"The development of cardiac allograft vasculopathy remains the Achilles heel of cardiac transplantation," commented working group leader, Mandeep R. Mehra, MD, Herbert Berger Professor and Head of Cardiology, University of Maryland School of Medicine, Baltimore, MD. "Unfortunately, the definitions of cardiac allograft vasculopathy are diverse and confusion abounds. There have been no uniform international standards for the nomenclature of this entity. The lack of a standard language has led to confusion in the interpretation of various studies and several unanswered questions persist. The ISHLT consensus statement is the first step in resolving these issues and improving cardiac transplant patient outcomes."

This consensus document, commissioned by the International Society for Heart and Lung Transplantation Board, is based on best evidence and clinical consensus derived from critical analysis of available information pertaining to angiography, intravascular ultrasound imaging, microvascular function, cardiac allograft histology, circulating immune markers, noninvasive imaging tests, and gene-based and protein-based biomarkers.

ISHLT President, John Dark, FRCS, stated, "The consensus document from the international working group led by Dr. Mehra defines the descriptors of the major clinical challenge late after cardiac transplantation. It also defines the ISHLT as the organization unifying all those, scientists and clinicians, working in this field, and able to put the stamp of authority on the recommendations. The topic is rapidly evolving, but Dr Mehra and his colleagues have undertaken to keep the data under close review. We can anticipate further definitive analyses in the future."

This article presents 5 consensus statements that describe how to best identify CAV and assess its severity. By developing a standard nomenclature, appropriate treatment options can be selected, depending on the level of CAV. Four levels of CAV are defined, ranging from CAV0 (not significant), where no angiographic lesions are detected, to CAV3 (severe), where multiple major heart vessels are involved. Key among the recommendations to define the severity of CAV is to view the anatomy of the allograft vasculature in concert with the physiological effects of the disease on cardiac allograft function.

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