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a Department of Internal Medicine and Geriatrics, Hôpital Gériatrique les Bateliers, Centre Hospitalier Régional, and University of Lille, France
François Puisieux, Service de M\|[eacute]\|decine Interne et de G\|[eacute]\|riatrie, H\|[ocirc ]\|pital G\|[eacute]\|riatrique les Bateliers, CHRU Lille, 59037 Lille Cedex, France E-mail: fpuisieux{at}nordnet.fr.
William B. Ershler, MD
| Abstract |
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Methods. Twenty-four-hour ABPM was performed in 156 inpatients (111 women, mean age 80.4 ± 8.1 years). Among them, 45 had been admitted for falls and 75 for syncope; 36 with no history of falls or syncope served as controls. Postprandial change in systolic blood pressure (
SBP) was calculated by subtracting the mean SBP within the 2 hours following the meal from the mean SBP within the 2 hours preceding the meal. PPH was defined by a
SBP
20 mm Hg.
Results. For the entire group, mean SBP decreased after the three meals. On average, the decline in SBP was greater after breakfast than after lunch or dinner, and the number of patients experiencing PPH was greater after breakfast. Average maximal
SBP was significantly larger in the syncope group than in the other groups ( p < .05). Moreover, the number of patients experiencing PPH was significantly higher in the syncope/fall group than in the control group (23% vs 9%; p = .03). Compared with patients without PPH, patients with PPH were more likely to have a history of diabetes mellitus (p < .01) or to use more than three different drugs daily ( p = .04), and they showed greater daytime SBP variability (p < .0001). Furthermore, there was a strong positive correlation between preprandial SBP and
SBP after breakfast.
Conclusions. About one out of four elderly patients with falls or syncope experiences PPH, usually after breakfast. Postprandial decline in BP contributes to BP variability.
SBP and preprandial SBP are positively correlated.
FALLS and syncope are common symptoms in elderly persons and may be caused by a large variety of disorders (1)(2)(3). Over the past decade, postprandial hypotension (PPH) (4)(5)(6)(7)(8) has been recognized as a common cause of syncope and falls in elderly persons. Noninvasive ambulatory blood pressure monitoring (ABPM) is considered a valuable and useful test for the management of patients with hypertension and particularly to eliminate "white-coat hypertension," to confirm the diagnosis of borderline hypertension, to assess the circadian rhythm of blood pressure (BP), or to evaluate treatment-resistant hypertension (9)(10)(11)(12)(13)(14)(15). Furthermore, ambulatory BP measurements have a better correlation with the presence of target organ complications of hypertensive disease than do office BP values, and ABPM is superior to office BP in predicting cardiovascular morbidity (9)(12). Because ABPM can produce considerable information about BP variations, it has been suggested that ABPM may be a useful test to detect abrupt changes in BP in elderly persons, especially after a meal or with changes in posture (7)(10)(14)(16). However, data are scanty in support of this assertion. Only a few studies using ABPM have been designed to assess postprandial changes in BP (17)(18)(19)(20)(21)(22). Only three of the studies reported on elderly patients (17)(20)(21), and to the best of our knowledge, none have addressed the particularities of BP profile in elderly patients with falls or syncopes. Our study investigates postprandial BP changes by means of ABPM in elderly patients with falls or syncopes and, for comparison, in control patients without such a history.
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Patients
Between February 1996 and January 1997, all patients who were admitted to our department of acute geriatric medicine for investigation of falls or syncope were invited to participate in the study provided they fulfilled the following criteria: (a) were
60 years old; (b) provided informed consent to participate in the study; and (c) had no history of myocardial infarction or stroke within the preceding 6 months. Thirty-four inpatients without a history of falls or loss of consciousness and who agreed to participate in the study served as controls.
Baseline Evaluation of Patients
For all patients, we obtained a complete history and physical examination, including details of medication use. A postural test was performed on each patient; orthostatic hypotension (OH) was defined by a systolic blood pressure (SBP) decline
20 mm Hg within 3 minutes after standing.
ABPM
During their hospitalization, all patients and controls underwent 24-hour ABPM using the Spacelabs 90207 monitor (SpaceLabs, Inc., Workingham, Beckshire, England), which has been validated according to British Hypertension Society criteria for use in elderly persons (23). The monitoring began at 10:00 AM. The monitor was programmed to take readings every 15 minutes during the day (7:00 AM to 10:00 PM) and every 30 minutes at night (10:00 PM to 7:00 AM). An appropriately sized cuff was applied to the left arm. For each patient, the average BP and the BP variability (SD of mean value) were calculated for 24 hours and for the periods corresponding to day and night. The circadian BP was considered as reversed when mean SBP during the day period was lower than mean SBP during the night period. In the hospital, meals are taken at set times; between 8:00 and 8:30 AM for breakfast; between 12:00 and 12:30 PM for lunch; between 6:00 and 6:30 PM for dinner. All patients took meals sitting, in their rooms. According to the definition of Grodziki and coworkers (21), postprandial SBP decline (
SBP) was defined by the following equation:
SBP = preprandial SBP - postprandial SBP where preprandial SBP = average SBP during the 2 hours preceding the meal, and postprandial SBP = average SBP during the 2 hours following the meal. PPH was defined by a
SBP
20 mm Hg. Only recordings with complete measurements of the BP variations at the time of the three meals were included (at least two readings per hour during the 2 hours before and the 2 hours after each meal). Each patient was asked about his or her waking time, time of falling asleep, and quality of his or her sleep.
Statistical Analysis
The results were expressed in mean values ± SD. The groups were compared by chi-square test for categorical variables and by analysis of variance or Student's t test for continuous variables for series, paired or not. The relation between postprandial change in BP and preprandial SBP for each patient was calculated using standard linear regression techniques. A value of p < .05 was considered statistically significant.
| Results |
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SBP) was assessed by comparing the mean SBP in the 2 hours before and after the meals, the decline in SBP, on average, was greater after breakfast (5.3 ± 13.4) than after lunch (3.4 ± 9.1) or after dinner (2.6 ± 10.5), but the difference did not reach statistical significance (p = .1).
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SBP was slightly greater among the patients with syncopes or falls than among the controls (respectively, 4.5 ± 5.7, and 3.8 ± 7.5 vs 1.8 ± 6.6 in the control group; p = .015) (Fig. 2). All patients experienced at least one (after one of the three meals) decline in SBP. For each patient, we obtained three measurements of postprandial SBP change (one for breakfast, one for lunch, one for dinner); thus we could consider the maximal postprandial decline in SBP (max
SBP). On average, max
SBP was significantly different between the three groups (13.4 ± 9.0 in the syncope group, 12.4 ± 11.2 in the fall group, and 8.6 ± 8.9 in the control group; p < .05). As illustrated by the histogram of the max
SBP for all patients (Fig. 3), 31 (20%) patients experienced PPH (defined by a
SBP
20 mm Hg). PPH was observed after breakfast in 14 patients, after lunch in eight patients, and after dinner in nine patients. The number of patients experiencing PPH was significantly greater in the syncope/fall group than in the control group (20 patients [27%] in the syncope group and 8 patients [18%] in the fall group vs 3 patients [8.5%] in the control group; p < .05).
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SBP
SBP after breakfast that fit a linear regression equation (r = .51, p < .0001). A significant positive relationship was also observed between preprandial SBP and
SBP after lunch (r = .38, p < .001).
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| Discussion |
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SBP
20 mm Hg) was high among elderly subjects hospitalized for falls or syncope (23%); (2) on average, the decline in SBP was greater after breakfast than after lunch or dinner, and the number of patients experiencing PPH was greater after breakfast; (3) compared with patients without PPH, those with PPH were more likely to have a history of diabetes mellitus or to use more than three different drugs daily; (4) PPH increased diurnal BP variability independently of nocturnal change in BP; and (5) preprandial SBP and
SBP were positively correlated, especially at breakfast time.
Although it has been suggested that ABPM may be a useful test to detect PPH in elderly persons, only a few studies have addressed this problem (17)(21)(22). There is no standardized definition for PPH (7). However, by analogy with OH, PPH is usually defined as a decrease in SBP of 20 mm Hg or more after meal ingestion (7). Because BP usually reaches a nadir within 15 to 75 minutes after the start of a meal (7), we took into account the mean BP during the 2 hours following the meal and, for comparison, the mean BP during the 2 hours preceding the meal. The definition used for PPH in the present study is identical to that used in a recent study by Grodziki and coworkers (21) and close to that used in a recent study by Kohara and coworkers (22), which allows for comparisons. Grodziki's study included 530 elderly patients (aged 60 to 100 years) participating in the Systolic Hypertension in Europe study, 70% of whom experienced some decline in BP after the main meal and one quarter of whom experienced a decrease of more than 16 mm Hg (21). Although our study population is rather different, we observed relatively similar results because approximately 20% of the subjects in our study experienced PPH (
SBP
20 mm Hg). In Kohara's study, which included 121 hospitalized, essential hypertensive, patients (65 patients were
60 years) (22), the postprandial BP decline showed age-dependent augmentation, and the mean postprandial BP decline was 7 ± 12.8 mm Hg among patients aged 70 years and older.
We observed that the maximal postprandial decline was significantly greater in the syncope group than in the fall group or in the control group (p < .05). We also found a higher prevalence of PPH in the fall/syncope group than in the control group (23% vs 8%; p < .05). This result is in agreement with other recent studies (5)(6)(7)(8) and constitutes a supplementary argument in favor of the hypothesis according to which PPH predisposes the elderly subject to falls and syncopes. In our study, PPH was significantly correlated with a history of diabetes mellitus. Previous studies have suggested that autonomic dysfunction caused by diabetes is a risk factor for PPH (7). We did not find any relationship between age, gender, BMI, ADL, and PPH. However, patients with PPH were more likely to use more than three different drugs daily. We failed to incriminate a therapeutic class in particular. In the literature, data concerning the link between drug use and PPH are scarce. In Aronow's study (6), which included 499 nursing home residents, the mean maximal reduction in postprandial SBP was significantly greater in patients treated with angiotension converting enzyme inhibitors, calcium blockers, diuretics, nitrates, and psychotropic drugs than in others. In Vaitkevicius's study (5), PPH occurred more frequently in patients using vasodilatators. Most of these drugs may promote PPH by reducing cardiac preload.
We observed a slightly higher prevalence of OH in the PPH group than in the non-PPH group, but the difference was not significant. Our results are in agreement with those of Jansen and colleagues (24) and indicate that OH and PPH do not occur necessarily in the same patients, suggesting that the mechanisms and causes of PPH differ at least partly from those of OH.
In our study, the average
SBP and the incidence of PPH were higher after breakfast than after lunch or after dinner. A similar observation was made by Kohara and coworkers (22) in their series of hypertensive patients. It has been demonstrated that the magnitude of the decrease in postprandial BP depends partly on the type of food ingested, especially on the quantity of glucose ingested and on the temperature of the meal (7). Because, in our study, the meals were not standardized, we can suppose that the breakfast composition was the most likely to induce PPH. We also can suspect a drug effect because a number of drugs are given at breakfast time. Our results suggest another possible explanation. Indeed, we observed a higher prevalence of PPH at breakfast time when preprandial SBP was highest and a positive correlation between preprandial SBP and
SBP. These findings suggest that the more elevated the preprandial SBP, the larger the postprandial BP decline and the higher the risk for PPH. Such a relationship between preprandial SBP and
SBP has been previously observed by Vaitkevicius and coworkers (5) in a series of 113 nursing-home residents and by Kohara and coworkers (22) using ABPM in a series of 121 hypertensive patients. Furthermore, Kohara and colleagues (22) observed a significant relationship between morning surge of BP and PPH at breakfast time.
The pathogenesis of PPH is not fully understood (7)(25)(26). Meal ingestion has been demonstrated to induce splanchnic vasodilatation and decrease in systemic vascular resistance, which may provoke a decrease in venous return and cause PPH (7). However, the amount of splanchnic blood pooling is not correlated with the magnitude of
SBP after meal ingestion (25), suggesting that excessive blood pooling during digestion is not the principal mechanism for PPH (7). There is evidence that PPH occurs when cardiovascular compensation for the meal-induced splanchnic vasodilatation is not adequate, because of inability to increase cardiac output or peripheral vascular resistance due to impaired baroreflex and/or peripheral sympathic nervous functions (7)(25). The exact role of insulin and other vasoactive peptides is still controversial (7)(26). Because hypertension impairs baroreflex sensitivity and diastolic ventricular filling that renders the heart more dependent on ventricular preload, it increases the risk for PPH (7)(26). We also observed a correlation between PPH and BP variability, which is considered as a cardiovascular risk factor (11). As baroreflex dysfunction has been shown to contribute to both morning surge in BP and BP variability (27)(28), our findings that
SBP, preprandial SPB, and BP variability are correlated support the involvement of baroreflex dysfunction in the pathogenesis of PPH.
In conclusion, the present study demonstrates that PPH is detected by ABPM in one out of four elderly patients with falls and syncope, usually after breakfast. It also suggests that PPH contributes to diurnal BP variability and that postprandial BP decline is positively related to preprandial SBP.
Received June 16, 1999
Accepted December 13, 1999
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