**Abstract**

We are living and fighting serious COVID-19 pandemic, which is caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) virus. Cardiovascular diseases are highly prevalent in the infected individuals, which modifies their treatment and prognosis. The injury of the myocardium is reported in over 15% of hospitalized severely ill patients, mostly presented in the form of acute heart failure, acute coronary syndrome, cardiac arrythmias, myocarditis and thromboembolic complications. All these complications may appear at early in the course of the disease, during the disease progress or in the later stage of the COVID-19 disease. Thromboembolic complications accompany more severe cases, caused by excessive inflammation, platelet activation, endothelial dysfunction, and stasis. This new virus pandemic is a global challenge for health care system where we still have much to learn.

**Keywords:** COVID-19, pandemic, myocardial injury, cardiovascular disease

## **1. Introduction**

The COVID-19 pandemic has opened up many serious challenges to the world. The pandemic has put enormous pressure on healthcare systems worldwide. There are many unknown puzzles the virus imposes to us as medical professionals. Most data we have come from China, Italy, France and USA and management is guided by the expert opinion. While COVID-19 primarily affects the lungs, causing interstitial pneumonitis and severe acute respiratory distress syndrome (ARDS), it can also affect multiple organs, particularly cardiovascular system. Mortality and complications risk is increased by the presence of several comorbidities: cardiovascular disease, hypertension, diabetes, obesity, chronic pulmonary disease, and cancer [1]. Cardiovascular system in COVID-19 infection is affected in up to 15% of severely ill patients on multiple levels, which leads to increased morbidity but also it might induce myocardial injury leading to myocardial dysfunction [2]. The most common complications include arrhythmia (atrial fibrillation, ventricular tachyarrhythmia, and ventricular fibrillation), cardiac injury (elevated highly sensitive troponin I (hs-TnI) and creatine kinase (CK) levels, NT pro-BNP levels), fulminant myocarditis, heart failure, pulmonary embolism, and disseminated intravascular coagulation (DIC) [3].

Patients with established heart disease constitute a particularly challenging group, with conditions that may be life-threatening if proper treatment or intervention is inadequately delayed, which is the base for increased complications risk and

worsened disease prognosis. COVID-19 case fatality rate is significantly different around the world. Patients with several comorbidities have significantly increased case fatality rate (CFR): 10.5% for cardiovascular disease (CVD); 7.3% for diabetes mellitus; 6.3% for chronic obstructive pulmonary disease (COPD); around 6% for hypertension patients with cancer [4]. The mortality rates are different in different world regions and are influenced by several technical and quality measures of the healthcare systems, number of tests performed, demographic characteristics of the tested population and their health status. These aspects underline the importance of the need for multidisciplinary assessment and treatment, including cardiovascular evaluation and therapy aimed to reduce the COVID-19 mortality.

#### **2. COVID-19 and cardiovascular system**

Published data about disease manifestation and progression showed that patients with established cardiovascular disease are among the highest risk individuals for severe manifestation of COVID 19 and death. In a series of 44 672 confirmed patients with COVID-19 from China, 14.2% were reported to have cardiovascular disease, but also 22,7% of all deaths were in patients with underlying cardiovascular disease [5, 6]. The presence of common risk factors, such as hypertension, diabetes, coronary artery disease (CAD) increase the risk for COVID-19 induced complications as shown in **Figure 1**. It is of greater concern and importance the fact that COVID-19 can lead to cardiac injury even in individual not reporting previous cardiovascular disease. There is a need for proper understanding of the pathophysiological mechanisms of the cardiovascular damage caused by COVID-19 disease. This will enable on time effective patient's management and mortality reduction. The affection of the cardiovascular system by the infection is followed by release of inflammatory markers such as highly sensitive troponin and natriuretic peptides, which modifies prognosis, particularly in patients with continuous rise of those markers [7]. Cytokines such as IL-6 causes inflammation of the vascular system that result in generalized endotheliopathy and immune induced thrombosis. Inflammation in the myocardium can lead to myocarditis, heart failure, cardiac arrhythmias, and sudden death [7, 8]. Down-regulation of ACE2 with viral infection may predispose to relatively unopposed angiotensin II effects, which and cause new or worsened hypertension. After infection with common RNA viruses, most infected patients may experience only a transient viral syndrome with no significant cardiac dysfunction. However, depending on the immune response it can manifest as acute myocarditis with heart failure or cardiogenic shock, accompanied by cytokine storm and inflammatory cell infiltration of the heart. With proper treatment some patients can recover, but others can develop inflammatory cardiomyopathy [9].

A place of the initial *SARS*-*CoV*-*2* virus entrance to our organism is virus attachment to the angiotensin converting-enzyme 2 (ACE-2) membrane-linked aminopeptidase receptor on the epithelial cells of the lungs. However, these receptors are expressed in many human organs including myocardium making them vulnerable to the virus [10]. The studies showed higher expression of ACE-2 receptors in diabetic and hypertensive patients, which might be one of the causes of more severe forms of the disease in those individuals. While ACE2 is essential for viral invasion, there is no evidence that ACE inhibitors or angiotensin receptor blockers (ARBs) worsen prognosis. Hence, patients should not discontinue their use, based on recommendations for COVID-19 and cardiovascular disease treatment from several cardiology associations. Moreover, renin–angiotensin–aldosterone system (RAAS) inhibitors might be beneficial in COVID-19 [10]. Initial immune and inflammatory

### *COVID-19 and Cardiovascular Disease: Mechanisms and Implications DOI: http://dx.doi.org/10.5772/intechopen.99332*

#### **Figure 1.**

*In COVID-19 disease patients' cardiovascular comorbidities are the cause of the increased mortality. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) which are established drugs for reduction of the cardiovascular risk have many positive effects that might modify the course of the COVID-19 disease. Nature Reviews Cardiology volume 17, pages 543–558(2020), ref. [7].*

responses induce a severe cytokine storm during the rapid progression phase of COVID-19. Early evaluation and continued monitoring of cardiac damage using the values of high sensitive cardiac troponin I (hs-cTn I), N-terminal *pro* b-type natriuretic peptide (NT-proBNP) and coagulation (D-dimer) after hospitalizationmay identify patients with cardiac injury and predict COVID-19 complications [11]. Severe inflammation is assumed as a cause of underlying generalized endothelial disfunction (endotheliopathy), which serves as a basis for development of microvascular thrombosis.
