Unmasking the Viral Veil: Exploring the Cardiovascular Intrigue of Pathogenic Infections

The intricate interplay between viral infections and cardiovascular complications has garnered significant attention from 2018 to 2023. Extensive research during this period has unveiled substantial connections between various viruses and cardiovascular diseases. Notable examples include cytomegalovirus (CMV), coxsackievirus, influenza, human immunodeficiency virus (HIV), Epstein-Barr virus (EBV), severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), as well as coxsackievirus A and B, enteroviruses, adenovirus, and parvovirus B19. These viruses exert diverse influences on cardiovascular health through various pathways, contributing to endothelial dysfunction, inflicting direct damage on cardiac tissue, and triggering inflammatory responses. The intricate interplay between viral infections and cardiovascular health underscores the importance of considering viral pathogens within the framework of cardiovascular disease development, clinical management practices, and future research initiatives. This systematic review comprehensively scrutinizes the cardiovascular impacts stemming from various viral infections, casting a revealing light on their underlying mechanisms and associated clinical implications. These valuable insights can guide clinical management strategies, preventive measures, and further investigations into the complex connection between viral infections and cardiovascular diseases, emphasizing the necessity for ongoing research and vigilance in comprehending and managing these pathogen-induced cardiac manifestations.

The intricate interplay between viral infections and cardiovascular complications has garnered increasing recognition in recent years. This systematic review is poised to comprehensively scrutinize the cardiovascular impacts stemming from various viral infections, casting a revealing light on their underlying mechanisms and associated clinical implications. From 2018 to 2023, research has unearthed intriguing correlations between viral infections and cardiovascular diseases. Notably, Cytomegalovirus (CMV), a member of the Herpesviridae family, has been closely associated with endothelial dysfunction and atherosclerosis, instigating apprehensions concerning its potential involvement in adverse cardiovascular outcomes [1,2]. Concurrently, Coxsackievirus strains A and B have been inextricably linked to myocarditis and dilated cardiomyopathy, thereby prompting thorough investigations into immune-mediated cardiac damage [3,4]. The influenza virus, traditionally recognized for its respiratory impact, has been acknowledged for its role in exacerbating cardiovascular risks, encompassing acute cardiovascular events [5].

Moreover, in a surprising twist, the Human Immunodeficiency Virus (HIV), primarily known for its immunological impact, has been identified as a contributor to an elevated risk of cardiovascular diseases, ostensibly due to chronic inflammation [6]. The Epstein-Barr Virus (EBV), conventionally associated with infectious mononucleosis, has drawn attention for its potential influence on endothelial dysfunction, vasculitis, and thrombosis [7,8]. The ongoing COVID-19 pandemic has unveiled the cardiovascular effects of SARS-CoV-2, giving rise to concerns regarding myocardial injury, myocarditis, and thromboembolic events [9]. Furthermore, enteroviruses, including Coxsackievirus A and B, adenovirus, and parvovirus B19, have emerged as noteworthy contributors to myocarditis and cardiomyopathy. Their direct effects on cardiac cells have triggered a call for further in-depth investigation [10-12]. This extensive exploration forms the foundation for our systematic review, which endeavors to delve deeper into the evolving landscape of these interrelationships and emphasizes the pressing necessity for ongoing research and vigilance in comprehending and managing these pathogen-induced cardiac manifestations.

Literature search and selection

In pursuit of a comprehensive exploration of the influence of viral infections on cardiovascular health, we conducted a systematic literature search. This investigation spanned from January 1, 2018, to August 14, 2023, encompassing renowned electronic databases, including Elsevier, PubMed, Scopus, and Web of Science. Our tailored search strategy meticulously integrated relevant keywords and Medical Subject Headings (MeSH) terms, aligning with the objective of probing viral infections and their potential impact on cardiovascular well-being [1-3].

Inclusion and exclusion criteria

In our review, we established precise inclusion and exclusion criteria to ensure a focused and rigorous analysis. Included were studies that delved into the cardiovascular effects of viral infections and exclusively involved human subjects. We limited our scope to publications released between 2018 and 2023, confined to those published in peer-reviewed journals and available in the English language. This rigorous selection process helped maintain the relevance and quality of the studies under consideration. Conversely, we deliberately excluded case reports, reviews and studies that lacked pertinent cardiovascular outcomes, adhering to a stringent approach aimed at ensuring that only studies with direct and substantial relevance to the cardiovascular impact of viral infections contributed to our comprehensive analysis. This approach guarantees the precision and depth of our investigation into this intricate interplay.

Data extraction and synthesis

Salient study attributes were meticulously extracted from diverse sources. These encompassed details such as the author, publication year, study design, specific viral infections under scrutiny, cardiovascular outcomes investigated, sample size, and key findings related to cardiovascular effects. The amassed data underwent a rigorous synthesis process to engender a comprehensive overview elucidating the impact of each viral infection on cardiovascular health [6,7]. Appropriate quality assessment tools were judiciously applied, contingent on the study design, to assess the reliability and validity of the included studies. The Newcastle-Ottawa Scale was employed for observational studies, while the Cochrane Collaboration tool was utilized for randomized controlled trials. The insights gleaned from this meticulous assessment process profoundly informed the interpretation of study findings [8,9]. Addressing the concern of low inter-rater reliability in the context of utilizing the Newcastle-Ottawa Scale (NOS) for observational studies involves a strategic reassessment of the scale’s application and the implementation of measures to enhance the consistency and agreement between raters. By meticulously adhering to these systematic methodologies, we aim to provide a robust and rigorous analysis of the interplay between viral infections and cardiovascular health, ensuring the validity and integrity of our findings.

Several viruses, including Cytomegalovirus (CMV), Coxsackievirus, Influenza, Human Immunodeficiency Virus (HIV), Epstein-Barr Virus (EBV), Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), Enteroviruses, Adenovirus and Parvovirus B19 viruses influence cardiovascular health.

Cytomegalovirus (CMV)

Research into CMV’s effect on cardiovascular health reveals compelling associations. Numerous studies have established a significant link between CMV infection and endothelial dysfunction, a key initiator of atherosclerosis [1,2]. Interestingly, CMV antigens have been detected within atherosclerotic plaques, suggesting its role in atherosclerosis progression [1]. Moreover, heightened anti-CMV antibody titers have been associated with tissue Plasminogen Activator Inhibitor 1 (tPAI-1), indicating CMV’s potential to disrupt clotting mechanisms and contribute to Acute Myocardial Infarction (AMI) [2]. CMV-induced immune activation may render plaques prone to rupture, precipitating acute coronary events [3].

Coxsackievirus

Extensive research has unveiled the cardiovascular effects of Coxsackieviruses, particularly A and B strains. These viruses can directly infect cardiac tissue, leading to myocarditis and inflammation in the heart muscles [9]. Such infections also damage cells and compromise heart function [9]. Studies have linked Coxsackievirus infections to an increased risk of acute cardiovascular events, including acute myocardial infarction [9]. The ability of Coxsackieviruses to target the heart and prompt inflammatory responses emphasizes their potential role in causing cardiovascular complications.

Influenza

The implications of influenza infections on cardiovascular health have undergone intense scrutiny. Extensive studies have demonstrated a link between influenza infections and an increased risk of acute cardiovascular events like heart attacks and strokes [12]. It is believed that the inflammatory response triggered by influenza can contribute to endothelial dysfunction and plaque instability [12]. Moreover, inflammation associated with influenza can worsen cardiovascular conditions, particularly among vulnerable populations, leading to unfavorable outcomes [12]. Recognizing the role of viral infections in cardiovascular health is crucial for understanding acute cardiovascular events caused by influenza [13,14].

Human Immunodeficiency Virus (HIV)

Examinations exploring the cardiovascular effects of HIV infection have revealed a complex interplay between viral infection, inflammation, and cardiovascular risk. People living with HIV are more susceptible to cardiovascular diseases such as atherosclerosis, myocardial infarction and stroke [15]. Persistent inflammation caused by HIV infection could contribute to endothelial dysfunction and plaque formation [15]. Although Antiretroviral Therapy (ART) has been effective in reducing certain cardiovascular risks, specific factors related to HIV, such as viral replication and immune dysregulation, may still impact health [15]. It is crucial to continue researching the multifaceted relationship between HIV and cardiovascular well-being [16-18].

Epstein-Barr Virus (EBV)

Recent studies have investigated potential links between EBV infection and cardiovascular disorders. Researchers have found associations between EBV infection, endothelial dysfunction, and atherosclerosis [19]. Moreover, studies have revealed a connection between EBV and myocarditis, an inflammatory condition that affects the heart muscle [20-22]. The ability of EBV to directly infect cardiomyocytes and disrupt immune regulation suggests its involvement in myocardial injury and autoimmune-mediated myocarditis [21]. Additionally, EBV has been associated with vasculitis and an increased risk of thrombosis, leading to a pro-thrombotic state [23]. The varied impact of EBV on endothelial function, myocardium, and thrombosis highlights its potential contribution to cardiovascular complications.

SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2)

The global emergence of the SARS-CoV-2 virus has brought attention to its potential cardiovascular implications. It is evident that SARS-CoV-2 can affect the cardiovascular system, leading to myocardial injury, myocarditis, and acute coronary syndromes [24]. The virus’s ability to directly infect cardiac cells and trigger an inflammatory response contributes to endothelial dysfunction and increased blood clotting [24]. Age and pre-existing cardiovascular conditions further amplify the virus’s impact on heart health [24]. Long-term studies also suggest lasting cardiovascular consequences among severe COVID-19 survivors [24]. The ever-evolving understanding of SARS-CoV-2’s impact on the cardiovascular system highlights the need for extensive research efforts and heightened clinical awareness [25,26].

Enteroviruses (including coxsackievirus)

Enteroviruses, particularly Coxsackieviruses, have become prominent contributors to various cardiovascular complications. Research highlights their involvement in myocarditis, where viral infection triggers heart muscle inflammation [9]. This inflammatory response can damage the heart and compromise cardiac function, potentially affecting heart health [9]. Moreover, enteroviruses may also contribute to the progression of atherosclerosis through inflammatory mechanisms [9]. The association of these viruses with acute cardiovascular events underscores their significance within the realm of cardiovascular diseases.

Adenovirus

Adenoviruses have garnered attention for their potential implications for cardiovascular health. Studies have revealed that adenoviral infections can lead to myocarditis and dilated cardiomyopathy [10]. The virus’s ability to directly infect cardiac tissue and elicit immune responses contributes to damage to the heart muscle and impaired cardiac function [10]. Moreover, there is evidence linking adenovirus infections with acute coronary syndromes and adverse cardiovascular outcomes, highlighting their significance within the realm of cardiovascular health [10].

Parvovirus B19

Parvovirus B19 infections can lead to cardiovascular manifestations, especially in individuals with pre-existing heart conditions. Recent research has demonstrated that parvovirus B19 can provoke myocarditis and worsen heart failure in susceptible individuals [11]. Moreover, the virus’s impact on endothelial function and inflammation furthers its potential involvement in cardiovascular complications [11]. These findings emphasize the intricate relationship between viral infections and heart health. Cardiac viruses have diverse but significant impacts on cardiovascular health, ranging from endothelial dysfunction and atherosclerosis to direct heart muscle infection and inflammation. Understanding these connections is vital for advancing patient care and preventing cardiovascular complications associated with viral infections.

Diverse type of viral infections is mounting day by day across the world [27-47]. The intricate relationship between viral infections and cardiovascular complications has garnered significant attention in recent years, particularly from 2018 to 2023. Extensive research during this period has unveiled substantial connections between various viruses and cardiovascular diseases. Notable examples include Cytomegalovirus (CMV), coxsackievirus, influenza, Human Immunodeficiency Virus (HIV), Epstein-Barr Virus (EBV), Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), as well as coxsackievirus A and B, enteroviruses, adenovirus, and parvovirus B19. These viruses exert diverse influences on cardiovascular health through various pathways, contributing to endothelial dysfunction, inflicting direct damage on cardiac tissue, and triggering inflammatory responses. The intricate interplay between viral infections and cardiovascular health underscores the importance of considering viral pathogens within the framework of cardiovascular disease development, clinical management practices and future research initiatives. This systematic review offers a comprehensive synthesis of recent research, shedding light on the cardiovascular effects of viral infections. Exploring the intricate relationships and underlying mechanisms deepens our understanding of how viral pathogens impact cardiovascular health. These valuable insights can guide clinical management strategies, preventive measures, and further investigations into the complex connection between viral infections and cardiovascular diseases.

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