Does hormone treatment alter arterial properties in postmenopausal women?

Arterial elastic properties and wave reflections constitute left ventricular pulsatile afterload and are directly related to cardiovascular morbidity and mortality. During the aging process, elastic arteries stiffen and increase pulse wave velocity, causing the reflected pressure wave to arrive at the heart during systole, and augment systolic and pulse blood pressure, resulting in left ventricular hypertrophy. The incidence of cardiovascular disease is much greater in men aged 30-50 years compared with women of a similar age. Among women, the incidence of cardiovascular disease increases dramatically after menopause, which occurs at an average age of 52 years. This observation has lead to the belief that sex hormones produced premenopausally impede or delay the progression of cardiovascular disease. Therefore, it appears logical that the administration of female sex hormones, hormone treatment (HT), estrogen alone or with progesterone should provide some degree of cardiovascular protection. This idea was supported by experiments in animals and isolated arterial segments demonstrating that HT increases plasma nitric oxide, decreases endothelin-1 levels and causes smooth muscle relaxation. Also, 17β-estradiol administration decreases collagen and increases elastin in the aortic wall of rats. These experimental studies suggest an improvement in both elastic and muscular artery properties and favorabe modifications of arterial wave reflection characteristics. Furthermore, HT improves lipoprotein metabolism and reduces coronary artery plaque formation in animal models. Unfortunately, observational and interventional studies in postmenopausal women that have evaluated the impact of HT on cardiovascular changes have produced inconsistent and inconclusive results. Most studies agree that arterial stiffness increases after menopause, partly due to advancing age and reduced estrogen production. Results from most studies that were designed to investigate the effects of HT on arterial properties have shown a selective decrease in elastic artery stiffness with little effect on muscular arteries. This beneficial effect was observed only if estrogen alone was administered. The main objective of this review is to discuss the ill effects of arterial stiffness in general and attempt to translate information from previous experimental studies to those in postmenopausal women and explain the beneficial effects of HT on arterial stiffness and improvement in left ventricular afterload.