Characteristics of patients with acute coronary syndrome in the covid-19 pandemic

Abstract

AimCoronavirus disease 2019 (COVID-19) has caused thrombotic disease. In this study, we aimed to determine the demographic and clinical characteristics of acute coronary syndrome (ACS) patients infected with COVID-19 and to investigate whether they differ from patients with ACS without COVID-19 in terms of these characteristics.MethodsThe study was designed as a single-center retrospective study. Thirty- three COVID-19 infected ACS patients (Group 1) and 100 ACS patients without COVID-19 infection (Group 2) were included in the study.ResultsThe groups were compared in terms of coronary angiographic data. Twenty-eight (84.8%) patients in Group 1 and 74 (74%) patients in Group 2 were presented as non-ST elevation myocardial infarctus. Patients were compared in terms of baseline Thrombolysis in Myocardial Infarctus (TIMI) flow, thrombus stage, myocardial blush (end), using of thrombus aspiration catheter, stent thrombosis, and TIMI flow after percutaneous coronary intervention, and it was observed that there was no statistical difference between the groups (P > .05).ConclusionCOVID-19 infection can cause plaque rupture, myocardial damage, coronary spasm and cytokine storm by triggering the coagulation and inflammation process. The fact is that we did not encounter an increased thrombus load in this study.

Keywords

Introduction

The new severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been affecting the entire world since December 2019, causing the 2019 coronavirus (COVID-19) epidemic. The virus primarily affects the respiratory system. Although some coronavirus carriers are asymptomatic, others experience severe pneumonia and acute respiratory distress syndrome (ARDS). During the clinical course or even after recovery, the virus can affect other organs, especially the cardiovascular system.¹
COVID-19 infection can cause acute myocardial damage, heart failure, arrhythmia, acute coronary syndrome, and thromboembolism during and after the disease process. SARS-COVID-2 binds to the transmembrane angiotensin-converting enzyme 2 (ACE2) protein. This protein is found in high amounts in pericytes. Once the virus attaches to this protein, it can enter the cell and disrupt the microvascular circulation. Thus, cardiovascular complications can occur. In addition, the current inflammatory process is believed to cause platelet activation, endothelial dysfunction, and stasis.^1,2
Mortality and morbidity rates are high in COVID-19 patients with cardiovascular disease. In this study, we aimed to determine the demographic and clinical characteristics of patients infected with COVID-19 and acute coronary syndrome and to investigate whether they differ from patients with acute coronary syndrome (ACS) who were not infected with COVID-19 in terms of these characteristics.

Materials and Methods

Patient SelectionThis single-center retrospective study included 33 patients with acute ACS and COVID-19 infection (Group 1) and 100 patients with ACS without COVID-19 infection (Group 2). The diagnosis of acute coronary syndrome was made according to the diagnostic criteria of the European Society of Cardiology (ESC) non-ST elevation myocardial infarction (NSTEMI) guideline published in 2020.³ and the ST-elevation myocardial infarction (STEMI) guideline published in 2017.⁴ The diagnosis of COVID-19 was first made on the basis of clinical findings and computed thoracic tomography, and then confirmed by COVID-19 swab test using real-time reverse transcriptase–polymerase chain reaction (RT-PCR). Patients with clinical and tomographic findings compatible with COVID-19 were found to be positive for COVID and treated accordingly. Patients who were not pregnant and aged> 18 years were included in the study. The medical history of patients was obtained from hospital records. Patients with out-of-hospital cardiac arrest who did not achieve return of spontaneous circulation were excluded from the study. This study was conducted by the COVID-19 Scientific Research Evaluation Commission of the Ministry of Health of the Republic of Turkey, with approval of the study on 31/05/2020 and the approval of the Ethics Committee of Sancaktepe Sehit Prof. Dr. Ilhan Varank Education and Research Hospital, Clinical Research Ethics Committee No. 1 (date: 18/11/2020, No. 2020-43).Evaluation of Blood Sample TestsTotal cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL), triglyceride, fasting blood glucose and thyroid-stimulating hormone were studied from the blood samples that were taken after at least 8 hours of fasting. Creatinine, albumin, C- reactive protein (CRP), procalcitonin, fibrinogen, D-dimer, high-sensitivity troponin I (hs troponin I), and complete blood count were studied from the blood tests taken immediately after admission to the hospital.Echocardiographic EvaluationHeart chamber diameters, valvular pathology, systolic pulmonary artery pressure, and ejection fraction (EF) (measured using the modified Simpson method) data were obtained from the apical and parasternal axes with a 2.5 MHz transducer and echocardiography machine (Vivid 5; GE Healthcare, Inc. Chicago, IL, USA).Coronary AngiographySTEMI patients had immediate coronary angiography, while those with NSTEMI who did not have high-risk criteria underwent coronary angiography within the first 24-48 hours. All patients received a loading dose of acetylsalicylic acid 300 mg and clopidogrel 600 mg, or ticagrelor 180 mg before the procedure. During the procedure, all patients were loaded with iv heparin at a rate of 70-100 IU / kg.
A panel of 2 interventional cardiologists, blinded to patient COVID-19 status, retrospectively reviewed cine-angiographic images of all patients and scored pre- and post-percutaneous coronary intervention (PCI) TIMI flow in the infarct-related artery, thrombus burden pre- and post-PCI, and myocardial blush grade.Follow-UpPatients in-hospital mortality, their admission to the hospital with acute coronary syndrome, cerebrovascular event, heart failure at the end of the first month, and combined total death rates were obtained from the medical records.Statistical AnalysisIBM SPSS Statistics for Windows, Version 18.0 (IBM Corp., Armonk, NY, USA) was used to perform the statistical analysis. Shapiro- Wilk test was used to assess the normality of distribution of the variables. Quantitative variables with normal distribution were specified as mean  ±  standard deviation, and non-normally distributed variables were specified as median (interquartile range). Categorical variables were shown as numbers and percentages. The non-normally distributed variables were assessed with the Mann-Whitney U test, while normally distributed variables were assessed with an independent sample Student’s t-test.

Results

The average age in Group 1 was 65.9 years, and 59.75 years in Group 2, and there was no significant difference. In Group 1, 21 (63%) individuals were males. In Group 2, 74 (74%) of the patients were male, and the two groups were considered similar in this respect. In the COVID-19 patient group, 19 (57.57%) patients had positive nasal swabs, on the other hand, lung involvement on non-contrast thoracic tomography was typical for COVID 19 pneumonia in 14 (42.43%) patients. The groups were compared in terms of chronic disease history. Patients with a history of coronary intervention were more common in the COVID 19 patient group. Hypertension (HT) was more common in the control group. There was a significant difference between the groups in terms of these two diseases (P = .001 and 0.024, respectively). Other demographic and clinical characteristics are summarized in Table 1.
The patients were compared in terms of laboratory test results. Hemoglobin, lymphocyte count, albumin, total cholesterol and triglyceride levels were higher in Group 2 (P = .041; 0.001; 0.000; 0.018; 0.05, respectively). In Group 1, the levels of CRP, and D-dimer were high (P < .001; 0.006, respectively), which led to a significant statistical result. Other laboratory results are summarized in Table 1. Patients were also compared in terms of coronary angiographic characteristics. Twenty-eight (84.8%) patients in the COVID 19 group and 74 (74%) in the control group presented with NSTEMI. On the other hand, 5 patients (15.2%) in Group 1 (15.2%) and 26 patients (26%) in Group 2 presented with STEMI. There was no statistical difference between the groups in terms of these characteristics (P > .05). Other angiographic features are summarized in Tables 2, 3.

Discussion

This study summarizes data from patients with and without COVID-19 who were admitted to a primary percutaneous intervention center and underwent coronary imaging. The patients included in the study were not divided into NSTEMI and STEMI groups. Therefore, this study differs from other coronary imaging studies.
The main finding of our study is that in patients with COVID-19 and ACS the thrombus burden was not higher than in ACS patients without COVID-19 infection.
One of the important features of COVID-19 infection is the microcirculatory endothelial damage in pulmonary circulation and other vascular beds.⁵ Since COVID-19 directly infects vascular endothelial cells, causing cellular damage and apoptosis, the antithrombotic activity of the luminal surface is remarkably decreased. Subsequently, damage of the endothelium leads to procoagulant changes in the vascular lumen, the formation of immunothrombosis, and organ malcirculation.⁶ Choudry et al. studied 39 STEMI patients with COVID-19 and 76 STEMI control patients. In this study, there were no significant differences between the groups in terms of basal TIMI, basal thrombus stage, or target vessel post-PCI TIMI, but differences were observed in terms of myocardial blush (end) stage, modified thrombus stage using an aspiration catheter, stent thrombosis, and multiple vessel intervention. It was observed that stent thrombosis and thrombus aspiration catheter use were more common, and the modified thrombus and myocardial blush stages were higher in the COVID-19 group.⁷ Unlike the study by Choudry et al., in two separate studies involving 28 and 18 STEMI patients, it was reported that lesions with high thrombus load were not more common in COVID patients.^8,9 In our study, there were no significant differences between the groups in terms of these parameters. Even after separating patients into STEMI and NSTEMI groups, there were no significant differences in our study. This may be due to the small study population. Similar to the study by Choundry et al., the duration of stay in the hospital and intensive care unit was longer in the COVID-19 group.⁷
It has been determined that HT is more common in COVID-19 patients, and the disease is more severe in those with HT.¹⁰ It has been suggested that HT causes the immune system to work irregularly. In our study, HT was more common in the control group, whereas past history of PCI was more common in the COVID-19 group.
COVID-19 infection is an inflammatory process that causes coagulation activation and endothelial dysfunction. It was observed that cardiac and coagulation biomarker levels were elevated during COVID-19 infection. Increased D-dimer and troponin levels have been associated with increased mortality and morbidity.¹¹ Although the groups in this study were found to be similar in terms of hs-troponin I, D-dimer levels were found to be higher in the COVID-19 patient group.
The bone marrow response to COVID-19 infection changes the course of the disease. Excessive immune reaction causes a cytokine storm, leading to increased risk of death.¹² CRP, procalcitonin, neutrophil, lymphocyte, albumin, and fibrinogen levels and the neutrophil/lymphocyte ratio can be used to predict this response and the course of the disease. In some studies, it has been found that lymphocyte levels are low and neutrophil levels are high in patients with severe COVID-19.^13,14 In addition, in severe cases, high levels of CRP, procalcitonin, and fibrinogen have been observed. On the other hand, albumin levels are low. In the study mentioned above, it was determined that hemoglobin, lymphocyte, and albumin levels were low in COVID-19 patients, whereas fibrinogen was higher and close to the statistically significant limits.
It has been previously shown that some viral infections affect cholesterol levels.¹⁵ It has been shown in a study conducted on pig testicular cells and hamster renal cells that the depletion of cholesterol from the cell membrane of the SARS-CoV-2 virus causes a decrease in the severity of viral infection.¹⁶ Wei et al. compared cholesterol levels of patients infected with COVID-19 with those of the normal population and showed that total cholesterol, HDL, and LDL were lower in the patient group.¹⁷ This result has been supported by other studies (Hu X, Chen D, Wu L, He G, Ye W. Low Serum Cholesterol Level Among Patients with COVID-19 Infection in Wenzhou, China. Available at: https://ssrn.com/abstract=3544826).¹⁸ In our study, it has been proven that total cholesterol levels and triglyceride levels are lower in patients infected with COVID-19.

Limitations

The small number of patients in the study is the greatest limitation. The inclusion of patients with high hs-troponin I and patients with ST-elevation or depression is an additional limitation.

Conclusion

In conclusion, although COVID-19 infection activates the coagulation and inflammation cascade and triggers thromboembolic events, we did not encounter increased thrombus burden among the groups in this study. This may be because the fact that the SARS-CoV-2 virus causes myocardial damage via plaque rupture, hypoxia, cytokine storm, coronary spasm.

Declarations

References

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