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N/A N=80

Genetic Determinants of the Coronary Microvascular Obstruction in PCI

Myocardial Infarction · No-Reflow Phenomenon

Enrolled (actual)
80
Serious AEs
0.0%
Results posted
Sep 2025
Primary outcome: Primary: Hospital Mortality Rate — 6; 2 Participants

Study Design & Population

Study type
Observational
Phase
N/A
Interventions
different variants of SNPs that may be associated with the coronary microvascular obstruction development (Genetic)
Age
Adult, Older Adult · 18+ yrs
Sex
All
Sponsor
Privolzhsky Research Medical University
Primary completion
Mar 2023

Outcome Measures

OutcomeResultp-value
PRIMARY
Hospital Mortality Rate
6; 2
SECONDARY
Left Ventricle Ejection Fraction
47; 50
SECONDARY
Six-minute Walk Test
395; 425
SECONDARY
N-terminal Pro-brain Natriuretic Peptide
1171; 530
SECONDARY
Ventricular Fibrillation
0; 0

Summary

Myocardial infarction (MI) remains one of the most common causes of death. Percutaneous coronary intervention (PCI) is the main treatment option to restore blood flow through the infarction-related coronary artery (IRA) in MI patients. Performing PCI significantly reduces mortality, but in 5-10% cases, PCI is complicated by the development of coronary microvascular obstruction (CMVO, "no-reflow"). CMVO is defined as the absence of adequate myocardial perfusion, despite the restoration of the IRA lumen. The development of CMVO significantly worsens the prognosis and increases mortality. CMVO has a complex pathogenesis and is development due to following mechanisms: distal microembolism, ischemia-reperfusion injury, persistent endothelial dysfunction, and individual predisposition. These mechanisms can be implemented simultaneously and have different severity. The most significant predictors of CMVO occurrence are: age, time from pain onset to reperfusion, severity of acute heart failure, ineffective thrombolytic therapy, collateral blood flow according to the Rentrop classification, severity of IRA thrombosis according to Thrombolysis in Myocardial Infarction (TIMI) thrombus grade, initial IRA blood flow according to TIMI flow grade, implantation of 3 or more stents, direct IRA stenting, neutrophil and blood glucose levels. Difficulties in CMVO predicting are caused by the pathogenetic heterogeneity of this complication. Even the best models are moderately accurate. This can be explained by the fact that the models don't use genetic factors that determine endothelial function, microcirculation, hemostasis, and inflammation. Identification of the genetic determinants of the CMVO development can help create a new diagnostic system for CMVO predicting.

Eligibility Criteria

Inclusion Criteria

  • informed consent to participate in the study;
  • male or female 18 years of age or older;
  • type 1 ST-segment elevation MI (according to the criteria of the fourth universal definition of myocardial infarction and current clinical guidelines);
  • blood sampling in the operating room (immediately after PCI) and signing the informed consent;
  • for the "CMVO+" group: CMVO because of PCI (CMVO is registered according to the criteria from the European Society of Cardiology clinical guidelines);
  • for the "CMVO-" group: absence of CMVO after PCI; patient should compliance by sex and age (±5 years) with pair in the "CMVO+" group.

Exclusion Criteria

  • late admission (more than 48 hours from the onset of anginal pain) or early post-infarction angina pectoris;
  • not 1 type MI;
  • complications during PCI (dissection, perforation or acute intraoperative thrombosis of the IRA);
  • death during PCI, not due to the CMVO development;
  • concomitant terminal pathology (not associated with MI) with a life expectancy less than 1 month.
View full record on ClinicalTrials.gov →

Data sourced from ClinicalTrials.gov (NCT05355532). Outcome figures and adverse-event rates are extracted automatically from the registry's posted results and are provided for clinician reference, not as a substitute for the primary publication.

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