Abnormal Subendocardial Perfusion in Cardiac Syndrome X Detected by Cardiovascular Magnetic Resonance Imaging
Jonathan R. Panting, M.B., M.R.C.P., Peter D. Gatehouse, Ph.D., Guang-Zhong Yang, Ph.D., Frank Grothues, M.D., David N. Firmin, Ph.D., Peter Collins, M.D., and Dudley J. Pennell, M.D.
Methods We performed myocardial-perfusion cardiovascular magneticresonance imaging in 20 patients with syndrome X and 10 matchedcontrols, both at rest and during an infusion of adenosine.Quantitative perfusion analysis was performed by using the normalizedupslope of myocardial signal enhancement to derive the myocardialperfusion index and the myocardial-perfusion reserve index (definedas the ratio of the myocardial perfusion index during stressto the index at rest).
Results In the controls, the myocardial perfusion index increasedin both myocardial layers with adenosine (in the subendocardium,from a mean [±SD] of 0.12±0.03 to 0.16±0.03[P=0.02]; in the subepicardium, from 0.11±0.02 to 0.17±0.05[P=0.002]); in patients with syndrome X, the myocardial perfusionindex did not change significantly in the subendocardium (0.13±0.02vs. 0.14±0.03, P=0.11; P=0.09 as compared with controls)but increased in the subepicardium (from 0.11±0.02 to0.20±0.04, P<0.001; P=0.11 for the comparison withcontrols). Adenosine provoked chest pain in 95 percent of patients with syndrome X and 40 percent of controls (P<0.001).
Between 10 and 20 percent of patients with typical anginal chestpain are found to have normal coronary angiograms.1 A subgroupof these patients, who also have classic downsloping ST-segmentdepression on exercise testing, are classified as having cardiacsyndrome X.2 The exact pathophysiological mechanisms underlyingthis condition are not well understood, and many mechanismsfor the chest pain have been suggested. In some studies, microvasculardysfunction has been proposed as the cause,3,4,5,6 whereas inothers, metabolic abnormalities, such as net myocardial lactateproduction,7,8,9,10,11 have been demonstrated. However, morerecent studies with stricter criteria for the selection of patientssuggest that lactate production is normal in patients with syndromeX.12
The lack of consistent findings in previous studies may suggesta predominantly nonischemic origin for the chest pain, but itmay also reflect a lack of sensitivity of the tests in detectinglimited subendocardial ischemia. Recently, the technique ofmyocardial-perfusion cardiovascular magnetic resonance imaginghas been developed and validated against the use of radioactivemicrospheres in animal models as a measure of transmural andsubendocardial blood flow.22,23 When compared with angiographyand PET, cardiovascular magnetic resonance imaging has beenshown to be accurate for the detection of ischemia in coronaryartery disease and has been shown to have higher resolutionthan conventional perfusion techniques.24,25,26,27 We thereforehypothesized that perfusion cardiovascular magnetic resonanceimaging would identify nontransmural ischemia in patients withsyndrome X.
Methods
Subjects
We studied 20 patients with syndrome X (16 women and 4 men;mean [±SD] age, 55.9±10.5 years) and 10 age- andsex-matched normal control subjects (8 women and 2 men; meanage, 57.9±7.4 years) (P=0.63 for both comparisons betweenthe groups). The patients were recruited from the Women's HeartDisease Clinic at Royal Brompton Hospital in London. All hada previously established diagnosis of classic syndrome X, witha typical history of exertional angina, an abnormal exerciseelectrocardiogram (0.1 mV horizontal or downsloping ST-segmentdepression of 80 msec after the J point), and completely normalresults on coronary angiography, with no inducible spasm onergonovine-provocation testing.28 The mean time from angiographyto the cardiovascular magnetic resonance imaging examinationwas 18±10 months. No patient had diabetes (defined bya fasting glucose level over 7.8 mmol per liter [141 mg perdeciliter] or a random-sample glucose level over 11.1 mmol perliter [200 mg per deciliter]), hypertension (defined as bloodpressure over 140/80 mm Hg), left ventricular hypertrophy (definedas a value above 35 mm for the sum of the height of the S wavein lead V1 and the height of the R wave in lead V5), or anychange in clinical condition between the investigations. Althoughthallium-perfusion single-photon-emission computed tomography(SPECT) was not performed in this study as part of the protocol,the results of SPECT were available for 14 patients (mean timefrom thallium SPECT to cardiovascular magnetic resonance imaging,12±7 months). These results showed normal perfusion in11 patients and a mild fixed defect in 3. The patients withsyndrome X received calcium-channel blockers (11 patients),nitrates (9 patients), hormone-replacement therapy (7 patients),beta-blockers (5 patients), potassium-channel openers (2 patients),or no treatment (1 patient). Some patients received more thanone medication.
The controls were all healthy, with no history of chest painor other cardiovascular symptoms. The profile of the controlswith respect to cardiovascular risk factors was as follows:none were smokers; the mean blood pressure was 127/76 mm Hg;the mean total cholesterol level was 5.7 mmol per liter (220mg per deciliter); the mean high-density lipoprotein (HDL) levelwas 1.8 mmol per liter (70 mg per deciliter); the mean ratioof total cholesterol to HDL cholesterol was 3.2. No patienthad diabetes or left ventricular hypertrophy, and the calculatedoverall 10-year mean risk of a coronary event was 4.5 percent.29None of the controls had undergone coronary angiography or thalliumSPECT. This study was approved by the institutional ethics committee,and all patients gave written informed consent.
Study Protocol
Cardiovascular magnetic resonance imaging was performed withuse of a 1.5-T scanner (Picker Edge) that used a gradient-echosequence with a 90-degree saturation pulse for T1 weighting.A cardiac phase-array receiver coil was used with sequence variablesas follows: time to echo, 1.2 msec; repetition time, 3 msec;phase matrix, 64; slice thickness, 10 mm; and field of view,450 by 225 mm, yielding a pixel size of 3.5 by 3.5 mm interpolatedto 1.75 by 1.75 mm. The two-slice sequence was started on theR wave for systolic gating and to ensure an adequate acquisitionwindow during any adenosine-induced tachycardia. Studies wereperformed at rest and during a six-minute infusion of adenosine(140 µg per kilogram of body weight per minute) to achieveintense coronary hyperemia. The two studies were separated by20 minutes to allow equilibration of the contrast agent afterthe first injection. Two short-axis left ventricular sliceswere placed one third and two thirds of the distance from baseto apex, with acquisition every cardiac cycle for 50 beats.A bolus of gadopentetate dimeglumine (0.05 mmol per kilogram)was injected at a rate of 5 ml per second for each first-passstudy by means of a power injector into a 14-gauge cannula inthe antecubital vein.
The images were analyzed quantitatively, in a masked fashion,and were presented in random order. Each series of images wasanalyzed by measuring the signal in regions of interest in theleft ventricular blood pool and myocardium. For analysis, themyocardium was divided into two subendocardial and subepicardialregions, which were drawn with the outer borders close to theendocardial and epicardial surfaces and with the inner bordersadjacent to each other in the mid-wall. The analysis was performedwith software designed in house (CMRtools, Imperial College).The regions of interest were drawn on a single image and propagatedautomatically throughout the perfusion series; each image wasthen checked for positioning, and adjustments were made forany respiratory movement. The intervals between images werecalculated from the electrocardiographic trace obtained duringacquisition, and from these measurements, curves showing signalintensity plotted against time were constructed for each regionof interest. An index of myocardial perfusion was then calculatedwith the use of myocardial slope measurements, as has been previouslyreported.24,26,27 In brief, curve fitting was used to obtainthe slope of the first-pass contrast enhancement for each ofthe myocardial regions of interest and the left ventricularblood-pool region of interest. The myocardial slope was thennormalized by dividing it by the left ventricular blood-poolslope. This method compensates for changes in the input functioncaused by the effects of adenosine on heart rate and systemiccirculation. The ratio of the myocardial perfusion index duringstress to that with the subject at rest was defined as the myocardial-perfusionreserve index. Subepicardial perfusion and subendocardial perfusionwere compared to determine the degree of heterogeneity acrossthe myocardial wall. Transmural perfusion was assessed by combiningthe subepicardial and subendocardial regions of interest. Heterogeneitywithin the subendocardial regions of interest was assessed byvisual scoring of 6 segments in each slice (total for the twoslices, 12 segments). In addition to undergoing magnetic resonanceimaging, all subjects graded the level of pain associated withthe adenosine infusion on the following scale: 1, no pain; 2,mild discomfort; 3, moderate but bearable pain; 4, severe pain;and 5, the worst pain ever experienced.
Statistical Analysis
Summary values are expressed as means ±SD. Differencesbetween means of continuous variables were tested by Wilcoxonnonparametric tests because of the small samples. The chi-squaretest was used to compare categorical data for pain. A P valueof less than 0.05 was considered to indicate statistical significance.
Results
Quantitative Analysis
There was no significant difference in the value of the myocardialperfusion index for transmural perfusion between controls andpatients with syndrome X either with the subjects at rest (0.12±0.03vs. 0.12±0.02, P=0.63) or during stress (0.16±0.04vs. 0.17±0.03, P=0.49). In the controls, the myocardialperfusion index increased significantly during adenosine infusionin both the subendocardium (from 0.12±0.03 to 0.16±0.03,P=0.02) and the subepicardium (from 0.11±0.02 to 0.17±0.05,P=0.002). However, in the patients with syndrome X, the myocardialperfusion index did not increase significantly in the subendocardiumduring the adenosine infusion (0.13±0.02 vs. 0.14±0.03,P=0.11; P=0.09 as compared with the controls) but did increasein the subepicardium (from 0.11±0.02 to 0.20±0.04,P<0.001; P=0.11 as compared with the controls) (Figure 1A).Subendocardial myocardial perfusion index normalized to heartrate fell in patients with syndrome X (from 1.7±0.5x10–3to 1.3±0.4x10–3 per heartbeat, P<0.001), butnot in the controls (1.8±0.7x10–3 vs. 1.7±0.4x10–3per heartbeat, P=0.38; P=0.13 as compared with the patientswith syndrome X). Examples of images obtained at the time ofmaximal contrast uptake in a control subject and in a patientwith syndrome X are shown in Figure 2 and Figure 3. The meannumber of abnormal myocardial segments in the patients withsyndrome X during stress was 5.6, representing 47 percent ofthe myocardium.
Figure 1. Measurements of Myocardial Perfusion Index in Controls and in Patients with Syndrome X.
Panel A shows the myocardial perfusion index at rest and during stress. Panel B shows the ratio of subendocardial to subepicardial myocardial-perfusion reserve index.
Figure 2. Images of Myocardium at Peak Myocardial Enhancement during the First Pass of Gadolinium in a Control Subject at Rest (Panel A) and during Stress (Panel B), Showing Uniform Myocardial Signal Enhancement.
Figure 3. Images of Myocardium at Peak Myocardial Enhancement during the First Pass of Gadolinium in a Patient with Syndrome X at Rest (Panel A) and during Stress (Panel B), Showing a Ring of Delayed Subendocardial Enhancement (Arrows in Panel B).
The results of the analysis of the myocardial-perfusion reserveindex are shown in Figure 1B. There was no significant differencein the myocardial-perfusion reserve index for the entire transmuralextent of myocardium between patients with syndrome X and controls(1.47±0.36 vs. 1.50±0.47, P=0.56). The differencesbetween the myocardial-perfusion reserve index in patients withsyndrome X and in controls were of borderline significance forboth the subendocardium (1.10±0.23 vs. 1.38±0.4,P=0.071) and the subepicardium (1.84±0.52 vs. 1.63±0.53,P=0.11), but the ratio of subendocardial to subepicardial myocardial-perfusionreserve index was significantly lower in patients with syndromeX (0.61±0.11 vs. 0.85±0.13, P=0.002). Accordingto analysis of the receiver-operating-characteristic curve,the optimal ratio of subendocardial to subepicardial myocardial-perfusionreserve index for distinguishing patients with syndrome X fromcontrols was 0.72, which yielded a sensitivity of 85 percent,a specificity of 100 percent, and an accuracy of 90 percentfor the test.
Pain Perception
Among the controls, four (40 percent) had chest pain duringadenosine infusion. The mean score for all controls was 1.3,indicating that the pain was mild at the worst. By contrast,19 of 20 of the patients with syndrome X (95 percent) had chestpain (2=26.1, P<0.001), and the majority reported that thepain was either severe or the worst ever experienced (mean score,4.2; P<0.001 for the comparison with the controls).
Discussion
Our results show that patients with syndrome X have significantlydifferent perfusion responses to adenosine than matched controls.Although values for the transmural myocardial perfusion indexat base line and under stress were equivalent between the groups,in the patients with syndrome X the subendocardial myocardialperfusion index did not increase with adenosine; in the controls,in contrast, a normal increase was seen. There was also a significantreduction in the subendocardial myocardial perfusion index normalizedto heart rate in the patients with syndrome X, which was notseen in the control group. The responses in the subepicardiumwere similar in both groups. Thus, the ratio of subendocardialto subepicardial myocardial-perfusion reserve index was significantlylower in patients with syndrome X. We found consistent evidencein patients with syndrome X of an abnormality of myocardialperfusion limited to the subendocardium. These results couldbe obtained because transmural resolution is higher with cardiovascularmagnetic resonance imaging than with other techniques.
Our results show that patients with syndrome X have a reductionin subendocardial myocardial perfusion index normalized to heartrate during stress and a reduction in the ratio of subendocardialto subepicardial myocardial-perfusion reserve index. These findings,combined with the occurrence of chest pain during stress inpatients with syndrome X, support the hypothesis that subendocardialischemia is the cause of the angina symptoms in these patients.However, whether there is an actual absolute reduction in subendocardialperfusion with stress in patients with syndrome X is unresolved,since current techniques for myocardial-perfusion cardiovascularmagnetic resonance imaging in humans do not generate reliableabsolute measures. This question might be resolved with furtherdevelopments in quantification with perfusion cardiovascularmagnetic resonance imaging, or possibly with the latest generationof high-resolution PET scanners. However, our findings are consistentwith data reported by Buchthal et al.,30 which showed reducedratios of phosphocreatine to adenosine triphosphate during handgripexercise in some women with chest pain and normal coronary arteries.This spectroscopic technique may detect cellular ischemia, butbecause of resolution constraints, it cannot currently determinethe distribution of ischemia or identify transmural variationsin ischemia. Other data that support our findings come fromBuffon et al.,31 who demonstrated release of lipoperoxides immediatelyafter pacing-induced tachycardia in all patients with syndromeX, a result consistent with ischemia–reperfusion injury.
In an open-chest dog model, subendocardial and subepicardialperfusion increased with adenosine infusion.32 However, at physiologicperfusion pressures, the ratio of subendocardial to subepicardialperfusion decreased during stress. Our results suggest thatin controls, subendocardial and subepicardial perfusion respondsto stress in a similar way. In patients with syndrome X, however,the perfusion responses were more similar to those seen in animalswith mild coronary-artery stenosis, except that in animals withcoronary disease the abnormality was confined to the territoryof the stenosed artery, whereas in patients with syndrome Xthe abnormality was more generalized. Although the perfusionabnormality was confined to the subendocardium, within thisregion the perfusion was variable, with a mean of 47 percentof segments affected. This result agrees with the findings ofLanza et al.,33 who showed impaired uptake of [123I]metaiodobenzylguanidinein patients with syndrome X, which was generalized in 4 andregional in 5 of the 12 patients studied.
The patients in our study had well-characterized syndrome X;however, other conditions may lead to microvascular dysfunction,and similar findings might be found in patients with hypertension,hypertrophic conditions, or diabetes. We were therefore carefulto exclude patients with these conditions from our study. Wehave not validated this protocol for perfusion cardiovascularmagnetic resonance in our own laboratory, but it has been validatedelsewhere.22,27 Electrocardiographic evidence of ST-segmentdepression during adenosine infusion could not be obtained,because of distortion due to the magnetic field, and no attemptwas made to interpret the ST segments. Left ventricular functionwas not measured, but other studies have not found this measurementhelpful.15,16 Further quantitative work on the heterogeneityof perfusion responses in patients with syndrome X would beuseful. Finally, we used only one type of scanner and one contrastprotocol in this study; further work is required to test whetherthese findings can be generalized.
Supported by grants from the Coronary Artery Disease ResearchAssociation (to Drs. Panting and Firmin) and from the WellcomeTrust (to Dr. Gatehouse).
We are indebted to Professor Paolo Camici and Dr. ChristineLorenz for their helpful comments on the manuscript, and toDr. Peter Burger for assistance in software development.
Source Information
From the Cardiovascular Magnetic Resonance Unit (J.R.P., P.D.G., F.G., D.N.F., D.J.P.) and the Department of Cardiovascular Medicine (P.C.), Royal Brompton Hospital and National Heart and Lung Institute, Imperial College, London; and the Department of Computing, Imperial College, London (G.-Z.Y.).
Address reprint requests to Dr. Pennell at the Cardiovascular Magnetic Resonance Unit, Royal Brompton Hospital, Sydney St., London SW3 6NP, United Kingdom.
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Cardiac Syndrome X
Huang M.-H., Ewy G. A., Bassan M., Collins A., Pennell D. J., Panting J. R., Collins P., Panza J. A.
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2=26.1, P<0.001), and the majority reported that the pain was either severe or the worst ever experienced (mean score, 4.2; P<0.001 for the comparison with the controls). 
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