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 Table of Contents  
ORIGINAL ARTICLE
Year : 2022  |  Volume : 10  |  Issue : 1  |  Page : 38-44

Cardiovascular involvement in patients with COVID-19 pneumonia: Observation from a tertiary care infectious disease Hospital


1 Department of Cardiology, R G Kar Medical College & Hospital, Kolkata, West Bengal, India
2 Department of Community Medicine, ID & BG Hospital, Kolkata, West Bengal, India
3 Department of Infectious diseases, IPGMER & SSKM Hospital, Kolkata, West Bengal, India
4 Department of Medicine, NRS Medical College & Hospital, Kolkata, West Bengal, India

Date of Submission13-Dec-2021
Date of Decision01-Feb-2022
Date of Acceptance08-Feb-2022
Date of Web Publication13-Apr-2022

Correspondence Address:
Dr. Rammohan Roy
Department of Cardiology, R G Kar Medical College & Hospital, Kolkata, West Bengal
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/heartindia.heartindia_103_21

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  Abstract 


Background: Covid 19 pneumonia presents with various cardiovascular manifestations. The proposed mechanisms of cardiovascular involvement in COVID-19 are direct invasion of myocardial cell by the virus, hyper- inflammatory state secondary to cytokine storm, increased angiotensin II, low ACE2 levels, antiphospholipid antibodies and increased platelet reactivity which contribute significantly to thrombus formation in systemic and pulmonary vasculature.
Objectives: To find out various cardiovascular manifestation of patients admitted with covid 19 pneumonia.
Methodology: A retrospective observational study had been conducted in a tertiary care infectious disease hospital from July 2020 to December 2020 that included a total of 108 patients.
Results: Most common risk factor were combination of hypertension and diabetes( 40.7%) followed by hypertension alone (28.7% )and diabetes in 18.5% patients. Most common presentation was asymptomatic myocarditis found in 37 patients followed by sinus tachycardia in 34, sinus bradycardia in 18, Orthostatic hypotensionin in 16, Atrial fibrillation in 14, cerebrovascular accident in 9, Acute limb ischemia in 7 , and acute coronary syndrome in 4 patients. Asymptomatic diastolic dysfunction (Grade 2 or more ) found in 17 patients without any overt features of heart failure (all have raised NTproBNP and HSTrop I along with clinical features ). A positive correlation was found between D- dimer level and severity of pneumonia by CT severity score.
Conclusion: A high index of suspicion and necessary investigation may be needed for early detection of myocarditis and to prevent any complication particularly fatal arrhythmia and sudden cardiac death.

Keywords: COVID, heart, pnemonia


How to cite this article:
Roy R, Maji B, Ray Y, Sinha A. Cardiovascular involvement in patients with COVID-19 pneumonia: Observation from a tertiary care infectious disease Hospital. Heart India 2022;10:38-44

How to cite this URL:
Roy R, Maji B, Ray Y, Sinha A. Cardiovascular involvement in patients with COVID-19 pneumonia: Observation from a tertiary care infectious disease Hospital. Heart India [serial online] 2022 [cited 2022 Dec 2];10:38-44. Available from: https://www.heartindia.net/text.asp?2022/10/1/38/343066




  Introduction Top


The COVID-19 pandemic has undoubtedly been one of the most important events of this century considering its impact on morbidity and mortality, impact on the economy, as well as the pace at which the human civilization prepares itself to fight against this virus. Severe acute respiratory syndrome coronavirus 2 (SARS CoV2) can involve several organs of the body including the heart. The most common being COVID-induced myocarditis and subsequent complications such as heart failure and arrhythmia. Another important cardiovascular complication vascular thrombosis and thrombo-embolic event occurred due to abnormal platelet reactivity which creates a hypercoagulable state. High incidence of vascular thrombosis (both venous and arterial) in critically ill COVID-19 pneumonia patients were reported that carry a high mortality rate.[1],[2] Anticoagulation along with corticosteroid had been the cornerstone of treatment of severe COVID-19 pneumonia. Anticoagulation was found to be associated with decreased cardiovascular mortality and no increase in the rate of bleeding.[3] Myocarditis can present with various manifestations, from subclinical to overt heart failure and fatal arrhythmia, thus it is difficult to estimate the incidence of myocarditis among hospitalized COVID-19 patients. Several observational studies have suggested that possible mechanisms of myocarditis may be direct virus entry and successive myocardial injury or an immune-mediated myocardial injury. The diagnosis is based on features of chest pain and elevation in Troponin levels to 3 times higher than normal serum concentrations and above the 99th percentile of the upper limit of the reference range in absence of any coronary artery obstruction. Features of myocarditis have been reported in 20%–30% of patients hospitalized due to severe COVID-19.[4],[5] Electrocardiogram (ECG) abnormalities in SARS-CoV-2 myocarditis may include sinus tachycardia, ST-segment and T-wave changes (pseudo-infarct pattern), premature ventricular complexes, bradyarrhythmia, and rarely advanced atrioventricular (AV) nodal block, new-onset bundle branch block, QT prolongation can be observed in myocarditis. Patients may present with chest pain, palpitation, tachycardia, and symptoms of heart failure like fatigue and dyspnoea. The pathophysiology of various arrhythmias in COVID myocarditis includes[1] direct injury to cardiomyocytes membrane causing disturbance of electrical conduction;[2] infection of the pericytes and microvascular dysfunction leading to ischemia; (3) myocardial fibrosis or scars forming a reentrant circuit; and (4) proinflammatory cytokines may enhance automaticity and arrhythmogenicity.[6] Pericardial effusion can also occur in a few patients with COVID myocarditis. Among different cardiac arrhythmias in COVID-19 patients, atrial fibrillation (AF) was most common and detected in approximately 19%–21% of all covid cases.[7] The underlying causes of AF in COVID-19 patients are largely unknown though it is presumed that electrical inhomogeneity, calcium handling, and structural remodeling may playa key role in AF pathophysiology.[8],[9]

It is well documented that human platelets express angiotensin-converting enzyme type 2 (ACE2) receptor as well as transmembrane protease serine 2 through which virus can gain entry and activate the platelets.[10] These lead to increased platelet aggregation, activation of the coagulation cascade, and resulting thromboembolic complications with increased morbidity and mortality.[11] A study has shown that COVID-19 patients with Acute respiratory distress syndrome (ARDS) had significantly more thrombotic events versus non-COVID ARDS patients (11.7% vs. 4.8%), as well as pulmonary embolism (11.7% vs. 2.1%).[12] In COVID pneumonia with SARS, there is the development of microthrombi in multiple organs predominantly in the lungs formed by a fibrin network and red blood cells (red thrombi) compared to white thrombi, the main types of thrombi in non-COVID SARS patients.[13]

Increased risk of myocardial involvement was noted in patients with hypertension, coronary artery disease, heart failure, or diabetes as evidenced by several studies.[14] Multisystem inflammatory syndrome in childhood (MIS-C) is a rare disease with a hyperinflammatory state and involvement of multiple organs including the heart resulting in acute heart failure and COVID-19 has been reported to cause severe inflammatory syndrome-like MIS-C in a small proportion of pediatric patients.[15]


  Materials and Methods Top


The study had been conducted in a tertiary care infectious disease hospital from July 2020 to December 2020. A total of 108 patients who had some form of cardiovascular manifestation were included in this study. Inclusion criteria: patients of at least moderate and severe disease defined as oxygen saturation of 93% or less at room air, tachypnoea (respiratory rate >24/min), mild disease with high risk for developing severe disease (age >60 years, obesity, cardiovascular disease, hypertension, coronary artery disease, diabetes mellitus and other immunocompromised states/chronic lung/kidney/liver disease/cerebrovascular disease or patients who need hospitalization for having symptoms such as severe weakness, persistent fever, rash, loose motion, persistent cough, chest pain, and diarrhea. Ethical approval is taken from the institutional ethics committee. Data were collected from record section regarding the demographic profile, ECG, various clinical cardiovascular presentations, any documented coronary events, or other vascular events just before hospitalization or during the hospital stay. high-resolution computed tomography (HRCT) thorax was done in most of the cases before or during admission. Quantitative estimation of biomarkers including D–dimer (a type of fibrin degradation product), N terminal pro B type natriuretic peptide (NT pro BNP) and high sensitivity troponin I (HS troponin I) were done in all patients. For NT Pro BNP and HS Troponin I, Vitrios 5600 machine was used (cut off value for NT pro-BNP was 300–450, 300–900, and 300–1800 for age group <50, 50–75 and >75 years, respectively, whereas HS troponin I cut off value was estimated as <9 ng/L for male and <12 ng/l for male). Routine echocardiography was done in all patients to find out systolic or diastolic dysfunction, appearance of any regional wall motion abnormality, any pericardial effusion, etc.


  Results and Analysis Top


A total of 108 patients were included in this study. The mean age of the patients was 50 (±5.6 years). The most common risk factor was the combination of hypertension and diabetes, found in 44 patients (40.7%) followed by hypertension alone found in 31 patients (28.7%) and diabetes in 20 patients (18.5%) [Figure 1]. The most common presentation was asymptomatic myocarditis found in 37 patients with elevated NT pro-BNP and HS Troponin I without any clinical features of heart failure [Figure 2]. Sinus tachycardia was found in 34 patients. Among them, 10 patients had elevated biomarkers of myocarditis and 15 patients had ARDS. Persistent sinus bradycardia was found in 18 patients. Only one patient had symptomatic bradycardia which responded well to injection atropine. Bradycardia reverted to sinus rhythm in an average of 3.1 days. None of the patients have symptoms of heart failure and biochemical evidence of myocarditis. Asymptomatic diastolic dysfunction (Grade 2 or more) occurs in 17 patients without any overt features of heart failure (all have raised NT pro-BNP and HS Trop I). Six patients had features of congestive heart failure including orthopnoea, highly elevated NT pro-BNP and HS troponin I and had severe COVID pneumonia with Grade 3 left ventricular diastolic dysfunction (LVDD). Heart failure responded to conservative therapy including diuretic. A total of 14 patients had AF but all have severe COVID pneumonia with ARDS and all required Bilevel positive airway pressure and high flow nasal cannula device. Eight of them died and were on mechanical ventilation before death. Orthostatic hypotension occurred in 16 patients among them only 4 patients were on one or more antihypertensive drugs. Temporary discontinuation of antihypertensive or decrease in dose, increased fluid intake, and adaptive training was required. On the other hand, 18 previously hypertensive patients had uncontrolled hypertension during the hospital stay and required increment of antihypertensive doses [Figure 2]. The ischemic cerebrovascular accident occurred in 9 patients. Four of them were on hemodialysis and were on unfractionated heparin. Two patients developed massive pulmonary embolism. Both of them were not given heparin because of contraindications. Four patients had sudden cardiac arrest with ventricular tachycardia, fibrillation, asystole and died. A total of 19 patients died. Most of them had severe ARDS and persistent hypoxemia. Acute limb ischemia occurred in 7 patients out of which 2 had digital ischemia. All the patients were on anticoagulant. Five of them died due to severe sepsis and septic shock. A total of 4 patients had acute myocardial infarction and among them, two had segment elevation Multisystem inflammatory and thrombolyzed but one of them died due to cardiogenic shock. Dynamic changes in ECG or change from baseline ECG helped in diagnosing non-ST segment elevation myocardial infarction as chest pain was a common symptom in severe COVID pneumonia and usually elevated cardiac enzymes happened because of associated myocarditis. A total of six patients developed venous thrombotic events of which 2 patients had severe pulmonary embolism and died. One 9-year-old boy had been admitted with MIS-C and had biventricular systolic dysfunction along with fever, rash, neutrophilia, and lymphopenia. He had acute decompensated heart failure with cardiogenic shock. Echo showed severe Right ventricular systolic dysfunction and moderate Left ventricular systolic dysfunction. He improved with conservative therapy and at the time of discharge had significant improvement in both left and right ventricular systolic function and normal echocardiogram after 4 weeks from discharge. He had been treated with IVIG as the disease often presents with Kawasaki Disease like symptoms.[16]
Figure 1: Risk factors for cardiovascular involvement

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Figure 2: Cardiovascular involvement in COVID-19 patients

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Another important observation was the association of D dimer with the severity of COVID pneumonia (by computed tomography [CT] severity score). There was a strong positive correlation (Pearson correlation coefficient r = 0.8613) [Figure 3]. However, no correlation was found with markers of myocarditis, i.e., HS Troponin I (r = 0.3276) and NT Pro BNP (r = 0.4424) with CT severity score. Mean NT Pro BNP in this study was 1626.68 pg/ml and mean HS Troponin I was 58.81 ng/ml whereas the mean CT severity was 12.06.
Figure 3: Relationship between computed tomography severity and D dimer

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  Discussion Top


The mechanisms of cardiovascular involvement in COVID-19 are considered to be excess synthesis of inflammatory mediators (cytokine storm), and certain other vasoreactive agents like angiotensin II. A low serum ACE2 levels, presence of antiphospholipid antibodies and increased platelet reactivity are other important factors. All these factors play a crucial role in disease progression particularly in patients with advanced age, diabetes, hypertension, and are intimately associated with severe COVID disease requiring hospitalization. Multiple case series and retrospective studies from different countries have shown that complications and mortality of COVID-19 increased if associated with cardiovascular risk factors. The incidence of these risk factors are quite high and hypertension is the most common risk factor followed by obesity and diabetes as corroborated by one study in New York City (USA) which included 5700 patients and hypertension was detected in 56.6% of patients followed by obesity (41.7%) and diabetes (33.8%).[17] However, another study from India as well as china showed that hypertension and diabetes were present in much less number of cases.[18],[19] The mode of entry of the SARS CoV2 virus involves spike S protein on the virus surface. The S protein has two subunits namely S1 and S2. The S1 helps in attachment of the virus with ACE2 receptor (present on the lung epithelial cell, vascular endothelial cell as well as cardiomyocytes) and S2 helps in fusion of the virion with the cell membrane and internalization with the help of TMPRSS2, a protease that cleaves and activates S2 subunit.[20],[21] After entry inside the cell, the virus replicates and destroys ACE2. The ACE2 or ACE2 is responsible for Ang-(1–7) synthesis from Ang II [Figure 4]. This enzyme can also form angiotensin 1-9 from hydrolysis of angiotensin I. Ang-(1–9) again can convert to Ang-(1–7) by ACE. angiotensin 1–7 works through Angiotensin II receptor type 2. It has antiproliferative and vasodilatory functions. A G protein couples receptor known as mitochondrial assembly receptor (MasR) bind to Ang-(1–7) and have antiapoptotic and vasodilatory property. Thus, the ACE2/Ang-(1–7)/MasR axis appears to counteract the harmful effect of ACE, Ang II, and AT1 receptors within the renin-angiotensin system.[22]
Figure 4: Role of angiotensin converting enzyme 2 on cardiovascular system

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In our study, asymptomatic myocarditis was the most common presentation as 34% of our patients had evidence of raised biomarker (NT Pro BNP and HS Troponin I) of myocardial inflammation and injury. Two separate studies conducted in Germany (one autopsy series and another magnetic resonance imaging (MRI) based study showed a high incidence of myocardial involvement among hospitalized patients (61% and 78%, respectively).[23],[24] In the MRI-based study 60% of patients had persistent inflammation and even few patients had regional scar and pericardial enhancement. MRI also detected significant myocardial interstitial edema involving both the ventricles with late gadolinium enhancement. There was no significant correlation between the severity of COVID pneumonia (as determined by clinical presentation and HRCT of Thorax severity index) and myocardial involvement in our study. Isolated cardiac involvement may be present in patients without any respiratory symptoms.[25] In a study in the USA more than 1 in 3 previously healthy college students showed features of pericardial inflammation and some myocardial involvement, all were asymptomatic or mildly symptomatic and no one had features of ongoing myocardial inflammation.[26] COVID-19-associated fulminant myocarditis and pericardial involvement with massive pericardial effusion were not detected in our study though reported in different literatures. Fulminant myocarditis can present with low left ventricular ejection and refractory heart failure and require prompt therapy with human immunoglobulin, methylprednisolone, and heart failure management.[27] In a resource-limited country like India, cardiac MRI or endomyocardial biopsy is not possible to be done in every case, particularly in the current situation thus, the diagnosis depends on clinical findings, ECG, echocardiography in association with elevated NT-pro BNP and troponin. It is noteworthy that some COVID pneumonia patients develop Sinus bradycardia which may not be directly related to myocardial injury and rather caused by direct inhibition of the Sino-atrial node by the virus (mediated by serum ACE2 receptor).[28] On the other hand, the cause of sinus tachycardia may be hypoxia and anxiety which may lead to a hyperadrenergic state. Myocarditis with intrinsic sinus node hyperactivity or autonomic dysfunction may also be an important cause. Inflammatory cytokines also may alter the function of myocardial ion channels and cause sinus tachycardia. Inappropriate sinus tachycardia should be treated with beta-blockers and/or ivabradine particularly in patients with preexisting heart failure or ischemic heart disease. AV block was not detected in any patient in our study though it was reported to be present in a good number of COVID-positive patients.[29] The mechanism of orthostatic hypotension is not exactly known and the possible hypothesis may be related to overexpression of ACE 2 receptor in vascular endothelium and increased responsiveness to ACEI. On the contrary uncontrolled hypertension may be related to increased activity of angiotensin II.[30]

Atrial arrhythmias, especially AF, are commonly detected in patients with COVID-19 pneumonia particularly in severe cases and associated ARDS. Patients often present with palpitation and worsening heart failure and shortness of breath. The proposed mechanisms AF include a reduction in ACE2 receptor, altered interaction of CD147 receptor and sialic acid-spike protein, enhanced automaticity because of the effect of inflammatory cytokines, hyperadrenergic state, and direct viral invasion on the myocardium. Increased production of reactive oxygen species may lead to atrial myocyte injury, structural remodeling, and alteration of electrical conduction, contributing to the development of AF.[31] Among other cardiac arrhythmia ventricular tachycardia and fibrillation were accountable for 6% of death in our study though the exact cause of death may be due to cardiac ischemia, acute myocardial infarction, respiratory failure, or pulmonary embolism.[29] Incidence of out of hospital sudden cardiac arrest also increased in the COVID-19 pandemic and high index of suspicion and risk stratification may be needed for early detection of myocarditis and to prevent further complications.[32] Asymptomatic diastolic dysfunction of grade 2 or more was found in 17 patients and among them, 10 patients had elevated NT pro-BNP and HS troponin I. COVID myocarditis also may lead to symptomatic heart failure (heart failure with preserved ejection fraction) or precipitate symptoms in a previous subclinical LVDD.[33]

Acute cerebrovascular disease was reported in 6% of severely affected COVID patients in a study done in Wuhan, China. The mechanism may be the development of a transient hypercoagulable state, especially in severe disease as also found in our study that there is a positive correlation of D dimer level and CT severity score.[34] Though the role of anticoagulant in severe COVID pneumonia is well established, combination of anticoagulants and antiplatelet is not in COVID pneumonia is not well documented. However, recent studies have shown improved outcomes in patients treated with antiplatelets.[35] Though there is a specific recommendation for anticoagulant (oral or injectable) in the management of moderate-to-severe COVID disease as well as prophylaxis in patients with raised D-dimer level, till now no state or national level guideline specifically mention the use of single or dual antiplatelets as thromboprophylaxis in the management of COVID-19 pneumonia.


  Conclusion Top


Asymptomatic myocarditis is a common finding in COVID pneumonia with moderate-to-severe disease. Often patients present with chest discomfort, palpitation, and occasionally shortness of breath on exertion. Careful clinical evaluation is essential to diagnose clinical or subclinical myocarditis and to exclude coronary artery disease and avoidance of strenuous exercise is usually advised to prevent serious complications such as arrythmia and sudden cardiac death. Patients with diastolic dysfunction along with myocarditis may present with congestive cardiac failure and require treatment. Sinus bradycardia and tachycardia occur transiently and may not be directly correlated to myocardial involvement by SARS-CoV2, but symptomatic patients should be treated. Antiplatelets may play a role in improved clinical outcomes with or without anticoagulation. Antiplatelets may be safely advised in mildly symptomatic hospitalized patients or patients in home isolation with one or more risk factors for cardiovascular complication and, who are at low risk of bleeding. Myocarditis can happen irrespective of COVID severity and our study showed no correlation between NT pro BNP level and CT severity index, but there is a positive correlation between D dimer level and CT severity index. Thus, maintaining anticoagulation is essential in patients with severe COVID pneumonia.

Ethical approval

Ethical Committee approval has been obtained.

Authors' contributions

Dr. Rammohan Roy : Conception and design, Data collection, Analysis, write up

Dr. Baisakhi Maji : Conception, data collection , data analysis, write up

Dr. Yogiraj Ray : Design, Data collection and analysis

Dr. Arijit Sinha: Design, Data collection and analysis

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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