Browsing by Subject "ventricular fibrillation"

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    The effects of remodeling with heart failure on mode of initiation of ventricular fibrillation and its spatiotemporal organization
    (Springer, 2015-09) Everett, Thomas H.; Hulley, George S.; Lee, Ken W.; Chang, Roger; Wilson, Emily E.; Olgin, Jeffrey E.; Department of Medicine, IU School of Medicine
    Purpose The effect of the heart failure substrate on the initiation of ventricular fibrillation (VF) and its resulting mechanism is not known. The objective of this study was to determine the effects of substrate on VF initiation and its spatiotemporal organization in the heart failure model. Methods Optical action potentials were recorded from LV wedge preparations either from structurally normal hearts (control, n = 11) or from congestive heart failure (CHF; n = 7), at the epicardial surface, endocardial surface which included a papillary muscle, and a transmural cross section. Action potential duration (APD80) was determined, and VF was initiated. A fast Fourier transform was calculated, and the dominant frequency (DF) was determined. Results The CHF group showed increased VF vulnerability (69 vs 26 %, p < 0.03), and every mapped surface showed an APD80 gradient which included islands of higher APDs on the transmural surface (M cells) which was not observed in controls. VF in the CHF group was characterized by stable, discrete, high-DF areas that correlated to either foci or spiral waves located on the transmural surface at the site of the papillary muscle. Overall, the top 10 % of DFs correlated to an APD of 101 ms while the bottom 10 % of DFs correlated to an APD of 126 ms (p < 0.01). Conclusions In the CHF model, APD gradients correlated with an increased vulnerability to VF, and the highest stable DFs were located on the transmural surface which was not seen in controls. This indicates that the CHF substrate creates unique APD and DF characteristics.
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    Role of apamin sensitive small conductance calcium-activated potassium currents in long term cardiac memory in rabbits
    (Elsevier, 2018) Yin, Dechun; Chen, Mu; Yang, Na; Wu, Adonis Z.; Xu, Dongzhu; Tsai, Wei-Chung; Yuan, Yuan; Tian, Zhipeng; Chan, Yi-Hsin; Shen, Changyu; Chen, Zhenhui; Lin, Shien-Fong; Weiss, James N.; Chen, Peng-Sheng; Everett, Thomas H., IV.; Medicine, School of Medicine
    Background Apamin-sensitive small conductance calcium-activated K current (IKAS) is upregulated during ventricular pacing and masks short-term cardiac memory (CM). Objective – To determine the role of IKAS in long-term CM. Methods – CM was created with 3-5 weeks of ventricular pacing and defined by a flat or inverted T-wave off pacing. Epicardial optical mapping was performed in both paced and normal ventricles. Action potential duration (APD80) was determined during RA pacing. Ventricular stability was tested before and after IKAS blockade. Four paced hearts and 4 normal hearts were used for western blotting and histology. Results – There were no significant differences in either the echocardiographic parameters or in fibrosis levels between groups. Apamin induced more APD80 prolongation in CM than in normal ventricles (9.6% [8.8%-10.5%] vs 3.1% [1.9%-4.3%], p<0.001). Apamin significantly lengthend the APD80 in the CM model at late activation sites, indicating significant IKAS upregulation at those sites. The CM model also had altered Ca2+ handling as the 50% Ca2+ transient duration and amplitude were increased at distal sites compared to a proximal site (near the pacing site). After apamin, the CM model had increased VF inducibility (paced vs control, 33/40 (82.5%) vs 7/20 (35%) P<0.001), and longer VF durations (124 vs 26 seconds, P<0.001). Conclusions Chronic ventricular pacing increases Ca2+ transients at late activation sites which activates IKAS to maintain repolarization reserve. IKAS blockade increases VF vulnerability in chronically paced rabbit ventricles.
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    Sudden Cardiac Arrest in a Young Patient with Severe Pectus Excavatum
    (Elsevier, 2018) Rachwan, Rayan Jo; Purpura, Andrea K.; Kahwash, Basil M.; Medicine, School of Medicine
    We report a case of sudden cardiac arrest in the setting of ventricular fibrillation in a previously healthy 19-year-old male. Chest imaging demonstrated severe pectus excavatum with Pectus Severity Index of 22.7. Extensive workup was unrevealing for other cardiopulmonary etiologies, including conduction and structural abnormalities. The patient was scheduled for a Ravitch procedure and was discharged on a wearable defibrillator vest for temporary protection against ventricular arrhythmias. Later, the patient underwent subcutaneous implantable cardioverter defibrillator placement. Sudden cardiac arrest as an initial presentation of pectus excavatum is a rare entity scarcely discussed in medical literature. In this patient-centered focused review, we explore this unique case and offer our management approach amid the lack of concrete guidelines.