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).
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).
Cardiac magnetic resonance (CMR) and 18F-2-fluoro-2-deoxyglucose positron emission tomography (FDG-PET) images were shown (figure 1).heartjnl;103/23/1922/F1F1F1Figure 1Cardiac magnetic resonance with a T1-weighted inversion recovery image (A) and 18F-2-fluoro-2-deoxyglucose positron emission tomography (B) in a 54-year-old man with new-onset ventricular fibrillation.
We have reported clinically relevant myocardial effects elicited by NHE-1 inhibitors given during resuscitation in animal models of ventricular fibrillation (VF).
A direction to explore could be to downgrade from CRT-D to CRT-P at the time of battery depletion in patients with large reverse remodeling and no ventricular tachycardia and ventricular fibrillation detected.
Ventricular tachycardia (VT)/ventricular fibrillation (VF) occurrence after cardiac resynchronization therapy-defibrillator (CRT-D) replacement is unknown; hence, there is no practical guideline to recommend either CRT-D or CRT-pacemaker at the time of device replacement.
Brugada syndrome is an inherited cardiac disorder caused by mutations in the cardiac sodium channel gene, SCN5A, that leads to ventricular fibrillation and sudden death.
The existence of SCN5A mutation and clinical variables (syncopal episode, documented ventricular fibrillation [VF], and family history of sudden death) were compared with spontaneous AF episodes.
Brugada syndrome is an inherited cardiac disorder caused by mutations in the SCN5A gene encoding the cardiac sodium channel alpha-subunit, and potentially leads to ventricular fibrillation and sudden death.
Dynamic change in ST-segment and spontaneous occurrence of ventricular fibrillation in Brugada syndrome with a novel nonsense mutation in the SCN5A gene during long-term follow-up.
Of the 27 candidate SNPs, one SNP (rs11720524) located in intron 1 of SCN5A which was previously associated with SCD was significantly associated with VF caused by first STEMI.