PREVENTION OF ATHEROSCLEROSIS AND END-ORGAN DAMAGE - A BASIS FOR ANTIHYPERTENSIVE INTERVENTIONAL STRATEGIES

Aim: To review the nature of the complex relationships between essenti al hypertension and cardiovascular end-organ damage, with a particular focus on the pathogenesis and prevention of coronary heart disease, t he major complication of untreated hypertension. Risk factors far coro nary heart disease: Both atherosclerosis and hypertension have their o rigins in childhood; in the second and third decades of life developme nt of the more advanced fibrous plaques accelerates, emphasizing the n eed for early diagnosis and intervention. Perplexing and complex relat ionships have been found among the principal risk factors for coronary heart disease, hyperinsulinemia, insulin resistance, dyslipidemia and hypertension. In the pathogenesis of atherosclerosis at the cellular and molecular level, the important features are the effects of monocyt e-macrophages, oxidant stress, lipoprotein modification, inflammatory mediators and the focal hemodynamic environment. Even brief periods of experimental hypertension can accentuate atherogenesis, the effects o f which are greatest but not limited to the cervical and cerebral arte ries. Further, acute hypertension lasting for even a few minutes cause s a 'leakage' of plasma proteins and particulate probes into the arter y wall, which has far-reaching implications for antihypertensive thera py. Recent work has shown that 24-h blood pressure variability is corr elated with target-organ damage in hypertensive patients. Therapy: Ant ihypertensive therapy should not only lower blood pressure but also pr event significant short-term blood pressure fluctuations. The trough:p eak ratio has been used to assess the effect of antihypertensive treat ment on blood pressure variability. Conclusion: More intensive researc h is required to clarify the nature of the interface between hypertens ion and atherogenesis.