Muhammad Torequl Islam :
Troponin I (TnI), the member of the troponin protein complex, binds to actin in thin myofilaments to hold the actin-tropomyosin complex in its right place. It prevents myosin from binding to actin in relaxed cardiac muscle. Calcium causes dislocation of TnI after binding to the troponin C, thus the tropomyosin leaves the binding site for myosin on actin and results contraction of cardiac muscle. TnI is an established biomarker of cardiac complications; leaks of it may be due to a demand ischemia or acute inflammation of the pateint’s myocardium. There is a well-established association between acute infections, especially those are frequently observed in Influenza patients and cardiac injury, including myocarditis and acute myocardial infarction.
Viral replication results an elevation of the TnI level in myocardium, leading to a cascade of inflammatory processes, results fibrosis and ultimately cardiac necrosis. Influenza infections during the 2017-2018 season resulted an increase in cardiac complications compared to previous years, where a frequency of TnI elevation was seen in the victims. However, an upregulation of it has been seen in chronic kidney failure, heart failure, inflammatory arthritis, subarachnoid hemorrhage, rheumatoid arthritis, and pulmonary embolus. The COVID-19 also found to link with an adverse prognosis and increased mortality in patients with myocardial injury. Two retrospective studies involving cohorts of patients from New York, USA, and Sichuan, China suggest that 36% of patients had a TnI level greater than the normal level. Only a minor elevation (30-90?pg/mL) of TnI level was associated with an increased risk of death by 95%, which was further increased by 95% in novel coronavirus disease 2019 (COVID-19) patients with a marked elevation in TnI levels (>90?pg/mL). Thus, arising the burning issue either a higher serum TnI level is associated with the high mortality rate among the cardiac patients with the COVID-19 or not!
First study also indicates a higher level of C-reactive protein (CRP), while the second predicts higher levels of lactate dehydrogenase (LDH) and interleukin 6 (IL-6) along with the serum TnI levels. These all are also well-known inflammatory biomarkers.
Generally, the reduced or lack of coronary artery blood flow leads to an accumulation of low molecular weight substances, such as lactate and phosphate that can pass through the interstitial space directly into the vascular space. LDH nearly presents in all living cells catalyzes the conversion of pyruvate to lactate (a waste product of glycolysis) and vice versa. An inhibition of LDH activity reduces lactate production, which can modulate the Warburg effect, immune response, acidification of the microenvironment, motility of cancer cells, and regeneration of nicotinamide adenine dinucleotide (NAD+). On the other hand, myocardial IL-6 mediates cardiac inflammation.
ACE2 is also evident for its lung protective capacity. Vitamin D has strong immunomodulatory effects and can be used in alveolar damage caused by acute respiratory distress syndrome (ARDS). It has been also evident that angiotensin II stimulates the melanogenesisprocess, therefore, a downregulation of ACE2 may stimulate melanin synthesis, which will negatively affect vitamin D synthesis in our body. Thus, the peoples having low levels of ACE2 will not get much defensive power over the high ACE2 content peoples. Taken together, high mortality rate of cardiac patients with COVID-19 may depend on various factors, not be associated only with higher serum levels of cardiac TnI.
Troponin I (TnI), the member of the troponin protein complex, binds to actin in thin myofilaments to hold the actin-tropomyosin complex in its right place. It prevents myosin from binding to actin in relaxed cardiac muscle. Calcium causes dislocation of TnI after binding to the troponin C, thus the tropomyosin leaves the binding site for myosin on actin and results contraction of cardiac muscle. TnI is an established biomarker of cardiac complications; leaks of it may be due to a demand ischemia or acute inflammation of the pateint’s myocardium. There is a well-established association between acute infections, especially those are frequently observed in Influenza patients and cardiac injury, including myocarditis and acute myocardial infarction.
Viral replication results an elevation of the TnI level in myocardium, leading to a cascade of inflammatory processes, results fibrosis and ultimately cardiac necrosis. Influenza infections during the 2017-2018 season resulted an increase in cardiac complications compared to previous years, where a frequency of TnI elevation was seen in the victims. However, an upregulation of it has been seen in chronic kidney failure, heart failure, inflammatory arthritis, subarachnoid hemorrhage, rheumatoid arthritis, and pulmonary embolus. The COVID-19 also found to link with an adverse prognosis and increased mortality in patients with myocardial injury. Two retrospective studies involving cohorts of patients from New York, USA, and Sichuan, China suggest that 36% of patients had a TnI level greater than the normal level. Only a minor elevation (30-90?pg/mL) of TnI level was associated with an increased risk of death by 95%, which was further increased by 95% in novel coronavirus disease 2019 (COVID-19) patients with a marked elevation in TnI levels (>90?pg/mL). Thus, arising the burning issue either a higher serum TnI level is associated with the high mortality rate among the cardiac patients with the COVID-19 or not!
First study also indicates a higher level of C-reactive protein (CRP), while the second predicts higher levels of lactate dehydrogenase (LDH) and interleukin 6 (IL-6) along with the serum TnI levels. These all are also well-known inflammatory biomarkers.
Generally, the reduced or lack of coronary artery blood flow leads to an accumulation of low molecular weight substances, such as lactate and phosphate that can pass through the interstitial space directly into the vascular space. LDH nearly presents in all living cells catalyzes the conversion of pyruvate to lactate (a waste product of glycolysis) and vice versa. An inhibition of LDH activity reduces lactate production, which can modulate the Warburg effect, immune response, acidification of the microenvironment, motility of cancer cells, and regeneration of nicotinamide adenine dinucleotide (NAD+). On the other hand, myocardial IL-6 mediates cardiac inflammation.
ACE2 is also evident for its lung protective capacity. Vitamin D has strong immunomodulatory effects and can be used in alveolar damage caused by acute respiratory distress syndrome (ARDS). It has been also evident that angiotensin II stimulates the melanogenesisprocess, therefore, a downregulation of ACE2 may stimulate melanin synthesis, which will negatively affect vitamin D synthesis in our body. Thus, the peoples having low levels of ACE2 will not get much defensive power over the high ACE2 content peoples. Taken together, high mortality rate of cardiac patients with COVID-19 may depend on various factors, not be associated only with higher serum levels of cardiac TnI.
(Muhammad Torequl Islam is Assistant Professor, Department of Pharmacy, Life Science Faculty, Bangabandhu Sheikh MujiburRahman Science and Technology University. E-mail: [email protected])
