Melatonin receptor activation protects against low potassium-induced ventricular fibrillation by preserving action potentials and connexin-43 topology in isolated rat hearts.
In hearts of PI3Kα-deficient mice, β-adrenergic stimulation in the presence of high Ca<sup>2+</sup> concentrations and 12-Hz burst pacing led to delayed afterdepolarizations and ventricular fibrillation.
We have reported clinically relevant myocardial effects elicited by NHE-1 inhibitors given during resuscitation in animal models of ventricular fibrillation (VF).
Using ambulance call reports and defibrillator files, we compared rates of VF termination (defined as the absence of VF at the rhythm check following defibrillation and two minutes of CPR) and VF termination to ROSC for patients who received standard defibrillation and those who received DSED (after on-line medical consultation).
VF influence on expression of p62, LC3BII/LC3BI, and Atg5-12 proteins was complex, possibly due to differential effects of VF-induced expression on proteins comprising the autophagic program.
Data revealed that VF induced degradation in AF, CF, CO, and SV, which prominently included-variable post-VF capacity for recovery of normal heart rhythm; increased extent of infarcted heart tissue; altered expression of cleaved-caspase-3 suggesting potential for VF-mediated amplification of apoptosis.
Family history of sudden cardiac death (SCD), prior syncope, spontaneous type 1 Brugada electrocardiogram (ECG), inducible ventricular fibrillation at electrophysiological study, and SCN5A mutations were present in 26%, 49%, 65%, 28%, and 58% of patients, respectively.
The study evaluates the microvascular density (MVD) and expression of hypoxia-induced factor (HIF-1α) in hypertrophic vocal fold (VF) lesions of different histopathological states including non-dysplastic, low-grade, high-grade dysplasia and invasive glottic cancer.
LV apical aneurysms are present in more than 20% MVOHCM cases and has been identified as an independent predictor of potentially lethal arrhythmic events, including non-sustained or sustained ventricular tachycardia (VT), and ventricular fibrillation (VF), as well as SCD.
The duration of ventricular fibrillation (VF) was higher in the lentiviral Tbx18 group compared with the GFP-injected controls (P = 0.02) and the Tbx18-pacemaker cell group (P = 0.02).
At 30 days, mortality was 13.9% and 3.6% in patients with and without primary ventricular fibrillation, respectively ( p<0.001), and median growth differentiation factor-15 concentration in patients with primary ventricular fibrillation was five-fold higher among those who died vs survivors (13,098 vs 2415 pg/ml, p<0.001).
LVEDV >158 mL and no use of angiotensin-converting-enzyme inhibitor/angiotensin receptor blocker were independent predictors of recurrences of VT/VF in ICM patients but not in DCM patients.
Compared to the without-STEMI subgroup, STEMI patients had more ventricular fibrillation (91 vs 50%; p<0.0001), and higher mean peak serum high-sensitivity troponin-T (8.25±14.7 vs 1.97±6.13 ug/L; p=0.006); in the context of higher median SS (18 vs 6.5; p=0.002) and target-lesion SS (tSS, 10 vs 0; p<0.001).