Summary
- •
Women who
Atherosclerosis-related cardiovascular events and cerebrovascular (CV) events are the cause of death in almost 50% of cases in developed countries [1]. The presence of atherosclerotic disease in more than one arterial system is associated with a higher risk of recurrent symptoms and complications. At three year follow-up, the rates of myocardial infarction, stroke, vascular death or rehospitalization are 25.5% for patients with symptomatic disease in one vascular system and 40.5% for multiple vascular systems [2], suggesting that atherosclerosis is a diffuse vascular disease whose effects are potentially additive. Indeed, patients with detectable disease in the coronary and peripheral arteries carry twice the level of risk as those presenting with coronary artery disease (CAD) alone [2]. Despite the fact that carotid atherosclerosis develops later in life compared to coronary disease [3], plaque morphology and their anatomical location at branching points and arterial curves is similar in the two arterial systems [4], [5], suggesting that development of the shared disease is likely to be influenced by similar systemic factors. However, the extent of association and concordance between the two arterial systems remains to be determined (Fig. 1).
This review will consider the various similarities and differences between atherosclerotic disease in the coronary and carotid arteries, comparing the pathomechanism of the conditions, their symptomatology, their risk factors, the mechanism of their acute syndromes and treatment (Table 1, Table 2).
The prevalence of severe carotid artery stenosis increases progressively concurrent with coronary artery stenosis and is a known predictor of worse CV outcome. A general review showed that the prevalence of >50, >60, >70, and >80% carotid stenosis was reported in 14.5%, 8.7%, 5.0%, and 4.5% of CAD patients respectively [6]. The prevalence of clinically significant severe carotid artery stenosis (>50%) was progressively increased among patients with either non-obstructive CAD, single vessel
Carotid and coronary atherosclerosis share common risk factors such as diabetes mellitus, hypertension, smoking, older age, high triglyceride levels and low high-density lipoprotein cholesterol levels [20]. Studies suggested that the classic CV risk factors have a different impact in different arterial systems, with cholesterol being particularly important in CAD, hypertension in ischemic stroke, whereas smoking and diabetes in intermittent claudication [21], [22]. Greater understanding of
Prevalence of carotid and coronary atherosclerosis increase gradually with age, and is more prevalent in man than in women [23]. The median age of MI and stroke onset is higher in females, with younger females having worse survival after MI compared with males [24], [25]. Among the older age (>64 years old) there is no gender difference for ischemic heart disease, whereas females have poorer short and long-term outcomes after stroke, independent of age and other covariates [26]. Women who Summary
Severity of CA stenosis does not predict acute future events [27]. The evidence suggests that in two thirds of acute coronary syndrome (ACS) patients the degree of stenosis associated with the culprit lesion is often <50% narrowing [28], [29], [30]. In contrast, the stroke risk in patients with symptomatic severe carotid stenosis (>50%) is directly related to extent of stenosis; a patient with 60–69% carotid stenosis has 11% risk of stroke within 3 years, compared with 32% for a patient with
It is well known that monocytes and T lymphocytes play a crucial role in atherosclerosis development [37]. A triggering event for this process may be the accumulation of oxidized LDL, which stimulates the overlying endothelial cells to produce a number of pro-inflammatory molecules, including adhesion molecules and cytokines such as macrophage colony-stimulating factor (M-CSF) [37]. It is unclear why atherosclerotic lesions remain quiescent for long periods of time and then suddenly undergo
The endothelium of coronary and carotid arteries responds not only to systemic and inflammatory factors in the circulation but also to the mechanical conditions created by blood flow and the cardiac cycle. Chronic exposure of endothelial cells to high levels of shear stress causes them to exhibit an atheroprotective phenotype [54]. Nitric oxide (NO) appears to be a key mediator of the atheroprotective effects of shear stress on the blood vessel wall. Low wall shear stress can cause arterial
The mechanisms that generate plaque disruption are similar in both the coronary and carotid arteries. These include rupture of the fibrous cap (60%), superficial erosion (35%) and thromboembolism formation on a calcium nodule (5%) [56]. Contact of blood elements (platelets and coagulation proteins) with the lipid core and other constituents of the atherosclerotic plaque (collagen and tissue factor) promote thrombosis. The exact relationship between plaque rupture and development of acute
The most common cause of ACS is hypoperfusion by plaque rupture and local thrombosis. Even though plaque rupture with luminal thrombosis is similarly considered to be the major etiology of carotid atherosclerosis, artery-to-artery embolism appears to be the dominant vascular mechanism causing brain ischemia [61]. While the heart is in continual motion of contraction and relaxation, the brain is in a steady state. This explains the difference in determinants of organ perfusion with coronary
The cerebral collateral circulation is recognized as an essential factor maintaining perfusion distal to the site of arterial occlusion [64]. The cerebral collateral circulation includes extracranial sources of cerebral blood flow and intracranial sources of ancillary perfusion that are commonly divided into primary and secondary pathways. Primary collaterals include arterial segments of the circle of Willis, whereas the ophthalmic and leptomeningeal vessels constitute secondary collaterals [63]
With a culprit lesion located in the coronary artery, thrombolytic therapy has been shown to improve survival rates in ST-segment elevation MI (STEMI) within the first 12 h after onset of symptoms, but the earlier therapy is begun, the greater the benefit. Fibrinolysis or percutaneous coronary intervention (PCI) are the definitive therapies for reperfusion in STEMI. The arrival to treatment (door-to-needle) should not be later than 30 min, and door-to-PCI balloon inflation less than 90 min [72]
There are many areas of correspondence between atherosclerosis in the coronary and carotid arteries, with prevalence and extent of stenosis in one artery being associated with prevalence and extent of stenosis in the other. Many stroke patients have severe coronary stenosis, while carotid occlusion is also a risk factor for MI. Yet there are also subtle differences in the disease appearance between the two arteries, with a different collateral recruitment rate, atherosclerosis treatment and