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Novel insights into an old controversy: is coronary artery ectasia a variant of coronary atherosclerosis?

ABSTRACT: Coronary artery ectasia (CAE) is defined as a localized or diffuse non-obstructive lesion of the epicardial coronary arteries with a luminal dilation exceeding 1.5-fold the diameter of the normal adjacent arterial segment. The incidence of CAE has been reported to range between 2% and 4%, which might be an overestimation of the true frequency. The coincidence of CAE with other systemic vascular dilatations has suggested that the mechanism underlying CAE is not only localized to coronary arteries, but also to other vascular compartments such as aorta or peripheral veins. Although the pathophysiology of CAE remains largely unknown, it was supposed to represent a variant of coronary atherosclerosis. This review focuses on this controversy of whether CAE and coronary artery disease (CAD) are two manifestations of the same underlying process. There are clear differences between CAD and CAE with respect to cardiovascular risk factors such as diabetes mellitus, and pathogenic steps in disease progress such as inflammation or extracellular matrix remodeling. As this review will underscore, the current knowledge of the field is insufficient to finally clarify the causative interrelation between CAE and CAD. The clinical course and treatment of CAE mainly depends on its coexistence with CAD. When coexisting with CAD, the prognosis and treatment of CAE are the same as for CAD alone. In isolated CAE, prognosis is better and anti-platelet drugs are the mainstay of treatment. Surgical treatment can be considered in selected patients. For clarifying the mechanism underlying CAE, additional clinical, histopathological and pathophysiological investigations are required. In fact, every patient with CAE should be evaluated systematically for pathological changes in other vascular territories, both in the arterial system as well as in the venous system, which might occur in the disease process.

SUBMITTER: Yetkin E

PROVIDER: S-EPMC2775118 | biostudies-other | 2007 Jun

REPOSITORIES: biostudies-other

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Project description:IntroductionAcute myocardial infarction (AMI) is a specific type of coronary artery disease (CAD) caused by the rupture of coronary atherosclerotic plaques. Coronary artery ectasia (CAE) is a rare phenotype of cardiovascular disease that may promote thrombosis and inflammatory responses leading to myocardial infarction due to abnormal dilatation of blood vessels and coronary blood flow disorders. It is a complicated disease and shows interaction between genetic and environmental factors.Patient concernsA 34-year-old male patient was admitted to our hospital on May 12, 2016, with complaints of chest pain for 1 hour duration.DiagnosisCoronary angiography through the emergency medical service (EMS) system showed 100% occlusion at the first turning point of the right coronary artery (RCA), along with tumor-like expansion of the proximal segment of the RCA and the end of the left main (LM) artery. The patient was diagnosed with AMI and CAE. Three-point mutations in the ATG16L1 gene were identified by direct sequencing.InterventionsAfter admission, the patient underwent emergency green channel coronary angiography and percutaneous coronary intervention (PCI) to assess and unblock the stenosis and occlusion of the RCA lumen, but no stenting was performed because the catheter could not pass the second inflection point of the RCA. Aspirin enteric-coated tablets, clopidogrel sulfate tablets, tirofiban hydrochloride, and low molecular weight heparin calcium were given as anticoagulant and antiplatelet therapy. Atorvastatin calcium tablets were used to regulate blood lipid levels. Perindopril and spironolactone were used to inhibit the renin-angiotensin-aldosterone system (RAAS) to reverse myocardial remodeling. Acetylcholinesterase inhibitors (ACEI) and beta blockers were administered to resist ventricular remodeling and improve cardiac function and prognosis after the patient's blood pressure and heart rhythm were stabilized.OutcomesAfter active rescue treatment, the patient recovered and was discharged. A coronary angiogram performed 2 years later showed that the RCA blood flow was restored, and the patient had recovered well.ConclusionThree-point mutations in the ATG16L1 gene were identified in a patient with AMI and CAE, which extended the mutation spectrum of the ATG16L1 gene. Hence, the etiology of coronary artery aneurysmal dilatation is worthy of further investigation.

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Novel insights into an old controversy: is coronary artery ectasia a variant of coronary atherosclerosis?

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