In the past, arterial and venous thrombosis have been accepted as two completely different diseases. Recently, the thesis of two separate pathogenetic mechanisms of venous and arterial thrombosis has ...been challenged by accumulation of evidence which suggest that patients with atherothrombosis are at increased risk for venous thrombosis. Pathophysiological studies indicated that etiopathogenetic mechanisms of both diseases are similar and that coagulation and platelet activation participate in both venous and arterial thrombogenesis. Inflammation most probably represents the basic etiopathogenetic mechanism of arterial as well as venous thromboembolic disease, being a common mechanism through which different risk factors trigger thrombus formation in both veins and arteries. Atherothrombosis is accepted as a chronic inflammatory disease and the association between circulating inflammatory markers and venous thromboembolism also indicates an involvement of the inflammatory process in venous thrombosis. During inflammation, there is an increase in the production of procoagulant factors, a down-regulation of the anticoagulant mechanisms and an inhibition of the endogenic fibrinolytic activity. In line with the arguments which support the link between arterial and venous thrombosis is also the recognition that different risk factors are common in both diseases, such as age, metabolic syndrome, hypercholesterolemia and thrombophilia. A relation was also found between subjects with preclinical or clinical atherosclerotic disease and venous thromboembolism. These findings indicate close interrelationship between arterial atherothrombotic and venous thromboembolic disease. It could mean that atherosclerosis may induce venous thrombosis or that these two diseases have common risk factors which promote the development of both diseases.
Atherosclerosis is a systemic disease with different faces. Despite identical or similar pathogenetic mechanisms, atherosclerotic lesions and their clinical manifestations vary in different parts of ...the vascular system. Peripheral arterial disease (PAD) represents one of the most frequent clinical manifestations of atherosclerosis with predominant location in the superficial femoral artery (SFA). Morphological characteristics of atherosclerotic plaques in peripheral arteries differ from lesions in the coronary and carotid arteries. Plaques in SFA have more fibrotic components, less lipids and inflammatory cells, which makes them more stable and less prone to rupture. Factors that determine the different structure of plaques in SFA compared to coronary arteries include hemodynamic forces, vasa vasorum and calcification. Low shear stress in SFA in the adductor canal is one of the factors which determines frequent atherosclerotic lesions in this region. Lower lipid content and fewer inflammatory cells explain higher stability of SFA plaques. The specific structure of SFA plaques may require preventive and therapeutic measures, which to some extent differ from prevention of coronary atherosclerosis and may include inhibition of fibrotic proliferation in SFA plaques and calcification. Revascularization of PAD differs from procedures used in coronary arteries and requires specific technical expertise and devices.
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•The atherosclerotic plaque structure of the superficial femoral artery (SFA) differs from plaque in other territories.•Plaques in SFA have more fibrotic components, and smooth muscle cells, less inflammatory cells and lipids. They are more stable.•Low shear stress and low density of vasa vasorum influence plaque structure in SFA, which differs from coronary arteries.•The growth of plaque in SFA is slower and relates to less thrombotic complications.•Different plaque structures in SFA may provoke different therapeutic measures e.g. inhibition of fibrotic proliferation.
Patients with intermittent claudication have significantly higher levels of inflammatory biomarkers, particularly interleukins, which is also a consequence of exercise limitation. Physical activity, ...which is one of the preventive measures against atherosclerosis, is associated with a decrease in inflammatory biomarkers. Therefore, in our study, we investigated the effects of revascularization of peripheral arteries in patients with intermittent claudication on functional capacity and levels of inflammatory markers. The study included 26 patients with intermittent claudication who underwent percutaneous transluminal angioplasty (PTA). Before the procedure and 2–4 months after successful revascularization, the ankle-brachial index (ABI), functional capacity using the treadmill test, and the walking impairment questionnaire (WIQ) were determined. Inflammatory biomarkers were also measured before and after procedures. Successful revascularization was associated with an increase in intermittent claudication: 120 (20–315) versus 300 (100–1000 m), P < 0.001. Treadmill testing showed a significant increase in initial and maximal walking distance. After revascularization, ABI increased significantly (0.55 vs 0.82, P < 0.003). Improvement in functional performance was also demonstrated by WIQ. Two to three months after revascularization, some inflammatory biomarkers decreased significantly: fibrinogen, interleukin-6 (IL-6), and interleukin-8 (IL-8). The high-sensitivity C-reactive protein (hsCRP) and tumor necrosis factor-alpha (TNFα) also did not decrease significantly. The levels of some inflammatory markers: IL-6, TNFα, and fibrinogen were significantly related to the improvement in patients’ functional capacity. The results of our study show that successful revascularization of the lower limb arteries not only improves the functional capacity of patients with intermittent claudication, but also reduces the systemic inflammatory response and may have a preventive effect on local and concomitant other atherosclerotic diseases.
Classical risk factors play a major role in the initiation and development of atherosclerosis. However, the estimation of risk for cardiovascular events based only on risk factors is often ...insufficient. Efforts have been made to identify biomarkers that indicate ongoing atherosclerosis. Among important circulating biomarkers associated with peripheral arterial disease (PAD) are inflammatory markers which are determined by the expression of different genes and epigenetic processes. Among these proinflammatory molecules, interleukin-6, C-reactive protein, several adhesion molecules, CD40 ligand, osteoprotegerin and others are associated with the presence and progression of PAD. Additionally, several circulating prothrombotic markers have a predictive value in PAD. Genetic polymorphisms significantly, albeit moderately, affect risk factors for PAD via altered lipoprotein metabolism, diabetes, arterial hypertension, smoking, inflammation and thrombosis. However, most of the risk variants for PAD are located in noncoding regions of the genome and their influence on gene expression remains to be explored. MicroRNAs (miRNAs) are single-stranded, noncoding RNAs that modulate gene expression at the post-transcriptional level. Patterns of miRNA expression, to some extent, vary in different atherosclerotic cardiovascular diseases. miRNAs appear to be useful in the detection of PAD and the prediction of progression and revascularization outcomes. In conclusion, taking into account one’s predisposition to PAD, i.e., DNA polymorphisms and miRNAs, together with circulating inflammatory and coagulation markers, holds promise for more accurate prediction models and personalized therapeutic options.
Atherosclerosis has a long preclinical phase, and the risk of cardiovascular (CV) events may be high in asymptomatic subjects. Conventional risk factors provide information for the statistical ...probability of developing CV events, but they lack precision in asymptomatic subjects. This review aims to summarize the role of some widely publicized indicators of early atherosclerosis in predicting CV events.
The earliest measurable indicator of the atherosclerotic process is endothelial dysfunction, measured by flow-mediated dilation (FMD) of the brachial artery. However, reduced FMD is a stronger predictor of future CV events in patients with existing CV disease than in apparently healthy persons.
Alternatively, measurement of carotid artery intima-media thickness does not improve the predictive value of risk factor scores, while detection of asymptomatic atherosclerotic plaques in carotid or common femoral arteries by ultrasound indicates high CV risk.
Coronary calcium is a robust and validated help in the estimation of vascular changes and risk, which may improve risk stratification beyond traditional risk factors with relatively low radiation exposure.
Arterial stiffness of the aorta, measured as the carotid-femoral pulse wave velocity is an independent marker of CV risk at the population level, but it is not recommended as a routine procedure because of measurement difficulties.
Low ankle-brachial index (ABI) indicates flow-limiting atherosclerosis in the lower limbs and indicates high CV risk, while normal ABI does not rule out advanced asymptomatic atherosclerosis.
Novel circulating biomarkers are associated with the atherosclerotic process. However, because of limited specificity, their ability to improve risk classification at present remains low.
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•Traditional risk factors for cardiovascular (CV) disease inform on the probability of developing atherosclerosis and related CV events.•Detecting preclinical atherosclerosis enables the identification of individuals with ongoing atherosclerosis.•Preclinical atherosclerosis can be identified by functional/morphologic deterioration of the arterial wall or by circulating biomarkers.•The predictive value of indicators of preclinical atherosclerosis for future CV events is not completely elucidated.•Ankle-brachial index, calcium score, and asymptomatic plaques may improve risk stratification for CV events beyond traditional risk factors.
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