Regional Dysfunction by MRI in Incident Heart Failure

心力衰竭是美国发病率和死亡率最重要的原因之一，减少其对社会负担的策略需要更全面地了解其自然史。 在美国，心力衰竭最常见的病因是冠状动脉疾病。 因此，在这个国家，心力衰竭发展之前的病理过程通常是区域性的。 然而，以前的研究，旨在阐明心力衰竭的病理生理学局限于利用全球指标的左心室扩张和功能障碍，或使用的方法与重现性差，以量化局部异常的左心室功能。 此外，症状性心力衰竭经常与保留的收缩功能共存，特别是在老年人中。 对于这种疾病，目前归因于与心室肥大、冠状动脉疾病和衰老相关的舒张功能障碍，没有亚临床标志物可用。 本研究旨在通过利用MRI组织标记来检测收缩功能障碍的最早体征以及舒张区域和整体损害，从而填补心力衰竭病理生理学方面的这些知识空白。 我们建议对NHLBI多种族动脉粥样硬化研究（梅萨）的参与者进行研究，以评估基线时的局部心肌收缩和舒张功能障碍，并将其与6-8年梅萨随访期间的整体LV功能障碍、症状性心力衰竭和死亡的发生联系起来。将MRI标记添加到梅萨MRI方案中仅需要5-10分钟的额外时间，并且将通过新的自动化方法进行分析。 最后，我们还建议研究左心室肥厚，临床缺血事件和亚临床动脉粥样硬化对亚临床和症状性心力衰竭发展的区域功能障碍的预测价值的影响。 亚临床动脉粥样硬化将作为梅萨的一部分通过使用CT的冠状动脉钙化和使用超声的颈动脉壁厚度来量化。我们期望阐明由整体收缩功能障碍引起的亚临床心力衰竭的前兆，并开发区域和/或整体心肌舒张功能障碍的新指标，作为与保留的收缩功能障碍相关的心力衰竭的亚临床标志物。

Heart failure is one of the most important causes of morbidity and mortality in the United States, and strategies to reduce its burden to society entail a more complete understanding of its natural history. The most common etiology of heart failure in the U.S. is coronary artery disease. Therefore, in this country, pathologic processes preceding the development of cardiac failure are commonly regional in nature. However, previous studies aimed at elucidating the pathophysiology of heart failure were limited to the utilization of global indices of LV dilatation and functional impairment, or used methods with poor reproducibility to quantify regional abnormalities of LV function. In addition, symptomatic heart failure frequently coexists with preserved systolic function, particularly in the elderly. For this condition, which is currently attributed to diastolic dysfunction associated with ventricular hypertrophy, coronary artery disease and aging, no sub-clinical markers are available. This study is designed to fill these knowledge gaps in the pathophysiology of heart failure by utilizing MRI tissue tagging to detect the earliest signs of systolic dysfunction, as well as diastolic regional and global impairment. We propose to study participants of the NHLBI Multi-Ethnic Study of Atherosclerosis (MESA) to assess regional myocardial systolic and diastolic dysfunction at baseline, and relate it to the development of global LV dysfunction, symptomatic heart failure and death over 6-8 years of MESA follow-up. The addition of MRI tagging to the MESA MRI protocol will entail only 5-10 extra minutes and analysis will be performed by a novel automated method. Finally, we also propose to study the impacts of left ventricular hypertrophy, clinical ischemic events and sub-clinical atherosclerosis on the predictive value of regional dysfunction for the development of sub-clinical and symptomatic heart failure. Sub-clinical atherosclerosis will be quantified as part of MESA by coronary calcification using CT, and carotid wall thickness using ultrasound. We anticipate to elucidate the precursors of sub-clinical heart failure caused by global systolic dysfunction, and develop novel indices of regional and/or global myocardial diastolic impairment, as sub-clinical markers of heart failure associated with preserved systolic dysfunction.