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 Table of Contents  
REVIEW ARTICLE
Year : 2020  |  Volume : 5  |  Issue : 2  |  Page : 50-57

Cardiovascular disease in the context of the COVID-19 pandemic


Geneva Learning Foundation, Geneva, Switzerland

Date of Submission25-May-2020
Date of Decision06-Jun-2020
Date of Acceptance08-Jun-2020
Date of Web Publication29-Jun-2020

Correspondence Address:
Prof. Shanthi Mendis
Geneva Learning Foundation, Avenue Louis-Casai 18, 1209 Geneve
Switzerland
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jncd.jncd_31_20

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  Abstract 


Emerging evidence indicate a close relationship between coronavirus disease 2019 (COVID-19) and cardiovascular diseases (CVDs). Age is a potent shared risk factor which links the two conditions. Although severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) principally affects the lungs, a sizeable number of patients develop new-onset cardiac dysfunction during the course of the illness. As outlined in this review, cardiovascular manifestations of COVID-19 are complex with patients presenting with one or more of the following: myocarditis, acute myocardial infarction, stroke, cardiomyopathy, heart failure, arrhythmias, acute pericarditis, and venous thromboembolism. Preexisting CVDs make people more vulnerable to SARS-CoV-2 infection and adversely impact clinical outcomes. The World Cardiology Associations have issued consensus-based guidance to ensure that cardiac and stroke care needs of people, are met effectively within the context of the COVID-19 burden. Clinicians caring for COVID-19 patients need to be aware of the potential cardiovascular side effects of various therapies used for treating SARS-CoV-2 infection, including chloroquine/hydroxychloroquine and azithromycin. Research is essential to better understand the mechanisms that shape the close interplay between SARS-CoV-2 infection and CVDs.

Keywords: Cardiomyopathy, cardiovascular disease, COVID-19, myocardial infarction, myocarditis, pandemic, stroke


How to cite this article:
Mendis S. Cardiovascular disease in the context of the COVID-19 pandemic. Int J Non-Commun Dis 2020;5:50-7

How to cite this URL:
Mendis S. Cardiovascular disease in the context of the COVID-19 pandemic. Int J Non-Commun Dis [serial online] 2020 [cited 2020 Aug 15];5:50-7. Available from: http://www.ijncd.org/text.asp?2020/5/2/50/288252




  Introduction Top


The deadly virus infection causing coronavirus disease 2019 (COVID-19), has become a global public health disaster as it rapidly spreads throughout the world.[1] Although the brunt of the severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection is on the respiratory system, evidence has rapidly emerged of its impact on the cardiovascular system. This article reviews the cardiovascular manifestations and the impact of preexisting and new-onset vascular disease on the clinical outcomes of COVID-19 patients. The manner in which COVID-19 has increased the delay in the diagnosis and treatment of cardiovascular emergencies is highlighted. The article also summarizes the general guidance issued by the World Cardiology Associations to ensure that the cardiac and stroke needs of people are efficiently met within the context of COVID-19.


  Methods Top


This review is based on a literature search done using PubMed and Google search engines for original and review articles and advisories from professional societies published since November 2019. The search terms “COVID-19” and “coronavirus” were used in combination with “cardiac,” “cardiovascular,” “arrhythmia,” “myocardial infarction,” “troponin,” “heart failure,” “cerebrovascular,” “stroke,” “thromboembolism,” and “cardiomyopathy.”


  Pathogenic Mechanisms Top


The virus uses the angiotensin-converting enzyme 2 (ACE2) receptor for internalization. The tissue localization of the receptors correlates with COVID-19 presenting symptoms and organ dysfunction. Potential explanations for the close relationship between COVID-19 and cardiovascular diseases (CVDs) include the high prevalence in those with advancing age, a weak immune system in those with advancing age, elevated levels of ACE2, or a predisposition to COVID-19 for those with CVD.

Preexisting CVDs may become unstable in the setting of a viral infection as a result of the imbalance between the infection-induced increase in metabolic demand and reduced cardiac reserve. This imbalance, coupled with an inflammatory response and myocardial injury, could raise the risk of acute coronary syndromes, heart failure, and arrhythmias.

The deleterious myocardial effects could also be propagated by the downregulation of myocardial and pulmonary ACE2 pathways, thereby mediating myocardial and lung inflammation.[2] Respiratory dysfunction and hypoxemia caused by COVID-19, can, in turn, cause damage to myocardial cells and increase the risk of arrhythmias. Other proposed mechanisms of myocardial injury include cytokine surge triggered by an imbalanced response by type 1 and 2 T-helper cells [3],[4] and interferon-mediated immunopathological processes.[5]


  Preexisting Cardiovascular Diseases and Coronavirus Disease 2019 Top


Preexisting cardiovascular diseases is a risk factor of coronavirus disease 2019

Emami et al.[6] performed a meta-analysis to estimate the prevalence of the underlying disorders in hospitalized COVID-19 patients. The data of 76,993 COVID-19 patients from ten studies were included in the analysis. The most prevalent underlying diseases were hypertension, CVD, and diabetes in 16.37% (95% confidence interval [CI]: 10.15%–23.65%), 12.11% (95% CI: 4.40%–22.75%), and 7.87% (95% CI: 6.57%–9.28%), respectively.

In another meta-analysis enrolling 1558 patients with COVID-19 from six studies, hypertension (odds ratio [OR]: 2.29, P < 0.001), CVD (OR: 2.93, P < 0.001), and cerebrovascular disease (OR: 3.89, P = 0.002) were independent risk factors associated with COVID-19.[7]

In a large intensive care unit (ICU) case series in Lombardy Italy, of 1591 patients with COVID-19 and severe illness, 49% had hypertension and 21% had CVD.[8]

Congestive cardiac failure is a common comorbidity of severe cases of COVID-19. In a case series of 21 patients with COVID-19, congestive heart failure was the second most common baseline comorbidity (42.9%).[9]

Preexisting cardiovascular disease is associated with greater severity of coronavirus disease 2019

A systematic review analyzed data from 13 studies (3027 patients with COVID-19) to investigate the effect of comorbidities on the outcomes of COVID-19.[10] The presence of CVD and hypertension was associated with a greater severity of illness and death (hypertension: OR = 2.72, 95% CI: 1.60, 4.64, P = 0.0002; CVD: OR = 5.19, 95% CI: 3.25, 8.29, P < 0.00001). Other comorbidities that adversely affected clinical outcomes were diabetes and respiratory disease. Male, older than 65 years, and smoking were risk factors for disease progression.

In another meta-analysis, the incidences of comorbidities were compared in ICU/severe and non-ICU/severe patients.[11] A total of six studies with 1527 patients were included in this analysis. The proportions of hypertension, cardio-cerebrovascular disease, and diabetes in patients with COVID-19 were 17.1%, 16.4%, and 9.7%, respectively. The incidences of hypertension, cardio-cerebrovascular diseases, and diabetes were about twofolds, threefolds, and twofolds, respectively, higher in ICU/severe cases than in their non-ICU/severe counterparts.

In an ICU case series,[8] the prevalence of hypertension was higher among patients who died in the ICU (63%, 195 of 309 patients) compared with those discharged from the ICU (40%, 84 of 212 patients) (difference, 23% [95% CI, 15%–32%]; P < 0.001).

Using an observational database from 169 hospitals in Asia, Europe, and North America, Mehra et al.[12] evaluated the relationship of CVD with in-hospital death among 8910 hospitalized patients with COVID-19. A total of 515 patients died in the hospital (5.8%). The factors independently associated with an increased risk of in-hospital death were coronary artery disease (10.2%, vs. 5.2% among those without disease; OR, 2.70; 95% CI, 2.08–3.51), heart failure (15.3%, vs. 5.6% among those without heart failure; OR, 2.48; 95% CI, 1.62–3.79), and cardiac arrhythmia (11.5%, vs. 5.6% among those without arrhythmia; OR, 1.95; 95% CI, 1.33–2.86).

A Clinical Risk Score Predicting the Occurrence of Critical Illness in Hospitalized Patients With COVID-19 demonstrates that hypertension, CVD, and diabetes are the top three comorbidities which identify patients with COVID-19 who may subsequently develop critical illness.[13]


  Cardiovascular Manifestations of Coronavirus Disease 2019 Top


The cardiovascular manifestations of COVID-19 are complex with patients presenting with one or more of the following: myocardial injury, acute myocardial infarction, stroke, myocarditis, stress cardiomyopathy, heart failure, arrhythmias, acute pericarditis, and venous thromboembolism [Table 1].
Table 1: Percentage of coronavirus disease 2019 patients affected by various cardiovascular manifestations in different case series

Click here to view


Myocardial injury

Retrospective data from Chinese cohorts,[14],[15],[16],[17] show that 7.2% of patients overall, and 23% that required intensive care developed acute myocardial injury, defined as an increase in troponin levels. Myocardial injury in patients with COVID-19 could be due to plaque rupture, cytokine storm, hypoxic injury, coronary spasm, microthrombi, or direct endothelial or vascular injury.

Myocardial infarction

Myocardial injury with ST-segment elevation has been reported in several case series.[18],[19],[20] In a case series of 18 patients with COVID-19,[20] the median age of the patients was 63 years, 83% were men, and 33% had chest pain around the time of ST-segment elevation. Fourteen patients (78%) had focal ST-segment elevation, five (36%) had a normal left ventricular ejection fraction, and six had regional wall-motion abnormalities. Half of the patients underwent coronary angiography, of whom two-thirds had obstructive disease. Those who had nonobstructive disease on coronary angiography or had normal wall motion on echocardiography in the absence of angiography were presumed to have noncoronary myocardial injury. The eight patients (44%) who received a clinical diagnosis of myocardial infarction had higher median peak troponin and d-dimer levels than the others with noncoronary myocardial injury. A total of 13 patients (72%) died in the hospital (4 patients with myocardial infarction and 9 with noncoronary myocardial injury).

Acute myopericarditis

Case reports show that myocarditis may occur with COVID-19 even without clinical features of respiratory infection.[21] Myocarditis results in focal or global myocardial inflammation, necrosis, and eventually ventricular dysfunction.

Acute myopericarditis has been documented in a case report of a 53-year-old female with COVID-19[22] presenting with severe fatigue with a history of fever and dry cough the week before. She was afebrile but hypotensive; electrocardiography showed diffuse ST elevation, and elevated high-sensitivity troponin T was detected. There was no evidence of obstructive coronary disease on coronary angiography. Cardiac magnetic resonance imaging showed increased wall thickness with diffuse biventricular hypokinesis and severe left ventricular dysfunction. Cardiac MRI showed biventricular myocardial interstitial edema, and there was also diffuse late gadolinium enhancement involving the entire biventricular wall. She also had a circumferential pericardial effusion.

Cardiac arrhythmia

In patients with COVID-19, arrhythmias may result from metabolic derangements, hypoxia, acidosis, intravascular volume imbalances, neurohormonal effects, and catecholaminergic stress.

In an early case series, comprising 137 patients, 7% presented with palpitations together with other initial symptoms such as fever, fatigue, and muscle pain.[23] In another case series, arrhythmia was noted in almost one-sixth of the patients and frequently occurred within the subgroup of patients needing intensive care, with almost half being affected.[15]

Atrial arrhythmias, namely, atrial flutter and atrial fibrillation, have been reported.[24] Among 393 patients with COVID-19 from New York, atrial arrhythmias were more common among patients requiring mechanical ventilation (17.7% vs. 1.9%).[25] Among 187 patients with COVID-19 from a Chinese cohort, 11 patients (5.9%) had ventricular tachyarrhythmias while hospitalized.[26]

Arrhythmias in COVID-19 patients may be drug induced.[27],[28] Chloroquine which is one of the drugs that is being tested in patients with COVID-19 may increase depolarization length duration and Purkinje fiber refractory period, ultimately leading to atrioventricular nodal and/or His system malfunction. Excessive QT prolongation, defined as prolongation to a QTc >500 ms, has already been reported for 11%–25% of COVID-19 patients treated with hydroxychloroquine/azithromycin.[29] Drug-induced torsade de pointes due to chloroquine therapy for COVID-19 has been reported in an 84-year-old female.[30]

Cardiomyopathy

Published studies indicate that cardiomyopathy developed in about 33% of severe COVID patients.[9] A minority of hospitalized patients with COVID-19 have developed an acute COVID-19 cardiovascular syndrome that can manifest as an acute cardiac injury with cardiomyopathy, ventricular arrhythmias, and hemodynamic instability in the absence of obstructive coronary artery disease. The etiology of this injury is uncertain, but is suspected to be related to myocarditis, microvascular injury, systemic cytokine-mediated injury, or stress-related cardiomyopathy.[31] There are several published case reports of acute stress cardiomyopathy (Takotsubo syndrome) in the setting of COVID-19 infection.[32],[33],[34],[35]

Cerebrovascular disease

The incidence of stroke among hospitalized COVID-19 patients in Wuhan, China, was about 5%.[14],[36] Oxley et al.[37] reported five cases of large-vessel stroke in COVID-19 patients younger than 50 years of age, who presented to the health system in New York City. Stroke may have been caused due to coagulopathy and vascular endothelial dysfunction.

Venous thromboembolism due to coagulation abnormalities

Coagulopathy is known to occur in the majority of patients who die of COVID-19. The incidence of venous thromboembolism in ICU patients with COVID-19 is 25%.[38] Al-Ani et al. (2020)[39] conducted a scoping review on thrombosis and coagulopathy in COVID-19 patients including in critically ill COVID-patients. A diagnosis of deep-vein thrombosis upon ICU admission adversely affected the duration of ICU and hospital stay and hospital mortality. Excessive inflammation, platelet activation, endothelial dysfunction, and stasis play a role in the pathogenesis of venous thromboembolism.[40]


  Cardiovascular Involvement Worsens Clinical Outcomes Top


Acute cardiac injury has been consistently shown to be a strong negative prognostic marker in patients with COVID-19.[4],[14],[15],[41] The association between cardiac injury and mortality was analyzed in a cohort of 416 hospitalized patients with COVID-19.[41] A total of 82 patients (19.7%) had cardiac injury, and compared with patients without cardiac injury, these patients were older and had more comorbidities such as hypertension. Significantly greater proportions of patients with cardiac injury required mechanical ventilation than those without cardiac injury. Complications were also more common in patients with cardiac injury than those without cardiac injury and included acute respiratory distress syndrome, acute kidney injury, and coagulation disorders. Patients with cardiac injury had higher mortality than those without cardiac injury (51.2% vs. 4.5%; P < 0.001].


  Effect of Angiotensin-Converting Enzyme Inhibitor/angiotensin Receptor Blockers on Coronavirus Disease 2019 Top


Initial epidemiological studies reported hypertension to have a significantly higher hazard ratio for mortality in patients with COVID-19.[14],[42] Several hypotheses have been proposed regarding the net effect of angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) on COVID-19 infections. Positive effects include ACE2 receptor blockade, disabling viral entry into the heart and lungs, and an overall decrease in inflammation secondary to ACEI/ARB. Negative effects include upregulation of ACE2 receptors through a retrograde feedback mechanism.

Meng et al.[43] enrolled COVID-19 patients with hypertension to evaluate the effect of ACEI and ARB therapy. They observed that patients receiving ACEI or ARB therapy had a lower rate of severe disease. In addition, ACEI or ARB therapy increased CD3 and CD8 T cell counts in peripheral blood and decreased the peak viral load compared to other antihypertensive drugs. This evidence supports the benefit of using ACEIs or ARBs to potentially contribute to the improvement of clinical outcomes of COVID-19 patients with hypertension. A case-population study which analyzed data for 1139 cases and 11,390 population controls, did not observe an increased risk of COVID-19 with either ACEI (OR: 0.80, 0.64–1.00) or ARB (OR: 1.10, 0.88–1.37).[44]

The risks of discontinuing ACEI and ARBs are well recognized and as recommended by World Cardiology Associations,[45],[46] patients with COVID-19 should not stop these drugs at this point of time.


  Collateral Effects of Coronavirus Disease 2019 on Cardiovascular Care Top


The effective triage of patients with CVD has become difficult in the context of COVID-19 environment as health-care workers have to weigh the risk of bringing susceptible patients into the hospital environment versus the risk of delaying treatment or a needed procedure.

The COVID-19 pandemic has also stretched health-care resources causing many health-care institutions to curtail elective procedures. This has resulted in the inability to care for patients with structural heart disease in a timely fashion, potentially subjecting them to increased risk of cardiovascular complications including congestive heart failure and death.

Any delay in care for patients with acute conditions such as myocardial infarction or stroke is consequential because timely treatment may decrease the incidence of disability.[47] Using a commercial neuroimaging database covering 856 hospitals in the United States, Kansagra et al.[48] compared the mean daily stroke imaging counts per hospital in an ostensibly prepandemic 29-day period, with the mean daily stroke imaging counts per hospital in a 14-day period during the early pandemic. The collateral effect of COVID-19 was a decrease of approximately 39% in the number of patients who received evaluations for acute stroke between these two epochs.


  Strategic Considerations Top


In many settings in the world, due to concerns over growing resource constraints, cardiologists are compelled to make drastic changes to their clinical practices, delaying elective cases and altering therapeutic strategies in high-risk patients. All hospital systems will need to ensure preparedness for dealing with a large volume of COVID-19 patients, many of whom would need ICU care and/or acute cardiac care.

Several cardiology associations have issued consensus-based guidance to ensure that cardiac and stroke care including echocardiography, imaging, electrophysiology, emergency care, cardiac revascularization, and cardiac surgery needs of people are effectively addressed within the context of the COVID-19 burden.[49],[50],[51],[52],[53],[54],[55],[56],[57] Guidance have been issued on the management of acute coronary syndromes and other cardiac manifestations.[58] Guidance is also available on re-organization of acute coronary syndrome networks, in-hospital emergency rooms, cardiac units, and catheterization laboratories to effectively handle the cardiovascular burden of COVID-19.

Key general points in these consensus-based guidance documents include the following:

  1. It is advised that cardiology consults be completed without a face-to-face visit by reviewing charts and monitoring data, to postpone nonurgent procedures and to increase the use of telehealth
  2. Specific guidance is available on how to triage patients in need of cardiovascular interventions and how to decide when it may be appropriate to proceed or postpone interventions. Some of the guidelines also deal with procedural issues and considerations for the function of heart/stroke/vascular teams during the COVID-19 pandemic
  3. Cardiovascular teams are advised to develop and rehearse context-specific protocols for rapid diagnosis, triage, isolation, and management of COVID-19 patients with cardiovascular complications. Rapid triaging and management of COVID-19 patients needing cardiovascular care is stressed, to allow efficient utilization of health-care resources, to minimize exposure to caregivers and prevent delays in delivering acute cardiac and stroke care
  4. Emphasis is placed on avoiding unwarranted diagnostic tests (e.g., cardiac troponin and echocardiography) to minimize unwarranted downstream diagnostic/therapeutic procedures which would further strain the already-stretched health-care resources and subject caregivers to the added risk of exposure to the infection
  5. Clinicians caring for COVID-19 patients are advised to be fully aware of the potential cardiovascular side effects of various therapies used for treating SARS-CoV-2 including chloroquine/hydroxychloroquine and azithromycin. Monitoring of QT interval is recommended, in patients with hepatic or renal dysfunction and in those receiving another drug with potential to prolong QT interval
  6. All health-care workers are advised to don personal protective equipment when dealing with any patients with suspected COVID-19. They are advised to have a high degree of suspicion for COVID-19 in any patient they interact within the hospital or outpatient setting, to take a travel history and assessment of contact with individuals/family members who were sick. Health workers are advised to take immediate steps to isolate patients with fever, cough, and upper respiratory symptoms and carry out tests for SARS-CoV-2. Recommendations have also been issued on measures for the protection of health-care providers involved with invasive cardiovascular procedures
  7. Doctors, nurses, and other health workers are encouraged to remain aware of their mental health and well-being needs and seek the right support as the health workforce is increasingly vulnerable to burnout, work-related fear of infection and stress, and mental illness during the pandemic.



  Future Directions Top


Rapidly aging populations and the growing global burden of CVD present a fertile substrate for the highly contagious SARS-CoV-2 virus, threatening global health security. A large number of patients with COVID-19 are bound to present with the preexisting CVD or develop new-onset cardiac dysfunction during the course of the illness. Future studies need to provide high-quality data on the incidence, prevalence, clinical manifestations, outcomes, and therapeutic modalities for CVD in the context of COVID-19. The diagnostic, therapeutic, and public health challenges posed by the concurrence of these two illnesses cannot be addressed without new knowledge. All stakeholders of global health security have a shared responsibility to support research that generates new and deeper insights on the mechanisms responsible for the interplay between CVD and COVID-19.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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