Regional Dysfunction by MRI in Incident Heart Failure

心力衰竭是美国发病率和死亡率的最重要原因之一，减轻其对社会的负担的战略需要对其自然历史有更全面的了解。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，心力衰竭发生之前的病理过程通常是区域性的。然而，以往关于心力衰竭病理生理机制的研究大多局限于利用整体指标评价左室扩张和功能损害，或采用重复性差的方法来量化左心功能的局部异常。此外，症状性心力衰竭经常与收缩功能保留并存，特别是在老年人。这种情况目前被归因于与心室肥厚、冠状动脉疾病和衰老相关的舒张期功能障碍，目前还没有亚临床标记物可用。这项研究旨在通过利用MRI组织标记来检测收缩功能障碍以及舒张期局部和整体损害的最早迹象，来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动脉粥样硬化多民族研究(MESA)的参与者进行研究，以评估基线下的局部心肌收缩和舒张期功能障碍，并将其与6-8年MESA随访期间全球左心功能不全、症状性心力衰竭和死亡的发生联系起来。将MRI标记添加到MESA MRI协议将只需要额外的5-10分钟，并且将通过一种新的自动化方法执行分析。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局部功能障碍对亚临床和症状性心力衰竭发展的预测价值的影响。亚临床动脉粥样硬化将通过CT冠状动脉钙化和超声颈动脉壁厚度来量化为MESA的一部分。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先兆，并开发新的局部和/或整体心肌舒张期损害指标，作为心力衰竭与保留的收缩功能障碍相关的亚临床标志物。

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.