Background: Risks and mechanisms of extension of conservatively managed spontaneous coronary artery dissection (SCAD) remain incompletely understood. Study objectives were to (1) evaluate mechanisms of early SCAD evolution through serial angiographic analysis, and (2) determine predictors of early SCAD progression. Methods and Results: Retrospective registry study of patients with SCAD managed with an initial conservative strategy (n=240). Patients who experienced significant SCAD progression within 14 days, defined as clinical worsening plus new critical coronary obstruction on repeat angiography, were compared with remaining controls. A total of 42 of 240 (17.5%) experienced significant SCAD progression after index conservative approach; 91% by day 6. Isolated intramural hematoma (IMH) at baseline (no intimal dissection) was observed more frequently in those experiencing progression compared with controls (69.1% versus 44.4%; P =0.004). Multivariable predictors of SCAD progression included lesion severity, multivessel involvement, and isolated IMH. To investigate mechanisms of SCAD evolution, all repeat angiograms ≤14 days were compared with corresponding baselines (n=82 patient angiogram pairs). Of those with isolated IMH at baseline, 20% developed intimal dissection at repeat study. IMH was associated with greater longitudinal lesion extension (11.5 versus 2.8 mm; P =0.01), worsening Thrombolysis in Myocardial Infarction flow (−0.8 versus 0.1; P =0.003), and a nonsignificant lower rate of angiographic improvement (20.0% versus 31.3%; P =0.16) compared with the group with baseline intimal dissection. Optical coherence tomography subgroup analysis (n=17) indicated intimo-medial thickness to be lowest at the midpoint of IMH. Conclusions: Conservatively managed SCAD carries a 1:6 hazard for serious deterioration within 6 days. The risk was higher in those with isolated IMH at baseline. IMH often precedes development of intimal dissection, which has implications for mechanisms of SCAD.
Coronary endothelial function and spontaneous coronary artery dissection
Objectives: To investigate the role of endothelial function in patients with previous spontaneous coronary artery dissection. Background: Mechanisms underlying spontaneous coronary artery dissection, including a possible contribution from endothelial dysfunction, remain poorly understood. Methods: This was a single center, retrospective study of patients with a prior spontaneous coronary artery dissection episode who underwent invasive endothelial function testing in the cardiac catheterization laboratory for evaluation of recurrent chest pain. Coronary epicardial and microvascular responses to acetylcholine, adenosine, and nitroglycerine were assessed. Findings were compared to a reference group of normal controls ( n=232). Results: A total of 10 patients with prior angiographically confirmed spontaneous coronary artery dissection were referred for coronary endothelial function testing. The median coronary flow reserve was 2.8 (interquartile range (IQR) 2.3, 3.6). The median change in coronary diameter with acetylcholine was −0.9% (IQR −23.9, 4.2). The median increase in peak coronary blood flow following acetylcholine administration was 91.4% (IQR 9.1, 105.7), which was similar to the response observed in a reference group of patients (median age 51 years, 96% women) from our laboratory with normal microvascular responses to acetylcholine: 107.4% (IQR 75.5, 165.7; P=0.20). Four patients (40%) had an abnormal microvascular response to acetylcholine, with less than a 50% increase in coronary blood flow, and all but one patient had left anterior descending artery or multivessel spontaneous coronary artery dissection. Conclusion: Coronary epicardial and microvascular vasomotor dysfunction is not a predominant feature of spontaneous coronary artery dissection. Endothelial dysfunction is not implicated as the principal underlying mechanism.
Techniques and outcomes of paravalvular leak repair after transcatheter aortic valve replacement
AbstractObjectivesTo investigate the feasibility, procedural success, and outcomes of paravalvular leak (PVL) closure in patients with prior transcatheter aortic valve replacement (TAVR).BackgroundPVL after TAVR is associated with adverse patient outcomes and increased mortality. Percutaneous PVL closure has emerged as a therapeutic strategy for addressing this issue, but data for transcatheter PVL repair after TAVR remains limited.MethodsThis is a single center retrospective review of PVL closure after TAVR. Patients with balloon‐expandable or self‐expanding prostheses were included. Baseline patient demographics, procedural characteristics, complications, and clinical outcomes were reviewed.ResultsA total of 18 patients with clinically significant PVL after TAVR referred for PVL closure were identified during the study period. Procedural success resulting in successful transcatheter occluder plug delivery was 78% (14 cases). Balloon postdilatation (2/4) and valve‐in‐valve (2/4) were used effectively in the remaining patients after an unsuccessful PVL closure attempt. PVL grading by echocardiography decreased from moderate or severe to < moderate in 13 patients (72%). Adverse events including cardiac tamponade and acute kidney injury occurred in 1 case each. One‐month all‐cause mortality was 11%.ConclusionIn selected patients, percutaneous PVL repair following TAVR is feasible and effective for both balloon‐expandable and self‐expanding prostheses. Most patients undergoing PVL closure after TAVR require a single occluder plug placement for reduction in PVL to mild or less.
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