COVID-19 and Acute Coronary Syndromes: From Pathophysiology to Clinical Perspectives.

Acute coronary syndromes (ACS) are frequently reported in patients with coronavirus disease 2019 (COVID-19) and may impact patient clinical course and mortality. Although the underlying pathogenesis remains unclear, several potential mechanisms have been hypothesized, including oxygen supply/demand imbalance, direct viral cellular damage, systemic inflammatory response with cytokine-mediated injury, microvascular thrombosis, and endothelial dysfunction. The severe hypoxic state, combined with other conditions frequently reported in COVID-19, namely sepsis, tachyarrhythmias, anemia, hypotension, and shock, can induce a myocardial damage due to the mismatch between oxygen supply and demand and results in type 2 myocardial infarction (MI). In addition, COVID-19 promotes atherosclerotic plaque instability and thrombus formation and may precipitate type 1 MI. Patients with severe disease often show decrease in platelets count, higher levels of d-dimer, ultralarge von Willebrand factor multimers, tissue factor, and prolongation of prothrombin time, which reflects a prothrombotic state. An endothelial dysfunction has been described as a consequence of the direct viral effects and of the hyperinflammatory environment. The expression of tissue factor, von Willebrand factor, thromboxane, and plasminogen activator inhibitor-1 promotes the prothrombotic status. In addition, endothelial cells generate superoxide anions, with enhanced local oxidative stress, and endothelin-1, which affects the vasodilator/vasoconstrictor balance and platelet aggregation. The optimal management of COVID-19 patients is a challenge both for logistic and clinical reasons. A deeper understanding of ACS pathophysiology may yield novel research insights and therapeutic perspectives in higher cardiovascular risk subjects with COVID-19.

SARS-CoV 2 Infection (Covid-19) and Cardiovascular Disease in Africa: Health Care and Socio-Economic Implications.

The current pandemic of SARS-COV 2 infection (Covid-19) is challenging health systems and communities worldwide. At the individual level, the main biological system involved in Covid-19 is the respiratory system. Respiratory complications range from mild flu-like illness symptoms to a fatal respiratory distress syndrome or a severe and fulminant pneumonia. Critically, the presence of a pre-existing cardiovascular disease or its risk factors, such as hypertension or type II diabetes mellitus, increases the chance of having severe complications (including death) if infected by the virus. In addition, the infection can worsen an existing cardiovascular disease or precipitate new ones. This paper presents a contemporary review of cardiovascular complications of Covid-19. It also specifically examines the impact of the disease on those already vulnerable and on the poorly resourced health systems of Africa as well as the potential broader consequences on the socio-economic health of this region.

Comprehensive Review of Cardiovascular Involvement in COVID-19.

COVID-19 has emerged as one of the most devastating and clinically significant infectious diseases of the last decade. It has reached global pandemic status at an unprecedented pace and has placed significant demands on health care systems worldwide. Although COVID-19 primarily affects the lungs, epidemiologic reports have shown that the disease affects other vital organs of the body, including the heart, vasculature, kidneys, brain, and the hematopoietic system. Of importance is the emerging awareness of the effects of COVID-19 on the cardiovascular system. The current state of knowledge regarding cardiac involvement in COVID-19 is presented in this article, with particular focus on the cardiovascular manifestations and complications of COVID-19 infection. The mechanistic insights of disease causation and the relevant pathophysiology involved in COVID-19 as they affect the heart are explored and described. Relevant practice essentials and clinical management implications for patients with COVID-19 with a cardiac pathology are presented in light of recent evidence.

Possible mechanisms responsible for acute coronary events in COVID-19.

The novel coronavirus (SARS-CoV-2) is primarily a respiratory pathogen and its clinical manifestations are dominated by respiratory symptoms, the most severe of which is acute respiratory distress syndrome (ARDS). However, COVID-19 is increasingly recognized to cause an overwhelming inflammatory response and cytokine storm leading to end organ damage. End organ damage to heart is one of the most severe complications of COVID-19 that increases the risk of death. We proposed a two-fold mechanism responsible for causing acute coronary events in patients with COVID-19 infection: Cytokine storm leading to rapid onset formation of new coronary plaques along with destabilization of pre-existing plaques and direct myocardial injury secondary to acute systemic viral infection. A well-coordinated immune response is the first line innate immunity against a viral infection. However, an uncoordinated response and hypersecretion of cytokines and chemokines lead to immune related damage to the human body. Human Coronavirus (HCoV) infection causes infiltration of inflammatory cells that cause excessive production of cytokines, proteases, coagulation factors, oxygen radicals and vasoactive molecules causing endothelial damage, disruption of fibrous cap and initiation of formation of thrombus. Systemic viral infections also cause vasoconstriction leading to narrowing of vascular lumen and stimulation of platelet activation via shear stress. The resultant cytokine storm causes secretion of hypercoagulable tissue factor without consequential increase in counter-regulatory pathways such as AT-III, activated protein C and plasminogen activator type 1. Lastly, influx of CD4+ T-cells in cardiac vasculature results in an increased production of cytokines that stimulate smooth muscle cells to migrate into the intima and generate collagen and other fibrous products leading to advancement of fatty streaks to advanced atherosclerotic lesions. Direct myocardial damage and cytokine storm leading to destabilization of pre-existing plaques and accelerated formation of new plaques are the two instigating mechanisms for acute coronary syndromes in COVID-19.

Care of acute coronary syndromes during the health contingency due to a SARS-CoV-2 outbreak.

The communications accumulated in the last weeks make it clear that there is no agreement to define the best treatment strategy in patients with acute coronary syndrome (SICA). In patients presenting with an acute myocardial infarction with ST-segment elevation (IAMCESST), it has been suggested to favor fibrinolysis (FL) over primary percutaneous coronary intervention (PCI), reserving ICP for cases of failed FL1,2; however, some societies have maintained the indication of the ICPp as the repercussion method of choice3. In SICAs without ST segment elevation (SICASESST) the recommendations are very similar, favoring medical treatment over percutaneous coronary intervention in this subgroup of patients1. Several companies consider the contagion status, particularly in the SICASESST, to decide which repercussion follow3. Anticipating that the epidemiological curve in Mexico will be similar to that observed in most countries, we recommend continuing the care of patients with SICA, the catheterization rooms must maintain their operation.

Las comunicaciones acumuladas en las últimas semanas dejan claro que no existe un acuerdo para definir la mejor estrategia de tratamiento en los pacientes con un síndrome coronario agudo (SICA). En los pacientes que se presentan con un infarto agudo del miocardio con elevación del segmento ST (IAMCESST) se ha sugerido privilegiar la fibrinólisis (FL) sobre la intervención coronaria percutánea primaria (ICPp), reservando el ICP para los casos de FL fallidar1,2; sin embargo algunas sociedades han mantenido la indicación de la ICPp como el método de repercusión de elecciónr3. En los SICA sin elevación del segmento ST (SICASESST) las recomendaciones son muy similares, favoreciendo el tratamiento medico sobre el intervencionismo coronario percutáneo, en este subgrupo de pacientes1. Varias sociedades consideran el estado de contagio, en particular en los SICASESST, para decidir que estrategia de repercusión seguir3. Anticipando que la curva epidemiológica en México será similar a la observada en la mayoría de los países, recomendamos continuar la atención de los pacientes con SICA, las salas de cateterismo deben mantener su funcionamiento.