INICSA   23916
INSTITUTO DE INVESTIGACIONES EN CIENCIAS DE LA SALUD
Unidad Ejecutora - UE
artículos
Título:
Risk of vascular disease in premenopausal women with diabetes mellitus.
Autor/es:
NESTOR H. GARCIA; HERNAN A. PEREZ; J. DAVID SPENCE; LUIS J. ARMANDO
Revista:
World Biomedical Frontiers
Editorial:
World Biomedical Frontiers
Referencias:
Año: 2015
ISSN:
2328-0166
Resumen:
The role of diabetes mellitus (DM) in the pathogenesis of cardiovascular disease is evident from the Framingham Heart Study identifying diabetes as a major cardiovascular risk factor . The last report from the AHA 2013 (1) indicated that of the estimated 19.7 million American adults with physician-diagnosed diabetes, more than 51% are women, and since 1984 the number of female deaths by cardiovascular disease (CVD) has exceeded those for males. In 2009, CVD in females represented 51.0% of deaths in United States. Another important observation is that 26% of women age 45 and older who have an initial recognized heart attack die within a year compared with 19% of men, more women than men have angina in total numbers (4.1 million vs. 3.7 million) and 64% of women who died suddenly of coronary heart disease had no previous symptoms, and finally the incidence for death stroke in 2009 was also superior in women (59.6% of total stroke deaths) than in men. All of these data indicate that women are at least equally sensitive to have a cardiovascular disease compared to men.Classically, in women, determination of cardiovascular risk is not intense and investigators have applied the term "bikini medicine" to actual preventive medicine practice in women (2), referring to a focus on the breasts and the reproductive system during premenopausal years, with cardiovascular prevention considered only after menopause.In women, as well in men, CAD events are the result of a complex interaction of multiple risk factors including diabetes mellitus (3). However, for women, up to 20% of all coronary events occur in the absence of these major risk factors (4), whereas many women with traditional risk factors do not experience coronary events, indicating that the algorithm used is not sensitive enough to prevent most of the cardiovascular events. In addition, physicians and other healthcare providers continue to underestimate cardiovascular risk in women, with consequent underutilization of preventive therapies (5), (6) such as statins at early age in the absence of evident target organ damage (intermittent claudication, coronary disease, etc).Diabetes accelerates the development of atherosclerosis, such that women with DM are at 2- to 4-fold increased risk of CVD compared with age-matched patients without DM (7). Coronary heart disease constitutes more than two-thirds of all deaths in older patients with DM. This has stimulated interest in reducing CHD and CVD-related morbidity and mortality through primary prevention among such patients (8). Despite this changing view of pathophysiology, variables included in current risk algorithms for women are largely unchanged from those recommended 40 years ago. Recently, the measurement of atherosclerosis burden as a predictor of cardiovascular event has been proposed, using the determination of total plaque area (9). Atherosclerosis develops silently over decades before symptoms occur. Thus there is opportunity for timely detection and personalized prevention. However, the period preceding development of symptoms (subclinical atherosclerosis) is not efficiently used, neither to prevent events, nor to categorize the risk of patients in primary care. Subclinical atherosclerosis can be detected, very accurately and non-invasively, by means of the determination of carotid total plaque area (TPA) by ultrasound (9). A recent meta-analysis showed that TPA was a stronger predictor of cardiovascular risk than the more widely used carotid intima-media thickness (10) and coronary calcium score (11). This well-developed technique can be used at the patient?s first visit and at follow-up visits to determine the effectiveness of different therapies. Figure 1 and 2 shows 2 different patients with regression and progression of an atherosclerosis plaque.