Author + information
- Received April 24, 2002
- Revision received June 21, 2002
- Accepted July 11, 2002
- Published online December 4, 2002.
- Woo-Young Chung, MD*,
- Dae-Won Sohn, MD*,* (, )
- Yong-Jin Kim, MD*,
- Seil Oh, MD*,
- I.n-H.o Chai, MD*,
- Young-Bae Park, MD* and
- Yun-Shik Choi, MD*
- ↵*Reprint requests and correspondence:
Dr. Dae-Won Sohn, Division of Cardiology, Department of Internal Medicine, Seoul National University College of Medicine, 28 Yongun-Dong, Chongno-Gu, Seoul 110-744, South Korea.
Objectives This study was designed to investigate a possible mechanism of postprandial angina.
Background Postprandial angina has been recognized for more than two centuries; however, its mechanism is still controversial. The most widely accepted mechanism involves increased myocardial oxygen demand after food intake. Recently, the redistribution in coronary blood flow (CBF) was suggested as a possible mechanism.
Methods Twenty young, healthy volunteer controls and 20 patients with significant stenosis in the left anterior descending (LAD) or left main coronary artery were enrolled in the study. Coronary blood flow was evaluated in the distal LAD by using transthoracic Doppler echocardiography before and 15, 30, 45, and 60 min after food intake. In the CBF curve, the time velocity integral of diastolic flow (Dtvi) and the product of Dtvi and heart rate (HR) were measured. In six patients, these measurements were repeated after successful coronary intervention.
Results In the healthy volunteer controls, Dtvi and Dtvi × HR increased after food intake with a peak value at 15 min, which indicates the presence of postprandial surge in the CBF. Fasting values and peak values at 15 min were significantly different (Dtvi: 15.1 ± 4.9 cm/s vs. 18.9 ± 5.9 cm/s, p = 0.04, Dtvi × HR: 862.2 ± 261.5 cm/min vs. 1,174.2 ± 307.5, p = 0.002). In contrast with the controls, despite postprandial increase in double product (HR × blood pressure), Dtvi and Dtvi × HR in the patient group decreased after food intake, with a nadir value at 45 min. Fasting values and nadir values at 45 min were significantly different (Dtvi: 24.0 ± 19.6 cm/s vs. 19.3 ± 17.1 cm/s, p < 0.001, Dtvi × HR: 1,449.6 ± 1,044.0 cm/min vs. 1,273.4 ± 1,000.9 cm/min, p = 0.002). In six patients, the CBF pattern resumed the normal pattern of postprandial surge in the CBF after successful coronary intervention.
Conclusions Results of our study suggest that “steal phenomenon” may play a role in the mechanism of postprandial angina.
The phenomenon of postprandial angina has been well recognized since it was first described by Herbeden in 1772 (1). However, its mechanism has not been clearly elucidated, though it has been postulated that increased myocardial oxygen demand after food intake precipitates angina (2–6).
In contrast with previous studies that have suggested increased myocardial oxygen demand as a mechanism of postprandial angina, a recent study (5)using positron emission tomography showed that myocardial blood flow decreases in the stenotic coronary artery territory during the postprandial period, suggesting a redistribution of myocardial blood flow as a possible cause of postprandial angina.
High-frequency pulse-wave Doppler echocardiography allows coronary blood flow (CBF) in the left anterior descending coronary artery (LAD) to be assessed non-invasively. Application of this modality in pathologic conditions is limited, as only the CBF in the LAD can be evaluated. However, given the modality’s non-invasiveness, it is suitable for evaluating coronary physiology. In this study, we compared changes in CBF in the controls with changes in CBF in patients having significant stenosis in the LAD or in the left main coronary artery. In addition, we evaluated changes in the CBF pattern after significant stenosis had been relieved. The effect of sham feeding was evaluated to exclude any effects of simple gastric distension.
Twenty patients with functionally significant stenosis of the LAD or the left main coronary artery were enrolled in the study. Functionally significant stenosis was defined as >75% stenosis by coronary angiogram and a reversible defect on sestamibi single photon emission computed tomography in the LAD territory during dipyridamole stress. Patients with resting angina, myocardial infarction, and previous percutaneous coronary intervention were excluded. Twenty healthy volunteers were enrolled as controls. Informed consent was obtained from all the volunteers and patients.
Transthoracic echocardiographic examinations were performed after fasting for at least 6 h, and all medications were discontinued for at least 12 h before examination. Before coronary flow was evaluated, left ventricular dimensions, ejection fractions, wall thicknesses, left atrial dimension, and mitral inflow Doppler parameters were obtained. Coronary blood flow was evaluated by using a 7 MHz transducer (Seqouia, Acuson, Mountain View, California) at the distal LAD during end-expiratory apnea before and 15, 30, 45, and 60 min after food intake, together with blood pressure (BP) and heart rate (HR). The time-velocity integral of the diastolic flow (Dtvi) was measured in the coronary flow velocity curve. The average value of three consecutive beats was used in the analysis. The standard meal was composed of 68 g of fat, 159 g of carbohydrate, and 37 g of protein, with a total calorie count of 1,382 Cal.
In six patients with successful percutaneous coronary intervention (two patients with balloon angioplasty and four with stenting), these measurements were repeated after the intervention. To evaluate the effect of simple gastric distension on the CBF, the CBF was assessed after the sham meal in five of the controls. Pure water (800 cm3) was used as a sham meal.
Continuous variables are reported as mean ± SD, and categorical variables as numbers and percentages. Differences in categorical variables were compared using the Fisher exact test and chi-squared test. Differences in continuous variables were compared by the Mann-Whitney Utest. The Wilcoxon signed-rank test was used in the analysis of the changes in continuous variables in a group. Statistical analysis was performed using SPSS 10.0 software (SPSS Inc., Chicago, Illinois), and a p value of <0.05 was considered statistically significant.
Clinical characteristics and echocardiographic parameters
All volunteer controls were men, and compared with the controls, the patients were older and had a higher prevalence of hypertension, diabetes, and history of smoking (Table 1). In the patient group, there were five patients with one-vessel disease, eight patients with two-vessel disease, six patients with triple-vessel disease, and one patient with left main disease. The controls showed lower ejection fractions and a lower prevalence of having abnormal relaxation (Table 2).
Postprandial changes in BP and HR
Controls and patients both showed similar trends in terms of changes in BP and HR after food intake. An increase in systolic BP and a decrease in diastolic BP—therefore, increase in pulse pressure—and increase in HR were observed after food intake (Fig. 1).
Changes in coronary blood flow after food intake
In the controls, Dtvi and Dtvi × HR increased after food intake, with the peak value 15 min after food intake. Fasting values and peak values at 15 min were significantly different (Dtvi: 15.1 ± 4.9 cm/s vs. 18.9 ± 5.9 cm/s, p = 0.04, Dtvi × HR: 862.2 ± 261.5 cm/min vs. 1,174.2 ± 307.5, p = 0.002). In patients, Dtvi and Dtvi × HR decreased after food intake with a nadir value 45 min after food intake. Fasting values and nadir values at 45 ⇓min were significantly different (Dtvi: 24.0 ± 19.6 cm/s vs. 19.3 ± 17.1 cm/s, p < 0.001, Dtvi × HR: 1,449.6 ± 1,044.0 cm/min vs. 1,273.4 ± 1,000.9, p = 0.002) (Figs. 2 and 3). ⇓
In six patients with successful percutaneous coronary interventions, the CBF pattern after food intake ⇓before intervention was similar to that of the whole patient group. However, the CBF pattern converted to that of the control group after intervention (Figs. 4 and 5). ⇓
Effects of sham meal on coronary flow
Inter- and intra-observer variability
Inter- and intra-observer variability was assessed in 10 of the controls and found to be 6.4% and 0.8%, respectively, for the measurement of Dtvi.
As the CBF dominates during the diastolic period, the CBF in one cardiac cycle can be represented by Dtvi multiplied by the cross-sectional area of the coronary artery. Assuming that the coronary artery has a constant cross-sectional area, changes in Dtvi represent changes in the CBF in one cardiac cycle. Therefore, changes in the CBF can be estimated from the product of Dtvi and HR.
After food intake, splanchnic vascular beds dilate and total vascular resistance decreases (4,7). To maintain BP and to meet the metabolic demands of digestion, there is a compensatory increase in cardiac output and HR (8–12). Regarding the changes in BP, it is reported that mean and diastolic BP decrease (4,11)after food intake, and may even cause syncope in the elderly (13,14). However, several studies (2,5,15)did not show significant change in BP after food intake. In our study, postprandial hemodynamics both in the controls and in patients showed an increase in systolic BP, a decrease in diastolic BP, and an increase in HR after food intake.
Pathophysiologic mechanism of postprandial angina
Several mechanisms have been suggested for postprandial angina. Redistribution of blood from the coronary artery to the splanchnic artery, or exercising muscles in the case of exertional postprandial angina, were once proposed (6). However, these mechanisms have not been proven in humans (16). Increased myocardial oxygen demand, associated with an increase in HR and sympathetic nervous activity after food intake, is a commonly believed mechanism (2,17,18). However, Figueras et al. (19)showed that there is no change in the product of HR and systolic BP at the onset of ischemic electrocardiographic abnormalities and suggested decreased myocardial perfusion as a possible mechanism of postprandial angina. Later, these investigators showed that myocardial ischemia was not induced when the patients were paced to the same HR observed during postprandial angina (20)and suggested that other factors such as coronary vasoconstriction, rather than increased oxygen demand, might play a role in producing postprandial angina.
Recently, Baliga et al. (5)showed reduced myocardial blood flow in the stenotic artery territory after food intake with an increase in blood flow in the normal artery territory, by using positron emission tomography. They suggested that the redistribution of myocardial blood flow might be the mechanism of postprandial angina.
In our study, in contrast with the control group, CBF distal to significant stenosis in patients did not show postprandial surge in CBF after food intake; rather, the CBF was significantly decreased after food intake. This absence of postprandial surge distal to the significant stenosis is not likely to be a global phenomenon, because when the stenosis was relieved by intervention, the normal pattern of postprandial surge in CBF was restored. Therefore, we speculate that the CBF is redistributed to territory of the normal or insignificantly stenotic coronary artery.
Although our study included patients with multivessel disease, functionally significant stenosis based on the sestamibi SPECT was confined to the LAD, and the inclusion of these patients would not affect the interpretation of our results.
Types of meals producing postprandial angina
The relationship between the components of a meal and the precipitation of postprandial angina is controversial. It has been proposed that postprandial angina is more likely to be precipitated by a fatty meal, which leads to postprandial endothelial dysfunction (21,22). However, other studies have suggested that a high-carbohydrate meal, rather than a fatty meal, is more likely to precipitate postprandial angina (11,23). In our study, we did not evaluate the effect of meal components. However, in contrast to a previous study (24), simple gastric distension by drinking water of the same volume as the standard meal did not affect the CBF, suggesting that a change in the CBF after food intake is not a vagally mediated response.
Because of the intrinsic limitation of the transthoracic Doppler echocardiographic evaluation of coronary flow, we could not measure the CBF in the right and left circumflex artery in our patients. Therefore, the presence of a “steal phenomenon” is postulated from the indirect evidence offered by the presence of postprandial surge in the CBF of healthy controls and of the restored normal pattern when stenosis is relieved. In addition, when estimating coronary blood flow, we neglected the flow during systole and assumed that the cross-sectional area of the coronary artery was constant during the study period.
We enrolled young, healthy volunteers as controls to minimize the possibility of their having coronary artery disease; therefore, age and gender ratio were not matched between the patient and control groups. Also, we did not limit the patient group to patients with postprandial angina.
Myocardial oxygen demand represented by the product of BP and HR increased after food intake. However, there was also a decrease in CBF distal to the significant stenosis, which suggests that steal phenomenon may play a role in the mechanism of postprandial angina.
☆ This study was financially supported by the Korean Society of Circulation.
- blood pressure
- coronary blood flow
- time velocity integral of the diastolic coronary flow
- heart rate
- left anterior descending artery
- single photon emission computed tomography
- Received April 24, 2002.
- Revision received June 21, 2002.
- Accepted July 11, 2002.
- American College of Cardiology Foundation
- Herbeden W.
- Goldstein R.E.,
- Redwood D.R.,
- Rosing D.R.,
- Beiser G.D.,
- Epstein S.E.
- Colles P.,
- Juneau M.,
- Gregoire J.,
- Larivee L.,
- Desideri A.,
- Waters D.
- ↵Fagan TC, Sawyer PR, Gourley LA, Lee JT, Gaffney TE. Postprandial alteration in hemodynamics and blood pressure in normal subjects. Am J Cardiol 1986;58:636–41
- Baliga R.R.,
- Rosen S.D.,
- Camici P.G.,
- Koner J.S.
- Berlinerbrau R.,
- Shani J.
- Kelbaek H.,
- Munck O.,
- Christensen N.J.,
- Godtfredsen J.
- Sidery M.B.,
- Macdonald I.A.,
- Cowley A.J.,
- Fullwood L.J.
- Kearney M.T.,
- Charlesworth A.,
- Cowley A.J.,
- Macnonald I.A.
- Lilley M.D.
- Regan T.J.,
- Binak K.,
- Gordon S.,
- DeFazio V.,
- Hellems H.K.
- Cowley A.J.,
- Fullwood L.J.,
- Stainer K.,
- Harrison E.,
- Muller A.F.,
- Hampton J.R.
- Figueras J.,
- Singh B.N.GanzW,
- Swan H.J.C.
- Nappo F.,
- Esposito K.,
- Cioffi M.,
- et al.