiological studies.ObjectivesTo prospectively assess the performance of noninvasive electrocardiographic mapping (ECM) in the pre-/periprocedural localization of OTVT origin to guide ablation and to compare the accuracy of ECM with that of published ECG algorithms.MethodsPatients with symptomatic OTVT/PVCs undergoing clinically indicated ablation were recruited. The OTVT/PVC origin was mapped preprocedurally by using ECM, and 3 published ECG algorithms were applied to the 12-lead ECG by 3 blinded electrophysiologists. Ablation was guided by using ECM. The OTVT/PVC origin was defined as the site where ablation caused arrhythmia suppression. Acute success was defined as abolition of ectopy after ablation. Medium-term success was defined as the abolition of symptoms and reduction of PVC to less than 1000 per day documented on Holter monitoring within 6 months.ResultsIn 24 patients (mean age 50 ± 18 years) recruited ECM successfully identified OTVT/PVC origin in 23/24 (96%) (right ventricular outflow tract, 18; left ventricular outflow tract, 6), sublocalizing correctly in 100% of this cohort. Acute ablation success was achieved in 100% of the cases with medium-term success in 22 of 24 patients. PVC burden reduced from 21,837 ± 23,241 to 1143 ± 4039 (P < .0001). ECG algorithms identified the correct chamber of origin in 50%–88% of the patients and sublocalized within the right ventricular outflow tract (septum vs free-wall) in 37%–58%.ConclusionsECM can accurately identify OTVT/PVC origin in the left and the right ventricle pre- and periprocedurally to guide catheter ablation with an accuracy superior to that of published ECG algorithms.
Background Bipolar electrogram voltage during sinus rhythm (V SR ) has been used as a surrogate for atrial fibrosis in guiding catheter ablation of persistent atrial fibrillation (AF), but the fixed rate and wavefront characteristics present during sinus rhythm may not accurately reflect underlying functional vulnerabilities responsible for AF maintenance. Objective The purpose of this study was determine whether, given adequate temporal sampling, the spatial distribution of mean AF voltage (V mAF ) better correlates with delayed-enhancement magnetic resonance imaging (MRI-DE)–detected atrial fibrosis than V SR . Methods AF was mapped (8 seconds) during index ablation for persistent AF (20 patients) using a 20-pole catheter (660 ± 28 points/map). After cardioversion, V SR was mapped (557 ± 326 points/map). Electroanatomic and MRI-DE maps were co-registered in 14 patients. Results The time course of V mAF was assessed from 1–40 AF cycles (∼8 seconds) at 1113 locations. V mAF stabilized with sampling >4 seconds (mean voltage error 0.05 mV). Paired point analysis of V mAF from segments acquired 30 seconds apart (3667 sites; 15 patients) showed strong correlation (r = 0.95; P <.001). Delayed enhancement (DE) was assessed across the posterior left atrial (LA) wall, occupying 33% ± 13%. V mAF distributions were (median [IQR]) 0.21 [0.14–0.35] mV in DE vs 0.52 [0.34–0.77] mV in non-DE regions. V SR distributions were 1.34 [0.65–2.48] mV in DE vs 2.37 [1.27–3.97] mV in non-DE. V mAF threshold of 0.35 mV yielded sensitivity of 75% and specificity of 79% in detecting MRI-DE compared with 63% and 67%, respectively, for V SR (1.8-mV threshold) . Conclusion The correlation between low-voltage and posterior LA MRI-DE is significantly improved when acquired during AF vs sinus rhythm. With adequate sampling, mean AF voltage is a reproducible marker reflecting the functional response to the underlying persistent AF substrate.
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