This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Even though CAD is the major cause of congestive heart failure (CHF), up to 30% of patients with CHF have a non-ischemic cardiomyopathy (IDC). A non-invasive tool that could discriminate between CAD and non-CAD etiology of CHF, and provide prognostic information in the latter would therefore be extremely valuable. Capillaries offer the most resistance to coronary blood flow (CBF) during hyperemia and limit the maximal increase in hyperemic CBF. Because they are laid in parallel, a greater number of capillaries allows a higher hyperemic CBF and vice versa. Conditions that are associated with capillary loss (either anatomically or functionally) such as myocardial infarction, hypertension, or diabetes, are associated with reduced CBF reserve despite the absence of coronary stenosis. Furthermore, the abnormal neurohormonal milieu that develops in patients with CHF may produce microvascular dysfunction which can also reduce CBF reserve. These conditions may lead to supply-demand mismatch and acute ischemic episodes during stress, and result in ventricular dysfunction despite the absence of CAD. Thus, reduced CBF reserve may play an important role in the development of LV dysfunction seen in these conditions even in the absence of CAD. Myocardial contrast echocardiography (MCE) is a technique that uses microbubbles as ultrasound contrast agents. This technique can non-invasively assess multiple aspects of the coronary microcirculation, including capillary density, and can also quantify CBF reserve. This proposal will test the hypothesis that in patients with nonischemic IDC, concurrent impairments in microcirculatory function detected by MCE may limit nutrient perfusion which can further worsen myocardial function and patient prognosis.
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