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COMMENTARY |
Geriatric Research, Education and Clinical Center–VA Medical Center, University of Florida, Gainesville.
In the current issue of The Journal of Gerontology: Medical Sciences, the article by Dr. James Goodwin on hypertension in the very old painstakingly examines many meta-analysis studies on hypertension in elderly people and a scant number of studies in those subjects over age 80 and 85 years (1). He convincingly presents a good case for the low morbidity and mortality in elderly people with hypertension and asserts that the tolerability of hypertension in the old-old is better than 85 years. It is related to the increase in physiologic vigor. Based on my experience as an exercise physiologist, we have data that show that older men and women (aged 70–79 years), after 6 months of aerobic exercise training at tolerated and low intensity, demonstrated a reduction in supine, sitting, and standing blood pressures. More recently published data showed that resistance training at lower levels of weight in healthy elderly men and women can result in a reduction in blood pressure (2). The persons who participated in these studies did not have hypertension. These data are pointed out because of the importance in the lay literature of nonpharmacological approaches, which are well known to the readership and include weight control, salt restriction, moderation of alcohol intake, and regular exercise. It is with regard to daily physical activities that physiological vigor be addressed. Similarly, a minimum number of comorbid entities also allow a patient to exert a degree of physiological vigor associated with his or her age. It is this writer's opinion that beginning a new activity at an old-old age, which includes physical activity, might result in adverse musculoskeletal injuries.
The article by Goodwin (1) stresses the issues of outcome. Outcome research is critical in hypertension because it provides data on the lack of treatment in young adult hypertensives, resulting in an increased incidence of stroke, heart failure, and renal insufficiency. Such outcome research measures are of critical need in the old-old patient. These types of clinical trials are of great significance especially when one considers vascular dementia, which may be related to late treatment of hypertension resulting in white matter demyelinization seen on magnetic resonance imaging in association with a clinical picture of cognitive disorder. There are no studies to date that have shown treatment for hypertension in the old-old that also improve cognitive function and help resolve demyelinization.
It is quite likely that vascular dementia can result from hypoperfusion of the brain due to a loss of autoregulation of cerebral vascular blood flow. This may also be a consequence of multiple episodes of stroke, which can be associated with cognitive dysfunction especially as one ages, wherein there are episodes of benign senile forgetfulness and age-associated cognitive dysfunction. Therefore, just as there are changes in renal, cardiac, and musculoskeletal function with age, so too are there benign changes in the brain manifested by some mild cognitive disorder not of the Alzheimer's type complicated possibly by poorly controlled blood pressure. In Goodwin's article (1), there are data cited that indicate that the old-old with hypertension have a degree of protection through maintenance of perfusion to vital organs including the brain.
The SHEP study (3) did show a reduction in the prevalence rate for stroke and the PROGRESS study (4) (perindopril), protection against recurrent stroke. These studies are 2 of the recorded clinical trials that show a reduction in the prevalence of first stroke and for recurrent stroke. In the SHEP study, long-term assessment showed that there was no impact of treatment on cognition (5). This has not been carried out for the PROGRESS study (6).
When the first studies were undertaken to assess the efficacy of antihypertensive therapy in elderly people, the principle concern was whether or not this caused a compromise in cerebral perfusion linked to ischemia due to the decreased efficiency of autoregulatory mechanisms. According to the J-point hypothesis, based on studies that demonstrated that very low levels of blood pressure can result in increased coronary events, and that blood pressure levels that are too high are associated with an increase in cerebrovascular mortality and mobility, it is, in fact, feared that this high blood pressure could damage the brain and therefore compromise cognitive function.
In 1983, Solomon and colleagues published a study on the cognitive performance of 33 elderly hypertensives with regard to the antihypertensive therapy taken (e.g., propranolol, methyldopa, hydrochlorothiazide). The results indicated an evident compromise of verbal memory but not visual memory when a subject was treated with beta blockers and methyldopa. A drug with central action similar to clonidine (7) can effect memory function.
Subsequent research showed that therapy with beta blockers resulted in an increase in reaction time. Other studies have demonstrated that their use resulted in an improvement in psychometric testing scores. In particular, metoprolol, given its increased lipophilic action, is regarded as having an anxiolytic effect (8).
A study of 300 elderly patients with signs of some compromised cognitive function was undertaken (9). The objective of this study was to evaluate the existence of a possible correlation with the pharmacological therapy that they were taking. This was documented in 35 patients, principally in relation to long-acting benzodiazepines and also some antihypertensive drugs (beta blockers, methodopa, and reserpine). Numerous studies have been done to evaluate the effect of antihypertensive drugs on cognitive status of hypertensive people; the majority of these studies provided limited useful information due to inadequacies in their methodology (10,11). The strength of Goodwin's article (1) is that it is based on the principles of evidence-based medicine, and as a final statement to doctors, the message is "Primum non nocere."
Acknowledgments
Address correspondence to David T. Lowenthal, MD, PhD, GRECC-VA Medical Center, University of Florida, 1601 SW Archer Road, Gainesville, FL 32608-1197. E-mail: dlowen4241{at}aol.com
REFERENCES
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