Potassium Disturbances and Risk of Ventricular Fibrillation Among Patients With ST-Segment-Elevation Myocardial Infarction

Background Potassium disturbances per se increase the risk of ventricular fibrillation (VF). Whether potassium disturbances in the acute phase of ST-segment-elevation myocardial infarction (STEMI) are associated with VF before primary percutaneous coronary intervention (PPCI) is uncertain. Methods and Results All consecutive STEMI patients were identified in the Eastern Danish Heart Registry from 1999 to 2016. Comorbidities and medication use were assessed from Danish nationwide registries. Potassium levels were collected immediately before PPCI start. Multivariate logistic models were performed to determine the association between potassium and VF. The main analysis included 8624 STEMI patients of whom 822 (9.5%) had VF before PPCI. Compared with 6693 (77.6%) patients with normokalemia (3.5-5.0 mmol/L), 1797 (20.8%) patients with hypokalemia (5.0 mmol/L) were older with more comorbidities. After adjustment, patients with hypokalemia and hyperkalemia had a higher risk of VF before PPCI (odds ratio 1.90, 95% CI 1.57-2.30, P<0.001) and (odds ratio 3.36, 95% CI 1.95-5.77, P<0.001) compared with normokalemia, respectively. Since the association may reflect a post-resuscitation phenomenon, a sensitivity analysis was performed including 7929 STEMI patients without VF before PPCI of whom 127 (1.6%) had VF during PPCI. Compared with normokalemia, patients with hypokalemia had a significant association with VF during PPCI (odds ratio 1.68, 95% CI 1.01-2.77, P=0.045) after adjustment. Conclusions Hypokalemia and hyperkalemia are associated with increased risk of VF before PPCI during STEMI. For hypokalemia, the association may be independent of the measurement of potassium before or after VF

Seasonality of ventricular fibrillation at first myocardial infarction and association with viral exposure

AIMS:To investigate seasonality and association of increased enterovirus and influenza activity in the community with ventricular fibrillation (VF) risk during first ST-elevation myocardial infarction (STEMI). METHODS:This study comprised all consecutive patients with first STEMI (n = 4,659; aged 18-80 years) admitted to the invasive catheterization laboratory between 2010-2016, at Copenhagen University Hospital, Rigshospitalet, covering eastern Denmark (2.6 million inhabitants, 45% of the Danish population). Hospital admission, prescription, and vital status data were assessed using Danish nationwide registries. We utilized monthly/weekly surveillance data for enterovirus and influenza from the Danish National Microbiology Database (2010-2016) that receives copies of laboratory tests from all Danish departments of clinical microbiology. RESULTS:Of the 4,659 consecutively enrolled STEMI patients, 581 (12%) had VF before primary percutaneous coronary intervention. In a subset (n = 807), we found that VF patients experienced more generalized fatigue and flu-like symptoms within 7 days before STEMI compared with the patients without VF (OR 3.39, 95% CI 1.76-6.54). During the study period, 2,704 individuals were diagnosed with enterovirus and 19,742 with influenza. No significant association between enterovirus and VF (OR 1.00, 95% CI 0.99-1.02), influenza and VF (OR 1.00, 95% CI 1.00-1.00), or week number and VF (p-value 0.94 for enterovirus and 0.89 for influenza) was found. CONCLUSION:We found no clear seasonality of VF during first STEMI. Even though VF patients had experienced more generalized fatigue and flu-like symptoms within 7 days before STEMI compared with patients without VF, no relationship was found between enterovirus or influenza exposure and occurrence of VF

Bundle branch block in cardiac arrest survivors without ischemic heart disease

Aims: Cardiac arrest (CA) survivors with left/right bundle branch block (LBBB/RBBB) and no ischemic heart disease (IHD) have not been previously characterized. The aim of this study was to describe heart failure, implantable cardioverter defibrillator (ICD) therapy and mortality in this population. Methods: Between 2009 and 2019 we consecutively identified all CA survivors with a consistent bundle branch block (BBB) defined as a QRS ≥ 120 ms, who had a secondary prophylactic ICD implanted. Patients with congenital and ischemic heart disease (IHD) were excluded. Results: Among 701 CA-survivors who survived to discharge and received an ICD, a total of 58 (8%) were free from IHD and had BBB; 46 (79%) had LBBB, 10 (17%) had RBBB and 2 (3%) had non-specific BBB (NSBBB). The prevalence of LBBB was 7%. Pre-arrest ECG were available in 34 (59%) patients; 20 patients (59%) had LBBB, 6 (18%) had RBBB, 2 (6%) had NSBBB, 1 had (3%) incomplete LBBB, and 4 (12%) without BBB. At discharge, patients with LBBB had a significantly lower left ventricular ejection fraction (LVEF) than patients with other types of BBB, p < 0.001. During follow-up, 7 (12%) died after a median of 3.6 years (IQR: 2.6–5.1) with no difference between BBB subtypes. Conclusion: We identified 58 CA-survivors with BBB and no IHD. The prevalence of LBBB among all CA-survivors was high, 7%. During CA hospitalization LBBB patients presented with a significantly lower LVEF than patients with other types of BBB (P < 0.001). ICD treatment and mortality did not differ between BBB subtypes during follow-up

Reassessment of Gene-Elusive Familial Dilated Cardiomyopathy Leading to the Discovery of a Homozygous AARS2 Variant—The Importance of Regular Reassessment of Genetic Findings

Background: AARS2 encodes the mitochondrial protein alanyl-tRNA synthetase 2 (MT-AlaRS), an important enzyme in oxidative phosphorylation. Variants in AARS2 have previously been associated with infantile cardiomyopathy. Case summary: A 4-year-old girl died of infantile-onset dilated cardiomyopathy (DCM) in 1996. Fifteen years later, her 21-year-old brother was diagnosed with DCM and ultimately underwent heart transplantation. Initial sequencing of 15 genes discovered no pathogenic variants in the brother at the time of his diagnosis. However, 9 years later re-screening in an updated screening panel of 129 genes identified a homozygous AARS2 (c.1774C &gt; T) variant. Sanger sequencing of the deceased girl confirmed her to be homozygous for the AARS2 variant, while both parents and a third sibling were all found to be unaffected heterozygous carriers of the AARS2 variant. Discussion: This report underlines the importance of repeated and extended genetic screening of elusive families with suspected hereditary cardiomyopathies, as our knowledge of disease-causing mutations continuously grows. Although identification of the genetic etiology in the reported family would not have changed the clinical management, the genetic finding allows genetic counselling and holds substantial value in identifying at-risk relatives

Erratum: Seasonality of ventricular fibrillation at first myocardial infarction and association with viral exposure (PLoS ONE (2020)15:2(e0226936)Doi: 10.1371/journal.pone.0226936)

The fifteenth author's initials are indexed incorrectly in PubMed. The correct initials are: Fischer TK