Cardiovascular System during SARS-CoV-2 Infection

SARS-CoV-2 virus can not only damage the respiratory system but may also pose a threat to other organs, such as the heart or vessels. This review focuses on cardiovascular complications of COVID-19, including acute cardiac injury, arrhythmias, biomarkers, accompanying comorbidities and outcomes in patients diagnosed with SARS-CoV-2 infection. The research was conducted on the databases: PubMed, Springer, ScienceDirect, UpToDate, Oxford Academic, Wiley Online Library, ClinicalKey. Fifty-six publications from 1 November 2020 till 15 August 2021 were included in this study. The results show that cardiac injury is present in about 1 in 4 patients with COVID-19 disease, and it is an independent risk factor, which multiplies the death rate several times in comparison to infected patients without myocardial injury. New-onset cardiac injury occurs in nearly every 10th patient of the COVID-19-suffering population. Comorbidities (such as hypertension, cardiovascular disease and diabetes) severely deteriorate the outcome. Therefore, patients with SARS-CoV-2 infection should be carefully assessed in terms of cardiac medical history and possible cardiological complications.


Introduction
After almost two years of global epidemics, we are certain that complications of COVID-19 do exist and have a tremendous impact on our psychical and mental condition [1,2]. SARS-CoV-2 has emerged as a life-threatening danger that damages the respiratory system resulting in pneumonia or acute respiratory distress syndrome (ARDS) [3], as well as the nervous system, causing headache, weakness, smell or taste loss [4,5]. In the vast majority of infected patients, the virus presents with mild symptoms, and a minority have a severe course of COVID-19, requiring hospitalisation or intensive care [6]. Aside from the respiratory and nervous systems, the cardiovascular system may be affected as well regarding short and long-term complications. The long-term results presumably will be subjected to further observation in the years following the epidemic. Thus, it is crucial to prepare for the challenges ahead and direct our research efforts to improve health care quality.
This review highlights possible cardiological complications in patients with SARS-CoV-2 infection and presents the outcome of patients with cardiovascular risk factors to illustrate what can be possibly encountered and should be expected during hospitalisation or ambulatory treatment.

Frequency and Characteristic
We used 15 articles in this section. Cardiac injury was present in 16.8% to 66.4% of subjects, and in the vast majority of reviewed articles, it was diagnosed based on elevated troponin level (cTn-cardiac troponin, hs-cTn-high sensitivity cardiac troponin) sometimes along with additional abnormality (for instance, new-onset abnormal ECG or echocardiography finding). A study in the group of 181 COVID-19-positive patients showed 23.2% of them had cardiac injury diagnosed on the basis of elevated biomarkers (high-sensitivity troponin I, myohemoglobin and creatine kinase myocardial (p < 0.001, >99th percentile)). The median age was 55 (IQR, 46-65) years [7]. A study of 2895 COVID-19-positive patients in New York University School of Medicine showed that cardiac injury was present in 16.8% of patients, and troponin levels (>99th percentile, adjusted for sex and age) were considered to be indicative of myocardial necrosis [8]. In the next study of 313 COVID-19positive patients in Italy, hs-cTnI (high-sensitivity cardiac troponin I) elevation was present in 85 patients (27.2%). The mean age for the whole group was 66.1 (55.1-79.4) [9]. There is one multi-centre study with higher percentages than others, carried out in the United Kingdom, which included 434 COVID-19-positive patients (mean age 66  years) and which demonstrated cardiac injury in 288 patients (66.4%). Median LVEF (left ventricle ejection fraction) was significantly lower for troponin(+) patients as compared to troponin(-) patients [10]. In research conducted in Istanbul, Turkey, 77 of 326 (23.8%) consecutive patients had a new acute cardiac injury (based on serum troponin I value >19.8 ng/mL, mean age 58.4 ± 15.2 years) [11]. In the last research of 270 COVID-19-positive patients, cardiac injury was present in 32.6% of infected patients during hospitalisation [12]. All six studies mentioned above can be seen in the figure below (Figure 3).

Frequency and Characteristic
We used 15 articles in this section. Cardiac injury was present in 16.8% to 66.4% of subjects, and in the vast majority of reviewed articles, it was diagnosed based on elevated troponin level (cTn-cardiac troponin, hs-cTn-high sensitivity cardiac troponin) sometimes along with additional abnormality (for instance, new-onset abnormal ECG or echocardiography finding). A study in the group of 181 COVID-19-positive patients showed 23.2% of them had cardiac injury diagnosed on the basis of elevated biomarkers (high-sensitivity troponin I, myohemoglobin and creatine kinase myocardial (p < 0.001, >99th percentile)). The median age was 55 (IQR, 46-65) years [7]. A study of 2895 COVID-19-positive patients in New York University School of Medicine showed that cardiac injury was present in 16.8% of patients, and troponin levels (>99th percentile, adjusted for sex and age) were considered to be indicative of myocardial necrosis [8]. In the next study of 313 COVID-19positive patients in Italy, hs-cTnI (high-sensitivity cardiac troponin I) elevation was present in 85 patients (27.2%). The mean age for the whole group was 66.1 (55.1-79.4) [9]. There is one multi-centre study with higher percentages than others, carried out in the United Kingdom, which included 434 COVID-19-positive patients (mean age 66  years) and which demonstrated cardiac injury in 288 patients (66.4%). Median LVEF (left ventricle ejection fraction) was significantly lower for troponin(+) patients as compared to troponin(-) patients [10]. In research conducted in Istanbul, Turkey, 77 of 326 (23.8%) consecutive patients had a new acute cardiac injury (based on serum troponin I value >19.8 ng/mL, mean age 58.4 ± 15.2 years) [11]. In the last research of 270 COVID-19-positive patients, cardiac injury was present in 32.6% of infected patients during hospitalisation [12]. All six studies mentioned above can be seen in the figure below (Figure 3). Critical or severe patients have higher levels of troponin during hospitalisation and are more likely to have a cardiac injury with the range from 28.3% to 51% [13][14][15][16]. In a study of 330 patients, cardiac injury (based on hs-cTnI levels) was diagnosed in 32.4% of patients (104), and the whole group consisted of only severe and critically ill COVID-19- Critical or severe patients have higher levels of troponin during hospitalisation and are more likely to have a cardiac injury with the range from 28.3% to 51% [13][14][15][16]. In a study of 330 patients, cardiac injury (based on hs-cTnI levels) was diagnosed in 32.4% of patients (104), and the whole group consisted of only severe and critically ill COVID-19-positive patients [14]. In the multi-centre study of 2878 SARS-CoV-2-positive critical patients in France, troponin was elevated above each centre's threshold in 32.4% and in 58.5% of the deceased group [16]. In the study of 243 intubated COVID-19-positive patients from five different hospitals, 51% had troponin levels above the upper limit [15]. Another paper of 201 SARS-CoV-2-positive patients with myocardial injury (based on cTnI) shows that troponin was elevated above the normal level of 0.04 ng/mL in mild patients and three times over the threshold (>0.12 ng/mL) in critical patients (28.3%, p < 0.001, critical patients were those who needed mechanical ventilation) [13]. In another article of 218 patients with myocardial injury, there were also major differences in troponin elevation between critical and mild COVID-19-positive patients (28.8% critical vs. 4.8% non-critical, p < 0.0001) [17].
The situation is different when speaking of first-detected cardiac injury. Here the numbers are lower with a range: 2.9-10.8%. A Chinese study has revealed that hs-cTnl (high-sensitivity cardiac troponin type I) was elevated in COVID-19-positive patients in 10.8% of 218 enrolled patients (mean age was 62 (IQR: 55, 69) years). These patients presented without previous cardiovascular symptoms or past medical history involving cardiovascular disease and were admitted to the hospital because of typical SARS-CoV-2 symptoms [17]. In the American study of 179 patients (mean age 59.8 ± 16.9 years), myocardial injury was present in only 7% of patients (significant troponin level elevation accompanied by new ventricular dysfunction or electrocardiographic abnormalities) [18]. Scientists from the King's College of London conducted a randomised study of 172 SARS-CoV-2-positive patients (mean age 55.1 ± 13.9 years), which showed that 10.2% developed a major cardiac injury (peak hs-cTnT >20× ULN) [19]. In the previously presented analysis, new cardiac abnormalities occurred in 3.9% of 434 COVID-19-positive patients [10]. Concerning athletes, a study showed that only 2.9% had abnormal newly-detected cTnI levels with no serious symptoms (laboratory 99th percentile, 0.035 ng/mL.). All these athletes were referred for CMR. No athlete had abnormal findings detected by CMR: no ventricular dysfunction, delayed myocardial enhancement, abnormal T2 weighted imaging or pericardial pathology. Limitations of this result could be that the authors did not use hs-cTnI [20]. The four previously mentioned studies [10,[17][18][19] are assembled in the figure below (Figure 4). The information from [20] is not included in the figure because it concerns athletes.
Int. J. Environ. Res. Public Health 2022, 19, x positive patients [14]. In the multi-centre study of 2878 SARS-CoV-2-positive critic tients in France, troponin was elevated above each centre's threshold in 32.4% a 58.5% of the deceased group [16]. In the study of 243 intubated COVID-19-positi tients from five different hospitals, 51% had troponin levels above the upper lim Another paper of 201 SARS-CoV-2-positive patients with myocardial injury (bas cTnI) shows that troponin was elevated above the normal level of 0.04 ng/mL in m tients and three times over the threshold (>0.12 ng/mL) in critical patients (28.3%, p < critical patients were those who needed mechanical ventilation) [13]. In another art 218 patients with myocardial injury, there were also major differences in troponin tion between critical and mild COVID-19-positive patients (28.8% critical vs. 4.8% critical, p < 0.0001) [17].
The situation is different when speaking of first-detected cardiac injury. Here the bers are lower with a range: 2.9-10.8%. A Chinese study has revealed that hs-cTnl sensitivity cardiac troponin type I) was elevated in COVID-19-positive patients in 10 218 enrolled patients (mean age was 62 (IQR: 55, 69) years). These patients presented out previous cardiovascular symptoms or past medical history involving cardiova disease and were admitted to the hospital because of typical SARS-CoV-2 symptom In the American study of 179 patients (mean age 59.8 ± 16.9 years), myocardial injur present in only 7% of patients (significant troponin level elevation accompanied b ventricular dysfunction or electrocardiographic abnormalities) [18]. Scientists fro King's College of London conducted a randomised study of 172 SARS-CoV-2-positi tients (mean age 55.1 ± 13.9 years), which showed that 10.2% developed a major c injury (peak hs-cTnT >20× ULN) [19]. In the previously presented analysis, new card normalities occurred in 3.9% of 434 COVID-19-positive patients [10]. Concerning athl study showed that only 2.9% had abnormal newly-detected cTnI levels with no s symptoms (laboratory 99th percentile, 0.035 ng/mL.). All these athletes were referr CMR. No athlete had abnormal findings detected by CMR: no ventricular dysfunctio layed myocardial enhancement, abnormal T2 weighted imaging or pericardial path Limitations of this result could be that the authors did not use hs-cTnI [20]. The four ously mentioned studies [10,[17][18][19] are assembled in the figure below (Figure 4). The mation from [20] is not included in the figure because it concerns athletes.   Critical or severe patients have higher levels of troponin during hospitalisation. In Wuhan, 40 (30.3%) consecutive patients displayed acute cardiac injury (based on hs-TnI above the 99th-percentile upper reference limit, mean age 61 ± 13 years) [21]. These could be due to more critical cases (62.1% severe or critical).
An interesting study showed that there is no association between the initial viral load (iVL) and cardiac injury (based on increased >100 ng/L hs-cTnI level); however, both iVL and cardiac injury were independent predictors of mortality [12].

Myocardial Infarction
We used three articles in this section. Myocardial infarction in COVID-19-positive patients is not common [9,25,34]. A study on 346 patients with elevated hs-cTnT conducted in the UK has demonstrated that there were no COVID-19-positive patients in the group of 115 patients with Type 1 MI, and in the group of 231 patients with Type 2 MI/myocardial Injury there were 36 (16%) patients who were COVID-19-positive. Cardiac causes of MI were more common in patients without SARS-CoV-2 virus (positive: 11.1% vs. negative: 33.3%, p = 0.22), of which tachyarrhythmia and heart failure were the most likely mechanisms (15.7% and 15.1%) [34]. Next, a study on 313 patients of whom elevation was present in 85 patients (27.2%) and of those 85 patients, only 11.7% had criteria for MI: 7% had type 2 MI, and 4.7% had type 1 MI [9]. In another work of 367 patients, only 5% of patients with elevated troponin (169) were adjudicated as acute MI, with three patients classified as type 1 MI and five patients as type 2 MI [25].

Comparison of the Situation before COVID-19 Pandemic and Now
We used three articles in this section. The articles show us that admission for acute cardiac syndrome decreased between 40.4% and 47% [35,36], the severity of cases increased between 1.2 and 2.5 times [35,36], admission time was prolonged between 21% and 22% [35], or there were more late presentations [37], mortality increased in COVID-period 3.4 times [35] compared to last year and cardiac complications after hospitalisation were between 2.8 and 4 times more frequent [35,37]. In Berlin, Germany, a study of 355 patients showed that although the admission for acute myocardial injury decreased (by 47%) during the pandemic, the mortality has risen significantly (5.2% to 17.7%, p < 0.05). Patients demographically did not differ comparing the pre-COVID-19 and COVID-19 periods; the cases were much more serious though (elevated troponin, lower LVEF (39 ± 16 in 2020 vs. 46 ± 16 in 2019, p < 0.05), higher demand for inotropic support). Admission time was also prolonged (22% for STEMI and 21% for NSTEMI). Cardiac complications developed much more often (17.6% vs. 6.3%), and the rehabilitation period was longer than in the pre-COVID-19 period [35]. In another paper from Japan, there were many more late presentations with STEMI compared with pre-COVID-19 times (25.4% vs. 14.2%, p = 0.03). Primary PCI was performed less often (68.3% vs. 82.5%, p = 0.009) and mechanical complications occurred much more often also (3.6% vs. 14.3%, p < 0.001) [37]. In Spain, the number of patients with acute cardiac syndrome decreased by 40.4% (2020 vs. 2019). A total of 11% of acute cardiac syndrome patients in 2020 were COVID-19-positive, and many more patients with SARS-CoV-2 virus (46.2%) had acute cardiac syndrome at admission compared to the COVID-19-negative patients (11.4%) in the group from 2020 (as a secondary diagnosis-SARS-CoV-2 infection was the primary). There were significantly more in-hospital patients in severe condition with acute cardiac injury in 2020 compared with a cohort from the same timeframe of 2019 (15.3% vs. 6.1%, p = 0.007). In the COVID-19-positive group of 118 patients (from 2020 with acute cardiac injury and SARS-CoV-2-positive) COVID-19-positivity was an independent mortality predictor, and the SARS-CoV-2 positive test was independently associated with 30-day mortality [36].

Myocarditis
We used five articles in this section. Acute myocarditis occurred in some COVID-19 patients and was usually focal but not common [25,38]. One of the studies with the biggest number of patients (1160) showed that acute myocarditis in COVID-19 patients developed in only 1% of cases [38]. Pericardial effusion was seen more frequently [21] (9%), [39] (9%). Another work of 367 patients showed that myocarditis was rare with clinical suspicion in only three patients in whom there was no definite confirmatory testing with cardiac magnetic resonance imaging or biopsy [25].
The situation is different in severe and critical COVID-19 patients. In a UK study concerning 148 severe COVID-19-positive and troponin(+) patients who underwent CMR (cardiac magnetic resonance), pericardial effusion was seen in 8/148 (5%). A total of 47/148 patients had a non-ischaemic pattern of myocardial injury, and 40/148 patients had a myocarditis-pattern injury (including four with coexisting inducible ischaemia and three with coexisting myocardial infarction). In the group of patients with myocarditispattern injury, only 12 (8% from the whole population) had findings consistent with active myocarditis (8 with a regional elevation of both native T1 and T2, 4 with a regional elevation of T2 only) [39].
creasing disease severity demonstrated in 28.6% of critical patients having new arrhythmia (p < 0.001) [42] and in another work, 25.2% of ICU patients [50]. The percentage of SARS-CoV-2-positive patients with both previous and new arrhythmias from previously selected studies [42][43][44][45][46][47] are presented in the next figure ( Figure 5). Study [48] was not presented in the figure because it has taken only atrial arrhythmias into account.

Accompanying Comorbidities
We used twenty-nine articles in this section. COVID-19-positive patients with more comorbidities are associated with a more severe duration of illness [13], more often require intensive care [55] or are at a higher risk of death [11,16,24,56]. Male sex is prevalent among patients who died during hospitalisation [23,24,27,57,58] and is associated with higher mortality [23,56]. Age is an independent predictor of higher mortality in COVID-19positive patients [16,55,56,59,60], increasing the risk of intensive care necessity [55] or illness severity [27]. Cardiovascular artery disease [55,56], diabetes mellitus and hypertension [55] are associated with higher mortality amongst COVID-19-positive patients and associated with intensive care or mechanical ventilation [55]. Critical patients are more likely to have the underlying cardiac disease [23], more comorbidities [13], to be male [13,23] and older [13,23,54]. About one-quarter of patients with heart failure die when they get infected with the SARS-CoV-2 virus [57]. There was a large study of 1,212,153 patients with a history of HF (heart failure), 8383 of which were COVID-19-positive (The Premier Healthcare Database), which concluded that patients with HF hospitalised with COVID-19 are at high risk for complications, with 24.2% dying during hospitalisation. Those who suffered from COVID-19 and had a past history of HF were more likely to have post-hospitalisation care (41% vs. 13%) or were referred to hospice (6.7% vs. 4.1%) than COVID-19-negative patients with HF. Patients with a previous history of HF and COVID-19 had significantly greater in-hospital resource use (mechanical ventilation, central venous catheter insertion) compared with patients hospitalised with acute HF and without COVID-19 (Intensive Care Unit care 29% vs. 15%, mechanical ventilation 17% vs. 6%, venous catheter 19% vs. 7%) Mortality amongst COVID-19 patients was greater in patients with acute heart failure 24.2% vs. 2.6% [57].
Here we present the percentage of infected patients with the most common comorbidities: Hypertension ( Figure 6), diabetes (Figure 7), cardiovascular disease ( Figure 8).
There are some values that are clearly different from the majority. This may be caused by population heterogeneity, such as higher percentage of male population presented in the study [24,33,53,62], higher age [24,53,56], higher percentage of black race [46,56] or ICU sample [62]. In paper [56], the authors selected patients with and without CAD to 14 There are some values that are clearly different from the majority. This may be caused by population heterogeneity, such as higher percentage of male population presented in the study [24,33,53,62], higher age [24,53,56], higher percentage of black race [46,56] or ICU sample [62]. In paper [56], the authors selected patients with and without CAD to compare these two groups. From six studies with the highest numbers, four were performed in the USA [33,46,56,62] and two in Italy [24,53]. In an article from Pakistan [14], the mean age of patients is lower than in the vast majority of other articles (44.6 ± 15.2). compare these two groups. From six studies with the highest numbers, four were performed in the USA [33,46,56,62] and two in Italy [24,53]. In an article from Pakistan [14], the mean age of patients is lower than in the vast majority of other articles (44.6 ± 15.2).
In paper [58], the percentage of patients with CAD is outstanding due to study design and chosen population sample: the authors compared SARS-CoV-2-infected patients with CAD to SARS-CoV-2-infected patients without CAD.
There are some values that are clearly outstanding and, similar as in Figure 6, this may be caused by population heterogeneity, such as higher percentage of the male population presented in the study [33,62], higher age [56], the higher percentage of black race [46,56] or ICU sample [62]. In paper [56], the authors selected patients with and without CAD to compare these two groups. All five studies with the highest numbers were performed in the USA [33,45,46,56,62].
In paper [58], the percentage of patients with CAD is outstanding due to study design and chosen population sample: the authors compared SARS-CoV-2-infected patients with CAD to SARS-CoV-2-infected patients without CAD.

Discussion
This work focuses on cardiological complications caused by the SARS-CoV-2 virus. There is a possibility that its mechanism of interaction of cells and the human organism can be similar or approximate to other well-known viruses: influenza, SARS-CoV-1 or MERS-CoV [63]. Cardiac injury amongst COVID-19 patients is quite common, and the numbers oscillate with the range of 16.8-66.4% for myocardial injury in general (with no regards to injury time or past medical history) [7][8][9][10][11][12] and with a range of 2.9-10.8% for new-onset cardiac injury [10,[17][18][19][20]. Those percentages are higher in patients with more severe/critical COVID-19 course [13][14][15][16][17]21], but we must remember that patients referred to intensive care wards usually have a more severe course of SARS-CoV-2 infection, as well as more risk factors such as age, male sex or comorbidities (hypertension or diabetes). Will it be temporary or permanent is a matter of research in the near future, but biomarkers of cardiac injury in SARS-CoV-2-infected patients usually decrease after a longer period of time, which can suggest direct cardiac damage caused by the virus [7]. However, it is known that there are various reasons for cardiac injury [64], and it can be caused by other viruses, for example, influenza virus [65,66]. Generally, infection increases the risk of cardiovascular events, such as acute myocardial infarction [67], and may deteriorate or trigger cardiovascular disease [68][69][70]. Nonetheless, there is a possibility that cardiovascular complications can be more severe for SARS-CoV-2 than other viruses, such as the influenza virus, mentioned before [63], and further research is needed to confirm this hypothesis. It is not a surprise that mortality is higher in patients with cardiac injury and/or elevated troponin levels comparing groups of COVID-19-positive patients with and without cardiac injury [7,9,10,15,16,32] but also those who are older [7,11,16,22,26], male [10,16,22] or have a more severe disease [7,22]. SARS-CoV-2-infected patients with more comorbidities are more likely to have cardiac injury [22,26]. The fact that cardiac injury [21,22], as well as elevated biomarkers [7,8,18,19,[28][29][30][31][32], are an independent risk factor for mortality in patients infected with SARS-CoV-2 is crucial. One of the works showed that cTnI is a better short-term morality marker than LDH, CRP or D-Dimers [31]. Mortality (magnitude), admission time (time from symptom onset to first medical contact), frequency of complications and severity of cases increased during the COVID-19 pandemic compared to non-pandemic years [35][36][37], but this situation applies not only to the cardiological field but to every sector of the healthcare system, for example, presentation of patients with cancers and lower number of cancer-screening examinations [71].
Although virus genetics are found in heart tissue, myocarditis is not common [38,40,41], pericardial effusion occurred more often [21], but SARS-CoV-2, like every virus, has a multiplicitous possibility to interfere with living cells. Like SARS-CoV-1 [72], SARS-CoV-2 uses its SPIKE protein to bind to the ACE2-receptor, which can also be found on the surface of a host cell [63,73,74] and in heart tissue [75]. COVID-19 illness is likely to be accompanied by a hypercoagulable state [76] and microangiopathy [77]. Whether cardiac injury is caused by thromboembolism phenomena [7], direct damage [78] or inflammation factors [79] is still a matter of question and further research.
Combining general arrhythmias, only-AF (atrial fibrillation) and only-AA (atrial arrhythmia) studies, we can summarise and say that arrhythmias occur during COVID-19-related hospitalisation with a range of 7.2-26.5% of the patient population [31][32][33][34]36,37]. The most common are atrial arrhythmias, with the majority being AF. [42,44,[46][47][48]. Brand-new arrhythmia occurs with a range of 5.3-13.3% of SARS-CoV2-infected patients [42][43][44][46][47][48]50]. Likewise, with cardiac injury, these patients are usually older and have more comorbidities than patients without arrhythmias [42,48,49,51], especially in the critical groups [13,42,53,54]. As we know, infections can be a cause of cardiac arrhythmias. It is not a rare sight when a patient with influenza virus, especially with more severe symptoms, develops atrial fibrillation [80], which seems to be one of the most common atrial arrhythmias. This applies not only to viral infections but pneumonia in general, which may initiate the phenomenon of arrhythmia in a patient [81] inter alia by triggering a reaction of the immune system, producing inflammation factors or increasing activation of the autonomic nervous system.
MRI is a very useful diagnostic device, and our research shows that abnormalities in the heart tissue were not common; however, the number of articles on this topic and patients who participated in such examinations were not sufficient [39].
The most common comorbidities in COVID-19-positive patients were hypertension (range:14.4-77%, median 47,8%) diabetes (range: 14-47%, median 23.7%) and cardiovascular disease (range: 8.7-56.7%, median 14.1%). The pathologies mentioned above were also popular amongst patients suffering from the MERS-CoV virus [82] and are possible to accompany every viral infection. Even if we are aware of the influence of viruses on our organisms, the SARS-CoV-2 virus seems to be unusually dangerous for the human population, and its long-term consequences are still uncertain.

Conclusions
Cardiac injury in the process of SARS-CoV-2 infection applies to approximately every fourth infected patient, whereas in nearly every tenth infected patient, it appears de novo. Myocarditis is not common and no different than in the healthy population. Nearly every seventh patient of the COVID-19-infected population has arrhythmias (which are mostly atrial), and almost every tenth patient has brand-new arrhythmias. The elevation of cardiac biomarkers (troponin, CK-MB, myoglobin) is an independent predictor of mortality in those patients. Comorbidities are crucial factors that worsen the outcome of a patient. Most common are hypertension, diabetes and cardiovascular disease. It is certain SARS-CoV-2 affects the cardiovascular system in many different ways and has an impact on the heart, electrical conduction system and vessels, which may suggest that we still need to continue research and expand our knowledge in order to better understand the virus itself.