Angina Postprandial

2002;40;1976-1983 J. Am. Coll. Cardiol.Young-Bae Park, and Yun-Shik Choi

Woo-Young Chung, Dae-Won Sohn, Yong-Jin Kim, Seil Oh, I. n-H. o Chai, stenosis: a possible mechanism of postprandial angina

Absence of postprandial surge in coronary blood flow distal to significant

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Angina Pectoris

Absence of Postprandial Surge in CoronaryBlood Flow Distal to Significant Stenosis:A Possible Mechanism of Postprandial AnginaWoo-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, MDSeoul, 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 increasedmyocardial oxygen demand after food intake. Recently, the redistribution in coronary bloodflow (CBF) was suggested as a possible mechanism.

METHODS Twenty young, healthy volunteer controls and 20 patients with significant stenosis in the leftanterior descending (LAD) or left main coronary artery were enrolled in the study. Coronaryblood flow was evaluated in the distal LAD by using transthoracic Doppler echocardiographybefore and 15, 30, 45, and 60 min after food intake. In the CBF curve, the time velocityintegral 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 peakvalue at 15 min, which indicates the presence of postprandial surge in the CBF. Fasting valuesand peak values at 15 min were significantly different (Dtvi: 15.1 � 4.9 cm/s vs. 18.9 � 5.9cm/s, p � 0.04, Dtvi � HR: 862.2 � 261.5 cm/min vs. 1,174.2 � 307.5, p � 0.002). Incontrast with the controls, despite postprandial increase in double product (HR � bloodpressure), Dtvi and Dtvi � HR in the patient group decreased after food intake, with a nadirvalue 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/minvs. 1,273.4 � 1,000.9 cm/min, p � 0.002). In six patients, the CBF pattern resumed thenormal 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 ofpostprandial angina. (J Am Coll Cardiol 2002;40:1976–83) © 2002 by the AmericanCollege of Cardiology Foundation

The phenomenon of postprandial angina has been wellrecognized 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 suggestedincreased myocardial oxygen demand as a mechanism ofpostprandial angina, a recent study (5) using positronemission tomography showed that myocardial blood flowdecreases in the stenotic coronary artery territory during thepostprandial period, suggesting a redistribution of myocar-dial blood flow as a possible cause of postprandial angina.

High-frequency pulse-wave Doppler echocardiographyallows coronary blood flow (CBF) in the left anteriordescending coronary artery (LAD) to be assessed non-invasively. Application of this modality in pathologic con-

ditions is limited, as only the CBF in the LAD can beevaluated. However, given the modality’s non-invasiveness,it is suitable for evaluating coronary physiology. In thisstudy, we compared changes in CBF in the controls withchanges in CBF in patients having significant stenosis in theLAD or in the left main coronary artery. In addition, weevaluated changes in the CBF pattern after significantstenosis had been relieved. The effect of sham feeding wasevaluated 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 arterywere enrolled in the study. Functionally significant stenosiswas defined as �75% stenosis by coronary angiogram and areversible 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 wereexcluded. Twenty healthy volunteers were enrolled as con-trols. Informed consent was obtained from all the volunteersand patients.

From the Clinical Research Institute and Division of Cardiology, Department ofInternal 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.

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



Echocardiographic examination. Transthoracic echocar-diographic examinations were performed after fasting for atleast 6 h, and all medications were discontinued for at least12 h before examination. Before coronary flow was evalu-ated, left ventricular dimensions, ejection fractions, wallthicknesses, left atrial dimension, and mitral inflow Dopplerparameters were obtained. Coronary blood flow was evalu-ated by using a 7 MHz transducer (Seqouia, Acuson,Mountain View, California) at the distal LAD duringend-expiratory apnea before and 15, 30, 45, and 60 minafter food intake, together with blood pressure (BP) andheart rate (HR). The time-velocity integral of the diastolicflow (Dtvi) was measured in the coronary flow velocitycurve. The average value of three consecutive beats was usedin the analysis. The standard meal was composed of 68 g offat, 159 g of carbohydrate, and 37 g of protein, with a totalcalorie count of 1,382 Cal.

In six patients with successful percutaneous coronaryintervention (two patients with balloon angioplasty and fourwith stenting), these measurements were repeated after theintervention. To evaluate the effect of simple gastric disten-sion on the CBF, the CBF was assessed after the sham mealin five of the controls. Pure water (800 cm3) was used as asham meal.Statistical analysis. Continuous variables are reported asmean � SD, and categorical variables as numbers andpercentages. Differences in categorical variables were com-pared using the Fisher exact test and chi-squared test.Differences in continuous variables were compared by theMann-Whitney U test. The Wilcoxon signed-rank test wasused in the analysis of the changes in continuous variables ina 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 withthe controls, the patients were older and had a higherprevalence of hypertension, diabetes, and history of smoking(Table 1). In the patient group, there were five patients withone-vessel disease, eight patients with two-vessel disease, sixpatients with triple-vessel disease, and one patient with leftmain disease. The controls showed lower ejection fractions anda 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 BPand HR after food intake. An increase in systolic BP and adecrease 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 thecontrols, Dtvi and Dtvi � HR increased after food intake,with the peak value 15 min after food intake. Fasting valuesand 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). Inpatients, Dtvi and Dtvi � HR decreased after food intakewith a nadir value 45 min after food intake. Fasting valuesand 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 �

Abbreviations and AcronymsBP � blood pressureCBF � coronary blood flowDtvi � time velocity integral of the diastolic coronary

flowHR � heart rateLAD � left anterior descending arterySPECT � single photon emission computed tomography

Table 1. Clinical Characteristics

Volunteers(n � 20)

Patients(n � 20) p Value*

Age (yrs) 24.5 � 3.1 59.8 � 8.0 � 0.001Men (%) 20 (100%) 16 (86%) 0.035HR (/min) 58 � 9 64 � 13 0.13HTN 0 7 (35%) 0.008DM 0 6 (30%) 0.02Smoking 6 (30%) 12 (60%) 0.06

*Continuous variables by the Mann-Whitney U test and categorical variables by theFisher’s exact test and chi-squared test.

DM � diabetes mellitus; HR � heart rate; HTN � hypertension.

Table 2. Echocardiographic Parameters in Healthy Volunteers and in Patients

Volunteers(n � 20)

Patients(n � 20) p Value*

LVESD (mm) 32.9 � 2.2 30.0 � 6.9 0.005LVEDD (mm) 49.5 � 3.6 49.2 � 6.1 0.647EF (%) 55.9 � 6.5 62.6 � 10.5 0.006IVS/LVPW (mm) 9.1 � 1.1/8.7 � 0.7 12.1 � 1.5/11.2 � 1.8 �0.001/�0.001LA (mm) 33.1 � 2.5 39.2 � 3.7 0.001E/A (m/s) 0.83 � 0.16/0.44 � 0.13 0.68 � 0.14/0.83 � 0.20 0.01/�0.001DT (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 ventricularend-diastolic dimension; LVESD � left ventricular end-systolic dimension; LVPW � left ventricular posterior wall thickness.

1977JACC Vol. 40, No. 11, 2002 Chung et al.December 4, 2002:1976–83 Mechanism of Postprandial Angina



Figure 1. Changes in systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR), and double product after food intake. Controls andpatients 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.

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



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 coronaryinterventions, the CBF pattern after food intake beforeintervention was similar to that of the whole patient group.However, the CBF pattern converted to that of the controlgroup after intervention (Figs. 4 and 5).Effects of sham meal on coronary flow. There were nosignificant changes in BP and HR after a sham meal. Inaddition, CBF did not change significantly after a shammeal (Figs. 6 and 7).

Inter- and intra-observer variability. Inter- and intra-observer variability was assessed in 10 of the controls andfound to be 6.4% and 0.8%, respectively, for the measure-ment of Dtvi.

DISCUSSION

As the CBF dominates during the diastolic period, the CBFin one cardiac cycle can be represented by Dtvi multiplied bythe cross-sectional area of the coronary artery. Assumingthat the coronary artery has a constant cross-sectional area,

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 foodintake. Numbers in each tracing denote the time velocity integral of diastolic flow velocity.




changes in Dtvi represent changes in the CBF in onecardiac cycle. Therefore, changes in the CBF can beestimated 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 metabolicdemands of digestion, there is a compensatory increase incardiac output and HR (8–12). Regarding the changes inBP, 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 showsignificant change in BP after food intake. In our study,postprandial hemodynamics both in the controls and inpatients showed an increase in systolic BP, a decrease indiastolic BP, and an increase in HR after food intake.Pathophysiologic mechanism of postprandial angina. S-everal mechanisms have been suggested for postprandialangina. Redistribution of blood from the coronary artery tothe splanchnic artery, or exercising muscles in the case ofexertional postprandial angina, were once proposed (6).However, these mechanisms have not been proven inhumans (16). Increased myocardial oxygen demand, associ-ated with an increase in HR and sympathetic nervousactivity after food intake, is a commonly believed mecha-nism (2,17,18). However, Figueras et al. (19) showed thatthere is no change in the product of HR and systolic BP atthe onset of ischemic electrocardiographic abnormalities

and suggested decreased myocardial perfusion as a possiblemechanism of postprandial angina. Later, these investiga-tors showed that myocardial ischemia was not induced whenthe patients were paced to the same HR observed duringpostprandial angina (20) and suggested that other factorssuch as coronary vasoconstriction, rather than increasedoxygen demand, might play a role in producing postprandialangina.

Recently, Baliga et al. (5) showed reduced myocardialblood flow in the stenotic artery territory after food intakewith an increase in blood flow in the normal artery territory,by using positron emission tomography. They suggestedthat the redistribution of myocardial blood flow might bethe mechanism of postprandial angina.

In our study, in contrast with the control group, CBFdistal to significant stenosis in patients did not showpostprandial surge in CBF after food intake; rather, theCBF was significantly decreased after food intake. Thisabsence of postprandial surge distal to the significant ste-nosis is not likely to be a global phenomenon, because whenthe stenosis was relieved by intervention, the normal patternof postprandial surge in CBF was restored. Therefore, wespeculate that the CBF is redistributed to territory of thenormal or insignificantly stenotic coronary artery.

Although our study included patients with multivesseldisease, functionally significant stenosis based on the sesta-mibi SPECT was confined to the LAD, and the inclusion

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 (upperpanel) and after (lower panel) successful intervention. Dtvi and Dtvi � HR changed to those of the healthy controls after intervention. *p � 0.05 comparedwith the fasting state by the Wilcoxon signed rank test.




of these patients would not affect the interpretation of ourresults.Types of meals producing postprandial angina. The re-lationship between the components of a meal and theprecipitation of postprandial angina is controversial. It hasbeen proposed that postprandial angina is more likely to beprecipitated by a fatty meal, which leads to postprandialendothelial dysfunction (21,22). However, other studieshave suggested that a high-carbohydrate meal, rather than afatty meal, is more likely to precipitate postprandial angina

(11,23). In our study, we did not evaluate the effect of mealcomponents. However, in contrast to a previous study (24),simple gastric distension by drinking water of the samevolume as the standard meal did not affect the CBF,suggesting that a change in the CBF after food intake is nota vagally mediated response.Study limitations. Because of the intrinsic limitation of thetransthoracic Doppler echocardiographic evaluation of cor-onary flow, we could not measure the CBF in the right andleft circumflex artery in our patients. Therefore, the pres-

Figure 5. Coronary flow velocities before (left panel) and after (right panel) successful intervention in patients with significant stenosis in the left anteriordescending 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 diastolicflow velocity.




ence of a “steal phenomenon” is postulated from the indirectevidence offered by the presence of postprandial surge in theCBF of healthy controls and of the restored normal patternwhen stenosis is relieved. In addition, when estimatingcoronary blood flow, we neglected the flow during systoleand assumed that the cross-sectional area of the coronaryartery was constant during the study period.

We enrolled young, healthy volunteers as controls tominimize the possibility of their having coronary artery

disease; therefore, age and gender ratio were not matchedbetween the patient and control groups. Also, we didnot limit the patient group to patients with postprandialangina.Conclusions. Myocardial oxygen demand represented bythe product of BP and HR increased after food intake.However, there was also a decrease in CBF distal to thesignificant stenosis, which suggests that steal phenomenonmay play a role in the mechanism of postprandial angina.

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

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 thediastolic flow velicity occurred after a sham meal. Numbers in each tracing denote time velocity integral of the diastolic flow velocity.




Reprint requests and correspondence: Dr. Dae-Won Sohn,Division of Cardiology, Department of Internal Medicine, SeoulNational University College of Medicine, 28 Yongun-Dong,Chongno-Gu, Seoul 110-744, Korea. E-mail: [email protected].

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2002;40;1976-1983 J. Am. Coll. Cardiol.Young-Bae Park, and Yun-Shik Choi

Woo-Young Chung, Dae-Won Sohn, Yong-Jin Kim, Seil Oh, I. n-H. o Chai, stenosis: a possible mechanism of postprandial angina

Absence of postprandial surge in coronary blood flow distal to significant

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