Systemic Hemodynamic Changes in Elderly Hypertensive Patients After Ingesting Foods With Lipid, Protein, and Carbohydrate Contents

Abstract

Aging is associated with changes in cardiovascular structure and function, which predisposes elderly people to reduced blood pressure levels after meals. The authors studied cardiac systolic function in elderly hypertensive patients after eating meals with different contents of lipids, proteins, and carbohydrates. Ten elderly male hypertensive patients were studied (mean age, 69 years; range 60–80 years). No patients had a previous history of orthostatic or postprandial hypotension. Patients ate 1 of 3 pre‐prepared meals: lipid meal (LM), protein meal (PM), or carbohydrate meal (CM), on different days. Mean arterial pressure, total peripheral resistance index (TPRi), cardiac index (CI), and stroke index were recorded at the end of the fasting period and then at 5, 15, 30, 45, and 60 minutes after food ingestion. After ingestion of a CM, the CI increased from 2.30±0.21 L/min/m² to 2.61±0.24 L/min/m² and the TPRi decreased from 3212±226 dynes/sec² to 2793±255 dynes/sec² at 45 minutes (P<.05). After the LM, the CI increased from 2.15±0.15 to 2.84±0.27 L/min/m² and the TPRi decreased from 3630±274 L/min/m² to 2666±282 dynes/sec² at 45 minutes (P<.05). After the PM, no systemic hemodynamic changes were observed. When all 3 meals were compared, the highest values of CI and the lowest values of TPRi were observed for the LM and CM. The authors’ results show that fat‐ and carbohydrate‐rich foods cause changes in the systemic hemodynamic of the elderly hypertensive patients.

There are several modifications that occur in the cardiovascular system after food ingestion. ¹ , ² The splanchnic blood vessels dilate to divert blood to the gastrointestinal tract ³ and heart rate and blood catecholamine levels increase in comparison to the basal values before eating. ⁴ , ⁵ These changes occur so that blood flow may be increased to the gut to ensure a continuous flow of metabolites to end organs such as the brain and kidneys. In healthy elderly individuals, arterial pressure shows little fluctuation in value during the digestive process. ¹ In order to maintain blood pressure (BP) levels despite vasodilatation of splanchnic vessels, other vascular beds increase their resistance in response to meals. ⁶ Aging is associated with physiologic changes in the cardiovascular and gastrointestinal systems such as a reduction in baroreflex activity, ⁷ a decrease in the autonomic responses to several stimuli, and a slowing of gastric emptying. ⁸ , ⁹ , ¹⁰ These modifications in structural and hormonal activity in elderly people can attenuate the expected changes in systemic hemodynamics after eating. In elderly individuals with arterial hypertension, these hemodynamic changes could be aggravated by the changes promoted by hypertensive disease. Thus, variations in BP levels after eating can be more severe than those observed in normotensive elderly individuals. Several hypotheses have been proposed to explain the mechanisms of postprandial variations in BP in this group of patients including excessive splanchnic pooling, ³ less of an increase in heart rate, ¹¹ an impairment of the sympathetic nervous system, ¹² decreased intravascular volume, and the release of peptides with vasodilator properties such as calcitonin gene–related peptide. ¹³ These changes can contribute to significant decreases in systemic arterial BP, which may result in a wide range of clinical symptoms, such as angina pectoris, stroke, falls, nausea, and dizziness. ¹⁴ Visvanathan and colleagues ¹⁵ demonstrated an increased risk of postprandial hypotension in older hypertensive individuals following consumption of glucose or the glucose‐releasing sugar sucrose when compared with nonglucose sugars. It has been suggested that insulin, which is secreted in response to carbohydrate ingestion, is one of the vasodilatory hormones with actions on the capacitance and resistance vessels. The normal protective responses of the adrenergic system are reduced and consequently the vasodilatory action can be more intense. From a clinical viewpoint, it is important to understand the BP response to different types of food in elderly hypertensive patients after food ingestion. This knowledge may prevent postprandial hypotension and provide guidance in the choice of meals for elderly patients. The objective of this study was to measure cardiac function in elderly hypertensive patients without postprandial hypotension, after eating different meals with different lipid, protein, and carbohydrate contents.

Methods

We enrolled 10 male hypertensive elderly patients between the ages of 60 and 80 years (mean ± standard error of the mean, 69±4.8 years) with systolic BPs (SBPs) of 140 to 160 mm Hg and diastolic BPs (DBPs) between 60 and 95 mm Hg. The patients were informed that the study was being conducted to determinate the modifications of systemic hemodynamics after eating different kinds of food. The protocol was approved prior to subject enrollment by the patients through oral consent and a hospital committee. All of the patients had a history of high BP levels for ≥10 years and they were not taking any hypotensive drugs for at least 2 weeks before the study. The reasons for spontaneous interruption of the medication were clinical side effects and costs of the hypotensive drugs. They did not have postural hypotension or report other comorbidities. BP was measured in the supine and orthostatic positions prior to the study. Patients who showed a decrease in BP values during the orthostatic position (>20 mm Hg in systolic levels and/or 10 mm Hg in diastolic levels) were excluded from the study. ¹⁶ BP values were taken throughout the study with the patients in a sitting position. Patients with serum creatinine levels >2.5 mg% were excluded. Heart rate (HR) and SBP and DBP were measured by a semiautomatic oscillometric device and are expressed in mm Hg. BP values were calculated using the average of 3 sequential readings. The cardiac index (CI) and stroke index (SI) were obtained by a thoracic bioimpedance instrument and were recorded every 15 seconds. The analyzed values were the average of the last 5 readings at each point. The first point was at the end of the fasting period and readings were then taken at 5, 15, 30, 45, and 60 minutes after the ingestion of food. The total peripheral resistance index (TPRi) was obtained using the equation (MAP – CVP/CI) × 80, where CVP is central venous pressure and MAP is mean arterial pressure. Total peripheral resistance was expressed in dynes⁻², CI in L/min/m², and SI in mL/beats/m². MAP was calculated using the equation: MAP = DBP + (SPB − DBP)/3 and CVP was considered to be zero for all patients.

Study Protocol

In the morning, after an overnight fast (8 pm–10 am), the patients arrived at the laboratory and anthropometric measurements were taken. They then rested for 30 minutes in a seated position, and during this time the bioimpedance electrodes were attached to their thoraces. At the end of the resting time, we gave each of the patients a randomized meal. There were 3 different meal compositions: high protein content (protein meal, PM), high lipid content (lipid meal, LM), and high carbohydrate content (carbohydrate meal, CM). Each meal had a total volume of 500 mL. The patient ate 1 of the 3 meals on day 1, a different meal on day 2, and the remaining type of meal on day 3. The average time required for eating was 20 minutes. After the ingestion of food, at the end of the resting time, we recorded the cardiac output, systolic volume, BP levels, and HR. After the fasting time, the patients were observed for an additional 60 minutes. We recorded the hemodynamic values at the end of the fasting time and at 5, 15, 30, 45, and 60 minutes after food ingestion.

Composition of the Meals

The PM was composed of foods rich in proteins: 400 g of grilled chicken, 200 mL of orange juice, 2 g of sodium, and 40 g of soybean protein. The total number of calories was 700 Kcal, potassium 55 mEq, and sodium 46 mEq, and the protein content represented 63% of the meal. The CM was composed of carbohydrates: 150 g of bananas, 30 g of honey, 50 g of sugar, 150 g of papaya, 2 g of sodium, 5 g of flour rice, and 200 mL of orange juice. The total number of calories was 700 Kcal, potassium 35.0 mEq, and sodium 35.9 mEq, and the carbohydrate content represented 96% of the meal. The LM was composed of foods rich in lipids: 40 g of bacon, 100 g of cooked potatoes, 20 g of margarine, 40 g of mayonnaise, 100 g of tomatoes, carrots, and lettuce, and 200 mL of orange juice. The total number of calories was 700 Kcal, potassium 27.3 mEq, and sodium 29.4 mEq, and the lipid content represented 75% of the meal. All of the food was eaten at room temperature.

Data Analyses

For comparisons within the same group, we used analysis of variance for repeated measures with the Dunnett test. For comparisons among different groups, we used the Tukey test. The data were analyzed using Prism 5 for Windows (GraphPad Software Inc, La Jolla, CA). P values <.05 were accepted as statistically significant. Data are presented as means ± standard error.

Results

At baseline, SBP and DBP were 152.8±5.3 mm Hg and 78.1±6.3 mm Hg, respectively. Our data showed that after eating different kinds of foods, the sitting BP did not change significantly but other hemodynamic parameters showed different responses (Table and Figure). The patients did not show any signs or symptoms related to systemic hemodynamic changes during the study period.

Table.

 Systolic Function of Heart After Eating Different Meals

Minutes	0	5	15	30	45	60
Cardiac index, L/min/m2
CM	2.30±0.21	2.35±0.20	2.57±0.21	2.80±0.18a	2.61±0.24a	2.62±0.18a
LM	2.15±0.15	2.49±0.19	2.65±0.25	2.70±0.21a	2.84±0.27a,b	2.82±0.21a
PM	2.28±0.14	2.48±0.17	2.40±0.16	2.47±0.18	2.47±0.18	2.45±0.15
Systolic index, mL/beat
CM	34.6±3.3	35.0±3.8	37.5±3.7	39.6±3.2a	37.0±4.5	37.3±4.0
LM	33.5±2.4	37.5±3.0	38.0±3.7	39.8±2.9a	40.4±3.3a,b	40.3±3.0a
PM	34.7±2.4	36.0±3.1	36.1±3.2	36.6±3.1	35.6±3.3	36.4±3.3
Mean arterial pressure, mm Hg
CM	94±2.4	96±2.0	91±2.6	87±2.4	90±3.0	85±2.4
LM	94±3.4	97±4.0	94±2.3	89±2.6	87±3.0	84±3.7
PM	96±2.1	99±4.0	96±4.7	93±2.2	90±3.6	95±4.5
Systolic blood pressure, mm Hg
CM	159±4.3	160±4.1	153±5.1	150±3.7	152±6.4	150±3.7
LM	160±4.1	155±4.2	154±4.7	153±3.3	151±6.7	149±5.1
PM	158±3.8	160±3.7	159±4.2	155±4.1	153±5.3	156±5.3
Diastolic blood pressure, mm Hg
CM	61±2.8	64±2.3	60±2.1	55±4.0	59±5.2	54±5.9
LM	61±3.0	68±3.0	64±1.9	57±5.2	55±3.6	56±4.9
PM	65±4.2	68±3.0	64±3.1	62±3.0	58±4.0	64±3.7
Peripheral total resistance index, dynes/sec−2
CM	3212±226	3219±205	2861±227	2537±166a	2793±255a	2636±181a
LM	3630±274	3296±281	3043±229	2738±187b	2666±282a,b	2529±247a,b
PM	3495±228	3347±270	3372±308	3174±301	3147±394	3222±267
Heart rate, beats per minute
CM	68±4.6	71±4.4	70±4.0	70±4.2	71±4.5	72±4.4
LM	65±3.9	70±3.7	69±3.5	69±3.3	71±4.0	70±3.0
PM	67±4.0	71±3.6	68±3.3	69±3.1	71±3.6	70±3.4

Values are expressed as means ± standard error of the mean. Abbreviations: CM, carbohydrate meal; LM, lipidic meal; PM, protein meal. ^a P<.05 (vs before eating – 0). ^b P<.05 (lipid vs protein).

Figure.

 Cardiac index (CI) (L/min/m²), mean arterial pressure (MAP) (mm Hg), and total peripheral resistance index (TPRi) (dynes⁻²) before (0) and after eating different types of meals (from 5 to 60 min). CM indicates carbohydrate meal; PM, protein meal; LM, lipid meal. *P<.05 (vs 0 – before eating) and ^† P<.05 (lipid vs protein).

After Eating a Protein‐Rich Meal

The MAP, CI, SI, and HR did not change significantly after the ingestion of a PM.

After Eating a Carbohydrate‐Rich Meal

After the ingestion of a CM, we observed an increase in CI, from 2.30±0.21 L/min/m² to 2.80±0.18 L/min/m² at 30 minutes. The values remained elevated from the basal values until the end of the study (P<.05). The SI increased from 34.6±3.3 mL/beat to 39.6±3.2 mL/beat at 30 minutes after the meal (P<.05). The TPRi decreased from 3212±226 dynes/sec⁻² to 2537±166 dynes/sec⁻² at 30 minutes and remained lower until 60 minutes (P<.05). MAP and HR did not change during the study.

After Eating a Lipid‐Rich Meal

We observed the greatest changes in systemic hemodynamics in this group of patients. The TPRi decreased from 3630±274 dynes/sec⁻² to 2666±282 dynes/sec⁻² (at 45 minutes) and 2529±247 dynes/sec⁻² (at 60 minutes) (P<.05). The SI increased from 33.5±2.4 mL/beat to 39.8±2.9 mL/beat (at 30 minutes) and remained significantly elevated until the end of the study (P<.05). The CI increased from 2.15±0.15 mL/min/m² to 2.70±0.21 mL/min/m² (at 30 minutes) (P<.05) to 2.84±0.27 mL/min/m² (at 45 minutes, P<.05) and 2.82±0.21 mL/min/m² (at 60 minutes, P<.05). The MAP changed significantly, from 94±3.4 mm Hg to 84±3.7 mm Hg (at 60 minutes, P>.05). The HR did not change from basal values to the end of study.

Comparison Among the Meals

The effects on systemic hemodynamics with the LM were more intense than those observed with the other meals at 45 minutes after food ingestion. At 45 minutes, the CI of the LM was 2.84±0.27 L/min/m² vs 2.47±0.18 L/min/m² for the PM and 2.61 0.24/L/min/m² for the CM (P<.05). In the same way, the decrease in TPRi after the LM was more intense than that observed for the PM and CM at 40 and 45 minutes (Table and Figure).

Discussion

The main finding of this study is that meals with high lipid and carbohydrate content can cause a significant decrease in peripheral resistance and an increase in CI in elderly hypertensive patients. A diet rich in protein did not cause any significant hemodynamic changes (Figure). Although the physiology of postprandial changes in the systemic circulation is not fully understood, it has been confirmed that the type of food content plays an important role in the digestive process and different macronutrients are able to cause specific responses in systemic hemodynamics. ³ , ⁴ This was also evident in our data. Although, the patients’ meals had the same caloric content (700 Kcal), the systemic hemodynamic responses were different (Table). This observation suggests that the caloric content is not the only factor that changes the systemic hemodynamics after food ingestion. The type of nutrients present in the food also plays a role. Many hormones from the gastrointestinal tract with vasodilatory properties, such as calcitonin gene–related peptide, seem to play a key role in systemic hemodynamic modifications. ¹⁷ , ¹⁸ These hormones are released into the bloodstream in response to food intake and are responsible for pooling of blood in the splanchnic circulation.

We could speculate on whether the intensity of liberation of these hormones by the gastrointestinal tract is or is not influenced by the type of nutrient ingested. Our data suggest that vasodilatation induced by an LM promoted a decrease in peripheral resistance and an increase in CI that were more significant than those observed with the CM and PM, mainly 45 minutes after eating. The rate of gastric emptying may be one of the factors that influenced the time and intensity of hemodynamic changes detected post‐ingestion of the different meals. The fatty foods that leave the stomach more slowly than carbohydrates could have promoted systemic hemodynamic changes at a later stage. Interestingly, the meal rich in protein did not change the systemic hemodynamics; CI, MAP, HR, and TPRi remained at basal values. These observations are important when considering the choice of meal for patients with postprandial hypotension, since the PM could become a better food alternative for these patients.

In healthy and young patients, oral glucose is able to increase cardiac output and peripheral vascular resistance to compensate for splanchnic blood pooling and to prevent significant BP reductions. Our data showed that in elderly hypertensive persons, the significant decrease in TPRi with the LM and CM were followed by only small compensatory increases in HR (P>.05). Lipsitz and colleagues ¹⁹ examined the systemic hemodynamics in 9 healthy elderly patients after eating a mixed meal. They observed an elevation in plasmatic levels of norepinephrine and increases in CI and forearm vessel resistance. In contrast, our data demonstrated decreases in TPRi, but our patients were hypertensive and the responsiveness of their vessels to vasoconstrictive hormones might not be the same as what was found by those authors. Other possible consequences of elevated plasma norepinephrine levels after eating could be an expected increase in HR, but, in our study, elderly patients did not demonstrate significant changes in HR. The well‐described age‐related decline in β‐adrenergic responsiveness may blunt the HR response to sympathetic activation induced by a meal. ²⁰ The absence of a postprandial increase in the HR suggests that the β‐adrenergic response is impaired by aging and hypertension, both of which reduce baroreflex sensitivity.

Kooner and colleagues ³ and Hoeldtke and Carabello ²¹ reported no postprandial changes in skin or forearm blood flow and a profound fall in BP in patients with autonomic failure. In our study, the patients did not have previous postural hypotension or other symptoms associated with autonomic failure. The decrease in TPRi was insufficient to reduce the MAP because it was followed by a simultaneous elevation in CI (Table and Figure).

It is also possible that different rates of gastric emptying and caloric delivery in the small intestine could explain the systemic hemodynamic responses. ²² , ²³ Although the total number of calories was the same for all the meals, it is possible that the time required for gastric emptying of these foods was not the same. Some gastrointestinal hormones and active peptides are released in the first step of digestion to prepare the organism for the digestive process, while others are secreted when the meal moves into the stomach and small intestine. Some hormones such as calcitonin gene–related peptide produce marked vasodilatation in the splanchnic and peripheral circulation by stimulating nitric oxide release. ²⁴ Others, such as gastrin‐releasing peptide, regulate cardiac function, and vasoactive intestinal peptide may be involved with reflex vasodilation in the small intestine. ²⁵ Thus, the systemic hemodynamic modifications observed after food ingestion could be partly attributed to the specific actions of vasoactive substances released by the gastrointestinal tract.

Conclusions

In our study, the changes in systemic hemodynamics were detected in the first hour after eating a meal. We demonstrated in a previous article that a mixed meal was able to induce systemic changes in cardiac function after eating. ²⁶ The present data demonstrate that an increase in CI occurs mainly due to the lipid and carbohydrate content in the meals. It is important to ask whether, if we added proteins in the LM or CM, would the effects on systemic hemodynamic be attenuated. This possibility is quite interesting for future studies.

The acute hemodynamic response caused by the ingestion of fat or carbohydrate meals promoted changes in the systemic hemodynamic of the elderly hypertensive patients. Unlike meals rich in lipids and carbohydrates, a meal with a high protein content did not cause these significant manifestations.