Abstract
Ruptured abdominal aortic aneurysms (AAA) are associated with overall mortality rates up to 90%. Despite extensive research, mechanisms leading to AAA formation and advancement are still poorly understood. Smooth muscle cells (SMC) are predominant in the aortic medial layer and maintain the wall structure. Apoptosis of SMC is a well-known phenomenon in the pathophysiology of AAA. However, remaining SMC function is less extensively studied. The aim of this study is to assess the in vitro contractility of human AAA and non-pathologic aortic SMC. Biopsies were perioperatively harvested from AAA patients (n = 21) and controls (n = 6) and clinical data were collected. Contractility was measured using Electric Cell-substrate Impedance Sensing (ECIS) upon ionomycin stimulation. Additionally, SMC of 23% (5 out of 21) of AAA patients showed impaired maximum contraction compared to controls. Also, SMC from patients who underwent open repair after earlier endovascular repair and SMC from current smokers showed decreased maximum contraction vs. controls (p = 0.050 and p = 0.030, respectively). Our application of ECIS can be used to study contractility in other vascular diseases. Finally, our study provides with first proof that impaired SMC contractility might play a role in AAA pathophysiology.
Highlights
Abdominal aortic aneurysms (AAA) are considered among the most severe surgical emergencies due to the overall mortality rate of 90% in case of rupture[1]
Genetic dysfunctions in Smooth muscle cells (SMC) contractile proteins and their devastating consequences for the aortic wall have been shown in cases of familial thoracic aneurysms[5,6]
SMCs are implicated in the pathogenesis of abdominal aortic aneurysms (AAA), due to their decreased density in the aortic media[3] and pathological apoptosis[20], little is known of their contractile function in the context of sporadic AAA pathogenesis
Summary
Abdominal aortic aneurysms (AAA) are considered among the most severe surgical emergencies due to the overall mortality rate of 90% in case of rupture[1]. Mutations in genes encoding for contractile proteins, such as smooth muscle myosin heavy chain (MYH11) and smooth muscle actin (ACTA2) have been associated with cases of hereditary thoracic aortic aneurysms and dissections[5,6]. This underscores a potential role of SMC contractile elements in aortic aneurysmal pathology[6,7,8]. To examine the role of SMC contractility in AAA pathophysiology, we measured the contractile properties of SMC isolated from aortic biopsies of controls and sporadic AAA patients. The aim of this study is to evaluate SMC contractility in patients with sporadic AAA
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