It is a pathological narrowing of the intima of the common or internal carotid artery, typically in focal areas called plaques or atheroma. Although the atheroma can remain stable for many years, its surface may rupture leading to formation of local thrombus with subsequent embolization to the territories of the ophthalmic artery, anterior cerebral, or medial cerebral artery.

The main symptoms depend on the affected territory. At the ophthalmic circulation, symptom of amaurosis fugax or retinal infarction may be seen. On the other hand, the medial cerebral artery embolism can be seen as transient symptoms in the contralateral hemisphere body (called ‘transient ischemic attack’) or even stroke.

However, it is usually diagnosed on non-invasive imaging studies in asymptomatic individuals [4].

Patients with atrial fibrillation have a threefold to fivefold increased risk of cardioembolic ischemic stroke . HyperlipidemiaHyperlipidemia is a risk factor for the disease development in this territory, being associated with the presence of atherosclerotic stenosis and the stroke occurrence observed when total cholesterol level is greater than 5.20 mmol/L (200 mg/dL) [5]. Hypertension is an independent risk factor for the development of cardiovascular disease and has a great association with hyperlipidemia [6]. The presence of diabetes mellitus is associated with increased chances of having ischemic stroke in two to three times and its proper control is related to risk reduction [7, 8].

Atherosclerosis reduces coronary blood flow leading to symptoms of myocardial ischemia. In recent years, advanced knowledge of the atheroma pathophysiology and the rupture of atherosclerotic plaques was have been achieved. The atheroma is responsible for acute coronary syndromes causes, in more than half of the cases, produces a stenosis lower than 50 % of the vessel diameter. Therefore, they are vulnerable plaques with a large lipid core, inflammatory cells and thin fibrous caps, subject to biomechanical stress. This knowledge of plaques vulnerability has led to change in treatment, with new therapeutic options such as antiplatelet, anti-thrombotic drugs, statins and beta-blockers drugs [9].

In this territory, the genetic factor is strongly associated with plaque formation and complication, especially in individuals with a history of premature familial disease. This correlation is significant for those with a first-degree relative who had atherosclerotic cardiovascular disease or died due to it before 55 years old for men or 65 years old for women [10]. Dyslipidemia is directly related to the occurrence of coronary artery disease due to its important role in the formation of atherosclerotic plaque. Higher levels of non-high density lipoprotein are associated with higher incidence of coronary events, particularly in patients with earlier manifestations [8, 11, 12]. Nicotine and tar are directly related to deaths from coronary artery disease and higher doses of these toxins are associated with progressive increase in mortality [13]. Patients with diabetes mellitus have higher chance of developing coronary artery disease and developing it in an early age when compared to the general population [14]. Diabetes mellitus also increases the risk of complications. The incidence of acute coronary syndrome is higher in patients with diabetes mellitus when compared to individuals without the disease [15]. Moreover, mortality of patients with diabetes mellitus is mostly related to coronary artery disease complications [16]. A study conducted in 52 countries showed a significant association between hypertension and coronary artery disease, consistent with the vast data related to the Framingham study. It shows that this is an important target for the reduction of myocardial infarction, especially when it occurs early in life [17, 18].

Atherosclerosis is the leading cause of peripheral arterial disease, in which there is a blockage or stenosis in the arteries that supply lower limbs . Approximately 80 % of patients with peripheral artery disease are asymptomatic. The main symptoms of the ischemia are muscular atrophy, ulcers, pallor and intermittent claudication, and the main finding in the physical examination is the reduction or absence of peripheral pulses. In some cases, the disease can have an acute worsening, characterized by severe pain, sudden onset, associated with reduced limb temperature, decreased temperature and paraesthesia, featuring acute arterial ischemia that must be treated immediately in an attempt to avoid amputation and death.

Advanced age is also a progressive risk for the disease in this territory. However, it becomes significant higher after 40 years. The risk greatly increases in patients older than 70 years, but only part of them present the symptomatic form of peripheral artery disease [20–22]. Smoking is strongly associated with the development of the disease. Studies like Framingham’s showed a two times increased risk of developing intermittent claudication among smokers when compared to non-smokers [23]. Such findings were confirmed by other epidemiological studies that also assigned the risk two to six times greater among smokers [24–26]. Diabetes mellitus is directly associated with the incidence and severity of peripheral artery disease. The prevalence is almost five times greater of peripheral artery disease in diabetic patients older than 40 years when compared to people without the comorbidity [27, 28]. Regarding the affected territory, diabetic patients generally have more distal involvement of the vessels, especially in the popliteal and tibial vessels [29, 30]. Regarding the outcome, the association of these two diseases correlates to a higher risk of lower limb amputations in elderly people [31]. It’s well known that patients with peripheral artery disease are more likely to have high levels non-high density lipoprotein cholesterol and/or triglycerides [32] as well as reduced levels of high density lipoprotein [33]. In addition, there is a significant association between hypertension and peripheral artery disease both in symptomatic and asymptomatic individuals [22, 34]. Those patients present a two times higher risk of developing symptoms such as claudication when compared to non-hypertensive patients [35].

The initial cause of the endothelial lesion not established that yet, though dyslipidemia, diabetes, hypertension and smoking certainly collaborate to the pathogenic process. It is the leading cause of renal artery stenosis in the elderly. This pathologic process is the main cause of renovascular hypertension, responding for 1–10 % of all hypertensive disease cases in the United States, and contributing importantly to chronic renal failure progression. The lumen of a renal artery with atherosclerosis gradually reduces, leading to decreased blood flow and renal ischemia. The kidney adaptation to atrophy and reduction of tubular cells, inflammation, fibrosis and glomerular atrophy generates a glomerular filtration rate angiotensin II dependent. This adaptation process can maintain a stable renal function until it reaches high grade renal artery stenosis [36].

The diagnosis of atherosclerosis is usually established after starting its symptoms in at least one of the above mentioned territories. However, the best approach is to diagnose it in a preclinical phase through risk stratification and laboratory tests, enabling the effective secondary prevention with the correct definition of individual therapeutic goals. Atherosclerotic disease risk stratification results from the sum of all potential increased risks identified in patients; therefore, the first step in clinical risk assessment is to identify any high-risk conditions that obviate the need for further risk assessment, these mainly include established atherosclerotic cardiovascular disease and diabetes. If none of such high-risk conditions is present, the second step is to apply a well stablished risk score, such as Framingham.