Space flight modulates the functions of the cardiovascular system. The exposure to space conditions can alter the cerebral blood flow, as well as the venous return. Anemia, cardiac output changes, and increased activity of the sympathetic nervous system can also be seen. Understanding cardiac changes prepares astronauts for both better in-flight adaptations and long-term protection against cardiovascular diseases. The heart could undergo radio-degenerative effects when exposed to space radiation, increasing the risk of cardiovascular diseases in the long run. A high frequency of arrhythmias, such as ventricular/atrial premature complexes, have been reported during the Gemini and Apollo missions. Additionally, microgravity can lead to progressive degeneration of the myocytes and muscle atrophy with altered gene expression and calcium handling, along with impaired contractility. This review summarizes the potential cardiovascular effects of spaceflight and prevention measures.

Sudden cardiac death due to arrhythmias, such as atrial fibrillation or ventricular tachycardia, account for 15–20% of all deaths. Myocardial infarction increases the burden of atrial fibrillation and ventricular tachycardia by structural and electrical remodeling of the heart. The current management of new-onset atrial fibrillation includes electric cardioversion with very high conversion rates and pharmacologic cardioversion, with less a than 50% conversion rate. If atrial fibrillation cannot be converted, the focus becomes the control of the symptoms ensuring a constant rhythm and rate control, without considering other contributory factors such as autonomic imbalance. Recently, a huge success was obtained by developing ablation techniques or addressing the vagal nerve stimulation. On the other hand, ventricular tachycardia is more sensitive to drug therapies. However, in cases of non-responsiveness to drugs, the usual therapeutic choice is represented by stereotactic ablative therapy or catheter ablation. This review focuses on these newly developed strategies for treatment of arrhythmias in clinical practice, specifically on vernakalant and low-level tragus stimulation for atrial fibrillation and stereotactic ablative therapy for drug-refractory ventricular tachycardia. These therapies are important for the significant improvement of the management of atrial fibrillation and ventricular tachycardia, providing: (1) a safer profile than current therapies, (2) higher success rate than current solutions, (3) low cost of delivery.

Ventricular tachycardia (VT) and ventricular fibrillation (VF) are the most frequent causes of death in the first 24 hours after myocardial infarction. Previous studies showed that depleting TRPV1 receptors with resiniferatoxin (RTX) led to a reduced risk of VT and VF post-myocardial infarction. Therefore, the question of resiniferatoxin as a cardioprotector against myocardial infarction (MI)-induced VT and VF was raised. The RNA sequence data from 3 groups of pigs, each having 4 animals (4 controls, 4 myocardial infarction - MI, and 4 RTX + MI) was analyzed through the lens of differentially expressed genes. The differential expression comparison was conducted in two ways: MI versus Control and RTX+MI versus MI. The results showed the downregulation of deleterious genes involved in inflammation and future plaque instability in the RTX group compared with the MI group. In the case of some of the genes, these findings were reinforced by obtaining the same trends in the MI versus Control group. All in all, we propose further investigation of RTX as a prophylactic method against cardiovascular complications of MI.

The incidence of cardiac implantable electronic device (CIED) malfunctions caused by radiotherapy (RT) is approximately 5%. Although individual national guidelines and expert consensus documents exist, the increased use of RT to treat various cancers points out the need for a standardized document to guide risk assessment and management of CIEDs during RT. We describe potential adverse RT-related events on CIEDs as well as the proposed mechanism of dysfunction. We review the main current guidelines and recommendations, emphasizing similarities and differences.