Left ventricular wall motion abnormalities as well as reduced wall thickness can cause false positive results of routine SPECT perfusion imaging for detection of myocardial infarction
Heiko Mahrholdt1,*,
Andreji Zhydkov1,
Stefan Hager1,
Gabriel Meinhardt1,
Holger Vogelsberg1,
Anja Wagner2 and
Udo Sechtem1
1Division of Cardiology, Robert-Bosch-Krankenhaus, Auerbachstrasse 110, 70376 Stuttgart, Germany
2Duke Cardiovascular MR Center, Durham, NC, USA
Received 21 October 2004; revised 3 May 2005; accepted 2 June 2005; online publish-ahead-of-print 8 July 2005.
* Corresponding author. Tel: +49 711 8101 3456; fax:+49 711 8101 3795. E-mail address: heiko.mahrholdt{at}rbk.de
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Abstract
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Aims The relationship between wall thickness, wall thickening, wall motion, and single-photon emission computed tomography (SPECT) results for detection of myocardial infarction has never been systematically evaluated in a clinical setting. In particular, the discussion whether non-ischaemic regional wall motion abnormalities and reduced wall thickness can cause SPECT to be false positive for infarct detection remains unsettled.
Methods and results We therefore evaluated patients presenting with left bundle branch block (LBBB) and only included them in the analysis if any coronary artery disease (CAD) had been ruled out by angiography. LBBB is known to cause septal wall motion abnormalities as well as to reduce systolic septal wall thickness. Thus, LBBB is a good non-ischaemic clinical model to evaluate the influence of wall thickness and wall motion on the homogeneity of tracer distribution in resting SPECT images. SPECT revealed fixed defects in all 139 patients initially identified for possible enrolment. CAD was found to be present by angiography in 120 patients. The remaining 19 patients without any CAD underwent cardiovascular magnetic resonance (CMR) and were included in the study. Evaluation of SPECT using a 72-segment model revealed septum-related fixed defects in all 19 patients. Every defect was interpreted as myocardial infarction by blinded observers. The comparison of nuclear results to the gold standard CMR demonstrated that none of the fixed SPECT defects did represent myocardial infarcts. Defects, however, exactly matched areas of wall motion abnormalities as well as regions with impaired wall thickness as demonstrated by CMR. On a segmental basis, we found a strong relationship between wall motion and reduced wall thickness on one hand and SPECT defects on the other hand. For example, only 5% of segments with normal wall motion were false positive by SPECT for myocardial infarction, whereas 93% of all dyskinetic segments were found to be false positive (P<0.01). Comparing wall thickness to SPECT results revealed that 58% of segment in which wall thickness was 1 SD below the mean and 93% of segments in which wall thickness was 2 SD below the mean showed fixed defects by SPECT. Conversely, only 0.5% of segments in which wall thickness was above the mean were affected by false positive SPECT results (P<0.01).
Conclusion Wall motion abnormalities as well as impaired myocardial wall thickening and wall thickness can cause false positive results of resting SPECT myocardial perfusion imaging for detection of myocardial infarction in the absence of myocardial infarct scars and CAD.
Key Words: Myocardial infarction Magnetic resonance imaging Left bundle branch block Single-photon emission computed tomography
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Introduction
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Single-photon emission computed tomography (SPECT) myocardial perfusion imaging is currently used in the clinical routine to rule out coronary artery disease (CAD) in patients presenting for workup of heart failure.1 In those patients, the diagnosis of CAD is frequently made if SPECT detects fixed perfusion defects presumably representing areas of previous myocardial infarction. However, there are some experimental and clinical reports indicating that wall motion abnormalities as well as reduced wall thickness may lead to fixed SPECT defects in the absence of myocardial infarction.25 Therefore, the assumption that the presence of fixed perfusion defects can be equated with the presence of myocardial infarction and hence ischaemic heart disease may be erroneous.
This is of clinical importance because reduced wall thickness and wall motion abnormalities are not limited to ischaemic heart disease, but are frequent findings in non-ischaemic heart diseases such as dilated or inflammatory cardiomyopathy. In those patients, the presence of resting perfusion defects on SPECT images could result in misinterpretation potentially causing suboptimal patient management decisions.
To our knowledge, the relationship between wall thickness, wall thickening, wall motion, and SPECT results for detection of infarction has not been systematically evaluated in a clinical setting. In particular, the discussion whether regional wall motion abnormalities and reduced wall thickness can cause SPECT to be false positive for infarct detection remains unsettled, because until recently, there was no non-invasive method available, which could serve as an in vivo gold standard to which SPECT results could be compared.
To further clarify the issue, we used cardiovascular magnetic resonance (CMR), which is a new technique allowing visualization and quantification of wall motion abnormalities as well as myocardial infarcts with
50-fold the spatial resolution of SPECT. This technique has been validated against histopathology as well as positron emission tomography and is considered to be a new gold standard for in vivo infarct assessment.69
Consequently, using CMR as gold standard, we evaluated whether regional wall motion abnormalities and reduced wall thickness can cause false positive results for SPECT detection of myocardial infarction in a clinical model of non-ischaemic wall motion abnormalities after any CAD was ruled out by angiography. Our study design consisted of both SPECT and CMR imaging in patients presenting with permanent left bundle branch block (LBBB), which is known to cause regional septal wall motion abnormalities as well as to reduce systolic septal wall thickness.10,11 Patients with non-ischaemic LBBB, thus, are excellent clinical models of those conditions suspected to affect the accuracy of SPECT.
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Methods
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Patient population
One-hundred and thirty-nine patients presenting with LBBB were initially identified for enrolment. All patients had fixed perfusion defects detected by technetium agent based SPECT (sestamibi or tetrofosmine) and underwent cardiac catheterization at our institution.
One-hundred and twenty patients were found to have CAD by angiography (stenosis>50% include 56 patients; plaques visible by angiography include 64 patients). Thus, these patients were excluded. The remaining 19 patients in whom any CAD was completely ruled out by coronary angiography were included in the study and underwent cine and contrast CMR imaging for detection of wall motion abnormalities and myocardial infarction.
SPECT imaging
Technetium-based routine rest and stress SPECT imaging was performed in every patient in an outpatient setting prior to inclusion. A standardized stress protocol using adenosine as pharmacological stressor was applied. For all nuclear scans, a dual-detector gamma camera (either ADAC Vertex or Siemens E-Cam) was used. SPECT images were acquired using a clinical routine protocol with 64 projections, each for 25 s, in a circular 180° orbit. After a qualitative clinical read by consensus of two observers, the presence of infarction by SPECT was determined for each segment applying an automated three-dimensional computer algorithm according to the method described by investigators at Cedars-Sinai Hospital in Los Angeles, California, USA1214 adapted for the use of a 72-segment model as displayed in Figure 1.

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Figure 1 Segmental model superimposed on cine CMR, SPECT, and contrast CMR images (from left to right). Cine and contrast CMR images were read in a 72-segment model (six slices with 12 segments). Wall motion was scored as 0=normal, 1=hypokinetic, 2=severe hypokinetic, 3=akinetic or 4=dyskinetic for each segment (left panel). Contrast enhancement was defined as mean signal±2SD and also assessed for each segment in a 72-segment model (right panel). SPECT images were analysed in the same segmental model. A SPECT defect was defined according to the method described by Kang et al.12 and Germano et al. (see text for detailed references).
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CMR imaging
CMR images of all patients were acquired using a clinical 1·5 T scanner (Siemens, Sonata, Erlangen, Germany) with a steady state free precession for cine- and an IR-FLASH pulse sequence for contrast imaging as previously described.6 Briefly, we obtained cine and contrast short-axis views from 1 cm below the level of the mitral-valve insertion throughout the whole left ventricle during repeated breath holds. Contrast images were acquired between 5 and 30 min after contrast administration (gadopentetate dimeglumine 0·10 mmol/kg bodyweight) constantly adjusting inversion time to null normal myocardium. In-plane image resolution was typically 1·2x1·6 mm and slice thickness was 6 mm with a 4 mm gap. We assessed images of patients and scored for the presence of infarction as well as wall motion abnormalities and wall thickness as previously described using a 72-segment model (12 segments per slice, six slices) displayed in Figure 1. Segments representing the left ventricular (LV) outflow tract were excluded from analysis (n=40). In brief, two observers scored all 1328 segments of cine images by consensus, according to the following scheme: 0, normal wall motion; 1, hypokinesia; 2, severe hypokinesia; 3, akinesia; 4, dyskinesia. They also measured systolic and diastolic wall thickness for each segment using a centreline method-based computer algorithm.15 Cumulative wall thickness during the cardiac cycle was introduced as an additional parameter in order to account for the fact that SPECT measures counts in a certain segment over a long period of time thus averaging the effects of wall thickness changes during the cardiac cycle. Cumulative wall thickness was therefore calculated as the average of systolic and diastolic wall thickness for each segment. All 1328 segments of contrast images were also scored by consensus as 0, no infarction or 1, infarction present.
Statistical analysis
Continuous data are expressed as mean±SD except where specified. To investigate the dependence of the probability of a false positive segment on either of the covariates wall motion score, systolic wall thickness, cumulative wall thickness, or diastolic wall thickness, four logistic regression models were fitted. The first one of the just mentioned variates is an ordered categorical variable with five levels. The three variates concerning thickness are basically continuous variables; however, for our analysis, we split them up in ordered categorical variables with five levels. These levels are given by mean, mean±SD, and mean±2SD. Mean and SD were computed for all three thickness variables across all patients. To account for the non-independence of the segmental data, a repeated-measures variable for the patient was added. Hence, we arrived at the following logistic mixed effects model with a random intercept ui:
Here, P(Yis=1|ui) is the conditional probability of the sth segment of the ith patient to be diagnosed as false positive given that the unknown random effect of the ith patient equals ui; Xisl equals one, if the respective covariate of patient i and segment s is found to be realized in covariate level l, and it equals zero otherwise; ui is considered to be the realization of the ith random variable of a sequence of I independent N(0, ó2)-distributed variables with unknown variance ó2 and a total number of I=19 patients.
is a deterministic intercept; ßl represents the strength of a segment on the probability of a false positive diagnosis, if the segment under consideration falls in covariate level l.
All statistical tests on difference of two proportions were two-tailed and were based on Wald statistics of the logistic regression models with random intercepts as described earlier; P<0.05 was regarded as statistically significant. The computations are performed with the Correlated Data Library under S-Plus (http://www.insightful.com/).16,17
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Results
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Patient characteristics
In 113 patients initially identified, the primary reason to seek medical attention and to undergo outpatient SPECT imaging was chest pain and/or dyspnea. The remaining 26 patients were evaluated because new LBBB was detected by ECG. SPECT imaging revealed fixed defects in all 139 patients and therefore all patients underwent cardiac catheterization for workup of suspected CAD. Coronary stenosis and/or plaques were found to be present in 120 patients by angiography. The remaining 19 patients in whom coronary angiography showed neither stenosis nor any visible plaque were included in the study. Clinical features of all included patients are summarized in Table 1.
SPECT results
The mid-rows of Figure 2 and the mid-columns of Figure 3 display typical SPECT images from this study. All patients presented with fixed SPECT perfusion defects located in the interventricular septum and the neighbouring either antero- or infero-septal segments, respectively. In the initial qualitative clinical read, all fixed septal defects had been interpreted as myocardial infarcts representing non-transmural lesions in most cases (Table 2). Only septum-related SPECT perfusion defects were present in the 19 patients (Table 2). In every patient, an average of 30±5 abnormal segments were detected by SPECT. Quantitative SPECT analysis results of all 1328 segments (12 segments per slice, six slices) confirmed the presence of all fixed defects visually identified and can be viewed in the lower mid-panel of Figure 4.

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Figure 2 Typical example of a patient (patient 7) presenting with LBBB and fixed septal defect as indicated by 99Tc-SPECT. The upper two panels demonstrate paradoxical septal wall motion and partial wall thinning in this area, which is typical in the setting of LBBB (see online Supplementary material for movies). In this case, CAD had been ruled out by cardiac catheterization. Furthermore, contrast CMR reveals no evidence for myocardial infarction (bottom panel).
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Figure 3 Three other examples of patients (patients 4, 10, and 11) presenting with LBBB and fixed septal defects in Tc99m sestamibi-SPECT. Note that the septal SPECT defect (rest and stress SPECT panel) matches the septal wall motion abnormality (left two panels) in all three cases (see online Supplementary material for movies). CAD had been ruled out by cardiac catheterization and contrast enhanced CMR reveals no evidence for myocardial infarction (right panel).
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Figure 4 Spatial distribution of the mean values for segmental wall motion (upper panel), cumulative wall thickness over the cardiac cycle, which was calculated as average of systolic and diastolic wall thickness (upper mid panel), fixed SPECT defects (bottom mid panel), and contrast enhancement (bottom panel) represented as grey-scale maps in basal, mid, and apical short-axis slices in all patients (n=19). Note that the septal SPECT defects match the septal wall motion abnormalities as well as impaired myocardial thickness. Contrast CMR reveals no evidence for myocardial infarction (bottom panel).
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CMR results
Cine and contrast CMR analysis was performed in all 1328 segments. The upper panel of Figure 2 and the left rows of Figure 3 display typical cine CMR images from this study. The full-motion cines corresponding to Figures 2 and 3 see online Supplementary material. All patients had typical septum-related wall motion abnormalities caused by LBBB. In most cases, the mid-area of the septum was dyskinetic, whereas the neighbouring antero- and infero-septal segments were akinetic or hypokinetic as displayed in the upper panel of Figure 4. The average systolic wall thickness in the left ventricle for all 1328 segments was 14±2.9 mm, the average diastolic wall thickness was 10±1.3 mm. Segments with reduced systolic wall thickening (<30% absolute thickening) and diastolic wall thickness were predominantly seen in the septal areas affected by LBBB. Segments with reduced systolic wall thickening were detected in all patients, whereas impaired diastolic wall thickness was present in 10 patients only. The derived parameter cumulative wall thickness was thus reduced in the segments affected by LBBB in all patients. This parameter can be viewed in the second row of Figure 4.
Subendocardial or transmural contrast enhancement, representing myocardial infarction, was not found in any patient. In two patients, initially suspected contrast enhancement in the LV lateral and inferior wall, which was revealed by computer analysis, could clearly be identified as artefact, as it matched areas of ghosting and was only detectable in one imaging plane (Table 2). One other patient showed remnants of subepicardial contrast enhancement in the LV lateral wall, indicative of myocarditis.18 All results of the segmental contrast CMR read can be viewed in the bottom panel of Figure 4.
Comparison between SPECT and CMR
The comparison of nuclear SPECT with the gold standard of in vivo infarct assessment contrast CMR revealed that in the setting of wall motion abnormalities and impaired wall thickness caused by LBBB, all fixed SPECT defects detected by quantitative analysis did not represent myocardial infarcts (Figure 4). SPECT defects, however, exactly matched areas of wall motion abnormalities as well as areas with impaired cumulative wall thickness as assessed by cine CMR (displayed in the upper and upper mid panel of Figure 4).
In addition, we found a strong relationship between wall motion score and cumulative wall thickness on one hand and the segments thought to be infarcted on the basis of SPECT imaging on the other hand. For example only 5% of all segments with normal wall motion were false positive by SPECT for myocardial infarction, whereas 93% of all dyskinetic segments were found to be false positive (P<0.01) (Figure 5, upper left panel). Comparing cumulative wall thickness with SPECT results showed, that nearly two-thirds of segments (58%) in which cumulative wall thickness was 1 SD below the mean cumulative wall thickness and nearly all (93%) segments in which cumulative wall thickness was 2 SD below the mean cumulative wall thickness showed fixed defects by SPECT. In contrast, only 0.5% of segments in which cumulative wall thickness was above the mean were affected by false positive SPECT results (P<0.01) (Figure 5 bottom left panel). The upper and lower right panels of Figure 5 display systolic and diastolic wall thickness plotted separately against fixed nuclear defects, indicating a weaker relationship between systolic wall thickness and SPECT defects. The weakest correlation was found between diastolic wall thickness and SPECT results.

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Figure 5 Results of the analysis comparing segments falsely identified as infarcted by SPECT and contrast CMR (gold standard cardiac catheterization) with the LV wall motion (upper left panel) as well as systolic (upper right panel), diastolic (bottom right panel), and cumulative wall thickness (bottom left panel). We found a progressive relationship between segments falsely identified as infarcted by SPECT and abnormal wall motion (upper left panel) as well as impaired wall thickness of at least 1 SD. Interestingly, nearly all segments thicker than the mean of myocardial segments were identified correctly as not infarcted by SPECT.
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Discussion
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This study is unique in that patients presenting with LBBB but without any CAD were used as a non-ischaemic clinical model to evaluate the influence of wall motion abnormalities, impaired wall thickening, and reduced wall thickness on SPECT results for detection of myocardial infarction. In addition, this is the first cohort of LBBB patients in whom contrast CMR was employed as an in vivo gold standard for SPECT infarct detection. Our data demonstrate that the commonly accepted concept of a reduced number of myocytes taking up tracer in areas of myocardial infarction19 is only one possible explanation for the presence of fixed SPECT defects in humans. In addition to this mechanism, wall motion abnormalities as well as reduced LV wall thickness may cause fixed SPECT defects due to partial volume effects in the absence of any myocardial infarct and in the absence of any CAD.
Effects of wall thickness on SPECT results
We found that fixed SPECT perfusion abnormalities correlated to segmental wall thickness. Nearly half of segments (40%) in which systolic wall thickness was 1 SD below the mean (11.1 vs. 14 mm) and more than two-thirds (68%) of segments in which systolic wall thickness was 2 SD below the mean (8.2 vs. 14 mm) showed fixed defects (Figure 5, upper right panel). For diastolic wall thickness, this relation was weaker. Only one-third of the segments (28%) in which diastolic wall thickness was 1 SD below the mean (8.7 vs. 10 mm) and less than half (43%) of those in which diastolic wall thickness was 2 SD below the mean (7.4 vs. 10 mm) showed fixed defects by resting SPECT imaging (Figure 5, right bottom panel).
As SPECT is an imaging technique, which integrates segmental counts over many cardiac cycles, we introduced an additional derived parameter cumulative wall thickness during the cardiac cycle. This parameter reflects the influence of mean segmental wall thickness, which is an important determinant of partial volume effects. Therefore, it is not surprising that cumulative wall thickness was most closely negatively related to the number of false positive SPECT results.
This finding is consistent with the concept that SPECT underestimates the concentration of radioactivity in small structures because of partial volume effects. Hassan et al.20 illustrated this point by applying a cardiac SPECT protocol to tubes of various diameters containing a constant concentration of radioactive tracer. Under such conditions, Hassan et al. found a 38% decrease in maximal voxel activity to be associated with a decrease in tube diameter from 12.3 to 8.8 mm corresponding to the difference in cumulative wall thickness between segments with and without fixed SPECT defects in the present study. This finding indicates that the magnitude of partial volume effect caused by wall motion abnormalities on patient SPECT images might be significant. However, the precise degree of that magnitude is still not known, because myocardial walls have a more complex shape than cylindric tubes. Nevertheless, the data from Hassan et al. strongly support our observation that SPECT defects detected in areas with thinned walls (measured by an independent imaging technique such as CMR) may be entirely explained by the decreased mass of myocardial tissue independent of an infarct.
Effects of wall motion and wall thickening on SPECT results
Furthermore, we found a strong correlation between the wall motion score and the segments indicated to be false positive by SPECT. In the present study, only 5% of all segments with normal wall motion by CMR were false positive, whereas 93% of all dyskinetic segments were found to be false positive by SPECT. This finding is also consistent with the literature, as it has been reported that SPECT defects decrease when LV function improves.20,21 Furthermore, on the basis of the relationship between wall thickness and SPECT results discussed earlier, the most likely mechanism for this effect can be explained, by the fact that lower contractility leads to a much lower systolic, cumulative wall thickness when compared with the normal contracting segments and thus to a decrease in the tracer uptake recorded by SPECT within those segments.22
We suggest that the main reason for the high frequency of false positive diagnosis of septal infarction by SPECT imaging in patients with LBBB is the significantly lower cumulative thickness of septal segments. Because nearly all defects described in the literature in the setting of LBBB are somewhere septal,24 other causes such as perfusion abnormalities due to microvascular disease affecting exclusively the septum and not any other region in the entire heart seem to be much less likely. In addition, several authors report the occurrence of LBBB in patients without structural heart disease, also contradicting the idea of exclusively septum-related microvascular disease.23,24 Our suggestion that lower cumulative wall thickness and thus a partial volume effect is the major cause for fixed SPECT defects in the setting of LBBB is further supported by animal studies demonstrating that the myocardial lactate extraction rate showed no significant change if LBBB is induced by right ventricular pacing.25 In addition, no lactate production or increased septal glucose uptake was observed under this condition,25 which clearly contradicts the concept of functional ischaemia caused by LBBB itself,26 because functional ischaemia would be expected to affect the lactate metabolism and glucose uptake in the septal myocardium.
A situation similar to that in patients with LBBB can be found in patients with Tako-tsubo cardiomyopathy (apical ballooning). This entity, which clinically mimics acute left anterior descending artery occlusion as patients present with chest pain, ECG abnormalities, and dyskinesia of the anterior wall and the apex in the absence of any coronary artery stenosis may also lead to fixed SPECT defects, which exactly match the areas of wall motion abnormality.27 However, just as in patients with LBBB without CAD, there is no myocardial scar in Tako-tsubo patients28 and the coronary angiogram is entirely normal.27 Furthermore, the wall motion abnormalities are completely reversible and only persist for a maximum of 2 weeks.27,29 Accordingly, it has been shown that the SPECT defects disappear when SPECT imaging is repeated after restoration of normal wall motion.27 This observation further supplements our finding that akinesia and dyskinesia lead to a much lower segment thickness during systole and even diastole in some cases, resulting in a decreased tracer uptake recorded by SPECT, independent of the underlying cause for the wall motion abnormality.
Pathophysiology case
The patient displayed in Figure 6 nicely illustrates the suspected pathophysiology for false positive SPECT results in the setting of wall motion abnormalities and impaired wall thickening. However, the patient displayed in Figure 6 has not been included in the analysis, because his LBBB is only present under stress conditions and not at rest. At rest (upper panel), when no LBBB is present and thus septal wall motion is nearly normal SPECT does reveal some decrease in tracer uptake caused by the thin septal wall. Under stress conditions, however (bottom panel), after the sudden appearance of LBBB, the entire septum becomes dyskinetic and therefore leads to a much lower segmental thickness during systole resulting in a significant decrease in tracer uptake recorded by SPECT when compared with rest, which was read as septal ischaemia in the qualitative clinical read. As a result of this SPECT scan, the patient underwent cardiac catheterization, which did reveal completely normal coronary arteries (bottom right panel).

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Figure 6 The case displayed in Figure 6 illustrates the suspected pathophysiology for false positive SPECT in the setting of wall motion abnormalities and wall thinning. However, the patient displayed has not been included in the analysis because in his case, LBBB is only present under stress conditions and not at rest. At rest (upper panel), when no LBBB is present and thus septal wall motion is nearly normal, SPECT does reveal some decrease in tracer uptake caused by the thin septal wall. Under stress conditions, however (bottom panel), after the sudden appearance of LBBB, the entire septum becomes dyskinetic. This results (i) in a much lower segmental thickness and (ii) a completely different position of the entire septum during systole. Thus, a technique averaging counts over the entire cardiac cycle will not receive signal from the septum during systole in the same location as during diastole. These two facts explain the significant decrease in tracer uptake recorded by SPECT when compared with rest, which was read as septal ischaemia in the qualitative clinical read. As a result of this SPECT scan, the patient underwent cardiac catheterization, which did reveal completely normal coronary arteries (bottom right panel).
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Clinical implications
The current study clearly indicates that in patients without CAD wall motion abnormalities as well as impaired myocardial wall thickness and thickening alone may cause false positive infarct detection in routine SPECT perfusion imaging. This is of clinical importance because wall thinning, impaired wall thickening, and wall motion abnormalities are not limited to ischaemic heart disease but are frequent findings in non-ischaemic cardiac diseases such as dilated or inflammatory cardiomyopathy. In those cases, SPECT may falsely indicate the presence of myocardial infarction, which may lead to incorrect patient management decisions. Thus, in patients with regional LV wall motion abnormalities and reduced wall thickness, CMR may be preferable to SPECT to evaluate the presence of myocardial infarction and to guide clinical patient management.
Conclusion
Wall motion abnormalities as well as impaired myocardial wall thickening and wall thickness can cause false positive results of resting SPECT myocardial perfusion imaging for detection of myocardial infarction in the absence of myocardial infarct scars and CAD.
Supplementary material
Supplementary material is available at European Heart Journal online.
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