ST Segment Elevation Myocardial Infarction in the COVID-19 Era: Appraisal of the Evidence

  • Clinical Medicine & Research
  • March 2022,
  • 20
  • (1)
  • 52-60;
  • DOI: https://doi.org/10.3121/cmr.2021.1707

Abstract

The COVID-19 pandemic continues to present a public health challenge and has had a significant impact on the presentation, time-dependent management, and clinical outcomes of ST elevation myocardial infarction (STEMI). Patients with COVID-19 and pre-disposing cardiovascular risk factors like hypertension, hyperlipidemia, and diabetes mellitus are at a higher risk of developing STEMI, and global trends have highlighted delayed management of STEMI, which may contribute to worse clinical outcomes. Prolonged time to intervention has also resulted in an increased rate of no reflow, which is an independent risk factor for worse outcomes in these patients. Timely primary percutaneous coronary intervention (PCI) remains standard of care for STEMI and can be attained within the recommended 90 minutes timeline from hospital presentation. A coordinated, safe, standardized, algorithmic approach among emergency medical services, emergency departments, and cardiac catheterization laboratory is needed to ensure optimal patient outcome during and after the COVID-19 pandemic. The focus of this case report is to highlight the challenges of PCI for ST elevation myocardial infarction in the COVID-19 era.

Keywords:

Primary percutaneous coronary intervention (PCI) is the recommended strategy to achieve reperfusion in the management of acute ST elevation myocardial infarction (STEMI).1 Patients exhibiting cardiac symptoms such as chest pain, shortness of breath, and lightheadedness should present to the emergency department (ED) in a timely manner. To achieve optimal clinical outcomes, the time from presentation to the ED to reperfusion should be less than 90 minutes.1 Infection with SARS-CoV-2, the virus that causes the coronavirus disease-2019 (COVID-19) affects diverse organ systems, including the cardiovascular system, and can precipitate STEMI.2 The SARS-CoV-2 virus triggers systemic inflammation that may result in the development of myocardial infarction (MI). Additionally, COVID-19 is associated with hypercoagulability and extensive microvasculopathy;3 thus, the occurrence of ST segment infarction in the context of a patient with COVID-19 can present a real challenge to the cardiologist. We present a case of a patient who had STEMI during the COVID-19 pandemic, and we discuss practical considerations for the diagnosis and treatment of patients with this cardiovascular emergency and concurrent COVID-19.

Case Presentation

A 70-year-old Hispanic man with a past medical history of hypertension, hyperlipidemia, type II diabetes mellitus, peripheral artery disease, and coronary artery disease (CAD) treated with a mid-left anterior descending artery (LAD) stent was brought to the ED by emergency medical service (EMS). The patient reported he had been in his usual state of health until the morning prior to presentation, when he developed throat pain and after several hours developed moderately intense retrosternal chest discomfort radiating up to his throat. His chest discomfort persisted, which prompted his wife to call EMS later in the day. He denied any preceding or associated fever, nasal congestion, cough, palpitations, shortness of breath, orthopnea, leg swelling, diaphoresis, dizziness or syncope, or contact with anyone with COVID-19, but his wife added that he had been looking fatigued for several days prior to presentation. His initial vital signs showed an elevated blood pressure of 240/100 mmHg, heart rate of 60 beats per minute, and respiratory rate of 20 cycles per minute. His oral temperature was 36.5°C, his body mass index was 23.0 kg/m², and his oxygen saturation level was normal on room air. Initial laboratory analysis of blood and serum samples revealed an elevated level of high-sensitivity troponin I at 865 ng/L (normal range: 0–57 ng/L) upon admission that rapidly increased to > 25,000 ng/L after a repeat blood draw at 2 hours. Elevated total white blood cell count (WBC) of 12.1x103 cells/µL (normal range: 4–11.0x103 cells/µl) and absolute neutrophil count (13.6 x103 cells/µL [normal range: 1.9–8.1x103 cells/µl]) with a low lymphocyte count (0.6x103 cells/µL [normal range: 1.0–3.9x103 cells/µL]) suggested an active infection. The patient’s SARS-CoV-2 virus screen was positive for infection, and his D-dimer was elevated at 3,404 ng/mL [normal range: 190–499 ng/mL]. His renal and liver function as well as coagulation profile were within normal ranges. A chest radiograph showed bilateral diffuse interstitial infiltrates consistent with COVID-19 (Figure 1).

Showing diffuse interstitial infiltrates throughout both lungs slightly more dense on the right (arrows).
Figure 1.

Showing diffuse interstitial infiltrates throughout both lungs slightly more dense on the right (arrows).

Due to his significantly elevated blood pressure, the patient was given 10 mg of intravenous (IV) hydralazine and a single dose of oral nitroglycerin for chest discomfort. An urgent electrocardiogram (EKG) showed sinus rhythm with first-degree AV block and acute inferior wall ST segment elevation myocardial infarction (Figure 2). He immediately received a full dose of aspirin and a 5,000 unit bolus of IV heparin and was prepared for emergent cardiac catheterization.

Electrocardiogram of a patient with COVID-19 and STEMI. Note the first-degree sinus rhythm, AV block, and ST elevation involving the inferior leads (denoted with arrows).
Figure 2.

Electrocardiogram of a patient with COVID-19 and STEMI. Note the first-degree sinus rhythm, AV block, and ST elevation involving the inferior leads (denoted with arrows).

While preparing for transfer to the cardiac catheterization laboratory, the patient became bradycardic and developed a high degree AV block that degenerated into a complete heart block. The patient became hypotensive with a decreased blood pressure of 84/53 mmHg and dyspneic requiring 10 L of oxygen. He subsequently received preload support with 3 L of IV fluid boluses and was started on a regimen of dopamine and phenylephrine infusion per protocol. An urgent cardiac catheterization was performed under maximum sterile techniques, using appropriate personal protective equipment based on institutional protocols. Coronary angiography revealed a large caliber right coronary artery that was totally occluded with a distal thrombus before bifurcation that was stented after a door to balloon time of 2 hours 40 minutes from ED presentation. A patent mid-left anterior descending artery (LAD) stent and multiple non-obstructive CAD of other epicardial coronary vessels were also visualized during the cardiac catheterization. The patient had a successful thrombectomy and placement of a drug eluting stent. Post-stent thrombolysis in myocardial infarction (TIMI) grade 2 flow and tissue blush grade 1 suggested a no reflow. Post-procedural echocardiography showed an estimated ejection fraction of 57% with abnormalities in the basal, mid inferior wall, septal segments, and inferolateral segments, apical inferior segment, and mid inferolateral segments.

Following revascularization, the patient showed significant improvement in his cardiac symptoms and overall oxygen requirements. He was treated with guideline directed therapy with aspirin, clopidogrel, beta blockers, and high intensity statins, as well as optimal management of his risk factors. He remained in sinus rhythm throughout his hospitalization. The patient was also managed for severe COVID-19 with IV dexamethasone and remdesivir and was discharged home in good condition after 5 days of hospitalization.

Discussion

This case typifies the high-risk demographics, clinical characteristics, and delays in the management of acute STEMI in the COVID-19 era. Patients who are elderly, from ethnic minorities, and with pre-existing cardiovascular conditions such as hypertension, hyperlipidemia and diabetes mellitus, have been shown in different single and multicenter studies to be at higher risk of critical presentations of COVID-19 and adverse clinical outcomes.3–8

Incidence and Clinical Characteristics of STEMI in the COVID-19 Era

Since the outbreak of COVID-19 in December 2019, there has been a global downtrend in STEMI activations and STEMI-related hospitalizations.3,8–10 Garcia et al9 demonstrated decreasing STEMI activations of 38% [95% confidence interval (CI): 26% – 49%; P < 0.001] in nine high volume (> 100 PCIs/year) cardiac catheterization laboratories in the United States from January 1, 2019, to March 31, 2020, during the early phases of the COVID-19 pandemic compared to before the pandemic. This reduction was similar to a 40% reduction in STEMI observed by Rodríguez-Leor et al11 in a Spanish cohort of patients. In another retrospective analysis of cardiovascular presentations from 15 hospitals in northern Italy, STEMI, which accounted for 45.3% of all acute coronary syndrome hospitalization during the pandemic, had an average admission rate of 6.1/day in the COVID-19 era, which was statistically lower than the rate of 8.0/day during a comparable pre COVID-19 time.12 In an 8-week single center evaluation of STEMI during the COVID-19 era, Simon et al10 observed a weekly decrease of STEMI presentations by 51.4% (95% CI, 23.6% – 70.2%) and PCI referral by a factor of 42.8% (95% CI, 23.7% – 57.6%), for a total weekly decrease of 53.1% (95% CI, 27.7% – 70.1%) in cardiac laboratory activations for STEMI (Table 1).

View this table:
Table 1:

Showing studies on COVID-19 positive STEMI patients and their outcomes.

Besides reduction in STEMI activation, several other studies have also demonstrated delays in patient presentation and in-hospital management, specifically an increase in door to balloon time.10,13 A single center Chinese study by Tam et al8 published in March 2020 reported a 300% increase in time from cardiac symptom onset to hospital presentation, a 30% increase in door to device time, and a 60% increase in time from arrival to the cardiac catheterization laboratory to revascularization. However, a recent high-powered, international, multicenter, prospective observational study from the North American COVID-19 myocardial infarction (NACMI) registry revealed that 58% of COVID-19 positive patients with STEMI achieved the recommended < 90 minutes door-to-balloon time, with a median time of 79 minutes (interquartile range IQR: 52 – 125 min), which was lower than the 73% rate achieved in the pre-COVID-19 era with age and sex matched control patients (median time of 66 min; IQR: 46 to 93 min [P = 0.006]).4 This may indicate some improvement in door to balloon time during the later portion of the pandemic, but in general, most reports showed a longer door to balloon time.

Further review of the NCAMI registry study highlights parallels in the pre-existing cardiovascular risk factors and ethnic background of the high-risk group to our patient. From that study, COVID-19 positive STEMI patients were typically male (71%) and ranged in age between 56-75 years, which did not differ from the pre-COVID-19 era controls.4 However, baseline cardiovascular risk differed between the two groups: COVID-19 positive patients in the STEMI group had a higher frequency of diabetes (46% versus 28%, [P < 0.001]), lower proportion of CAD (24% versus 31%, [P = 0.045]), and a lower proportion of dyslipidemia (46% versus 60%, [P = 0.001]) compared to age- and sex-matched patients with STEMI in the pre-COVID-19 era.4 Like the index patient, a majority of COVID-19 positive patients in this study were ethnic minorities: Hispanics (23%), Blacks (24%), and Asian (6%). White/Causasian individuals comprised the remaining population at 39% (Figure 3A). This contrasted from the ethnic distribution of COVID-19 negative patients with STEMI who were mainly White (76%) with smaller populations of Black (10%), Hispanic (6%), and Asian (5%) patients (Figure 3B).4 Based on these results, we propose that STEMI occurs with a higher frequency in COVID-19 positive patients, though whether these conditions occur concurrently due to higher rates of SARS-CoV-2 transmission in these populations or in response to other factors is unclear.

(A) The demographic distribution of COVID-19 positive patients with STEMI from the North American COVID-19 myocardial infarction (NACMI) registry study.4 (B) The demographic distribution of COVID-19 negative patients with STEMI from the North American COVID-19 myocardial infarction (NACMI) registry study.4 Ethnic minorities [Black, Hispanic, Asian]
Figure 3.

(A) The demographic distribution of COVID-19 positive patients with STEMI from the North American COVID-19 myocardial infarction (NACMI) registry study.4 (B) The demographic distribution of COVID-19 negative patients with STEMI from the North American COVID-19 myocardial infarction (NACMI) registry study.4 Ethnic minorities [Black, Hispanic, Asian]

Patient-related factors noted to have likely contributed to delays in presentation include delays in health-seeking behavior due to public health restrictions, overall fear of COVID-19 exposure during transportation to hospitals for public commuters, dismissal of cardiac symptoms as benign in comparison with a higher risk of contracting the virus, hospital phobia exacerbated by intense media coverage of the virus, general health care avoidance to prevent disease exposure, or presentation to less crowded, low volume hospital facilities to minimize exposure risk.3,8–10,14 Health system-related factors that may contribute to delays are increased time for ED investigations, including patient triage, COVID-19 testing or imaging for risk stratification, lower emphasis on other cardiovascular diseases compared to COVID-19 during peaks of the pandemic, and additional time needed by health care providers to use personal protective equipment (PPE).3,8–10,14 Several other factors that might have contributed to a decline in incidence of STEMI in the COVID-19 era are restricted public movement and transition to an online platform for social activities, which may have resulted in fewer physical activities that might promote atherosclerotic plaque complication or rupture.14

Clinical presentation of STEMI in the setting of SARS-CoV-2 infection has been shown to be variable. A single center study in northern Italy by Stefanini et al15 found that in 85.7% of patients, STEMI represented the first clinical presentation of COVID-19, similar to our patient. About 78.6% of these patients presented with typical chest pain with or without dyspnea, while 21.4% presented with dyspnea without chest pain.15 Dyspnea was also a predominant presenting symptom in 54% of COVID-19 positive patients with STEMI who were analyzed in the NCAMI registry study, which differed from the 26% rate of dyspnea observed in COVID-19 negative patients with STEMI (P < 0.001).4 This may be related to the pathophysiology of SARS-CoV-2 infection which initially affects the lungs.16 Chest pain was the major complaint in 52% of COVID positive patients with STEMI in the NCAMI study, which differed from the 78% of COVID-19 negative patients with STEMI (P < 0.001),4 suggesting the possibility of other pathophysiological mechanisms responsible for STEMI in the context of COVID-19. Pre-PCI cardiogenic shock was observed with 18% of COVID-19 positive patients with STEMI, which differed from the 10% rate observed during the pre-COVID-19 era (P = 0.002). Cardiac arrest pre-PCI was observed in 11% of COVID-19 positive patients with STEMI, compared to 7% observed in the pre-COVID-19 era (P = 0.095).4 These high-risk cohort of COVID-19 positive patients presenting with complicated STEMI may end up requiring mechanical circulatory support and higher levels of care which further complicates their management and clinical outcome.

Pathogenicity and Pathophysiologic Mechanisms of STEMI in COVID-19 Patients.

Acute myocardial injury in COVID-19 patients may result from several recognized indirect and direct pathogenic mechanisms including systemic inflammatory response syndrome, also known as cytokine storm,17,18 myocarditis,19 hypoxic injury,20 stress or Takotsubo cardiomyopathy,21 ischemic injury caused by small vessel vasculitis, and cardiac or microvascular dysfunction from microemboli and endotheliitis.22,23 Other additional mechanisms include epicardial coronary artery disease atherosclerotic plaque disruption, demand ischemia, and right heart strain resulting from pulmonary embolism and adult respiratory distress syndrome or pneumonia.23–26 Recognized direct mechanisms of cardiac injury from COVID-19 include viral myocarditis resulting in myocardial death and inflammation, as well as indirect mechanisms like cardiac stress due to respiratory failure. Hypoxemia and cardiac inflammation secondary to severe systemic hyper-inflammation have also been described.17–23 The resultant myocardial injury can manifest as cardiac or respiratory symptoms, elevated levels of cardiac injury biomarkers (cardiac troponin I and brain-type natriuretic peptide), acute MI, arrhythmias, and heart failure symptoms.16

SARS-CoV-2 has been shown to penetrate infected cells through the angiotensin-converting enzyme (ACE) 2 receptor, a membrane bound carbioxypeptidase that converts angiotensin II into angiotensin.16 This enzyme is homologous to ACE, but it has a crucial role in cardiovascular hemostasis and is highly expressed in the lungs and heart.16,28,29 The resultant invasion of the alveolar epithelial cells via the ACE2 receptor at the initial phase of infection leads to respiratory symptoms that might proceed with cardiac manifestations as observed in 54% of patients.4 The resulting local and systemic inflammation and low cell counts triggered by the infection, as well as imbalanced host response that leads to respiratory dysfunction and hypoxemia, may also contribute to myocardial damage.16,28,29 This relationship between viral entry and ACE 2 forms the basis of the argument against the use of renin-angiotensin-aldosterone system antagonists, which have been shown in animal studies to increase ACE 2 expression and could theoretically increase susceptibility to infection.26,28 However, this adverse association between ACE2 antagonist use and increased susceptibility has not been proven. Several studies have shown that ACE inhibitors are clinically safe to use in patients with COVID-19, and recommendations from several clinical guidelines are to continue this class of medication for management of cardiovascular disease, although we acknowledge that discontinuation of these medications might be necessary for patients with contraindications like hypotension or acute kidney injury.30–33

Evidence-Based Management and Reperfusion Strategies of COVID-19 Positive Patients with STEMI

In an observational study in Lombardy, Italy that evaluated the angiographic findings and clinical outcomes of STEMI patients with COVID-19, of the 28 patients that underwent urgent angiography, 17 patients (60.7%) had evidence of a culprit lesion requiring revascularization, and 11 patients (39.3%) did not have obstructive CAD, which excluded a type I myocardial infarction.15 This finding supports primary PCI as an initial revascularization strategy, as systemic fibrinolysis would not be required or contraindicated in about 40% of patients from the study. Similar findings were also seen from the multicenter NACMI registry study from 106 COVID-19 positive STEMI patients, which showed that 23% of these patients did not have any culprit vessels compared to 1% of control patients from pre-COVID-19 era [P < 0.001] and 11% observed in COVID-19 negative STEMI control patients [P < 0.001].4 In addition, the systemic inflammation associated with SARS-CoV-2 infection increases the risk of life-threatening hemorrhagic complications from thrombolysis and makes PCI the preferred reperfusion strategy in PCI capable hospitals.34–38

In a recently published position statement, the American College of Cardiology (ACC), Society for Cardiovascular Angiography and Interventions (SCAI), and the American College of Emergency Physicians (ACEP), recommended that, “during the COVID-19 pandemic, primary PCI remains the standard of care for patients with STEMI at PCI-capable hospitals where it could be provided in a timely manner, with an expert team outfitted with PPE in a dedicated cardiac catheterization laboratory room. A fibrinolysis-based strategy may be entertained at non- PCI capable referral hospitals or in specific situations where primary PCI cannot be executed or is not deemed the best option.”37 This multi-society recommendation recognizes the complex cardiovascular manifestations of COVID-19 positive patients with STEMI and encourages the consideration of STEMI simulators or mimics like myocarditis, stress cardiomyopathy, non- ischemic cardiomyopathy, nonspecific myocardial injury, and coronary spasm in the initial evaluation of these patients, especially in the ED prior to choosing a reperfusion strategy.37 It further emphasizes the value of appropriate PPE for health care workers, coordination of EMS, ED, and cardiac catheterization laboratory members, and application of an efficient algorithmic approach by regional STEMI care networks to ensure a balanced and standardized approach towards STEMI care in patients with COVID-19.37

Clinical Outcomes

The occurrence of STEMI in COVID-19 positive patients generally confers a poor prognosis, as evidence has shown that about one-third of patients succumbed to the disease regardless of revascularization options.4,27,39,40 In the NACMI registry study, in-hospital mortality of COVID- 19 positive patients was 33% compared to 11% of COVID-19 negative patients with STEMI (P < 0.001) and 4% of patients with STEMI in the pre-COVID-19 era (P < 0.001). Mortality was also found to be higher for COVID-19 positive cohorts who did not undergo coronary angiography, 48% compared to those who did receive coronary angiography 28% (P = 0.006). Also statistically significantly different between COVID-19 positive and negative patients with STEMI was the primary endpoint, defined as a composite of in-hospital death, stroke, recurrent MI, or unplanned revascularization, which was observed in 36% of COVID-19 positive patients and 13% of COVID-19 negative patients with STEMI, compared to 5% of patients with STEMI in the pre-COVID-19 era (all P values < 0.001).4 Besides the primary outcome, COVID-19 positive patients were also found to have a longer intensive care unit stay and overall length of hospitalization4,5 (Figure 4).

The frequency of in hospital outcomes from the North American COVID-19 myocardial infarction (NACMI) registry study.4 Primary Endpoint includes composite of in- Hospital mortality, Stroke, Recurrent MI, or unplanned revascularization.
Figure 4.

The frequency of in hospital outcomes from the North American COVID-19 myocardial infarction (NACMI) registry study.4 Primary Endpoint includes composite of in- Hospital mortality, Stroke, Recurrent MI, or unplanned revascularization.

Post intervention, COVID-19 STEMI patients who are hemodynamically stable without associated clinically significant respiratory symptoms or hypoxemia can be considered for early discharge based on clinical, laboratory and epidemiological criteria outlined by healthcare authorities.41,42 This is especially important for low risk, mildly-symptomatic COVID-19 patients as this practice will help decongest the healthcare facilities already strained by the pandemic. If this is considered, appropriate post-hospitalization monitoring should be ensured for public health safety and to prevent clinical deterioration.41 A randomized trial has demonstrated that early discharge of low risk STEMI patients post revascularization is safe and feasible with clinical outcomes of mortality, myocardial infarction, unstable angina and stroke, unexpected re-hospitalization at 90 days comparable to patients with delayed discharge.43

A key angiographic finding during cardiac catheterization of our patient was the occurrence of no reflow due to post-stent TIMI grade 2 flow and tissue blush grade 1. This observation of myocardial tissue hypoperfusion in the presence of a revascularized epicardial coronary artery suggested a microvascular obstruction.44–46 This phenomenon occurs in more than 20% of patients undergoing PCI and in fewer than 2% of elective PCI cases.44 No reflow is a serious prognostic sign, as it can result in poor healing of infarcts, adverse left ventricular remodeling, congestive heart failure, major adverse cardiac events, and death.44–46 The underlying pathophysiologic mechanisms proposed for this pathological finding include ischemic reperfusion injury, endothelial swelling or dysfunction, capillary obstruction, muscle spasm, or inflammatory response and distal coronary embolization.44–47

However, coronary microvascular obstruction seen in the pathophysiology of STEMI in the context of COVID-19 may suggest this phenomenon is more common in COVID-19 positive patients with STEMI. This speculation is supported by observations in the NACMI registry study, which documented a significant difference between post-PCI TIMI flow in COVID-19 positive patients with STEMI when compared to patients with STEMI in the pre-COVID-19 era: TIMI flow grade 0/1 of 6% versus 2% (P = 0.010) and TIMI flow of 2/3 (94% versus 98%) (P = 0.010), respectively.4 The degree of interventional or reperfusion with no reflow has been associated with the duration of the preceding myocardial ischemia, infarct size, procedural variables and patient characteristics.44 Delayed patient presentation, delayed door to balloon time, and higher risk of diabetes may contribute to increased rate of no reflow and poor outcomes in COVID-19 positive patients with STEMI. Clinical strategies to prevent the development of no reflow during STEMI may include public health awareness regarding prompt hospital presentation or EMS consult for cardiac symptoms, reduction in door to balloon time per guideline recommendation, and optimal management of pre-intervention risk factors like diabetes. Intraprocedural strategies to prevent no reflow phenomenon would include intracoronary thrombectomy in patients with angiographic evidence of large thrombus burden and intracoronary administration of medications like adenosine, nitroprusside, and nicorandil, as these therapeutics have produced beneficial effects in some reports.44–48 Further studies are needed to evaluate the effectiveness of these interventions to improve patient outcomes post- STEMI in the context of COVID-19.

Conclusion

Besides the general threat to public health, the COVID-19 pandemic has adversely impacted the clinical presentation, management, and outcomes of STEMI globally. Timely PCI is necessary to improve patient outcomes in the context of concurrent COVID-19. A coordinated, standardized approach to care of patients with COVID-19 and symptoms of cardiac distress at the EMS, inpatient, and cardiology department levels may facilitate care transitions and ensure optimal patient outcome.

Author Contributions

Both authors contributed to the concept/design, data collection and analysis, writing of the manuscript, and provided subjects. Both authors had full access to the data included in this report.

Acknowledgements

The authors would like to thank Emily Andreae, PhD and Marie Fleisner for assistance in preparing this manuscript.

Footnotes

  • Disclosures: The authors have reported no conflicts of interest or financial support related to this work. No part of this work has been previously published or presented at a scientific meeting.

  • Received July 12, 2021.
  • Accepted November 10, 2021.

References

  1. 1.
    ↵
    Levine GN, Bittl JA. Focused update on primary percutaneous coronary intervention for patients with st-elevation myocardial infarction. JAMA Cardiol. 2016;1(2):226.
    Google Scholar
  2. 2.
    ↵
    Rezkalla SH, Kloner RA. Viral myocarditis: 1917–2020: From the Influenza A to the COVID- 19 pandemics. Trends Cardiovasc Med. 2021;31(3):163-169.
    Google Scholar
  3. 3.
    ↵
    Jain V, Gupta K, Bhatia K, Management of STEMI during the COVID-19 pandemic: Lessons learned in 2020 to prepare for 2021. Trends Cardiovasc Med. 2021;31(3):135-140.
    Google Scholar
  4. 4.
    ↵
    Garcia S, Dehghani P, Grines C, Initial findings from the North American COVID-19 Myocardial Infarction Registry. J Am Coll Cardiol. 2021;77(16):1994-2003.
    Google Scholar
  5. 5.
    ↵
    Zhou F, Yu T, Du R, Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. Lancet. 2020;395(10229):1054-1062.
    Google ScholarCrossRefPubMed
  6. 6.
    Rosenthal N, Cao Z, Gundrum J, Sianis J, Safo S. Risk factors associated with in-hospital mortality in a us national sample of patients with covid-19. JAMA Netw Open. 2020;3(12):e2029058.
    Google Scholar
  7. 7.
    Wu Z, McGoogan JM. Characteristics of and important lessons from the coronavirus disease 2019 (COVID-19) outbreak in China: summary of a report of 72 314 cases from the Chinese center for disease control and prevention. JAMA. 2020;323(13):1239.
    Google ScholarCrossRefPubMed
  8. 8.
    ↵
    Tam CF, Cheung KS, Lam S, Impact of Coronavirus Disease 2019 (COVID-19) Outbreak on ST-Segment-Elevation Myocardial Infarction Care in Hong Kong, China. Circ Cardiovasc Qual Outcomes. 2020 Apr;13(4):e006631.
    Google ScholarCrossRefPubMed
  9. 9.
    ↵
    Garcia S, Albaghdadi MS, Meraj PM, Reduction in ST-segment elevation cardiac catheterization laboratory activations in the United States during COVID-19 pandemic. J Am Coll Cardiol. 2020;75(22):2871-2872.
    Google ScholarCrossRefFull TextPubMed
  10. 10.
    ↵
    Wilson SJ, Connolly MJ, Elghamry Z, Effect of the COVID-19 pandemic on ST- segment–elevation myocardial infarction presentations and in-hospital outcomes. Circ Cardiovasc Interv. 2020;13(7):e009438.
    Google ScholarCrossRefPubMed
  11. 11.
    ↵
    Rodríguez-Leor O, Cid-Álvarez B, Pérez de Prado A, Impact of COVID-19 on ST- segment elevation myocardial infarction care. The Spanish experience. Rev Esp Cardiol (Engl Ed). 2020;73(12):994-1002.
    Google ScholarCrossRef
  12. 12.
    ↵
    De Filippo O, D’Ascenzo F, Angelini F, Reduced rate of hospital admissions for ACS during COVID-19 outbreak in northern Italy. N Engl J Med. 2020;383(1):88-89.
    Google ScholarCrossRefPubMed
  13. 13.
    ↵
    Coughlan JJ, Chongprasertpon N, Arockiam S, Arnous S, Kiernan TJ. COVID-19 and STEMI: A snapshot analysis of presentation patterns during a pandemic. Int J Cardiol Heart Vasc. 2020;30:100546.
    Google ScholarPubMed
  14. 14.
    ↵
    Zitelny E, Newman N, Zhao D. STEMI during the COVID-19 pandemic - an evaluation of incidence. Cardiovasc Pathol. 2020;48:107232.
    Google ScholarPubMed
  15. 15.
    ↵
    Stefanini GG, Montorfano M, Trabattoni D, ST-elevation myocardial infarction in patients with COVID-19: clinical and angiographic outcomes. Circulation. 2020;141(25):2113-2116.
    Google ScholarPubMed
  16. 16.
    ↵
    Akhmerov A, Marbán E. COVID-19 and the Heart. Circ Res. 2020 May 8;126(10):1443-1455.
    Google ScholarCrossRefPubMed
  17. 17.
    ↵
    Tersalvi G, Vicenzi M, Calabretta D, Biasco L, Pedrazzini G, Winterton D. Elevated Troponin in Patients With Coronavirus Disease 2019: Possible Mechanisms. J Card Fail. 2020;26(6):470-475.
    Google ScholarCrossRefPubMed
  18. 18.
    ↵
    Akhmerov A, Marbán E. COVID-19 and the Heart. Circ Res. 2020 May 8;126(10):1443-1455.
    Google ScholarCrossRefPubMed
  19. 19.
    ↵
    Shi S, Qin M, Shen B, Association of Cardiac Injury With Mortality in Hospitalized Patients With COVID-19 in Wuhan, China. JAMA Cardiol. 2020;5(7):802-810.
    Google Scholar
  20. 20.
    ↵
    Zheng YY, Ma YT, Zhang JY, Xie X. COVID-19 and the cardiovascular system. Nat Rev Cardiol. 2020;17(5):259-260.
    Google ScholarCrossRefPubMed
  21. 21.
    ↵
    Giustino G, Croft LB, Oates CP, Takotsubo Cardiomyopathy in COVID-19. J Am Coll Cardiol. 2020;76(5):628-629.
    Google ScholarCrossRefFull TextPubMed
  22. 22.
    ↵
    Varga Z, Flammer AJ, Steiger P, Endothelial cell infection and endotheliitis in COVID- 19. Lancet. 2020;395(10234):1417-1418.
    Google ScholarCrossRefPubMed
  23. 23.
    ↵
    Huette P, Beyls C, Guilbart M, Acute Cor Pulmonale in COVID-19-Related ARDS: Improvement With Almitrine Infusion. JACC Case Rep. 2020;2(9):1311-1314.
    Google Scholar
  24. 24.
    Poissy J, Goutay J, Caplan M, Pulmonary embolism in patients with covid-19: awareness of an increased prevalence. Circulation. 2020;142(2):184-186.
    Google ScholarPubMed
  25. 25.
    Tersalvi G, Vicenzi M, Calabretta D, Biasco L, Pedrazzini G, Winterton D. Elevated Troponin in Patients With Coronavirus Disease 2019: Possible Mechanisms. J Card Fail. 2020;26(6):470-475.
    Google ScholarCrossRefPubMed
  26. 26.
    ↵
    Danzi GB, Loffi M, Galeazzi G, Gherbesi E. Acute pulmonary embolism and COVID-19 pneumonia: a random association? Eur Heart J. 2020 May 14;41(19):1858.
    Google ScholarPubMed
  27. 27.
    ↵
    Xiang D, Xiang X, Zhang W, Management and Outcomes of Patients With STEMI During the COVID-19 Pandemic in China. J Am Coll Cardiol. 2020;76(11):1318-1324.
    Google ScholarCrossRefFull TextPubMed
  28. 28.
    ↵
    Zheng YY, Ma YT, Zhang JY, Xie X. COVID-19 and the cardiovascular system. Nat Rev Cardiol. 2020;17(5):259-260.
    Google ScholarCrossRefPubMed
  29. 29.
    ↵
    Turner AJ, Hiscox JA, Hooper NM. ACE2: from vasopeptidase to SARS virus receptor. Trends Pharmacol Sci. 2004 Jun;25(6):291-294.
    Google ScholarCrossRefPubMed
  30. 30.
    ↵
    American Heart Association: Newsroom. Patients taking ACE-i and ARBs who contract COVID-19 should continue treatment, unless otherwise advised by their physician. Statement from the American Heart Association, the Heart Failure Society of America and the American College of Cardiology. March 2020. https://newsroom.heart.org/news/patients-taking-ace-i-and-arbs-who-contract-covid-19-should-continue-treatment-unless-otherwise-advised-by-their-physician. Last accessed March 18, 2022.
    Google Scholar
  31. 31.
    International Society of Hypertension. A statement from the International Society of Hypertension on COVID-19. 2020. https://ish-world.com/a-statement-from-the-international-society-of-hypertension-on-covid-19/. Last accessed March 18, 2022.
    Google Scholar
  32. 32.
    European Society of Cardiology. Position Statement of the ESC Council on Hypertension on ACE-Inhibitors and Angiotensin Receptor Blockers. March 13, 2020. https://www.escardio.org/Councils/Council-on-Hypertension-(CHT)/News/position-statement-of-the-esc-council-on-hypertension-on-ace-inhibitors-and-ang. Last accessed March 18, 2022.
    Google Scholar
  33. 33.
    ↵
    Hypertension Canada. Statement on: Hypertension, ACE-Inhibitors and Angiotensin Receptor Blockers and COVID-19. March 13, 2020. https://hypertension.ca/wp-content/uploads/2020/03/2020-30-15-Hypertension-Canada-Statement-on-COVID-19-ACEi-ARB.pdf. Last accessed March 18, 2022.
    Google Scholar
  34. 34.
    ↵
    Keeley EC, Cigarroa JE. Facilitated primary percutaneous transluminal coronary angioplasty for acute ST segment elevation myocardial infarction: rationale for reuniting pharmacologic and mechanical revascularization strategies. Cardiol Rev. 2003;11(1):13-20.
    Google ScholarCrossRefPubMed
  35. 35.
    Huynh T, Perron S, O’Loughlin J, Comparison of primary percutaneous coronary intervention and fibrinolytic therapy in ST-segment-elevation myocardial infarction: bayesian hierarchical meta-analyses of randomized controlled trials and observational studies. Circulation. 2009;119(24):3101-3109.
    Google ScholarCrossRefAbstract/Full TextPubMedWeb of Science
  36. 36.
    Gurwitz JH, Gore JM, Goldberg RJ, Risk for intracranial hemorrhage after tissue plasminogen activator treatment for acute myocardial infarction. Participants in the National Registry of Myocardial Infarction 2. Ann Intern Med. 1998;129(8):597-604.
    Google ScholarCrossRefPubMedWeb of Science
  37. 37.
    ↵
    Mahmud E, Dauerman HL, Welt FGP, Management of Acute Myocardial Infarction During the COVID-19 Pandemic: A Position Statement From the Society for Cardiovascular Angiography and Interventions (SCAI), the American College of Cardiology (ACC), and the American College of Emergency Physicians (ACEP). J Am Coll Cardiol. 2020;76(11):1375-1384.
    Google ScholarCrossRefFull TextPubMed
  38. 38.
    ↵
    Vrachatis DA, Deftereos S, Stefanini GG. STEMI in COVID-19 patients: thrombolysis-first approach could yield more risk than benefit. Eur Heart J. 2020;41(42):4141-4142.
    Google Scholar
  39. 39.
    ↵
    Roffi M, Guagliumi G, Ibanez B. The obstacle course of reperfusion for ST-segment– elevation myocardial infarction in the COVID-19 pandemic. Circulation. 2020;141(24):1951-1953.
    Google ScholarPubMed
  40. 40.
    ↵
    Guagliumi G, Sonzogni A, Pescetelli I, Pellegrini D, Finn AV. Microthrombi and ST- Segment-Elevation Myocardial Infarction in COVID-19. Circulation. 2020;142(8):804-809.
    Google Scholar
  41. 41.
    ↵
    European Center for disease prevention and control. Novel coronavirus (SARS-CoV-2) Discharge criteria for confirmed COVID-19 cases – When is it safe to discharge COVID-19 cases from the hospital or end home isolation? https://www.ecdc.europa.eu/sites/default/files/documents/COVID-19-Discharge-criteria.pdf. Last accessed March 18, 2022.
    Google Scholar
  42. 42.
    ↵
    Center for disease control and prevention. Interim Clinical Guidance for Management of Patients with Confirmed Coronavirus Disease (COVID-19). February 16, 2021. https://www.cdc.gov/coronavirus/2019-ncov/hcp/clinical-guidance-management-patients.html. Last accessed March 18, 2022.
    Google Scholar
  43. 43.
    ↵
    Novobilsky K, Stipal R, Cerny P, Safety of early discharge in low risk patients after acute ST-segment elevation myocardial infarction, treated with primary percutaneous coronary intervention. Open label, randomized trial. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub. 2019;163(1):61-66.
    Google Scholar
  44. 44.
    ↵
    Jaffe R, Charron T, Puley G, Dick A, Strauss BH. Microvascular obstruction and the no- reflow phenomenon after percutaneous coronary intervention. Circulation. 2008;117(24):3152-3156.
    Google ScholarCrossRefFull TextPubMedWeb of Science
  45. 45.
    Morishima I, Sone T, Okumura K, Angiographic no-reflow phenomenon as a predictor of adverse long-term outcome in patients treated with percutaneous transluminal coronary angioplasty for first acute myocardial infarction. J Am Coll Cardiol. 2000;36(4):1202-1209.
    Google ScholarCrossRefFull TextPubMed
  46. 46.
    ↵
    Rezkalla SH, Stankowski RV, Hanna J, Kloner RA. Management of no-reflow phenomenon in the catheterization laboratory. JACC: Cardiovasc Interv. 2017;10(3):215-223.
    Google ScholarCrossRefAbstract/Full Text
  47. 47.
    ↵
    Fugit MD, Rubal BJ, Donovan DJ. Effects of intracoronary nicardipine, diltiazem and verapamil on coronary blood flow. J Invasive Cardiol. 2000;12(2): 80-85.
    Google ScholarPubMedWeb of Science
  48. 48.
    ↵
    Rezkalla SH, Dharmashankar KC, Abdalrahman IB, Kloner RA. No-reflow phenomenon following percutaneous coronary intervention for acute myocardial infarction: incidence, outcome, and effect of pharmacologic therapy. J Interv Cardiol. 2010;23(5):429-436.
    Google ScholarCrossRefPubMedWeb of Science
Loading
PDF
Back to top

In this Issue

Clinical Medicine & Research

Clinical Medicine & Research

Vol. 20, Issue 1

1 Mar 2022

Table of Contents Cover (Photo) Index by author
  • Share

    Share This Article

    ST Segment Elevation Myocardial Infarction in the COVID-19 Era: Appraisal of the Evidence
    • Clinical Medicine & Research
    • Mar 2022,
    • 20
    • (1)
    • 52-
    • 60;
    • DOI: 10.3121/cmr.2021.1707
  • Bookmark this Article

    SAVE ITEM IN SELECTED FOLDER.

Jump to

Keywords

COVID-19, STEMI, PCI, Pandemic, No reflow