Ventricular Fibrillation Publications (35759)
Ventricular Fibrillation Publications
What makes this presentation original is that the pre-ablation spontaneous heart rate in AF was slow (84 bpm), and that VF occurred after ablation despite a minimal heart rate drop of only 14 bpm. VF is the most feared complication of AVN ablation, but it had previously only been described in case of acute heart rate drop after ablation of at least 30 bpm (and more frequently>50 bpm). This case report highlights the fact that VF may occur after AVN ablation regardless of the heart rate drop, rendering temporary fast ventricular pacing mandatory whatever the pre-ablation heart rate.
The aim of this study was to assess the diagnostic yield of NGS in IVF patients.
A total of 33 patients initially diagnosed with IVF were included (mean age 53±15; 42% male). In all included patients NGS of 33 genes + the DPP6 haplotype were screened and normal in a previous stage. Genetic screening comprised NGS of a panel of 179 additional genes. Variants with a minor allele frequency of <0.05% were assessed for pathogenicity using existing mutation databases and in silico predictive algorithms.
In one out of 33 patients, a likely pathogenic mutation was detected. The added yield of genetic testing with NGS of 179 additional genes is 3% in IVF patients. In 15% of the patients one or multiple variants of uncertain clinical significance were detected.
The added yield of genetic screening of extended NGS panels in patients initially diagnosed with IVF is minimal. Routine analysis of large diagnostic NGS panels is therefore not recommended.
We investigated the VF events, prevalence of J waves, and relationship between the VF events and J waves.
J waves were observed in 16 patients (26%) and VF events were documented in 11 (18%). The incidence of VF in the patients with J waves was significantly higher than that in those without J waves (38% vs 11%, p=0.026). J waves were observed in the inferior leads in 14 patients, lateral leads in 5, and anterior leads in 3. A univariate analysis indicated that the incidence of VF in the inferior leads of J wave positive patients (46%=6/14) was significantly (p=0.01) higher than that in the inferior leads of J wave negative patients (10%=5/48). The J waves in the anterior and/or lateral leads were not related to the incidence of VF. Notched type and slurred type J waves were not associated with VF. A multivariate analysis revealed that J waves in VSA patients were associated with VF [odds ratio (OR) 6.41, 95% confidence interval (CI) 1.37-29.93, p=0.02] and organic stenosis (OR 6.98, 95% CI 1.39-35.08, p=0.02). Further, J waves in the inferior leads were strongly correlated with VF (OR 11.85, 95% CI 2.05-68.42, p=0.006).
The results suggest that the existence of J waves, especially in the inferior leads, might be a risk factor for VF in VSA patients.
We analyzed 27 single nucleotide polymorphisms (SNP) previously associated with SCD/VF in other cohorts, and examined whether these SNPs were associated with VF caused by first STEMI in the GEnetic causes of Ventricular Arrhythmias in patients with first ST-elevation Myocardial Infarction (GEVAMI) study on ethnical Danes. The GEVAMI study is a prospective case-control study involving 257 cases (STEMI with VF) and 537 controls (STEMI without VF).
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. The major C-allele of rs11720524 was present in 64% of the cases and the C/C genotype was significantly associated with VF with an odds ratio (OR) of 1.87 (95% CI: 1.12-3.12; P = 0.017). After controlling for clinical differences between cases and controls such as age, sex, family history of sudden death, alcohol consumption, previous atrial fibrillation, statin use, angina, culprit artery, and thrombolysis in myocardial infarction (TIMI) flow, the C/C genotype of rs11720524 was still significantly associated with VF with an OR of 1.9 (95% CI: 1.05-3.43; P = 0.032). Marginal associations with VF were also found for rs9388451 in HEY2 gene. The CC genotype showed an insignificant risk for VF with OR = 1.50 (95% CI: 0.96-2.40; P = 0.070).
One common intronic variant in SCN5A suggested an association with VF caused by first STEMI. Further studies into the functional abnormalities associated with the noncoding variant in SCN5A may lead to important insights into predisposition to VF during STEMI.
He postulated that such a device "when adapted for clinical use, might be implanted temporarily or permanently in selected patients particularly prone to develop ventricular fibrillation and thus provide them with some degree of protection from sudden coronary death". In 1980 he reported on the first human implants of an "electronic device designed to monitor cardiac electrical activity, to recognise ventricular fibrillation and ventricular tachyarrhythmias … and then to deliver corrective defibrillatory discharges". Through innovations in circuitry, battery, and capacitor technologies, the current implantable cardioverter-defibrillator is 10 times smaller and exponentially more sophisticated than that first iteration. This article will review the inner workings of the implantable cardioverter-defibrillator and outline several features that make it the wonder in technology that it has become.
Owing to the relatively high prevalence of asymptomatic Wolff-Parkinson-White pattern and availability of catheter ablation, there has been a need to identify risk among asymptomatic patients. Recent guidelines recommend invasive evaluation for such patients where pre-excitation clearly does not disappear during exercise testing. This strategy has a high negative predictive value only. The accuracy of this approach is under continued investigation, especially in light of other considerations: Patients having intermittent pre-excitation, once thought to be at minimal risk may not be, and the role of isoproterenol in risk assessment.
Anomalous origin of coronary artery from the opposite sinus occurs in 0.7% of the young general population aged between 11 and 15 years. If the anomalous coronary artery courses between the pulmonary artery and the aorta, sudden cardiac death may occur during or shortly after vigorous exercise, especially in patients where the anomalous left coronary artery originates from the right sinus of Valsalva. Symptomatic patients with evidence of ischaemia should have surgical correction. No treatment is needed for asymptomatic patients with an anomalous right coronary artery from the left sinus of Valsalva. At present, there is no consensus regarding how to manage asymptomatic patients with anomalous left coronary artery from the right sinus of Valsalva and interarterial course. Myocardial bridging is commonly observed in cardiac catheterisation and it rarely causes exercise-induced coronary syndrome or cardiac death. In symptomatic patients, refractory or β-blocker treatment and surgical un-bridging may be considered.
We retrospectively analyzed 104 consecutive CRT patients. A responder was defined as a patient with a relative reduction in the LVESV ≥15% at 6 months after CRT. Fifty-six responders participated in this study. A transient responder was defined as a responder without a relative reduction in the LVESV ≥15% at 2 years after CRT or who died of cardiac events during the 24-month follow-up period.
Of 56 responders, 16 (29%) were transient responders. Multivariable logistic regression analysis showed that chronic atrial fibrillation (AF) (odds ratio [OR] = 19.2, 95% confidence interval [CI] [1.93, 190], P = 0.012) and amiodarone usage (OR = 60.9, 95% CI [4.18, 886], P = 0.003) were independent predictors of transient responses. Hospitalizations for heart failure were significantly higher among the transient responders than among the lasting responders during a mean follow-up period of 7.6 years (log-rank P < 0.001), and all-cause mortality tended to be higher among the transient responders (log-rank P = 0.093).
One-third of the responders were transient responders at 2 years after CRT, and their long-term prognoses were poor. Careful attention should be paid to maintain the reduction in LVESV especially in patients with chronic AF. This article is protected by copyright. All rights reserved.
We present the unusual case of a young Afghan male, who presented to us with painful, tender and swollen legs three days after a heavy alcohol binge on a Saturday night. He was diagnosed as a case of acute limb ischemia secondary to massive abdominal aorta and bilateral femoral artery thrombosis. He also had acute renal failure secondary to rhabdomyolysis. Cardiac workup revealed new onset paroxysmal atrial fibrillation and a large thrombus in the left ventricular cavity. His blood ethanol level was high. He was treated by a multidisciplinary team; urgent surgical thrombectomy for thrombotic complications, intravenous fluid hydration and later renal replacement therapy for acute renal failure. To the best of our knowledge, such a constellation of clinical features in association with severe acute alcohol intoxication has not been reported in the literature. We believe, the procoagulant nature of high blood ethanol levels and the onset of atrial fibrillation after the heavy alcohol binge, known as the holiday heart syndrome, precipitated the thrombotic events leading to rhabdomyolysis and acute renal failure. Through this case, we conclude that a very heavy alcohol binge may cause thrombotic occlusion of the abdominal aorta and femoral arteries resulting in ischemic rhabdomyolysis and acute renal failure. A high index of suspicion must be kept, especially for a patient presenting with tender, swollen lower limbs and acute renal failure after an alcohol binge.