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Can low pulse pressure have an adverse effect in octogenarians?

Bursztyn, Michael

doi: 10.1097/HJH.0000000000000481
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Hypertension Unit, Department of Medicine, Hadassah-Hebrew University Medical Center, Mount-Scopus, Jerusalem, Israel

Correspondence to Michael Bursztyn, MD, FAHA, Hypertension Unit, Department of Medicine, Hadassah-Hebrew University Medical Center, Mount-Scopus, P.O. Box 24035, Jerusalem 912400, Israel. Tel: +972 2 5844706; fax: +972 2 5844705; e-mail: bursz@mail.huji.ac.il

After the publication of the landmark randomized Veteran Administration study on severe hypertension, the hypertension community focused mainly on DBP [1]. Later on, SBP regained its position as the most important determinant of risk associated with hypertension [2]. This transition took a few decades, although already in the 1970s, some authors had suggested DBP need not be measured [3].

Indeed, there are well known problems with measuring DBP, and there was quite a controversy whether the fourth or the fifth Korotkoff's sound should define DBP [4,5]. There is also some evidence that measurement of elevated DBP may frequently be artefactual [6]. As a matter of fact, a slower heart rate was found to be related to a lower DBP already at the beginning of the twentieth century [4].

During the past decade, pulse pressure (PP) – that is the arithmetic difference between SBP and DBP – was suggested as a major determinant of outcome [7]. In part, this reflects the increasing aortic and general vascular rigidity with age at a time when the aged are becoming the majority of the hypertensive population. With aging, there is a parallel process of rising SBP and decreasing DBP, that is increase in PP, and because the slope of SBP rise is usually steeper than the DBP decrease, PP frequently follows SBP.

In elderly hypertensive patients, PP has become a readily available surrogate of aortic rigidity, but limitations in its assessment were scarcely considered. The effect of bradycardia was already mentioned [6], and bradycardia may also be associated with higher blood pressure (BP) variability, especially in the face of a constant rate of deflating the measurement cuff [8,9]. The ‘white-coat’ response may not affect SBP and DBP to the same extent, thus leading to a ‘white-coat’ PP [10].

While low SBP (hence low PP [7]) is generally associated with a better outcome [11] (though with some limitations in octogenarians [12]), this may not be the case in the setting of acute events. Dramatic decreases in cardiac output and peripheral vascular resistance may occur in acute coronary syndromes, heart failure, severe aortic stenosis, and septic or anaphylactic shock. Indeed, low SBP and PP were found as predicting adverse outcome in variety of studies of acute cardiovascular events such as acute coronary syndromes [13–15] and heart failure [16–19].

Nevertheless, most of these studies, with some exceptions [19], examined mainly middle-aged and younger elderly. Octogenarians, who fill today medical wards, were under-represented in the majority of previous research.

The study by Li et al.[20], in this issue of the journal, is therefore most welcome. The authors have examined 353 consecutive admissions of patients 80 years of age or older with acute coronary syndrome to university hospitals in Gothenburg, Sweden, and followed them for all-cause mortality for 5 years [20]. BP was measured on admission in the emergency department or in a medical ward (if directly admitted) by trained personnel, who measured it by the auscultatory method, presumably with an aneroid sphygmomanometer, as in Sweden, the use of mercury sphygmomanometers has been forbidden [21] (http://www.kemi.se/Documents/Publikationer/Trycksaker/PM/PM2-11-Phase-out-of-mercury.pdf). Not withstanding all reservations about BP measurements and definition of PP, ‘white-coat’ effect, and so on, the authors found that those with PP below 50 mmHg on admission had a significantly increased mortality relative to other PP groups. This is in sharp contrast with the association of higher PP with adverse outcome [7] in the outpatient setting. Those with a PP greater than 70 mmHg also had increased mortality relative to those with PP between 50 and 70 mmHg. Also, after a myocardial infarction, a higher PP predicted an adverse outcome [22]. It may be suggested that, during an acute coronary syndrome, the decrease in myocardial perfusion (typical of the syndrome) causing myocardial ischemia usually brings about a decrease in cardiac output (CO). In the face of decreased CO, homeostatic mechanisms, mainly secretion of pressor substances, such as norepinephrine, angiotensin II, and so on, typically cause peripheral vasoconstriction and elevation of total peripheral resistance. The net combined effect is frequently associated with lower SBP and higher-than-baseline DBP, hence lower PP. Indirect evidence for such a mechanism comes from the authors’ observation that a PP lower than 50 mmHg was associated with a lower ejection fraction (43 ± 12% vs. 49 ± 10%) than in those with higher PP (P < 0.001). This difference was eliminated by propensity scoring. Propensity scoring may equalize differences and thus allow comparison between the two PP groups, but may also introduce some distortion: whereas 80% of patients with PP below 50 mmHg were represented in the propensity-scored subcohort, only 36% of the patients with higher PP were represented there. In the propensity-scored subcohort, those with lower PP had higher ejection fraction than those with lower PP in the whole cohort, indicating that those with a higher ejection fraction had no suitable matches. Despite this bias, which might diminish predictive effect of low PP, PP lower than 50 mmHg was still predictive of mortality. We are not told when was the ejection fraction measured, and as this is an observational study of consecutive patients, in all likelihood, ejection fraction was not measured in all patients at the same time during their clinical course. So we cannot put too much weight on this measurement. Similarly, we have no detail regarding BP measurement and early mortality, and no data regarding morbidity.

Low PP on admission may not necessarily mean a subsequent low PP. In a study of old patients with aortic stenosis and acute heart failure, those who had survived a year after the index admission had higher PP on admission, than those who died within a year, but at hospital discharge, their PP was similar [19]. Moreover, PP measured within a fortnight after myocardial infarction was a strong predictor of all-cause mortality and recurrent infarction [22]. This stresses the immense difference between BP variables determined during a cardiovascular event and those prevailing in the outpatient setting. Indeed ‘ …low or even normal BP at presentation, which may be the goal of treatment in the ambulatory setting, may be a more ominous finding, reflecting a low cardiac output and suboptimal or inadequate end-organ perfusion’ [17]. The authors mention several times the effects of reducing PP; nevertheless, in real life, there is very little we can do about lowering PP. Frequently, even in the successful case of reducing severe hypertension, say 180/110 mmHg, to well controlled hypertension (say 140/70 mmHg), we end up with very similar PP.

Low PP on admission may predict adverse long-term outcome, not on the basis of long-term effects of low PP, but as a reflection of an unfavorable acute hemodynamics, seriousness of the acute cardiac injury, and consequent peripheral vasoconstriction.

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ACKNOWLEDGEMENTS

Conflicts of interest

There are no conflicts of interest.

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