**5. Post-cardiac arrest syndrome (PCAS)**

In 2015, the ERC and the European Society of Intensive Care Medicine developed the first combined resuscitation treatment guidelines, which were jointly published in Resuscitation and Intensive Care Medicine [16]. The latest version, published in 2021, including the directive with new results since 2015, supplemented by further recommendations [17].

In post-resuscitation care, ensuring adequate oxygenation, ventilation, and circulating cardiac output remain one of the cornerstones of care, and cerebral protection is paramount. The Recommendation describes the four key components of the PCAS to be focused on during early treatment that are still accepted today. These include post-circulatory central nervous system damage, post-circulatory myocardial dysfunction, systemic ischemic and reperfusion responses, and persistent underlying disease-causing circulatory arrest.

If the patient's spontaneous circulation has returned, treatment of PCAS is initiated on-site, with the pillars of stabilization of the hemodynamic state, prevention of arrhythmia recurrence, prevention of cellular damage, and normalization of organ perfusion. Following on-site stabilization, patient care will be continued in specialized centers capable of providing full diagnostic and therapeutic care, which will include a high-level intensive care, angiography, and electrophysiology laboratory, CT/MRI, neurology, mechanical circulatory support, and cardiac surgery.

One of the most important elements of intensive PCAS treatment is controlled targeted temperature management, which is essential to prevent hypoxic and further secondary damage to the brain. Neurological damage is exacerbated during hyperpyrexia, epileptiform seizure activities, and hypoglycemia during PCAS [6]. The quality of treatment applied in the early post-resuscitation period significantly determines the outcome, especially concerning neurological recovery [18].

**Figure 3.**

*Phases of return of spontaneous circulation (ROSC) [19].*

#### *Out-of-Hospital Cardiac Arrest in General Population and Sudden Cardiac Death in Athletes DOI: http://dx.doi.org/10.5772/intechopen.101813*

The consecutive phases of PCAS and the intervals of care are illustrated in **Figure 3**. Time intervals may vary from patient to patient after the first 20 minutes after a spontaneous return of circulation (ROSC), depending on the severity of the PCAS, the rate of recovery, or any progression that may occur. At each stage, care is aimed at limiting ongoing injuries and preventing recurrence of cardiac arrest.


#### **6. Sudden cardiac death in athletes**

Sudden cardiac death is rare among athletes, but it is still a devastating phenomenon, as athletes are associated with the image of a strong, healthy, resilient body. These cases usually get into the focus of media attention, and even if, for a short time, SCD gets in the spotlight. This is also of great importance to the public because it draws attention to having expertise in resuscitation.

The likelihood of OHCA in athletes is also influenced by age, gender, the type of sport, and the existing diseases. The incidence is between 1/50,000 and 1/100,000 in young athletes on an annual basis [20]. An athlete is considered to be young under the age 35. Among them, SCD is usually a consequence of some congenital disease. The incidence rises between 1/15,000 and 1/18,000 in elderly athletes [21]. In these cases, sudden cardiac death is usually associated with coronary disease [20]. Similar to the general population, male athletes have a higher risk of SCD compared with their female counterparts (5:1) [21].

The type of sport and the intensity of the activity performed are also influencing factors. Observations suggest that basketball, football, and athletics have the highest risk of SCD [21]. Hobby athletes who have congenital disorders should choose a sport that can be pursued at a constant energy level, avoiding a sudden increase in the heart rate. In addition, it is also worth avoiding extreme environment during sports, such as high temperature and high humidity. These can adversely affect blood pressure and electrolyte balance [20].

In some cases, the underlying cardiovascular disease in athletes remains asymptomatic, and the first symptom is sudden cardiac arrest. Although in the minority of the cases, syncope, chest pain, and ventricular arrhythmias appear as warning symptoms.

Cardiac and non-cardiac diseases leading to sudden cardiac death in athletes, grouped by age, are listed in **Table 1**.


#### **Table 1.**

*Causes of SCD based on age.*

#### **6.1 Etiology**

Hypertrophic cardiomyopathy is a genetic disorder associated with left ventricular hypertrophy that can lead to SCD via ventricular tachycardia/fibrillation. Basso et al. have found that in athletes, arrhythmogenic right ventricular cardiomyopathy (ARVD) causes sudden cardiac arrest even more often than hypertrophic cardiomyopathy. This genetic disease causes a fatty-fibrous remodeling of the right ventricular wall muscle, and sometimes it affects the left ventricle or the interventricular system as well, which can lead to the aneurysm-like dilation of the ventricular free wall [22].

Congenital coronary abnormalities may also be in the background of sudden cardiac death. According to one study, these are responsible for 17% of athletes' deaths from cardiovascular disease. One of the most severe coronary malformations is the origin of the coronary artery from behind the pulmonary trunk, which causes severe symptoms from an early age. However, other lesions with less pronounced symptoms can also cause SCD, especially during increased exercise. In these cases, the coronary can be derived from the sinus on the opposite side, which will make its course abnormal. During exercise, an abnormally grown coronary artery cannot increase blood flow sufficiently, leading to the development of ischemic episodes. As a result, the myocardium will be injured, and the resulting scar tissue will serve as a basis for ventricular arrhythmias and ventricular fibrillation [23].

Pathologists do not find any myocardial lesion that causes SCD in 30% of autopsies. In such cases, cardiac arrest may have been caused by ion channel mutations (long QT syndrome, Brugada syndrome), which may eventually result in ventricular fibrillation. Mutation of ion channels may be alerted by ECG abnormality. The disease is inherited by autosomal dominant, and the mutation is found in genes encoding sodium and potassium channels. Catecholaminergic polymorphic ventricular tachycardia can develop due to a mutation in calcium receptors. In this case, we do not see any difference in the resting ECG. However, with increased sympathetic activity during sports activities, arrhythmias may occur above a heart rate of 120–130/min [22].

Among the valve defects, mitral valve prolapse and aortic stenosis, which are arrhythmogenic, should be highlighted. The most common cause of aortic stenosis is calcareous disease of the aortic valve, with manifestation at a much younger age in addition to bicuspid aortic valves [22].

Acquired cardiac abnormalities may also be among the underlying causes, such as myocarditis due to a viral infection, vascular disease, and aortic dissection [23].

*Out-of-Hospital Cardiac Arrest in General Population and Sudden Cardiac Death in Athletes DOI: http://dx.doi.org/10.5772/intechopen.101813*

#### **6.2 Why is screening important?**

Sport activity can trigger sudden cardiac death in individuals who already have some kind of heart disease. Existing disease (e.g., hypertrophy, fibrosis) can be considered as a substrate and sport may be a trigger, which can cause arrhythmias, increased catecholamine release, acidosis, and dehydration [23].

The American Heart Association and the Sports Cardiology Study Group of the European Society of Cardiology recommend physical examination of high school and college students before a sporting activity in addition to their own and family history recordings. The European guidelines complement this with an ECG registration. The effectiveness of this screening method is supported by observation published by Corrado et al.; they found that the incidence of sudden cardiac death between 1979 and 1980 decreased from 3.6 athletes/100,000 people/year to 0.4 athletes/100,000 people/year for the year 2004 due to the introduction of screening.

### **7. COVID-19 and sports**

In our experience to date, COVID-19 can damage heart itself and its function in at least two basic ways. Directly, when the virus enters the body by binding to human ACE-2 receptors, which are expressed not only in the lungs but also in the myocardium and several other areas of the cardiovascular system. In the early stages of COVIDassociated myocarditis, the virus replicates within myocytes, followed by a subacute immunological response including both the T-cell and B-cell immune responses. At this time, the host's immune system may even worsen myocardial damage through cytokine activation and the production of antibodies to viral proteins. In the chronic phase of myocarditis, fibrosis and dilatation of the ventricles may occur. This may manifest as deterioration in pump function and may lead to heart failure [24]. According to a study presented by Linder et al. [25], the presence of Sars-Cov-2 in the myocardium (24/39 autopsy pattern, 61.5%) and active viral replication suggested that direct viral invasion may be more common than previously it was previously assumed. In these studies, the samples were taken from patients treated in hospitals; therefore, their applicability to athletes in the younger population has not been established. The other way in which an intense "cytokine storm" during a severe disease leads to a decrease in heart function, similarly to other forms of sepsis, with mechanisms that are overlapping the development of "stress" or catecholamine-induced cardiomyopathy [25].

Although hospitalization for acute infection in young, healthy individuals is uncommon, there is concern that subclinical myocardial damage may be present in several cases and may manifest as prolonged malaise, or even more may develop malignant arrhythmias and may act as substrate for cardiac death. Exercise during the acute phase of myocarditis caused by a viral infection can accelerate or prolong the disease and trigger malignant and nonmalignant arrhythmias (**Figure 4**) [20].

Therefore, it is important to emphasize that training started before the recommended recovery period of time may contribute to involve cardiovascular system even in asymptomatic individuals. Athletes must undergo a full cardiological examination before returning to daily training. Transthoracic echocardiography is currently considered the first line in post-COVID-19 monitoring in athletes. In addition, exercise ECG and 24-hour Holter monitoring are also a useful help in the "return-to-play" algorithm to detect possible supraventricular and ventricular arrhythmias but have low sensitivity to identify myocarditis [26]. Finally, the levels of serum biomarkers (troponin, CK-MB, BNP) should be monitored thoroughly.

Athletes having positive COVID 19 test or experienced symptoms should abstain from sports and strenuous physical activity for 2 weeks. In the case of myocarditis

**Figure 4.** *COVID-19 disease progression in the heart.*

or myopericarditis, athletes need to be withheld in sport activity for up to 3–6 months depending on the course and severity of the disease [27]. Thereafter, if the left ventricular systolic function has returned to normal, serum biomarkers for myocardial damage started to decrease, and no clinically significant supraventricular or ventricular arrhythmia has been observed in the 24-hour Holter monitoring or during exercise test, the athlete can return to sport activity [28].

#### **8. Summary**

More than half of cardiovascular deaths in the 35–49-year-old population are out-of-hospital non-traumatic sudden cardiac arrest. The rate, for men, is 3–4 times higher than for women; and it gradually increases with age. The classical cardiovascular risk factors are obesity, hypertension, diabetes mellitus, hyperlipidemia, and smoking, in addition to cardiac morphology as known coronary disease or cardiac myopathies can cause sudden cardiac death.

Regular screening significantly reduced the incidence of sudden cardiac death among athletes as well.

A growing number of studies suggest that many COVID-19 survivors experience some type of heart damage, including arrhythmias, heart failure, and myocarditis, even if they were asymptomatic. Congenital structural diseases and myocarditis are a leading cause of sudden cardiac death in competitive athletes so they must be properly treated by their cardiologists before the return to sports.

Exponentially increasing number of scientific data on OHCA and IHCA are available to help with prevention as well. Future studies processing histopathological and toxicological data from autopsy may provide adequate medical data to develop a strategy to prevent cardiovascular death.

*Out-of-Hospital Cardiac Arrest in General Population and Sudden Cardiac Death in Athletes DOI: http://dx.doi.org/10.5772/intechopen.101813*
