aneurysm/nicotine

Elevated elastase activity in patients with chronic obstructive pulmonary disease (COPD) is attributable to the direct effect of nicotine. COPD is also known to be an independent predictor of abdominal aortic aneurysm (AAA) growth and rupture. The purpose of this study is to determine the effect of

Aortic aneurysms (AAs) are without effective pharmacologic therapy, in clinical usage, in part because of the limited understanding of factors leading to AA development. The objectives of this study were to examine the evidence that cigarette smoking induces AAs through altering matrix

Aim: Smoking is a major risk factor for abdominal aortic aneurysm (AAA). Among the components of smoke, nicotine is known to exert pro-atherosclerotic, prothrombotic, and proangiogenic effects on vascular smooth muscle cells (VSMCs). The current study was designed to investigate the

BACKGROUND We determined the predictive power of tobacco smoking on aortic aneurysm as opposed to other risk factors in the general population. METHODS We recorded tobacco smoking and other risk factors at baseline, and assessed hospitalization and death from aortic aneurysm in 15,072 individuals

Aim: Arterial stiffness is a significant risk factor for many cardiovascular diseases, including abdominal aortic aneurysms (AAA). Nicotine, the major active ingredient of e-cigarettes and tobacco smoke, induces acute vasomotor effects that may temporarily increase arterial stiffness. Here, we

Nicotine, a major chemical component of cigarettes, plays a pivotal role in the development of abdominal aortic aneurysm (AAA). c-Jun N-terminal kinase (JNK) has been demonstrated to participate in elastase-induced AAA. This study aimed to elucidate whether the JNK inhibitor SP600125 can attenuate

Background and Purpose- Tobacco cigarette smoking is considered to be a strong risk factor for intracranial aneurysmal rupture. Nicotine is a major biologically active constituent of tobacco products. Nicotine's interactions with vascular cell nicotinic acetylcholine receptors containing α7 subunits

Identification and treatment of abdominal aortic aneurysm (AAA) remains among the most prominent challenges in vascular medicine. MicroRNAs are crucial regulators of cardiovascular pathology and represent possible targets for the inhibition of AAA expansion. We identified microRNA-21 (miR-21) as a

Inflammation, proteolysis, smooth muscle cell apoptosis, and angiogenesis have been implicated in the pathogenesis of abdominal aortic aneurysms (AAAs), although the well-defined initiating mechanism is not fully understood. Matrix metalloproteinases (MMPs) such as MMP-2 and -9 and other proteinases

Smoking is the only modifiable risk factor that is associated with the development, expansion and rupture of abdominal aortic aneurysm (AAA). However, the causative link between cigarette smoke and AAA is unknown. Here we report a causative link between smoking and AAA in vivo. Acute infusion of

Several studies have found that smoking increases the risk of abdominal aortic aneurysm, however, the strength of the association has differed between studies and data from cohort studies have not yet been summarized. A systematic review and meta-analysis was therefore conducted to clarify this

BACKGROUND The goal of the study was to analyse retrospectively the impact of risk factors for subarachnoid haemorrhage (SAH) on the size of ruptured intracranial aneurysms in order to identify variables that might influence the discrepancy between average sizes of ruptured and unruptured

Background: The prevalence of unruptured intracranial aneurysms (UIA) in females who smoke cigarettes and the association between smoking and hypertension with purely incidental UIAs have been unexplored.