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Cardiovascular-Kidney Effects of Dapagliflozin in Patients at Cardiovascular Risk With or Without Type 2 Diabetes:
Vikas S Sridhar1,2, Luxcia Kugathasan3,2, Yuliya Lytvyn3,2
1Division of Nephrology, Department of Medicine, University of British Columbia, Vancouver, Canada (V.S.S.).
Background:
We investigated the impact of 12 weeks of sodium-glucose cotransporter-2 inhibition (dapagliflozin 10 mg daily) on vascular stiffness, cardiac and kidney function, and neurohormonal pathways in participants at cardiovascular risk.
Methods:
This randomized double-blind, parallel-group, placebo-controlled study enrolled 51 participants with at least 1 established cardiovascular condition or cardiovascular risk factor. Participants underwent 3 sequential assessments under clamped euglycemia (4-6 mmol/L): at baseline, at 1 week and 12 weeks of treatment. The primary outcome was vascular arterial stiffness, quantified as augmentation index and pulse-wave velocity. Secondary outcomes included: blood pressure, body fluid composition, noninvasive cardiac output monitoring, arterial vasodilatation tests, heart rate variability, echocardiography, iohexol-measured glomerular filtration rate, and natriuresis.
Results:
Dapagliflozin decreased vascular arterial stiffness, as measured by aortic augmentation index (placebo-adjusted change of -7.4±2.8%, P=0.01) after 12 weeks. Dapagliflozin acutely decreased extracellular fluid (-0.8±0.3 L, P=0.004), with sustained reductions in thoracic fluid content at 12 weeks (-3.3±1.5 kΩ-1, P=0.03). Reductions in measured glomerular filtration rate (-5.8±2.1 mL/min per 1.73m2, P=0.008) were accompanied by acute increases in proximal sodium excretion (5.1±2.2%, P=0.03), absolute fractional distal sodium reabsorption (4.4±2.1%, P=0.04), and urine adenosine (0.21±0.08 mmol/L per μmol Cr, P=0.01).
Conclusions:
Dapagliflozin induced early cardiorenal changes in individuals at varying levels of cardiovascular risk in whom evidence of clinical protection is lacking. Clinical trials in lower-risk populations, particularly in the context of primary prevention, are needed to determine whether these effects of sodium-glucose cotransporter-2 inhibition translate into improved clinical cardiorenal outcomes.
Registration:
URL: https://www.clinicaltrials.gov; Unique identifier: NCT04258371.
Insights
Sodium-glucose cotransporter-2 inhibition with dapagliflozin reduced vascular stiffness and improved cardiorenal function in high-risk patients. Further trials are needed to confirm clinical benefits in primary prevention populations.
Area of Science:
- Cardiology
- Nephrology
- Pharmacology
Background:
- Investigated the effects of sodium-glucose cotransporter-2 (SGLT2) inhibition using dapagliflozin (10 mg daily) over 12 weeks.
- Focused on participants at cardiovascular risk, assessing impacts on vascular stiffness, cardiac and kidney function, and neurohormonal pathways.
Purpose of the Study:
- To evaluate the efficacy of dapagliflozin in improving cardiorenal parameters in individuals with cardiovascular risk factors.
- To assess changes in vascular stiffness, cardiac output, renal function, and fluid balance.
Main Methods:
- Randomized, double-blind, placebo-controlled study with 51 participants.
- Sequential assessments at baseline, 1 week, and 12 weeks under clamped euglycemia.
- Primary outcome: vascular arterial stiffness (augmentation index, pulse-wave velocity). Secondary outcomes: blood pressure, fluid composition, cardiac output, vasodilatation, heart rate variability, echocardiography, glomerular filtration rate (GFR), natriuresis.
Main Results:
- Dapagliflozin significantly reduced aortic augmentation index (-7.4±2.8%, P=0.01) after 12 weeks.
- Acute reduction in extracellular fluid (-0.8±0.3 L, P=0.004) and sustained decrease in thoracic fluid content.
- Reduced GFR (-5.8±2.1 mL/min per 1.73m², P=0.008) with increased sodium excretion and urine adenosine.
Conclusions:
- Dapagliflozin demonstrated early cardiorenal benefits in individuals at cardiovascular risk.
- The study highlights potential benefits but calls for trials in lower-risk populations for primary prevention outcomes.
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