Implantable Defibrillator Use for De Novo Ventricular Tachyarrhythmias Encountered After Cardiac Surgery

2002 ◽  
Vol 25 (6) ◽  
pp. 951-956 ◽  
Author(s):  
EDWARD A. TELFER ◽  
ANDREW MECCA ◽  
MAUWIA MARTINI ◽  
BRIAN OLSHANSKY
2017 ◽  
Vol 26 (1) ◽  
pp. 47-53 ◽  
Author(s):  
Raul A Borracci ◽  
Miguel Rubio ◽  
Julio Baldi ◽  
Jose L Barisani

1986 ◽  
Vol 57 (1) ◽  
pp. 57-59 ◽  
Author(s):  
Eric J. Topol ◽  
Bruce B.L. Lerman ◽  
Kenneth L. Baughman ◽  
Edward V. Platia ◽  
Lawrence S.C. Griffith

2020 ◽  
Vol 6 (5) ◽  
Author(s):  
Nabil El-Sherif ◽  
Mohamed Boutjdir ◽  
Gioia Turitto

Sudden cardiac death accounts for approximately 360,000 annually in the United States and is the cause of half of all cardiovascular deaths. Ischemic heart disease is the major cause of death in the general adult population. Sudden cardiac death can be due to arrhythmic or non-arrhythmic cardiac causes, for example, myocardial rupture. Arrhythmic sudden cardiac death may be caused by ventricular tachyarrhythmia (ventricular tachycardia/ventricular fibrillation) or pulseless electrical activity/asystole. The majority of research in risk stratification centers on ventricular tachyarrhythmias simply because of the availability of a successful management strategy, the implantable cardioverter/ defibrillator. Currently the main criterion of primary defibrillator prophylaxis is the presence of organic heart disease and depressed left ventricular systolic function assessed as left ventricular ejection fraction. However, only one third of eligible patients benefit from the implantable defibrillator, resulting in significant redundancy in the use of the device. The cost to the health care system of sustaining this approach is substantial. Further, the current low implantation rate among eligible population probably reflects a perceived low benefit-to-cost ratio of the device. Therefore, attempts to optimize the selection process for primary implantable defibrillator prophylaxis are paramount. The present report will review the most recent pathophysiology and risk stratification strategies for sudden cardiac death beyond the single criterion of depressed ejection fraction. Emphasis will be placed on electrophysiological surrogates of conduction disorder, dispersion of repolarization, and autonomic imbalance, which represent our current understanding of the electrophysiological mechanisms that underlie the initiation of ventricular tachyarrhythmias. Further, factors that modify arrhythmic death, including noninvasive risk variables, biomarkers, and genomics will be addressed. These factors may have great utility in predicting sudden cardiac arrhythmic death in the general public.


1991 ◽  
Vol 68 (10) ◽  
pp. 1099-1100 ◽  
Author(s):  
Peter M. Sapin ◽  
Alan K. Woelfel ◽  
James R. Foster

2011 ◽  
Vol 109 (suppl_1) ◽  
Author(s):  
Murray H Kwon ◽  
Jennifer Q Zhang ◽  
Ani Abrahamyan ◽  
Zilu K Zhang ◽  
David W Gjertson ◽  
...  

Purpose: To clarify patterns of anti-HLA antibody expression (sensitization) occurring in patients bridged to transplantation (BTT) with ventricular assist devices (VADs). Methods: The study is a retrospective review of 68 patients undergoing BTT with either Heartmate II (HMII) axial flow LVAD or paracorporal BIVAD from January 2007 to July 2010 at UCLA Medical Center. Results: Five of 15 (33.3%) HMII pts became sensitized during treatment compared to 29 of 53 (54.7%) BIVAD patients, p=0.24. Table 1 shows common etiologies for patient sensitization of which only PRBC transfusion was statistically significant. [ table 1 ] Multiple variable analysis comparing BIVAD vs. HMII while controlling for previous cardiac surgery, pregnancy, and PRBC transfusion demonstrated an Odds Ratio of 5.20, p=0.029 (robust variance estimator). Of sensitized patients, all 5 (100%) of the HMII patients had pre-existing antibodies prior to VAD placement compared to 11 of 29 (62.1%) BIVAD patients, p=0.016. Maximum cumulative MFIs for BIVAD were 46,259 ± 66,349 vs. 42540 ± 12840 for HMII, p=0.90. Time to maximum antibody expression was shorter for the HMII group (34 ± 28 days vs. 5.8 ± 9 days, p=0.04). Table 1. Sensitization Risk Factors Antibodies + Antibodies − p-value Previous Cardiac Surgery 23.5% 8.8% 0.19 Pregnancy 20.6% 2.9% 0.05 PRBC 52.1±34.7 35.9±22.3 0.04 FFP 29.4±14.4 23.6±15.2 0.15 Platelets 9.8±9.7 6.8±6.7 0.20 Cryoprecipitate 3.2±2.6 3.1±2.6 0.74 Blood products expressed as mean units ± std dev Conclusion: BIVADs were associated with a five fold increased risk for sensitization when accounting for other risk factors. HMII patients required pre-sensitization to express antibodies during their treatment interval whereas BIVAD patients developed de novo antibodies. Although the peak cumulative MFIs were similar for both VAD types, the days to reach this peak were significantly less in the HMII group. These data suggest that sensitization in HMII patients may not be due to antigenic stimulation from the device itself.


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