Background: Extracellular matrix (ECM) remodeling contributes to in-stent restenosis and thrombosis. Despite its important clinical implications, little is known about ECM changes post–stent implantation. Methods: Bare-metal and drug-eluting stents were implanted in pig coronary arteries with an overstretch under optical coherence tomography guidance. Stented segments were harvested 1, 3, 7, 14, and 28 days post-stenting for proteomics analysis of the media and neointima. Results: A total of 151 ECM and ECM-associated proteins were identified by mass spectrometry. After stent implantation, proteins involved in regulating calcification were upregulated in the neointima of drug-eluting stents. The earliest changes in the media were proteins involved in inflammation and thrombosis, followed by changes in regulatory ECM proteins. By day 28, basement membrane proteins were reduced in drug-eluting stents in comparison with bare-metal stents. In contrast, the large aggregating proteoglycan aggrecan was increased. Aggrecanases of the ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) family contribute to the catabolism of vascular proteoglycans. An increase in ADAMTS-specific aggrecan fragments was accompanied by a notable shift from ADAMTS1 and ADAMTS5 to ADAMTS4 gene expression after stent implantation. Immunostaining in human stented coronary arteries confirmed the presence of aggrecan and aggrecan fragments, in particular, at the contacts of the stent struts with the artery. Further investigation of aggrecan presence in the human vasculature revealed that aggrecan and aggrecan cleavage were more abundant in human arteries than in human veins. In addition, aggrecan synthesis was induced on grafting a vein into the arterial circulation, suggesting an important role for aggrecan in vascular plasticity. Finally, lack of ADAMTS-5 activity in mice resulted in an accumulation of aggrecan and a dilation of the thoracic aorta, confirming that aggrecanase activity regulates aggrecan abundance in the arterial wall and contributes to vascular remodeling. Conclusions: Significant differences were identified by proteomics in the ECM of coronary arteries after bare-metal and drug-eluting stent implantation, most notably an upregulation of aggrecan, a major ECM component of cartilaginous tissues that confers resistance to compression. The accumulation of aggrecan coincided with a shift in ADAMTS gene expression. This study provides the first evidence implicating aggrecan and aggrecanases in the vascular injury response after stenting.

Background: Whereas the efficacy and safety of intravascular lithotripsy (IVL) have been confirmed in de novo calcified coronary lesions, little is known about its utility in treating stent underexpansion. This study aimed to investigate the impact of IVL in treating stent underexpansion. Methods and Results: Consecutive patients with stent underexpansion treated with IVL entered the multicenter IVL-Dragon Registry. The procedural success (primary efficacy endpoint) was defined as a relative stent expansion >80%. Thirty days device-oriented composite endpoint (DOCE) (defined as a composite of cardiac death, target lesion revascularization, or target vessel myocardial infarction) was the secondary endpoint. A total of 62 patients were enrolled. The primary efficacy endpoint was achieved in 72.6% of patients. Both stent underexpansion 58.5% (47.5–69.7) vs. 11.4% (5.8–20.7), p < 0.001, and the stenotic area 82.6% (72.4–90.8) vs. 21.5% (11.1–37.2), p < 0.001, measured by quantitative coronary angiography improved significantly after IVL. Intravascular imaging confirmed increased stent expansion following IVL from 37.5% (16.0–66.0) to 86.0% (69.2–90.7), p < 0.001, by optical coherence tomography and from 57.0% (31.5–77.2) to 89.0% (85.0–92.0), p = 0.002, by intravascular ultrasound. Secondary endpoint occurred in one (1.6%) patient caused by cardiac death. There was no target lesion revascularization or target vessel myocardial infarction during the 30-day follow-up. Conclusions: In this real-life, largest-to-date analysis of IVL use to manage underexpanded stent, IVL proved to be an effective and safe method for facilitating stent expansion and increasing luminal gain.

Drug-eluting stents (DES) demonstrated superior efficacy when compared to bare metal stents and plain-old balloon angioplasty and are nowadays used in almost all percutaneous revascularization procedures. The design of the stent platforms is constantly improving to maximize its efficacy and safety. Constant development of DES includes adoption of new materials used for scaffold production, new design types, improved overexpansion abilities, new polymers coating and, finally, improved antiproliferative agents. Especially nowadays, with the immense number of available DES platforms, it is crucial to understand how different aspects of stents impact the effect of their implantation, as subtle differences between various stent platforms could impact the most important issue—clinical outcomes. This review discusses the current status of coronary stents and the impact of stent material, strut design and coating techniques on cardiovascular outcomes.

Background: Autopsy studies have established that thin-cap fibroatheromas (TCFAs) are the most frequent cause of fatal coronary events. In living patients, optical coherence tomography (OCT) has sufficient resolution to accurately differentiate TCFA from thick-cap fibroatheroma (ThCFA) and not lipid rich plaque (non-LRP). However, the impact of OCT-detected plaque phenotype of nonischemic lesions on future adverse events remains unknown. Therefore, we studied the natural history of OCT-detected TCFA, ThCFA, and non-LRP in patients enrolled in the prospective multicenter COMBINE FFR-OCT trial (Combined Optical Coherence Tomography Morphologic and Fractional Flow Reserve Hemodynamic Assessment of Non-Culprit Lesions to Better Predict Adverse Event Outcomes in Diabetes Mellitus Patients). Methods: In the COMBINE FFR-OCT trial, patients with diabetes and ≥1 lesion with a fractional flow reserve >0.80 underwent OCT evaluation and were clinically followed for 18 months. A composite primary end point of cardiac death, target vessel-related myocardial infarction, target-lesion revascularization, and hospitalization for unstable angina was evaluated in relation to OCT-based plaque morphology. Results: A total of 390 patients (age 67.5±9 years; 63% male) with ≥1 nonischemic lesions underwent OCT evaluation: 284 (73%) had ≥1 LRP and 106 (27%) non-LRP lesions. Among LRP patients, 98 (34.5%) had ≥1 TCFA. The primary end point occurred in 7% of LRP patients compared with 1.9% of non-LRP patients (7.0% versus 1.9%; hazard ratio [HR], 3.9 [95% CI, 0.9–16.5]; P =0.068; log rank- P =0.049). However, within LRP patients, TCFA patients had a much higher risk for primary end point compared with ThCFA (13.3% versus 3.8%; HR, 3.8 [95% CI, 1.5–9.5]; P <0.01), and to non-LRP patients (13.3% versus 1.9%; HR, 7.7 [95% CI, 1.7–33.9]; P <0.01), whereas ThCFA patients had risk similar to non-LRP patients (3.8% versus 1.9%; HR, 2.0 [95% CI, 0.42–9.7]; P =0.38). Multivariable analyses identified TCFA as the strongest independent predictor of primary end point (HR, 6.79 [95% CI, 1.50–30.72]; P =0.013). Conclusions: Among diabetes patients with fractional flow reserve-negative lesions, patients carrying TCFA lesions represent only one-third of LRP patients and are associated with a high risk of future events while patients carrying LRP-ThCFA and non-LRP lesions portend benign outcomes. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT02989740.

Background: Diagnosis of myocardial infarction with non-obstructive coronary arteries (MINOCA) requires both clinical evidence of acute myocardial infarction (AMI) and demonstration of non-obstructive coronary arteries using angiography. We compared the clinical features, treatments, and three-year outcomes in patients with MINOCA and myocardial infarction with obstructive coronary artery disease (MI-CAD). Methods: We retrospectively analyzed data for 205,606 hospitalized patients with AMI. MINOCA was indicated as a working diagnosis in 6063 patients (2.94% of all AMI patients). For the control group we included 160,886 patients with MI-CAD. We evaluated the baseline characteristics, medication management options, outcomes, and readmission causes at 36 months follow-up. Results: Patients in the MINOCA group were younger. Females constituted a greater proportion of patients in the MINOCA group when compared to MI-CAD patients. STEMI during admission was diagnosed less frequently in the MINOCA group when compared to the MI-CAD group. All-cause mortality at 12 months was higher in the MINOCA group (10.94% vs. 9.54%, p < 0.001). At 36 months, there was no difference in the all-cause mortality rates (MINOCA 16.18% vs. MI-CAD 14.93%, p = 0.081). All-cause readmission rates were lower in the MINOCA group when compared to the MI-CAD group at both 12 months (45.19% vs. 54.33%, p < 0.001) and 36 months follow-up (56.42% vs. 66.66%, p < 0.001). Conclusions: This is the first description of the clinical features, treatments, and three-year outcomes in a large population of Polish patients. The main finding of this study was a relatively low rate of MINOCA, with high rates of adverse events both at 12 and 36 months follow-up.