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Billah, M.; Naz, A. COVID-19 and Coronary Heart Disease. Encyclopedia. Available online: https://encyclopedia.pub/entry/8489 (accessed on 16 November 2024).
Billah M, Naz A. COVID-19 and Coronary Heart Disease. Encyclopedia. Available at: https://encyclopedia.pub/entry/8489. Accessed November 16, 2024.
Billah, Muntasir, Adiba Naz. "COVID-19 and Coronary Heart Disease" Encyclopedia, https://encyclopedia.pub/entry/8489 (accessed November 16, 2024).
Billah, M., & Naz, A. (2021, April 07). COVID-19 and Coronary Heart Disease. In Encyclopedia. https://encyclopedia.pub/entry/8489
Billah, Muntasir and Adiba Naz. "COVID-19 and Coronary Heart Disease." Encyclopedia. Web. 07 April, 2021.
Peer Reviewed
COVID-19 and Coronary Heart Disease
This is a peer-reviewed entry published in Encyclopedia Journal, full entry can be found at 10.3390/encyclopedia1020028

Coronary heart disease (CHD) is the leading cause of mortality worldwide. One of the main contributions of mortality and morbidity in CHD patients is acute myocardial infarction (AMI), which is the result of abrupt occlusion of an epicardial coronary artery due to a sudden rupture of atherosclerotic plaque, causing myocardial ischemia. In the initial stage of myocardial ischemia, lack of oxygen and nutrient supply results in biochemical and metabolic changes within the myocardium. Depletion of oxygen switches the aerobic cellular metabolism to anaerobic metabolism and impairs the oxidative phosphorylation pathway eventually leading to cardiomyocyte death. Several studies suggest an interlink between COVID-19 and ischemic heart disease. An increased ACE2 receptor expression in the myocardium may partly contribute to the myocardial injuries that are observed in patients affected by SARS-CoV-2. Furthermore, pre-existing cardiovascular disease, in conjunction with an aggravated inflammatory response which causes an up-regulation in pro-inflammatory cytokines. Moreover, patients with atherosclerosis are observed to be more prone to ischemic attacks when affected by COVID-19, due to hypercoagulation in the blood as well as elevated pro-inflammatory markers.

COVID-19 SARS-CoV-2 ischemic heart disease ischemia coronary heart disease
Ischemia is caused due to a reduction in blood flow in an area, as a result of a blockage in the blood vessel. Ischemic heart disease, commonly referred to as coronary heart disease (CHD), generally leads to the narrowing of coronary arteries, which primarily supply oxygenated blood to the cardiac muscles [1][2][3]. One of the main contributions of mortality and morbidity in CHD patients is acute myocardial infarction (AMI) [4]. Acute-ST segment elevation myocardial infarction (STEMI), which is the result of abrupt occlusion of an epicardial coronary artery due to a sudden rupture of atherosclerotic plaque, most commonly affects the left anterior descending artery (LAD) (50%), right coronary artery (30%) and left circumflex artery (20%) [5]. Atherosclerosis is a multifactorial progressive disease of the arterial wall and is demonstrated by focal development of atherosclerotic lesion or plaque within the arterial wall. Smooth muscle cells (SMCs) and mononuclear phagocytes (MPs) as well as inflammatory cells such as macrophages, T cells, dendritic cells and mast cells accumulate in the lesions as the disease progresses [6]. Multiple risk factors including dyslipidemia, incriminated vasoconstrictor hormones, hyperglycemia, pro-inflammatory cytokines, and smoking facilitate the progression of almost 50% of the arterial lesions. In the absence of systemic hypercholesterolemia, stimulated T lymphocytes, certain heat shock proteins and plasma lipoprotein induces inflammation that helps the atherosclerotic plaque formation [7][8]. Chronic inflammation can rupture the plaque and may lead to ischemia and myocardial infarction [9][10]. Delay in the restoration of the coronary blood flow leads to cardiac cell death. If acute myocardial ischemia is prolonged, cardiomyocyte death begins in the sub-endocardium, and over time, spreads towards the epicardium [11]. In the initial stage of myocardial ischemia, lack of oxygen and nutrient supply results in biochemical and metabolic changes within the myocardium. Depletion of oxygen switches the aerobic cellular metabolism to anaerobic metabolism and impairs the oxidative phosphorylation pathway leading to mitochondrial membrane potential loss and subsequently decreases in production and inhibits the contractile function of the cardiomyocytes. This process is exacerbated by the hydrolysis of the available Adenosine triphosphate (ATP) due to the reverse function of F1F0 ATPase to maintain the mitochondrial membrane potential. Anaerobic glycolysis results in the accumulation of lactic acid, which increases the intracellular acidity by reducing the pH (to <7.0) and leads to ionic imbalances [12]. Acidic environment damages the mitochondria and ATP production eventually ceases [13]. Accumulation of intracellular protons activates the Na+-H+ ion exchanger and it drives the protons out of the cell in exchange for Na+. The intracellular Na+ overload in conjunction with cell membrane depolarization reverses the Na+-Ca2+ exchanger function and expels Na+ out of the cell for Ca2+ into the cell [14]. Eventually, cellular membrane ion pumps such as Na+/K+ ATPase, sarcoplasmic reticulum ATPase Ca2+ (SERCA) and active Ca2+ excretion fail due to the drop in ATP level and ion gradients across the cell membranes collapse leading to the cell to death [15].
A clinical syndrome, named angina pectoris, is the chest pain or discomfort that persists as a result of failure to acquire the required amount of oxygen to the cardiac muscles. National Health and Nutrition Examination (NHANES) states that as of the time frame between 2003 to 2006, it has been estimated that 17.6 million Americans of age 20 and above have had CHD. The annual incidence of myocardial infarction was 935,000, and the overall prevalence of angina pectoris was found to be 4.6%. In 2006, CHD was responsible for every one in six deaths and is the leading cause of death in both of the sexes.
It has been observed that there is a significant correlation between myocardial injury and fatal outcomes of COVID-19 [16]. In a study conducted with 187 patients that tested positive for COVID-19, 52% had a myocardial injury, which was observed by detecting higher levels of troponin T (TnT). This marker was seen to be elevated in cases of mortality from COVID-19. Furthermore, it has been noted that light should be shone onto the protection of the cardiovascular system while treating patients with COVID-19, as when severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infects the host cell, acute myocardial injury is seen to take place, along with chronic damage to the cardiovascular system [17]. The National Health Commission of China (NHC) had mortality data showing that 35% of the patients that tested positive for COVID-19 had hypertension and 17% had a history of CHD. Hence it is suggested that cardiovascular diseases can provoke pneumonia and further worsen other symptoms in patients that are infected with SARS-CoV-2.
Severe respiratory conditions such as respiratory failure and infectious diseases may induce a mismatch between oxygen demand and supply. Acute respiratory failure causes hypoxemia (reduced oxygen supply) and activates the sympathetic nervous system which increases the heart rate, cardiac output and myocardial contractility—leading to increased oxygen demand. This imbalance can lead to myocardial injury or MI, termed as type 2 MI [18][19][20]. According to recent reports, about 7% of the COVID-19 patients have an acute cardiac injury and may present as type 2 MI or myocarditis [21]. Atheroma was found in only a small percentage of STEMI patients after coronary angiogram [22][23][24]. COVID-19 patients can present with cardiac conditions such as STEMI, non-STEMI (NSTEMI), heart failure, cardiac arrhythmia, thromboembolism and cardiac arrests. Hence, it is crucial to differentiate between the type 2 MI patients from the other urgent management requiring conditions.
This paper is aimed to understand the correlation between COVID-19 and ischemic heart diseases or CHD, and possibly propose a mechanism of action behind their interrelationship.

References

  1. Billah, M.; Ridiandries, A.; Allahwala, U.K.; Mudaliar, H.; Dona, A.; Hunyor, S.; Khachigian, L.M.; Bhindi, R. Remote Ischemic Preconditioning induces Cardioprotective Autophagy and Signals through the IL-6-Dependent JAK-STAT Pathway. Int. J. Mol. Sci. 2020, 21, 1692.
  2. Billah, M.; Ridiandries, A.; Allahwala, U.; Mudaliar, H.; Dona, A.; Hunyor, S.; Khachigian, L.M.; Bhindi, R. Circulating mediators of remote ischemic preconditioning: Search for the missing link between non-lethal ischemia and cardioprotection. Oncotarget 2019, 10, 216–244.
  3. Billah, M.; Ridiandries, A.; Rayner, B.S.; Allahwala, U.K.; Dona, A.; Khachigian, L.M.; Bhindi, R. Egr-1 functions as a master switch regulator of remote ischemic preconditioning-induced cardioprotection. Basic Res. Cardiol. 2019, 115, 3.
  4. Mozaffarian, D.; Benjamin, E.J.; Go, A.S.; Arnett, D.K.; Blaha, M.J.; Cushman, M.; de Ferranti, S.; Despres, J.P.; Fullerton, H.J.; Howard, V.J.; et al. Heart disease and stroke statistics-2015 update: A report from the American Heart Association. Circulation 2015, 131, e29–e322.
  5. Sutton, P. Cardiovascular System, 3rd ed.; Elsevier Health Sciences: London, UK, 2008; p. 252.
  6. Gown, A.M.; Tsukada, T.; Ross, R. Human atherosclerosis. II. Immunocytochemical analysis of the cellular composition of human atherosclerotic lesions. Am. J. Pathol. 1986, 125, 191–207.
  7. Millonig, G.; Malcom, G.T.; Wick, G. Early inflammatory-immunological lesions in juvenile atherosclerosis from the Pathobiological Determinants of Atherosclerosis in Youth (PDAY)-study. Atherosclerosis 2002, 160, 441–448.
  8. Libby, P.; Ridker, P.M.; Hansson, G.K. Inflammation in atherosclerosis: From pathophysiology to practice. J. Am. Coll. Cardiol. 2009, 54, 2129–2138.
  9. Hansson, G.K.; Robertson, A.K.; Soderberg-Naucler, C. Inflammation and atherosclerosis. Annu. Rev. Pathol. 2006, 1, 297–329.
  10. Lusis, A.J. Atherosclerosis. Nature 2000, 407, 233–241.
  11. Reimer, K.A.; Lowe, J.E.; Rasmussen, M.M.; Jennings, R.B. The wavefront phenomenon of ischemic cell death. 1. Myocardial infarct size vs duration of coronary occlusion in dogs. Circulation 1977, 56, 786–794.
  12. Venardos, K.M.; Perkins, A.; Headrick, J.; Kaye, D.M. Myocardial ischemia-reperfusion injury, antioxidant enzyme systems, and selenium: A review. Curr. Med. Chem. 2007, 14, 1539–1549.
  13. Monassier, J.P. Reperfusion injury in acute myocardial infarction: From bench to cath lab. Part II: Clinical issues and therapeutic options. Arch. Cardiovasc. Dis. 2008, 101, 565–575.
  14. Avkiran, M.; Marber, M.S. Na(+)/H(+) exchange inhibitors for cardioprotective therapy: Progress, problems and prospects. J. Am. Coll. Cardiol. 2002, 39, 747–753.
  15. Grace, P.A. Ischaemia-reperfusion injury. Br. J. Surg. 1994, 81, 637–647.
  16. Guo, T.; Fan, Y.; Chen, M.; Wu, X.; Zhang, L.; He, T.; Wang, H.; Wan, J.; Wang, X.; Lu, Z. Cardiovascular Implications of Fatal Outcomes of Patients With Coronavirus Disease 2019 (COVID-19). JAMA Cardiol. 2020, 5, 811–818.
  17. Zheng, Y.Y.; Ma, Y.T.; Zhang, J.Y.; Xie, X. COVID-19 and the cardiovascular system. Nat. Rev. Cardiol. 2020, 17, 259–260.
  18. Thygesen, K.; Alpert, J.S.; Jaffe, A.S.; Chaitman, B.R.; Bax, J.J.; Morrow, D.A.; White, H.D.; Executive Group on behalf of the Joint European Society of Cardiology /American College of Cardiology /American Heart Association /World Heart Federation Task Force for the Universal Definition of Myocardial, I. Fourth Universal Definition of Myocardial Infarction (2018). J. Am. Coll. Cardiol. 2018, 72, 2231–2264.
  19. Januzzi, J.L.; Sandoval, Y. The Many Faces of Type 2 Myocardial Infarction. J. Am. Coll. Cardiol. 2017, 70, 1569–1572.
  20. Smilowitz, N.R.; Weiss, M.C.; Mauricio, R.; Mahajan, A.M.; Dugan, K.E.; Devanabanda, A.; Pulgarin, C.; Gianos, E.; Shah, B.; Sedlis, S.P.; et al. Provoking conditions, management and outcomes of type 2 myocardial infarction and myocardial necrosis. Int. J. Cardiol. 2016, 218, 196–201.
  21. Wang, D.; Hu, B.; Hu, C.; Zhu, F.; Liu, X.; Zhang, J.; Wang, B.; Xiang, H.; Cheng, Z.; Xiong, Y.; et al. Clinical Characteristics of 138 Hospitalized Patients with 2019 Novel Coronavirus-Infected Pneumonia in Wuhan, China. JAMA 2020, 323, 1061–1069.
  22. Lippi, G.; Sanchis-Gomar, F.; Cervellin, G. Chest pain, dyspnea and other symptoms in patients with type 1 and 2 myocardial infarction. A literature review. Int. J. Cardiol. 2016, 215, 20–22.
  23. Sandoval, Y.; Smith, S.W.; Sexter, A.; Schulz, K.; Apple, F.S. Use of objective evidence of myocardial ischemia to facilitate the diagnostic and prognostic distinction between type 2 myocardial infarction and myocardial injury. Eur. Heart J. Acute Cardiovasc. Care 2020, 9, 62–69.
  24. Arlati, S.; Brenna, S.; Prencipe, L.; Marocchi, A.; Casella, G.P.; Lanzani, M.; Gandini, C. Myocardial necrosis in ICU patients with acute non-cardiac disease: A prospective study. Intensive Care Med. 2000, 26, 31–37.
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Subjects: Cardiac & Cardiovascular Systems
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Muntasir Billah
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Adiba Naz
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Entry Collection: COVID-19
Online Date: 07 Apr 2021
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