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Published on: January 28, 2020
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.
Abstract:
Spontaneous coronary artery dissection (SCAD) is increasingly recognized as an important cause of myocardial infarction (MI). Currently there is little knowledge about prognostic factors for unfavorable outcome at long term follow-up; furthermore, there is also little knowledge about the genetics of these patients.
Aims:
This observational and retrospective study describes long-term cardiovascular outcomes of a population affected by SCAD and assesses predictors of recurrent de novo SCAD and major adverse cardiovascular events (MACE). Furthermore, a correlation between genotype and adverse events at follow-up was sought.
Methods:
Baseline characteristics, angiographic features, use of medication and long-term cardiovascular events were systematically ascertained between 2000 and 2019. Next generation sequencing was performed with a panel consisting of twenty genes of interest. Variants found were filtered based on their frequency and only frequencies <1% in the general population were considered as "positive".
Results:
Seventy patients were enrolled and followed for a median time of 39.1 months. Median age was 52 years and the majority were women (86%). Use of hormone therapy (HT) (OR 3.64, p = 0.041) and presence of malignant ventricular arrhythmias (VAs) at onset (OR 7.03, p = 0.0073) were associated with a greater risk of recurrent de novo SCAD. Proximal type SCAD (OR 8.47, p < 0.0001) and presence of VAs at onset (OR 9.97, p = 0.047) were associated with a greater risk of MACE. A potential SCAD-associated mutation was detected in 27 patients (44%); 6 patients (22%) defined as genetically "positive" developed MACE vs. 2 patients (6%) defined as "negative" (p = 0.06 at univariate analysis). MACE at follow-up is reached earlier in genetically positive patients (7.9 vs. 42.5 months).
Conclusion:
use of HT and VAs at SCAD onset are prognostic factors for recurrent de novo SCAD. Proximal SCAD site and VAs at SCAD onset were prognostic factors for MACE. Analysis by molecular genetics seems to be a promising tool for the possible additional role it could play in MACE prediction.
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