ABC of Arterial and Venous Disease
ABC of Arterial and Venous Disease
Pathogenesis of Atherosclerosis and Methods of Arterial and Venous Assessment
Mario De Nunzio1 and Timothy J. England2
1Derby Hospitals NHS Foundation Trust, Royal Derby Hospital, UK
2Division of Medical Sciences & GEM, School of Medicine, University of Nottingham, UK
Atherosclerosis is a chronic inflammatory disorder
The ankle-brachial pressure index (ABPI), calculated from the ratio of ankle systolic blood pressure (SBP) to brachial SBP, is a sensitive marker of arterial insufficiency in the lower limb
Blood velocity increases through an area of narrowing. Typically, a 2-fold increase in peak systolic velocity compared with the velocity in a proximal adjacent segment of the same artery usually signifies a stenosis of 50% or more
In detecting femoral and popliteal artery disease, duplex ultrasonography has a sensitivity of 80% and a specificity of 90-100%
The introduction of multidetector computed tomography (MDCT) has had a dramatic effect on vascular imaging. Computed tomography pulmonary angiography (CTPA) for suspected pulmonary embolism (PE) is a good example, but computed tomography angiography (CTA) and magnetic resonance angiography (MRA) are widely used to investigate large artery pathology
Colour duplex scanning is both sensitive and specific (90-100% in most series) for detecting proximal deep vein thrombosis (DVT). Pathogenesis of atherosclerosis
Atherosclerosis is a chronic inflammatory disorder that results in hardening and thickening of arterial walls. Although it inevitably accompanies aging, it is not a degenerative process. The initial insult, called a 'fatty streak', is a purely inflammatory lesion and has been observed in infants. Over many years, circulating monocyte-derived macrophages adhere to and invade the arterial wall. An inflammatory response, proliferation of vascular smooth muscle cells and deposition of cholesterol and other lipids create arterial plaques. The insult creates a prothrombotic environment and induces the release of inflammatory mediators including cytokines, growth factors and hydrolytic enzymes. Over time, the plaques narrow the arterial lumen (and at times dilate it) and subsequently rupture, causing platelet activation, aggregation and resultant thrombus and embolus formation ( Figure 1.1 ). It remains unclear as to what causes a stable plaque to rupture but it may be due to mechanical stress (e.g. hypertension) and the large lipid core redistributing shear stress over weakened areas of a thin fibrous cap.
Figure 1.1 Spontaneous rupture or fissuring of an atherosclerotic plaque exposes the lipid-rich core and triggers platelet activation and platelet aggregation. The platelet GP IIb/IIIa receptor activation binds fibrinogen and leads to intravascular thrombus formation, resulting in complete or near-complete vessel occlusion. Clinically, this often presents with a life-threatening unstable event such as an acute coronary syndrome, acute limb ischaemia or stroke.
It is recognised that increasing age, a genetic predisposition, male sex, hypertension, lipid abnormalities (in particular, LDL-cholesterol), diabetes, chronic high alcohol intake and cigarette smoking (causing an increase in free radicals) increase the risk of atherogenesis and endothelial dysfunction. Atherosclerosis mainly affects large and medium-sized arteries at places of arterial branching (e.g. carotid bifurcation). Symptoms occur when there is insufficient blood flow to the vascular bed as a result of
in situ thrombotic arterial occlusion,
low flow distal to an occluded or severely narrowed artery or
embolism from an atherosclerotic plaque or thrombus.
Clots occurring in the venous syst