Beyond the myocardium? SGLT2 inhibitors target peripheral components of reduced oxygen flux in the diabetic patient with heart failure with preserved ejection fraction
Autor: | Robert J. Chilton, Mouhamed Nashawi, Ayman Battisha, Omar Sheikh, Mahnoor Mir |
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Rok vydání: | 2020 |
Předmět: |
medicine.medical_specialty
Disease 030204 cardiovascular system & hematology 03 medical and health sciences 0302 clinical medicine Internal medicine Diabetes mellitus Diabetes Mellitus medicine Empagliflozin Humans 030212 general & internal medicine Endothelial dysfunction Sodium-Glucose Transporter 2 Inhibitors Heart Failure Canagliflozin business.industry Myocardium Stroke Volume Hypoxia (medical) medicine.disease Oxygen Heart failure Cardiology medicine.symptom Cardiology and Cardiovascular Medicine Heart failure with preserved ejection fraction business medicine.drug |
Zdroj: | Heart Failure Reviews. 27:219-234 |
ISSN: | 1573-7322 1382-4147 |
DOI: | 10.1007/s10741-020-09996-y |
Popis: | Recent cardiovascular outcome trials have highlighted the propensity of the antidiabetic agents, SGLT2 inhibitors (SGLT2is or -flozin drugs), to exert positive clinical outcomes in patients with cardiovascular disease at risk for major adverse cardiovascular events (MACEs). Of interest in cardiac diabetology is the physiological status of the patient with T2DM and heart failure with preserved ejection fraction (HFpEF), a well-examined association. Underlying this pathologic tandem are the effects that long-standing hyperglycemia has on the ability of the HFpEF heart to adequately deliver oxygen. It is believed that shortcomings in oxygen diffusion or utilization and the resulting hypoxia thereafter may play a role in underlying the clinical sequelae of patients with T2DM and HFpEF, with implications in the long-term decline of extra-cardiac tissue. Oxygen consumption is one of the most critical factors in indexing heart failure disease burden, warranting a probe into the role of SGLT2i on oxygen utility in HFpEF and T2DM. We investigated the role of oxygen flux in the patient with T2DM and HFpEF extending beyond the heart with focuses on cellular metabolism, perivascular fibrosis with endothelial dysfunction, hematologic changes, and renal effects with neurohormonal considerations in the patient with HFpEF and T2DM. Moreover, we give a commentary on potential therapeutic targets of these components with SGLT2i to gain insight into disease burden amelioration in patients with HFpEF and T2DM. |
Databáze: | OpenAIRE |
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