Link Between Macrocirculation and Microcirculation in Isolated Systolic Hypertension of Older Subjects

The arteries have two functions—first as a conduit, and second as a cushion.1 Arteries distribute blood to the systemic organs and tissues (the conduit function) but they must also cushion pulsations from the left ventricle so that blood may flow evenly into the microcirculation (cushion function). Obstruction of an artery usually causes obvious ischemia or infarction of a tissue or organ, whereas stiffening causes more subtle changes predominantly upstream, where pulsatile pressure is increased in central arteries. Changes are not fully apparent in peripheral arteries such as the brachial.1,2 Increase in central pulsatile pressure adversely affects the heart, because the left ventricle must pump harder in systole, and has lower pressure to perfuse it during diastole through the coronary arteries. Consequences are left ventricular hypertrophy and predisposition to myocardial ischemia and heart failure.1 Effects of arterial stiffness on cushioning function have only recently been appreciated.3 In the arteries of young people, pulsations are effectively cushioned in the large elastic arteries so that energy lost in arterial pulsation is very low—perhaps 5–10% of energy lost driving blood through the narrow arterioles and capillaries.4 With aging, the elastic arteries stiffen and cannot cushion pulsations of flow. The flow pulsations extend down into vasodilated high flow organs—notable in the brain and kidneys. In consequence, pulsatile energy is absorbed in the microvessels of these organs, and this may be increased fourfold.3 Magnetic resonance imaging studies have noted increase in pulsatile flow in small cerebral vessels, even extending into cerebral veins of older subjects, most marked in persons with dementia.5 The term “Pulse Wave Encephalopathy”3,5 has been introduced to explain the plexiform lesions seen in the brain of such persons, with evidence of edema, endothelial damage with thrombosis, and medial damage causing microhemorrhage. White matter hyperintensities may be the major manifestations of these vascular lesions.3,5 In this issue of the journal, Triantafyllidi and colleagues6 describe a relationship between arterial stiffening and cognitive impairment in older persons with never treated hypertension. They also describe a similar relationship between arterial stiffening and microalbuminuria of older persons. Other studies have shown similar problems in the brain and kidney. They are explicable on the basis of principles described above. But they also fit in with other observations—of similar lesions in the brain and kidneys when blood pressure is acutely elevated in malignant hypertension, and their disappearance when hypertension is controlled.1,3 They fit in with development over years of similar plexiform lesions (with organized thrombosis and microhemorrhage) in small vessels in the lungs as a cause of pulmonary hypertension in untreated left to right cardiac shunting, where pulmonary pulsations are markedly increased.7 They may explain the apparent shedding of endothelial cells in older persons with stiffened arteries, and their appearance in peripheral blood. The widespread damage and associated inflammatory process of repair may explain elevation of CRP and ESR. New studies in this field link disease of the macrovessels with disease of the microvessels in brain and kidney, and may explain how effective treatment of hypertension, and especially isolated systolic hypertension, may delay development of cerebral microvascular lesions and of intellectual deterioration, together with microalbuminuria and renal dysfunction in older subjects. Michael F. O'Rourke is a founding director of AtCor Medical Pty Limited, Sydney, Australia, manufacturer of systems for analyzing the arterial pulse.