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

Glinge, Charlotte; Engstrøm, Thomas; Midgley, Sofie; Tanck, Michael W.T.; Madsen, Jeppe Ekstrand Halkjær; Pedersen, Frants; Jacobsen, Mia Ravn; Lodder, Elisabeth M.; Al-Hussainy, Nour R.; Stampe, Niels Kjær; Trebbien, Ramona; Køber, Lars; Gerds, Thomas Alexander; Torp‐Pedersen, Christian; Fischer, Thea Kølsen; Bezzina, Connie R.; Tfelt-Hansen, Jacob; Jabbari, Reza

doi:10.1371/journal.pone.0226936

Cited by 4 publications

(1 citation statement)

References 45 publications

(65 reference statements)

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“…Furthermore, data in the literature suggested that SCD may occur as a consequence of a trigger factor in the context of electrical or structural heart disorder (genetic or acquired), which acts as a predisposing condition. Known exogenous triggers resulting in the fatal event of SCD may be fever, alcohol intake, electrolyte disorders, hypertensive crisis, infection, cytotoxic drugs, and pregnancy [ 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 ]. Moreover, regular physical activity is an important exogenous factor affecting the risk of SCD in predisposed subjects.…”

Section: Introductionmentioning

confidence: 99%

The Hidden Fragility in the Heart of the Athletes: A Review of Genetic Biomarkers

Barretta

Mirra

Monda

et al. 2020

IJMS

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Sudden cardiac death (SCD) is a devastating event which can also affect people in apparent good health, such as young athletes. It is known that intense and continuous exercise along with a genetic background that predisposes a person to the risk of fatal arrhythmias is a trigger for SCD. Therefore, knowledge of the athlete’s genetic conditions underlying the onset of SCD must be extended, in order to develop new effective prevention and/or therapeutic strategies. Arrhythmic features occur across a broad spectrum of cardiac diseases, sometimes presenting with overlapping phenotypes. The genetic basis of arrhythmogenic disorders has been greatly highlighted in the last 30 years, and has shown marked heterogeneity. The advent of next-generation sequencing has constantly updated our understanding of the genetic basis of arrhythmogenic diseases and is laying the foundation for precision medicine. With the exception of a few clinical cases involving a single athlete showing a highly suspected phenotype for the presence of a heart disease, there are few studies to date that analysed the applicability of genetic testing on cohorts of athletes. This evidence shows that genetic testing can contribute to the diagnosis of up to 13% of athletes; however, the presence of clinical markers is essential. This review aims to provide a reference collection on current knowledge of the genetic basis of sudden cardiac death in athletes and to review updated evidence on the effectiveness of genetic testing in early identification of athletes at risk for SCD.

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Section: Introductionmentioning

confidence: 99%

The Hidden Fragility in the Heart of the Athletes: A Review of Genetic Biomarkers

Barretta

Mirra

Monda

et al. 2020

IJMS

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Influenza associated cardiac arrhythmia- a systematic review

Alam,

Paul,

Aggarwal

et al. 2024

The American Journal of the Medical Sciences

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Circulating virome and inflammatory proteome in patients with ST-elevation myocardial infarction and primary ventricular fibrillation

Oliveras

Revuelta‐López

García-García

et al. 2022

Sci Rep

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Primary ventricular fibrillation (PVF) is a life-threatening complication of ST-segment elevation myocardial infarction (STEMI). It is unclear what roles viral infection and/or systemic inflammation may play as underlying triggers of PVF, as a second hit in the context of acute ischaemia. Here we aimed to evaluate whether the circulating virome and inflammatory proteome were associated with PVF development in patients with STEMI. Blood samples were obtained from non-PVF and PVF STEMI patients at the time of primary PCI, and from non-STEMI healthy controls. The virome profile was analysed using VirCapSeq-VERT (Virome Capture Sequencing Platform for Vertebrate Viruses), a sequencing platform targeting viral taxa of 342,438 representative sequences, spanning all virus sequence records. The inflammatory proteome was explored with the Olink inflammation panel, using the Proximity Extension Assay technology. After analysing all viral taxa known to infect vertebrates, including humans, we found that non-PVF and PVF patients only significantly differed in the frequencies of viruses in the Gamma-herpesvirinae and Anelloviridae families. In particular, most showed a significantly higher relative frequency in non-PVF STEMI controls. Analysis of systemic inflammation revealed no significant differences between the inflammatory profiles of non-PVF and PVF STEMI patients. Inflammatory proteins associated with cell adhesion, chemotaxis, cellular response to cytokine stimulus, and cell activation proteins involved in immune response (IL6, IL8 CXCL-11, CCL-11, MCP3, MCP4, and ENRAGE) were significantly higher in STEMI patients than non-STEMI controls. CDCP1 and IL18-R1 were significantly higher in PVF patients compared to healthy subjects, but not compared to non-PVF patients. The circulating virome and systemic inflammation were not associated with increased risk of PVF development in acute STEMI. Accordingly, novel strategies are needed to elucidate putative triggers of PVF in the setting of acute ischaemia, in order to reduce STEMI-driven sudden death burden.

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

Cited by 4 publications

References 45 publications

The Hidden Fragility in the Heart of the Athletes: A Review of Genetic Biomarkers

The Hidden Fragility in the Heart of the Athletes: A Review of Genetic Biomarkers

Influenza associated cardiac arrhythmia- a systematic review

Circulating virome and inflammatory proteome in patients with ST-elevation myocardial infarction and primary ventricular fibrillation

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