T1 mapping in cardiac MRI

Quantitative myocardial and blood T1 have recently achieved clinical utility in numerous pathologies, as they provide non-invasive tissue characterization with the potential to replace invasive biopsy. Native T1 time (no contrast agent), changes with myocardial extracellular water (edema, focal or diffuse fibrosis), fat, iron, and amyloid protein content. After contrast, the extracellular volume fraction (ECV) estimates the size of the extracellular space and identifies interstitial disease. Spatially resolved quantification of these biomarkers (so-called T1 mapping and ECV mapping) are steadily becoming diagnostic and prognostically useful tests for several heart muscle diseases, influencing clinical decision-making with a pending second consensus statement due mid-2017. This review outlines the physics involved in estimating T1 times and summarizes the disease-specific clinical and research impacts of T1 and ECV to date. We conclude by highlighting some of the remaining challenges such as their community-wide delivery, quality control, and standardization for clinical practice

Coronary microvascular dysfunction in cardiovascular disease:Lessons from large animal models

The coronary microvasculature is responsible for maintaining local matching of myocardial blood flow to myocardial demand of oxygen and nutrients. Long term adjustment of myocardial blood flow involves structural changes in microvascular density and diameter while fine-tuning of flow is achieved via adaptations in vascular smooth muscle tone in the coronary microvasculature.In the past several decades, considerable research efforts have been directed at understanding structural and functional microvascular adaptations involved in matching myocardial oxygen supply and demand and how these mechanisms are affected by various diseases. In this review we will discuss our current understanding of the mechanisms underlying the regulation of coronary microvascular tone under healthy physiological conditions, and the role of microvascular dysfunction in obstructive and non-obstructive coronary artery disease, as studied in large animal (particularly swine) models and confirmed in human studies. Future studies should be directed at further unraveling the mechanisms of coronary microvascular dysfunction in different disease entities in order to, and ultimately directed at improving microvascular function as a therapeutic target in patients with ischemic heart disease