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In 2009, the "Guidelines for diagnosis and treatment of myocarditis (JCS 2009)" were issued by the Japanese Circulation Society (JCS). 1 Although this guideline has been widely used in clinical practice for more than a decade, it is certain that they now require adjustment in line with recent trends.Recent Position Statements and Expert Consensuses published in Europe 3 and the USA 2 have shown a shift to general classification of myocarditis into acute myocarditis and chronic inflammatory cardiomyopathy, resulting in a decrease in the use of the term "chronic myocarditis" worldwide. This is attributable to the fact that the understanding of the etiology, pathological condition, and clinical course of myocarditis has gradually deepened through AKIN Acute Kidney Injury Network APACHE Acute Physiology and Chronic Health Evaluation AST aspartate aminotransferase BNP B-type natriuretic peptide BTT bridge to transplantation BiVAD biventricular assist device CK creatine kinase CK-MB creatine kinase myocardial bound COVID-19 COronaVirus Infectious Disease, emerged in 2019 CRP C-reactive protein CRT-D cardiac resynchronization therapy defibrillator CTLA-4 cytotoxic T lymphocyte-associated protein 4 CQs Clinical Questions DI disagreement index DIC disseminated intravascular coagulation DLST drug-induced lymphocyte stimulation test 1. Process of Preparation ▋ 1.1 Purpose, Users, and Targeted Patients of the Guidelines ▋ 1.1.1 Purpose To provide practice guidelines for appropriate diagnosis and treatment management to physicians engaged in clinical care of patients with myocarditis. ▋ 1.1.2 Expected Users The present Guidelines were prepared in the expectation that cardiologists, cardiovascular surgeons, pediatricians, intensive care physicians, general internists, general practitioners, nurses, and other medical personnel who are engaged in the clinical care of myocarditis patients would use them when devising treatment strategies. It is alsoStep 4: Evaluation and Finalization of the Clinical Practice Guidelines The content of the Guidelines was reviewed by external reviewers and based their reports, modifications were made as necessary. ▋ 1.5 PublicationThe final draft was published after approval of the JCS Clinical Practice Guidelines Committee. ▋ 1.6 Conflict of Interest (COI)Conflict of interest, if any, was declared according to the rules prescribed by the JCS. The declaration covered 3 years from 2020 to 2022.

Conversion to EVL from MMF in maintenance periods after HTx may decrease the rate of CAV progression based on IVUS indices.

BackgroundThe influence of preexisting donor-transmitted atherosclerosis (DA) on cardiac allograft vasculopathy (CAV) development remains unclear.MethodsWe performed 3-dimensional intravascular ultrasound (3D-IVUS) analysis in 42 heart transplantation (HTx) recipients at 2.1 ± 0.9 months (baseline) and 12.2 ± 0.4 months post-HTx, as well as consecutive 3D-IVUS analyses up to 3 years post-HTx in 35 of the 42 recipients. Donor-transmitted atherosclerosis was defined as a maximal intimal thickness of 0.5 mm or greater at baseline. Changes in volumetric IVUS parameters were compared in recipients with (DA group) and without DA (DA-free group) at baseline, 1 year, and 3 years post-HTx.ResultsDonor-transmitted atherosclerosis was observed in 57.1% of 42 recipients. The DA group exhibited a significantly greater increase in plaque volume at 1 year post-HTx (P < 0.001), leading to increased percent plaque volume (plaque volume/vessel volume, [%]) (P < 0.001) and decreased luminal volume (P = 0.021). Donor-transmitted atherosclerosis was independently associated with a greater increase in percent plaque volume during the first post-HTx year (P = 0.011). From 1 to 3 years post-HTx, the DA group underwent continuous reduction in luminal volume (P = 0.022). These changes resulted in a higher incidence of angiographic CAV at 3 years post-HTx in the DA group (58.8% vs 5.6%, P = 0.002).ConclusionsThis volumetric IVUS study suggests that DA correlates with the worsening change in CAV several years post-HTx. Donor-transmitted atherosclerosis recipients may require more aggressive treatment to prevent subsequent CAV progression.

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