- Email: [email protected]
Occasionally increased 18F-fluorodeoxyglucose uptake in apical hypertrophic cardiomyopathy with mid-ventricular obstruction
G Model
JCCASE-841; No. of Pages 4 Journal of Cardiology Cases xxx (2017) xxx–xxx
Contents lists available at ScienceDirect
Journal of Cardiology Cases journal homepage: www.elsevier.com/locate/jccase
Case Report
Occasionally increased 18F-fluorodeoxyglucose uptake in apical hypertrophic cardiomyopathy with mid-ventricular obstruction Hideya Yamamoto (MD, FJCC)a,*, Toshiro Kitagawa (MD)a, Hitoshi Susawa (MD)a, Ryoichiro Hata (MD)b, Fuminari Tatsugami (MD)c, Toru Higaki (PhD)c, Kazuo Awai (MD)c, Yasuki Kihara (MD, FJCC)a a
Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan Department of Radiology, Chugoku Electric Power Corporation Hospital, Hiroshima, Japan c Department of Diagnostic Radiology, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan b
A R T I C L E I N F O
A B S T R A C T
Article history: Received 6 January 2017 Received in revised form 29 March 2017 Accepted 11 April 2017
We report on a 77-year-old man who was diagnosed with apical hypertrophic cardiomyopathy (HCM) with mid-ventricular obstruction. He had a cured hepatitis C infection. We detected occasionally increased 18F-fluorodeoxyglucose (18F-FDG) uptake on whole-body positron emission tomography (PET)/ computed tomography (CT) performed to examine the involvement of bladder carcinoma. 18F-FDG-PET was restudied following specific preparation involving an 18-h low-carbohydrate diet and following 15-h fasting plus heparin pre-administration. Increased uptake of 18F-FDG was observed reproducibly in the hypertrophic apical to mid left ventricular myocardium, with a maximum standardized uptake value of 6.2. In contrast, relatively lower 18F-FDG-uptake areas tended to match areas of late gadolinium enhancement on cardiac magnetic resonance (CMR). Histopathological examination of myocardial biopsy showed disarried hypertrophic myocytes with cellular infiltration. Increased uptake of 18F-FDG may reflect the phenomenon of increased glucose utilization in hypertrophied myocardium. The increasing clinical utility of whole-body PET/CT for evaluating malignancies may increase the detection of occasional abnormal 18F-FDG uptake in the heart. It is necessary to clarify that 18F-FDG myocardial PET in combination with CMR may provide a more detailed risk assessment in patients with HCM. © 2017 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.
Keywords: 18 F-Fluorodeoxyglucose Hypertrophic cardiomyopathy Late gadolinium enhancement Cardiac magnetic resonance
Introduction
with mid-ventricular obstruction, with occasionally increased F-FDG uptake in the apex of the heart on whole-body PET/ computed tomography (CT). 18
18
F-Fluorodeoxyglucose (18F-FDG)-positron emission tomography (PET) is used clinically to diagnose the systemic involvement of malignancies or inflammatory diseases by virtue of their ability to metabolize glucose [1]. Increased uptake of 18F-FDG in the myocardium may indicate the presence of cardiac tumors or inflammatory diseases, such as cardiac sarcoidosis [2]. Herein, we report a patient with apical hypertrophic cardiomyopathy (HCM)
* Corresponding author at: Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical & Health Sciences, 1-2-3 Kasumi, Minami-Ku, Hiroshima 734-8551, Japan. Fax: +81 82 257 1569. E-mail address: [email protected] (H. Yamamoto).
Case report A 77-year-old man had been diagnosed with apical to midventricular-type HCM at Hiroshima University Hospital. He had experienced dyspnea with chest discomfort since his 60s. This case was complicated by interstitial pneumonitis and a history of cerebral infarction due to paroxysmal atrial fibrillation. He had a history of hepatitis C viral infection but the viral antigen disappeared after antiviral agents. He had no remarkable family history. His blood pressure was 116/70 mmHg and his pulse was regular at 60 bpm. Auscultation revealed systolic ejection murmur
http://dx.doi.org/10.1016/j.jccase.2017.04.004 1878-5409/© 2017 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.
Please cite this article in press as: Yamamoto H, et al. Occasionally increased 18F-fluorodeoxyglucose uptake in apical hypertrophic cardiomyopathy with mid-ventricular obstruction. J Cardiol Cases (2017), http://dx.doi.org/10.1016/j.jccase.2017.04.004
G Model
JCCASE-841; No. of Pages 4 H. Yamamoto et al. / Journal of Cardiology Cases xxx (2017) xxx–xxx
2
Fig. 1.
Electrocardiography (A) showed deep negative T waves in I, aVL, and precordial leads (V2–6) (7 mm depth in V5). Echocardiography (B) showed marked mid to apical left ventricular hypertrophy (maximum thickness 19 mm) with a left ventricular ejection fraction of 71%. Continuous Doppler examination showed accelerated late systolic peak flow (3.8 m/s) in the left ventricular cavity of the mid-obliterans portion during the Valsalva maneuver (C).
(Levine II/VI) at the apex area, and fine crackle in bilateral lung fields. Electrocardiography showed deep negative T waves in I, aVL, and V2–6 leads (7 mm depth in V5), while Doppler echocardiography showed marked left ventricular hypertrophy in the mid to apical portion, and accelerated late systolic peak flow (3.8 m/s) in the left ventricular cavity of the mid-obliterans portion during the Valsalva maneuver (Fig. 1). His serum creatinine kinase-MB level was slightly elevated (9 U/L) and plasma N-terminal B-type natriuretic peptide level was elevated (1,074 pg/mL), but serum C-reactive protein and lysozyme levels were normal. Cine cardiac magnetic resonance (CMR) performed in June 2016 revealed normal myocardial blood flow and a patchy pattern of late gadolinium enhancement in the inner layer of the mid to apical hypertrophic myocardium. There was no obvious high-intensity signal in the T2-weighted image. He received bisoprolol 2.5 mg/ day, cibenzoline 300 mg/day, and apixaban 10 mg/day. The patient visited a urological clinic in October 2016 because of hematuria. He was diagnosed with bladder carcinoma and scheduled to receive surgical treatment. Prior to surgery, he underwent whole-body 18F-FDG-PET/CT at Chugoku Electronic Hospital to evaluate the involvement of the bladder carcinoma. PET/CT was performed following the usual 12-h fasting preparation. A marked increase in 18F-FDG uptake was occasionally found in the apex of the heart, but no other abnormal uptake was detected (Fig. 2A and B). 18 F-FDG-PET was repeated at Hiroshima University Hospital after resection of the bladder cancer, following specific preparation involving an 18-h low-carbohydrate diet and following 15-h fasting
plus heparin pre-administration 15 min prior to 18F-FDG injection (50 IU/kg) [3]. The CMR and 18F-FDG/CT images are compared in Fig. 2C–H. Increased uptake of 18F-FDG was observed reproducibly in the hypertrophic apical left ventricular myocardium, with a maximum standardized uptake value of 6.2. In contrast, relatively lower 18F-FDG-uptake areas tended to match the areas with late gadolinium enhancement. Histopathological examination of the myocardial biopsy obtained from the endocardium of the right ventricular apex showed disarray of hypertrophic myocytes with mononuclear cell aggregation and mild fibrosis, but no signs of granuloma or malignancies (Fig. 3). Discussion In the present case with apical HCM with mid-ventricular obstruction, increased 18F-FDG uptake was occasionally found in the apex of the heart on whole-body PET/CT performed to evaluate bladder cancer involvement. Abnormal 18F-FDG uptake in HCM has been sporadically reported, and they speculated that the increased uptake of 18FFDG in HCM is caused by increased glucose utilization, complementary to impaired fatty acid metabolism [4,5]. In addition, Takeishi et al. demonstrated increased uptake of 18F-FDG and relatively low uptake in the late gadolinium enhancement area in the apex [5]. However, the current patient showed mild to moderate mononuclear cell aggregation in the myocardial biopsy. Then, increased uptake of 18F-FDG may reflect the phenomenon that inflammation caused the increased glucose utilization in hypertrophied myocardium. In contrast, a previous study reported
Please cite this article in press as: Yamamoto H, et al. Occasionally increased 18F-fluorodeoxyglucose uptake in apical hypertrophic cardiomyopathy with mid-ventricular obstruction. J Cardiol Cases (2017), http://dx.doi.org/10.1016/j.jccase.2017.04.004
G Model
JCCASE-841; No. of Pages 4 H. Yamamoto et al. / Journal of Cardiology Cases xxx (2017) xxx–xxx
Fig. 2.
In whole-body positron emission tomography (PET)/computed tomography (CT), increased 18F-fluorodeoxyglucose (18F-FDG) uptake was occasionally detected in the apex area of the heart (A). Panel (B) shows merged axial image of 18F-FDG-PET/CT. The T1-weighted cardiac magnetic resonance (CMR) images in long-axis (C) and sagittal views (D) at end-diastole showed remarkable hypertrophy in the mid to apical left ventricular myocardium. Myocardial blood flow was normal. Patchy pattern of late gadolinium enhancement (arrows) was observed in the inner to mid layer of the apical myocardium in the long-axis (E) and short-axial (F) views. 18F-FDG-PET following specific preparation involving an 18-h low-carbohydrate diet and following 15-h fasting, plus intravenous heparin preadministration. Merged image of 18F-FDG-PET and CT showed reproducibly increased 18F-FDG uptake in the apical left ventricle. Maximum standardized uptake value was 6.2 (G). Reconstructed short-axis view of 18F-FDG-PET corresponding to (F) showed increased 18F-FDG uptake but relatively lower uptake overlapping the area of late gadolinium enhancement (arrows) (H).
that mild inflammation is related to pathogenesis of HCM [6]. However, in this case, histopathological findings of inflammatory cell accumulation were weak and not specific for hepatitis C
infection, and their association remains unclear. Therefore, we suggest that increased uptake of 18F-FDG is owing to the possibility of myocardial stress or overload, which is caused by intraventricular pressure gradient, and induces these histopathological findings including cell infiltration or mild fibrosis rather than the hepatitis C virus-induced inflammation. The presence of late gadolinium enhancement has been associated with increased mortality in HCM patients [7]. Late gadolinium enhancement was reported in 40% of patients with apical HCM, compared with 70% with asymmetric septal HCM [8]. Increased 18F-FDG uptake was observed in the apical to mid hypertrophic myocardium, whereas late gadolinium enhancement was limited to the focal area. Taken together, it is necessary to further evaluate the clinical significance of the increase in F-FDG uptake in this case with HCM. The increasing clinical utility of whole-body PET/CT for evaluating malignancies may increase the chance of occasionally detecting abnormal 18F-FDG uptake in the heart. On the other hand, increased uptake of 18F-FDG suggests that chronic inflammation due to myocardial stress or overload probably caused by intraventricular pressure gradient. Finally, the usefulness of 18FFDG-PET for assessing the severity or prognosis in HCM patients remains unclear. It is necessary to clarify that 18F-FDG myocardial PET in combination with CMR may provide a more detailed risk assessment. Conflict of interest
Fig. 3.
3
Microscopic image of myocardial biopsy (hematoxylin–eosin stain, original magnification, 20) showed disarrayed hypertrophic myocardium with mononuclear cell aggregation (arrow) and mild fibrosis. There were no signs of granuloma or malignancy.
Authors have no conflict of interest. Acknowledgment None.
Please cite this article in press as: Yamamoto H, et al. Occasionally increased 18F-fluorodeoxyglucose uptake in apical hypertrophic cardiomyopathy with mid-ventricular obstruction. J Cardiol Cases (2017), http://dx.doi.org/10.1016/j.jccase.2017.04.004
G Model
JCCASE-841; No. of Pages 4 H. Yamamoto et al. / Journal of Cardiology Cases xxx (2017) xxx–xxx
4
References [1] Lowe VJ, Naunheim KS. Positron emission tomography in lung cancer. Ann Thorac Surg 1998;65:1821–9. [2] Youssef G, Leung E, Mylonas I, Nery P, Williams K, Wisenberg G, et al. The use of 18 F-FDG-PET in the diagnosis of cardiac sarcoidosis: a systematic review and meta-analysis including the Ontario experience. J Nucl Med 2012;53:241–8. [3] Manabe O, Yoshinaga K, Ohira H, Masuda A, Sato T, Tsujino I, et al. The effects of 18-h fasting with low-carbohydrate diet preparation on suppressed physiological myocardial 18F-fluorodeoxyglucose (FDG) uptake and possible minimal effects of unfractionated heparin use in patients with suspected cardiac involvement sarcoidosis. J Nucl Cardiol 2016;23:244–52. [4] Uehara T, Ishida Y, Hayashida K, Shimonagata T, Miyake Y, Sago M, et al. Myocardial glucose metabolism in patients with hypertrophic cardiomyopathy: assessment by F-18-FDG PET study. Ann Nucl Med 1998;12:95–103.
[5] Takeishi Y, Masuda A, Kubo H, Tominaga H, Oriuchi N, Takenoshita S. Cardiac imaging with 18F-fluorodeoxyglucose PET/MRI in hypertrophic cardiomyopathy. J Nucl Cardiol 2016 [in press]. [6] Kuusisto J, Ka¨rja¨ V, Sipola P, Kholova´ I, Peuhkurinen K, Ja¨a¨skela¨inen P, et al. Lowgrade inflammation and the phenotypic expression of myocardial fibrosis in hypertrophic cardiomyopathy. Heart 2012;98:1007–13. [7] Minami Y, Kajimoto K, Terajima Y, Yashiro B, Okayama D, Haruki S, et al. Clinical implications of midventricular obstruction in patients with hypertrophic cardiomyopathy. J Am Coll Cardiol 2011;57:2346–55. [8] Green JJ, Berger JS, Kramer CM, Salerno M. Prognostic value of late gadolinium enhancement in clinical outcomes for hypertrophic cardiomyopathy. JACC Cardiovasc Imaging 2012;5:370–7.
Please cite this article in press as: Yamamoto H, et al. Occasionally increased 18F-fluorodeoxyglucose uptake in apical hypertrophic cardiomyopathy with mid-ventricular obstruction. J Cardiol Cases (2017), http://dx.doi.org/10.1016/j.jccase.2017.04.004
JCCASE-841; No. of Pages 4 Journal of Cardiology Cases xxx (2017) xxx–xxx
Contents lists available at ScienceDirect
Journal of Cardiology Cases journal homepage: www.elsevier.com/locate/jccase
Case Report
Occasionally increased 18F-fluorodeoxyglucose uptake in apical hypertrophic cardiomyopathy with mid-ventricular obstruction Hideya Yamamoto (MD, FJCC)a,*, Toshiro Kitagawa (MD)a, Hitoshi Susawa (MD)a, Ryoichiro Hata (MD)b, Fuminari Tatsugami (MD)c, Toru Higaki (PhD)c, Kazuo Awai (MD)c, Yasuki Kihara (MD, FJCC)a a
Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan Department of Radiology, Chugoku Electric Power Corporation Hospital, Hiroshima, Japan c Department of Diagnostic Radiology, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan b
A R T I C L E I N F O
A B S T R A C T
Article history: Received 6 January 2017 Received in revised form 29 March 2017 Accepted 11 April 2017
We report on a 77-year-old man who was diagnosed with apical hypertrophic cardiomyopathy (HCM) with mid-ventricular obstruction. He had a cured hepatitis C infection. We detected occasionally increased 18F-fluorodeoxyglucose (18F-FDG) uptake on whole-body positron emission tomography (PET)/ computed tomography (CT) performed to examine the involvement of bladder carcinoma. 18F-FDG-PET was restudied following specific preparation involving an 18-h low-carbohydrate diet and following 15-h fasting plus heparin pre-administration. Increased uptake of 18F-FDG was observed reproducibly in the hypertrophic apical to mid left ventricular myocardium, with a maximum standardized uptake value of 6.2. In contrast, relatively lower 18F-FDG-uptake areas tended to match areas of late gadolinium enhancement on cardiac magnetic resonance (CMR). Histopathological examination of myocardial biopsy showed disarried hypertrophic myocytes with cellular infiltration. Increased uptake of 18F-FDG may reflect the phenomenon of increased glucose utilization in hypertrophied myocardium. The increasing clinical utility of whole-body PET/CT for evaluating malignancies may increase the detection of occasional abnormal 18F-FDG uptake in the heart. It is necessary to clarify that 18F-FDG myocardial PET in combination with CMR may provide a more detailed risk assessment in patients with HCM.
Keywords: 18 F-Fluorodeoxyglucose Hypertrophic cardiomyopathy Late gadolinium enhancement Cardiac magnetic resonance
Introduction
with mid-ventricular obstruction, with occasionally increased F-FDG uptake in the apex of the heart on whole-body PET/ computed tomography (CT). 18
18
F-Fluorodeoxyglucose (18F-FDG)-positron emission tomography (PET) is used clinically to diagnose the systemic involvement of malignancies or inflammatory diseases by virtue of their ability to metabolize glucose [1]. Increased uptake of 18F-FDG in the myocardium may indicate the presence of cardiac tumors or inflammatory diseases, such as cardiac sarcoidosis [2]. Herein, we report a patient with apical hypertrophic cardiomyopathy (HCM)
* Corresponding author at: Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical & Health Sciences, 1-2-3 Kasumi, Minami-Ku, Hiroshima 734-8551, Japan. Fax: +81 82 257 1569. E-mail address: [email protected] (H. Yamamoto).
Case report A 77-year-old man had been diagnosed with apical to midventricular-type HCM at Hiroshima University Hospital. He had experienced dyspnea with chest discomfort since his 60s. This case was complicated by interstitial pneumonitis and a history of cerebral infarction due to paroxysmal atrial fibrillation. He had a history of hepatitis C viral infection but the viral antigen disappeared after antiviral agents. He had no remarkable family history. His blood pressure was 116/70 mmHg and his pulse was regular at 60 bpm. Auscultation revealed systolic ejection murmur
http://dx.doi.org/10.1016/j.jccase.2017.04.004 1878-5409/© 2017 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.
Please cite this article in press as: Yamamoto H, et al. Occasionally increased 18F-fluorodeoxyglucose uptake in apical hypertrophic cardiomyopathy with mid-ventricular obstruction. J Cardiol Cases (2017), http://dx.doi.org/10.1016/j.jccase.2017.04.004
G Model
JCCASE-841; No. of Pages 4 H. Yamamoto et al. / Journal of Cardiology Cases xxx (2017) xxx–xxx
2
Fig. 1.
Electrocardiography (A) showed deep negative T waves in I, aVL, and precordial leads (V2–6) (7 mm depth in V5). Echocardiography (B) showed marked mid to apical left ventricular hypertrophy (maximum thickness 19 mm) with a left ventricular ejection fraction of 71%. Continuous Doppler examination showed accelerated late systolic peak flow (3.8 m/s) in the left ventricular cavity of the mid-obliterans portion during the Valsalva maneuver (C).
(Levine II/VI) at the apex area, and fine crackle in bilateral lung fields. Electrocardiography showed deep negative T waves in I, aVL, and V2–6 leads (7 mm depth in V5), while Doppler echocardiography showed marked left ventricular hypertrophy in the mid to apical portion, and accelerated late systolic peak flow (3.8 m/s) in the left ventricular cavity of the mid-obliterans portion during the Valsalva maneuver (Fig. 1). His serum creatinine kinase-MB level was slightly elevated (9 U/L) and plasma N-terminal B-type natriuretic peptide level was elevated (1,074 pg/mL), but serum C-reactive protein and lysozyme levels were normal. Cine cardiac magnetic resonance (CMR) performed in June 2016 revealed normal myocardial blood flow and a patchy pattern of late gadolinium enhancement in the inner layer of the mid to apical hypertrophic myocardium. There was no obvious high-intensity signal in the T2-weighted image. He received bisoprolol 2.5 mg/ day, cibenzoline 300 mg/day, and apixaban 10 mg/day. The patient visited a urological clinic in October 2016 because of hematuria. He was diagnosed with bladder carcinoma and scheduled to receive surgical treatment. Prior to surgery, he underwent whole-body 18F-FDG-PET/CT at Chugoku Electronic Hospital to evaluate the involvement of the bladder carcinoma. PET/CT was performed following the usual 12-h fasting preparation. A marked increase in 18F-FDG uptake was occasionally found in the apex of the heart, but no other abnormal uptake was detected (Fig. 2A and B). 18 F-FDG-PET was repeated at Hiroshima University Hospital after resection of the bladder cancer, following specific preparation involving an 18-h low-carbohydrate diet and following 15-h fasting
plus heparin pre-administration 15 min prior to 18F-FDG injection (50 IU/kg) [3]. The CMR and 18F-FDG/CT images are compared in Fig. 2C–H. Increased uptake of 18F-FDG was observed reproducibly in the hypertrophic apical left ventricular myocardium, with a maximum standardized uptake value of 6.2. In contrast, relatively lower 18F-FDG-uptake areas tended to match the areas with late gadolinium enhancement. Histopathological examination of the myocardial biopsy obtained from the endocardium of the right ventricular apex showed disarray of hypertrophic myocytes with mononuclear cell aggregation and mild fibrosis, but no signs of granuloma or malignancies (Fig. 3). Discussion In the present case with apical HCM with mid-ventricular obstruction, increased 18F-FDG uptake was occasionally found in the apex of the heart on whole-body PET/CT performed to evaluate bladder cancer involvement. Abnormal 18F-FDG uptake in HCM has been sporadically reported, and they speculated that the increased uptake of 18FFDG in HCM is caused by increased glucose utilization, complementary to impaired fatty acid metabolism [4,5]. In addition, Takeishi et al. demonstrated increased uptake of 18F-FDG and relatively low uptake in the late gadolinium enhancement area in the apex [5]. However, the current patient showed mild to moderate mononuclear cell aggregation in the myocardial biopsy. Then, increased uptake of 18F-FDG may reflect the phenomenon that inflammation caused the increased glucose utilization in hypertrophied myocardium. In contrast, a previous study reported
Please cite this article in press as: Yamamoto H, et al. Occasionally increased 18F-fluorodeoxyglucose uptake in apical hypertrophic cardiomyopathy with mid-ventricular obstruction. J Cardiol Cases (2017), http://dx.doi.org/10.1016/j.jccase.2017.04.004
G Model
JCCASE-841; No. of Pages 4 H. Yamamoto et al. / Journal of Cardiology Cases xxx (2017) xxx–xxx
Fig. 2.
In whole-body positron emission tomography (PET)/computed tomography (CT), increased 18F-fluorodeoxyglucose (18F-FDG) uptake was occasionally detected in the apex area of the heart (A). Panel (B) shows merged axial image of 18F-FDG-PET/CT. The T1-weighted cardiac magnetic resonance (CMR) images in long-axis (C) and sagittal views (D) at end-diastole showed remarkable hypertrophy in the mid to apical left ventricular myocardium. Myocardial blood flow was normal. Patchy pattern of late gadolinium enhancement (arrows) was observed in the inner to mid layer of the apical myocardium in the long-axis (E) and short-axial (F) views. 18F-FDG-PET following specific preparation involving an 18-h low-carbohydrate diet and following 15-h fasting, plus intravenous heparin preadministration. Merged image of 18F-FDG-PET and CT showed reproducibly increased 18F-FDG uptake in the apical left ventricle. Maximum standardized uptake value was 6.2 (G). Reconstructed short-axis view of 18F-FDG-PET corresponding to (F) showed increased 18F-FDG uptake but relatively lower uptake overlapping the area of late gadolinium enhancement (arrows) (H).
that mild inflammation is related to pathogenesis of HCM [6]. However, in this case, histopathological findings of inflammatory cell accumulation were weak and not specific for hepatitis C
infection, and their association remains unclear. Therefore, we suggest that increased uptake of 18F-FDG is owing to the possibility of myocardial stress or overload, which is caused by intraventricular pressure gradient, and induces these histopathological findings including cell infiltration or mild fibrosis rather than the hepatitis C virus-induced inflammation. The presence of late gadolinium enhancement has been associated with increased mortality in HCM patients [7]. Late gadolinium enhancement was reported in 40% of patients with apical HCM, compared with 70% with asymmetric septal HCM [8]. Increased 18F-FDG uptake was observed in the apical to mid hypertrophic myocardium, whereas late gadolinium enhancement was limited to the focal area. Taken together, it is necessary to further evaluate the clinical significance of the increase in F-FDG uptake in this case with HCM. The increasing clinical utility of whole-body PET/CT for evaluating malignancies may increase the chance of occasionally detecting abnormal 18F-FDG uptake in the heart. On the other hand, increased uptake of 18F-FDG suggests that chronic inflammation due to myocardial stress or overload probably caused by intraventricular pressure gradient. Finally, the usefulness of 18FFDG-PET for assessing the severity or prognosis in HCM patients remains unclear. It is necessary to clarify that 18F-FDG myocardial PET in combination with CMR may provide a more detailed risk assessment. Conflict of interest
Fig. 3.
3
Microscopic image of myocardial biopsy (hematoxylin–eosin stain, original magnification, 20) showed disarrayed hypertrophic myocardium with mononuclear cell aggregation (arrow) and mild fibrosis. There were no signs of granuloma or malignancy.
Authors have no conflict of interest. Acknowledgment None.
Please cite this article in press as: Yamamoto H, et al. Occasionally increased 18F-fluorodeoxyglucose uptake in apical hypertrophic cardiomyopathy with mid-ventricular obstruction. J Cardiol Cases (2017), http://dx.doi.org/10.1016/j.jccase.2017.04.004
G Model
JCCASE-841; No. of Pages 4 H. Yamamoto et al. / Journal of Cardiology Cases xxx (2017) xxx–xxx
4
References [1] Lowe VJ, Naunheim KS. Positron emission tomography in lung cancer. Ann Thorac Surg 1998;65:1821–9. [2] Youssef G, Leung E, Mylonas I, Nery P, Williams K, Wisenberg G, et al. The use of 18 F-FDG-PET in the diagnosis of cardiac sarcoidosis: a systematic review and meta-analysis including the Ontario experience. J Nucl Med 2012;53:241–8. [3] Manabe O, Yoshinaga K, Ohira H, Masuda A, Sato T, Tsujino I, et al. The effects of 18-h fasting with low-carbohydrate diet preparation on suppressed physiological myocardial 18F-fluorodeoxyglucose (FDG) uptake and possible minimal effects of unfractionated heparin use in patients with suspected cardiac involvement sarcoidosis. J Nucl Cardiol 2016;23:244–52. [4] Uehara T, Ishida Y, Hayashida K, Shimonagata T, Miyake Y, Sago M, et al. Myocardial glucose metabolism in patients with hypertrophic cardiomyopathy: assessment by F-18-FDG PET study. Ann Nucl Med 1998;12:95–103.
[5] Takeishi Y, Masuda A, Kubo H, Tominaga H, Oriuchi N, Takenoshita S. Cardiac imaging with 18F-fluorodeoxyglucose PET/MRI in hypertrophic cardiomyopathy. J Nucl Cardiol 2016 [in press]. [6] Kuusisto J, Ka¨rja¨ V, Sipola P, Kholova´ I, Peuhkurinen K, Ja¨a¨skela¨inen P, et al. Lowgrade inflammation and the phenotypic expression of myocardial fibrosis in hypertrophic cardiomyopathy. Heart 2012;98:1007–13. [7] Minami Y, Kajimoto K, Terajima Y, Yashiro B, Okayama D, Haruki S, et al. Clinical implications of midventricular obstruction in patients with hypertrophic cardiomyopathy. J Am Coll Cardiol 2011;57:2346–55. [8] Green JJ, Berger JS, Kramer CM, Salerno M. Prognostic value of late gadolinium enhancement in clinical outcomes for hypertrophic cardiomyopathy. JACC Cardiovasc Imaging 2012;5:370–7.
Please cite this article in press as: Yamamoto H, et al. Occasionally increased 18F-fluorodeoxyglucose uptake in apical hypertrophic cardiomyopathy with mid-ventricular obstruction. J Cardiol Cases (2017), http://dx.doi.org/10.1016/j.jccase.2017.04.004