Key result
Diabetic mice show no difference in passive aortic mechanics versus controls at equivalent blood pressures.
Why the study?
Mean arterial pressure confounds pulse wave velocity (PWV), prompting an investigation into whether increased aortic PWV in type 2 diabetic mice is driven by blood pressure rather than vascular biomechanics.
Does increased blood pressure drive the elevation in aortic pulse wave velocity in type 2 diabetic mice rather than intrinsic vascular biomechanics?
Does increased blood pressure drive the elevation in aortic pulse wave velocity in type 2 diabetic mice rather than intrinsic vascular biomechanics?
Elevated pulse wave velocity in diabetic mice is driven by concomitant increases in blood pressure rather than intrinsic vascular stiffness, suggesting caution when interpreting PWV as a pure marker of vascular stiffness.
Answers are grounded in this paper and cite their sources.
BP may drive PWV elevation in diabetic mice rather than intrinsic stiffness; leaves open human translation and clinical PWV interpretation.
Introduction: Vascular stiffness is a predictor of cardiovascular disease and pulse wave velocity (PWV) is the current standard for measuring in vivo vascular stiffness. Mean arterial pressure is the largest confounding variable to PWV; therefore, in this study we aimed to test the hypothesis that increased aortic PWV in type 2 diabetic mice is driven by increased blood pressure rather than vascular biomechanics. Methods and Results: Using a combination of in vivo PWV and ex vivo pressure myography, our data demonstrate no difference in ex vivo passive mechanics, including outer diameter, inner diameter, compliance (Db/db: 0.0094 ± 0.0018 mm 2 /mmHg vs. db/db: 0.0080 ± 0.0008 mm 2 /mmHg, p > 0.05 at 100 mmHg), and incremental modulus (Db/db: 801.52 ± 135.87 kPa vs. db/db: 838.12 ± 44.90 kPa, p > 0.05 at 100 mmHg), in normal versus diabetic 16 week old mice. We further report no difference in basal or active aorta biomechanics in normal versus diabetic 16 week old mice. Finally, we show here that the increase in diabetic in vivo aortic pulse wave velocity at baseline was completely abolished when measured at equivalent pharmacologically-modulated blood pressures, indicating that the elevated PWV was attributed to the concomitant increase in blood pressure at baseline, and therefore “stiffness.” Conclusions: Together, these animal model data suggest an intimate regulation of blood pressure during collection of pulse wave velocity when determining in vivo vascular stiffness. These data further indicate caution should be exerted when interpreting elevated PWV as the pure marker of vascular stiffness.
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McCallinhart et al. (2023) studied Type 2 Diabetes Mellitus (T2DM) and Vascular Stiffness (n=22). Type 2 diabetes (db/db mutation) vs. Non-diabetic heterozygous Db/db mice was evaluated on Ex vivo aortic compliance at 100 mmHg (mm2/mmHg) (p=>0.05). In diabetic db/db mice, elevated in vivo aortic pulse wave velocity was completely abolished when measured at equivalent blood pressures, demonstrating no difference in ex vivo passive aortic mechanics compared to controls.
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