Pericardial fat volume is an independent risk factor for the severity of coronary artery disease in patients with preserved ejection fraction.

OBJECTIVES: The aim of this study was to assess the relationship between the pericardial fat volume (PFV) and the characteristics of coronary plaques in patients with ischemic heart disease (IHD). BACKGROUND: It has been suggested that pericardial adipose tissue promotes plaque development in coronary artery disease (CAD). METHODS: We analyzed the cardiac computed tomography scans in consecutive patients suspected of CAD. PFV was quantified using validated software and indexed to body surface area, and the severity of coronary stenosis was evaluated in the patients who underwent coronary angiography. A total of 105 subjects (mean age, 68±10 years) with IHD were categorized into tertiles of body surface area-indexed PFV values (PFVi, cm3/m2): low-tertile, PFVi < 81.2 cm3/m2; mid-tertile, 81.2 cm3/m2 ≤ PFVi ≤ 114 cm3/m2; high-tertile, PFVi > 114 cm3/m2. Their body mass index (BMI), waist circumference, Gensini score (GS), and coronary plaque component were evaluated. RESULTS: The GS was significantly different between the high-tertile and the low-tertile groups, indicating a stepwise decrease in GS from high-tertile to mid-tertile and to low-tertile. PFVi had a significant positive correlation with BMI (p=0.0001) and GS (p<0.0001). However, no significant association was found between GS and BMI. On the multivariate analysis, high PFVi remained an independent predictor for the coronary artery disease severity (p<0.001), while BMI and waist circumference were not independent predictors. CONCLUSIONS: Obese patients were found to have more PFVi, and the characteristics of their coronary lesions were more severe. Pericardial adipose tissue as unique ectopic fat might be more highly associated with IHD progression.

Fluorodeoxyglucose accumulation in the left atrial appendage of a patient with paroxysmal atrial fibrillation.

A 69-year-old man with a history of paroxysmal atrial fibrillation (PAF) and subsequent cerebral infarction was referred to our hospital because of an abnormal accumulation of 18F-fluorodeoxyglucose (FDG) in the left atrial appendage (LAA) that was detected on positron emission tomography-computed tomography (PET-CT) imaging during a health screening. Transesophageal echocardiography (TEE) demonstrated thrombus formation in the LAA. Even after the thrombus disappeared by strictly guided oral anticoagulant therapy, intense abnormal FDG uptake in the LAA on PET-CT imaging persisted. In low-risk patients such as this, inflammation may have played some role in LAA thrombus formation.

Survival after acute necrotizing eosinophilic myocarditis complicating a massive left ventricular mural thrombus: a case report.

An 81-year-old man was referred to our hospital with exertional dyspnea following cold-like symptoms. Electrocardiography revealed ST elevation and positive T wave in leads I, II, aVL, aVF, and V2-V6. The diagnosis was acute myocarditis complicating heart failure. He was conservatively managed. On hospital day 8, brain infarction developed and echocardiography disclosed massive mural thrombus in the left ventricle. Left ventriculotomy was performed on hospital day 21 and histological examination showed inflammatory cell infiltration mainly composed of eosinophils and monocytes, degeneration of myocytes with replacement fibrosis, and fresh fibrin thrombus overlaying the endocardium. These findings were compatible with a diagnosis of acute necrotizing eosinophilic myocarditis(ANEM). He recovered uneventfully without specific therapy. This case suggests that a subtype of ANEM might be self-limiting.

A precise pharmacodynamic study showing the advantage of a marked reduction in cardiotoxicity in continuous infusion of doxorubicin.

We have already shown that the antileukemic activity of daunorubicin that had been reported to be dependent on the area under the concentration - time curve (AUC) was actually peak concentration (Cmax) dependent. The antitumor activity of doxorubicin (DXR) has also been reported to be dependent on AUC, whereas its cumulative cardiotoxicity has been reported to be Cmax dependent. In this study, we evaluated whether the antileukemic and cardiotoxic effects of DXR were AUC or Cmax dependent, and compared their cytotoxic effects, utilizing the computer-controlled in vitro pharmacokinetic simulation system or a conventional culture system for a leukemic cell line and measuring the intracellular ATP amount or the proportion of beating cells for the cardiotoxicity. In leukemic cells, the cytotoxic rate decreased as the simulated infusion time or exposure time increased with the same AUC value in the simulation and conventional culture system (P < 0.05 and <0.01, respectively). The intracellular ATP and proportion of beating cells also increased with prolonged DXR exposure time with the same constant concentration - time product value (P < 0.05 and <0.0001, respectively) in heart cells. These results indicated that both the antileukemic effects and the cardiotoxicity were Cmax dependent. However, a comparison of the two showed that cardiotoxicity was more Cmax dependent than the antileukemic effect. These results suggested that the continuous infusion treatment schedule of DXR may have the clinical advantage of reducing cardiotoxicity more markedly than the antileukemic effect.

Reversible defect of 123I-15-(p-iodophenyl)-9-(R,S)-methylpentadecanoic acid indicates residual viability within infarct-related area.

To evaluate the relationship between the reversible defect of 123I-15-(p-iodophenyl)-9-(R,S)-methylpentadecanoic acid (9MPA) and residual viability within an infarct-related area, we performed resting single photon emission computed tomography (SPECT) with 9MPA and positron emission tomography (PET) with 18F-deoxyglucose (FDG) and 13N-ammonia (NH3) in 7 patients with prior myocardial infarction. 9MPA-SPECT was obtained 2 min (early) and 50 min (delayed) after tracer injection. Tomographic images of the left ventricle were divided into 13 segments to correlate the regional uptake of each tracer. Residual viability within an infarct-related segment was confirmed by NH3- and FDG-PET. Twenty-six infarct-related segments, confirmed by NH3-PET, showed reduced uptake of 9MPA on early images. In these 26 segments, 6 showed reversible defect of 9MPA and 20 showed fixed defect on delayed images. Residual viability was present in all segments exhibiting reversible 9MPA defect and 7 segments (35%) exhibiting fixed defect (p < 0.05). The sensitivity, specificity and accuracy of reversible 9MPA defect for the detection of myocardial viability were 46%, 100%, and 73%, respectively. Myocardial clearance of 9MPA was significantly slower in non-viable segments than in ischemic but viable segments (4.9+/-5.1% vs. 10.1+/-5.3%; p < 0.05). These data suggest that a reversible 9MPA defect indicates residual viability within the infarct-related area.