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Original Research |
1 Department of Radiology, Prefectural Ehime Imabari Hospital, Ishii-cho 4-5-5,
Imabari-city, Ehime 794-0006, Japan.
2 Department of Cardiology, Prefectural Ehime Imabari Hospital, Ehime,
Japan.
3 Department of Radiology, Ehime University Medical School, Ehime, Japan.
4 Department of Medical Engineering, Division of Allied Health Sciences, Osaka
University Medical School, Osaka, Japan.
Received July 24, 2007;
accepted after revision January 18, 2008.
Address correspondence to M. Nagao
(i-minagao{at}epnh.pref.ehime.jp).
Abstract
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SUBJECTS AND METHODS. We performed cardiac MDCT at rest and stress/rest 201Tl myocardial perfusion scintigraphy (MPS) in 34 patients with suspected coronary artery disease. We reconstructed 2D long- and short-axis cardiac images in diastolic and systolic phases using raw data from coronary CT angiography. The attenuation value (in Hounsfield units) in the myocardium was used as an estimate of myocardial perfusion. We measured the subendocardial intensity of 17 segments according to the American Heart Association classification. Systolic perfusion or diastolic perfusion was calculated by dividing the subendocardial intensity at systole or diastole, respectively, for each segment by the mean value across all segments for each patient. We used stress/rest MPS to evaluate the variation in myocardial perfusion at systole and diastole for the segments diagnosed as ischemic or nonischemic.
RESULTS. Systolic perfusion for ischemic segments was significantly lower than that for nonischemic segments in 15 of 17 segments. The difference between systolic perfusion and diastolic perfusion in ischemic segments was significantly lower than that in nonischemic segments (14 of 17 segments). There was no significant difference in diastolic perfusion between ischemic and nonischemic segments (15 of 17 segments).
CONCLUSION. Our results suggest that a pattern of subendocardial hypoperfusion at systole and normal perfusion at diastole characterizes ischemic myocardium.
Keywords: cardiac imaging • coronary artery disease • ischemia • myocardium • perfusion imaging
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Contrast-enhanced MDCT has been proposed as a means of evaluating coronary artery stenosis [7, 8]; investigators have reported that contrast-enhanced MDCT enables noninvasive assessment of coronary artery disease in the clinical setting [9, 10]. Myocardial perfusion imaging with pharmacologic stress CT has been used to evaluate subendocardial ischemia in patients with coronary artery disease [11, 12]; however, assessment of hemodynamic changes on myocardial ischemia at rest using cardiac CT has yet to be performed. Progressive improvements in temporal resolution from technologic advances enable cardiac imaging with 64-MDCT to be used for assessment of myocardial blood flow during the first or second pass of contrast medium. We hypothesized that alterations in subendocardial perfusion during the cardiac cycle may be related to appearances of ischemia. In the present study, we investigated to characterize myocardial perfusion during the cardiac cycle on ischemic myocardium using contrast-enhanced 64-MDCT.
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The entry criteria were as follows: first, effort or rest stable angina (documented ST-T change on ECG or angina relieved by administration of nitroglycerin); and, second, asymptomatic patients with a high probability of coronary artery disease (i.e., multiple coronary risk factors) or abnormal findings on exercise ECG.
The exclusion criteria were as follows: first, acute myocardial infarction (within 3 months); second, unstable angina (recent onset of angina within 1 month and severe and worsening clinical symptoms); third, chronic atrial fibrillation; fourth, deteriorated renal function (serum creatinine > 1.5 mg/dL); fifth, pregnancy, hyperthyroidism, or known allergic reaction to contrast medium; sixth, severe left ventricular dysfunction (left ventricular ejection fraction < 20%); seventh, known history of bronchial asthma; eighth, congestive heart failure (class IV according to the New York Heart Association classification); ninth, greater than first-degree atrioventricular block; and, tenth, patients with areas of subendocardium with decreased attenuation approaching attenuation levels of fat (negative value) on reconstructed 2D cardiac images because this finding suggests prior subendocardial infarction.
A total of 73 patients at our institutes were enrolled in the current study from March 2006 to February 2007. After the exclusion criteria were taken into account, 34 patients (25 men, nine women; age range, 51–84 years; mean age, 69.5 years) were included in the study group; they underwent contrast-enhanced MDCT and stress/rest 201Tl MPS.
The interval between contrast-enhanced MDCT and stress MPS was within 2 weeks. During that interval, no coronary event, such as acute myocardial infarction or drug refractory angina, requiring percutaneous coronary intervention occurred.
The clinical symptoms of the study patients were effort angina (n = 14) or rest angina (n = 8). The remaining patients were symptom-free (n = 12). The patients' coronary risk factors were hypertension (n = 28), diabetes mellitus (n = 20), dyslipidemia (n = 13), and cigarette smoking (n = 8). None of the patients had a history of myocardial infarction. There were no differences in age, clinical symptoms, or coronary risk factors between men and women.
Control Group
Twenty-eight subjects (11 men, 17 women; age range, 54–84 years; mean
age, 67.9 years) were derived from the same community population to serve as a
control group. Contrast-enhanced 64-MDCT was perform ed using the same
protocol as that used for imaging the patient group; stress/rest MPS was not
performed. No significant coronary artery stenosis was observed on
contrast-enhanced 64-MDCT coronary angiography. The control subjects underwent
an evaluation similar to that of the patients, including a general medical
examination; they had no symptoms or heart illnesses and were not taking any
medication for any specific condition.
Contrast-Enhanced MDCT Protocol
A 64-MDCT scanner (LightSpeed VCT 64, GE Healthcare) was used with the
following scanning parameters: retrospective ECG gating, 912-channel detectors
along the gantry and 64-channel detectors along the z-axis, tube
voltage of 120 kV, tube current of 550–750 mA (depending on patient
size), scan field of view (SFOV) of 50 cm, gantry rotation of 0.35 second per
rotation, matrix of 512 x 512, slice width of 0.625 mm, and range of
helical pitch of 0.18–0.24. The pitch was selected on the basis of the
patient's heart rate.
A single oral dose of 25–50 mg of atenolol was administered 4 hours before MDCT if the patient's heart rate before scanning was > 65 beats per minute.
Patients were scanned in a fasting and asymptomatic state in the supine position and received oxygen at a rate of 3 L/min inhaled through a mask in preparation for scanning. The scan delay was calculated using a bolus injection of nonionic contrast medium (320 mg I/mL, 4 mL/s x 10 mL of ioversol 320; Optiray 320 syringe, Tyco Healthcare); attenuation monitored the proximal part of the ascending aorta as the region of interest (ROI). The true scan was obtained after IV injection of 40–60 mL, depending on the patient's body weight, of contrast medium at a rate of 4 mL/s.
Stress/Rest 201Tl MPS
Stress/rest 201Tl MPS was performed according to the guidelines
established by the American College of Cardiology (ACC), American Heart
Association (AHA), and American Society of Nuclear Cardiology (ASNC) for the
clinical use of cardiac radionuclide imaging
[13]. For each patient, stress
was induced pharmacologically via an IV infusion of adenosine (6-minute
infusion of 140 µg/kg/min), as described by Nishimura et al.
[14]. The patient's standard
ECG, vital signs, and general condition were continuously monitored during the
stress protocol. Three minutes after the continuous infusion of adenosine, 111
MBq of thallium-201 was injected IV and flushed with saline.
Early SPECT was performed 10 minutes after the adenosine stress test; late SPECT was performed 4 hours after early SPECT.
SPECT images were acquired using a three-headed SPECT system (GCA 9300, Toshiba Medical Systems). Tomographic reconstruction was performed using a standard filtered back-projection technique with a ramp filter to produce a transaxial tomogram. No scatter or attenuation correction was applied. From these transaxial tomograms, the long axis of the left ventricle was identified and oblique-angled tomograms were generated (i.e., vertical long- and short-axis and horizontal long-axis tomograms).
The SPECT images were visually and independently analyzed by two experienced cardiologists. The slices were displayed sequentially to assess myocardial perfusion in each vascular territory [15]. The presence or absence of re distribution related to the early images was judged visually in the 4-hour images, which were read as showing positive or negative findings for ischemia.
Analysis of Perfusion CT
Transaxial images were reconstructed using a slice thickness of 0.625 mm
and 0.4-mm increments, thereby optimizing the position of the reconstruction
window by increments or decrements of 5% of the cardiac cycle. The volume data
were transferred to a dedicated workstation (Advantage Workstation 4.2, GE
Healthcare) for postprocessing. A commercially available program (Cardiac IQ
in Advantage Windows 4.2, GE Healthcare) was used to create long-axis and
short-axis images through reconstruction with an R-R interval of 40–55%
and 70–85% of the cardiac cycle to minimize motion artifacts. Most of
the cardiac images were selected with R-R intervals of 40% and 75% for
end-systole and enddiastole, re spectively. Assignment of the left ventricular
segments was based on the ASNC/AHA statement
[15].
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Analysis of Coronary CT Angiography
Coronary CT angiograms were analyzed on a workstation (Advantage
Workstation 4.2) using the same data as those used for perfusion CT. Scans
were analyzed by consensus of two observers who were unaware of the clinical
data and were blinded to the results of stress/rest MPS.
A previously described 15-segment AHA model of the coronary tree was used [16]. Each identified lesion was examined using maximum-intensity-projection and multiplanar reconstruction techniques along multiple longitudinal axes and in the transverse plane. Lesions were classified by the maximal luminal diameter stenosis seen in any plane. Quantitative CT angiographic analysis was performed on the most severe well-defined lesion in each segment, using a previously described digital caliper method [17]. In the case of multiple lesions in a given segment, the segment was classified by the worst lesion. In the case of multiple abnormal segments per artery, the vessel was classified by the worst segment. Significant stenosis was defined as a greater than 50% reduction in diameter.
Statistical Analysis
We compared systolic perfusion, diastolic perfusion, and the difference
between systolic perfusion and diastolic perfusion in ischemic seg ments with
those values in non ischemic segments using Mann-Whitney's U test. A
probability value of less than 0.05 was considered statistically
significant.
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Comparison of Myocardial Perfusion in Ischemic and Nonischemic Segments
Systolic perfusion for ischemic segments was significantly lower than that
for nonischemic segments in 15 of 17 segments (88%). There was no significant
difference in systolic perfusion in the basal inferior and mid inferolateral
segments (Fig. 4).
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The difference between systolic perfusion and diastolic perfusion for ischemic segments was significantly lower than that for nonischemic segments in 14 of 17 segments (82%). There was no significant difference in the mid anteroseptal, apical septal, and apical lateral segments (Fig. 6).
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Comparison of Perfusion CT and Coronary CT Angiography
Representative perfusion CT images, stress/rest MPS images, and CT
angiography images for myocardial ischemia are shown in Figures
7A,
7B and
8A,
8B. Myocardium was shown using
a color scale that depicts faint low-attenuation areas more clearly than
gray-scale. The color scales were classified into six steps using mean + 2 SD,
mean + SD, mean, mean – SD, and mean – 2 SD for each case.
Perfusion CT images showed a pattern of endocardial hypoperfusion at systole
and normal perfusion at diastole in the most ischemic segments. We defined
this appearance as the ischemic pattern.
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Several physiologic studies have revealed the influence of cardiac contraction on systolic coronary flow and transmural blood flow distribution [2, 3, 18]. Cardiac contraction predominantly affects subendocardial vessels and impedes subendocardial flow more than subepicardial flow regardless of left ventricular pressure [2]. Flynn et al. [3] pointed out that the decrease in subendocardial flow and the increase in subepicardial flow are caused by retrograde pumping of blood from the deep layer to the superficial layer of the left ventricle because little or no blood enters the myocardium from the extramural arteries during systole. Retrograde systolic blood flow contributes to the vulnerability of the subendocardium to ischemia [6]. Microvascular resistance is affected by ischemia, with the effects most prominent in the subendocardium during systole and in the subepicardium during diastole [1, 4]. The capillary microvessels showed a larger phasic change in microvascular resistance, which may function to maintain the capillary patency during systole [19]; consequently, the increase in subendocardial resistance induced by ischemia causes a decrease in the capacitance of microvessels during systole.
Adenosine stress on MPS is not exactly the same as systolic strain at rest on myocardial CT. The increase in capillary flow velocity with adenosine was less than the increase in arterial flow [20]. A widely accepted explanation for adenosine-induced ischemia is the pre sence of coronary steal, either intercoronary dependent or epicardial steal from the endocardium [21]. The decrease in pressure caused by a coronary stenosis results in a greater decrease in the diameter of the subendocardial arter ioles than in the subepicardial arterioles; furthermore, stenosis selectively reduces the dilatory response of subendocardial arterioles [5]. Therefore, adenosine decreases in the predominant subendocardial blood flow in the territory with epicardial coronary stenosis.
As indicated by the results of the present study, perfusion CT at rest shows systolic endocardial hypoperfusion in most territories of stenosed coronary arteries. This finding suggests that the effect of adenosine resembles the influence of cardiac contraction at rest in ischemic myocardium.
Study Limitations
We acknowledge the following limitations of this study: First, motion
artifact caused by myocardial wall movement occasionally occurs, especially in
systole, thereby affecting the diagnostic accuracy of imaging for the
detection of coronary artery stenosis
[22]. Horizontal bands caused
by the motion artifact were sometimes seen on the reconstructed 2D cardiac
images. The horizontal bands artifactually decrease the intensity in the
inferior and anterior walls more than in the septal and lateral walls. This
might make no significant difference in systolic perfusion between ischemia
and nonischemia in part of the inferior wall
(Fig. 4).
Second, systolic perfusion in the cranial portions of the left ventricle tended to be higher than those in the caudal portions. Depending on the temporal resolution of the scanner, there is usually a delay in imaging the more caudal portion of the heart. This delay could account for the fact that ischemia was less commonly identified in the inferior heart (78%) in the RCA territory than in 93% of the LAD territory.
An additional limitation in evaluating the subendocardium only, which is adjacent to the left ventricle, is the phenomenon of pseudoenhancement—that is, when attenuation values from a hyperattenuating structure "bleed into" a nearby low-attenuation structure. Pseudoenhancement could confound assessment of vasculature in the wall of the ventricle, especially along the subendocardial surface and would be expected to artifactually elevate measured attenuation values in the subendocardium, which would make our method less sensitive.
Using the mean values for control subjects separated ischemic segments from nonischemic segments with a sensitivity of more than 80% and with a specificity of more than 60%. The systolic perfusion and diastolic perfusion values and the difference between systolic and diastolic perfusion for control subjects varied among regions, which might be related to anatomic characterization in left ventricular contractile function. This regional variation might make our method have a lower specificity. When comparing CT with MPS for the assessment of myocardial perfusion, we should discuss sensitivity and specificity of analysis by patient rather than by segment. However, there were only two patients without ischemic segments that were assessed on MPS. Because of small sample size, the sensitivity and specificity of MPS in detecting ischemia were not elucidated. In future studies, we will add many nonischemic patients and evaluate the diagnostic accuracy by patient.
Conclusion
Quantification of perfusion CT images with 64-MDCT allows characterization
of intramural myocardial perfusion in patients with myocardial ischemia. The
results of the present study suggest that myocardial ischemia is characterized
as systolic endocardial hypoperfusion with normal perfusion at diastole.
Perfusion CT has potential as a noninvasive method for detecting myocardial
ischemia at rest.
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