Dynamic Trend of Myocardial Edema in Takotsubo Syndrome: A Serial Cardiac Magnetic Resonance Study.

BACKGROUND: The wall motion abnormalities of the left ventricle (LV) in takotsubo syndrome (TTS) are known to be transient and completely recover within a few weeks. However, there is little information about the relationship between functional recovery and tissue characteristics. The aim of this study was to investigate the recovery process of TTS using cardiovascular magnetic resonance (CMR). METHODS: Consecutive patients with TTS were prospectively enrolled. We performed serial CMR in the acute phase (<72 h after admission), the subacute phase (7-10 days after admission) and the chronic phase (3 months later). To assess the degree of myocardial edema quantitatively, we evaluated the signal intensity of myocardium on T2-weighted images and calculated the signal intensity ratio compared with the skeletal muscle. RESULTS: Fifteen patients with TTS were enrolled. CMR demonstrated reduced LV ejection fraction in the acute phase, and it recovered almost completely by the subacute phase. On the other hand, severe myocardial edema was still observed in the subacute phase, associated with increased LV mass. The highest signal intensity ratio in the subacute phase was correlated with the maximum voltage of negative T wave on electrocardiogram (r = 0.57, p = 0.03). CONCLUSIONS: In patients with TTS, myocardial edema associated with increased LV mass still remained in the subacute phase despite functional recovery of the LV. Electrocardiogram may be useful to assess the degree of myocardial edema in the subacute phase. Our study suggests that myocardial ischemia might have a central role in developing TTS.

Case Report: Sustained mitochondrial damage in cardiomyocytes in patients with severe propofol infusion syndrome.

Introduction: Propofol infusion syndrome (PRIS) is rare but a potentially lethal adverse event. The pathophysiologic mechanism is still unknown. Patient concerns: A 22-year-old man was admitted for the treatment of Guillain-Barré syndrome. On day six, he required mechanical ventilation due to progressive muscle weakness; propofol (3.5 mg/kg/hour) was administered for five days for sedation. On day 13, he had hypotension with abnormal electrocardiogram findings, acute kidney injury, hyperkalemia and severe rhabdomyolysis. Diagnosis and interventions: The patient was transferred to our intensive care unit (ICU) on suspicion of PRIS. Administration of noradrenaline and renal replacement therapy and fasciotomy for compartment syndrome of lower legs due to PRIS-rhabdomyolysis were performed. Outcomes: The patient gradually recovered and was discharged from the ICU on day 30. On day 37, he had repeated sinus bradycardia with pericardial effusion in echocardiography. Cardiac 18F-FDG PET on day 67 demonstrated heterogeneous 18F-FDG uptake in the left ventricle. Electron microscopic investigation of endomyocardial biopsy on day 75 revealed mitochondrial myelinization of the cristae, which indicated mitochondrial damage of cardiomyocytes. He was discharged without cardiac abnormality on day 192. Conclusions: Mitochondrial damage in both morphological and functional aspects was observed in the present case. Sustained mitochondrial damage may be a therapeutic target beyond the initial therapy of discontinuing propofol administration.

Right ventricular sugars and fats in chronic thromboembolic pulmonary hypertension.

BACKGROUND/OBJECTIVES: Several studies have already shown the correlation between the right ventricle (RV) hemodynamic values and either glucose uptake or fatty acid uptake in the RV, respectively. However, there are few studies to compare the RV metabolic alteration before and after treatment for pulmonary hypertension. The aims of this study are to assess right ventricular glucose and fatty acid in chronic thromboembolic pulmonary hypertension (CTEPH) patients before and after pulmonary thromboendarterectomy and to examine whether there is a correlation between right ventricular glucose and fatty acid uptake. METHODS: To assess glucose and fatty acid accumulation in the RV, [(18)F] fluoro-2-deoxyglucose (FDG)-positron emission tomography (PET) and (123)I-ß-methyl iodophenyl pentadecanoic acid (BMIPP) imaging were performed in CTEPH patients before (FDG: n=20, BMIPP: n=13) and after (FDG: n=12, BMIPP: n=8) thromboendarterectomy. RESULTS: Both [(18)F] FDG uptake and (123)I-BMIPP uptake in RV of post-PEA patients obviously decreased after this operation procedure (p<0.01). The right ventricle [(18)F] FDG uptake was also significantly correlated with (123)I-BMIPP uptake (r=0.45, p=0.04). CONCLUSIONS: In this study, we observed that both glucose and fatty acid accumulated in the RV of patients with CTEPH. Although the exact details of the altered energy metabolism in the stressed RV remain unknown, this is the first study to evaluate both glucose and fatty acid uptake before and after thromboendarterectomy in patients with CTEPH, even though the number of the patient is limited.

Transient semi-circumferential mid-ventricular ballooning: An atypical variant of takotsubo cardiomyopathy.

Although apical ballooning is the most common morphological type of takotsubo cardiomyopathy, variants have been reported. Several case reports have demonstrated focal takotsubo cardiomyopathy. Most cases had left ventricular wall motion abnormality in the anterolateral segment. We present a case of focal ventricular ballooning localized especially in the inferior mid-ventricular segment. .

Determination of optimum periods between onset of suspected acute myocarditis and ¹8F-fluorodeoxyglucose positron emission tomography in the diagnosis of inflammatory left ventricular myocardium.

PURPOSE: To determine optimum periods for (18)F-fluorodeoxyglucose (FDG) positron emission tomography (PET) examination in subjects with suspected acute myocarditis, we compared (18)F-FDG PET with endomyocardial biopsy (EMB) using the latest definition of (18)F-FDG PET for inflammatory left ventricular (LV) myocardium. MATERIALS AND METHODS: Retrospective analysis of 29 subjects (18 male, 48 ± 18 years) who have symptoms or LV dysfunction underwent both (18)F-FDG PET (Advance NXi, GE-Healthcare) under fasting conditions and EMB from LV posterior wall within 3 months. RESULTS: When we defined (18)F-FDG PET positive inflammatory LV posterior wall as 'focal on diffuse' pattern, sensitivity, specificity, and positive predictive values (PPV), and negative predictive values (NPV) of (18)F-FDG PET for detecting active inflammatory LV posterior wall compared with EMB were 46.2, 81.3, 66.7, and 65.0%, respectively. Receiver operating characteristic curve of periods (days) between onset of clinically suspected acute myocarditis and performance of (18)F-FDG PET for detecting inflammatory LV posterior wall demonstrated 17 days as a best cut off values with area under the curve (0.497, P=0.982) with sensitivity=21.1% and specificity=100%. Sensitivity, specificity, PPV and NPV of (18)F-FDG PET for detecting inflammatory LV posterior wall on EMB were all 100% when (18)F-FDG PET was performed at 1-14 days after onset of suspected acute myocarditis. CONCLUSIONS: In our definition, (18)F-FDG PET showed excellent agreement with EMB for detecting active inflammatory LV posterior wall in subjects with clinically suspected active acute myocarditis. If possible, (18)F-FDG PET should be performed within 14 days after the onset to maintain high diagnostic accuracy compared with EMB.

Cardiac sarcoidosis evaluated by multimodality imaging.

An asymptomatic 62-year-old female patient with sarcoidosis was referred to our hospital for new-onset right bundle-branch block by electrocardiogram (ECG). She had been diagnosed with sarcoidosis by lymph node biopsy 3 years previously, and followed up by chest X-ray and ECG from then onward. Chest X-ray on admission showed bilateral lymph node enlargement, which was unchanged. Transthoracic echocardiogram showed wall thinning and severe hypokinesis in the basal portion of the left ventricular (LV) posterior-inferior wall, and coronary heart disease was excluded by conventional coronary angiogram. ECG-gated enhanced 320 slice multislice computed tomography revealed contrast defects in the basal portion of the LV posterior-inferior wall with reduced wall thickness in the early phase, which were conversely abnormally enhanced in the late phase, suggesting fibrosis or edema with inflammation. Late gadolinium enhancement in contrast-enhanced magnetic resonance imaging (MRI) was observed in the same region. To evaluate for evidence of inflammation, we performed 67-gallium-citrate scintigraphy, T2-weighted MRI, and fasting 18F-fluoro-deoxyglucose (FDG) positron emission tomography (PET). Although the 67-Ga scintigram showed no significant uptake, T2-weighted MRI revealed high intensity images, and fasting 18F-FDG PET identified increased uptake of FDG in the basal portion of the LV posterior-inferior wall, suggesting inflammation. We started corticosteroid therapy, diagnosing her condition as active cardiac sarcoidosis.

Comprehensive evaluation of characteristics of left ventricular myocardium in a subject with non-coronary arterial cardiac dysfunction through segment by segment analysis using various diagnostic modalities.

We performed segment by segment analysis for comprehensive evaluation of the characteristics of the left ventricular (LV) myocardium by multislice CT (MSCT), magnetic resonance imaging (MRI), single photon emission computed tomography (SPECT) and positron emission tomography (PET) in a patient with non-coronary arterial cardiac dysfunction. If diagnosis had been performed only by transthoracic echocardiogram and conventional coronary angiography, this subject might have been diagnosed as having dilated cardiomyopathy. However, we succeeded in the detailed evaluation of characteristics of LV myocardium non-invasively. Because of the difference in spatial resolution, MSCT and MRI could only detect focal fibrosis and MSCT could only detect fatty changes in the LV myocardium with an accurate ratio of thickness of lesions in comparison with the thickness of the whole LV myocardium. Conversely, a drawback of PET and SPECT was the partial volume effect and these methods could visualize the lesions as only diffuse decrements of attenuation and could not provide detailed information. Furthermore in MSCT, LV wall motion abnormality could be visualized by showing the ribs, sternum and descending aorta and in particular MSCT could obtain much information, including extra cardiac findings.

Active myocarditis in a patient with chronic active Epstein-Barr virus infection.

Chronic active Epstein-Barr virus (CAEBV) infection is characterized by chronic or recurrent infectious mononucleosis-like symptoms and the prognosis of CAEBV infection is quite poor. The incidence of myocarditis as a complication of EBV infection is not so high and it is unusual that heart failure appears as the initial symptom. However, it is very important to detect and treat chronic active myocarditis in the early phase of CAEBV infection because chronic active myocarditis disorganizes and decreases cardiomyocytes, resulting in the progression to heart failure. We report a case of a 45-year-old man with CAEBV infection for 5 years. Echocardiography revealed moderate left ventricular systolic dysfunction with mild pericardial effusion. Endomyocardial biopsies demonstrated massive lymphocytic infiltration with adjacent myocytolysis and necrosis of cardiomyocytes suggesting active myocarditis. Immunohistological analysis of biopsies revealed that the infiltrating cells were mainly T lymphocytes. And some of the infiltrating cells showed a positive signal for the EBV-encoded small nuclear RNA by in situ hybridization. Positron emission tomography using (18)F-fluoro-2-deoxyglucose ((18)F-FDG) performed revealed increased uptake of (18)F-FDG of whole left ventricular wall with mild heterogeneity.

Hemangioma located just above the left main coronary artery, in a subject who had cardiac arrest due to ventricular fibrillation, led to a diagnosis of Brugada syndrome.

We report the case of a 38-year-old Asian man with a pericardial hemangioma on the left main coronary artery. The patient presented initially at our hospital after cardiopulmonary resuscitation following an episode of ventricular fibrillation (VF). Because of spontaneous coved-type ST segment elevation on the higher intercostal space V1 to V2 in a 12-lead electrocardiogram, documented VF in the absence of structural heart disease, and a family history of sudden death, he was diagnosed with Brugada syndrome. Transesophageal echocardiography showed a smooth-surfaced mass with well-demarcated borders, directly above the left main coronary artery. Computed tomography confirmed the presence of the mass, which showed no enhancement at early phase, but did demonstrate homogenous enhancement at delay phase by contrast material. There were no findings from either the nuclear medicine or the tumor marker investigations which indicated that the mass located just above the main coronary arteries was malignant. Therefore, taken together, these findings suggested that the tumor might be a pericardial hemangioma. The relationship between the location of the hemangioma just above the left main coronary artery and the occurrence of VF was not clear, i.e. whether the presence of the hemangioma caused the stimulation of the left main coronary artery and as a result, led to the spasm of the left main coronary artery and the occurrence of VF. Furthermore, as the tumor did not extend into any of the adjacent structures, such as the coronary arteries or the right ventricular outflow tract, surgical resection was not performed; instead, the patient received a dual chamber implantable cardioverter-defibrillator.