Clinical and laboratory features of primary acute myocardial infarction in patients with obstructive and non-obstructive coronary atherosclerosis

According to the literature, 40-60% of patients with acute myocardial infarction (AMI) have obstructive multivessel coronary artery disease (CA) and 8.8% of patients have non-obstructive CA lesions. And it is around these two groups of patients that there are active discussions and disputes regarding the choice of optimal treatment tactics and further prognosis. The aim of the study was to study clinical and laboratory features of development and course of primary AMI in patients with multi-and single-vessel obstructive lesion of the CA compared with patients with non-obstructive CA lesions. Methods. The study has included patients hospitalized "through the ambulance channel" in the Department of cardiac intensive care of municipal clinical hospital named after S. S. Yudin Moscow with a diagnosis “primary acute myocardial infarction”, ACS with and without ST segment elevation, unstable angina in 2015-2016. The diagnosis of acute myocardial infarction (AMI) was established at the hospital stage according to the criteria of the "Third universal definition of myocardial infarction" in 2012. The study included 1240 patients who underwent coronary angiography (CAG) no later than 12 hours from the time of admission. The first group (comparison group) consisted of patients with AMI and the first detected multivessel obstructive atherosclerotic lesion of CA (664 patients), the second (interest group) consisted of patients with AMI and non-obstructive atherosclerotic lesion of CA (96 patients) meeting the MINOCA criteria. The third group consisted of patients with single-vessel obstructive lesion and complete acute occlusion of the CA (272 patients). Patients with hemodynamically significant lesions of the left CA trunk were not included in the study. The clinical and laboratory features of the course of acute primary myocardial infarction in patients with obstructive and non-obstructive coronary atherosclerosis were studied. The generally accepted statistical processing methods were used. A year after discharge from the hospital, 727 patients (468 patients from the 1^st group, 78 from the 2nd group, 181 from the 3rd group) were interviewed by means of a structured telephone survey about the course of the disease (collection of medical history). The median follow-up was 12 months. (interquartile range 11-13 months). The endpoints were: re-hospitalization for any reason, re-coronary event, death. The received answers are entered into questionnaires and statistically processed. Results and conclusions. In patients with AMI and non-obstructive atherosclerotic CA lesion, pain behind the sternum is observed one and a half times less often (54.2%) than in patients with obstructive CA lesion (MOAPCA 86.1%, OAPCA 89.7%) and the cardiac co duction system is almost three times more likely to be affected ( 30% versus 8.4% and 12%). Only 12.5% of patients in this group had an abnormal Q wave (Q – myocardial infarction) on the ECG, therefore, a smaller volume of myocardial damage and a lower level of troponin than in patients of groups 1 and 3. During the first year after the development of AMI, patients with obstructive coronary atherosclerosis did not experience repeated coronary events, there were no indications for conducting CAG, PCI or CABG, in contrast to patients with obstructive lesion of CA. For multivascular obstruction (group 1), PCI was performed in 9.6% of patients and 3.8% of CABG. PCI was performed in group 3 with obstructive single-vessel lesion of CA in 7.7% of patients. In patients with AMI and obstructive single-vessel atherosclerotic lesion of CA (group 3), two and a half times less often (9.1%) myocardial reperfusion injury is observed, while in patients with multivascular obstructive CA defeat, this syndrome was observed in 21.3%.

1. Cruveilhier J. Anatomie pathologique du corps humain, ou description, avec figures lithographiées et colorieés, des diverses alterations morbides dont le corps humain est susceptible. 2 text volumes et 2 volumes atlas. -Paris: Baillière;1829.

2. Obraztsov V.P. Symptomatology and diagnosis of coronary thrombosis. Proceedings of the First Russian Congress of therapists. – M.: Printing house A.E. Mamontov;1910. – 26–40 p.

3. Dyatlov N.V., Lykov Yu.V., Zhelnov V.V., Dvoretsky L.I. Some peculiarities of acute myocardial infarction pathogenesis in non-obstructive coronary arteries. Medical news of the North Caucasus. 2017;12 (3):260–5. DOI: 10.14300/mnnc.2017.12078

4. Pasupathy S, University of Adelaide, Central Adelaide Local Health Network, Tavella R, University of Adelaide, Central Adelaide Local Health Network et al. Myocardial Infarction with Nonobstructive Coronary Arteries — Diagnosis and Management. European Cardiology Review. 2015;10(2):79–82. DOI: 10.15420/ecr.2015.10.2.79

5. Pasupathy S, Tavella R, Beltrame JF. Myocardial Infarction with Nonobstructive Coronary Arteries (MINOCA): The Past, Present, and Future Management. Circulation. 2017;135(16):1490–3. DOI: 10.1161/CIRCULATIONAHA.117.027666

6. Planer D, Mehran R, Ohman EM, White HD, Newman JD, Xu K et al. Prognosis of Patients with Non–ST-Segment–Elevation Myocardial Infarction and Nonobstructive Coronary Artery Disease: Propensity-Matched Analysis from the Acute Catheterization and Urgent Intervention Triage Strategy Trial. Circulation: Cardiovascular Interventions. 2014;7(3):285–93. DOI: 10.1161/CIRCINTERVENTIONS.113.000606

7. Pais JL, Izquierdo B, González V, Magana JG, Caballero RM, Pascual MJE et al. Incidence, clinical profile and prognosis of patients with myocardial infarction with non-obstructive coronary arteries in the real world. Journal of the American College of Cardiology. 2017;69(11):142. DOI: 10.1016/S0735-1097(17)33531-3

8. Scalone G, Niccoli G, Crea F. Pathophysiology, diagnosis and management of MINOCA: an update. European Heart Journal: Acute Cardiovascular Care. 2019;8(1):54–62. DOI: 10.1177/2048872618782414

9. Thygesen K, Alpert JS, Jaffe AS, Simoons ML, Chaitman BR, White HD. Third Universal Definition of Myocardial Infarction. Circulation. 2012;126(16):2020–35. DOI: 10.1161/CIR.0b013e31826e1058

10. Agewall S, Beltrame JF, Reynolds HR, Niessner A, Rosano G, Caforio ALP et al. ESC working group position paper on myocardial infarction with non-obstructive coronary arteries. European Heart Journal. 2016;38(3):143–53. DOI: 10.1093/eurheartj/ehw149

11. Windecker S, Kolh P, Alfonso F, Collet J-P, Cremer J, Falk V et al. ESC / EACTS recommendations for myocardial revascularization 2014. Russian Journal of Cardiology. 2015;20(2):5–81. DOI: 10.15829/1560-4071-2015-02-5-81

12. O’Gara PT, Kushner FG, Ascheim DD, Casey DE, Chung MK, de Lemos JA et al. 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction: Executive Summary: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2013;127(4):529–55. DOI: 10.1161/CIR.0b013e3182742c84

13. Unikas R, Budrys P. Association between clinical parameters and ST-segment resolution after primary percutaneous coronary intervention in patients with acute ST-segment elevation myocardial infarction. Medicina. 2016;52(3):156–62. DOI: 10.1016/j.medici.2016.03.004

14. Fröhlich GM, Meier P, White SK, Yellon DM, Hausenloy DJ. Myocardial reperfusion injury: looking beyond primary PCI. European Heart Journal. 2013;34(23):1714–22. DOI: 10.1093/eurheartj/eht090

15. Simonis G, Strasser RH, Ebner B. Reperfusion injury in acute myocardial infarction. Critical Care. 2012;16(Suppl 2): A22. DOI: 10.1186/cc11280

16. Reimer KA, Lowe JE, Rasmussen MM, Jennings RB. The wavefront phenomenon of ischemic cell death. 1. Myocardial infarct size vs duration of coronary occlusion in dogs. Circulation. 1977;56(5):786–94. DOI: 10.1161/01.CIR.56.5.786

17. Kingma Jg. Acute Myocardial Injury: A Perspective on Lethal Reperfusion Injury. Cardiovascular Pharmacology: Open Access. 2017;6(5):216. DOI: 10.4172/2329-6607.1000216

18. Lau JK, Pennings GJ, Yong A, Kritharides L. Cardiac Remote Ischaemic Preconditioning: Mechanistic and Clinical Considerations. Heart, Lung and Circulation. 2017;26(6):545–53. DOI: 10.1016/j.hlc.2016.11.006

19. Iliodromitis EK, Andreadou I, Iliodromitis K, Dagres N. Ischemic and Postischemic Conditioning of the Myocardium in Clinical Practice: Challenges, Expectations and Obstacles. Cardiology. 2014;129(2):117–25. DOI: 10.1159/000362499

20. Li X, Liu M, Sun R, Zeng Y, Chen S, Zhang P. Protective approaches against myocardial ischemia reperfusion injury. Experimental and Therapeutic Medicine. 2016;12(6):3823–9. DOI: 10.3892/etm.2016.3877

21. Matsuzawa Y, Lerman A. Endothelial dysfunction and coronary artery disease: assessment, prognosis, and treatment. Coronary Artery Disease. 2014;25(8):713–24. DOI: 10.1097/MCA.0000000000000178

22. Bairey Merz CN, Pepine CJ, Walsh MN, Fleg JL, Camici PG, Chilian WM et al. Ischemia and No Obstructive Coronary Artery Disease (INOCA): Developing Evidence-Based Therapies and Research Agenda for the Next Decade. Circulation. 2017;135(11):1075–92. DOI: 10.1161/CIRCULATIONAHA.116.024534

23. Grodzinsky A, Arnold SV, Gosch K, Spertus JA, Foody JM, Beltrame J et al. Angina frequency after acute myocardial infarction in patients without obstructive coronary artery disease. European Heart Journal - Quality of Care and Clinical Outcomes. 2015;1(2):92–9. DOI: 10.1093/ehjqcco/qcv014