Aims Predictive models for heart failure patients are widely used in the clinical practice to stratify patients' mortality and enable clinicians to tailor and intensify their approach. However, such models have not been validated internationally. In addition, biomarkers are now frequently measured to obtain prognostic information, and the implications of this practice are not known. In this study, we aimed to validate the model performance of the Meta‐analysis Global Group in Chronic Heart Failure (MAGGIC) score in a Japanese acute heart failure registry and further explore the incremental prognostic value of discharge B‐type natriuretic peptide (BNP) level. Methods and Results In this study, we evaluated the registered data of 2215 consecutive acute HF patients (with 694 119 person‐years follow‐up) from a prospective multicentre registry (the West Tokyo Heart Failure) conducted in Japan from April 2006 to August 2016. The mean age was 73.0 ± 13.0, and 61.2% were male. The MAGGIC score demonstrated modest discrimination (c‐index = 0.71, 95% confidence interval 0.67–0.74) and good calibration (R² value = 0.97); there was constant overestimation for 1 year mortality. However, when the BNP level was added to the original MAGGIC variables, the model demonstrated good discrimination (c‐index = 0.74, 95% confidence interval 0.70–0.78) with adequate calibration (R² value = 0.91). The modified MAGGIC BNP score was externally validated in a separate Japanese registry (NaDEF) and demonstrated moderate discrimination (c‐index = 0.69, 95% confidence interval 0.65–0.73) and calibration (R² value = 0.85). Conclusion The original MAGGIC score performed modestly in Japanese patients, but the addition of discharge BNP level enhanced model performance. The addition of objective biomarkers may result in effective modification of preexisting internationally recognized risk models and aid in multinational comparisons of heart failure patients' outcomes.

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Autoimmune abnormalities, as well as viral infection and genetic abnormalities, appear to be major predisposing factors for dilated cardiomyopathy (DCM). Abnormalities of cell-mediated immunity are mainly involved in the onset of cardiomyopathy secondary to myocarditis. However, various antimyocardial antibodies are detected in the serum of patients with DCM. The appearance of these antibodies was considered to be an epiphenomenon associated with myocyte injury resulting from myocarditis, but recent findings have suggested that at least some of them are directly related to the pathophysiology of DCM. In particular, an autoantibody targeting the β1-adrenergic receptor that exhibits an agonist-like effect is related to the persistent myocardial damage resulting in DCM and provides substrates for fatal ventricular arrhythmias. In addition, an antibody for the muscarinic M2 receptor is related to atrial fibrillation, an antibody targeting Na-K-ATPase is closely related to sudden cardiac death as a result of fatal ventricular arrhythmias, and an autoantibody for troponin I increases the L-type calcium current and is related to the myocardial damage. Based on these findings, immunoadsorption therapy was developed to remove such autoantibodies in patients with refractory heart failure as a result of DCM. (Circ J 2009; 73: 602 - 607)

Heart failure (HF) is a syndrome with global clinical and socioeconomic burden worldwide owing to its poor prognosis. Accumulating evidence has implicated the possible contribution of gut microbiota-derived metabolites, short-chain fatty acids (SCFAs), on the pathology of a variety of diseases. The changes of SCFA concentration were reported to be observed in various cardiovascular diseases including HF in experimental animals and humans. HF causes hypoperfusion and/or congestion in the gut, which may lead to lowered production of SCFAs, possibly through the pathological changes of the gut microenvironment including microbiota composition. Recent studies suggest that SCFAs may play a significant role in the pathology of HF, possibly through an agonistic effect on G-protein-coupled receptors, histone deacetylases (HDACs) inhibition, restoration of mitochondrial function, amelioration of cardiac inflammatory response, its utilization as an energy source, and remote effect attributable to a protective effect on the other organs. Collectively, in the pathology of HF, SCFAs might play a significant role as a key mediator in the gut–heart axis. However, these possible mechanisms have not been entirely clarified and need further investigation.