European Journal of Cardiovascular Medicine

In terms of world health and history, 2020 was a historic year. The pandemic of the coronavirus disease 2019 (COVID-19) has brought attention to the risks associated with deadly diseases that can spread quickly throughout the world. Pneumonia of unknown etiology became prevalent in Wuhan, China, in December 2019. It was shown that SARS CoV-2, a novel beta coronavirus, was the source of COVID-19. This virus produced unprecedented levels of morbidity and mortality on a global scale [1].

These people's bronchoalveolar lavage fluid samples were used to extract and sequence RNA. It was found that a novel beta coronavirus called SARSCoV-2 was the cause of COVID19, resulting in unprecedented levels of morbidity and mortality around the globe [2]. For over two years, there has been no sign of an end to the COVID-19 pandemic in the near future. Numerous and continuing investigations on COVID-19 have led to the discovery of a large variety of organ dysfunctions. Health communities must deal with a unique condition encountered by some COVID-19 survivors while the pharmaceutical arsenal for COVID-19 is still being created in an effort to limit morbidity and death in COVID-19 patients. Known as long haulers, long COVID, or post-acute COVID-19 syndrome (PACS), this syndrome is linked to delayed or long-term consequences that continue more than four weeks after the beginning of symptoms [3]. Roughly 42% of PACS symptoms are associated with cardiovascular issues, which are one cause of several of the symptoms and indicators seen in long-term COVID-19 patients. Additionally, in long-term COVID patients, imaging and laboratory data suggest cardiovascular issues [4]. As far as we are aware, PACS still lacks sufficient data on cardiovascular outcomes. As a result, this narrative review carefully examined the evidence that was at hand, highlighted the pathomechanisms that cause acute COVID-19 and may also contribute to long-term COVID, and developed tenable theories based on the data that was at hand. Clinical research and epidemiological studies have demonstrated the complicated biochemical mechanisms and related behavioral aspects that underlie the intersection of diet, COVID-19, and CVD. In the post-pandemic environment, diet may be a vital tool for altering risk of both communicable and non-communicable illnesses.

Hypothesized Mechanisms of Extended COVID-19 in the cardiovascular system-

On March 11, 2020, SARS-CoV-2 is already known to have caused the global COVID-19 pandemic [5]. Given that both viruses have positive-stranded RNA and have four structural proteins that bind to the viral envelope, this entity and SARS-CoV-1 are similar in many respects [6]. The most crucial structure among these structural proteins, the spike (S) glycoprotein, is in charge of the host cell entrance mechanism. The S glycoprotein binds to the host cell's angiotensin-converting enzyme-2 (ACE2) receptor, mainly in type 2 pneumocytes, initiating the SARS-CoV-2 entrance pathway and causing viral membrane and host cell fusion [7]. The type II transmembrane serine protease (TMPRSS2) helps to speed up the process by causing the S protein to become active. Many organs, including the kidneys, lungs, intestines, and-most importantly-the heart and endothelium, express ACE2 receptors widely [8]. While SARS-CoV-1 and 2 bind to the same receptors (ACE), SARS-CoV-2 has been shown to have increased infectivity. There are two causes. S1 and S2, the two units of the S glycoprotein, are present in SARS-CoV-2 [9]. Subsequently, SARS-CoV-2's affinity for ACE-2 was significantly increased by 10-20 times over SARS-CoV-1 due to modifications in the virus's receptor binding area [10]. As we'll see later in the review, SARS-CoV-2's increased virulence also means that it can do more damage. It is well established that PACS plays a role in the ongoing organ damage that results from an acute COVID-19 infection.

While multiple organs are impacted and contribute to the prolonged duration of symptoms in long COVID, in this narrative review, we solely address the cardiovascular (CV) aftereffects of long COVID, mainly concerning their potential underlying pathophysiology. direct SARS-CoV-2 invasion, aberrant immunological and the cardiovascular side effects of prolonged COVID were mostly caused by five pathomechanisms: inflammatory response, dysregulation of ACE2, abnormalities of the lungs, and adverse effects associated with the COVID-19 treatment itself [3].