Prognostic significance of right ventricular dimension on acute decompensation in chronic left-sided heart failure.

Right ventricular (RV) dysfunction has been discussed in relation to an adverse outcome in heart failure (HF). The aim of this study was to analyze the relationship between RV function with HF exacerbation and its subsequent long-term outcome in patients with chronic left-sided HF.We studied 122 consecutive patients who were admitted for dyspnea due to exacerbated left-sided HF with a left ventricular (LV) ejection fraction of less than 40%. Conventional echocardiography was performed in the study subjects on admission and at discharge. Cox proportional hazards analysis revealed that RV end-diastolic dimension (RVDd) (hazard ratio 1.131, P = 0.005, 95% confidence interval 1.039-1.231) and the serum level of creatinine on admission were independent predictors of subsequent cardiac-related death, but RVDd at discharge and other LV parameters were not. Thus, patients were divided into tertiles on the basis of RVDd on admission: < 32 mm (n = 37), 32-40 mm (n = 43), and ≥ 40 mm (n = 42). According to the increase in the RVDd category, the cardiac-related death-free rate significantly decreased. Among the 3 groups, the pulse pressure and serum total bilirubin levels that demonstrated low cardiac output syndrome (LOS) parameters had significant differences.RVDd on admission could be measured noninvasively and easily to predict a worse long-term prognosis of chronic left-sided HF on admission, and showed correlations with LOS parameters.

99mTc-Hynic-annexin V imaging to evaluate inflammation and apoptosis in rats with autoimmune myocarditis.

Inflammation and cell death are two important components of myocarditis. We evaluated the distribution of inflammation and apoptotic cell death in rats with autoimmune myocarditis using two radiotracers - technetium-99m Hynic-annexin V ((99m)Tc-annexin) as a marker of apoptotic cell death and carbon-14 deoxyglucose ((14)C-DG) as a marker of inflammation - in comparison with histologic findings. Three, 7 and 14 weeks after immunization with porcine cardiac myosin (acute, subacute, and chronic phases, respectively) (99m)Tc-annexin and (14)C-DG were injected. The uptake in the total heart was determined as the percentage of injected dose per gram (% ID/g) by tissue counting. Dual-tracer autoradiography with (99m)Tc-annexin and (14)C-DG was performed. The distribution of each of these agents was compared with the results of hematoxylin and eosin staining to identify areas of inflammation, and TUNEL staining to identify areas of apoptosis. Total cardiac uptake of (99m)Tc-annexin in the acute phase of myocarditis was significantly higher than that in normal rats (1.28%+/-0.30% vs 0.46%+/-0.01%; P<0.0001); it then decreased in the subacute phase and reached normal levels (0.56%+/-0.08% vs 0.60%+/-0.08%; P=NS). Total cardiac uptake of (14)C-DG in the acute phase of myocarditis was significantly higher than that in normal rats (2.78%+/-0.95% vs 1.02%+/-0.25%; P<0.0001); it then decreased in the subacute phase, but still remained higher than in controls (2.06%+/-0.52% vs 1.37%+/-0.46%; P<0.05). Using autoradiography and staining of tissue specimens, it was found that most histologic inflammatory foci corresponded to areas of high (14)C-DG uptake; some also corresponded to areas of high (99m)Tc-annexin uptake in the acute phase of myocarditis. (99m)Tc-annexin localization was strongly correlated with the number of TUNEL-positive cells (P<0.0001, r=0.83), but the uptake of (14)C-DG showed no relationship with it. There is a marked difference in the distribution of inflammation and apoptotic cell death in the myocardium of animals with immune myocarditis. These changes are mirrored by the localization of (14)C-DG and (99m)Tc-annexin. Sites of inflammation and zones of apoptotic cell death change over the course of immune myocarditis.

[No 123I-BMIPP accumulation in the myocardium and type I CD36 deficiency in a patient with acute subendocardial infarction: a case report].

This patient was a 70-year-old man had acute subendocardial infarction in the inferior wall. 123I-BMIPP myocardial scintigraphy showed no accumulation in the myocardium. 123I-MIBG myocardial scintigraphy on the early and delay images and 99mTc-tetrofosmin myocardial scintigraphy at rest showed slightly decreased accumulation of the tracer in the apical region and in middle inferior wall of the left ventricle, indicating subendocardial infracted area. In the examinations of CD36 in platelets and monocytes, the patient had negative CD36 in platelets and monocytes, and type I CD36 deficiency was diagnosed. We supposed that no 123I-BMIPP accumulation may be related closely to type I CD36 deficiency.