Cardiac sarcoidosis, the complete atrioventricular block of which was completely recovered by intravenous steroid pulse therapy

AbstractAtrioventricular block (AVB) in individuals with cardiac sarcoidosis (CS) is one of the major complications caused by inflammation of the conducting system of the heart, as a sign of worse prognosis. We report the case of a 53-year-old Japanese woman whose electrocardiogram showed complete AVB by the clinical diagnosis of CS. We administered intravenous methylpredonisolone (1g/day) for 3 days. On the second day of steroid pulse therapy, the complete AVB improved to sinus rhythm of 1st degree AVB and complete right bundle branch block. Normal sinus rhythm was then observed after oral steroid therapy. These results suggest that in cases of complete AVB, steroid pulse therapy with a strong anti-inflammatory effect may be recommended first.<Learning objective: This case illustrates a typical case of CS with complete AVB, but the cardiac contraction was normal. In this setting, steroid pulse therapy may be effective when (1) the active inflammation of the conduction system can be suppressed by steroid pulse therapy; (2) the time to start steroid therapy is short enough to recover.

Value of late gadolinium enhancement by magnetic resonance in patients with cardiac sarcoidosis: characteristic findings and clinical utility

73rd Annual Scientific Meeting of the Japanese Circulation Society 2009年03月 Osak

Case Report: Acute Eosinophilic Myocarditis With a Low-Flow Heart Failure With Preserved Ejection Fraction Phenotype

Eosinophilic myocarditis is a rare subtype of myocarditis characterized by myocardial eosinophilic infiltration, and it is potentially fatal if left untreated. Although endomyocardial biopsy (EMB) is a cornerstone for the histological diagnosis of acute eosinophilic myocarditis (AEM), as it is an invasive procedure and has a low diagnostic accuracy, the diagnosis of AEM with hemodynamic instability remains challenging. We describe a case of AEM presenting as low-flow heart failure with preserved ejection fraction (HFpEF), with rapid progression to cardiogenic shock. The constellation of peripheral eosinophilia, increased left ventricular wall thickness, and HFpEF raised the suspicion of AEM. Contrast-enhanced computed tomography (CT) scan revealed heterogeneous hypoenhancement localized in the basal-to-mid septal and mid anterolateral walls of the left ventricle, strongly suggestive of acute inflammation. Based upon these findings, we performed CT-guided EMB, which lead to a definitive diagnosis. Subsequent high-dose corticosteroids allowed a rapid and dramatic recovery and normalization of cardiac structure and function. This case highlights the clinical importance of assessing AEM as a rare cause of HFpEF and the usefulness of CT-guided EMB in patients with hemodynamic instability

Value of late gadolinium enhancement by magnetic resonance in patients with cardiac sarcoidosis: characteristic findings and clinical utility

73rd Annual Scientific Meeting of the Japanese Circulation Society 2009年03月 Osak

14-Cmethionine uptake as a potential marker of inflammatory processes after myocardial ischemia and reperfusion

A relationship between L-[methyl-11C]methionine (11C-methionine) uptake and angiogenesis has been suggested in gliomas. However, methionine uptake in myocardial ischemia and reperfusion has received little attention. We investigated the serial changes and mechanisms of 14-Cmethionine uptake in a rat model of myocardial ischemia and reperfusion. Methods: The left coronary artery was occluded for 30 min, followed by reperfusion for 1-28 d. At the time of the study, 14-Cmethionine (0.74 MBq) and 201Tl (14.8 MBq) were injected intravenously at 20 and 10 min before sacrifice, respectively. One minute before sacrifice, the left coronary artery was reoccluded, and 99mTc-hexakis-2-methoxyisobutylisonitrile (150-180 MBq) was injected to verify the area at risk. Histologic sections of the heart were immunohistochemically analyzed using anti-CD68, anti-smooth-muscle a-actin (SMA), and antitroponin I and compared with the autoradiography findings. Results: Both 14Cmethionine (uptake ratio, 0.71 ± 0.13) and 201Tl uptake were reduced in the area at risk at 1 d after reperfusion. However, 3 d after reperfusion, an increased 14-Cmethionine uptake (1.79 ± 0.23) was observed corresponding to the area of still-reduced 201Tl uptake, and the 14-Cmethionine uptake gradually declined until 28 d. The increased 14-Cmethionine uptake area at 3 and 7 d corresponded well to the macrophage infiltrations demonstrated by positive CD68 staining. Anti-SMA staining appeared at 7 d, after which CD68 staining was gradually replaced by the SMA staining, suggesting that methionine uptake in the early phase after ischemia and reperfusion might reflect inflammatory activity. Conclusion: 14-Cmethionine accumulated in the infarcted area, and its uptake corresponded closely to macrophage infiltration at 3-7 d after reperfusion. Methionine imaging may be useful for inflammatory imaging early after myocardial infarction. COPYRIGHT © 2013 by the Society of Nuclear Medicine and Molecular Imaging, Inc

Effect of postconditioning on dynamic expression of tenascin-C and left ventricular remodeling after myocardial ischemia and reperfusion

金沢大学疾患モデル総合研究センターBackgroundTenascin-C (TNC), an extracellular matrix glycoprotein, is expressed transiently in distinct areas in association with active tissue remodeling. This study aimed to explore how ischemic postconditioning (PC) affects myocardial expression of TNC and ventricular remodeling using 125I-labeled anti-TNC antibody (125I-TNC-Ab) in a rat model of ischemia and reperfusion.MethodsIn control rats (n = 27), the left coronary artery (LCA) was occluded for 30 min followed by reperfusion for 1, 3, 7, and 14 days. PC (n = 27) was performed just after the reperfusion. At the time of the study, 125I-TNC-Ab (1.0 to 2.5 MBq) was injected. Six to 9 h later, to verify the area at risk, 99mTc-MIBI (100 to 200 MBq) was injected intravenously just after the LCA reocclusion, with the rats sacrificed 1 min later. Dual tracer autoradiography was performed to assess 125I-TNC-Ab uptake and area at risk. To examine the ventricular remodeling, echocardiography was performed 2 M after reperfusion in both groups.ResultsIn control rats, 125I-TNC-Ab uptake ratio at 1 day after reperfusion was 3.73 ± 0.71 and increased at 3 days (4.65 ± 0.87), followed by a significant reduction at 7 days (2.91 ± 0.55, P < 0.005 vs 3 days) and14 days (2.01 ± 0.17, P < 0.005 vs 1 and 3 days). PC attenuated the 125I-TNC-Ab uptake throughout the reperfusion time from 1 to 14 days; 2.59 ± 0.59 at 1 day, P < 0.05: 3.10 ± 0.42 at 3 days, P < 0.005: 1.93 ± 0.37 at 7 days, P < 0.05: 1.40 ± 0.07 at 14 days, P < 0.001. In echocardiography, PC reduced the ventricular end-diastolic and systolic dimensions (1.00 ± 0.06 cm to 0.83 ± 0.14 cm (P < 0.05) and 0.90 ± 0.15 cm to 0.62 ± 0.19 cm (P < 0.05), respectively) and prevented a decline of ventricular percentage fractional shortening (10.5 ± 3.7 to 28.2 ± 10.7, P < 0.005).ConclusionsThese data indicate that 125I-TNC-Ab imaging may be a way to monitor myocardial injury, the subsequent repair process, and its response to novel therapeutic interventions like PC by visualizing TNC expression

Dynamic expression of tenascin-C after myocardial ischemia and reperfusion: Assessment by125i-anti-tenascin-c antibody imaging

金沢大学疾患モデル総合研究センターTenascin-C, an extracellular matrix glycoprotein, appears only in the early stages of embryonic development. It is not normally expressed in the adult heart but does reappear transiently in distinct areas in association with active tissue remodeling. The aim of this study was to explore serial changes in the expression of tenascin-C after myocardial ischemia and reperfusion, using 125I-labeled anti-tenascin-C antibody (125I-TNC-Ab) in a rat model of acute ischemia and reperfusion. Methods: The left coronary artery was occluded for 20or30min, followedbyreperfusion for 1, 3, or 7 d in rats with 20 min of ischemia and for 1, 3, 7, 14, or 28 d inrats with30min ofischemia.Atthe timeofthe study,125I-TNC-Ab (1.0-2.5 MBq) was injected. Three to 5 h later, to verify the area at risk,99mTc- methoxyisobutylisonitrile (100-200 MBq) was injected intravenously just after the left coronary artery reocclusion and the rats were sacrificed 1 min later. Dual-tracer autoradiography was performed to assess125I-TNC-Ab uptake and the area at risk. Results: In rats with 20 min of ischemia, 125I-TNC-Ab uptake peaked at 3 d after reperfusion, followed by faint uptake after 7 d (uptake ratios at 1, 3, and 7 d after reperfusion were 1.81 ± 0.53, 2.46 ± 0.79, and 1.23 ± 0.17, respectively [P < 0.05 vs. 3 d]). In rats with 30 min of ischemia, uptake was high at 1 and 3 d after reperfusion (2.99 ± 0.90 and 2.71 ± 0.80, respectively), decreased at 7 and 14 d (1.94 ± 0.23 and 2.06 ± 0.37, respectively), and was weak at 28 d (1.47 ± 0.27, P < 0.005 vs. 1 d, P < 0.05 vs. 3 d). Conclusion: These data indicate that125I-TNC-Ab imaging may be a way to monitor myocardial injury and its repair process after ischemia and reperfusion by visualizing tenascin-C expression. COPYRIGHT © 2010 by the Society of Nuclear Medicine, Inc