No abstract

Serum IL-10 levels on admission enabled one to predict subsequent CS requiring MCSS and mortality of fulminant myocarditis patients.

SummaryThe recommended treatment for eosinophilic myocarditis (EM), pathologically defined as myocardial inflammation with eosinophil infiltration, is corticosteroids. Although EM has a wide variety of clinical features including the degree of eosinophilic infiltration, there have been no reports on how patients with EM should be treated with corticosteroids irrespective of their pathological findings.Thirty-seven consecutive patients with acute myocarditis hospitalized in our institute between 1996-2009 were enrolled. Excluding those with secondary EM such as Loeffler's endocarditis, hypereosinophilic syndrome, and ChurgStrauss Syndrome, together with drug-induced allergic myocarditis, the subjects were divided into 2 groups according to the existence of eosinophils in the myocardial interstitium observed in endomyocardial biopsy specimens. There were no differences in the clinical characteristics on admission between the 2 groups: with (group EM, n = 22) and without (group lymphocytic myocarditis (LM), n = 7) eosinophilic infiltrates irrespective of pathological differences. The treatment policy has been consistent in our institution: intensive hemodynamic observation and support without corticosteroid administration, not only in LM but also in idiopathic EM. There was no significant difference in clinical recovery in the acute phase as indicated by the hospitalization period, left ventricular ejection fraction, or long-term prognosis in EM compared to LM.A conventional management strategy for idiopathic EM without corticosteroid administration can improve the prognosis in the acute and chronic phases, similar to that of LM. (Int Heart J 2011; 52: 110-113) Key words: Eosinophilic myocarditis, Endomyocardial biopsy, Corticosteroid therapy E osinophilic myocarditis (EM) is a relatively rare condition. Although the etiology of EM is not always apparent, several causes have been identified, including hypersensitivity to medicine or some other substance with the heart as the target organ. The spectrum of clinical presentation is wide, and EM is likely to lead to progressive myocardial damage with destruction of the conduction system and then refractory heart failure. It is widely known that EM demonstrates cardiac symptoms with pathological findings of infiltration of eosinophils and degranulation in the myocardium. It has been recommended EM be treated with corticosteroid therapy, according to the guidelines 1) but such is not the case regarding viral myocarditis. In previous reports, some cases of EM, including those with a history of severe left ventricle (LV) dysfunction and aborted sudden death, showed dramatic responses to corticosteroid therapy.2,3) In one case report, an intravenous bolus of methylprednisolone (1 g/day for three days) followed by 1 mg/kg/day oral prednisolone with gradual tapering for one year resulted in an improvement of symptoms, a reduction in the eosinophil count, and increased LV ejection fraction as shown by echocardiography. 4) Also, some reports have shown that conventional managem...

An interaction between the intestine and cardiovascular disease has been suggested. We thought to clarify the association between intestinal conditions and clinical outcomes in patients with heart failure (HF). Hemodynamic parameters in intestinal vessels [superior mesenteric artery (SMA), inferior mesenteric artery (IMA), and portal vein (PV)] and average colon wall thickness (aCWT) from the ascending colon to sigmoid colon were evaluated in 224 hospitalized HF patients. Echocardiographic parameters and composite event rates (all-cause mortality, readmission for HF deterioration, major ventricular arrhythmias) were also examined. Higher PV congestion index (CI) and aCWT were observed in patients with New York Heart Association (NYHA) class III/IV. Higher PVCI [hazard ratio (HR) per + 1 standard deviation (SD) 1.50, p < 0.01] and aCWT (HR per + 1 SD 1.45, p < 0.01) were independently associated with higher composite event rates during the follow-up of 122 ± 68 days. None of SMA/IMA hemodynamic parameters were associated with NYHA class or composite event rates. Higher right ventricular end-diastolic dimension (38 ± 7 vs 34 ± 9 mm, p < 0.01) and lower tricuspid annual plane systolic excursion (15 ± 5 vs 19 ± 5 mm, p < 0.001) were observed in patients with higher PVCI (> 0.031 cm s) and aCWT (> 2.8 mm) relative to those in others. In conclusion, increased portal congestion and intestinal edema were associated with severe HF symptoms and poor outcomes in hospitalized HF patients, in addition to being associated with impaired right-sided cardiac function.

This study aimed to identify the association between the time course of left ventricular reverse remodeling (LVRR) and late gadolinium enhancement in cardiac magnetic resonance imaging (LGE-cMRI) in patients with idiopathic dilated cardiomyopathy (IDCM). We identified 214 IDCM patients treated by optimal pharmacotherapies. LVRR was defined as ≥10 % increment in LV ejection fraction along with ≥10 % reduction in LV end-diastolic dimension. Findings of LGE-cMRI focusing on presence and extent of LGE were evaluated at baseline. Echocardiographic evaluation for detecting LVRR was performed in all patients for 3 years. The primary endpoint was defined as composite events (CEs) including readmission for heart failure, detection of major ventricular arrhythmia, and all-cause mortality. LVRR was found at <1 year in 59 patients (28 %, early responder), ≥1 year in 56 patients (26 %, late responder), and was absent in 99 patients (46 %, non-responder). Multivariate Cox-proportional hazards analysis revealed that both early responders (P = 0.02) and late responders (P < 0.001) had lower incidence of CEs than non-responders. Among 66 subjects (23 %) with complete cMRI evaluation, LGE was detected more often in late and non- than early responders (65, 83 vs. 23 % P < 0.001, respectively), whereas the LGE area was smaller in both early and late than non-responders (2 ± 3, 4 ± 3 vs. 12 ± 10 %, P < 0.001, respectively). In conclusion, evaluating the presence and the extent of LGE is useful for predicting the clinical differences of LVRR time course and subsequent long-term outcomes.