EDITORIAL
Year : 2020 | Volume
: 2 | Issue : 1 | Page : 1--2
COVID-19 and Cardiovascular diseases
Govindan Vijayaraghavan
Sr Consultant, Department of Cardiology, Dean, Post Graduate Medical Education, Thiruvananthapuram, Kerala, India
Correspondence Address:
Prof. Govindan Vijayaraghavan
Kerala Institute of Medical Sciences, Thiruvananthapuram - 695 029, Kerala
India
How to cite this article:
Vijayaraghavan G. COVID-19 and Cardiovascular diseases.Ann Clin Cardiol 2020;2:1-2
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How to cite this URL:
Vijayaraghavan G. COVID-19 and Cardiovascular diseases. Ann Clin Cardiol [serial online] 2020 [cited 2023 Jun 4 ];2:1-2
Available from: http://www.onlineacc.org/text.asp?2020/2/1/1/284927 |
Full Text
In December 2019, the city of Wuhan in Mainland China reported a cluster of cases with pneumonia who had consumed food from a seafood market. By the month's end, several more cases from neighboring parts of this city were reported. These cases were subsequently found to be caused by a previously unknown betacoronavirus. At the time of writing, this infection now has spread to 250 countries worldwide resulting in global case count (April 15, 2,018,351 infections; 128,062 deaths (6.3%). About 492,176 patients have recovered (24.4%) from this illness. While data on this illness have accumulated rapidly, they were apparent early on that persons with cardiovascular disease who had substantially higher mortality than persons without.[1]
We have to examine the evidence one by one. In one of the largest reported series of 1099 patients from China, 15% of the patients had preexisting systemic hypertension. About 40% of the patients admitted with pneumonia had preexisting cardiovascular disease. Another report states that 26% of the patients required intensive cardiac care. Acute coronary syndrome, with dynamic electrocardiographic changes and elevated troponins and cardiac arrhythmias, were the most common cause of admission to intensive cardiac care. In many others, palpitations and chest pain were the presenting symptoms. Other published and anecdotal reports indicate the presence of myocarditis, cardiac arrest, and acute heart failure.[2],[3]
Angiotensin Converting Enzymes 2 and COVID-19
It is well established that higher levels of angiotensin-converting enzymes 2 (ACE 2) are present in patients receiving ACE inhibitors (ACEIs) or angiotensin II receptor blockers (ARBs) which is known to facilitate entry of the COVID-19 virus into the human body, especially through the lungs. We do not have adequate proof that ACEIs, ARBs, and other renin–angiotensin–aldosterone system (RAAS) inhibitors affect lung-specific expression of ACE2 in animal models or humans and whether higher ACE 2 activity facilitates greater engagement and entry of severe acute respiratory syndrome-CoV-2 spike protein. Future studies may probe into the mechanisms of RAAS inhibition and similar viral infections. Given these uncertainties, the recommendation would be to continue ACEIs and ARBs in patients with heart failure, ischemic heart disease, and systemic hypertension and rather than face the additional burden of these comorbidities during the COVID-19 pandemic. Until further data are available, we recommend that RAAS inhibitors be continued in patients in otherwise stable condition who are at risk for, being evaluated for, or with COVID-19.[4]
COVID-19 and Myocarditis
Acute myocardial involvement in COVID-19 infection is currently described as "acute cardiac injury" characterized by sudden elevation of cardiac biomarkers, namely high sensitivity troponin T or I above the 99th percentile upper reference limit, and is described in more than 20% of patients and associated with an increased mortality. The exact pathophysiology behind acute myocardial injury in COVID-19 is not known. The identification of the etiology, either myocardial inflammation (myocarditis or myopericarditis) or necrosis, is clinically relevant for the correct diagnostic and therapeutic management of these patients, especially those with concomitant infections. Since COVID-19 virus can localize in organs/tissues other than the lung anon-ischemic acute myocardial injury may be due to viremia or migration of macrophages from the lung. Hence, the treatment strategy should be planned according to the type of myocardial injury.[5]
Electrocardiogram and COVID-19
The electrocardiogram (ECG) is an integral part of any clinical work up including COVID-19 infection and can be helpful in diagnosing myocarditis, arrhythmias, and conduction abnormalities. The ECG is also an important tool in health workers who are on prophylactic hydroxychloroquine (HCQ) and in patients with COVID-19 who are treated with this drug since HCQ is known to increase the QT interval. This and other drugs that prolong the QT interval should be avoided in subjects with a baseline QTc of >500 ms (assuming the QRS duration is<120 ms). Although rapidly changing, chloroquine and azithromycin are currently given in combination to combat COVID-19 infection. Both these drugs can prolong the QT interval, and hence, monitoring with an ECG is important in these patients. We have to remember that a controlled trial done in China, use of HCQ, failed to relieve symptoms of COVID-19 patients more than the standard care alone and patients who received HCQ had more serious side effects compared to controls. However, the authors (Tang et al.) concluded that there was a significant reduction of symptoms and the inflammatory marker C-reactive protein, after adjusting for the confounding effects of the antiviral agents.
It is important to a good history from patient's systemic hypertension or ischemic heart disease regarding their drug treatment. We have to remember that the ACEIs, ARBs, and the diuretics can alter the QT interval and the results are to be interpreted accordingly.
Echocardiography
As soon as the COVID-19 infection became a pandemic, the American Society of Echocardiography issued guidelines for conducting echo Doppler in these patients. A dedicated echo machine and a technician should be posted for screening COVID cases. Point-of-care or bedside echo is the preferred mode of imaging. Off-axis echo imaging planes are suggested to avoid, if possible, transesophageal echocardiography with its attendant aerosol dispersion into the surroundings. All the personnel should conform to the WHO stipulations for wearing the personal protective equipment (PPE) as well as cleaning the equipment's before and after the procedure.
Cardiology during the COVID–19 Pandemic
We have to remember that ischemic heart disease with all its manifestations, systemic hypertension and its complications, heart failure, valvular heart disease and children with heart disease will have their share of outpatient and emergency attendance in every hospital, and we cannot slow down our approach to these diseases. COVID–19 has imposed a major burden on health-care workers and cardiologists cannot forget our commitment toward other cardiovascular illnesses at this time.
Cardiologists during the COVID–19 Epidemic
It is very important that all medical personnel safeguard against this infection by adopting guideline-directed prophylactic measures in dealing with patients during this epidemic. This is true in the outpatient settings, inpatient settings, as well as in various cardiology laboratories. Intensive cardiology rooms should to have institutional guidelines published in this regard. The use of PPE should be stressed at this moment. You have to prevail on your institution in providing adequate quantities of protection equipment in times of need. All the staff should rigorously follow the instructions which may be modified from time to time.
References
| 1 | Ferrari R, Di Pasquale G, Rapezz C. 2019 coronavirus: What are the implications for cardiology? Eur J Prev Cardiol 2020;2020:1-4. |
| 2 | Wang D, Hu B, Hu C, Zhu F, Liu X, Zhang J, et al. Clinical characteristics of 138 hospitalized patients with 2019 novel coronavirus infected pneumonia in Wuhan, China. JAMA 2020;323:1061-9. |
| 3 | Huang C, Wang Y, Li X, Ren L, Zhao J, Hu Y, et al. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet 2020;395:497-506. |
| 4 | Vaduganathan M, Vardeny O, Michel T, McMurray JJ, Pfeffer MA, Solomon SD. Renin-angiotensin-aldosterone system inhibitors in patients with COVID-19. N Engl J Med 2020;382:1653-9. |
| 5 | Tavazzi G, Pellegrini C, Maurelli M, Belliato M, Sciutti F, Bottazzi A et al. Myocardial localization of coronavirus in COVID 19 cardiogenic shock. Eur J Heart Fail. 2020 April 10 (Epub ahead of print). DOI: 10.1002/ejhf.1828. |
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