Cholesterol crystals at the culprit lesion in patients with acute coronary syndrome are associated with worse cardiovascular outcomes at two years follow up - results from the translational OPTICO-ACS study program.

BACKGROUND: Cholesterol crystals (CCs) represent a feature of advanced atherosclerotic plaque and may be assessed by optical coherence tomography (OCT). Their impact on cardiovascular outcomes in patients presenting with acute coronary syndromes (ACS) is yet unknown. METHODS: The culprit lesion (CL) of 346 ACS-patients undergoing preintervention OCT imaging were screened for the presence of CCs and divided into two groups accordingly. The primary end-point was the rate of major adverse cardiac events plus (MACE+) consisting of cardiac death, myocardial infarction, target vessel revascularization and re-hospitalization due to unstable or progressive angina at two years. RESULTS: Among 346 patients, 57.2% presented with CCs at the CL. Patients with CCs exhibited a higher prevalence of ruptured fibrous caps (RFC-ACS) (79.8% vs. 56.8%; p < 0.001) and other high-risk features such as thin cap fibroatheroma (80.8% vs. 64.9%; p = 0.001), presence of macrophages (99.0% vs. 85.1%; p < 0.001) as well as a greater maximum lipid arc (294.0° vs. 259.3°; p < 0.001) at the CL as compared to patients without CCs. MACE+ at two years follow-up occurred more often in CC-patients (29.2% vs. 16.1%; p = 0.006) as compared to patients without CCs at the culprit site. Multivariable cox regression analysis identified CCs as independent predictor of MACE+ (HR 1.705; 1.025-2.838 CI, p = 0.040). CONCLUSIONS: CCs were associated with conventional high-risk plaque features and associated with increased MACE+-rates at two years follow up. The identification of CCs might be useful as prognostic marker in patients with ACS and assist "precision prevention" in the future.

Coexistence of calcified- and lipid-containing plaque components and their association with incidental rupture points in acute coronary syndrome-causing culprit lesions: results from the prospective OPTICO-ACS study.

AIMS: Rupture of the fibrous cap (RFC) represents the main pathophysiological mechanism causing acute coronary syndromes (ACS). Destabilization due to plaque biomechanics is considered to be importantly involved, exact mechanisms triggering plaque ruptures are, however, unknown. This study aims at characterizing the relation between plaque components and rupture points at ACS-causing culprit lesions in a large cohort of ACS-patients assessed by high-resolution intracoronary imaging. METHODS AND RESULTS: Within the prospective, multicentric OPTICO-ACS study program, the ACS-causing culprit plaques of 282 consecutive patients were investigated following a standardized optical coherence tomography (OCT) imaging protocol. Each pullback was assessed on a frame-by-frame basis for the presence of lipid components (LC), calcium components (CC), and coexistence of both LC and CC (LCC) by two independent OCT-core labs. Of the 282 ACS-patients, 204 patients (72.3%) presented with ACS caused by culprit lesions with rupture of the fibrous cap (RFC-ACS) and 27.7% patients had ACS caused by culprit lesions with intact fibrous cap (IFC-ACS). When comparing RFC-ACS to IFC-ACS, a preferential occurrence of all three plaque components (LC, CC, and LCC) in RFC-ACS became apparent (P < 0.001). Within ruptured culprit lesions, the zone straight at the rupture point [extended rupture zone (RZ)] was characterized by similar (24.7% vs. 24.0%; P = ns) calcium content when compared with the proximal and distal border of the culprit lesion [border zone (BZ)]. The RZ displayed a significantly higher amount of both, LC (100% vs. 69.8%; P < 0.001) and LCC (22.7% vs. 6.8%; P < 0.001), when compared with the BZ. The relative component increase towards the RZ was particularly evident for LCC (+233.8%), while LC showed only a modest increase (+43.3%). CONCLUSIONS: Calcified- and lipid-containing components characterize ruptured fibrous cap ACS-causing culprit lesions. Their coexistence is accelerated directly at the ruptured point, suggesting a pathophysiological contribution in the development of RFC-ACS.

A Patient with Quadricuspid Aortic Valve and Ischemic Stroke.

Quadricuspid aortic valve (QAV) is a rare congenital cardiac defect. Aortic regurgitation is the predominant hemodynamically relevant abnormality in patients with QAV, and the main reason for patients requiring valve surgery. Calcific valve disease of the left heart valves is classified as 'low embolic risk' according to current guidelines. However, it remains an important risk factor of cardiovascular events, including ischemic stroke. A 71-year-old woman presented with new-onset aphasia and hemiparesis of the right side of her body. A magnetic resonance imaging scan of the brain showed acute infarction in the supply area of the left middle cerebral artery. Transesophageal echocardiography revealed a QAV with thickening of the leaflet tips and focal calcifications, especially in the coaptation zones. The four cusps were of equal size and symmetrically affected by sclerosis and calcific deposits, and the aortic valve area was 3.2 cm2 with moderate aortic valve regurgitation.