Medical Journal of Dr. D.Y. Patil Vidyapeeth

: 2020  |  Volume : 13  |  Issue : 3  |  Page : 269--273

Late presentation of acute coronary syndrome during COVID-19

Snehangsh Dash1, Ashish Kumar Dhiman1, Pushkar Pandey1, Anil Kumar2,  
1 Department of Medicine, Air Force Hospital, Gorakhpur, Uttar Pradesh, India
2 Department of Medicine, Air Force Hospital, Kanpur, Uttar Pradesh, India

Correspondence Address:
Anil Kumar
Department of Medicine, Air Force Hospital, Nathu Singh Road, Kanpur Cantt, Kanpur - 208 004, Uttar Pradesh


During the pandemic of coronavirus disease (COVID 19), anecdotal reports have been emerging all over the world that cases of acute cardiovascular emergencies such as ST-elevation myocardial infarction (MI) have decreased to the extent of 30%–70% at various hospitals. The number of primary percutaneous interventions has significantly decreased all over the world including developed nations. We present case reports of acute coronary syndromes (ACS) who presented to our hospital after the period of lockdown during the COVID-19 pandemic. These patients presented late to the hospital when we compare the ACS presentation before the lockdown period. Because of the late presentation, these patients developed heart failure and other complications leading to their death.

How to cite this article:
Dash S, Dhiman AK, Pandey P, Kumar A. Late presentation of acute coronary syndrome during COVID-19.Med J DY Patil Vidyapeeth 2020;13:269-273

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Dash S, Dhiman AK, Pandey P, Kumar A. Late presentation of acute coronary syndrome during COVID-19. Med J DY Patil Vidyapeeth [serial online] 2020 [cited 2020 Oct 19 ];13:269-273
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Full Text


The coronavirus disease 2019 (COVID-19) pandemic has spread all over the world in the last few months affecting the way of life including transport, movement, and medical treatment for various emergencies. By the end of December 2019, a new coronavirus, SARS-CoV-2, was identified as the cause of a disease outbreak that originated in the city of Wuhan, China. The disease it causes was called COVID-19. The infection spread rapidly, and the World Health Organization, on March 11, declared COVID-19 a pandemic. On April 11, 2020, more than 1.6 million cases were diagnosed in five continents.[1] During the last month, anecdotal reports have been emerging that cases seeking emergency treatment and reaching various hospitals all over world have decreased by 30%–70%. A nationwide analysis in 73 Spanish centers involved in ST-elevation myocardial infarction (MI) care networks revealed a 40% decrease in patients treated for STEMI when comparing activity before and during the current outbreak.[2] In the same direction, an American study revealed an estimated 38% reduction in catheterization laboratories' STEMI activations in nine high-volume centers during the early phase of the COVID-19 pandemic.[3]

We report five cases of acute coronary syndromes (ACS) during the COVID-19 lockdown.

 Case Reports

Case 1

A 59-year-old woman who was a known case of hypertension and Type 2 diabetes mellitus sustained acute ST-elevation anterior wall MI on March 16, 2020, and she was managed at a local hospital in Patna with thrombolysis using streptokinase. coronary angiography (CAG) was done on March 21, 2020, which was suggestive of triple-vessel disease, and percutaneous coronary intervention (PCI) to right coronary artery (RCA) was done. The patient again had chest pain on March 26, 2020, and was brought to the hospital on March 28 2 days late and on arrival, she was having dyspnea with features of heart failure. On examination, she had tachycardia, hypoxia, and hypotension. She had bilateral extensive crackles. Her electrocardiogram (ECG) was suggestive of left-axis deviation with QS in the anterior leads [Figure 1]. Troponin T was positive. She was managed as a case of acute myocardial infarction (MI) (delayed presentation) with severe left ventricular (LV) dysfunction in acute LV failure with noninvasive ventilator (NIV) support, inotrope infusion, diuretics, heparin, antiplatelets, lipid-lowering agents, anti-anginals, and antibiotics symptomatically. She had Hb 9.1 g/dl, TLC 18800/mm [3], Neutrophils 82%, urea 58 mg/dl, creatinine 1.8 mg/dl, Serum Bilirubin 1.2 mg/dl, AST 111 IU/L, ALT 114 IU/L, sodium 130 meq/L, potassium 4.5 meq/L, CKMB 53 IU/L. Gradually, she had oliguria followed by anuria with severe metabolic acidosis and refractory hypotension. She was managed with ventilator support, sodium bicarbonate, and escalation of inotropes and supportive treatment continued. Despite all measures, she had cardiac arrest on March 30 and succumbed to her illness on the next day.{Figure 1}

Case 2

A 75-year-old male patient who was a known case of old inferior wall MI with triple-vessel disease with mild LV dysfunction with post-PCI to RCA and left anterior descending (LAD) 1 year back presented to the hospital. Additional comorbidities were Type 2 diabetes mellitus and hypertension, and the patient was admitted on April 6, 2020, with a history of 7 days of chest pain and dyspnea with orthopnea of 5 days' duration presented with heart failure at the hospital. On examination, he had tachycardia, tachypnea, and hypoxia (SpO2 76%) with bilateral crackles on the chest. His ECG [Figure 2] revealed ST depression in leads V4 to V6, chest X-ray was suggestive of acute heart failure (pulmonary edema), and Troponin T was positive. His Hb was 9.3 g/dl, TLC 9800/mm [3], Platelets 1.7 lakh, Urea 65 mg/ dl, Creatinine 2.0 mg/dl, Bilirubin 0.9 mg/dl, AST 19 IU/ L, ALT 25 IU/L, Sodium 136 meq/L & Potassium 4.5 meq/. He was managed with oxygen support, heparin, diuretics, morphine, antiplatelets, antianginals, broad-spectrum antibiotics, and supportive care. The next day, he had become severely breathless and restless followed which he had a spontaneous cardiorespiratory arrest, and he was revived with cardiopulmonary resuscitation (CPR) within 10 min. Post-CPR, he was placed on ventilator support and other supportive care continued. Post-CPR survival, he had a poor glasgow coma scale (GCS) of E1VTM1 and also had myoclonus. He was continued on life support and despite all aggressive measures, he succumbed to his illness on April 8, 2020.{Figure 2}

Case 3

A 70-year-old male who was a known case of coronary artery disease with triple-vessel disease and post-post percutaneous intervention (PCI) status to left anterior descending coronary artery (LAD), left circumflex artery (LCX), and right coronary artery (RCA) was admitted on April 11, 2020, with a history of chest pain 5 days back and now dyspnea of 1 day. He had tachycardia, hypoxia, and hypotension with bilateral crept on chest. His ECG was suggestive of sinus tachycardia and ST depression in lead I, aVL, and V2 to V6 [Figure 3]. His Troponin T was positive. On investigation, he had Hb of 10 gm/dl and CKMB of 94, and he was managed as a case of acute MI with cardiogenic shock, acute kidney injury with heparin infusion, dual antiplatelet, inotropes, oxygen inhalation, and other supportive therapy. Despite all efforts, he succumbed to his illness on April 13, 2020.{Figure 3}

Case 4

A 58-year-old woman who was a known case of Type 2 diabetes mellitus and hypertension was admitted with acute-onset anginal chest pain with dyspnea and autonomic symptoms of 24 h duration (hospital admission pain settled, but dyspnea continued) on April 16, 2020. She had tachycardia, hypertension, and hypoxia (SpO2 80%) with bilateral crept on the chest. ECG had QS complex in leads V1 to V4 [Figure 4], and Troponin T was positive. Chest X-ray [Figure 5] had cardiomegaly with bilateral alveolar opacities of acute heart failure. She was managed as a case of acute MI with LV failure with oxygen support, heparin, diuretics infusion, insulin infusion, antiplatelets, and lipid-lowering agents with other symptomatic care. Her Hb was 8.0 g/dl, TLC was 16,000/mm [3], platelet count was 1.6 lacs, urea was 32, creatinine was 1.0, serum bilirubin was 0.9, AST was 60, and ALT was 78. She responded well to treatment with chest pain and breathlessness relieved after 3 days, and chest X-ray had gradual clearing of opacities. She was finally discharged on April 24, 2020.{Figure 4}{Figure 5}

Case 5

A 69-year-old male presented with no comorbid conditions but chest pain of more than 12 h duration on April 20, 2020. Clinically, he had a blood pressure of 100/80 mmHg, and ECG [Figure 6] done revealed STEMI anterior wall. As he was having ongoing chest pain, he was taken for primary percutaneous intervention (antiplatelet loading was done) immediately, which revealed normal right coronary artery (RCA) and Left coronary artery revealed ostial Left anterior descending artery (LAD) 100 percent occlusion [Figure 7] with very poor filling retrogradely from RCA. He was taken up for PCI (percutaneous intervention) to LAD and repeated thrombosuction was carried out as the whole artery was full of thrombus because of late presentation to the hospital where left main coronary artery to left anterior descending artery (LAD) drug eluding coronary stent was placed with final TIMI 3 flow [Figure 8]. He was managed thereafter with standard antiplatelets and ionotropes. ECG after PCI showed resolution of ST-elevation and also pain was reduced, but he developed refractory pulmonary edema for which initially NIV support was given and later mechanical ventilation, but despite all efforts, he succumbed to his illness after 12 h.{Figure 6}{Figure 7}{Figure 8}


All cases were ACS who presented later than 12 h (four out of five died probably because of late presentation). In fact, only one case presented <24 h with ongoing chest pain where he was taken for primary PCI; rest of all the cases presented well beyond 2 days after the onset of chest pain that too when chest pain subsided and patients developed breathlessness. Now, the window period for intracoronary thrombolysis is 3–6 h (earlier the better) and if chest pain is ongoing, then thrombolysis may be considered at 12 h also if no primary PCI facility is available in the hospital. Patient can also be taken for Primary PCI even after 12 hours of presentation if ongoing chest pain is there indicating viable myocardium. The survival benefit of recanalization of myocardium is maximum in the window period (0–6 h or maximum 12 h) by thrombolysis or primary PCI, and the benefit goes down rapidly after that.

Now, there may be many reasons for late presentation which include fear of going to hospital where COVID-19 patients are treated and nonavailability of transport. Reports are already emerging in western literatures of reduction in number of STEMI coming to hospital by as high as 50 percent, despite the availability of transport in those developed countries. Preliminary analysis has shown an important and disturbing decrease in the number of STEMI patients attending hospitals in Europe and in North America during COVID-19 outbreak. A nationwide analysis at 73 Spanish centers involved in STEMI care networks revealed a 40% decrease in patients treated for STEMI when comparing activity before and during the current outbreak.[2] Similarly, an American study revealed an estimated 38% reduction in catheterization laboratories' STEMI activations in nine high-volume centers during the early phase of the COVID-19 pandemic.[4] In both cases, STEMI care networks were working normally, so potential etiologies for this decrease should be a combination of avoidance of medical care due to social distancing and concerns of contracting COVID-19 in the hospital.

A recent study by Tam et al.[4] during the actual COVID-19 outbreak in Hong Kong, China, showed an almost 4-fold increase in median time from symptom onset to first medical contact (from 82.5 to 318 min) and more than a 2-fold increase in median time from door to device (from 84.5 to 110 min). Lack of or delayed access to reperfusion treatment will lead to an increase in short-term STEMI complications, such as left ventricle systolic dysfunction, cardiogenic shock, intraventricular thrombus formation, and peripheral embolism or mechanical complications.[5] In the long term, suboptimal revascularization and larger infarct size will lead to an increase in complications related to worse ventricular remodeling, such as chronic heart failure or ventricular arrhythmias.[6]


Some of the concerns regarding STEMI care during COVID-19 or for that matter outbreak of any contagious disease are decrease in patients seeking emergency medical care due to fear or lack of transport; increase in out-of-hospital sudden cardiac arrest; delay from the onset of symptoms to reperfusion; increase in the use of thrombolysis as reperfusion therapy; short- and long-term complications and mortalities; what revascularization strategies to be used; and control of nosocomial infections.

We recommend that each hospital should have a contingency plan including telemedicine services and better liaison with regional administrative authorities to deal with such situations during an outbreak to prevent avoidable deaths.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


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