Abstract: TH-OR44
Renal Revascularization Attenuates Myocardial Mitochondrial Damage and Improves Diastolic Function in Pigs with Metabolic Syndrome and Renovascular Hypertension
Session Information
- Hypertension and Cardiovascular Risk in CKD
November 04, 2021 | Location: Simulive, Virtual Only
Abstract Time: 04:30 PM - 06:00 PM
Category: Hypertension and CVD
- 1403 Hypertension and CVD: Mechanisms
Authors
- Eirin, Alfonso, Mayo Clinic Minnesota, Rochester, Minnesota, United States
- Farahani, Rahele A, Mayo Clinic Minnesota, Rochester, Minnesota, United States
- Ferguson, Christopher M., Mayo Clinic Minnesota, Rochester, Minnesota, United States
- Zhu, Xiang yang, Mayo Clinic Minnesota, Rochester, Minnesota, United States
- Tang, Hui, Mayo Clinic Minnesota, Rochester, Minnesota, United States
- Jordan, Kyra L., Mayo Clinic Minnesota, Rochester, Minnesota, United States
- Saadiq, Ishran M., Mayo Clinic Minnesota, Rochester, Minnesota, United States
- Herrmann, Sandra, Mayo Clinic Minnesota, Rochester, Minnesota, United States
- Chade, Alejandro R., The University of Mississippi Medical Center, Jackson, Mississippi, United States
- Lerman, Amir, Mayo Clinic Minnesota, Rochester, Minnesota, United States
- Lerman, Lilach O., Mayo Clinic Minnesota, Rochester, Minnesota, United States
Background
Percutaneous transluminal renal angioplasty (PTRA) may improve renal and cardiac function in renovascular hypertension (RVH), but its effect on the biological mechanisms implicated in cardiac damage remains unknown. We hypothesized that restoration of kidney function by PTRA ameliorates myocardial mitochondrial damage and preserves cardiac function in pigs with metabolic syndrome (MetS) and RVH.
Methods
Pigs were studied after 16 weeks of MetS+RVH, MetS+RVH treated 4 weeks earlier with PTRA, and Lean and MetS Sham controls (n=6 each). Cardiac and renal function was assessed by multi-detector CT, whereas cardiac mitochondrial morphology and function, and injury pathways were assessed ex vivo.
Results
RVH induced renal and cardiac diastolic (albeit not systolic) dysfunction (Table). PTRA improved renal function but not RVH. It preserved myocardial mitochondrial structure and function, ameliorated oxidative stress and fibrosis (Fig.A), attenuated left ventricular remodeling (LVMM), and restored diastolic function (E/A ratio). Myocardial mitochondrial damage did not correlate with blood pressure but correlated directly with renal dysfunction (Fig.B).
Conclusion
Improved renal function by PTRA preserves myocardial mitochondria and enhances cardiac recovery regardless of RVH, underscoring reno-cardiac crosstalk in experimental MetS+RVH.
Funding
- NIDDK Support