scholarly journals Nonspecific Intraventricular Conduction Delay by ECG Finding

2020 ◽  
Author(s):  
Keyword(s):  
Conduction Delay ◽  
Intraventricular Conduction ◽  
Intraventricular Conduction Delay

scholarly journals Physiological pacing to improve cardiac resynchronization therapy non-responder and a tryst with calcified septum—a case report

2021 ◽  
Vol 73 (1) ◽  
Author(s):  
Vanita Arora ◽  
Francesco Zanon ◽  
Viveka Kumar ◽  
Vivek Kumar ◽  
Pawan Suri
Keyword(s):  
Case Report ◽  
Cardiac Resynchronization Therapy ◽  
Ischemic Cardiomyopathy ◽  
Cardiac Resynchronization ◽  
Conduction Delay ◽  
Resynchronization Therapy ◽  
Intraventricular Conduction ◽  
Technological Approach ◽  
Intraventricular Septum ◽  
Intraventricular Conduction Delay

Abstract Background As per the literature, patients with intraventricular conduction delay (IVCD) do not respond well to cardiac resynchronization therapy (CRT) alone. They need advanced technological approach and out of the box thinking for a good response. Case Ours is a case of ischemic cardiomyopathy with wide QRS-IVCD, a non-responder to CRT. While planning for replacement of the device for early replacement indicator (ERI), we decided to do His-optimized CRT/left bundle optimized CRT (HOT-CRT/LOT-CRT) for the patient. Conclusion The challenges we faced with the present available hardware paved a way for insisting on the limitation of the available lumenless lead to penetrate calcified the septum and importance of the pre-procedure evaluation of intraventricular septum (IVS) for calcification by more than just echocardiography.

Abstract 13286: Non-Specific Intraventricular Conduction Delay and Risk of Sudden Death

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Audrey Uy-Evanado ◽  
Carmen Teodorescu ◽  
Kyndaron Reinier ◽  
Kumar Narayanan ◽  
Harpriya Chugh ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
General Population ◽  
Left Bundle Branch Block ◽  
Cardiac Death ◽  
Conduction Delay ◽  
Bundle Branch Block ◽  
Intraventricular Conduction ◽  
Qrs Morphology ◽  
Qrs Duration ◽  
Intraventricular Conduction Delay

Introduction: We and others have reported an independent association between prolonged QRS duration and risk of sudden cardiac death (SCD) in the general population. Left and right bundle branch block have been studied previously, but there is little information regarding non-specific intraventricular conduction delay and risk of SCD. Hypothesis: Completed conduction defects, including non-specific IVCD, are associated with increased SCD risk. Methods: Sudden cardiac death cases and controls from an ongoing large population based study in the Northwestern US (2002 to 2010) were included if age ≥ 35 years with a non-paced 12-lead ECG (recorded prior and unrelated to SCD in cases). QRS morphology was subcategorized as normal, intermediate [left anterior fascicular block (LAFB), left posterior fascicular block (LPFB), and incomplete right or left bundle branch block (IRBBB/ILBBB)] or completed conduction defects [left bundle branch block (LBBB), right bundle branch block (RBBB), or nonspecific intraventricular conduction delay (IVCD)]. Comparisons were conducted using chi-square tests for categorical variables and independent samples t-tests for continuous variables. Logistic regression was used to evaluate the association of QRS morphology with SCD. Results: We evaluated 761 SCD cases (64% male) and 539 controls (65% male). Cases were significantly older (69.7 vs 66.3 years, p<0.0001) with greater QRS duration (102 vs. 98 ms, p=0.001). For conduction categories, intermediate or completed conduction defects were significantly more common in cases whereas normal QRS morphology was more common among controls (p=0.01). And for specific morphology overall, QRS morphology patterns differed between cases and controls (p=0.03); abnormal QRS morphologies were more frequent in cases than controls except for LAFB. After adjustment for age and gender, however, only a finding of LBBB or non-specific IVCD remained a significant predictor of SCD [OR 1.34 (95% CI 1.03-1.75)]. Conclusions: LBBB and non-specific IVCD, but not RBBB, are significant predictors of SCD in the general population. These findings contribute to the utility of the 12-lead EKG for SCD risk stratification.

scholarly journals Intraventricular Conduction Delay as a Determinant of Atrial Echo Beats

Circulation ◽  
1974 ◽  
Vol 49 (5) ◽  
pp. 805-810 ◽  
Author(s):  
P. JACOB VARGHESE ◽  
ANTHONY N. DAMATO ◽  
ANTONIO R. CARACTA ◽  
JOHN J. GALLAGHER ◽  
MARK E. JOSEPHSON ◽  
...  
Keyword(s):  
Conduction Delay ◽  
Intraventricular Conduction ◽  
Intraventricular Conduction Delay

Intraventricular conduction delay after bupropion overdose

2005 ◽  
Vol 29 (3) ◽  
pp. 299-305 ◽  
Author(s):  
Steven C. Curry ◽  
John S. Kashani ◽  
Frank LoVecchio ◽  
William Holubek
Keyword(s):  
Conduction Delay ◽  
Intraventricular Conduction ◽  
Intraventricular Conduction Delay

scholarly journals Multiple arrhythmic syndromes in a newborn, owing to a novel mutation in SCN5A

2011 ◽  
Vol 89 (10) ◽  
pp. 723-736 ◽  
Author(s):  
Kirstine Calloe ◽  
Nicole Schmitt ◽  
Soren Grubb ◽  
Ryan Pfeiffer ◽  
Jens-Peter David ◽  
...  
Keyword(s):  
Qt Interval ◽  
Atrial Tachycardia ◽  
Novel Mutation ◽  
Post Partum ◽  
Conduction Delay ◽  
Interval Prolongation ◽  
Intraventricular Conduction ◽  
Qt Interval Prolongation ◽  
Window Current ◽  
Intraventricular Conduction Delay

Background. Mutations in the SCN5A gene have been linked to Brugada syndrome (BrS), conduction disease, Long QT syndrome (LQT3), atrial fibrillation (AF), and to pre- and neonatal ventricular arrhythmias. Objective. The objective of this study is to characterize a novel mutation in Nav1.5 found in a newborn with fetal chaotic atrial tachycardia, post-partum intraventricular conduction delay, and QT interval prolongation. Methods. Genomic DNA was isolated and all exons and intron borders of 15 ion-channel genes were sequenced, revealing a novel missense mutation (Q270K) in SCN5A. Nav1.5 wild type (WT) and Q270K were expressed in CHO-K1 with and without the Navβ1 subunit. Results. Patch-clamp analysis showed ∼40% reduction in peak sodium channel current (INa) density for Q270K compared with WT. Fast and slow decay of INa were significantly slower in Q270K. Steady-state activation and inactivation of Q270K channels were shifted to positive potentials, and window current was increased. The tetrodotoxin-sensitive late INa was increased almost 3-fold compared with WT channels. Ranolazine reduced late INa in WT and Q270K channels, while exerting minimal effects on peak INa. Conclusion. The Q270K mutation in SCN5A reduces peak INa while augmenting late INa, and may thus underlie the development of atrial tachycardia, intraventricular conduction delay, and QT interval prolongation in an infant.

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