First published online September 27, 2006
British Journal of Radiology (2007) 80, 3-11
© 2007 British Institute of Radiology
doi: 10.1259/bjr/92105597
Benign variations and incidental abnormalities of myocardial FDG uptake in the fasting state as encountered during routine oncology positron emission tomography studies
K Fukuchi, MD1,3,
H Ohta, MD2,
K Matsumura, MD2 and
Y Ishida, MD3
1 PET Imaging Center, Shizuoka General Hospital, Shizuoka, 2 Higashitemma Clinic, Osaka, 3 Department of Nuclear Medicine and Radiology, National Cardiovascular Center, Suita, Osaka, Japan
Correspondence: Kazuki Fukuchi, PET Imaging Center, Shizuoka General Hospital, 4-27-1 Kita-andoh, Aoi-ku, Shizuoka, 420-8527, Japan. E-mail: kfukuchi{at}ga2.so-net.ne.jp
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Abstract
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Increased 18fluoro-2-deoxyglucose (FDG) uptake in the myocardium is frequently observed while performing clinical positron emission tomography (PET) body scans for oncology under fasting conditions. This article reviews the normal variations and abnormal appearances of myocardial FDG accumulation which are likely to be encountered in the routine PET studies. Knowledge about the myocardial glucose metabolism and specific abnormalities are indispensable in the interpretation of myocardial FDG uptake.
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Introduction
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The recent advances in positron emission tomography (PET) capability and the widespread recognition of the value of 18fluoro-2-deoxyglucose (FDG) PET in oncology have led to routine whole-body imaging for most oncological indications. Although non-specific uptake in the myocardium is a common finding as well as in the stomach and bowels in whole-body FDG-PET [1], patients with cancer or cancer screening incidentally have some heart disease. Thus, every PET physician has the opportunity to encounter various types of myocardial FDG accumulation, including specific heart diseases.
In this article, we review a basic knowledge of the myocardial metabolism and present some cases with benign variations and incidental abnormalities of myocardial FDG uptake in the fasting state.
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Benign variations of FDG uptake in the heart
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With a sufficiently long fasting period (typically more than 12 h), the myocardial metabolism shifts to fatty acids as a source of energy and the myocardial FDG uptake becomes largely indistinguishable from the blood pool tracer activity. However, the image quality of the myocardial FDG uptake in the fasting healthy subjects varied under the clinical fasting conditions (6 h to overnight) [2, 3]. While a significant negative linear correlation between the myocardial metabolic rates of glucose and serum free fatty acid levels is observed, increased FDG uptake in the myocardium does not significantly correlate with the blood glucose level, age, or duration of fasting in non-diabetic patients [2, 4]. Only in the uncontrolled diabetic patients did high levels of blood glucose (>7.5 mmol l–1) always result in absent or faint myocardial uptake of FDG.
We can classify the FDG distribution patterns in the normal myocardium into three types (no to faint uptake; regional uptake; and diffuse uptake), but there may be no specific meaning in the myocardial distribution patterns of FDG [4] (
Figures 1–3). In addition, even in the same individual, the myocardial FDG uptake is neither stable nor reproducible unless under similar fasting conditions (Figure 2). The transition from the intense FDG uptake of a dominantly glycolytic myocardial metabolism to the absent FDG uptake of a dominantly fatty acid metabolism is not entirely uniform either temporally or regionally. Gropler et al reported that myocardial accumulation in the septum and anterior wall averaged 80% of that in the lateral and posterior walls in the subjects with regional uptake [5]. Moreover, the base of the heart is often the last to lose FDG uptake (Figure 3).
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Figure 1. No apparent left ventricular FDG uptake in a patient with non-cardiac disease. Weak FDG activity is seen in the left ventricular cavity as a blood pool. (a) Coronal section and (b) transaxial section.
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Figure 2. Serial FDG coronal images of the same patient at different examinations.(a,b) No apparent cardiac uptake is seen in the first examination. (c,d) Relatively diffuse cardiac uptake is seen in the second examination, which was performed approximately 4 months after the first examination.
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Figure 3. Non-homogeneous but physiological FDG uptake in the left ventricle. The base of the heart is often the last to lose FDG uptake, resulting in focal uptake (arrow). (a) Maximal intensity projection image and (b) transaxial section.
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The right ventricle can be seen as a thin linear tracer uptake in patients without right heart diseases and, on occasion, even the atria can be noted (Figure 4). The reason for this is not clear, but may be related to atrial overload in chronic heart failure [6].
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Figure 4. Atrial muscle FDG uptake. FDG uptake in the left atrium is often detected, can be irregular and may be associated with somewhat focal activity(arrow).
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Lipomatous hypertrophy of the interatrial septum
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Lipomatous hypertrophy of the interatrial septum (LHIS) is a relatively uncommon disorder of the heart. LHIS is a histologically benign process in which adipose tissue, a normal component of the interatrial septum, increases and infiltrates between the myocardial fibres [7]. Fan et al noted marked preferential FDG uptake within the atrial septa in patients with CT or MRI confirmation of LHIS [8]. FDG uptake in LHIS could be explained by the presence of a variable amount of brown fat in LHIS. The diagnosis is confirmed by detection of non-enhanced fat density on CT, or fat signal intensity within the characteristically shaped lesion on MRI. Fusion PET/CT also helps to clarify the region of localized FDG uptake and confirm that it lies in the region of LHIS (Figure 5) [9].
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Figure 5. A case with lipomatous hypertrophy of the interatrial septum(LHIS). (a) An unenhanced CT scan showing fat density in the interatrial septum. (b) PET image and (c) fused PET/CT image showing increased FDG uptake in LHIS.
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Ischaemic heart disease
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When patients with stable angina on exercise are examined at rest, the regional myocardial glucose utilization is homogeneously low and comparable with that of the healthy subjects [10]. On the other hand, in patients with severe re-perfused myocardial injury, unstable angina, or ischaemic cardiomyopathy, the myocardial glucose utilization at rest is increased because the oxidative metabolism is reduced and the primary substrate for energy metabolism becomes glucose to support adenosine triphosphate production from glycolysis [11, 12]. However, since glucose metabolism in the fasting state is quite heterogeneous even in the normal myocardium [4, 5], it is difficult to diagnose the presence of ischaemic myocardium by fasting FDG-PET imaging alone.
Sustained reductions in the flow may also lead to myocardial dysfunction with preservation of the cell viability. This reduction in myocardial function has been thought to be a protective chronic down regulation mechanism to reduce oxygen utilization and ensure myocyte survival. The myocardial perfusion–metabolism mismatch pattern seen on perfusion weighted FDG PET imaging supported this hypothesis; i.e. the sustained reduction in flow with maintained glucose utilization is considered to represent hibernating (ischaemic but viable) myocardium [3]. Thus, it has been well known that FDG uptake indicates the myocardial viability. If regional FDG uptake in the left ventricle is observed in ordinary fasting routine PET studies, this part of the myocardium can be judged as viable. However, sometimes no FDG uptake in the myocardium is noticed regionally. Although the uptake of FDG indicates viability, the lack of uptake may indicate either non-viable tissue or viable tissue that is utilizing substrates other than glucose in the fasting status. Therefore, the myocardial FDG uptake should be carefully evaluated for assessing the myocardial viability in the fasting studies. Only in cases with relatively diffuse FDG uptake in unprepared patients can the myocardial viability be occasionally assessed (Figure 6). To obtain precise information about the myocardial viability from FDG-PET, glucose loading, oral administration of acipimox and/or insulin protocol to optimize FDG uptake in the viable myocardium is considered preferable [3].
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Figure 6. A patient with old myocardial infarction.(a) Myocardial FDG uptake is observed in the entire left ventricular wall, but a decreasing uptake is seen in the anteroseptal region (black arrow). (b) CT scan from PET/CT demonstrating linear fat deposition (white arrow). (c) Fused PET/CT clearly depicts the decreased FDG uptake corresponding to fat deposited myocardial infarction (white arrow).
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Atrial fibrillation
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We sometimes encounter increased FDG activity in the wall of the enlarged right atrium (Figure 7). In such cases, electrocardiography (ECG) probably shows atrial fibrillation (AF). Fujii et al reported encountering 10 patients with increased activity in the wall of the right atrium among a total of 2367 examinees who participated in a cancer screening programme with whole-body FDG-PET (0.4%), and that all cases suffered from cardiac disorders, especially AF [13]. Interestingly, the average size of the right atria in such cases was significantly enlarged as compared with other cases without cardiac disease.
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Figure 7. A patient with atrial fibrillation.(a) Coronal section and (b) transaxial section. Increased FDG uptake is clearly noticed in the enlarged right atrial wall (arrow).
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The relationship between right atrial enlargement and atrial arrhythmias has been previously analysed in both human and experimental animal studies [14, 15]. These studies revealed that electrical remodelling and right atrial dilation promote the inducibility and perpetuation of AF. Although the exact mechanism of FDG uptake in the right atrial wall is still unclear and all patients with AF do not show this pattern of uptake, increased FDG activity in the wall of the right atrium may be associated with AF.
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Complete left bundle branch block
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Complete left bundle branch block (CLBBB) occurs when transmission of the cardiac electrical impulse is delayed or fails to conduct along the rapidly conducting fibres of the main left bundle branch. It has been well known that patients with CLBBB show a unique metabolic alteration in their ventricular septum (Figure 8). Zanco et al reported that all CLBBB patients without significant coronary stenosis have reduced uptake of FDG in comparison with the myocardial perfusion by 13-nitrate ammonia PET in the septum [16].
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Figure 8. A patient with complete left bundle branch block.(a) The myocardial perfusion in the septal wall is decreasing in Technetium-99m sestamibi single photon emission tomography. (b) FDG uptake is also decreasing more greatly and widely than the perfusion abnormality.
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Non-ischaemic cardiomyopathy
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Hypertrophic cardiomyopathy is a mostly genetically determined disease and results in abnormal hypertrophy of the myocardium, which is often regionally heterogeneous and especially pronounced in the septum [17]. In the fasting images, regionally increased FDG uptake is often seen in the hypertrophic septal areas (Figure 9), but sometimes its uptake is observed diffusely in the left ventricular wall [18]. On the other hand, dilated cardiomyopathy shows enlarged left ventricle but more regional homogeneity, and fewer and lesser severe defects in FDG as compared with ischaemic cardiomyopathy (Figure 9) [19].
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Figure 9. Cases with cardiomyopathy.(a) A patient with hypertrophic cardiomyopathy. Intense FDG uptake in the hypertrophic septal wall is observed (arrow). (b) A patient with dilated cardiomyopathy. Enlarged left ventricular cavity and relatively homogeneous FDG uptake are seen.
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Right ventricular uptake due to pulmonary hypertension
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Long-term ventricular pressure or volume overload has been shown to alter the myocardial energy substrate metabolism. In patients with pulmonary hypertension, apparent tracer uptake in the enlarged right ventricular free wall is often seen in FDG studies (Figure 10) [20]. In follow-up PET studies on patients with pneumonectomy due to lung carcinomas, positive FDG accumulation in the right ventricular wall is often seen because pneumonectomy is associated with post-operative elevation of the pulmonary artery systolic pressure and right ventricular dilatation [21].
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Figure 10. A patient with primary pulmonary hypertension. Enlarged right ventricular wall and increased FDG uptake are demonstrated.(a) Transaxial section of FDG PET and (b) contrast enhanced CT image.
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Cardiac sarcoidosis
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Sarcoidosis is a multisystemic inflammatory disorder of unknown cause, characterized by the presence of non-caseating epitheloid cell granulomas in the affected tissue [22]. Patients with sarcoidosis are incidentally examined by PET on suspicion of having malignant lymphoma or primary unknown mediastinal lymphadenopathy. Although sarcoidosis is generally associated with a low mortality rate, the cardiac involvement may carry a poor prognosis. Thus, if patients with sarcoidosis are examined by PET, the presence or absence of active cardiac involvement is an important diagnostic clue to be considered in the treatment.
In cases with active cardiac sarcoidosis, focal intense FDG uptake is frequently observed in the basal septal region [23]. This finding is consistent with the findings of previous pathological and morphological studies, indicating that the cardiac involvement in sarcoidosis is common in the basal septal region [24]. Multifocal abnormal FDG uptake including the right ventricular wall may indicate cardiac involvement (Figure 11).
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Figure 11. A patient with cardiac sarcoidosis and complete atrioventricular block. Multifocal FDG uptake in the basal left ventricular wall is seen(arrow). Right ventricular non-homogeneous uptake is also visualized (arrowhead).
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According to a previous paper, the sensitivity and specificity of FDG-PET for cardiac sarcoidosis were 100% and 81.5%, respectively, following administration of heparin prior to FDG injection. This protocol could increase the serum FFA levels and possibly minimize the background myocardial FDG uptake [25].
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Cardiac tumours
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Three quarters of primary cardiac tumours are benign, nearly half are myxomas and approximately 10% are lipoma. The PET literature has suggested that significant uptake of FDG is indicative of malignant tissue. Thus, myxoma is supposed to show no significant-to-weak FDG accumulation [26].
A quarter of all cardiac tumours exhibit some features of malignancy or behave in a malignant way; 95% of these are sarcomas, the other 5% being lymphoma. Metastatic heart tumours may be epicardial, myocardial, or endocardial, but the vast majority are epicardial (Figure 12). They frequently originate from carcinomas of the lung, breast, malignant melanoma, leukaemia and lymphoma. Carcinomas of the lung or breast may spread by local infiltration to the pericardium, leading usually to pericardial effusion. For reasons which are not clear, melanoma has a particular predilection for metastasising to the heart. Half of the cases of disseminated melanoma have cardiac deposits at necropsy [27]. Lymphomas metastasise to the heart with regularity, forming discrete intramyocardial masses (Figure 13). Several case reports describing FDG patterns in cardiac tumours have been published [28–31]. However, the usefulness of FDG in differentiation between benign (including thrombi) and malignant tumours is still unclear because cardiac tumours are rare and there are no data pertaining to a reasonable size of patient cohort.
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Figure 12. A patient with right ventricular metastasis from uterine cervical carcinoma.(a) Broad intense FDG accumulation is seen in the right ventricular wall. (b) Contrast enhanced CT scan revealing that the mass is located in the epicardial portion of the right ventricle and invading toward the pericardium.
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Figure 13. A patient with malignant lymphoma in the right atrium.(a) Transaxial image depicting dense FDG uptake in the right heart system. (b) Contrast enhanced CT revealing that the huge mass is located in the right atrium.
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Conclusion
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The physiological FDG uptake in the myocardium is common in PET oncology, but noteworthy FDG uptake is sometimes observed (Table 1). Abnormal myocardial FDG uptake may be of clinical significance as it can indicate specific cardiac disorders, even in the fasting condition. In those cases, further examinations including echocardiography, MRI and/or enhanced CT may be required.
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Acknowledgments
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We thank the PET imaging technicians and the chemistry staff at the National Cardiovascular Center and Higashitemma Clinic for their excellent technical assistance. The fruitful discussion with Mitsuaki Tatsumi, MD, and Keisuke Kanao, RT, is well appreciated.
Received for publication April 24, 2006.
Revision received July 7, 2006.
Accepted for publication August 25, 2006.
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Abstract
Introduction
