Absence of postprandial surge in coronary blood flow distal to significant

stenosis: a possible mechanism of postprandial angina

Woo-Young Chung, Dae-Won Sohn, Yong-Jin Kim, Seil Oh, I. n-H. o Chai,
Young-Bae Park, and Yun-Shik Choi
J. Am. Coll. Cardiol. 2002;40;1976-1983

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Journal of the American College of Cardiology Vol. 40, No. 11, 2002
© 2002 by the American College of Cardiology Foundation ISSN 0735-1097/02/$22.00
Published by Elsevier Science Inc. PII S0735-1097(02)02533-0

Angina Pectoris

Absence of Postprandial Surge in Coronary

Blood Flow Distal to Significant Stenosis:
A Possible Mechanism of Postprandial Angina
Woo-Young Chung, MD, Dae-Won Sohn, MD, Yong-Jin Kim, MD, Seil Oh, MD, In-Ho Chai, MD,
Young-Bae Park, MD, Yun-Shik Choi, MD
Seoul, 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. (J Am Coll Cardiol 2002;40:1976 – 83) © 2002 by the American
College of Cardiology Foundation

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 eluci-
dated, though it has been postulated that increased myo-
cardial 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 myocar-
dial 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 con-
From the Clinical Research Institute and Division of Cardiology, Department of
Internal Medicine, Seoul National University College of Medicine, Seoul, Korea.
This study was financially supported by the Korean Society of Circulation.
Manuscript received April 24, 2002; revised manuscript received June 21, 2002,
accepted July 11, 2002.
Downloaded from content.onlinejacc.org by on May 17, 2010
ditions 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.
METHODS
Study subjects. Twenty patients with functionally signifi-
cant 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 com-
puted tomography in the LAD territory during dipyridam-
ole stress. Patients with resting angina, myocardial infarc-
tion, and previous percutaneous coronary intervention were
excluded. Twenty healthy volunteers were enrolled as con-
trols. Informed consent was obtained from all the volunteers
and patients.
JACC Vol. 40, No. 11, 2002 Chung et al. 1977
December 4, 2002:1976–83 Mechanism of Postprandial Angina

Table 1. Clinical Characteristics

Abbreviations and Acronyms Volunteers Patients
BP ⫽ blood pressure (n ⴝ 20) (n ⴝ 20) p Value*
CBF ⫽ coronary blood flow
Age (yrs) 24.5 ⫾ 3.1 59.8 ⫾ 8.0 ⬍ 0.001
Dtvi ⫽ time velocity integral of the diastolic coronary
Men (%) 20 (100%) 16 (86%) 0.035
flow
HR (/min) 58 ⫾ 9 64 ⫾ 13 0.13
HR ⫽ heart rate
HTN 0 7 (35%) 0.008
LAD ⫽ left anterior descending artery
DM 0 6 (30%) 0.02
SPECT ⫽ single photon emission computed tomography
Smoking 6 (30%) 12 (60%) 0.06
*Continuous variables by the Mann-Whitney U test and categorical variables by the
Fisher’s exact test and chi-squared test.
Echocardiographic examination. Transthoracic echocar- DM ⫽ diabetes mellitus; HR ⫽ heart rate; HTN ⫽ hypertension.

diographic 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 evalu-
ated, left ventricular dimensions, ejection fractions, wall
thicknesses, left atrial dimension, and mitral inflow Doppler
parameters were obtained. Coronary blood flow was evalu-
ated 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 disten-
sion 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.
Statistical analysis. Continuous variables are reported as
mean ⫾ SD, and categorical variables as numbers and
percentages. Differences in categorical variables were com-
pared using the Fisher exact test and chi-squared test.
Differences in continuous variables were compared by the
Mann-Whitney U test. 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.
RESULTS
Clinical characteristics and echocardiographic param-
eters. 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 pa-
tients 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 pres-
sure—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 ⫻

Table 2. Echocardiographic Parameters in Healthy Volunteers and in Patients

Volunteers Patients
(n ⴝ 20) (n ⴝ 20) p Value*
LVESD (mm) 32.9 ⫾ 2.2 30.0 ⫾ 6.9 0.005
LVEDD (mm) 49.5 ⫾ 3.6 49.2 ⫾ 6.1 0.647
EF (%) 55.9 ⫾ 6.5 62.6 ⫾ 10.5 0.006
IVS/LVPW (mm) 9.1 ⫾ 1.1/8.7 ⫾ 0.7 12.1 ⫾ 1.5/11.2 ⫾ 1.8 ⬍0.001/⬍0.001
LA (mm) 33.1 ⫾ 2.5 39.2 ⫾ 3.7 0.001
E/A (m/s) 0.83 ⫾ 0.16/0.44 ⫾ 0.13 0.68 ⫾ 0.14/0.83 ⫾ 0.20 0.01/⬍0.001
DT (ms) 153 ⫾ 32 227 ⫾ 52 ⬍0.001
*By the Mann-Whitney U test.
A ⫽ peak velocity of late mitral inflow; DT ⫽ deceleration time of early mitral inflow; E ⫽ peak velocity of early mitral
inflow; EF ⫽ ejection fraction; IVS ⫽ interventricular septal thickness; LA ⫽ left atrial dimension; LVEDD ⫽ left ventricular
end-diastolic dimension; LVESD ⫽ left ventricular end-systolic dimension; LVPW ⫽ left ventricular posterior wall thickness.

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1978 Chung et al. JACC Vol. 40, No. 11, 2002
Mechanism of Postprandial Angina December 4, 2002:1976–83

Figure 1. Changes in systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR), and double product after food intake. Controls and
patients both showed similar patterns of change. Solid line ⫽ patients; dotted line ⫽ controls.

Figure 2. Changes in time velocity integral of the diastolic coronary flow (Dtvi) and Dtvi ⫻ heart rate (HR) after food intake in controls (upper panel)
and in patients (lower panel). Dtvi and Dtvi ⫻ HR increased in controls after food intake. In patients, Dtvi and Dtvi ⫻ HR decreased after food intake.
*p ⬍ 0.05, †p ⬍ 0.005 compared with the fasting state by the Wilcoxon signed rank test.

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JACC Vol. 40, No. 11, 2002 Chung et al. 1979
December 4, 2002:1976–83 Mechanism of Postprandial Angina

Figure 3. Coronary flow velocities in a healthy control (left panel) and in a patient (right panel) at the fasting state and 15, 30, 45, and 60 min after food
intake. Numbers in each tracing denote the time velocity integral of diastolic flow velocity.

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. There were no
significant changes in BP and HR after a sham meal. In
addition, CBF did not change significantly after a sham
meal (Figs. 6 and 7).
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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 measure-
ment of Dtvi.
DISCUSSION
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,
1980 Chung et al.
Mechanism of Postprandial Angina
Figure 4. Changes in time velocity integral of the diastolic flow velocity (Dtvi) and Dtvi ⫻ heart rate (HR) after food intake in six patients before (upper
panel) and after (lower panel) successful intervention. Dtvi and Dtvi ⫻ HR changed to those of the healthy controls after intervention. *p ⬍ 0.05 compared
with the fasting state by the Wilcoxon signed rank test.
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.
Postprandial hemodynamics. After food intake, splanch-
nic vascular beds dilate and total vascular resistance de-
creases (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. S-
everal 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, associ-
ated with an increase in HR and sympathetic nervous
activity after food intake, is a commonly believed mecha-
nism (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
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JACC Vol. 40, No. 11, 2002
December 4, 2002:1976–83
and suggested decreased myocardial perfusion as a possible
mechanism of postprandial angina. Later, these investiga-
tors 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 ste-
nosis 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 sesta-
mibi SPECT was confined to the LAD, and the inclusion
JACC Vol. 40, No. 11, 2002 Chung et al. 1981
December 4, 2002:1976–83 Mechanism of Postprandial Angina

Figure 5. Coronary flow velocities before (left panel) and after (right panel) successful intervention in patients with significant stenosis in the left anterior
descending artery in the fasting state and 15, 30, 45, and 60 min after food intake. Numbers in each tracing denote time velocity integral of the diastolic
flow velocity.

of these patients would not affect the interpretation of our
results.
Types of meals producing postprandial angina. The re-
lationship 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
Downloaded from content.onlinejacc.org by on May 17, 2010
(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.
Study limitations. Because of the intrinsic limitation of the
transthoracic Doppler echocardiographic evaluation of cor-
onary flow, we could not measure the CBF in the right and
left circumflex artery in our patients. Therefore, the pres-
1982 Chung et al. JACC Vol. 40, No. 11, 2002
Mechanism of Postprandial Angina December 4, 2002:1976–83

Figure 6. Changes in time velocity integral of the diastolic flow velocity (Dtvi) and Dtvi ⫻ heart rate (HR) after sham feeding. No significant changes in
Dtvi or Dtvi ⫻ HR were observed after sham feeding.

ence 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.
Conclusions. 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.

Figure 7. Coronary flow velocities in the fasting state and 15, 30, and 45 min after the sham meal. No significant changes in time velocity integral of the
diastolic flow velicity occurred after a sham meal. Numbers in each tracing denote time velocity integral of the diastolic flow velocity.

Downloaded from content.onlinejacc.org by on May 17, 2010

JACC Vol. 40, No. 11, 2002
December 4, 2002:1976–83
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, Korea. E-mail: dwsohn@snu.ac.kr.
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 Absence of postprandial surge in coronary blood flow distal to significant
stenosis: a possible mechanism of postprandial angina
Woo-Young Chung, Dae-Won Sohn, Yong-Jin Kim, Seil Oh, I. n-H. o Chai,
Young-Bae Park, and Yun-Shik Choi
J. Am. Coll. Cardiol. 2002;40;1976-1983
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