Spontaneous coronary artery dissection: Role of prognostic markers and relationship with genetic analysis

Marco Antonutti1, Federica Baldan2, Corrado Lanera3

  • 1Division of Cardiology, Department of Cardiothoracic Sciences, Azienda Sanitaria Universitaria Friuli Centrale - Ospedale Santa Maria della Misericordia, Piazzale Santa Maria della Misericordia 15, 33100 Udine, Italy; Institute of Applied and Basic Clinical Research (IRCAB Foundation), Piazzale Santa Maria della Misericordia 11, 33100 Udine, Italy.

Insights

Spontaneous coronary artery dissection (SCAD) patients using hormone therapy or experiencing ventricular arrhythmias face higher risks of recurrence. Genetic analysis may aid in predicting major adverse cardiovascular events (MACE) in SCAD survivors.

Area of Science:

  • Cardiology
  • Genetics
  • Internal Medicine

Background:

  • Spontaneous coronary artery dissection (SCAD) is an emerging cause of myocardial infarction (MI).
  • Limited understanding exists regarding long-term prognostic factors and genetic predispositions in SCAD patients.
  • This study addresses these knowledge gaps by examining long-term outcomes and genetic correlations.

Purpose of the Study:

  • To describe long-term cardiovascular outcomes in SCAD patients.
  • To identify predictors of recurrent SCAD and major adverse cardiovascular events (MACE).
  • To explore the correlation between patient genotype and adverse cardiovascular events.

Main Methods:

  • An observational, retrospective study design was employed.
  • Data on baseline characteristics, angiographic features, and medication use were collected from 2000-2019.
  • Next-generation sequencing was performed on a panel of 20 genes, considering variants with <1% population frequency as potentially significant.

Main Results:

  • Seventy patients were followed for a median of 39.1 months; 86% were women.
  • Hormone therapy use and ventricular arrhythmias (VAs) at onset predicted recurrent SCAD (OR 3.64, p=0.041 and OR 7.03, p=0.0073, respectively).
  • Proximal SCAD and VAs at onset predicted MACE (OR 8.47, p<0.0001 and OR 9.97, p=0.047, respectively). A potential SCAD-associated mutation was found in 44% of patients, with genetically "positive" patients experiencing MACE earlier.

Conclusions:

  • Hormone therapy and VAs at SCAD onset are prognostic factors for recurrent SCAD.
  • Proximal SCAD location and VAs at onset are prognostic factors for MACE.
  • Molecular genetic analysis shows promise for predicting MACE in SCAD patients.

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