Gender differences in biological substrates of disease determine different clinical manifestations of CV disease with important implications for prevention, diagnosis and therapy in the two sexes. In women, the activity of sex hormones reduces the influence of CV risk factors during the reproductive age, and delays the onset of CHD of 2 decades compared to men. However, women as men suffer from CV events, and in women mortality from all CV causes and have greater than the sum of the others 7 causes of death together. Women are more likely than men to die of a first myocardial infarction a probability of developing heart failure or a second infarction than their male counterparts. The levels of lipid components vary in different ages of life and in the two genders. TC and LDL increase in men between 35 and 50 years of age. On the contrary LDL levels do not change significantly in fertile women in which they have a lower predictive value for CHD than in men, HDL levels are higher in premenopausal women than in men of the same age and their role in predicting CHD is considerably higher in women. High triglycerides and Lp(a) are more important as a risk factor in women than in men. Because of the greater incidence of cardiovascular diseases in men until the early 80s, the information about the importance of risk factors associated with an increased risk of cardiovascular events has been gathered mainly in men and transferred to women. Most studies on lipid-lowering therapy did not have the adequate statistical power to show significant reductions in CV events in women. Regarding the indications for use of statins in daily practice, current data suggest that in secondary prevention statins are equally effective in both genders while in primary prevention the CV benefits of lipid-lowering therapy in women are less clear than in men and therefore should be used according to the degree of risk calculated from the available score systems.
The use of Lys-HA in the healing process of decubitus ulcers provides an improved efficacy with respect to SH in hospitalized patients, suggesting its use from the early phases of ulceration.
In this study the authors sought to determine the prevalence and long-term prognostic value of low triiodothyronine levels in elderly patients with heart failure and no thyroid disease. Lower levels of triiodothyronine are more prevalent in patients with advanced heart failure without thyroid disease, and this may have prognostic implications. However, this hormonal milieu has not been investigated in elderly patients. The authors prospectively followed a consecutive sample of 69 elderly patients aged 76.5+/-5.9 years with heart failure and 44 age-matched controls without heart failure between March 1997 and September 2000 at the Geriatric Cardiology Outpatient Clinic of the Heart Institute of Sao Paulo, Brazil. Events analyzed included death, hospitalization, and the combined end point of death or hospitalization. The study revealed that levels of triiodothyronine were lower in heart failure patients than in controls (89+/-23 vs. 101+/-16 ng/dL, p=0.001). During the follow-up period of 14.3+/-8.1 months there were 19 deaths and 33 hospitalizations in the heart failure group. The combined end point of death or hospitalization occurred in 38 patients. Triiodothyronine levels were lower in heart failure patients who had a cardiovascular event than in event-free patients (82.7+/-24.8 vs. 96.7+/-19.2 ng/dL, p=0.012). The odds ratio for events was 9.8 (95% confidence interval, 2.2-43, p=0.004) for patients in the lowest tertile of triiodothyronine, that is, lower than 80 ng/dL, compared with patients with levels above 80 ng/dL. The authors conclude that among elderly patients with heart failure, lower triiodothyronine concentrations are more prevalent and are associated with a worse prognosis.
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