Seven types of coronaviruses are known to cause human infection, four of which cause mainly mild symptoms, while the remaining three can cause fatal diseases (SARS, MERS and the ongoing COVID-19).
COVID-19. ; It is a fatal disease that spreads very quickly and mostly progresses with acute respiratory distress syndrome or fulminant pneumonia in symptomatic cases.
The disease is transmitted from infected people due to the spread of droplets through the air during coughing, sneezing or speaking. It can also be transmitted after touching infected surfaces and contacting mucosa. Fever, cough, fatigue, muscle pain, headache, abdominal pain, diarrhea and respiratory distress occur 3-7 days after the virus enters the body. In patients with infection, extensive filtration areas are revealed on tomography.
However, the presence of other pre-existing respiratory diseases or infections and cardiovascular diseases in the patient constitute important risk factors for contracting the disease and the development of vital complications.
COVID-19 and The underlying cardiovascular diseases mutually increase each other's severity. Complications related to both diseases may flare up.
This infection enters cells by binding to angiotensin-converting enzyme 2 (ACE2), a membrane-bound aminopeptidase that is highly expressed in the heart and lungs.
Primarily lung type 2 alveolar cells. It has been shown that ACE2 is present in myocardium, kidney proximal tubule, esophagus, ileum epithelial cells, and bladder urethelial cells. This situation explains the mechanism by which disorders occur in other organs other than the lungs.
ACE2 plays an important role in the neuro-humoral regulation of the cardiovascular system in normal health and in various disease states. Binding of SARS-CoV-2 to ACE2 can lead to alteration of ACE2 signaling pathways and acute heart and lung injury. ACE inhibitors and ACE receptor blockers used in the treatment of high blood pressure increase ACE levels. In this case, it theoretically suggests that the COVID infection may cling more to the lungs and increase lung damage.
It has been observed that COVID-19 increases arrhythmia. It is thought that this develops as a result of hypokalemia (low potassium) that develops as a result of the interaction of this virus with the renin-angiotensin-aldosterone system. Hypokalemia increases susceptibility to various tachyarrhythmias. They also increase the severity in patients with pre-existing arrhythmias. Current studies have shown that 16% of these patients develop arrhythmia. In patients followed in intensive care, this rate can reach up to 40%.
Various cardiovascular risk factors also negatively affect the prognosis of these patients. A meta-analysis of six studies including 1527 patients with COVID-19 published from China reported that diabetes, cardio-cerebrovascular disease and hypertension were observed in 9.7%, 16.4% and 17.1%, respectively. Here, cardiovascular risk factors may have an impact on the severity of the disease in patients rather than on the disease itself. More importantly, the presence of diabetes, cardio-cerebrovascular disease and hypertension increases the development of serious disease or the need for intensive care by 2-3 times. Hypertension was found in 27% of patients who developed acute respiratory distress syndrome due to severe lung involvement, diabetes was found in 19%, and cardiovascular disease was found in 6%. The reason for the high hypertension in these patients is explained by the fact that hypertension is common in the elderly patient population and these people are more vulnerable to infection.
While the mortality rate in COVID-19 cases is 2.3% in general, it is significant in hypertension, diabetes and CVD patients. are higher and are 6%, 7.3% and 10.5%, respectively.
The incidence of cardiovascular diseases and their effects on clinical outcomes vary significantly in different geographical regions.
It has been shown that COVID-19 infection causes damage to the heart as well as the lungs. Studies have shown that severe/critical COVID-19 patients have high levels of pro-inflammatory cytokines in circulation. As a result, severe systemic inflammation and multiple organ failure may develop. It is thought that the risk of plaque rupture and thrombosis in the coronary arteries due to this inflammatory process, that is, the risk of heart attack, may increase. More It can affect the respiratory system and cause damage to the heart muscle due to serious decreases in blood oxygen levels.
Due to these mechanisms, it has been shown that there are significant increases in troponin levels, which indicate myocardial damage in patients. It is known that roughly 8-12% of positive cases develop significant troponin I elevation. This rate increases to 17% in patients admitted to intensive care. In the group with mild disease, this rate is observed as 1-2%. Despite the increase in these enzyme levels, no ECG changes were detected in the patients. Studies have shown that 52% of patients who died and 12% of those who were discharged developed heart failure.
There is a concern about the safety of ACE inhibitors (ACEi) and angiotensin receptor blockers (ARB) with COVID-19 infection. . These agents regulate ACE2 expression in various tissues, including cardiomyocytes. Because SARS-CoV-2 binds to ACE2 to enter human cells, it is thought that the development of COVID-19 or the severity of the disease may be increased in patients already treated for hypertension with ACEi/ARB. However, to date, no experimental or clinical data has emerged to support these concerns.
The potential side effects of agents used to treat COVID-19 also need to be fully known. Chloroquine / hydroxychloroquine and azathioprine have been recommended for treatment. Both of these drugs are known to prolong the QT interval, and caution should be exercised when prescribing these agents. The combination of these is best avoided, and even when chloroquine/hydroxychloroquine is used alone, a daily electrocardiogram is required to monitor the QT interval, esp. in patients with liver or kidney dysfunction and in patients taking another drug that has the potential to prolong the QT interval.
As a result, ACE inhibitor or receptor blocker agents used in the treatment of high blood pressure and the covid-19 infectious agent interact using the same receptors. is passing. Theoretically, it is predicted that Covid-19 may progress more seriously with the use of these blood pressure medications. However, clinical findings supporting this have not been fully demonstrated. Under these conditions, it is not yet necessary to convert these blood pressure drugs into another group of drugs. It has not been clarified yet. However, for people in the high-risk group and using ACE inhibitors or receptor blockers, it would be appropriate to replace the drugs with another group.
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