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Cardiac Manifestations Of Coronavirus (COVID-19)

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Last Update: May 2, 2022.

Continuing Education Activity

Coronaviruses are a large family of single positive-stranded, enveloped RNA viruses that can infect many animal species and humans. Human coronaviruses can be divided based on their pathogenicity. The types with high pathogenicity include SARS-CoV, MERS-CoV, and the current novel SARS-CoV2. Cross-species transmission is the most likely model of the initial transmission from bat to human. The initial transfer is believed to have happened in Wuhan, China. This activity reviews the evaluation and treatment of victims of COVID-19. It highlights the role of the interprofessional team in evaluating and treating patients with this condition and, in particular, those with cardiac manifestations.


  • Review the epidemiology of COVID-19.
  • Describe the signs and symptoms of a patient with COVID-19.
  • Summarize the treatment options for a patient with COVID-19.
  • Outline the prognosis of a patient with cardiac manifestations of COVID-19.
Access free multiple choice questions on this topic.


Coronaviruses are a large family of single positive-stranded, enveloped RNA viruses that can infect many animal species and humans. Human coronaviruses can be divided based on their pathogenicity. The types with high pathogenicity including SARS-CoV, MERS-CoV, and the current novel SARS-CoV2.[1] Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has led to possibly the worst pandemic of this century in the form of Coronavirus disease 2019 (COVID-19). Initially recognized as a respiratory system disease, COVID-19 has been found to interact with and affect the cardiovascular system leading to myocardial damage and cardiac and endothelial dysfunction mainly via the Angiotensin-converting enzyme 2 (ACE-2) receptor.[2][3][4][5]In fact, cardiac damage has been noted even without clinical features of respiratory disease. On the one hand, respiratory symptoms are worse in COVID-19 affected patients with preexisting cardiac ailments; however, new-onset cardiac dysfunction is common in this subset. In fact, cardiac damage has been noted even without clinical features of respiratory disease. On the one hand, respiratory symptoms are worse in COVID-19 affected patients with preexisting cardiac ailments; however, new-onset cardiac dysfunction is common in this subset.[6][7][8][9]


As early as December 2019, cases of unusual pneumonia presented and were diagnosed in Wuhan, China. A novel SARS-CoV2 virus was identified as the cause of the new Corona disease 2019 (COVID-19). [2]



The involvement of cardiac factors was recognized early in the pandemic in reports from China. A retrospective analysis of 187 patients treated in a Wuhan hospital between January 23 and February 23, 2020, found that 35% had existing cardiovascular comorbidities such as hypertension, coronary disease, and cardiomyopathy, and 28% exhibited myocardial injury indicated by elevated troponin T levels [9]. Other Chinese reports found rates of baseline cardiovascular disease ranging from 5% to 16%, hypertension ranging from 15% to 31%, coronary artery disease of 11%, and diabetes of 10%.[2][3][8][10] 

World Scenario

Beyond China, even higher rates of these comorbidities have been reported. A retrospective case series from Italy presented results from 1,591 critically ill patients with COVID-19 who were admitted to the intensive care unit (ICU): 49% of patients had hypertension, 21% had cardiovascular disease, and 17% had diabetes.[11] In a study from New York between March 2 and April 1, 2020, 1150 adults with COVID-19 were admitted to two hospitals; 257 were critically ill. Of these, 82% had at least one chronic illness, the most common of which were hypertension (63%), diabetes (36%), obesity (46%), and heart disease (19%).[12] In a large case series of 5700 patients with COVID-19 admitted to 12 hospitals in New York, the prevalence of hypertension, diabetes, and coronary artery disease was 57%, 34%, and 11%, respectively.[13]


ACE2 Receptor

SARS-CoV-2 uses its S-spike to bind to ACE2 receptors as the point of entry into the cell. These ACE2 receptors are expressed in type 1 and type 2 pneumocytes and other cell types, including endothelial cells. ACE2 is an inverse regulator of the renin-angiotensin-aldosterone system. Like other coronaviruses, SARS-CoV-2 uses these ACE2 receptors to target the respiratory system primarily. [2][14][15]

SARS-CoV-2 and the Immune Response

There are two immune-response phases of COVID-19 disease. Phase 1 occurs during the incubation stage of the disease, during which the adaptive immune system works to eliminate the virus; if any defects occur at this stage, SARS-CoV-2 will disseminate and induce systemic organ damage, with more significant destruction of organs with higher expression of ACE2 receptors, including lung, endothelial cells, the heart, and the kidneys. This massive damage leads to phase 2: severe inflammation in the affected organs.[16]

Diabetes, atherosclerosis, and obesity, which are risk factors for cardiovascular disease, downregulate the immune system. These have been associated with a poor prognosis in COVID-19.[17]

Mechanisms of Cardiac Damage in COVID-19 

Multiple mechanisms have been suggested for cardiac damage, based on studies conducted during the previous SARS and MERS epidemics and the ongoing COVID-19 epidemic. Part of the systemic inflammatory response in severe COVID-19 is the release of high levels of cytokines (known as cytokine release syndrome) that can injure multiple tissues, including vascular endothelium and cardiac myocytes.[14][15][18][19]

Cytokine Release Syndrome

Cytokine release syndrome occurs in patients with severe COVID-19 infection. Many proinflammatory cytokines are significantly elevated in severe cases, including interleukin (IL)-2, IL-10, IL-6, IL-8, and tumor necrosis factor (TNF)-α.[16][18] Cytokines play an important role during infection with the virus (phase 1) and during ongoing severe inflammation (phase 2), resulting in acute respiratory distress syndrome (ARDS) and other end-organ damage.[16][20]

Direct Myocardial Cell Injury

The interaction of SARS-CoV-2 with ACE2 can cause changes to the ACE2 pathways, leading to acute injury of the lung, heart, and endothelial cells. A small number of case reports have indicated that SARS-CoV2 might directly infect the myocardium, causing viral myocarditis. However, in most cases, myocardial damage appeared to be caused by increased cardiometabolic demand associated with the systemic infection and ongoing hypoxia caused by severe pneumonia or ARDS.[18]

Acute Coronary Syndrome

Plaque rupture leading to acute coronary syndrome can result from the systemic inflammation and catecholamine surge inherent in this disease.[18][21] Coronary thrombosis also has been identified as a possible cause of acute coronary syndrome in COVID-19 patients.[22]

Other Possible Mechanisms

Certain medications such as corticosteroids, antiviral medications, and immunological agents may have cardiotoxic side effects. Electrolyte disturbances can occur in any critical systemic illness and trigger arrhythmias, for which patients with underlying cardiac disease are at higher risk. There is particular concern about hypokalemia in patients with COVID-19, given the interaction of SARS-CoV-2 with the renin-angiotensin-aldosterone system. Hypokalemia is well known to increase vulnerability to various kinds of arrhythmia.[9][18]

History and Physical

COVID-19 disease mostly affects middle-aged and elderly patients. Children seem to be asymptomatic or get a mild form of the disease. The mean incubation period is about 5 days from exposure but ranges between 2 to 14 days. A higher risk of infection has been noticed in older patients, male sex, patients with medical comorbidities, patients with chronic pulmonary or chronic cardiac or chronic kidney disease, and patients with diabetes.[2][23]U.S experience indicates that up to one-fifth of infected people are between the ages of 20 to 44 years who have been hospitalized, including 2% to 4% who required intensive care unit admission. The symptoms of COVID-19 are akin to other viral upper respiratory illnesses. Initial presentation can, however, be vague. GI symptoms are present in 10% of cases, including nausea, vomiting, or diarrhea. Patients may also experience rarely headaches and confusion. Atypical presentations of infection may be more common in the elderly and immunocompromised, who may not mount a febrile response. Alteration of taste and smell, anosmia, is suspected as an early symptom of COVID-19 and is occasionally reported as a phenomenon of upper respiratory viral infection. Presently it is unclear how common it is in COVID-19. In current literature, no known reports exist in which the presenting symptoms were exclusively cardiac.[24][23]Three major trajectories for COVID-19 have been described: a mild disease with upper respiratory symptoms, non-severe pneumonia, and severe pneumonia complicated by acute respiratory distress syndrome (ARDS), necessitating aggressive resuscitative measures. Based on current reports, which could be biased by available data, only hospitalized patients were noted to have cardiac involvement. Though, as alluded to earlier, this number is significant and did correlate with increased morbidity and mortality several notches higher than those without ARDS.[24]


Blood Investigations

Certain laboratory anomalies have corresponded to cardiovascular involvement and severe illness. These include lymphopenia, elevated lactate dehydrogenase, liver enzymes, ferritin and C-reactive protein, prothrombin time, troponin, creatine phosphokinase, serum creatinine, and D-dimer.[2][25][26]


Transthoracic echocardiography is recommended for inpatients with heart failure, arrhythmia, ECG changes, or newly diagnosed cardiomegaly on chest X-ray or chest CT.[27] Cardiac MRI has been used to diagnose cardiac dysfunction in COVID-19. [28][29]

Coronary angiography should be performed depending on the patient's presentation and only if indicated.[30]

Treatment / Management

Comprehensive Cardiovascular Care for COVID-19 Patients

Cardiac care needs to be optimized for COVID-19 patients with an aim for early detection and management of cardiac ailments with the simultaneous aim at triaging cases and proper protection to prevent or minimize COVID-19 exposure.[31] As Bonow et al. have rightly put, the message to the patients should be clear that prompt emergency care to be sought in case of warning cardiac symptoms. Mask-wearing, physical distancing remains as essential as ever. Simultaneously, doctors and researchers are finding the best practices for COVID-19 related cardiovascular disease.[32]

ACE inhibitors (ACEI)/ Angiotensin Receptor Blockers (ARB)

Early in 2020, a controversy grew regarding the safe usage of these drugs in COVID-19 patients. The current consensus agrees to the continued use of these medications.[33][34] BRACE CORONA trial was presented in ESC Congress 2020, which found no significant difference in the number of days alive and out of hospital through 30 days among subjects receiving continuous ACEI/ARB and hospitalized for COVID-19 compared to those in whom these medicines were temporarily suspended.[35] Five common classes of antihypertensive medications are safe in patients of COVID-19 and do not increase the likelihood of infection.[36] 


Remdesivir is an antiviral (RNA polymerase inhibitor) drug used to treat COVID-19. A multicenter, double-blind RCT from China studied Remdesivir for adult patients hospitalized for severe COVID-19. The study showed a reduction in clinical improvement in the treatment group compared with controls, but the difference was not significant.[37] A subsequent trial, sponsored by the US National Institute of Allergy and Infectious Disease, assessed 1063 hospitalized COVID-19 patients in a remdesivir treatment trial. Results published in the New England Journal of Medicine indicated a faster time to recovery for patients who received remdesivir vs. placebo. [38]

The US Food and Drug Administration (FDA) has issued an emergency use authorization for remdesivir in all patients hospitalized with COVID-19. Thus far, no prominent cardiovascular side effects have been reported with Remdesivir, although these may become apparent with future use during the COVID-19 pandemic.

Hydroxychloroquine and Chloroquine

Hydroxychloroquine was introduced as a potential treatment for COVID-19 patients based on an open-label, single-group study from France.[39] However, an observational study of hospitalized COVID-19 patients conducted at a large medical center in New York City found no apparent benefit from hydroxychloroquine.[40] The use of hydroxychloroquine alone or hydroxychloroquine plus azithromycin did not improve a composite endpoint of intubation or death.

Chloroquine has been noted to cause atrioventricular blocks and prolonged QTc, especially when combined with azithromycin.[41] The lack of benefit seen in clinical trials and the potential for cardiovascular side effects has led the FDA to revoke its emergency use authorization of hydroxychloroquine and chloroquine for patients in COVID-19.


Azithromycin was commonly used in combination with hydroxychloroquine as a treatment early in the pandemic. However, several studies of this combination have not shown any clinical benefit. [42][43]Azithromycin is a macrolide and is known to prolong the QTc interval. Combining azithromycin with chloroquine or hydroxychloroquine increases QTc prolongation and potentially the risk for torsade de points.[41] The lack of clinical benefit and the potential for cardiac arrhythmias has discouraged physicians from using azithromycin in COVID-19.[44]


Lopinavir and ritonavir are protease inhibitors approved by the FDA for HIV-1 infection. In a recent study published in the New England Journal of Medicine, researchers observed no survival benefit after treatment with lopinavir-ritonavir in hospitalized adults with severe COVID-19.[45] Lopinavir-ritonavir can interact with cardiovascular drugs such as antiarrhythmic agents, antiplatelet drugs, and anticoagulants that are metabolized by cytochrome P-450 3A4; therefore, it should be used with caution, especially in patients with underlying cardiovascular disease.[46]


The World Health Organization has recommended using systemic steroids to treat COVID-19 infection.[47] Corticosteroids are known to possess potent anti-inflammatory effects, and they have been studied extensively in the treatment of sepsis and ARDS. However, they are also known to cause fluid retention, electrolyte derangement, hyperglycemia, and hypertension.[48][49] [48]At the onset of the COVID-19 pandemic, concerns about potential harm from steroids in COVID-19 were based on data collected and extrapolated during the previous SARS-CoV outbreak.[50][51] Nonetheless, the recent RECOVERY (Randomized Evaluation of COVID-19 Therapy) trial compared dexamethasone 6 mg once daily for up to 10 days versus usual care alone in hospitalized patients with COVID-19 receiving invasive mechanical ventilation or oxygen. Dexamethasone reduced 28-day mortality by one-third in patients on a mechanical ventilator and by one-fifth in patients requiring oxygen therapy.[52]


In a retrospective study, the use of low-dose Aspirin in patients hospitalized with COVID-19 was associated with better outcomes. [53]


Tocilizumab, an anti–IL-6 receptor antibody, has been investigated to treat hospitalized COVID-19 patients.[3] IL-6 levels are elevated in COVID-19 patients and significantly elevated in patients with severe disease. Tocilizumab’s potential efficacy lies in its ability to reduce the inflammatory response, including the cytokine storm that contributes to ARDS and death.[3] As for cardiac side effects, tocilizumab is known to increase cholesterol levels, but there are conflicting reports on its effect on long-term cardiac morbidity and mortality.[54][55]

Convalescent Plasma 

Convalescent plasma for the treatment of COVID-19 patients is obtained from individuals who have recovered from COVID-19 and have generated an immune response. Small randomized trials and case studies have shown some benefit from convalescent plasma in hospitalized patients with severe COVID-19, especially if given early in the disease course.[56][57][58] The FDA has granted emergency use authorization for convalescent plasma in hospitalized patients with COVID-19. 


Ivermectin was introduced as a potential treatment for COVID-19 patients. Ivermectin is an antiparasitic drug used to treat Strongyloides and onchocerciasis infection. A Meta-analysis by Dr. Andrew Hill investigated Ivermectin in 18 randomized clinical trials. There was a 75% reduction in mortality found in moderate or severe infection in six randomized trials. In another randomized trial of 476 patients, Ivermectin did not shorten the duration of the infection. Multiorgan failure was reported in four patients. The FDA has issued a warning against using Ivermectin to prevent or treat COVID-19 infection. [59]


The SARS-CoV-2 genetic sequence was published in January 2020, and since then, researcher teams worldwide have been working actively to develop a vaccine against SARS-CoV-2. More than 90 vaccines are being developed at this time.[60][61] Vaccination has already started in various countries. The mRNA- based vaccines developed by Pfizer and Moderna have been granted emergency use authorization (EUA) by the US Food and Drug Administration (FDA). Many healthcare workers have already received these vaccines. 

Immune thrombotic thrombocytopenia developed after ChAdOx1nCov-19 Vaccination was reported as a rare complication developed in several cases. Mechanism of the thrombocytopenia similar to heparin-induced thrombocytopenia. [62]

No significant cardiac complication has been reported with any of the vaccines thus far.

Differential Diagnosis

The differential diagnosis for COVID-19 should be tailored to the patient and their presenting symptoms and comorbidities. Influenza, respiratory syncytial virus (RSV), other viral illnesses, and bacterial pneumonia should be considered and other pulmonary diseases. Given the well-known epidemiology, antecedent travel or other sources of exposure, if present, must be elicited. The cardiac presentation includes cardiac injury, heart failure, and myocarditis also are not specific and have already been reported with other virus infections, including influenza.

Pertinent Studies and Ongoing Trials

Ongoing research in different aspects of COVID-19 will shed more light on the pathophysiology and treatment of cardiovascular sequelae of COVID-19. Cardiac complications and side effects of the disease per se, drugs, and vaccines will also become more apparent as time passes and more data is available. Newer therapies and improved vaccines will arise, leading to better treatment and eradicating the virus. As we gain more data, more extensive retrospective studies will guide us regarding what caused higher morbidity and mortality and better prognosis.


Most of the patients (80%) will get a mild form of the disease. The severe form of the disease occurs in about 15% of patients requiring hospitalization and the critical form occurs in about 5% of patients requiring intensive care. The current mortality rate ranges between 2% to 5% of all patients with COVID-19 but is much higher in patients requiring invasive mechanical ventilation. The major cause of death in COVID-19 is acute respiratory distress (ARDS); however, there is also significant other vital organ involvement, including the cardiovascular system and shock.[2][14][15] The presence of chronic cardiac diseases or cardiac involvement leads to a higher mortality rate in comparison to patients without cardiovascular disease.[8][63]

In this COVID-19 pandemic, fewer cardiac patients have attended clinics or hospitals due to the fear of contracting the infection. On the contrary, cardiac patients irrespective of SARS-CoV-2 infection need prompt evaluation and management, more so during this pandemic as the resources and workforce are often compromised.[64][65]

The prognostic significance of cardiovascular disease was amply illustrated in a cohort of 191 patients in which 30% had hypertension and constituted 48% of nonsurvivors, whereas 8% had cardiovascular disease and constituted 13% of nonsurvivors.[24] In a report of 44672 confirmed cases of COVID-19 from the Chinese Center for Disease Control and Prevention, the overall case-fatality rate was 2.3% for the entire cohort but significantly higher for patients with hypertension (6%), diabetes (7%), or cardiovascular disease (11%).[66]


Myocarditis, Myocardial Injury, and Elevated Cardiac Enzymes

The myocardial injury appears to be a common feature in COVID-19 and portends a poor prognosis when present. A meta-analysis of six published studies from China found that 8% of patients with COVID-19 had associated cardiac injury.[8] Several case series have examined cardiac enzyme elevations indicating myocardial damage that could be secondary to ischemic or non-ischemic causes. Other studies have reported patients with viral myocarditis, myocardial injury, and inflammation without an ischemic cause. 

Early reports from China noted that 7%–20% of patients had increased levels of cardiac biomarkers or electrocardiographic (ECG) abnormalities indicating underlying myocardial injury. These patients with myocardial involvement had worse outcomes.[67] In a case series of 41 patients with COVID-19 in Wuhan, five patients (12%) had a myocardial injury with elevated levels of high-sensitivity cardiac troponin I and four were in critical condition [2]. A study of 191 patients with COVID-19 reported that 17% had an acute cardiac injury and that all but one of these died.[24] Similarly, a retrospective study of 416 COVID-19 hospitalized patients found that 20% had an underlying myocardial injury; these patients had a much higher mortality rate (51%) than did patients without cardiac injury (5%).[10]

The association between myocardial injury and fatal outcomes was examined in a retrospective single-center case series of 187 COVID-19 patients from Wuhan, 28% of whom had elevated troponin T levels indicating myocardial injury. In-hospital mortality was 60% in these patients versus 9% in patients with normal troponin T levels. Further, mortality was 8% in patients without underlying cardiovascular disease and normal troponin T levels, 13% in patients with underlying cardiovascular disease but normal troponin T levels, 38% in patients without underlying cardiovascular disease but elevated troponin T levels, and much higher at 69% for those with underlying cardiovascular disease and elevated troponin T. The authors concluded that the presence of myocardial damage was associated with increased mortality in COVID-19 patients and that the absence of myocardial injury led to a better prognosis.[68]

Myocardial injury was predictive of the risk for in-hospital mortality in patients with severe COVID-19.[69] In a study of 671 hospitalized patients with severe COVID-19, the mortality rate was 9%; myocardial injury was seen in 76% of the patients who died, versus 10% of survivors.[70] 

Most of the early studies did not report echocardiographic or cardiac magnetic resonance imaging (MRI) results. Later studies have identified patients with myocardial injury elicited abnormal cardiac imaging and cardiac contractile dysfunction.[71][72][73] Even after recovery from confirmed SARS-CoV-2 infection, cardiac magnetic resonance imaging has shown left ventricular dilatation, lower ejection fraction, myocardial edema, and inflammation.[74] However, in a cohort study of 112 patients with COVID-19, 14 patients had clinical abnormalities indicating myocarditis but no signs of myocardial injury on ECG or echocardiogram. This suggests myocardial damage being secondary to systemic effects rather than direct viral involvement.[75]

A 53-year-old woman without any history of cardiovascular disease presented with severe fatigue in a case report from Italy. She was found to have evidence of acute myopericarditis with elevated levels of cardiac biomarkers. Her ECG showed diffuse ST elevation. Imaging with cardiac MRI revealed a slew of gross abnormalities, including biventricular hypokinesis, ventricular interstitial edema, circumferential pericardial effusion, and a left ventricular ejection fraction of 35%. The patient was treated with lopinavir/ritonavir, steroids, and chloroquine, along with dobutamine for heart failure, and showed clinical improvement.[6]

Another case report from China described a 37-year-old man with COVID-19 complicated by fulminant myocarditis and cardiogenic shock. Troponin T was elevated, and ECG showed ST elevation. Emergency computed tomography (CT) coronary angiography revealed no coronary stenosis. Echocardiography showed an enlarged heart with a left ventricular ejection fraction of 27%. The patient was treated with glucocorticoids and immunoglobulins, resulting in clinical recovery with the restoration of normal cardiac size and function.[76]

Histopathological evidence of COVID-19 affecting the myocardium is limited. In one case report, a patient with COVID-19 developed ARDS, hypotension, and cardiogenic shock. Endomyocardial biopsy showed low-grade myocardial inflammation with coronavirus particles observed in the myocardial interstitium.[77] An autopsy series from 12 consecutive confirmed COVID-19 deaths showed that SARS-CoV-2 RNA was detected in the lungs in all patients, with five patients showing high viral titers in the heart.[78] Portmann et al. reported active lymphocytic infiltration on myocardial biopsy of COVID-19 recovered patients with severe cardiac magnetic resonance abnormalities.[74] However, in a case report of a patient with COVID-19 and ARDS who died of sudden cardiac arrest, an autopsy showed no evidence of myocardial structural involvement, suggesting that COVID-19 did not directly impair the heart.[14]

Currently, the exact mechanism of action of myocardial injury by SARS CoV-2 is not precisely understood. Some evidence suggests an indirect effect of the virus, with myocardial injury appearing to be mostly related to systemic inflammation and hypoxia. In a few cases, the myocytes' direct viral involvement may lead to viral myocarditis.[79]

Heart Failure

Heart failure has been well described in patients with pneumonia, and now multiple studies have shown an association between heart failure and COVID-19. In a case series of 21 severely ill patients with COVID-19 in an ICU, one-third developed new-onset cardiomyopathy with globally decreased left ventricular ejection fraction on transthoracic echocardiogram with clinical signs of cardiogenic shock and elevated creatine kinase or troponin I.[80][80] In a cohort of 191 patients with COVID-19 from Wuhan, 23% were diagnosed with heart failure; of the 54 patients who died, 52% had heart failure.[24] In another study of 799 COVID-19 patients from Wuhan, heart failure was observed in 24% of patients and 49% of those who died.[81][81]

Patients with COVID-19 may develop right-sided heart failure secondary to pulmonary hypertension due to hypoxia and ARDS. In a cohort of 105 COVID-19 patients hospitalized at one center, right ventricular dilation was present in 31% of intubated patients. Right ventricular hypokinesia was observed in 66% of COVID-19 patients with right ventricular enlargement versus 5% of COVID-19 patients without right ventricular enlargement.[82]

A few studies have reported takotsubo (stress-induced) cardiomyopathy as a complication of COVID-19. Most cases occurred in women older than 65 years of age. The association with COVID-19 infection is not clear, but it has been suggested that the emotional distress and anxiety associated with the pandemic may have a role in the onset of this disease.[83][84]

The etiology of heart failure in COVID-19 disease is unclear whether it is a direct effect of SARS-CoV-2 on the myocardium or indirectly caused by hypoxia, cytokine release, volume overload, renal failure, stress, or overwhelming critical illness. Further, some patients with risk factors for heart disease (diabetes, hypertension, hyperlipidemia, coronary artery disease) may have had underlying subclinical heart failure uncovered or exacerbated by COVID-19 infection and associated illness. Acute coronary syndromes triggered by COVID-19 can also result in heart failure or worsen the preexisting disease.[67]

Diagnostic workup for suspected heart failure includes brain natriuretic peptide, troponin markers, transthoracic echocardiography, and cardiac MRI. Cardiac MRI may help look for changes induced by COVID-19 in patients with diastolic heart failure.[85][86]

Knowledge of the presence or absence and degree of cardiomyopathy is crucial for managing patients in shock status and determining the need for circulatory support and type of extracorporeal membranous oxygenation. The management of heart failure in patients with COVID-19 should be initiated and continued as per current guidelines.[87][88]

Arrhythmias and Sudden Cardiac Arrest 

Arrhythmias and sudden cardiac arrest have been reported with COVID-19. In a report of 138 hospitalized patients with COVID-19 in Wuhan, 17% had arrhythmias [1], although the specific types of arrhythmias were not described. In another study of hospitalized COVID-19 patients in Wuhan, 6% had developed ventricular tachycardia or ventricular fibrillation. More patients with elevated troponin T levels (17%) than normal troponin T levels (2%) had ventricular tachycardia or ventricular fibrillation.[68]

In patients with COVID-19, a cardiac injury that induces arrhythmia can be due to various causes, such as hypoxia, a worsening of coronary perfusion, direct tissue damage, hyperacute systemic inflammatory response syndrome, or the effects of medications used to manage the COVID-19. Hypokalemia can occur in patients with COVID-19 due to the interaction of SARS-CoV-2 with the renin-angiotensin-aldosterone system and increases vulnerability to various kinds of arrhythmia.[9][18]Recommendations for managing arrhythmias are similar to those for non-COVID patients, including electrolyte optimization, avoidance of triggers, and medication modification. Concomitant ECG monitoring for patients who have long QTc or taking medications known to prolong the QTc interval is mandated.[89]

Cardiac arrest was reported in 11% of COVID-19 patients with ECG evidence of ST elevation in a case series from New York.[90] A study from Italy looked at local out-of-hospital cardiac arrests during the first 40 days of the COVID-19 outbreak and compared the rate with that from the same period a year ago. During the study period, there was a 58% increase in out-of-the hospital cardiac arrests (362 cases compared to 229 cases the year before) correlating to the incidence of COVID-19. Of the 362 cases of out-of-hospital cardiac arrest, 28% had, or were suspected of having, COVID-19.[91]

Thromboembolism and Coagulation Abnormalities 

COVID-19 infection has been associated with venous and arterial thromboembolism. Studies have shown abnormalities of the coagulation cascade, with elevated D-dimer, thrombocytopenia, slightly elevated prothrombin time, and higher levels of fibrinogen and von Willebrand factor. The hypercoagulable state in COVID-19 infection is thought to be related to severe inflammatory response, cytokine storm, and endothelial damage, along with underlying patient comorbidities.[92][93]

In a retrospective cohort study from China, a D-dimer >1 mcg/mL was reported in 42% of patients and in 81% of those who died from COVID-19; as such, it was identified as one of the risk factors for death and was associated with 18-times increased risk for mortality.[24] A Wuhan study found elevated D-dimer in 46% of patients, 60% of patients with severe illness, and up to 70% of patients in a composite group with ICU admission, mechanical ventilation, or death. Platelet count was <150,000/mm3 (signifying thrombocytopenia) in 36% of patients and 58% of patients with severe disease.[23] In an autopsy series of COVID-19 patients from Germany, deep venous thrombosis was found in 58% of patients in whom venous thromboembolism was not suspected before death. Pulmonary embolism was found in 4 of the patients and was the direct cause of death.[94]

COVID-19 infection has been associated with cerebrovascular accidents. The incidence of acute ischemic stroke in patients with COVID-19 is approximately 1%–3%. A review of 37 studies with 370 patients with COVID-19 who had developed acute ischemic stroke or transient ischemic attack found that most patients had underlying comorbidities predisposing them to ischemic stroke.[95] However, case reports describe large-vessel strokes in young adults with COVID-19 who did not have any cardiovascular risk factors.[94] In a case series from the United Arab Emirates, 22 patients with confirmed COVID-19 infection presented with ischemic stroke symptoms as the first evidence of their COVID-19 infection; most were male and younger than 55 years of age.[96] Patients with COVID-19 and stroke are reported to have significantly higher mortality than historical controls.[97] In addition to arterial strokes, cerebral venous sinus thrombosis has been reported in 13 patients in 9 studies.[92]

Peripheral arterial thromboembolism causing acute limb ischemia also has been described in COVID-19. Two young patients without any known risk factors have been diagnosed with acute thrombosis involving the aorta presenting as acute limb ischemia.[98] A report from Italy described four patients with COVID-19 who developed acute limb ischemia; two had comorbidities, but the other two were young and active, without any comorbidities.[99] In another Italian case series, 20 patients were diagnosed with COVID-19-related pneumonia before acute limb ischemia was detected; revascularization was less successful than expected, possibly secondary to a virus-related hypercoagulable state.[100] A case series from Spain described acute limb ischemia in four patients infected with COVID-19 secondary to a hypercoagulable state. None of these patients had known cardiovascular disease or comorbidities that could have predisposed them to arterial embolisms.[101]

There is increasing evidence that anticoagulation is of benefit in COVID-19 illness. A study from New York demonstrated that treatment-dose anticoagulation was associated with reduced mortality. In the study, 786 out of 2773 patients (28%) were administered systemic anticoagulation. In-hospital mortality for patients who received anticoagulation was 23%, and median survival was 21 days, compared with 23% and median survival of 14 days in patients who did not receive treatment-dose anticoagulation. In patients who needed mechanical ventilation, in-hospital mortality was 29% for those who received treatment-dose anticoagulation, and median survival was 21 days, versus 63% and median survival of 9 days in patients who did not receive treatment-dose anticoagulation.[102] A retrospective study from China showed that the use of low molecular weight heparin was associated with better prognosis in severe COVID-19 patients meeting sepsis-induced coagulopathy criteria or with markedly elevated D-dimer.[103]

At this time, most centers have incorporated anticoagulation into the treatment protocol for COVID-19 patients, especially if they have elevated D-dimer levels. However, it is unknown which anticoagulation agent (unfractionated heparin, low-molecular-weight heparin, warfarin, or direct oral anticoagulants) is most efficacious in preventing thromboembolic events in COVID-19 patients. As always, the risks and benefits of anticoagulation treatment must be weighed for each patient. Future clinical trials may shed more light on the benefits of anticoagulation in COVID-19 infection.[104]

Acute Coronary Syndrome 

Several studies and case reports have established an association between COVID-19 and acute coronary syndrome. In a letter to the editor, investigators from New York reported their experience with COVID-19 patients who showed ST-segment elevation on ECG.[90] Ten patients had ST-segment elevation at the time of presentation, whereas the other eight developed ST changes during hospitalization. Nine patients underwent coronary angiography, and six were found to have an obstructive disease; five of these six patients needed percutaneous coronary intervention. Overall, eight patients were diagnosed as having an acute myocardial infarction, and the other ten were deemed to have a noncoronary myocardial injury. Of the 13 patients (72%) who passed away during hospitalization, four had a myocardial infarction, and the other nine had a noncoronary myocardial injury.

In Italy, researchers published a study of 28 patients with confirmed COVID-19 who had undergone with coronary angiogram for ST-elevation myocardial infarction. Of these, 79% had typical chest pain, while 21% presented with dyspnea without any chest pain; 86% had ST-elevation myocardial infarction as the initial presentation of COVID-19. This suggests that COVID-19 caused acute coronary syndrome (ACS) without substantial systemic inflammation.[105] The pathophysiology of ACS in COVID-19 is not clear, but it may be related to direct endothelial injury by the SARS-CoV-2 virus, microthrombi formation, or systemic inflammation and cytokine storm resulting in plaque rupture or coronary spasm.[106]

Despite the association between COVID-19 and ACS, the reported incidence of ACS has been lower during the pandemic than in the pre-COVID-19 period. Reports indicate a 42%–48 % reduction in ACS hospitalizations and 38%–40% fewer percutaneous coronary interventions performed for ST-elevation myocardial infarction. This could be due to patients being reluctant to present to hospitals and clinics out of fear of contracting COVID-19. Unavailability of beds has also been a reason, as hospitals have been flooded with sick COVID-19 patients precluding many other admissions, particularly non-urgent cases.[64][65] 

Deterrence and Patient Education

During this pandemic time, patients should avoid close contact with another patient with suspected or confirmed COVID-19 or having signs and symptoms of respiratory infection. Get vaccinated, wearing masks, hand washing, and social distancing are principles to reduce the risk of infection. Patients with underlying cardiac disease, hypertension, cardiac transplant patients, or patients taking immunosuppressive medications should take extra caution to avoid getting infected, considering the data we already explained above. CDC also supports these recommendations.

Enhancing Healthcare Team Outcomes

The SARS-CoV-2 infection has been often reported to be complicated with cardiac dysfunction. Preexisting cardiac diseases predispose to the severity of the disease and worsening of the cardiac condition. Early detection of cardiovascular disease by clinical and laboratory parameters and treatment is of paramount importance. Clinical trials are underway, and more research will follow to evaluate the disease and its therapies, which will guide the clinicians in treatment and policymakers to set the guidelines for better management of cardiovascular aspects of COVID-19.

Review Questions

This illustration, created at the Centers for Disease Control and Prevention (CDC), reveals ultrastructural morphology exhibited by coronaviruses


This illustration, created at the Centers for Disease Control and Prevention (CDC), reveals ultrastructural morphology exhibited by coronaviruses. Note the spikes that adorn the outer surface of the virus, which impart the look of a corona surrounding (more...)

Clinical Presentation of Patients with CoVID-19


Clinical Presentation of Patients with CoVID-19. Contributed by Rohan Bir Singh, MD; Made with Biorender.com


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