Dr. Kumaresan’s Research

Characterization of Cardiac Atrophy Among the Critically Ill

Over 5 million Americans are admitted to intensive care units annually in the United States alone. Of survivors, 40-60% will suffer from significant morbidity and functional decline associated with their ICU admission. Skeletal muscle wasting, resulting from the persistent inflammation associated with critical illness, is a major contributor to this morbidity and functional disability after discharge. Although cardiac muscle is similar to skeletal muscle on a cellular and functional level, the role of cardiac muscle atrophy in functional disability after discharge has not been established. Based on previous studies, this study hypothesizes that critical illness leads to an endogenous inflammatory environment, driven by eicosanoid signaling pathways, that promotes cardiac muscle wasting and contributes to adverse ICU outcomes. To test this hypothesis, a prospective study design will be used to assess changes in left ventricular mass using echocardiography, its determinants related to acute disease in ICU patients, clinically relevant outcomes, and serial eicosanoid profiles to examine possible underlying mechanisms. This study aims to establish the impact of critical illness in promoting and accelerating cardiac muscle atrophy, determine how this phenomenon relates to outcomes after ICU admission, and lay the groundwork for further investigation into the role of inflammation in driving this process. This research represents the next logical step in understanding the physiologic impact of critical illness and will serve as the basis for subsequent, more extensive clinical trials and mechanistic studies of muscle wasting and cardiac atrophy, ultimately leading to interventions that improve quality of life for ICU survivors.