Background-Age-related alterations of left ventricular (LV) structure and function that may predispose to cardiovascular events are not well understood. Methods and Results-We used cardiac MRI to examine age-related differences in LV structure and function in 5004 participants without overt cardiovascular disease when enrolled in the Multi-Ethnic Study of Atherosclerosis; 1099 participants received additional strain analyses by MRI tagging. We also assessed the relation of age-associated remodeling with cardiovascular outcomes using Cox proportional hazard models adjusting for cardiovascular risk factors. Although LV mass decreased with age (Ϫ0.3 g per year), the mass-to-volume ratio markedly increased (ϩ5 mg/mL per year, PϽ0.0001), driven by a substantial reduction in end-diastolic volume (Ϫ0.8 mL per year, PϽ0.0001).Age was also associated with a significant fall in stroke volume (Ϫ0.4 mL per year, PϽ0.0001), along with strain patterns reflecting systolic (PϽ0.0001) as well as diastolic (PϽ0.01) myocardial dysfunction-despite a modestly enhanced ejection fraction (ϩ0.1% per year, PϽ0.0001). Increased mass-to-volume ratio conferred a significant risk for total cardiovascular events; this trend was strongest among younger (Ͻ65 years; hazard ratio, 3.69 [CI, 1.34 to 10.10]) versus older (Ն65 years; hazard ratio, 1.68 [CI 0.77 to 3.68]) individuals with the highest compared to lowest mass-to-volume ratio quintile (P interaction ϭ0.013). Conclusions-Age is associated with a phenotype of LV remodeling marked by increased mass-to-volume ratio and accompanied by systolic as well as diastolic myocardial dysfunction that is not reflected by preserved ejection fraction. This pattern of ventricular remodeling confers significant cardiovascular risk, particularly when present earlier in life. Key Words: aging Ⅲ MRI Ⅲ myocardium Ⅲ remodeling W hile age is one of the most powerful risk factors for cardiovascular disease, the mechanisms by which aging predisposes to cardiovascular morbidity and mortality remain incompletely understood. [1][2][3] It is well known that age is associated with left ventricular (LV) hypertrophy, but less clear is the degree to which this remodeling is accompanied by age-specific relative changes in LV mass, 4 -11 volumes, 11-17 chamber performance, 13,15,16 and intrinsic myocardial function in humans. 10,11,14,18 Recent work has described aging-related cellular 8,19,20 and molecular [21][22][23] processes that likely contribute to myocardial dysfunction. Although the relation of advancing age with diastolic dysfunction is widely recognized, associated changes in systolic function are less clear. 11,16,24 -27 Conventional diagnostic methods may be limited in their ability to detect intrinsic age-associated changes in human myocardial function in relation to structural chamber remodeling. Furthermore, their link to cardiovascular morbidity and mortality remains elusive. Clinical Perspective on p 198In a large cohort of ethnically diverse individuals free of cardiovascular disease at baseline, we s...
Background-The ability to distinguish dysfunctional but viable myocardium from nonviable tissue has important prognostic implications after myocardial infarction. The purpose of this study was to validate the accuracy of contrast-enhanced multidetector computed tomography (MDCT) for quantifying myocardial necrosis, microvascular obstruction, and chronic scar after occlusion/reperfusion myocardial infarction. Methods and Results-Ten dogs and 7 pigs underwent balloon occlusion of the left anterior descending coronary artery (LAD) followed by reperfusion. Contrast-enhanced (Visipaque, 150 mL, 325 mg/mL) MDCT (0.5 mm ϫ 32 slice) was performed before occlusion and 90 minutes (canine) or 8 weeks (porcine) after reperfusion. MDCT images were analyzed to define infarct size/extent and microvascular obstruction and compared with postmortem myocardial staining (triphenyltetrazolium chloride) and microsphere blood flow measurements. Acute and chronic infarcts by MDCT were characterized by hyperenhancement, whereas regions of microvascular obstruction were characterized by hypoenhancement. MDCT infarct volume compared well with triphenyltetrazolium chloride staining (acute infarcts 21.1Ϯ7.2% versus 20.4Ϯ7.4%, mean difference 0.7%; chronic infarcts 4.15Ϯ1.93% versus 4.92Ϯ2.06%, mean difference Ϫ0.76%) and accurately reflected morphology and the transmural extent of injury in all animals. Peak hyperenhancement of infarcted regions occurred Ϸ5 minutes after contrast injection. MDCT-derived regions of microvascular obstruction were also identified accurately in acute studies and correlated with reduced flow regions as measured by microsphere blood flow. Conclusions-The
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