Background We assessed the relation between the severity ofstenosis in a coronary artery and the degree of impairment ofmyocardial blood flow. Studies in laboratory animals have shownthat as the degree of coronary-artery stenosis increases, themaximal coronary flow measured after maximal vasodilatationprogressively decreases, with a concomitant decrease in basalflow. However, this relation has not been carefully documentedin humans through measurement of myocardial blood flow.
Methods We studied 35 patients with single-vessel coronary arterydisease and normal left ventricular function and 21 age-matchedcontrols. Regional myocardial blood flow in the area suppliedby the stenosed artery was measured by positron-emission tomographywith oxygen-15-labeled water while the subject was at rest (basalflow) and during hyperemia induced by the intravenous administrationof the vasodilator adenosine (140 µg per kilogram of bodyweight per minute) or dipyridamole (0.56 mg per kilogram).
Results The mean (±SD) basal myocardial blood flow was1.14 ±0.42 ml per minute per gram of tissue in the patientsand 1.13 ±0.26 ml per minute per gram in the controls;during hyperemia, myocardial flow was 2.10 ±1.16 and3.37 ±1.25 ml per minute per gram (P<0.001), respectively.Basal flow was unchanged regardless of the severity of stenosis,expressed as a percentage of the diameter of the affected vessel(range of degrees of stenosis, 17 to 87 percent). In contrast,flow during hyperemia correlated inversely and significantlywith the degree of stenosis and correlated directly with theminimal luminal diameter. The coronary vasodilator reserve (definedas the ratio of flow during hyperemia to flow at base line)began to decline when the degree of stenosis was about 40 percentand approached unity when stenosis was 80 percent or greater.
Conclusions In humans, basal myocardial blood flow remains constantregardless of the severity of coronary-artery stenosis. However,during hyperemia, flow progressively decreases when the degreeof stenosis is about 40 percent or more and does not differsignificantly from basal flow when stenosis is 80 percent orgreater.
Studies in animals have shown that the coronary vasodilatorreserve (defined as the ratio of maximal to basal coronary bloodflow) can be used as a functional index of the severity of coronary-arterystenosis1,2. Additional studies have demonstrated that the coronaryvasodilator reserve also correlates with the geometry of thestenosis assessed by quantitative arteriography and consideredalong with all the physiologic variables determining coronaryflow3,4. To date, several investigations of the relation betweencoronary vasodilator reserve and the severity of stenosis inpatients have produced conflicting results,5,6 perhaps in partbecause of technical factors7,8.
Recent studies by different groups of investigators have shownthat positron-emission tomography can be used to quantitateregional myocardial blood flow accurately and noninvasively9,10,11,12.To determine the relation between the severity of coronary-arterystenosis and absolute myocardial blood flow, we measured stenosisby quantitative coronary arteriography and myocardial bloodflow by positron-emission tomography at rest and during maximalvasodilatation, in patients with coronary artery disease.
Methods
Study Population
We studied 35 patients with single-vessel coronary artery diseaseand normal left ventricular function; the mean (±SD)age of the 6 women and 29 men was 59 ±9 years (range,37 to 77). None had a clinical history or electrocardiographicevidence of previous myocardial infarction, evidence of valvularor primary myocardial disease, or a history of diabetes or systemichypertension; no patient had evidence of left ventricular hypertrophyon echocardiographic examination. All patients underwent coronaryarteriography with left ventriculography and positron-emissiontomography. The index artery was the left anterior descendingartery in 30 patients, a dominant right coronary artery in 4patients, and a dominant left circumflex artery in 1 patient.
Twenty-one normal subjects served as controls; the mean ageof the 6 women and 15 men was 57 ±13 years (range, 41to 79) (P = 0.42 for the comparison with the patients). Thecontrols also underwent positron-emission tomography. They wereselected because their history and physical examinations hadshown them to be at low risk for coronary disease; all had normalresting electrocardiograms and negative exercise tests in responseto a high workload.
Study Protocol
The study protocol was approved by the Ethics Committee of theUniversity of Louvain Medical School, Brussels, and the Onze-Lieve-VrouwHospital, Aalst, Belgium, and the Research Ethics Committeeof Hammersmith Hospital, London. All patients gave informedconsent to the study.
Quantitative Coronary Arteriography and Left Ventriculography
Selective arteriography of the right and left coronary arteriesin multiple views was performed according to the Judkins technique.The coronary arteriograms were analyzed by an automated edgecontourdetection system (Cardiovascular Angiographic Analysis System,Pie Medical Equipment, Maastricht, the Netherlands)13. The luminaldiameter of the stenosed artery in the projection showing maximalseverity, along with the adjacent reference segments, was measuredat end-diastole. The degree of stenosis was expressed as thepercent reduction of the internal luminal diameter in relationto the estimated diameter interpolated from the diameters atthe proximal and distal boundaries of the stenosis. The cross-sectionalarea of the vessel and the percentage of area represented bythe stenosis were also calculated from orthogonal views by thismethod. The patients were grouped according to their degreeof stenosis: less than 40 percent, 40 to 59 percent, 60 to 79percent, and 80 percent or more of the vessel diameter.
The global and regional left ventricular ejection fraction wasmeasured from a cineangiogram obtained in a 30-degree rightanterior oblique projection. An automated hard-wired endocardial-contourdetector linked to a microcomputer was used to measure leftventricular end-systolic and end-diastolic volumes accordingto the modified Simpson's rule, to determine the computed regionalcontribution to the ejection fraction14,15.
Positron-Emission Tomography
The patients did not receive antianginal medication (exceptnitrates) for at least 48 hours before positron-emission tomography.Scanning was performed at two centers: at the University ofLouvain, Brussels (27 patients and 4 controls), with an ECAT911/01 single-slice tomograph (CTI, Knoxville, Tenn.), whichhas been described previously16; and at the Medical ResearchCouncil Cyclotron Unit, Hammersmith Hospital, London (8 patientsand 17 controls), with an ECAT 931-08/12 15-slice tomographgiving a 10.5-cm axial field of view (CTI)17. In both scanners,emission scans were reconstructed with a Hanning filter thathad a cutoff frequency of half maximum, resulting in a transaxialresolution with a full width of 8 mm at half maximum for theemission data at the center of the field of view16,17.
Regional myocardial blood flow (expressed in milliliters perminute per gram of tissue) was measured on transaxial images;the flow tracer was intravenously infused oxygen-15-labeledwater (University of Louvain) or inhaled oxygen-15-labeled carbondioxide, which is rapidly converted to oxygen-15-labeled waterby carbonic anhydrase in the lung (Medical Research CouncilCyclotron Unit). Both agents give similar results,12,18 andtheir use has been validated at the respective centers12,19.Flow was measured at rest and two minutes after the end of theintravenous administration of dipyridamole (0.56 mg per kilogramof body weight, given over a period of four minutes, in 8 patientsand 20 controls) or during the infusion of adenosine (140 µgper kilogram per minute, in 27 patients and 1 control), accordingto standard practice12,18,19. The vasodilator response to dipyridamoleor adenosine in the controls at the Brussels center did notdiffer significantly from the response in the controls at theLondon center.
Data analysis was performed as previously reported12,19. Inbrief, either three or four regions of interest were selected:one region in the interventricular septum and two or three regionsin the left ventricle -- the anterior wall and the lateral freewall (University of Louvain) or the anterior wall, the lateralwall, and the inferoposterior wall (Medical Research CouncilCyclotron Unit). In patients with stenosis of the left anteriordescending artery on arteriography, the anterior region wasdesignated as the stenosis-related region. In patients withstenosis of the right coronary or left circumflex artery (MedicalResearch Council Cyclotron Unit only), the inferoposterior regionwas designated as the stenosis-related region. Among patientswith stenoses of similar severity, there were no significantdifferences in blood flow in the anterior and in the inferoposteriorregions. The coronary vasodilator reserve was defined as theratio of myocardial blood flow during hyperemia to flow at baseline. Flow in the patients was compared with the average flowin all regions in the controls.
Because basal myocardial blood flow is closely related to therate-pressure product,20 an index of myocardial oxygen consumption,values for basal flow in each patient were also corrected forthe respective rate-pressure product, by multiplying basal flowby the mean rate-pressure product in the patients as a group,divided by the rate-pressure product in the individual patient.Total coronary resistance at base line was calculated by dividingthe mean arterial pressure by the flow at base line, and resistanceat maximal vasodilatation by dividing the mean arterial pressureby the flow during hyperemia.
Statistical Analysis
All values are expressed as means ±SD. Two-tailed pairedand unpaired Student's t-tests were used to compare group means.One-way analysis of variance was used for simultaneous comparisonof more than two mean values, and Fisher's method of least significantdifferences was subsequently applied to localize the sourceof the difference21. Regression analyses were performed to detectcorrelations between flow variables (Y) and angiographic variables(X; stenosis expressed as a percentage of the vessel diameter,or the minimal luminal diameter) in the patients. If a nonconstantincrease or decrease in values for a flow variable in relationto values for an angiographic variable was identified, a nonlinearstatistical model was used, chosen on the basis of a diagnosticbox plot of the SD of Y against the mean of Y in equally spacedintervals of X. If no functional relation was found betweenthe SD of Y and the mean, the statistical model for regressionwas linear. If the SD of Y increased in proportion to the mean,the regression model was log-linear. If the square of the SDof Y increased in proportion to the mean, the regression modelwas quadratic. The fitted regression curves and correspondingcorrelation coefficients are shown in the figures. A P valuebelow 0.05 was considered to indicate statistical significance.
Results
Coronary-Artery Stenoses
In the 35 patients, the mean stenosis expressed in terms ofthe vessel diameter was 56 ±20 percent (range, 17 to87), the mean area of stenosis 76 ±18 percent (range,30 to 98), the mean minimal luminal diameter of the artery 1.21±0.61 mm (range, 0.35 to 2.54), and the mean cross-sectionalarea of the artery 1.43 ±1.27 mm2 (range, 0.10 to 5.00)(Table 1). The mean global left ventricular ejection fractionwas 70 ±7 percent (range, 58 to 84). Individual valuesfor these variables are shown in Table 1.
Table 1. Hemodynamic Characteristics of 35 Patients with Coronary-Artery Stenosis.
Hemodynamic Measurements during Positron-Emission Tomography
There were no significant differences between the patients andthe controls in the increase in the heart rate from base lineto maximal vasodilatation, although the increase itself wassignificant (from 63 ±10 to 88 ±16 beats per minutein patients, P<0.001; and from 65 ±7 to 84 ±10beats per minute in controls, P<0.001). Systolic blood pressurewas significantly higher in the patients than in the controlsat base line (148 ±22 vs. 132 ±19 mm Hg, P = 0.01)and during maximal vasodilatation (153 ±21 vs. 140 ±20mm Hg, P = 0.03). However, the rate-pressure product in thepatients was similar to that in the controls both at base line(9333 ±2167 and 8605 ±1848 mm Hg per minute, respectively)and during maximal vasodilatation (13,570 ±3280 and 11,950±2710 mm Hg per minute, respectively). Diastolic bloodpressure was similar in both groups at base line and duringmaximal vasodilatation (74 ±11 and 72 ±12 mm Hg,respectively, in the patients, and 76 ±8 and 75 ±12mm Hg, respectively, in the controls). Likewise, the mean arterialpressure was similar in both groups at base line and duringmaximal vasodilatation (98 ±13 and 98 ±13 mm Hg,respectively, in the patients; 100 ±11 and 97 ±13mm Hg, respectively, in the controls).
Regional Myocardial Blood Flow
Myocardial blood flow was similar in the patients and controlsat base line (1.14 ±0.42 and 1.13 ±0.26 ml perminute per gram of tissue) but significantly lower in the patientsduring hyperemia (2.10 ±1.16 vs. 3.37 ±1.25 mlper minute per gram, P<0.001). Coronary vasodilator reserve(the ratio of flow during hyperemia to flow at base line) wassignificantly lower in the patients than in the controls (2.11±1.45 vs. 3.16 ±1.4, P = 0.01). Basal flow correctedfor the rate-pressure product was similar in both groups (1.15±0.44 and 1.19 ±0.32 ml per minute per gram inthe patients and controls, respectively); the corrected vasodilatorreserve was significantly lower in the patients (2.08 ±1.32vs. 3.00 ±1.36, P = 0.02). Total coronary resistancewas similar in the patients and controls at base line (95.3±37.8 and 90.9 ±20.3 mm Hg • min • gper milliliter, respectively) but significantly higher in thepatients during hyperemia (57.2 ±26.6 and 32.1 ±12.0mm Hg • min • g per milliliter, P<0.001).
Table 2 shows myocardial blood flow at base line and duringhyperemia in the study groups defined according to the degreeof stenosis. Basal flow and basal flow corrected for the rate-pressureproduct remained constant in the patients irrespective of theseverity of stenosis. Flow during hyperemia in the patientswith stenoses of less than 40 percent was not significantlydifferent from flow in the controls (Table 2). Among the patientswith stenoses of 40 percent or more of the luminal diameter,flow during hyperemia and coronary vasodilator reserve progressivelydecreased as the degree of stenosis increased (Table 2 and Figure 1).For stenoses equal to 80 percent or more of the luminaldiameter, flow at base line and during hyperemia was similar-- i.e., the coronary vasodilator reserve approached unity.When the degree of stenosis was expressed as a percentage ofthe vessel area, a similar pattern became apparent, with a reductionin flow during hyperemia when the area of stenosis was at least60 percent, and exhaustion of the coronary vasodilator reservewhen the area of stenosis was just over 90 percent. When stenosiswas expressed as an absolute measurement, a similar relationwas found, with no change in flow at base line but a progressivereduction in flow during hyperemia (Figure 2). A similar relationwas observed when stenosis was expressed in terms of cross-sectionalarea (data not shown).
Figure 1. Myocardial Blood Flow, Coronary Vasodilator Reserve, and Coronary Resistance in Relation to Stenosis Expressed as a Percentage of Vessel Diameter.
There was no significant correlation between blood flow in the 35 patients at base line (top panel, open circles) and their degree of stenosis; flow during hyperemia (solid circles) decreased significantly as stenosis increased. Similarly, coronary vasodilator reserve (the ratio of flow during hyperemia to flow at base line) decreased significantly as stenosis increased (middle panel). Minimal total coronary resistance increased significantly with the severity of the stenosis (bottom panel).
The values in the 21 controls are shown at 0 percent stenosis in each panel; some circles represent more than 1 control. The values for flow and vasodilator reserve in all subjects were corrected for the rate-pressure product (see the Methods section).
Figure 2. Myocardial Blood Flow, Coronary Vasodilator Reserve, and Coronary Resistance in Relation to Stenosis Expressed as the Minimal Luminal Diameter.
There was a significant correlation between blood flow in the 35 patients during hyperemia and their degree of stenosis (top panel). Similarly, coronary vasodilator reserve correlated significantly with stenosis, with almost complete exhaustion of the reserve when the diameter was 0.5 mm (middle panel). Minimal total coronary resistance increased significantly as the luminal diameter decreased (bottom panel).
Discussion
We have demonstrated a significant inverse relation betweenthe severity of coronary-artery stenosis and absolute myocardialblood flow during hyperemia, a finding consistent with previouswork in both animals1,2,3,4 and patients22,23,24,25. Basal flowremains constant despite any increase in the severity of stenosis,and maximal flow starts to diminish progressively if stenosesare 40 percent or greater. This agrees with the finding thatbasal flow to collateral-dependent myocardium is preserved inpatients with complete coronary occlusion and normal regionalwall motion26. Although a relatively small number of patientswere studied whose stenoses were more than 80 percent (whichare equivalent to 96 percent or more if stenoses are expressedin terms of area), very few patients with normal left ventricularfunction have stenoses of more than 80 percent and normal anterogradeflow; such patients usually appear to have functional occlusionswith reduced flow and well-developed collateral vessels3.
Although the overall relation between the anatomical and functionalmeasurements of the degree of stenosis was statistically significant,our data show that maximal myocardial blood flow and vasodilatorreserve can vary appreciably among patients whose coronary stenosesare of comparable severity. This may reflect either a true variabilityor limitations of our measurements of the stenosis, myocardialperfusion, or both. There was also substantial variability amongthe controls in this study, as in previous studies12,20. Thismay be due to differences in the responsiveness of individualsubjects to pharmacologic vasodilatation27,28. Although thestudy remains limited in that vasodilatation may have been submaximalin a minority of the patients,28 intravenous dipyridamole andadenosine, at the doses used, have comparable vasodilating effects,29similar to those of intracoronary papaverine30. Furthermore,the maximal flows in controls and patients with stenoses ofless than 40 percent were similar to those previously reportedin subjects of similar age20,31.
Despite our correcting for the rate-pressure product, therestill may have been variability (particularly in the vasodilatorresponse) because loading conditions and coronary perfusionpressures may differ from patient to patient32,33,34. However,a similar relation was observed when coronary resistance wasused to correct for coronary perfusion pressure. Although weselected patients without extensive collateralization, individualvariations in intramyocardial wall tension and resistive vesselfunction may have accounted for differences in regional myocardialperfusion.
Previous investigators have attempted to integrate all the geometriccharacteristics of a coronary-artery stenosis, including thepercentage of stenosis and the cross-sectional area and lengthof the lesion, by studying dogs with induced epicardial stenoses4.That study demonstrated a strong correlation between the flowreserve predicted from an arteriogram and the value measuredwith an epicardial Doppler probe. In humans, an intracoronaryDoppler catheter has been used to measure blood-flow velocity22,27.Absolute blood flow can be estimated from flow velocity if thecross-sectional diameter of the vessel is known, but severalfactors limit this method, above all the fact that measurementwith a Doppler catheter does not take into account collateralflow, flow to side branches proximal to the stenosis, and expansionof the distal vascular bed during vasodilatation and thus cannotdetermine nutritive tissue perfusion35. This has led to theuse of positron-emission tomography to assess the functionalseverity of coronary artery disease36,37 with different flowtracers9,10,11,12,38,39.
In a study using rubidium-82 and nitrogen-13-labeled ammonia,the relative perfusion reserve (the ratio of maximal to basalradioactivity in the stenosis-related region divided by theratio in a remote region) correlated well with the value forstenosis expressed as a percentage of vessel diameter or arearepresented curvilinearly23. Perfusion reserve could also becorrelated with cross-sectional area by comparing lesions inthe same index artery, and with flow reserve predicted froman arteriogram. However, not all patients had single-vesseldisease and some had previously had myocardial infarction orundergone coronary angioplasty,23 which is known to affect myocardialblood flow in stenosis-related regions40. The subjectively determinedseverity of perfusion defects during positron-emission tomographyof the stenosis-related region has been found to correlate withthe arteriographically predicted flow reserve of the stenosis24.However, a stenosis flow reserve has been found to vary widelyamong patients with stenoses of 50 to 60 percent (in terms ofvessel diameter); 38 percent of patients with stenoses greaterthan 50 percent have only a slightly decreased or even normalestimated coronary flow reserve. This underscores the problemof defining myocardial perfusion in terms of the severity ofthe stenosis alone, even though estimated stenosis flow reserveis uninfluenced by prevailing hemodynamic conditions23.
Because the effective resistance at the site of the stenosisis proportional to the fourth power of the radius, small changesundetectable by arteriographic assessment may cause larger changesin resistance at the stenosis, particularly more severe lesions2.Computer-assisted edge-detection methods have been developedto reduce the error and inaccuracy inherent in visual assessment41.Nevertheless, several groups of investigators have reporteda poor correlation between the effect of a stenosis on function,measured with an epicardial suction Doppler probe, and its anatomicalcharacteristics expressed as the percentage of the vessel diameteror lesion area,5,6 particularly for moderate-to-severe stenoses42.This is probably due to the difficulty in ascertaining the normalreference segment of coronary artery because of diffuse intimalatherosclerosis proximal and distal to the stenosis, and itmay account for the stronger correlation between coronary flowvelocity and cross-sectional area,5 albeit dependent on thesize of the artery studied23. Furthermore, the orientation ofthe vessel to the x-ray plane and asymmetrical narrowing maylead to further inaccuracy. However, although errors can bemade when quantitative arteriography is used, our study showsthat the severity of stenosis as assessed by these methods correlateswell with absolute myocardial perfusion as measured by positron-emissiontomography.
In patients with single-vessel coronary disease and normal leftventricular function, basal myocardial blood flow remains constantdespite increasing severity of stenosis. Maximal flow beginsto decrease progressively if the stenosis is more than about40 percent, leading to exhaustion of coronary vasodilator reserveif the stenosis is 80 percent or more. Our study demonstratesthe power of positron-emission tomography to quantify myocardialblood flow and flow reserve noninvasively and thus allow thefunctional importance of coronary-artery stenosis to be assessed.
Supported by a grant (3-4522-89) from the Fonds National dela Recherche Scientifique et Medicale, a grant (91/96-146) fromthe Action de Recherche Concertee, and by the European EconomicCommunity Concerted Action on PET Investigation of CellularRegeneration and Degeneration.
We are indebted to Patrick Royston, D.Sc. (Department of MedicalPhysics, Royal Postgraduate Medical School), Christopher G.Rhodes, M.Sc. (Medical Research Council Cyclotron Unit), andAnnie Robert, Ph.D. (Division of Cardiology, University of Louvain),for their statistical advice.
Source Information
From the Cyclotron Unit, Medical Research Council Clinical Sciences Centre and Royal Postgraduate Medical School, Hammersmith Hospital, London (N.G.U., P.G.C.); the University of Louvain Medical School, Brussels, Belgium (J.A.M., W.W., T.B.); and the Cardiovascular Center, Aalst, Belgium (B.D.B.). Presented in part at the 66th Scientific Sessions of the American Heart Association, Atlanta, November 7-11, 1993.Dr. Baudhuin is deceased.
Address reprint requests to Dr. Camici at the MRC Cyclotron Unit, Hammersmith Hospital, Du Cane Rd., London W12 0HS, United Kingdom.
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