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Table of Contents
Year : 2020  |  Volume : 10  |  Issue : 3  |  Page : 101-104

COVID-19 targeting heart: The perspective of injuring the vulnerable

Department of Cardiology, Division of Cardiac Imaging, Kiran Multisuperspecialty Hospital and Research Center, Surat, Gujarat, India

Date of Submission28-Mar-2020
Date of Decision07-Jun-2020
Date of Acceptance10-Jun-2020
Date of Web Publication23-Dec-2020

Correspondence Address:
Keyur P Vora
Department of Cardiology, Division of Cardiac Imaging, Kiran Multisuperspecialty Hospital and Research Center, Surat, Gujarat
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/JICC.JICC_16_20

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In a clinical bulletin published by American College of Cardiology in February 2020, it was revealed that the case fatality rate of coronavirus disease 2019 (COVID-19) pandemic for patients with cardiovascular disease is 10.5%. Heart failure (HF) is a global pandemic affecting at least 26 million people worldwide and is increasing in prevalence. Looking at the historical prospectus of practice of clinical cardiology in most countries, patients with left ventricular ejection fraction (LVEF) < 40% presented periodically to exhibit worsening signs and symptoms. The superimposition of novel respiratory tract pathogens like COVID-19 can have accelerated inflammatory injury. Immunosenescense, overactive immune response or direct viral toxicity are hypothetical mechanisms of cardiac injury. Undoubtedly, all countries have to proactively approach their cardiovascular disease (CVD) patient population due to high vulnerability from individual and epidemiological risk factors.

Keywords: COVID-19, Immunology, Myocarditis, ACS, Heart Failure

How to cite this article:
Vora KP. COVID-19 targeting heart: The perspective of injuring the vulnerable. J Indian coll cardiol 2020;10:101-4

How to cite this URL:
Vora KP. COVID-19 targeting heart: The perspective of injuring the vulnerable. J Indian coll cardiol [serial online] 2020 [cited 2022 Dec 7];10:101-4. Available from: https://www.joicc.org/text.asp?2020/10/3/101/304372

  Introduction Top

The coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS CoV2), which first started in Wuhan, China.[1] As a result of expeditious escalation of this virus with consequences on an international scale, COVID-19 was declared a pandemic by the World Health Organization on March 11, 2020.[2] The current situation is so intensive that clinicians and researchers of all disciplines should now become aware about the potential impact of this disease on our respective practice guidelines. In a clinical bulletin published by the American College of Cardiology (ACC), it was revealed that the case fatality rate of COVID-19 for patients with cardiovascular disease was 10.5%. Data also point to a greater likelihood that individuals over the age of 65 with ischemic heart disease or hypertension can contract the illness, as well as experience more severe symptoms that will require critical care management. Every country has to proactively approach its cardiovascular patient population due to the high vulnerability from individual and epidemiological risk factors.

  Coronavirus Disease 2019 and Decompensated Heart Failure Top

In many countries, heart failure (HF) was considered to be an episodic disorder that was present only when patients sought medical consultation. Due to availability of better diagnostic modalities, pharmacological interventions and lifestyle modifications, the life expectancy is increasing among these patient populations. Many of these patients are of elderly age and present at the emergency room with acute decompensation of chronic heart failure. High percentage of these patients have acute elevation of pulmonary hypertension where intensive care management is mandatory. The high risk triggers include moderate to severe physical exertion, chronic and acute psychological stress, uncontrolled diabetes, exposure to respiratory tract infections, deterioration of renal function and drug non-compliance. All these factors can induce tachycardia, increased oxygen demand, tachypnea, acute pulmonary edema and decreased oxygen saturation, setting a vicious cycle for air hunger. Especially the respiratory tract infections can rapidly deteriorate the delicate balance of reflex mechanisms and pharmacological support systems. Among all such patients, acute aggravation of pulmonary artery pressure and pulmonary edema is unequivocally present.

The current event of COVID-19 pandemic exposes HF population to a unique life-threatening clinical deterioration. Chronic pulmonary hypertension by reduced LVEF (Group II: Updated PAH Classification 2012) can enhance the vulnerability to respiratory tract infections due to chronically elevated pulmonary arteriolar hydrostatic pressure, interstitial edema and impairment of alveolar fluid clearance. Reduction in the pulmonary diffuse capacity of lung for carbon monoxide (DLCO) is well documented in heart failure.[3] Under such primed conditions, direct viral toxicity and recruitment of inflammatory cells by overactive immune response can be intensified. Further experiments and basic science research are crucial for this potential hypothesis. These patients may develop either natural active acquired immunity or artificially acquired active immunity by the commercially available vaccines. However, in the current COVID-19 pandemic, there is neither herd immunity or acquired immunity in the absence of vaccines.

Current observations indicate that coronaviruses are particularly adapted to evade immune detection and dampen human immune responses. This could be a part of explanation why they tend to have a longer incubation period, 2-11 days on average compared to influenza, 1-4 days.[4] At present, the survival after COVID-19 exposure depends upon the individual immune response to develop natural active immunity. This very needed immune response is very low in HF patients by two factors: 1) immunosenescence and altered cytokine profile in elderly age;[5] 2) Chronic pulmonary hypertension induced suboptimal alveolar fluid clearance.[6] The viral load and immunological cascade with cytokine storm leads to disruption of alveolar-capillary barrier and promotes microalveolar pulmonary edema leading to respiratory failure. All these are hallmark signs of acute lung injury and acute respiratory distress syndrome (ARDS). At any point of time in the evolution of respiratory pathology, compensated HF can become decompensated, leading to elevate pulmonary artery pressure, elevated right atrial pressure, central venous pressure and thus increased preload status. In addition to ionotropic support, the reflex mechanisms of circulatory failure leads to increased afterload status. The vicious cycle of overload of preload and afterload of cardiopulmonary circulation combined with poor peripheral circulation predisposes to acute renal injury and decreased urine output. The renal involvement leads to metabolic acidosis which again leads to myocardial suppression and further decline of LVEF. The prolonged acidosis can also involve right ventricular suppression and decline of RVEF as well. Positive pressure ventilation with elevated positive end-expiratory pressure (PEEP) becomes less effective at this point. Sustained myocardial suppression also causes poor inotropic response, arrhythmogenicity and sudden cardiac death. In the current era of novel respiratory tract infections like H5N1, SARS, MERS and COVID-19, the HF population is not only vulnerable but also the carrier for such infectious agents.

  Coronavirus Disease 2019 and Myocarditis Injury Top

Both ischemic and nonischemic myocardial damage leads to cardiomyocyte injury and elevated serum troponin levels.[7],[8] In a meta-analysis of four studies including a total of 341 patients, the standardized mean difference of cardiac troponin I levels were significantly higher in those with severe COVID-19-related illness compared to those with nonsevere disease (25.6, 95% confidence interval [CI] 6.8–44.5).[9] Significant higher troponin levels were reported among patients who died as compared to patients who survived.[10],[11] Furthermore, this patient population had significant electrocardiographic and echocardiography abnormalities with low ejection fraction (EF). Especially, EF was an important prognostic parameter during advanced stages of myocarditis.

The research focus in COVID-19 myocarditis is to determine the potential direct viral toxicity and cardiac injury, especially by endomyocardial biopsy. Moreover, the advanced stage of systemic viral infection leads to septicemic shock, acute renal injury, metabolic acidosis, and myocardial suppression. This vicious cycle sets resistant myocardial suppression and eventual mortality. This vicious cycle is highly likely among elderly patients especially with diabetes and preexisting left ventricular dysfunction due to low contractile reserve. However, troponin levels can be exacerbated in patients with renal insufficiency due to delayed excretion, which is common in patients with advanced stages of the viral pneumonitis. It would be an important research question to answer whether the myocarditis is the consequence of viral immunological cascade or direct viral toxicity to cardiomyocytes. The study of 41 hospitalized patients with high-levels of proinflammatory cytokines including IL-2, IL-7, IL-10, G-CSF, IP-10, MCP-1, MIP-1A, and TNFα were observed in the COVID-19 severe cases.[12] These findings are identical with SARS and MERS in that the presence of lymphopenia and “cytokine storm” may have a major role in the pathogenesis of COVID-19.[13]

The deterioration of preexisting left ventricular dysfunction, new right ventricular dysfunction, myocarditis induced cardiomyopathy or stress induced cardiomyopathy remains to be studied as we collect more data from hospitalised COVID-19 patients. The diagnosis, prognosis and understanding of pathophysiological mechanisms of novel viral infections have been improved by molecular genetics essays of endomyocardial biopsy samples and advances in cardiac MRI study methods during last decade. Prior studies in other coronavirus species (MERS-CoV) have demonstrated evidence of acute myocarditis using cardiac MRI.[14] Therefore, the COVID-19 infection is expected to induce significant myocardial inflammation and injury for eventual life-threatening cardiopulmonary circulatory failure.

  Coronavirus Disease 2019 and Vulnerable Plaques Top

It is interesting to study the impact of profound inflammatory response of COVID-19 on underlying vulnerable plaques of coronary arteries. There are no data published yet on the pathophysiology of COVID-19 on acute coronary syndrome (ACS). However, the higher risk of acute myocardial infarction (MI) has been reported after the acute respiratory viral infections such as influenza (incidence ratio [IR]: 6.1; 95% CI: 3.9–9.5) and noninfluenza viral illnesses including other coronavirus species (IR: 2.8; 95% CI: 1.2–6.2).[15] Interestingly, there are multiple reports of acute electrocardiographic and echocardiographic changes identical to MI with acute chest pain where coronary angiography reveals absence of any obstructive coronary artery lesions and patients are eventually found COVID-19 positive. It is an important clinically relevant information to identify the prevalence of ACS among COVID-19-positive patients. As it is an evolving pandemic, if the patients with significant CV risk factors or preexisting CAD with multivessel disease get exposure to COVID-19, the probability of ACS is anticipated to be high.

Recent autopsy reports of COVID-19 patients reveals presence of thrombi in major pulmonary arteries especially in patients with pre-existing conditions like hypertension, type 2 diabetes mellitus, obesity, chronic obstructive pulmonary disease, coronary heart disease, cancer, history of cerebrovascular ischemic stroke and pulmonary embolism.[16] It is an important research question to determine whether these findings result from acute thrombus formation or thrombus migration as embolism and whether it is the consequence of different stages of COVID-19 specific immunological response.

  Plea for Proactive Approach During Pandemic Top

Heart failure (HF) is a global pandemic affecting at least 26 million people worldwide and is increasing in prevalence.[17] The widespread availability of echocardiography based cardiac evaluation over the last decade has promoted identification of HF cardiomyopathies in both adult and elderly populations. In a clinical bulletin published by American College of Cardiology on February 13th 2020, it was revealed that the case fatality rate of COVID-19 pandemic for patients with cardiovascular disease is 10.5%. Among chronic HF patients, high prevalence of elderly age, drug non-compliance, smoking and unregulated dietary practices can pose additional burden on the index HF issue. Due to these additional risk factors, the COVID-19 exposure can create accelerated inflammatory response as well as increase the risk for high viral load, profound tissue injury and need for ICU treatment including ventilatory support systems. Considering the economic issues, current ICU beds availability and resources for invasive ventilation, the hypothetical calculation of even one million of ICU beds just for the HF population is not a pragmatic solution. The clinical care of cardiac patients with COVID-19 will require the expertise of many specialty services including pulmonology/critical care, infectious diseases, cardiology, surgery, pharmacy, and hospital administration.

As per centers for disease control & prevention (CDC) precautionary guidelines, co-morbid conditions like systemic hypertension, diabetes, obesity or immunocompromised status as in HIV or immunosuppressive medications are considered vulnerable for severe forms of disease. Under the ongoing lockdown opportunity to break the chain of community spread of COVID-19 in many countries around globe, mandate for self-quarantine measures for the HF population are more intensive as compared to the general public. Even the developed nations are facing a grave escalation of morbidity and mortality rates. The burden of COVID-19 on the world has now been projected to a common clinical decision system to admit only those patients who have a better chance to survive and this is the great ethical dilemma for every hospital with limited resources. Targeted quarantine measures for the vulnerable population is not only needed in current time but also for emergency preparedness during future endemic and pandemic infection waves in order to reduce the healthcare burden and reserve the medical resources for new patients. Our healthcare system as a whole is vulnerable for acute decompensation if we do not prevent our clinically vulnerable populations from community acquired infections. Under such grave situations, it would not be an overstatement to mandate that 'Prevention is the Best Treatment' for the CV patient population all over the world.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

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.  Back to cited text no. 1
World Health Organization. WHO Director-General's opening remarks at the media briefing on COVID-19 - 11 March 2020.  Back to cited text no. 2
Guazzi M. Alveolar gas diffusion abnormalities in heart failure. Journal of Cardiac Failure 2008;14:695-702.  Back to cited text no. 3
Lessler J, Reich NG, Brookmeyer R, Perl TM, Nelson KE, Cummings DA. Incubation periods of acute respiratory viral infections: a systematic review. Lancet Infect Dis. 2009;9:291-300.  Back to cited text no. 4
Busse PJ, Mathur SK. Age-related changes in immune function: effect on airway inflammation. The Journal of allergy and clinical immunology. 2010;126:690-701.  Back to cited text no. 5
Brauer R, Chen P. Influenza leaves a TRAIL to pulmonary edema. J Clin Invest 2016;126: 1245–7.  Back to cited text no. 6
Sarkisian L, Saaby L, Poulsen TS, Gerke O, Jangaard N, Hosbond S, et al. Clinical Characteristics and Outcomes of Patients with Myocardial Infarction, Myocardial Injury, and Non-elevated Troponins. Am J Med 2016;129:446 e5-446 e21.  Back to cited text no. 7
Thygesen K, Alpert JS, Jaffe AS, Chaitman BR, Bax JJ, Morrow DA, et al. Fourth Universal Definition of Myocardial Infarction. J Am Coll Cardiol 2018;72:2231-64.  Back to cited text no. 8
Lippi G, Lavie CJ, Sanchis-Gomar F. Cardiac troponin I in patients with coronavirus disease 2019 (COVID-19): Evidence from a meta-analysis. Prog Cardiovasc Dis 2020; S0033-0620(20)30055-4.  Back to cited text no. 9
Ruan Q, Yang K, Wang W, Jiang L, Song J. Clinical predictors of mortality due to COVID-19 based on an analysis of data of 150 patients from Wuhan, China. Intensive Care Med 2020.  Back to cited text no. 10
Yang X, Yu Y, Xu J, Shu H, Xia J, Liu H, et al. Clinical course and outcomes of critically ill patients with SARS-CoV- 2 pneumonia in Wuhan, China: a single-centered, retrospective, observational study. Lancet Respir Med 2020.  Back to cited text no. 11
Tufan A, Avanoğlu Güler A, Matucci-Cerinic M. COVID-19, immune system response, hyperinflammation and repurposing antirheumatic drugs. Turk J Med Sci. 2020;50(SI-1):620-632. Published 2020 Apr 21. doi:10.3906/sag-2004-168  Back to cited text no. 12
Felsenstein S, Herbert JA, McNamara PS, Hedrich CM. COVID-19: Immunology and treatment options [published online ahead of print, 2020 Apr 27]. Clin Immunol. 2020;215:108448. doi:10.1016/j.clim.2020.108448  Back to cited text no. 13
Alhogbani T. Acute myocarditis associated with novel Middle east respiratory syndrome coronavirus. Ann Saudi Med 2016;36:78-80.  Back to cited text no. 14
Kwong JC, Schwartz KL, Campitelli MA, Chung H, Crowcroft NS, Karnauchow T, et al. Acute Myocardial Infarction after Laboratory- Confirmed Influenza Infection. N Engl J Med 2018;378:345-53.  Back to cited text no. 15
Deshpande C. Thromboembolic Findings in COVID-19 Autopsies: Pulmonary Thrombosis or Embolism? Ann Intern Med. doi:10.7326/M20-3255.  Back to cited text no. 16
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