Marco Antonutti1, Federica Baldan2, Corrado Lanera3, Leonardo Spedicato4, Davide Zanuttini4, Teodoro Bisceglia4, Enrico Favaretto4, Stefano Poli4, Chiara Tioni4, Dario Sut4, Dario Gregori3, Giuseppe Damante5, Alessandro Proclemer6. 1. Division 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. Electronic address: marcoantonutti@hotmail.it. 2. Department of Medicine, University of Udine, Via Colugna 51, 33100 Udine, Italy. 3. Unit of Biostatistics, Epidemiology and Public Health, DCTVPH, University of Padova, Via 8 Febbraio 1848, 2, 35122 Padova, PD, Italy. 4. Division 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. 5. Department of Medicine, University of Udine, Via Colugna 51, 33100 Udine, Italy; Institute of Medical Genetic, Azienda Sanitaria Universitaria Integrata di Udine - Ospedale Santa Maria della Misericordia, Piazzale Santa Maria della Misericordia 15, 33100 Udine, Italy. 6. Division 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.
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.
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.