Vascular Stiffness and Pulmonary Congestion (PREDICT)

Pulmonary Congestion and Vascular Stiffness (PREDICT)

In this study we hypothesize that increased aortic stiffness during dobutamine stress is predictive of future flash pulmonary edema warranting hospitalization independent of other causes of flash pulmonary edema. We also hypothesize that the mechanism by which aortic stiffness heightens the risk of future pulmonary edema as by limiting the ability of the left ventricular stroke volume to increase during stress. In addition, we hypothesize that increased aortic stiffness my have a genetic component, and therefore may be associated with genetic variations in candidate genes. To gather evidence in support of our hypotheses, we will implement (in 608 subjects at risk for the development of flash pulmonary edema) a novel form of cardiovascular magnetic resonance (CMR) that will allow the simultaneous rest and stress assessments of aortic and LV structure and function. After the CMR stress test, we will follow our participants over time to ascertain the post-testing outcome of the occurrence of flash pulmonary edema warranting hospitalization.

Our design will allow us to determine if change in aortic stiffness during dobutamine independently predicts flash pulmonary edema after controlling for other factors that promote pulmonary edema (e.g., age, LV hypertrophy, or increased aortic wall thickening). In addition, our study design will allow us to determine if change in aortic stiffness during intravenous dobutamine (10 mcg/kg/min x 5 minutes, if inducible ischemia is absent at this level of stress, dobutamine 20 to 40 mcg/kg/min x 5 min) is an independent predictor of flash pulmonary edema after controlling for its effect on LV stroke volume reserve (the stress-rest ratio of LV stroke volume). Our results will be significant in that we will define the relationship between factors affecting aortic stiffness and LV performance and the future occurrence of flash pulmonary edema warranting hospitalization. With this understanding, we will gain mechanistic insight into the pathophysiology of flash pulmonary edema that will be useful for developing interventions prevent the morbidity and mortality associated with this disorder. In order to measure the contribution to genetic components, we will collect DNA samples from whole blood samples from eligible and willing subjects for future genetic studies.

Last Updated: 02-18-2015
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