415.5 - Metabolic Changes in Heart Disease, as Exemplified by Barth Syndrome Cardiomyopathy
Tuesday, April 5, 2022
2:35 PM – 2:55 PM
Room: 201 C - Pennsylvania Convention Center
Introduction: It is increasingly recognized that comorbidities, particularly age, metabolic derangement and chronic kidney disease, contribute to heart failure with preserved ejection fraction (HFpEF) as well as ischemia with no obstructive coronary artery disease (INOCA), with coronary microvascular dysfunction being a common denominator in both. Indeed, recent studies indicate that patients with INOCA are at risk for development of HFpEF, further confirming an intricate relation between coronary microvascular function and diastolic cardiac function. Moreover, it has recently been proposed that HFpEF is not one disease, but that the underlying processes may differ between different patient groups, resulting in very different outcomes and potentially also requiring different treatment strategies.
Open questions in the field are how the cardiomyocytes and the coronary microvasculature communicate, and how co-morbidities and disease progression impact this communication. Furthermore, it is known that inflammation and oxidative stress are increased in HFpEF and INOCA, but the mechanisms responsible for their induction and the relation with comorbidities are incompletely understood.
We believe that a translational integrative approach is required to put the different pieces of this puzzle together, not just focusing on the cardiomyocyte or the coronary microvasculature, but looking beyond the heart to the influence of dysfunction of other organs, such as the kidneys. In this symposium, we have therefore put together a program with experts investigating multiple aspects of the relation between different comorbidities and cardiac and/or microvascular dysfunction. Their experimental approaches range from clinically-relevant large animal models with different comorbidities to study onset, progression, and reversibility of disease (Goodwill, Sorop, Lerman) to experiments on coronary microvessels (Sorop) and cardiomyocytes (Maack) obtained during cardiac surgery to investigate the source(s) and downstream consequences of inflammation and oxidative stress in advanced disease. An important, underrecognized, aspect therein is the role of mitochondria, which may be impacted by altered circulating substrates, but have also been shown to change their structure and function in various disease states and may contribute to the production of oxygen radicals.
With this combination, we think we have put together an interesting symposium that combines the strengths of the APS Cardiovascular Section and the Microcirculatory Society using a truly integrative approach to address an important public health problem.
