Risk Stratification by Adenosine Stress Cardiac Magnetic Resonance in Patients With Coronary Artery Stenoses of Intermediate Angiographic Severity
Christina Doesch, MD*,
Achim Seeger, MD ,
Jörg Doering, MD,
Christian Herdeg, MD*,
Christof Burgstahler, MD*,
Claus D. Claussen, MD,
Meinrad Gawaz, MD*,
Stephan Miller, MD,
Andreas E. May, MD*,*
* Department of Cardiology, Eberhard Karls University, Tübingen, Germany
Department of Radiology, Eberhard Karls University, Tübingen, Germany
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Abstract
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Objectives: The purpose of this study was to determine the role of adenosine stress cardiac magnetic resonance (CMR) for risk stratification in patients with coronary artery stenoses of intermediate angiographic severity.
Background: Coronary angiography only provides a morphological description of coronary lesions. As the patient's prognosis is closely related to the functional significance of angiographically detected coronary lesions, a functional assessment is desirable in patients with coronary artery stenoses of intermediate severity.
Methods: Myocardial perfusion measurements at rest and adenosine stress were performed on 81 patients (75.6% male, mean age 64.2 years) with stable angina pectoris (AP) and coronary artery stenoses of intermediate angiographic severity (50% to 75%). Regardless of the CMR result, all patients were treated conservatively with an intensified medical treatment, and a follow-up was performed after 18 ± 8 months and 30 ± 8 months. The primary end point was defined as a major adverse cardiac event (MACE): all-cause death, stroke, acute coronary syndrome; the secondary end point was defined as target vessel revascularization. Furthermore, AP and dyspnea were evaluated.
Results: After the follow-up period of 30 ± 8 months, 9 patients with perfusion deficit (PD) suffered from MACE, whereas no MACE occurred among the 36 patients without PD (p = 0.014). Among patients who had MACE, the number of ischemic segments (2.3 ± 1.6 vs. 1.4 ± 1.6, p = 0.0025) was significantly higher, whereas the number of delayed enhancement segments did not differ (1.4 ± 1.6 vs. 1.6 ± 2.3, p = 0.4). Target vessel revascularization was required in 38% of patients with PD and 6% of patients without PD (p = 0.005). In addition, the percentage of freedom from AP and dyspnea at the follow-up after 18 ± 8 months was significantly lower among patients without perfusion deficit (69.4% vs. 15.6%; p = 0.0001). After a follow-up period of 30 ± 8 months, the rate of AP (11.1% vs. 8.3%, p = 0.33) as well as the percentage of patients free of symptoms was similar in both groups (77.8% vs. 88.9%, p = 0.82).
Conclusions: Adenosine stress CMR may help to identify patients at risk who benefit from intensified medical treatment and close follow-up.
Key Words: CAD • intermediate angiographic severity • perfusion • adenosine stress CMR • prognosis
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Abbreviations and Acronyms
| | ACS = acute coronary syndrome | | AP = angina pectoris | | CA = coronary angiography | | CAD = coronary artery disease | | CMR = cardiac magnetic resonance | | FFR = fractional flow reserve | | MACE = major adverse cardiac event | | PCI = percutaneous coronary intervention | | PD = perfusion deficit | | QCA = quantitative coronary angiography | | SPECT = single-photon emission computed tomography | | TVR = target vessel revascularization |
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Coronary angiography (CA) is the gold standard for the evaluation of coronary artery stenoses. In patients with mild or severe stenoses, the angiographic assessment is usually straightforward. However, the correct interpretation of coronary lesions of intermediate severity (diameter of stenosis 50% to 75%) is challenging (1–3). CA only provides a morphological description of coronary lesions. The patient's prognosis, however, is closely related to the functional significance of angiographically detected coronary lesions (4–7). Therefore, a functional assessment is desirable in patients with coronary artery stenoses of intermediate severity.
Former stress single-photon emission computed tomography (SPECT) studies (8–11) proved that inducible ischemia is a predictor of future cardiac events in patients with known or suspected coronary artery disease. However, it requires the exposure to ionizing radiation. Adenosine stress cardiac magnetic resonance (CMR) is a noninvasive imaging modality that has been shown to accurately predict coronary artery disease (CAD) in patients scheduled for CA (12–14). A study (15) comparing adenosine stress CMR with fractional flow reserve (FFR) as the gold standard could prove that stress rest perfusion CMR is able to distinguish hemodynamically relevant from nonrelevant coronary lesions with high sensitivity and specificity. Therefore, adenosine stress CMR might facilitate patient selection, especially among patients with diabetes or with diffuse CAD and several intermediate coronary artery stenoses, in whom symptoms cannot reliably be attributed.
As the ischemic burden correlates with the cardiac event rate (16), the aim of our study was to determine the role of adenosine stress CMR for the identification of patients at risk with coronary artery stenoses of intermediate angiographic severity. Therefore, we investigated whether perfusion CMR is a suitable technique to distinguish between patients for whom an intensive medical treatment is the optimal strategy and patients who may profit from close follow-up and—potentially—from early revascularization.
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Methods
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Study design and patients.
Patients referred to our hospital for elective surgery were consecutively screened between January 2006 and May 2007. Patients were eligible if they had 1 or more target lesions of  50% to  75% diameter stenoses. Patients with multivessel disease were also included if no other main epicardial vessel showed a lesion suitable for percutaneous coronary intervention (PCI) beyond the target vessel.
All patients who met the study criteria agreed to participate and had no contraindication to CMR (e.g., pacemaker, claustrophobia) or to adenosine (e.g., more than second-degree atrioventricular block, severe obstructive pulmonary disease) were recruited. An adenosine stress CMR was performed in 85 patients. In 4 patients, adenosine stress CMR was discontinued because of claustrophobia (n = 2), angina (n = 1), and amblyacousia (n = 1).
All patients gave written consent for participation, and the study was approved by the local ethics committee. Adenosine stress CMR was performed 7.4 ± 8.0 days after CA to determine the functional significance of the intermediate stenoses. To ensure minimal basal blood flow and a maximal vasodilatory response to adenosine, patients were instructed to refrain from smoking and ingesting tea, coffee, and chocolate 24 h before the adenosine stress CMR. Patients were monitored for potential complications throughout the imaging procedure. Heart rate and blood pressure were continuously monitored during rest-stress examinations. All adenosine stress CMR and angiograms were reassessed by 2 experienced readers for clinical and angiographical stability. All patients with intermediate stenoses that seemed to be angiographically stable were discharged with optimized medical therapy that was intensified during the following weeks to maximally tolerated doses. The intensity of medical therapy was evaluated on the ranking of medications by drug class modified according to Mahmarian et al. (5).
At 18 ± 8 months and 30 ± 8 months, clinical information was obtained from patient telephone interviews, contact with the patients' physicians, and hospital records. A standardized questionnaire was used during the telephone interviews to assess patient symptoms, major adverse events, secondary end points, and medications. Typical angina pectoris (AP) was classified according to the Canadian Cardiovascular Society classification of AP as I to IV (17) by experienced cardiologists who were blinded to the CMR results.
Primary end points were defined as all causes of deaths, stroke, and acute coronary syndrome (ACS). According to the American College of Cardiology/American Heart Association (ACC/AHA) guidelines (18,19), ACS comprises unstable angina, non–ST-segment elevation myocardial infarction, and ST-segment elevation myocardial infarction. Non–ST-segment elevation myocardial infarction was defined as typical chest pain with no ST-segment elevation and an increase in creatine kinase and creatine kinase-myocardial band to >2 times the upper limit of normal, with a creatine kinase-myocardial band fraction of 4% or more of total creatine kinase or a positive troponin I or T. An ST-segment elevation myocardial infarction was diagnosed if ST-segment elevation of 1 mm in 2 or more leads or ST-segment depression of at least 2 mm was present. Patients with new angina or worsening angina without significant ST-segment elevation or increased troponin were classified as unstable angina. The secondary end points included TVR and AP or dyspnea at follow-up.
CA and image interpretation.
CA was performed with a conventional angiography unit (Integris H, Philips Medical Systems, Hamburg, Germany). Coronary artery stenoses were imaged in the center of the field from multiple projections, and overlap of side branches and foreshortening of relevant coronary arteries were avoided as much as possible.
Quantitative coronary angiography.
QCA was performed by 2 experienced interventional cardiologists unaware of the CMR results using the QCA software (ACA, Philips Medical Systems). The diameter of the guiding catheter, which ranged from 5- to 7-F, was used as the calibration reference.
Measurements were made in the frame that clearly demonstrated the stenotic lesion and included the reference sites. From the QCA images, the angiographic percent area stenosis was calculated by selecting the angiographically normal proximal and distal segments as the reference sites. Under these conditions, the minimal diameter of the stenosis was also determined. The maximal and minimal distances from the center of the stenotic lesion to the outline of the vessel wall were measured. Finally, the angiographic length of the stenosis was determined by measuring the distance between the proximal and distal shoulders of the stenosis. A reduction in the luminal diameter of 50% to 75% was considered as stenosis of intermediate severity.
CMR imaging protocol.
The CMR imaging was performed by using 1.5-T system (Magnetom Sonata, Siemens Medical Systems, Erlangen, Germany) equipped with high-performance gradients (maximum amplitude 40 mT/m, slew rate 200 mT/m) (20). An 18-gauge catheter was inserted into an antecubital vein for injection of the contrast agent and into an antecubital vein of the contralateral arm for the adenosine infusion. CMR-compatible electrocardiography leads were placed on the patient's chest. Imaging was performed by using a phased-array surface coil as a receiver.
Adenosine perfusion CMR.
Left ventricular short-axis orientation was used for perfusion CMR. For myocardial perfusion measurements, 3 representative short-axis sections were obtained, 1 each in the basal, midventricular, and apical regions of the left ventricle according to the segment model of the AHA (21). Pharmacological stress was applied using adenosine, which was administered intravenously at 140 µg/kg body weight over 4 to 5 min under electrocardiographic and blood pressure monitoring. Acquisition of perfusion CMR images was started a few seconds after the injection of 0.1 mmol gadopentetate dimeglumine per kilogram of body weight (Magnevist, Schering, Berlin, Germany); perfusion images were obtained by using a 2-dimensional saturation-recovery turbo-flash sequence (field of view 300 to 340 mm, time to repeat/time to echocardiogram 2.4 ms/1.08 ms, flip angle 15°, bandwidth 840 Hz/pixel, voxel size 2.1 x 1.6 x 8 mm) in parallel acquisition mode with an acceleration factor of 2. Parallel imaging to shorten the acquisition time was used. The bolus injection of gadopentetate dimeglumine (at a flow rate of 4 ml/s) was followed with a 25-ml flush of 0.9% NaCl (at a flow rate of 4 ml/s).
A delay of 10 min after the stress examination allowed residual gadopentetate dimeglumine to be washed out of the myocardium. A second bolus of 0.1 mmol gadopentetate dimeglumine was injected, and rest perfusion images were obtained with the same orientation and position before and after the administration of adenosine.
Late enhancement.
Ten minutes after resting perfusion, delayed enhancement images were acquired in continuous short-axis and 4- and 2-chamber long-axis views using an inversion-recovery gradient-recalled echocardiogram MR sequence. Parameters for inversion-recovery turbo-flash 2-dimensional sequences were as follows: field of view 300 to 340 mm, time to repeat/time to echocardiogram 9.56 ms/4.38 ms, TI 200 to 360 ms, flip angle 25°, matrix 166 x 256, and section thickness 6 mm. The inversion time was chosen to minimize the signal from normal myocardium.
Image analysis.
Myocardial segments were assigned to the 3 coronary arterial territories according to the 17-segment model of the AHA standardized myocardial segmentation (21). An abnormal CMR study was defined by the presence of a perfusion defect during adenosine infusion. Perfusion scans were interpreted qualitatively by consensus of 2 experienced readers blinded to angiography. A perfusion deficit was defined as abnormal if it was darker than the surrounding myocardium and if it persisted more than 5 images beyond initial peak enhancement of the segment that appeared most normal. Delayed enhancement images were displayed with a gray scale to optimally show normal myocardium as dark and regions of delayed enhancement or fat as bright tissue. Myocardial ischemia was defined as a segment with a perfusion deficit at stress and no hyperenhancement at delayed enhancement. A myocardial scar was defined as a segment with a hyperenhancement at delayed enhancement.
Statistical analysis.
Mean values between 2 categories were compared with a 2-tailed unpaired t test. The chi-square test was used for dichotomous analysis of categorical data. Chi-square statistics were used to compare baseline characteristics between patients with intermediate coronary stenoses and perfusion deficits on CMR and normal CMR images. The log-rank test (Mantel-Cox) was applied for the evaluation of secondary end points. Multivariate Cox regression analysis was used to compare the association of TVR with perfusion deficits seen on CMR, cardiovascular risk factors, sex, and age. Kaplan-Meier survival was used to estimate event-free survival and survival of death from cardiovascular causes. All probability values reported are 2-sided, and a p value <0.05 was considered to indicate statistical significance. Statistical analysis was done with SPSS software, version 15 for Windows (SPSS, Inc., Chicago, Illinois). Event classification was performed by an investigator blinded to the result of the CMR and the angiogram.
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Results
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Baseline characteristics.
Eighty-one consecutive patients with intermediate stenoses assessed by CA and stable AP were enrolled. According to the adenosine stress CMR result, patients were assigned either to the group with perfusion deficit or to the group without perfusion deficit, as illustrated in Figure 1. The baseline characteristics of the 2 study groups were comparable (Table 1). Moreover, there was no difference in the severity or length of the stenotic lesion assessed by quantitative CA between the 2 groups (Table 2). The medication during follow-up was not significantly different in both groups, either (Table 3). Telephone follow-up was obtained for all patients (100%) after 18 ± 8 months and 30 ± 8 months.
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Figure 1 Examples of 2 Representative CMR Studies
The coronary angiograms (upper panel) of 2 representative patients with stenoses of intermediate angiographic severity of the right coronary artery (arrows). In both patients, a cardiac magnetic resonance (CMR) study including adenosine stress and rest perfusion as well as delayed enhancement was performed to determine the hemodynamic relevance of the stenosis. One patient (left panels) shows no perfusion deficit (PD) on stress perfusion and a normal delayed enhancement. The other patient (right panels) also has a normal delayed enhancement but exhibits a perfusion deficit on the inferior wall during adenosine stress (arrow), indicating stress-induced myocardial ischemia. The example illustrates that CMR is able to provide information about the functional significance of angiographically detected intermediate coronary lesions.
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Extent of PD.
The extent, type, and location of the ischemic PD, the delayed enhancement (DE), and the total PD is displayed in Table 4. There is no difference in the extent and location of DE in both groups (1.9 ± 2.4 vs. 1.2 ± 2.1, p = 0.7). However, only 45 patients display an ischemic PD of 2.4 ± 1.4 segments, and therefore present with a significantly extended total PD (4.3 ± 2.6 vs. 1.2 ± 2.1, p < 0.001). The ischemic PD is equally distributed to all 3 coronary artery territories, and there is no correlation between the number of ischemic PD segments assessed by CMR and the degree of stenosis analyzed by QCA.
The presence and extent of ischemia did not influence medial therapy or the decision for TVR. All patients were assigned to an optimized medical therapy regardless of their PD. Analyzing the number of ischemic segments and segments with DE, it becomes evident that the number of ischemic segments (2.3 ± 1.6 vs. 1.4 ± 1.6, p = 0.0025) was significantly increased in the 9 patients who had a subsequent major adverse cardiac event (MACE) during the follow-up period of 30 ± 8 months, whereas the number of DE segments did not differ (1.4 ± 1.6 vs. 1.6 ± 2.3, p = 0.4). At the first follow-up after 18 ± 8 months, the number of ischemic PD segments in the 28 patients complaining of persistent stable angina was significantly elevated (3.0 ± 1.9 vs. 2.0 ± 2.1, p = 0.04); however, there was no difference in the number of DE segments (2.1 ± 2.8 vs. 1.3 ± 2.0, p = 0.18). After the follow-up period of 30 ± 8 months, only 8 patients still complained about stable angina. Comparing the number of ischemic segments at initial presentation of these patients with the 73 symptom-free patients, the number of ischemic PDs did not vary (2.3 ± 2.3 vs. 2.3 ± 2.2, p = 0.97). Analyzing the patients who underwent TVR during the follow-up period of 30 ± 8 months, there was also no significant difference regarding the number of ischemic segments in patients who underwent TVR during follow-up and patients who did not need TVR during follow-up (1.9 ± 1.6 vs. 1.4 ± 1.6, p = 0.29).
Incidence of major adverse events.
Table 5
shows the incidence of major adverse events (primary end point). During the follow-up period of 30 ± 8 months, no patient died or had a stroke. In the group of patients without a PD, no patient had any major adverse event. In contrast, in the group of patients with a PD, 9 of 45 (20%) had an ACS (p = 0.014 for comparison with the group without a PD). Figure 2
shows the cumulative event-free survival from major adverse events depending on the result of the initial CMR.
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Figure 2 Primary End Points
Primary end points: Kaplan-Meier curves demonstrate the event-free survival (%) of patients without perfusion deficit (orange line) and of patients with perfusion deficit (PD) (brown line) on adenosine stress test during the follow-up period of 30 ± 8 months. Differences between curves are statistically significant (p = 0.014 by log-rank test). As all major adverse events (death, stroke, acute coronary syndrome) occur in the patient group with a PD on adenosine stress test, the occurrence of a PD during adenosine stress cardiac magnetic resonance seems to indicate an enhanced risk of developing adverse cardiac events.
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Incidence of secondary end points.
Secondary end points in both groups are described in Table 6
after 18 ± 8 months and after 30 ± 8 months. It should be noted that in patients with PD, the rate of TVR after 18 ± 8 months (28.9% vs. 5.5%, p = 0.05) and after 30 ± 8 months (37.8% vs. 5.5%, p = 0.05) was significantly higher. The result from multivariate Cox regression analysis for TVR at 30 ± 8 months, including sex, age, and cardiovascular risk factors, and ischemic PD identified the existence of ischemic PD as the only independent factor influencing the occurrence of TVR during follow-up (0.14, 95% confidence interval: 0.031 to 0.627, p = 0.01). At a follow-up period of 18 ± 8 months, AP was more frequent among patients with PD (53.3% vs. 11.1%, p = 0.01) (Fig. 3). At this time, patients with PD also seemed to suffer more frequently from dyspnea; however, this was not significantly different (p = 0.08). Despite optimal medical therapy in both groups, the percentage of patients free from AP or dyspnea after 18 ± 8 months was significantly higher in the patient cohort without PD (69.4% vs. 15.6%, p = 0.0001). However, after a follow-up period of 30 ± 8 months, the rate of AP in patients who presented initially with PD and patients without PD was not different any more (11.1% vs. 8.3%, p = 0.33). This result also applied to the percentage of patients free of symptoms that aligned in both groups (77.8% vs. 88.9%, p = 0.82).
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Figure 3 Secondary End Points
Secondary end points: the percentage of patients with target vessel revascularization (TVR), angina, and dyspnea as well as patients free of symptoms during follow-up is illustrated. At the follow-up period of 18 ± 8 months (A), the occurrence of TVR (28.9% vs. 5.5%, p = 0.005) and AP (53.5% vs. 11.1%, p = 0.01) was significantly more frequent among patients with perfusion deficit (PD) (brown bars); whereas among patients without PD (orange bars), the percentage of patients free of symptoms was significantly elevated (69.4% vs. 15.6%, p = 0.0001). At the follow-up period of 30 ± 8 months (B), TVR was required for 37.8% of patients with PD (brown bars) but for only 5.5% of patients without PD (orange bars) (p = 0.005). However, the percentage of patients free from angina and patients without symptoms was not significantly different for both groups.
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Discussion
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The primary objective of this study was to analyze the prognostic value of PD detected on adenosine stress CMR in patients with intermediate coronary lesions. Our study suggests that patients with intermediate coronary artery stenoses and a normal CMR represent a patient cohort with an excellent prognosis who benefit from intensive medical treatment and do not require coronary revascularization. In contrast, PD on adenosine stress CMR in patients with intermediate stenoses seem to depict a patient cohort that at least requires a close follow-up. Patients with a PD detected on adenosine stress CMR seem to be at enhanced risk for the development of adverse cardiac events and to have a more pronounced need for TVR.
These findings are in line with previous studies demonstrating that stress-induced myocardial ischemia is a valuable prognostic marker for patients with stable AP as proven by various studies using the SPECT technique (4,22–24) or pharmacological stress echocardiography (25–28). In patients with intermediate stenoses, the DEFER (Deferral Versus Performance of PTCA in Patients Without Documented Ischemia) study (6) showed that the 5-year outcome of patients after deferral of PCI was excellent and could not be improved by stenting. However, the decision to defer PCI in this study was based on invasive functional flow reserve measurement, and the majority of patients in the DEFER study had a single stenosis. Our results suggest that this also seems to be valid for adenosine stress CMR in patients with intermediate stenoses and even in patients with multivessel disease, since 75% of our patients had 2- or 3-vessel disease.
All MACE occurred in the patient subgroup with a PD on CMR, and the rate of TVR after 30 ± 8 months accounted for 37.8% versus 5.5% in the group with a normal CMR (p = 0.005). Conversely, 62% of patients with a PD on the initial CMR did well with intensified medical treatment alone. These results indicate that among patients with functionally relevant intermediate coronary stenoses, optimized medical therapy is a successful strategy for the majority of patients. The significant reduction in stable angina to only 8 of 81 (9.9%) and the increased number of patients free from symptoms, 64 of 81 (79%), after the follow-up period of 30 ± 8 months suggests that the optimal medical treatment and PCI, if indicated, was effective in suppressing ischemia in our patient cohort. Our data indicate that adenosine stress CMR is able to determine the ischemic significance of an intermediate stenosis and allows a prognostic evaluation. It helps to identify patients who are at enhanced risk and, therefore, may profit from close follow-up.
Study limitations.
The current number of 81 patients did not allow us to additionally randomize patients with a PD for conservative versus interventional treatment. Therefore, we can only demonstrate that patients with a PD are at higher risk for adverse events. Thus, this study does not allow the drawing of conclusions that interventional treatment is superior for patients with PD. Future prospective randomized trials will have to clarify this aspect.
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Conclusions
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Our study suggests that patients with coronary artery stenoses of angiographic intermediate severity causing a PD in the initial CMR are at higher risk for MACE within the following year and a half. Therefore, these patients should receive intensified medical treatment, and close follow-up is necessary. Whether these patients would further benefit from coronary revascularization has to be clarified in the future. Nevertheless, deferring PCI in patients with intermediate coronary artery stenoses and no PD on CMR seems to be safe.
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Acknowledgments
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The authors thank Dr. Stephan Lindemann, Prof. Dr. Stephen Schroeder, and the staff of the Cardiac Catheterization Laboratory for help in the performance of this study. Special thanks go to Dr. Bernhard Klumpp, Dr. Michael Fenchel, and Dr. Ulrich Kramer of the Radiology Department of the University of Tübingen for their assistance with CMR image reading.
* Reprint requests and correspondence: Prof. Dr. Andreas E. May, Department of Cardiology, Eberhard Karls University, Otfried-Müller Strasse 10, D-72076, Tübingen, Germany (Email: Andreas.May{at}med.uni-tuebingen.de).
Manuscript received May 22, 2008;
revised manuscript received November 5, 2008,
accepted November 10, 2008.
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E. Nagel
Taking the Last Hurdles: Magnetic Resonance Myocardial Perfusion Imaging
J. Am. Coll. Cardiol. Img.,
April 1, 2009;
2(4):
434 - 436.
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Abstract
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