Blood pressure (BP) values are subjected to continuous dynamic changes throughout one individual's life. Some of these changes are apparently random in nature and may be related to individual characteristics in cardiovascular regulation, whereas others depend on well defined causes and mechanisms . Typical examples of the latter are the BP fall observed during sleep, the BP increases in response to physical or emotional stress, and also the BP fall which occurs in most people after meals . This postprandial BP fall appears to be primarily a result of neurohormonal changes induced by food intake, leading to vasodilation in the splanchnic vascular bed [2,3]. Whereas its extent is normally limited by compensatory mechanisms, in particular by increased sympathetic activity, in some individuals this compensation is not adequate, leading to postprandial hypotension (Fig. 1). This is more likely in elderly people, in whom arterial baroreflex control of the circulation is impaired and BP variability is enhanced also because of increased large arteries stiffness [4,5]. This phenomenon is commonly, although arbitrarily, defined as a SBP fall of at least 20 mmHg, compared with baseline BP levels, occurring after a meal (or a postprandial decrease in SBP below 90 mmHg from a baseline level ≥100 mmHg). The time frame when the maximal postprandial BP response occurs is between 30 and 60 min after a meal in most individuals, but it may extend to 120 min in some . Although this phenomenon is well known to clinicians dealing with the elderly (in this age group it is most common, especially in the presence of diabetes or Parkinson's disease), its pathophysiological background and clinical importance are still not fully understood.
The study by Tabara et al. published in the current issue of Journal of Hypertension was aimed at improving the understanding of clinical and epidemiological relevance of postprandial BP decline and hypotension. To this aim, the data on postprandial BP obtained in 1308 participants participating in a general health check-up were related to the presence of vascular lesions in brain MRI. The authors report a higher prevalence of lacunar infarctions in patients with postprandial hypotension compared with controls, and a significant relationship between the size of postprandial BP fall and the number of lacunar infarctions, independent of major confounders, including basal BP levels.
Whereas the study of Tabara et al. basically confirms previous findings in an institutionalized population, coming from the same group , it has the merit of extending them to a community-dwelling population, at lower risk of cerebrovascular disease.
A major strength of the study is the extensive and standardized phenotyping, including a brain MRI scan, performed in a large sample of patients. This sample, owing to the lack of specific selection criteria and to the recruitment based on population-scale health initiative, appears to be reasonably representative of a middle-aged and elderly Japanese population .
A major interpretative difficulty in this study lies in understanding the direction of relationship between postprandial BP pattern and cerebral outcome. In fact, the cross-sectional nature of this study does not allow authors to prove that the observed association reflects a cause–effect relationship. Nonetheless, the authors in the discussion make a good case in favour of the hypothesis that postprandial hypotension is the cause of brain ischaemic lesions rather than being their consequence or just an epiphenomenon. Although their arguments are mostly valid, they do not necessarily preclude alternative possible explanations, however. One, the impairment of baroreflex cardiovascular modulation, frequent in the elderly, may contribute to development of postprandial hypotension (e.g. in diabetic patients), and, on the other hand, it may also be associated with cerebral damage (either as its cause or consequence) [8,9]. The authors argue that, because the observed relationship between postprandial hypotension and brain lacunae was independent from carotid intima–media thickness and from arterial stiffness (as evaluated through brachial–ankle pulse wave velocity assessment), it is unlikely that it depended to a large extent on altered baroreflex function. However, this reasoning is quite speculative since arterial wall structure and stiffness are not the only determinants of cardiovascular modulation by afferent arterial baroreflex signalling [10,11]. It also does not consider the possible alterations in the efferent or central portions of the arterial baroreflex loop, nor in the activity of other baroreceptor areas (venous, cardiopulmonary). Thus the possibility of postprandial hypotension being an epiphenomenon cannot be excluded, even if in one study which directly assessed this issue, no changes in baroreflex sensitivity were found in response to oral glucose loading either in young or in elderly patients . Secondly, cerebral ischaemic lesions might cause an impairment in cardiovascular regulation (by affecting the central portion of baroreflex, but also other mechanisms involved in the control of vascular tone), thus leading to postprandial hypotension . This possibility could only be verified in a prospective study in individuals with no previous ischaemic lesions. Unfortunately, in the only longitudinal study which demonstrated an increased risk of stroke in patients with postprandial hypotension, brain imaging at baseline was not performed .
An important and possibly critical aspect of the study by Tabara et al. is the methodology of BP assessment. Postprandial BP fall was assessed based on just two measurements: one before lunch and one 30 min after lunch. Considering the well known instability of casual BP measurements and the fact that BP nadir may occur after 60 or even 120 min after food intake , such an approach was likely to reduce the power of the study. This may also have contributed to the somewhat surprising lack of independent relationship between baseline SBP and the presence of lacunae. Together with the fact that patients with postprandial hypotension had much higher baseline SBP than controls, this methodological limitation thus creates some difficulties in interpreting study results. Data obtained with a more robust approach (ambulatory BP monitoring or at least repeated conventional measurements) would have strengthened the study results.
Notwithstanding the above limitations, the study of Tabara et al. provides an important contribution to a better understanding of the clinical importance of postprandial hypotension (Fig. 1) and raises a number of interesting research questions, clinically relevant and still unanswered: How does postprandial hypotension relate to nocturnal nondipping, or to ‘extreme dipping’, a phenomenon reported to be associated with excess cerebrovascular risk in the elderly?  What is the relative contribution to the so-called ‘siesta dipping’ phenomenon by BP reaction to food ingestion (’true’ postprandial BP fall) on one hand and by BP changes due to reduced activity on the other? To what extent may postprandial hypotension contribute to increased overall BP variability, another BP pattern related to cerebrovascular outcomes? Can therapeutic interventions aimed at reducing postprandial hypotension reduce the risk of cerebrovascular sequelae? Considering that in the developed countries the number of elderly people prone to develop postprandial hypotension is constantly increasing, these questions deserve to be answered by future ad hoc studies.
Conflicts of interest
There are no conflicts of interest.
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