Isolated Systolic Hypertension in the Young

The patient is a 16‐year old male who, during a routine physical examination at his school, was found to have a blood pressure of 150/80 mm Hg. This was a cause of consternation for both his parents and his teachers. On several repeat measurements the same thing was found—a high systolic but normal diastolic pressure. A subsequently purchased home monitor originally gave systolic readings of about 135 mm Hg, but these quickly settled to about 120 mm Hg. He reported no symptoms that might be related to high systolic blood pressure and was physically active and a member of the football team. Investigations for secondary causes of hypertension were negative and there was no evidence of target organ damage. A 24‐hour blood pressure recording showed a daytime average pressure of 129/62 mm Hg, which was considered normal. He was diagnosed as having white coat hypertension, and no treatment was prescribed.

Another diagnosis, which does not necessarily exclude the possibility of white coat hypertension, is isolated systolic hypertension of youth. This phenomenon was first described in 2000 by O'Rourke et al. ¹ It appears that O'Rourke did not consider this a major finding at the time because it was published in a journal that is subscribed to by only 24 libraries worldwide. The article describes six young men between ages 14 and 23 years who had systolic pressures ranging from 150 to 176 mm Hg and diastolic pressures from 50 to 85 mm Hg. They were all asymptomatic and otherwise quite healthy, and all were relatively tall for their age. The key investigation tool was applanation tonometry, a technique for recording the pressure waveform at the radial artery and deriving the central aortic pressure from it. In all subjects, the pressure wave recorded at the radial artery had a sharper‐than‐usual systolic peak and mean arterial pressure was normal. The estimated central aortic pressure was considered normal (less than 126 mm Hg), implying that the abnormality in these young men was an exaggerated amplification of the arterial pressure wave as it traveled to the periphery.

A second study, by Mahmud and Feely, ² suggests that this condition is not at all uncommon. These researchers measured the blood pressure and radial artery waveform in 174 consecutive medical students (half of whom were men). Eleven of the men (but none of the women) had systolic pressure above 140 mm Hg, giving a prevalence of about 12%. Average brachial artery pressure was 147/70 mm Hg, and estimated aortic pressure was 116/70 mm Hg, which was thought to be normal. None of the systolic hypertensives smoked, compared with 15% of the normotensive men, and all were engaged in active sports, whereas only 40% of the normotensive men were. The systolic hypertensive men also had slower resting heart rates. Thus, with the notable exception of elevated systolic pressure, these young men appeared to be exceptionally healthy. As in O'Rourke's cases, applanation tonometry showed exaggerated amplification of the pulse pressure in the peripheral circulation. The difference between the aortic and brachial systolic pressure was 31 mm Hg in the systolic hypertensives, but only 20 mm Hg in the normotensives.

What is the explanation for this phenomenon? At any point in the circulation, the recorded pressure wave is the result of the outgoing incident wave and the returning reflected wave. ³ If the peaks of the two waves coincide, there will be an exaggerated systolic pressure. This occurs in older persons with isolated systolic hypertension, where the brachial artery and aortic waves show a late systolic peak that causes an amplification of the more central waveform, but clearly some other explanation is needed to explain systolic hypertension of the young.

The factors that determine where the reflected wave will impinge on the incident wave are those that influence the timing of the reflected wave. If the reflected wave comes back quickly, it will hit the systolic peak of the next incident wave, but if it takes longer it will arrive in the diastolic downslope of the wave. The three principal factors are the velocity of the wave (pulse wave velocity), the distance the wave has to go before it is reflected, and the heart rate. As our arteries, like other parts of our bodies, become stiffer with age, pulse wave velocity increases, resulting in more rapid wave reflection and the late systolic peak of the pressure wave that is characteristic of older subjects (in whom there is little or no amplification of the wave as it travels to the periphery). In younger subjects the wave takes longer to return, and so ends up in the diastolic component of the pressure wave. The second factor, distance traveled, is related to the height of an individual: in a tall person the reflected wave will take longer to return than in a short person, so it is less likely to affect the systolic peak. Third, it has been observed that a high heart rate is associated with an increased amplification of the wave in the peripheral circulation. This happens because when the heart rate is rapid, the duration of systole is shortened and the reflected wave will begin to impinge on the diastolic portion of the wave. ⁴

In young systolic hypertensives it took significantly longer for the reflected wave to return to the ascending aorta than in normotensives. Thus two of these three factors—low pulse wave velocity (indicating elastic vessels) and increased body height (which was observed in these young men)—tended to enhance the amplification of the pressure wave, while the third—slow heart rate—tended to reduce it. But why should the brachial artery pressure actually be increased? One possibility is that the subjects had a high stroke volume. If the resting cardiac output is normal and the heart rate is slow, there must be a compensatory increase in stroke volume; the systolic hypertensives were all engaged in active sports and may have had some degree of "athlete's heart." If the aorta is very compliant in these subjects it may be able to accommodate the increased stroke volume without any increase of aortic systolic pressure, but the enhanced amplification of the pressure wave in these subjects may lead to an increased systolic pressure in the periphery to above‐normal values. We will undoubtedly hear more about this condition in the coming years. If Mahmud and Feely's ² observations are confirmed, it may occur in as many as 10% of healthy young men. If our case is typical, there may be a large white coat effect contributing to the phenomenon (the white coat effect predominantly affects systolic pressure). White coat hypertension certainly occurs in children. In one study of children with systolic pressures above the 95th percentile, 44% were classified as having white coat hypertension. ⁵ We would like to know more about the hemodynamics of the condition (is stroke volume increased, for example?), and the $64,000 question is whether or not the prognosis is benign. O'Rourke et al. ¹ labeled this condition “spurious” hypertension, which certainly implies a benign prognosis, although direct confirmation is lacking. Given the recent attention to prehypertension (systolic pressure between 120 and 139 mm Hg), it may be hard to convince anxious parents that their athletic son's systolic pressure of 160 mm Hg is no cause for alarm, that he can continue to indulge in active sports programs, and that he will grow out of it. The best advice is to follow these individuals carefully, but not to start them precipitately on medication.