COVID-19-associated myocardial infarction
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Haddadi, M.D.[2]
Synonyms and keywords: Novel coronavirus, covid-19, COVID-19, SARS-CoV-2, Wuhan coronavirus, myocardial infarction, MI, Acute coronary syndrome, ACS
Overview
COVID-19 patients with cardiovascular comorbidities have higher mortality. According to a recent systematic review and meta-analysis,acute cardiac injury with troponin levels greater than 28 pg/ml was detected in 12.4% of confirmed COVID-19 patients.[1] Acute Myocardial Infarction is defined as an acute myocardial injury with clinical evidence of acute myocardial ischemia plus rise and/or fall of cardiac troponin values with at least one value above the 99th percentile upper reference limit and at least one of the following:Symptoms of myocardial ischemia including new ischemic ECG changes, development of pathological Q waves, imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischemic etiology. Identification of a coronary thrombus by angiography or autopsy (not for type 2 or 3 MI).[2]
Classification
Myocardial infarction may be classified according to two subtypes:
- Non ST Elevation Myocardial Infarction (non-STEMI)
- ST Elevation Myocardial Infarction (STEMI)
ST-Elevation Myocardial Infarction (STEMI) and COVID-19:
A US model from 9 major centers showed a 38% drop in total STEMI activations during the COVID-19 pandemic. There is a 40% reduction noted in Spain as well. there was also a delay between the first presentation to a medical encounter up to 318 min. This is important since COVID-19 can potentially be a cause of STEMI through microthrombi, cytokine storm, coronary spasm, or direct endothelial injury.[3][4]
- Potential etiologies for the reduction in STEMI PPCI activations:
- avoidance of medical care due to social distancing or concerns of contracting COVID-19 in the hospital
- STEMI misdiagnosis
- increased use of pharmacological reperfusion due to COVID-19
It is very important to realize if patients' anxiety is the reason behind decreasing the presentation of STEMI to U.S. hospitals.[5][2]
- Treatment of STEMI & COVID-19: The specific protocols for the treatment have been evolving. Early recommendations showed intravenous thrombolysis as first-line therapy for STEMI patients with confirmed COVID-19 since most hospitals do not have protected cardiac catheterization labs.[3]
Pathophysiology
The mechanism of COVID-19 cardiovascular injury has not been fully understood and is likely multifactorial.
- The cytokine release caused by the virus may lead to vascular inflammation, plaque instability, myocardial inflammation, a hypercoagulable state, or direct myocardial suppression. For hypercoagulable state in COVID-19, click here
- increased inflammatory response may also lead to endothelial dysfunction causing the microthrombi formation.[6]
- ACE-2 is the receptor of SARS-CoV 2 which is highly expressed on cardiac pericytes. Therefore it can be speculated that the pericyte damage by the virus results in endothelial cell damage which at the end leads to microvascular impairment.[7]
- This video shows plaque rupture or disruption of the atherosclerotic plaque in the mid left anterior descending artery (LAD) .
Pathological changes:
- In the level of cardiac tissue: findings include a range of minimal change to interstitial inflammatory infiltration and myocyte necrosis
- In the level of vasculature: micro-thrombosis and vascular inflammation[8]
Causes
According to the Fourth Universal Definition of MI, there are two clinical classifications of the disease based on the causes:
- Type 1: MI caused by acute atherothrombotic CAD precipitated by atherosclerotic plaque disruption (rupture or erosion).
- Type 2: MI due to a mismatch between oxygen demand and supply, possible causes are hypotension due to septic state and hypoxemia due to respiratory failure
Most of the MIs associated with COVID-19 are type 2 indicating the causes to be the primary infection, hemodynamic disturbance, or respiratory deterioration.[2] [9][6]
Differentiating Myocardial infarction from other Diseases
Differentiating ST Elevation Myocardial Infarction from other Diseases
Differentiating Unstable Angina/Non-ST Elevation Myocardial Infarction from other Disorders
Epidemiology and Demographics
- Hospitalized patients with COVID-19 and Cardiovascular disease seem to be more prevalent in both the USA and China. [8]
- Studies have shown reduction of incidence and hospitalization of acute MI during COVID-19 Pandemic.[10][5][11][12]
- A study in Italy showed up to a 49.4 percent reduction in admissions for acute MI to coronary care units from March 12th to 19th in 2020 compared to the equivalent time in 2019. [10]
Prognosis
In a case series with 187 patients who had confirmed COVID-19, 27.8% of patients had a myocardial injury, which caused cardiac dysfunction and arrhythmias. The result was significantly higher mortality among patients with myocardial injury. It seems to be advisable to triage patients with COVID-19 based on their underlying CVD for a more aggressive treatment plan. The mortality during hospitalization was shown to be 7.62% for patients without underlying CVD and normal TnT levels, 13.33% for those with underlying CVD and normal TnT levels, 37.50% for those without underlying CVD but elevated TnT levels, and 69.44% for those with underlying CVD and elevated TnTs.[4]
Diagnosis
History and Symptoms
- Substernal chest pain
- Occurs at rest or exertion
- Radiation to neck, jaw, left shoulder and left arm
- Aggravated by physical activity and emotional stress
- Relieved by rest, nitroglycerin or both
- Chest discomfort described crushing, squeezing, burning, choking, tightness or aching
- Dyspnea
- Diaphoresis
- Nausea and vomiting
- Fatigue
- Syncope[13]
Laboratory Findings
Unstable angina / non ST elevation myocardial infarction biomarkers
ST elevation myocardial infarction laboratory findings
Imaging
Treatment
In patients with ACS, and COVID-19, treatment should follow the guidelines of the updated Society for Cardiovascular Angiography and Interventions.[8] [14]
References
- ↑ Nasiri, Mohammad Javad; Haddadi, Sara; Tahvildari, Azin; Farsi, Yeganeh; Arbabi, Mahta; Hasanzadeh, Saba; Jamshidi, Parnian; Murthi, Mukunthan; Mirsaeidi, Mehdi (2020). doi:10.1101/2020.03.24.20042903. Missing or empty
|title=(help) - ↑ 2.0 2.1 2.2 Thygesen K, Alpert JS, Jaffe AS, Chaitman BR, Bax JJ, Morrow DA; et al. (2018). "Fourth Universal Definition of Myocardial Infarction (2018)". J Am Coll Cardiol. 72 (18): 2231–2264. doi:10.1016/j.jacc.2018.08.1038. PMID 30153967.
- ↑ 3.0 3.1 Ullah W, Sattar Y, Saeed R, Ahmad A, Boigon MI, Haas DC; et al. (2020). "As the COVID-19 pandemic drags on, where have all the STEMIs gone?". Int J Cardiol Heart Vasc. 29: 100550. doi:10.1016/j.ijcha.2020.100550. PMC 7261452 Check
|pmc=value (help). PMID 32550258 Check|pmid=value (help). - ↑ 4.0 4.1 Guo T, Fan Y, Chen M, Wu X, Zhang L, He T; et al. (2020). "Cardiovascular Implications of Fatal Outcomes of Patients With Coronavirus Disease 2019 (COVID-19)". JAMA Cardiol. doi:10.1001/jamacardio.2020.1017. PMC 7101506 Check
|pmc=value (help). PMID 32219356 Check|pmid=value (help). - ↑ 5.0 5.1 Garcia S, Albaghdadi MS, Meraj PM, Schmidt C, Garberich R, Jaffer FA; et al. (2020). "Reduction in ST-Segment Elevation Cardiac Catheterization Laboratory Activations in the United States During COVID-19 Pandemic". J Am Coll Cardiol. 75 (22): 2871–2872. doi:10.1016/j.jacc.2020.04.011. PMC 7151384 Check
|pmc=value (help). PMID 32283124 Check|pmid=value (help). - ↑ 6.0 6.1 Montone, Rocco A; Iannaccone, Giulia; Meucci, Maria Chiara; Gurgoglione, Filippo; Niccoli, Giampaolo (2020). "Myocardial and Microvascular Injury Due to Coronavirus Disease 2019". European Cardiology Review. 15. doi:10.15420/ecr.2020.22. ISSN 1758-3764.
- ↑ Xiong, Chenglong; Feng, Yi; Chen, Mingquan; Li, Xiangjie; Chen, Liang (2020). "The ACE2 expression in human heart indicates new potential mechanism of heart injury among patients infected with SARS-CoV-2". Cardiovascular Research. 116 (6): 1097–1100. doi:10.1093/cvr/cvaa078. ISSN 0008-6363.
- ↑ 8.0 8.1 8.2 Kang Y, Chen T, Mui D, Ferrari V, Jagasia D, Scherrer-Crosbie M; et al. (2020). "Cardiovascular manifestations and treatment considerations in covid-19". Heart. doi:10.1136/heartjnl-2020-317056. PMC 7211105 Check
|pmc=value (help). PMID 32354800 Check|pmid=value (help). - ↑ Template:Cite website
- ↑ 10.0 10.1 De Rosa S, Spaccarotella C, Basso C, Calabrò MP, Curcio A, Filardi PP; et al. (2020). "Reduction of hospitalizations for myocardial infarction in Italy in the COVID-19 era". Eur Heart J. 41 (22): 2083–2088. doi:10.1093/eurheartj/ehaa409. PMC 7239145 Check
|pmc=value (help). PMID 32412631 Check|pmid=value (help). - ↑ Solomon MD, McNulty EJ, Rana JS, Leong TK, Lee C, Sung SH; et al. (2020). "The Covid-19 Pandemic and the Incidence of Acute Myocardial Infarction". N Engl J Med. doi:10.1056/NEJMc2015630. PMID 32427432 Check
|pmid=value (help). - ↑ De Filippo O, D'Ascenzo F, Angelini F, Bocchino PP, Conrotto F, Saglietto A; et al. (2020). "Reduced Rate of Hospital Admissions for ACS during Covid-19 Outbreak in Northern Italy". N Engl J Med. doi:10.1056/NEJMc2009166. PMC 7224608 Check
|pmc=value (help). PMID 32343497 Check|pmid=value (help). - ↑ Abidov A, Rozanski A, Hachamovitch R, Hayes SW, Aboul-Enein F, Cohen I; et al. (2005). "Prognostic significance of dyspnea in patients referred for cardiac stress testing". N Engl J Med. 353 (18): 1889–98. doi:10.1056/NEJMoa042741. PMID 16267320. Review in: Evid Based Med. 2006 Jun;11(3):91
- ↑ Szerlip M, Anwaruddin S, Aronow HD, Cohen MG, Daniels MJ, Dehghani P; et al. (2020). "Considerations for cardiac catheterization laboratory procedures during the COVID-19 pandemic perspectives from the Society for Cardiovascular Angiography and Interventions Emerging Leader Mentorship (SCAI ELM) Members and Graduates". Catheter Cardiovasc Interv. doi:10.1002/ccd.28887. PMID 32212409 Check
|pmid=value (help).