Sinus node dysfunction and atrial fibrillation-Relationships, clinical phenotypes, new mechanisms, and treatment approaches.

Although the anatomical basis of the pathogenesis of sinus node dysfunction (SND) and atrial fibrillation (AF) is located primarily in the left and right atria, increasing evidence suggests a strong correlation between SND and AF, in terms of both clinical presentation and formation mechanisms. However, the exact mechanisms underlying this association are unclear. The relationship between SND and AF may not be causal, but is likely to involve common factors and mechanisms, including ion channel remodeling, gap junction abnormalities, structural remodeling, genetic mutations, neuromodulation abnormalities, the effects of adenosine on cardiomyocytes, oxidative stress, and viral infections. Ion channel remodeling manifests primarily as alterations in the "funny" current (If) and Ca2+ clock associated with cardiomyocyte autoregulation, and gap junction abnormalities are manifested primarily as decreased expression of connexins (Cxs) mediating electrical impulse propagation in cardiomyocytes. Structural remodeling refers primarily to fibrosis and cardiac amyloidosis (CA). Some genetic mutations can also cause arrhythmias, such as SCN5A, HCN4, EMD, and PITX2. The intrinsic cardiac autonomic nervous system (ICANS), a regulator of the heart's physiological functions, triggers arrhythmias.In addition, we discuss arrhythmias caused by viral infections, notably Coronavirus Disease 2019 (COVID-19). Similarly to upstream treatments for atrial cardiomyopathy such as alleviating CA, ganglionated plexus (GP) ablation acts on the common mechanisms between SND and AF, thus achieving a dual therapeutic effect.

Prehospital Sinus Node Dysfunction and Asystole in a Previously Healthy Patient with COVID-19.

We report a case of a previously healthy 47-year-old female with syncope due to multiple episodes of nodal dysfunction and asystole. During these brief episodes, she was hypoxic in the mid-80's as a result of COVID-19 pneumonia. The patient was admitted and treated for viral pneumonia and found to have normal electrocardiograms (ECG's), normal troponin levels and a normal echocardiogram during her hospital stay. As she recovered from COVID-19, no further episodes of bradycardia or bradyarrhythmia were noted. This case highlights a growing body of evidence that arrhythmias, specifically bradycardia, should be anticipated by prehospital providers as a potential cardiac complication of SARS-CoV-2 infection.