Spontaneous coronary artery dissection: Role of prognostic markers and relationship with genetic analysis. (1st March 2021)

• Record Type: Journal Article
• Authors: Antonutti, Marco; Baldan, Federica; Lanera, Corrado; Spedicato, Leonardo; Zanuttini, Davide; Bisceglia, Teodoro; Favaretto, Enrico; Poli, Stefano; Tioni, Chiara; Sut, Dario; Gregori, Dario; Damante, Giuseppe; Proclemer, Alessandro
• Is Part Of: International journal of cardiology. Volume 326(2021)
• Page Start: 19
• Page End: 29
• Publication Date: 2021-03-01
• Subjects: SCAD -- Spontaneous -- Coronary -- Dissection -- Genetics; Cardiology -- Periodicals; Electronic journals; 616.12
• DOI: 10.1016/j.ijcard.2020.10.040
• Languages: English
• ISSNs: 0167-5273

Abstract

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. Highlights: The strong point of our work is represented from two new cornerstones for better understanding this disease. First, we have shown that there are several prognostic factors that can predict both recurrent de novo SCAD (use of hormonal therapy and ventricular arrhythmias) and major adverse cardiovascular events (MACE) (ventricular arrhythmias and proximal coronary site of the lesion at the first event). Second, we have highlighted how there may be a relationship between MACE development and genetic mutations sought through next generation sequencing.