|Year : 2022 | Volume
| Issue : 1 | Page : 5-10
Acute coronary syndrome in COVID-19: Obstacles and management challenges
Anas Mohmoud Musa1, Omar Yousef Al-Assaf2, Nouha Azaza2, Rahaf Wardeh2, Reem Ahmad Awad2
1 Department of Cardiology, Rashid Hospital, Dubai, United Arab Emirates
2 Department of Internal Medicine, Rashid Hospital, Dubai, United Arab Emirates
|Date of Submission||10-Jun-2021|
|Date of Decision||15-Nov-2021|
|Date of Acceptance||16-Nov-2021|
|Date of Web Publication||25-Mar-2022|
Omar Yousef Al-Assaf
Department of Internal Medicine, Rashid Hospital, Dubai
United Arab Emirates
Source of Support: None, Conflict of Interest: None
Introduction: Severe Acute Respiratory Syndrome Coronavirus has caused a pandemic in 2019 causing a significant increase in mortality. Varied cardiac manifestations have been reported and variety of management plan used in different parts of the world. Methodology: A review process using PubMed and Google scholars was conducted for articles reporting any cardiac disease in SARS-CoV-2 and SARS-CoV patients. Discussion: In this review, we focus the discussion on diagnosis and management of acute coronary syndrome and its association with COVID-19. In addition to ways improving patient care in such diseases.
Keywords: Acute coronary syndrome, COVID, sudden death
|How to cite this article:|
Musa AM, Al-Assaf OY, Azaza N, Wardeh R, Awad RA. Acute coronary syndrome in COVID-19: Obstacles and management challenges. Hamdan Med J 2022;15:5-10
|How to cite this URL:|
Musa AM, Al-Assaf OY, Azaza N, Wardeh R, Awad RA. Acute coronary syndrome in COVID-19: Obstacles and management challenges. Hamdan Med J [serial online] 2022 [cited 2022 May 28];15:5-10. Available from: http://www.hamdanjournal.org/text.asp?2022/15/1/5/340815
| Introduction|| |
Since the World Health Organisation announcement of a coronavirus pandemic and naming of the associated disease as coronavirus disease 2019 (COVID-19), caused by the new virus strain labelled as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), associated cardiac manifestations have been frequently reported.,,,, Many published researches reported variable cardiovascular manifestations with arrhythmic and non arrhythmic presentations.,, The development of acute coronary syndrome (ACS) is further associated with increased mortality due to the challenges posed by infection control policies, patient's factors and the pathophysiology of COVID-19. In this article, we discussed the obstacles and challenges in management challenges caused by COVID-19 infection. In addition, we discuss ways to improve ACS care to reduce morbidity and mortality and to avoid unnecessary exposure to the virus preventing the spread of infection to staff.
| Methodology|| |
A review process using the electronic database of published articles in PubMed and Google scholars to search for articles reporting any cardiac disease in SARS-CoV-2 and SARS-CoV patients was performed. The articles published prior to 1st January 2021 in the English language were taken. After which the articles were grouped into several groups and the review analysis was done accordingly; COVID and chest pain, ST-elevated myocardial infarction (STEMI), non-ST-elevated myocardial infarction (NSTEMI) and sudden death.
| Acute Coronary Syndrome Clinical Presentation in Coronavirus Disease 2019|| |
Pain is very common in patients with COVID-19 being present in nearly 70%, of which 25% is chest pain, and it was a primary symptom in 46.6%. Another report quoted chest tightness in 35.7% of patients. There is a wide range of differential diagnosis of chest pain associated with COVID-19 [Table 1]. It could be related to pleurisy, pulmonary emboli, pericarditis, myocarditis or myocardial infarction.,, It is important to differentiate chest pain due to pleurisy, which can be the first presentation of COVID-19 and indicate either viral pleurisy or pulmonary embolism (PE), with unstable angina particularly in patients with high cardiovascular risks. There are few cases reported with pleurisy as the first manifestation of COVID-19 and it was diagnosed by the characteristic of the pain, being lateralized sharp agonizing pain that is aggravated by breathing, in the absence of other possible causes of chest pain including acute cardiac insult and PE.,, Pericarditis can obscure the diagnosis further as cases of COVID-19 present atypically with chest pain without fever or other respiratory symptoms due to pericarditis.,
|Table 1: Differential diagnosis of elevated troponin in coronavirus disease 2019|
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As patients with ACS-NSTEMI usually present with chest pain and elevated troponin with the characteristic electrocardiogram (ECG) changes of ST-depression and T-wave changes; myocardial injury and myocarditis associated with COVID-19 can pose difficulty in diagnoses and management. Troponin rise with ECG changes can be found in cases of PE, myocarditis or acute myocardial infarction (AMI). Although the presentation of PE usually is known, PE in COVID-19 presents atypically. The available literature suggests a high index of suspicion, particularly in critically ill with pleuritic chest pain, higher D-dimer or disproportionate elevation in comparison to ferritin, later deterioration with atrial fibrillation, hypotension, right ventricular strain or desaturation.,, Myocarditis is another possible obstacle being presenting with chest pain, heart failure and arrhythmia. The literature of COVID-19-related myocarditis suggests three main courses of presentations as subclinical with atypical symptoms, the symptomatic clinical presentation with fatigue and dyspnoea with or without exertional chest pain or chest tightness, and deteriorating course showing tachycardia and overt heart failure with cardiogenic shock.,,,,,,
Careful utilization and clinical interpretation of cardiovascular imaging with ECG, transthoracic echocardiography, cardiac magnetic resonance (CMR), cardiac-computed tomography (CT) angiogram and CT-pulmonary angiogram can alleviate these obstacles and help optimising patient care [Table 2] and [Figure 1].,
|Table 2: Usefulness of cardiovascular imaging and their interpretation in coronavirus disease 2019|
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|Figure 1: Illustration of findings and their interpretation in COVID-19 on cardiovascular imaging with electrogram, transthoracic echocardiography, cardiac magnetic resonance and endomyocardial biopsy|
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| Characteristics of ST-elevated Myocardial Infarction in Coronavirus Disease 2019|| |
The diagnosis of STEMI in COVID-19 patients did not change much as it might be the primary presentation of COVID-19; although some patients developed STEMI while in hospital. Many reports have marked out the delay in the management of these patients and mostly is due to regional and local infection control policy and guidelines. A pan- London heart attack group review reported a 5 - 23 minute delay in the ambulance response time and 21% reductions in STEMI admissions. Another report from Poland has concluded an absolute reduction in both acute and elective interventional procedures during 2020 compared to the prepandemic year of 2019. A report from China concluded reductions in STEMI patients' access to care, increased mortality and heart failure and changes in reperfusion strategies.
Although the presenting symptoms can include chest pain associated with ST elevation in the ECG, there is an increasingly reported high clot burden., The pathophysiology of STEMI associated with COVID-19 is attributed to underlying atherosclerotic cardiovascular disease as evidenced by a multicentre report from Italy identifying four major cardiovascular risks present in these patients like dyslipidaemia, hypertension, smoking and diabetes. Another possible mechanism leading to STEMI in COVID-19 is that; SARS-CoV2 use angiotensin-converting enzyme-2 receptor, presenting in the endothelium of vasculature, for cellular invasion, can lead to plaque instability and rupture and or can increase the myocardial oxygen demand causing type-2 myocardial infarction. A recent report found that patients with STEMI have higher troponin, elevated dimer and C-reactive protein levels, lower lymphocyte count, as well as increased coronary thrombosis that might point to a hyper-coagulable state that is well known associated with COVID-19.
Current clinical guidelines recommend rapid perfusion therapy to patients with STEMI either primary percutaneous intervention or fibrinolysis and set door to balloon and door to needle targets. However, there is a continuous delay in performing timely STEMI management due to the COVID-19 pandemic as reported in the literature. Hamadeh A et al.have reported in a multicentre study that there is a delayed door to balloon at a median of 128 min while maintaining door to needle time at a median of 27 min with fibrinolysis predominance in 76% of cases. Moreover, it was also found that patients in the fibrinolysis arm have a better outcome and reduced mortality and in-hospital morbidity compared to those in the percutaneous coronary intervention arm. Higher stent thrombosis and re-infarction despite standard management of STEMI with dual antiplatelet therapy and addition of an intravenous glycoprotein IIA-IIIB inhibitor whenever required as per the current STEMI guidelines is increasingly reported and has led to the conclusion of requirement to adjust antiplatelet therapy with anticoagulation.,, There were initial concerns regarding increased myopathy and renal complications with concomitant use of statin and COVID-19 with many reports suggesting that starting statin therapy in critically ill patients might increase renal complications and thus mortality., However, later new research concluded a mortality benefit with statin especially in diabetic patients with COVID-19.,
| Diagnoses and Management of Non-ST-elevated Myocardial Infarction in Coronavirus Disease 2019|| |
COVID-19 pandemic has resulted in an unexpected major decline in presentations of AMI. It is hypothesised that several personal, social, clinical and environmental factors contributed to this decline. Of these, patients' avoidance to seek medical services concerned about contracting COVID-19, focus on COVID-19 awareness lead to misinterpreting chest symptoms as pulmonary related, postponement of seeking needed medical care and interventions for AMI by a threefold from the onset of symptoms to revascularisation after hospital discharge due to COVID-19 protocols, reduction in stressors in life as individuals remained on 'lockdown', and reducing triggers of AMI.,, In addition to changes in air pollution and reductions in exposure to pollution, specifically nitric oxide, in the air during the lockdown phase may explain the reductions in NSTEMI presentations.
The challenge facing physicians in diagnosing AMI associated with COVID-19 infection happens because some patients present with clinical syndrome and ECG changes of myopericarditis mimicking ACS, resulted in an increased number of false-positive ACS calls. In addition, troponin elevations have been observed in hospitalised COVID-19 patients, even without chest pain, with fulminant myocarditis reported as accountable for up to 7% of deaths related to COVID-19-making the discrimination more difficult. The presentation of ACS associated with SARS-CoV-2 is characterised by a high percentage of cardiac arrest on admission, the incidence of no-reflow and in-hospital mortality as reported in the literature.
As the elevation of cardiac troponin can be associated with COVID-19, the management should be individualised according to the clinical presentation. Thus, when the syndrome is typical of infective COVID-19-specific cardiology input, targeted ACS treatment, or invasive angiography is of no need. However, left ventricle function assessment can be of prognostic value in patients with high-risk, yet routine studies should be avoided to reduce the risk of transmission in compliance with local infection control policies. Therefore, bedside echocardiography should be offered for those patients with a clear clinical indication; clinical heart failure or valvular disease suspicion, especially if it can be of value to the management plan.
In the context of AMI with COVID-19 presenting as typical of ACS, standard management should be given for stable patients, regardless of COVID-19 status; pharmacological therapy initiation and transfer to a catheterization lab. The timing for invasive management should be guided by the patient's COVID-19 status and infectivity as in acute viral symptoms with high fever, cough, and sepsis. Thus, delaying the procedure until such markers are settled will be safer for staff and should also theoretically reduce immediate procedural complications, for example stent thrombosis.
Patients with raised cardiac biomarkers, high-risk ECG features or regional ventricular abnormalities on echocardiography should be offered invasive angiography before discharge. Early conservative discharge on medical therapy alone would reduce hospital stay but holds a considerable risk of re-infarction. Moreover, a good number of patients will be unwilling to seek hospital attention because of fears of acquiring COVID-19, early medical discharges could pose a higher mortality risk during the pandemic. Management of very high risk NSTEMI should be similar to STEMI, but it's wise for high risk NSTEMI cases to be tested for COVID19 before subjecting them to coronary angiography. Moreover, patients with intermediate risk NSTEMI could be evaluated noninvasively with CCTA if feasible. In such cases and to reduce the risk of infection among the staff, the addition of CCTA protocol to thorax CT scan performed will be of great benefit.
It is reported that more AMI patients during the outbreak had complications in their hospital course and had worse clinical outcomes due to treatment delay, which was attributed to a lack of public education and COVID-free hospitals. These were necessary to overcome patients' fear of seeking healthcare services and might be the reason behind the increased risk of major adverse coronary events.,,,,,,, Another reason for the significantly higher incidence of in-hospital mortality could be attributed to old age and multiple co-morbidities, as compared to non-COVID-19 counterparts with AMI. It was found that patients with ACS and COID 19 had a high prevalence of occluded artery and no-reflow phenomenon, suggesting a high thrombotic burden leading to higher complications and mortality.
| Sudden Cardiac Death in Coronavirus Disease 2019|| |
Since the start of the pandemic in December 2019, there is a higher incidence of out of hospital cardiac arrest (OHCA) in comparison to the same times in prepandemic years which have been linked to many factors including the infection's controls policies of lockdown and limitations to access for elective management, as well as due to COVID-19 itself. An Italian report has quoted a 58% increase in the prevalence of OHCA in the year 2020 compared to 2019. A French population survey has reported a maximum weekly cumulative incidence increase from 13.42 to 26.64 per million inhabitants.
Nevertheless, in-hospital sudden cardiac death (SCD) associated with COVID-19 is being reported interestingly in stable patients despite improvement of their clinical condition and attributed to many reasons. An autopsy and review report from Houston, Texas, and other American cities support a multi organ induced direct viral injury including the heart with frequently reported lymphocytic infiltrates in the myocardium and pericardium. Shirazi et al., reported 3 cases of SCD occurred while their general conditions are improving and suggested direct viral myocardial involvement, arrhythmic event, cytokine storm, or adverse drug effects as possible causes. Murt A, and his colleagues blamed the use of hydroxychloroquine in 2 dialysis patients to cause SCD of their patients.
On the other hand, SCD occurs in very sick patients, is relatively common and many mechanisms are proposed. Myocarditis, cardiac tamponade, ACS, drugs related QTs prolongation and arrhythmogenesis, electrolytes abnormalities, severe hypoxia, high grade inflammatory response, and co-agulopathy; are the most common causes., The risks of SCD increase in patients with elevated Troponin-C, presence of medical co-morbidities especially cardiovascular disease and hypertension, genetic predisposition, and associated use of face mask during exercise particularly strenuous exercises.,,,, Giudicessi et al., found a potential pro-arrhythmic genetic variant (p. Ser1103-Tyr-SCN5A) in 1/4th of African-American that has potential to increase the risks of fatal arrhythmia derived by hypoxia and drugs. Lee et al., hypothesized that exercise with facemasks can induce hypoxia and hypercapnia leading to increased adrenergic stimulation and oxidative stress that promote arrhythmias through re-entry or nonre-entry ways.
There is no enough evidence to support specific recommendations to prevent SCD in COVID-19, but knowledge and thus treatment of the known risk factors associated with arrhythmia which is the main drive for SCD can help reduce this deadly complication. The general management of SCD in patients with Long QTc, Brugada, cardiomyopathies and those at high risks for SCD would be a reasonable modality till further evidence becomes available as suggested by Yamin M and Demili AU.
| Conclusion|| |
The challenges of diagnosis of ACS in COVID-19 are due to similar and sometimes atypical presentations of associated underlying myocardial or pulmonary disease implicated by COVID-19. Careful and clinically directed use of CMR and cardiac CT is very helpful in the diagnosis and management specifically in patients with suspected myocardial infarction and myocarditis. Anticoagulation and antiplatelet therapy need to be re-evaluated, especially in patients presenting with AMI and COVID-19 due to associated higher thrombus burden. The abundant use of fibrinolysis in patients presenting with COVID-19 appears to be safe with good clinical outcome in comparison with cardiac intervention and reduce staff exposure. Further studies are needed to evaluate whether the paradigm of standard management of ACS could be changed in reference to optimising antiplatelet therapy and use of fibrinolysis as first choice in COVID-19 patients.
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Conflicts of interest
There are no conflicts of interest.
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[Table 1], [Table 2]