Clinical and Anamnestic Characteristics of Acute Coronary Syndrome after Suffering COVID-19

Cover Page


Cite item

Full Text

Abstract

Background. COVID-19 increases the risk of developing thromboembolic complications, including acute myocardial infarction, in the acute period of the disease. The long-term consequences of COVID-19 are poorly understood. At the same time, the available data on an increased risk of acute coronary syndrome after infectious diseases allow us to make an assumption about a similar risk in COVID-19. The aim of the study was to study the anamnestic and laboratory diagnostic data in patients with acute coronary syndrome after COVID-19. Methods. The study included 185 patients with acute coronary syndrome who were admitted to the State Clinical Hospital No. 13 in Moscow in the period from May to December 2020. 2 groups were identified: group 1 — 109 patients with ACS who had previously suffered COVID-19, group 2 — 76 patients with ACS without COVID-19 in the past. The patients were collected anamnesis, including: the fact of smoking and alcohol consumption, heredity, previous diseases, including diabetes mellitus, acute myocardial infarction, previously performed PCI. Information about the COVID-19 infection has been collected (the duration of the disease, the course of the disease). A clinical and laboratory examination was conducted, including the determination of body mass index (BMI), examination for antibodies to COVID-19, determination of the lipid profile level (total cholesterol, LDL, HDL, triglycerides), blood glucose level, C-RB. The analysis was performed on automatic biochemical analyzers Hitachi-902, 912 (Roche Diagnostics, Japan). All patients underwent coronary angiography. Results. In patients with ACS with previously transferred COVID-19, the development of the disease occurred at a younger age compared to patients without transferred COVID-19. Among the patients with COVID-19, body weight was significantly lower, there were fewer smokers, concomitant type 2 diabetes mellitus and transferred ONMC were less common. In laboratory parameters, lower triglyceride levels were observed in patients with ACS with COVID-19 compared with those of patients without COVID-19. In the laboratory parameters of blood clotting in patients with ACS with COVID-19, higher APTT, thrombin time, fibrinogen level, D-dimer were noted. The indicated laboratory parameters in the groups had statistically significant differences. In ACS patients with a previous COVID-19, compared with patients without COVID-19, the lesion of 2 or more coronary vessels was more common in the anamnesis. Conclusion. According to the results of our study, it was revealed that multivessel coronary artery damage in patients after COVID-19 in comparison with patients without COVID-19 develops significantly more often, while these patients are significantly less likely to have DM and previously suffered ONMC, the level of TG is significantly lower.

Full Text

Justification

The COVID-19 pandemic has affected millions of people around the world and caused many deaths. Moreover, 40% of deaths from COVID-19 are caused by complications from the cardiovascular system [1]. It becomes obvious that, along with the respiratory organs, COVID-19 affects the cardiovascular system [2, 3, 4]. Among the cardiovascular complications of COVID-19, pulmonary embolism (PE), cardiac arrhythmias, myocarditis, pericarditis, and cardiovascular failure are identified [3]. Musher DM et al. described an increased risk of acute coronary syndrome (ACS) in patients with COVID-19 [6].
In previous studies, an association of the development of acute coronary syndrome with previous infectious diseases was revealed. Elevated titers of antibodies to C. pneumoniae and cytomegalovirus have been identified as independent risk factors for acute myocardial infarction (AMI) [6, 7]. The relationship between the development of AMI and acute cerebrovascular accident (ACVA) with a previous respiratory infection is known: influenza, parainfluenza, rhinovirus, respiratory syncytial virus, adenovirus. The strongest association is found in patients over 65 years of age [8]. Based on the results of 10 studies, a twofold increase in the risk of developing AMI after suffering from influenza was revealed [9]. The risk of AMI in patients with influenza was noted not only during the acute period of the disease, but also within 1 year after recovery [10]. ClaytonT et al. consider that patients are at the greatest risk of AMI in the first 5-10 days after influenza A and B [11]. Analysis of the incidence of AMI after an influenza epidemic showed that the risk of acute coronary events persists in patients for several months [12, 13]. In the pathogenesis of the development of ACS, researchers noted an increase in the activity of intravascular inflammation against the background of influenza, which was accompanied by the destabilization of the atherosclerotic plaque [14, 15]. Another mechanism for increasing the risk of developing ACS against the background of a respiratory infection is an increase in blood coagulation activity with an increase in thrombus formation [16].
Stefanini GG et al. based on the results of a clinical study, it was concluded that SARS-CoV-2 infection not only contributes to the development of ACS, but in some cases COVID-19 can manifest with ST elevation AMI [17]. Currently, there are few data in the literature on the level of risk of developing ACS after suffering COVID-19.

Methods
Study design
The study included 185 patients with acute coronary syndrome. According to the history of the presence of a previous coronavirus infection, the patients were divided into 2 groups: group 1 - 109 patients with ACS who had previously undergone COVID-19, group 2 - 76 patients with ACS without previous coronavirus infection. In the course of the study, a comparative assessment of the history, clinical course of ACS, data of laboratory and instrumental examination methods was carried out.
Compliance criteria
Inclusion criteria: presence of ACS. The study did not include patients with COVID-19 at the time of admission (positive PCR test), viral myocarditis, systemic diseases, antiphospholipid syndrome, cancer and hematological diseases.
Conditions of conducting
The study was carried out in the cardiology department and the cardiac intensive care unit of the City Clinical Hospital No. 13 of the city of Moscow.
Study duration
The study included patients with ACS who were admitted to the hospital between May and December 2020.
Description of the medical intervention
The patients underwent anamnesis collection, including: the fact of smoking and drinking alcohol, heredity, past diseases, incl. diabetes mellitus, acute myocardial infarction, previously performed PCI. Information about the previous COVID-19 infection was collected (the duration of the disease, the course of the disease). A clinical and laboratory examination was carried out, including the determination of body mass index (BMI), examination for antibodies to COVID-19, determination of the level of lipid profile (total cholesterol, LDL, HDL, triglycerides), blood glucose, C-RB. The analysis was performed on automatic biochemical analyzers Hitachi-902, 912 (Roche Diagnostics, Japan). Conducted electrocardiography, ECHO - cardiography ("Acuson", USA). All patients underwent coronary angiography (CAG) as part of the examination for acute coronary syndrome. Based on the performed CAG, ACS was confirmed and another mechanism of pain syndrome, laboratory changes, changes in ECG and ECHO of CG was excluded, incl. viral myocarditis. Coronary angiography was used to assess atherosclerotic lesions of the coronary arteries. The number of coronary arteries with stenosis of more than 50% was taken into account.
Ethical review
The ethical examination of the study was carried out at the Federal State Autonomous Educational Institution of Higher Education. N.I. Pirogov, Ministry of Health of Russia. The study was carried out in accordance with the Declaration of Helsinki.
Statistical analysis
The obtained data were processed on a personal computer based on Intel Celeron in the Microsoft Excel software environment using the built-in "Analysis Package", which is specially designed for solving statistical problems. Comparison of average indicators was performed using standard methods of variation statistics of a biomedical profile.

results
The patients included in the study suffered from COVID-19 on average 2-3 months before the development of ACS. Comparison of the anamnesis data and the results of clinical examination revealed that in patients with ACS with previous COVID-19, the development of the disease occurred at a younger age in comparison with patients without COVID-19, there were fewer smokers among patients with COVID-19, and was lower body mass index (BMI), concomitant type 2 diabetes mellitus was significantly less common, earlier AMI, stroke, and previous PCI were less common (Table 1).
Table 1. Anamnesis data and results of anthropological research

 

Groups

Indicators

Group 1

(n=109)

Group 2

(n=76)

p

Average age, years

64,4 [62, 0; 66, 9]

68,2 [66, 2; 71, 4]

0,1

Previous AMI,%

35,8

41,2

0,12

Previous PCI, %

90,8

91,4

0,14

ONMK, %

35,8

41,2

0,047

History of diabetes,%

21,8

35,3

0,045

Body mass (kg)

84,5 [78, 7; 90, 4]

79,4 [77, 2; 80, 4]

0,04

Height (cm)

168,5 [166, 1; 170, 9]

161,4 [158, 5; 164, 1]

0,1

BMI (kg / m²)

29,6 [27, 9; 31, 5]

31,4 [29, 1; 34, 0]

0,2

Smoking (%)

18,3

24,8

0,2

      


In laboratory parameters, patients with ACS with previous COVID-19 showed lower levels of serum glucose, total cholesterol, LDL, VLDL, triglycerides in comparison with those of patients without COVID-19. Differences in triglyceride levels were significantly significant (Table 2). The CRP level was higher in ACS patients without previous COVID-19.
Table 2. Laboratory indicators in 2 groups

 

Groups

Indicators

Groups 1

 (n=109)

Groups 2

 (n=76)

p

Serum glucose blood (mmol / l)

6,44 [6, 01; 6, 87]

7,1 [6, 8; 7, 92]

0,22

TOC (mmol / l)

4,39 [4, 02; 4, 75]

4,91 [4, 12; 5, 41]

0,51

TG (mmol / l)

1,7 [1, 39; 2, 01]

2,02 [1, 92; 2, 4]

0,045

HDL (mmol / l)

1,49 [1, 02; 1, 97]

1,71 [1, 45; 1, 98]

0,51

LDL (mmol / l)

2,33 [2, 03; 2, 63]

2,61 [2, 12; 3, 0]

0,5

LDLP (mmol / l)

2 [0, 45; 4, 46]

2,45 [1, 78; 4, 01]

0,6

CRP

6,36 [3, 57; 9, 14]

8,7 [4, 93; 10, 3]

0,03

 

      The study of the results of the performed CAG revealed that in patients with ACS without previous COVID-19, in half of the cases, there is a single-vessel lesion of the coronary arteries. ACS patients with previous COVID-19 compared with patients without a history of COVID-19 are more likely to have lesions of 2 or more coronary vessels (Figure 1).

Figure 1. Damage to coronary vessels according to coronary angiography

Discussion
Until now, there is little information about the development of ACS in patients with COVID-19. At the same time, based on the data on the high risk of thromboembolic complications in patients with COVID-19, scientists consider the likelihood of an increased risk of AMI both in the acute and postcoid periods [3, 18]. A significant increase in the risk of ACS in patients with COVID-19 is indicated in their work by Kochi AN et al. [nineteen]. The authors found that the severity of the course of COVID-19 also affects the risk of developing AMI [5].
It is known that patients with COVID-19 have an increased risk of arterial thrombosis: AMI, stroke, peripheral arterial thrombosis. An increase in the incidence of strokes was noted at a relatively young age - up to 50 years [20]. In patients with COVID-19, an increase in the risk of an unfavorable outcome of ischemic stroke was revealed [21]. Hamadeh A, et al. also indicate an increased risk of a poor prognosis of AMI in the presence of COVID-19. The authors note the difficulties in diagnosing ACS: low specificity of symptoms and diagnostic parameters, incl. ECG and troponin levels [22].
Considering the pathogenesis of the development of acute coronary events in patients with COVID-19, researchers note the presence of risk factors for AMI type 1 and 2. Scientists have identified the ability of the SARS-CoV-2 virus to cause inflammatory reactions in the vascular endothelium. This can contribute to intravascular thrombosis as well as destabilize atherosclerotic plaques. The consequence of these processes is an increased risk of developing acute coronary syndrome [23, 24]. The development of AMI type 2 is predisposed by the presence of hypoxemia, hypotension, tachycardia and fever in patients with COVID-19, which leads to oxygen deficiency in cardiomyocytes [3, 25, 26].
In our study, we found that COVID-19 is an independent risk factor for the development of ACS. The results obtained agree with the data of other researchers. Belanis P et al. studied the risk factors for the development of stroke in patients with COVID-19. It was found that in the presence of traditional CVD risk factors, SARS-CoV-2 infection is an independent risk factor and significantly increases the risk of stroke [27].
In a study by J.Y. Xiao et al, evaluated the effect of CVD risk factors on the degree of atherosclerotic coronary artery disease. In a study that included 1729 patients, an association of the severity of coronary sclerosis with gender, age, arterial hypertension, and impaired lipid and carbohydrate metabolism was revealed [28]. The risk of developing ACS and multivessel coronary artery disease was also influenced by smoking [29]. The results of our study indicate that COVID-19 significantly affects the severity of coronary artery disease regardless of the presence of traditional CVD risk factors: type 2 diabetes, dyslipidemia, etc.

Conclusion
Based on the results of the study, it can be concluded that the transferred COVID-19 disease increases the risk of multivessel coronary artery disease and the development of acute coronary syndrome, regardless of the presence of risk factors for cardiovascular complications: obesity, smoking, age, type 2 diabetes mellitus, dyslipidemia.
Conclusion. COVID-19 is an acute respiratory viral disease with cardiovascular complications. Damage to the cardiovascular system is possible not only in the acute period of the disease, but also in the postcoid period. The results of the study indicate the impact of COVID-19 on the risk of developing ACS in patients who have undergone a viral infection, regardless of whether patients have traditional risk factors for cardiovascular diseases. Past infection with SARS-CoV-2 affects atherogenesis, thrombogenesis and contributes to multivessel coronary artery disease. Further study of the impact of COVID-19 on the development and course of ACS will determine the duration and scope of preventive and rehabilitation measures.

×

About the authors

Natalia V. Orlova

Pirogov Russian National Research Medical University

Email: vrach315@yandex.ru
ORCID iD: 0000-0002-4293-3285
SPIN-code: 8775-1299

MD, PhD, Professor

Russian Federation, 1 Ostrovityanova str., 117997, Moscow

Valerij V. Lomajchikov

Pirogov Russian National Research Medical University

Email: lomaychikov@yandex.ru

Assistant

Russian Federation, 1, Ostrovityanova str., 117997, Moscow

Tatyana I. Bonkalo

Research Institute for Healthcare Organization and Medical Management

Email: bonkalotatyanaivanovna@yandex.ru
ORCID iD: 0000-0003-0887-4995
SPIN-code: 6572-7417

MD, PhD in Psychology, Professor

Russian Federation, Moscow

Grigorij A. Chuvarayan

Pirogov Russian National Research Medical University

Email: grigoriy.chuvarayan@gmail.com
ORCID iD: 0000-0002-4503-6280

MD, PhD, Assistant Professor

Russian Federation, 1, Ostrovityanova str., 117997, Moscow

Yana G. Spiryakina

Pirogov Russian National Research Medical University

Email: janezo@yandex.ru
ORCID iD: 0000-0002-1006-4118
SPIN-code: 5620-6667

MD, PhD, Assistant Professor

Russian Federation, 1, Ostrovityanova str., 117997, Moscow

Anna P. Petrenko

Pirogov Russian National Research Medical University

Email: petrenkoAnna5@yandex.ru

Clinical Resident

Russian Federation, 1, Ostrovityanova str., 117997, Moscow

Tatyana V. Pinchuk

Pirogov Russian National Research Medical University

Author for correspondence.
Email: doktor2000@inbox.ru
ORCID iD: 0000-0002-7877-4407
SPIN-code: 1940-2017

MD, PhD, Assistant Professor

Russian Federation, 1, Ostrovityanova str., 117997, Moscow

References

  1. Patel VD, Patel KH, Lakhani DA, Desai R, Mehta D, Mody P, Pruthi S. Acute pericarditis in a patient with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection: a case report and review of the literature on SARS-CoV-2 cardiological manifestations. AME Case Rep. 2021 Jan 25;5:6. doi: 10.21037/acr-20-90. PMID: 33634246; PMCID: PMC7882268.
  2. Chen C, Zhou Y, Wang DW. SARS-CoV-2: a potential novel etiology of fulminant myocarditis. Herz. 2020 May;45(3):230-232. doi: 10.1007/s00059-020-04909-z. PMID: 32140732; PMCID: PMC7080076.
  3. Driggin E, Madhavan MV, Bikdeli B, Chuich T, Laracy J, Bondi-Zoccai G, et al. Cardiovascular considerations for patients, health care workers, and health systems during the coronavirus disease 2019 (COVID-19) pandemic. J Am Coll Cardiol. (2020) 75:2352–71. doi: 10.1016/j.jacc.2020.03.031.
  4. Guzik TJ, Mohiddin SA, Dimarco A, Patel V, Savvatis K, Marelli-Berg FM, et al. COVID-19 and the cardiovascular system: implications for risk assessment, diagnosis, and treatment options. Cardiovasc Res. (2020) 116:1666–87. doi: 10.1093/cvr/cvaa106.
  5. Musher DM, Abers MS, Corrales-Medina VF. Acute Infection and Myocardial Infarction. N Engl J Med. 2019 Jan 10;380(2):171-176. doi: 10.1056/NEJMra1808137. PMID: 30625066.
  6. Saikku P. Epidemiologic association of Chlamydia pneumoniae and atherosclerosis: The initial serologic observation and more J Infect Dis 2000 Jun;181 Suppl 3:S411-3. doi: 10.1086/315625.
  7. Prasad A, Zhu J, Halcox JP, Waclawiw MA, Epstein SE, Quyyumi AA. Predisposition to atherosclerosis by infections: role of endothelial dysfunction. Circulation. 2002 Jul 9;106(2):184-90. doi: 10.1161/01.cir.0000021125.83697.21. PMID: 12105156.
  8. Blackburn R, Zhao H, Pebody R, Hayward A, Warren-Gash C. Laboratory-Confirmed Respiratory Infections as Predictors of Hospital Admission for Myocardial Infarction and Stroke: Time-Series Analysis of English Data for 2004-2015. Clin Infect Dis. 2018 Jun 18;67(1):8-17. doi: 10.1093/cid/cix1144. PMID: 29324996; PMCID: PMC6005111.
  9. Barnes M, Heywood AE, Mahimbo A, Rahman B, Newall AT, Macintyre CR. Acute myocardial infarction and influenza: a meta-analysis of case-control studies. Heart. 2015 Nov;101(21):1738-47. doi: 10.1136/heartjnl-2015-307691. Epub 2015 Aug 26. PMID: 26310262; PMCID: PMC4680124.
  10. Guan X, Yang W, Sun X, Wang L, Ma B, Li H, Zhou J. Association of influenza virus infection and inflammatory cytokines with acute myocardial infarction. Inflamm Res. 2012 Jun;61(6):591-8. doi: 10.1007/s00011-012-0449-3. Epub 2012 Feb 29. PMID: 22373653.
  11. Clayton TC, Capps NE, Stephens NG, Wedzicha JA, Meade TW. Recent respiratory infection and the risk of myocardial infarction. Heart. 2005 Dec;91(12):1601-2. doi: 10.1136/hrt.2004.046920. PMID: 16287745; PMCID: PMC1769237.
  12. Kwong JC, Schwartz KL, Campitelli MA, Chung H, Crowcroft NS, Karnauchow T, et al. Acute Myocardial Infarction after Laboratory-Confirmed Influenza Infection. N Engl J Med. 2018 Jan 25;378(4):345-353. doi: 10.1056/NEJMoa1702090. PMID: 29365305.
  13. Caussin C, Escolano S, Mustafic H, Bataille S, Tafflet M, Chatignoux E, et al. CARDIO-ARSIF Registry Investigators. Short-term exposure to environmental parameters and onset of ST elevation myocardial infarction. The CARDIO-ARSIF registry. Int J Cardiol. 2015 Mar 15;183:17-23. doi: 10.1016/j.ijcard.2015.01.078. Epub 2015 Jan 28. PMID: 25662048.
  14. Auer J, Berent R, Weber T, Eber B. Influenza virus infection, infectious burden, and atherosclerosis. Stroke. 2002 Jun;33(6):1454-5. doi: 10.1161/01.str.0000018667.77849.95. PMID: 12052970.
  15. Madjid M, Aboshady I, Awan I, Litovsky S, Casscells SW. Influenza and cardiovascular disease: is there a causal relationship? Tex Heart Inst J. 2004;31(1):4-13. PMID: 15061620; PMCID: PMC387426.60.
  16. Liu PP, Blet A, Smyth D, Li H. The Science Underlying COVID-19: Implications for the Cardiovascular System. Circulation. 2020 Jul 7;142(1):68-78. doi: 10.1161/CIRCULATIONAHA.120.047549. Epub 2020 Apr 15. PMID: 32293910.
  17. Stefanini GG, Montorfano M, Trabattoni D, Andreini D, Ferrante G, Ancona M, et al. ST-Elevation Myocardial Infarction in Patients With COVID-19: Clinical and Angiographic Outcomes. Circulation. 2020 Jun 23;141(25):2113-2116. doi: 10.1161/CIRCULATIONAHA.120.047525. Epub 2020 Apr 30. PMID: 32352306; PMCID: PMC7302062.
  18. Long B, Brady WJ, Koyfman A, Gottlieb M. Cardiovascular complications in COVID-19. Am J Emerg Med. 2020 Jul;38(7):1504-1507. doi: 10.1016/j.ajem.2020.04.048. Epub 2020 Apr 18. PMID: 32317203; PMCID: PMC7165109.
  19. Kochi AN, Tagliari AP, Forleo GB, Fassini GM, Tondo C. Cardiac and arrhythmic complications in patients with COVID-19. J Cardiovasc Electrophysiol. 2020 May;31(5):1003-1008. doi: 10.1111/jce.14479. Epub 2020 Apr 13. PMID: 32270559; PMCID: PMC7262150.
  20. Yaghi S, Ishida K, Torres J, Mac Grory B, Raz E, Humbert K, et al. SARS-CoV-2 and Stroke in a New York Healthcare System. Stroke. 2020 Jul;51(7):2002-2011. doi: 10.1161/STROKEAHA.120.030335. Epub 2020 May 20. Erratum in: Stroke. 2020 Aug;51(8):e179. PMID: 32432996; PMCID: PMC7258764.
  21. Escalard S, Maïer B, Redjem H, Delvoye F, Hébert S, Smajda S, et al. Treatment of Acute Ischemic Stroke due to Large Vessel Occlusion With COVID-19: Experience From Paris. Stroke. 2020 Aug;51(8):2540-2543. doi: 10.1161/STROKEAHA.120.030574. Epub 2020 May 29. PMID: 32466736; PMCID: PMC7282400.
  22. Hamadeh A, Aldujeli A, Briedis K, Tecson KM, Sanz-Sánchez J, Al Dujeili M, et al. Characteristics and Outcomes in Patients Presenting With COVID-19 and ST-Segment Elevation Myocardial Infarction. Am J Cardiol. 2020 Sep 15;131:1-6. doi: 10.1016/j.amjcard.2020.06.063. Epub 2020 Jul 3. PMID: 32732010; PMCID: PMC7333635.
  23. Varga Z, Flammer AJ, Steiger P, Haberecker M, Andermatt R, Zinkernagel AS, et al. Endothelial cell infection and endotheliitis in COVID-19. Lancet. 2020 May 2;395(10234):1417-1418. doi: 10.1016/S0140-6736(20)30937-5. Epub 2020 Apr 21. PMID: 32325026; PMCID: PMC7172722.
  24. Mauriello A, Sangiorgi G, Fratoni S, Palmieri G, Bonanno E, Anemona L, et al. Diffuse and active inflammation occurs in both vulnerable and stable plaques of the entire coronary tree: a histopathologic study of patients dying of acute myocardial infarction. J Am Coll Cardiol. 2005 May 17;45(10):1585-93. doi: 10.1016/j.jacc.2005.01.054. Epub 2005 Apr 25. PMID: 15893171.
  25. Long B, Brady WJ, Koyfman A, Gottlieb M. Cardiovascular complications in COVID-19. Am J Emerg Med. 2020 Jul;38(7):1504-1507. doi: 10.1016/j.ajem.2020.04.048. Epub 2020 Apr 18. PMID: 32317203; PMCID: PMC7165109.
  26. Sandoval Y, Jaffe AS. Type 2 Myocardial Infarction: JACC Review Topic of the Week. J Am Coll Cardiol. 2019 Apr 16;73(14):1846-1860. doi: 10.1016/j.jacc.2019.02.018. PMID: 30975302
  27. Belani P, Schefflein J, Kihira S, Rigney B, Delman BN, Mahmoudi K, et al. COVID-19 Is an Independent Risk Factor for Acute Ischemic Stroke. AJNR Am J Neuroradiol. 2020 Aug;41(8):1361-1364. doi: 10.3174/ajnr.A6650. Epub 2020 Jun 25. PMID: 32586968; PMCID: PMC7658882.
  28. Xiao JY, Zhang HN, Cao L, Cong HL. [An analysis of relationship between the severity of coronary artery lesion and risk factors of cardiovascular events in Tianjin]. Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2013 Nov;25(11):650-4. Chinese. doi: 10.3760/cma.j.issn.2095-4352.2013.11.014. PMID: 24225217.
  29. Castela S, Duarte R, Reis RP, Correia MJ, Toste J, Carmelo V, Cardim N, Adão M, Correia JM. Acute coronary syndromes in smokers: clinical and angiographic characteristics. Rev Port Cardiol. 2004 May;23(5):697-705. English, Portuguese. PMID: 15279454.

Supplementary files

Supplementary Files
Action
1. JATS XML
Download
2. Fig. 1. Damage to coronary vessels according to coronary angiography,%

Download (119KB)
Indexing metadata

Copyright (c) 2021 "Paediatrician" Publishers LLC



This website uses cookies

You consent to our cookies if you continue to use our website.

About Cookies