ST-Segment Elevation in Patients with COVID-19: A Late Complication

Dear Editor

Acute Myocardial Infarction (AMI) in Coronavirus disease – 2019 (COVID-19) can result from coronary plaque rupture secondary to exaggerated inflammatory response, endothelial dysfunction and demand ischemia from hypoxemia. We report a case series of four COVID-19 patients who had ST segment elevation myocardial infarction (STEMI) with a median of 12 days after COVID-19 symptom onset. Early identification of Acute Coronary Syndrome is of utmost importance during hemodynamic instability in COVID-19 patients. The treatment options for STEMI during the pandemic should be based on availability of resources and individual patient prognosis.

The Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) pandemic that has developed in late 2019 and 2020 has caused thousands of deaths and enormous impact on our health systems and economies. COVID 19 caused by SARS-COV-2 is mainly a respiratory illness but it can cause multiple direct and indirect cardiovascular complications in the form of acute myocardial injury, myocarditis, arrhythmias and thromboembolism.¹ We collected data from medical charts from 3 different hospitals of North Jersey, the epicenter of Pandemic from April 1, 2020 to April 26, 2020, there were 4 patients who had STEMI and also tested positive for COVID-19. Table 1 shows demographics, clinical, laboratory and radiological features of these patients, the median age of the patients was 60 years, all were men, two were Hispanic and two were Caucasian. One of the patients was a known hypertensive and two patients were diagnosed with new onset diabetes mellitus on hospitalization. All the four patients had STEMI during the course of COVID-19 infection, three were hospitalized at the time of STEMI and fourth patient came back with STEMI, five days after discharge for treatment of COVID-19. One study showed that the median time from hospitalization to STEMI onset was 6 days.² The median time between onset of COVID-19 symptoms and STEMI in our case series was 12 days. Initial COVID-19 symptoms were similar in all four patients and included fever, shortness of breath, and cough; half reported myalgias as well. Three patients had acute chest pain during STEMI and fourth patient was intubated and became hypotensive and electrocardiogram (EKG) showed ST segment Elevation (Table 1). Two patients had inferolateral STEMI, one had Inferolateral and posterior STEMI and fourth patient had antero-lateral STEMI. Echocardiogram in the patient with anterolateral STEMI showed apical septal, apical anterior and apical lateral wall hypokinesia with ejection fraction of 40–45%. Echocardiogram in two showed inferolateral wall hypokinesia. In three patients echocardiogram showed corresponding regional wall motion abnormalities to ST segment changes on electrocardiogram, while in one patient echocardiogram was done after reperfusion and showed normal myocardial wall motion (Table 1). D-dimer levels obtained in two of the patients were found to be significantly elevated in comparison to presentation. Two patients received intravenous alteplase and heparin drip was continued for 48 h post thrombolysis. One of the patients had significant epistaxis after second dose of alteplase, so it was stopped. The patient with anterolateral STEMI given large myocardial territory involvement was taken for cardiac catherization and was found to have 100% occlusion of the mid left anterior descending artery, underwent percutaneous coronary intervention. One patient was not a candidate for thrombolytics and received medical management with dual antiplatelets and anticoagulation. In this series of COVID-19 patients with STEMI, there was variability in clinical course and management. Higher the troponin level, was associated with worse prognosis in COVID 19 patients. Case fatalities rates have been reported to be higher in patients with underlying cardiovascular disease and hypertension as compared to those without these underlying comorbidities (10.5 and 6 percent mortality, respectively, compared with 0.9 percent mortality without underlying comorbidities.² In our case series, three patients who died had more comorbidities and higher troponin levels.

TABLE 1.

Demographic, clinical, laboratory, electrocardiogram, and clinical features of 4 COVID-19 patients who developed STEMI.

	Patient 1	Patient 2	Patient 3	Patient 4
Age (years)	53	81	55	52
Sex	Male	Male	Male	Male
Race	Hispanic	White	White	Hispanic
Past Medical History	Diabetes Mellitus Chronic Kidney Disease and Tobacco abuse	Hypertension	Diabeted Mellitus	No
Initial COVID Symptoms	Fever, shortness of breath and cough	Fever, shortness of breath, cough and myalgia	Fever, shortness of breath and cough	Fever, shortness of breath and cough
Signs and Symptoms at the time of STEMI	Hypotension (patient was intubated)	Chest pain	Chest pain, Left arm numbness	Chest pain radiating to arm and diaphoresis
Initial Labs
WBC (4.5 × 103 – 11.0 × 103 mm3)	8.2	8	11	7.9
Ferritin (16.4– 294.0 ng/mL)	N/A	1456	924	1389
LDH (140 – 271 units/L)	407	525	525	562
CRP (≤9.9 mg/L)	16.8	124.6	213.3	250.6
ESR (0 – 10 mm/h)	56	28	55	84
CK (30 – 223 units/L)	N/A	453	132	278
D-Dimer ≤0.50 mcg/mL)	2.75	2.33	2.4	0.7
Troponin (<0.030 ng/mL)	0.06	0.055	0.038	0.029
Fibrinogen (183 – 503 mg/dL)	N/A	N/A	726	N/A
PCT (0.010 – 0.49 ng/mL)	N/A	1.64	1.84	0.96
IL-6 (< 15.5 pg/mL)	N/A	118.2	71.4	N/A
Chest X ray	Fluffy perihilar airspace opacities	Multifocal pneumonia:	Multifocal pneumonia	Bilateral patchy infiltrates
Initial EKG	Normal sinus rhythm, Rate 84/min, left axis deviation, poor R wave progression in precordial leads	Normal sinus rhythm, rate 92/min, normal axis	Normal sinus rhythm, Rate 98/min, left axis deviation	Normal sinus rhythm, Rate 100/min, normal axis
Duration between Covid symptom and onset of STEMI (days)	12	12	7	17
STEMI Labs
WBC (4.5 × 103 – 11.0 × 103 mm3)	20.8	18	11	8.5
Ferritin (16.4 – 294.0 ng/mL)	NA	4298	575	779
LDH (140 – 271 units/L)	925	933	444	218
CRP (≤9.9 mg/L)	16.8	156.2	149.3	3.4
ESR (< 10 mm/h)	56	80	32	20
CK (30 – 223 units/L)	1853	90	333	N/A
D-Dimer (≤0.50 mcg/mL)	N/A	>20.0	>20	N/A
Peak Troponin (< 0.030 ng/mL)	80	57.995	43.915	13.711
STEMI EKG	ST Elevation in inferolateral leads II, III, aVF, V7-V8	ST Elevation in inferolateral leads II, III, aVF, V4-V6 and ST depression in V1-V2	ST elevation in anterolateral Leads V1-V5	ST Elevation in inferolateral leads II, III, aVF, V5-V6
Transthoracic echocardiogram- ejection fraction (EF) and wall motion abnormalities	50–55% EF Hypokinesis of mid to base of inferolateral wall	60–65% EF Basal and mid inferior wall and basal and mid inferolateral; regional wall motion abnormalities;	50–55% EF Hypokinesis of the mid to apical septal and apical lateral walls.	55–60% EF No wall motion abnormalities (Echo done post Thrombolysis)
STEMI treatment	Dual antiplatelets and anticoagulation with Heparin	Thrombolysis	Percutaneous coronary intervention	Thrombolysis
Outcome	Expired	Expired	Expired	Discharged home

Abbreviations: CK, creatine kinase; CRP, c-reactive protein; EKG, electrocardiogram; ESR, erythrocyte sedimentation rate; IL-6, interleukin −6; LDH, lactate dehydrogenase; N/A, not available; PCT, procalcitonin; STEMI, ST-elevation myocardail infacrtion; WBC, white cell count.

Acute myocardial infarction (AMI) is defined as acute myocardial injury with clinical evidence of acute myocardial ischaemia and with detection of a rise and/or fall of cTn values with at least one value above the 99th percentile URL and at least one of the following:

• •Symptoms of myocardial ischaemia;
• •New ischaemic 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 ischaemic etiology;
• •Identification of a coronary thrombus by angiography or autopsy.³

AMI in COVID 19 can result from coronary plaque rupture in the milieu of increased inflammatory response from cytokine storm, endothelial dysfunction, vasospasm and demand ischemia from hypoxemia and hemodynamic instability.⁴ Less frequent STEMI activations have been reported during this pandemic. An analysis of data from nine high-volume (>100 PPCI per year) cardiac catheterization laboratories in the Unites States from January 1, 2019 to March 31, 2020, reported an estimated 38% reduction in cardiac catheterization laboratory STEMI activations after declaration of COVID-19 pandemic. The potential reasons being fear of contracting COVID 19 and increased use of pharmacological reperfusion due to COVID-19.⁵ Also, there have been delays reported in STEMI care. The possible reasons for delays in STEMI care being delay from patient side secondary to fear of getting Covid 19 from hospitals, appropriate screening in emergency department for COVID-19 with history and chest X ray before transferring patient to cardiac catheterization lab. In catheterization lab, staff needs time to be in proper personal protective equipment and while performing PCI in full protective gear leads to longer times.⁶ Ensuring adequate protection of all healthcare workers in including emergency medical serives, transfer hospitals, cardic cath lab team is critical. Cardiovascular procedures in the safest possible environment to optimize clinical outcomes and minimize the risk of infection is crucial. This includes access to rapid testing protocols for the diagnosis of COVID-19, separate donning and doffing areas, deep cleaning team will then prepare the lab for the next patient, use of a negative pressure room and limiting staff in the room. For patients with confirmed or suspected COVID-19, the decision regarding fibrinolysis versus cardiac catherization versus conservative management should be based on availability of resources and patient related factors including age, co-morbidities, respiratory status, infarct location and bleeding risk. During the early rise of COVID, thrombolysis was usually considered first choice for STEMI in patients with COVID-19.^{7 , 8} As per recent guidelines from European Society of cardiology and American Society of cardiology for management of AMI during COVID 19 Pandemic, Primary PCI should be the standard of care for COVID 19 confirmed or probable patients at PCI capable hospitals in a dedicated cardiac catheterization laboratory with STEMI team geared in appropriate attire and IVthrombolysis should be considered at a non PCI capable center if patient cannot be transferred within 120 min of first medical contact.⁹ In conclusion, with increasing COVID-19 cases hospitals should prepare for management of these patients based on their local resources and high index of suspicion should be kept for Acute Coronary Syndrome in COVID-19 patients with risk factors during events of hemodynamic instability.

Declaration of Competing Interest

“The authors certify that there is no conflict of interest with any financial organization regarding the material discussed in the manuscript.”

Funding

None.

Author Contributions

P.K. and P.P.: original draft preparation. B.S., N.G. and R.V.: conceptualization. H.S.V., F.S. and M.B.: review and editing.