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Pulse pressure and cardiovascular risk in diseased patients

Journal of Human Hypertension volume 30, pages 293–294 (2016)Cite this article

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High blood pressure (BP) is considered a major cardiovascular risk factor. Data from observational studies involving more than 1 million individuals without pre-existing vascular disease have indicated that coronary and cerebrovascular mortality increases progressively with increasing systolic and diastolic brachial BP.1 This relation not necessarily is the same in ‘diseased’ subjects. In patients with coronary artery disease, the relation may be J- or U-shaped, with higher event rates at very low and very high blood pressures.2, 3 In addition, brachial pulse pressure (PP), the difference between systolic and diastolic BP, is a major cardiovascular risk factor directly related to cardiovascular events.4 However, these findings are not without exception. Several studies in patients with systolic heart failure showed an inverse relationship between PP and the cardiovascular risk.5, 6 In addition, in the study published in the present issue of the Journal of Human Hypertension, Theilade et al.7 failed to show an independent relationship between brachial PP and cardiovascular events in a high-risk population with diabetes, chronic kidney disease and anemia. Importantly, systolic and diastolic BP were not related to cardiovascular risk in this highly selected population as well. These results may suggest that BP in general and PP in particular is useless in risk stratification in patients with diabetes, chronic kidney disease and anemia.

Several potential pathophysiological mechanisms are appropriately discussed by the authors to explain the existence of the above discrepancies. The first explanation could be an epiphenomenon of chronic illness, which increases noncardiovascular mortality. Second, medical treatment may alter the relationship between BP components and cardiovascular risk. Indeed, study participants were adequately treated with a high proportion receiving renin–angiotensin–aldosteron system blockers, and median BP was 136/71 mm Hg. In addition, it is reasonable to suspect that BP-lowering treatment was modified during the observational period. Probably, this occurred more often in subjects with high BP leading to a blunted prognostic value of the baseline BP. Third, brachial PP is only a crude estimate of arterial stiffening, inferior to direct measures of central hemodynamics and aortic stiffness.8 Fourth, following the same lines of argument, the central-to-brachial pressure wave amplification should be taken into account. There is increasing evidence that the difference between central and peripheral BP impacts the predictive value of brachial BP. Although the difference between central and peripheral BP is smaller in older subjects9 as well as in those with diseases leading to reduced arterial wall compliance (for example, renal insufficiency, diabetes), the difference still may have clinical significance. The last and most likely explanation is the relationship between left ventricular (LV) systolic function and PP. In contrast to normal systolic function, where measures of pulsatile function (PP, wave reflection parameters) are related to aortic and arterial elastic properties, when systolic function is severly impaired, the left ventricle cannot cope with pulsatile afterload, ejection ceases early, and PP and wave reflection parameters decline. The net result is an inverse relationship between ejection fraction (and other measures of LV function) and pulsatile hemodynamics.10, 11, 12 Supporting this concept, pulse wave velocity, a direct measure of aortic stiffness, was directly related to cardiovascular mortality in patients with severly impaired systolic function, but PP showed an inverse relationship.13

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  1. First Department of Cardiology and Hypertension, Institute of Cardiology, Jagiellonian University Medical College, Kraków, Poland

    P Jankowski

  2. Cardiology Department, Klinikum Wels-Grieskirchen, Wels, Austria

    T Weber

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Correspondence to P Jankowski.

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Jankowski, P., Weber, T. Pulse pressure and cardiovascular risk in diseased patients. J Hum Hypertens 30, 293–294 (2016). https://doi.org/10.1038/jhh.2015.83

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