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Central hemodynamic modifications in diabetes mellitus
Davide Agnoletti1, Ari Lieber, Yi Zhang
1Paris Descartes University, AP-HP, Diagnosis and Therapeutic Center, Hôtel-Dieu, 1 place du Parvis Notre Dame, 75004 Paris, France; Department of Internal Medicine, University of Bologna, Via Albertoni 15, 40138 Bologna, Italy.
Insights
Hypertensive diabetics exhibit greater arterial stiffness than non-diabetics, with insulin therapy potentially worsening this condition independently of blood pressure control.
Area of Science:
- Cardiovascular Medicine
- Endocrinology
- Hypertension Research
Background:
- Arterial stiffness is influenced by age, MAP, and HR in hypertension.
- Factors affecting arterial stiffness in diabetes mellitus are not fully understood.
Purpose of the Study:
- To compare central hemodynamics in diabetics versus non-diabetic controls with similar MAP.
- To investigate factors influencing arterial stiffness in diabetic patients.
Main Methods:
- Compared central hemodynamics (central blood pressure, PWV, AIx, PPA) in 126 diabetics and 203 controls using applanation tonometry.
- Collected anthropometric, laboratory, and clinical data.
- Adjusted for age, gender, MAP, heart rate, and metabolic syndrome.
Main Results:
- Diabetics showed significantly higher PWV and AIx after adjusting for age, gender, MAP, and HR.
- PWV remained significantly higher in diabetics after further adjustment for metabolic syndrome.
- PWV in diabetics did not correlate with MAP, suggesting non-hemodynamic factors contribute to arterial stiffening.
- Insulin therapy was associated with increased PWV, independent of other variables.
Conclusions:
- Hypertensive diabetics have greater arterial stiffness than hypertensive controls.
- Arterial stiffening in diabetes is influenced by multiple factors beyond hemodynamics.
- Insulin therapy is linked to increased arterial stiffness, warranting further investigation into its direct or indirect effects.
Abstract:
Arterial stiffness in hypertension is markedly influenced by age, mean arterial pressure (MAP) and heart rate, whereas factors influencing this parameter in diabetes mellitus are not yet fully understood. The aim of our study was to compare central hemodynamics in diabetics (n = 126) versus non-diabetic controls (n = 203), most of whom were hypertensive, and with similar MAP. Anthropometric, laboratory and clinical measurements were collected. Hemodynamic parameters (central blood pressure, aortic pulse wave velocity [PWV], augmentation index [AIx] and pulse pressure amplification [PPA]) were measured using applanation tonometry. PWV and AIx were significantly higher in diabetics, after adjustment for age, gender, MAP, and heart rate. After further adjustment for metabolic syndrome, only the difference in PWV persisted (P < 0.0001). PPA was marginally altered though not significantly. In diabetics, PWV did not correlate with MAP, suggesting that other structural alterations, resulting from insulin resistance, may account for diabetic arterial stiffening to a greater extent than, and independently of, blood pressure. Chronic treatment with insulin was associated with increased PWV, independently of blood pressure, diabetes control and duration, or other common confounding variables. In conclusion, hypertensive diabetics had greater arterial stiffness than hypertensive controls. In diabetes, multiple factors affect arterial stiffening independently of hemodynamic status. Notably, insulin therapy (IT) is associated with more severe arterial stiffness, suggesting a consistent relationship between these parameters. It remains to be determined whether IT should be considered as a marker of diabetes severity that leads to increased arterial stiffness, or whether it has a direct/indirect effect on arterial wall modifications.
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