Chronic coronary artery disease

Abstract

State of the ArtCoronary insufficiency (CI) is the state in which an imbalance occurs between the supply and demand of oxygen, which prevents adequate maintenance of the metabolic needs of the myocardium, resulting in ischemia of several degrees of intensity.CI has numerous causes among which are cardiac valvular diseases (aortic stenosis), hypertrophic cardiomyopathy, microvasculature diseases (diabetes mellitus, syndrome X), anomalous origin of coronary arteries, and coronary fistulas. However, the most important cause, because of its frequency and the resulting morbidity and mortality, is atherosclerotic obstructive CI. Therefore, this discussion will be specifically about coronary atherosclerosis. The main objective is not to suggest practical applications for specific situations, but to outline concepts, based on critical analysis of data in the literature, which may provide a basis for conducting further investigation and for providing treatment of coronary artery disease (CAD). PathophysiologyHuman atherosclerosis is a chronic, progressive and systemic process characterized by an inflammatory and fibroproliferative response of the arterial wall caused by aggression against the arterial surface. As a systemic process, it frequently attacks all arterial beds, including the aorta and its main branches: carotid, renal, iliac and femoral arteries. Among the risk factors (RF) for arterial lesions are hypercholesterolemia, arterial hypertension (AH), diabetes, smoking, immunological and inflammatory reactions, and individual genetic susceptibility 1 . The coronary vascular alterations present in atherosclerosis derive from three fundamental components: 1) endothelial dysfunction, which starts early, altering the reactivity of the vessel and causing paradoxical vasoconstriction following stimuli with acetylcholine, and exacerbation of reactivity to epinephrine and angiotensin; endothelial dysfunction also leads to loss of the natural antithrombotic properties and of the selective permeability of the endothelium; 2) obstruction of the lumen of the vessel by the atherosclerotic plaque and 3) thrombosis at the location of the lesion. Any of these could individually trigger CI, but they often occur at the same time. Response of the arterial wall to aggressive agentsEndothelial cells play several physiological roles in maintaining the integrity of the arterial wall and constitute a permeable barrier through which diffusion and exchanges or active transportation of several substances occur. They provide a non-thrombogenic and non-adhesive surface for platelets and leukocytes; they operate to maintain vascular tonus by releasing nitric oxide (NO), prostacyclin (PGI 2 ) and endothelin-1; they produce and discharge growth factors and cytokines and maintain the integrity of the basal membrane rich in collagen and proteoglycans on which they are supported 2 . Alterations in one or more of these functions represent initial manifestations of endothelial dysfunctions and may trigger cellular interactions with monocytes, platel...

Obesity and Cytokines in Childhood-Onset Systemic Lupus Erythematosus

“…Previous studies have shown that visceral fat accumulation is associated with increased risk of CV risk [37]. In addition, with an increase in TNF- α , a reduction in lipoprotein lipase activity in adipose tissue is observed [39]. There is also evidence that TNF- α has a local effect, regulating adipocyte size in the face of increasing energy consumption [40, 41].…”

“…Cytokines, such as TNF- α and IL-6, are primarily involved in the early stages of the inflammatory response culminating in atherosclerosis [39, 42]. Increased TNF- α levels in the endothelium promote initial atheroma plaque [39, 42].…”

“…Increased TNF- α levels in the endothelium promote initial atheroma plaque [39, 42]. However, so far, studies were not able to conclude whether TNF- α is a causative factor of atherosclerosis.…”

Prinzmetal angina in a patient with previous coronary artery disease.Topic review and case report

“…A prazosina, um bloqueador seletivo de alfa-adrenorreceptores, também tem se mostrado eficaz em alguns pacientes, sendo considerada uma droga de segunda linha no tratamento da angina de Prinzmetal. 16 Um possível fator que contribui para o espasmo coronário é a deficiência de magnésio, pois este tem um efeito bloqueador nos canais de cálcio e pode prevenir a contração do músculo liso vascular. Daí a infusão de magnésio ser proposta para reduzir os ataques de espasmos nesses pacientes.…”

“…Daí a infusão de magnésio ser proposta para reduzir os ataques de espasmos nesses pacientes. 16 Existe uma associação do uso do ácido acetilsalicílico com vasoespasmo coronariano, fato especialmente importante em pacientes que realizaram ICP prévia. A admi nistração de altas doses de aspirina (>325mg por dia) é conhecida por bloquear a produção de prostaciclina, que é um potente vasodilatador endógeno e, por tal motivo, pode agravar o vasoespasmo da artéria coronária, 17 porém mesmo a administração de baixas doses de aspirina é conhecida por bloquear o tromboxano A2, que também está implicado no espasmo da artéria coronária.…”