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

      research-article

      , MD, , MD PhD

      Clinical Research in Cardiology

      Steinkopff-Verlag

      coronary artery ectasia, coronary artery disease, atherosclerosis

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          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.

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          Most cited references 109

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          Based on 20 years of surveillance of the Framingham cohort relating subsequent cardiovascular events to prior evidence of diabetes, a twofold to threefold increased risk of clinical atherosclerotic disease was reported. The relative impact was greatest for intermittent claudication (IC) and congestive heart failure (CHF) and least for coronary heart disease (CHD), which was, nevertheless, on an absolute scale the chief sequela. The relative impact was substantially greater for women than for men. For each of the cardiovascular diseases (CVD), morbidity and mortality were higher for diabetic women than for nondiabetic men. After adjustment for other associated risk factors, the relative impact of diabetes on CHD, IC, or stroke incidence was the same for women as for men; for CVD death and CHF, it was greater for women. Cardiovascular mortality was actually about as great for diabetic women as for diabetic men.
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            Nitric oxide, superoxide, and peroxynitrite: the good, the bad, and ugly.

            Nitric oxide contrasts with most intercellular messengers because it diffuses rapidly and isotropically through most tissues with little reaction but cannot be transported through the vasculature due to rapid destruction by oxyhemoglobin. The rapid diffusion of nitric oxide between cells allows it to locally integrate the responses of blood vessels to turbulence, modulate synaptic plasticity in neurons, and control the oscillatory behavior of neuronal networks. Nitric oxide is not necessarily short lived and is intrinsically no more reactive than oxygen. The reactivity of nitric oxide per se has been greatly overestimated in vitro because no drain is provided to remove nitric oxide. Nitric oxide persists in solution for several minutes in micromolar concentrations before it reacts with oxygen to form much stronger oxidants like nitrogen dioxide. Nitric oxide is removed within seconds in vivo by diffusion over 100 microns through tissues to enter red blood cells and react with oxyhemoglobin. The direct toxicity of nitric oxide is modest but is greatly enhanced by reacting with superoxide to form peroxynitrite (ONOO-). Nitric oxide is the only biological molecule produced in high enough concentrations to out-compete superoxide dismutase for superoxide. Peroxynitrite reacts relatively slowly with most biological molecules, making peroxynitrite a selective oxidant. Peroxynitrite modifies tyrosine in proteins to create nitrotyrosines, leaving a footprint detectable in vivo. Nitration of structural proteins, including neurofilaments and actin, can disrupt filament assembly with major pathological consequences. Antibodies to nitrotyrosine have revealed nitration in human atherosclerosis, myocardial ischemia, septic and distressed lung, inflammatory bowel disease, and amyotrophic lateral sclerosis.
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              Simple scoring scheme for calculating the risk of acute coronary events based on the 10-year follow-up of the prospective cardiovascular Münster (PROCAM) study.

              The absolute risk of an acute coronary event depends on the totality of risk factors exhibited by an individual, the so-called global risk profile. Although several scoring schemes have been suggested to calculate this profile, many omit information on important variables such as family history of coronary heart disease or LDL cholesterol. Based on 325 acute coronary events occurring within 10 years of follow-up among 5389 men 35 to 65 years of age at recruitment into the Prospective Cardiovascular Münster (PROCAM) study, we developed a Cox proportional hazards model using the following 8 independent risk variables, ranked in order of importance: age, LDL cholesterol, smoking, HDL cholesterol, systolic blood pressure, family history of premature myocardial infarction, diabetes mellitus, and triglycerides. We then derived a simple point scoring system based on the beta-coefficients of this model. The accuracy of this point scoring scheme was comparable to coronary event prediction when the continuous variables themselves were used. The scoring system accurately predicted observed coronary events with an area under the receiver-operating characteristics curve of 82.4% compared with 82.9% for the Cox model with continuous variables. Our scoring system is a simple and accurate way of predicting global risk of myocardial infarction in clinical practice and will therefore allow more accurate targeting of preventive therapy.
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                Author and article information

                Contributors
                +31-4 33 87 51 06 , +31-4 33 87 51 04 , j.waltenberger@cardio.azm.nl
                Journal
                Clin Res Cardiol
                Clinical Research in Cardiology
                Steinkopff-Verlag (Darmstadt )
                1861-0684
                1861-0692
                26 April 2007
                June 2007
                : 96
                : 6
                : 331-339
                Affiliations
                Department of Cardiology, University Hospital of Maastricht and Cardiovascular Research Institute of Maastricht (CARIM) University of Maastricht, P. Debyelaan 25, 5800, 6202 AZ Maastricht, The Netherlands
                Article
                521
                10.1007/s00392-007-0521-0
                2775118
                17453130
                b1401b78-1c15-48d5-8529-20b94a1b8e9e
                © Steinkopff-Verlag 2007
                Categories
                Review
                Custom metadata
                © Steinkopff-Verlag 2007

                Cardiovascular Medicine

                coronary artery disease, atherosclerosis, coronary artery ectasia

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