Atherosclerotic Plaque Biomarkers: Beyond the Horizon of the Vulnerable Plaque

Cardiovascular disease (CVD) is the number one cause of death globally, and the majority of CVD is caused by atherosclerosis. Atherosclerosis is a systemic inflammatory disease that leads to myocardial infarction, stroke and lower limb ischemia. Pathological studies have given insight to development of atherosclerosis and the importance of local plaque vulnerability, leading to thrombus formation and cardiovascular events. Due to the burden of cardiovascular disease, identification of patients at risk for cardiovascular events and treatment stratification is needed. The predictive power of classical risk factors is limited, especially in patients with manifest atherosclerosis. Imaging modalities have focused on the characteristics of the vulnerable plaque. However, it has become evident that not all so-called vulnerable plaques lead to rupture and subsequent thrombosis. The latter obviously limits the positive predictive value for imaging assessment of plaques and patients at risk. Serum biomarkers have also been studied extensively, but have very limited application in a clinical setting for risk stratification. In line with the important relation between vulnerable plaques and cardiovascular events, plaque biomarker studies have been initiated. These longitudinal studies are based on the concept, that a vulnerable plaque contains predictive information for future cardiovascular events, also in other territories of the vascular tree. Results look promising and plaque markers can be used to develop imaging modalities to identify patients at risk, or to monitor treatment effect. Plaque biomarker studies do not challenge the definition of the vulnerable plaque, but use its concept in favor of prediction improvement for vascular patients

Outcomes of open repair of postdissection abdominal aortic aneurysms

Background: Evidence to guide management of postdissection abdominal aortic aneurysms (PDAAA) is lacking. This study describes the outcomes of open repair of PDAAA. Methods: A retrospective cohort study was conducted of all consecutive patients treated with open repair for PDAAA after a Stanford type A or type B thoracic aortic dissection between January 2006 and December 2017 in two vascular referral centers. Preceding type B dissection treatment could include conservative or surgical management. Primary outcomes were 30-day mortality, complication rates, survival, and reintervention-free survival. Survival and reintervention-free survival were analyzed using the Kaplan-Meier method. Reintervention was defined as any endovascular or surgical intervention after the index procedure. Results: Included were 36 patients (27 men [75%]) with a median age of 64 years (range, 35-81 years). The 30-day mortality was 2.7%. The median follow-up was 16 months (range, 0-88 months). The postoperative course was uneventful in 21 patients (58%). The most frequent complications were postoperative bleeding requiring repeat laparotomy (n = 4), pneumonia (n = 3), congestive heart failure (n = 2), new-onset atrial fibrillation (n = 2), mesenteric ischemia requiring left hemicolectomy (n=1), and ischemic cerebrovascular accident (n = 1). Renal failure requiring hemodialysis developed in one patient. The overall survival at 1 year was 88.8%. Reintervention-free survival was 95.5% after 1 year and 88.6% after 2 years. Conclusions: Open repair of PDAAA can be performed with a low mortality rate and an acceptable complication rate, comparable with elective open repair of abdominal aortic aneurysms without dissection

Different stages of intraplaque hemorrhage are associated with different plaque phenotypes: A large histopathological study in 794 carotid and 276 femoral endarterectomy specimens

BACKGROUND AND PURPOSE: Intraplaque hemorrhage (IPH) is an important determinant of progression and destabilization of atherosclerotic plaque. We recently demonstrated that IPH is an independent predictor of cardiovascular events. IPH has become more clinically relevant since magnetic resonance imaging (MRI) technique is able to visualize IPH in vivo. Different stages of IPH have been described. However, etiology of the different stages is not known and it is unclear if these detected different stages are all associated with the vulnerable plaque phenotype. METHODS AND RESULTS: 1070 patients who underwent a carotid (n=794) or femoral (n=276) endarterectomy were included. Histopathological presence of IPH was determined and divided into 3 types: recent, organized and amorphous IPH. Carotid IPH was observed in 644/794 (81%) plaques, divided into 14 (2%) recent, 70 (11%) organized and 560 (87%) amorphous. Femoral IPH was observed in 175/276 (63%) plaques, divided into 2 (1%) recent, 89 (51%) organized and 84 amorphous (48%). Overall presence of carotid IPH was associated with a large lipid core, no or minor staining of smooth muscle cells, no or minor calcification and high microvessel density. Overall presence of femoral IPH was associated with moderate to heavy staining of macrophages. Plaques with organized IPHs revealed more macrophages, a larger lipid core, less smooth muscle cells, less calcification and higher microvessel density than plaques with amorphous IPHs. CONCLUSIONS: IPH is a significant characteristic of carotid and femoral atherosclerotic plaque and can be classified into different types. Organized IPH is associated with unstable and amorphous IPH with stable plaque characteristics.status: publishe