Arterial Stiffness and Type 1 Diabetes: The Current State of Knowledge

2021 ◽  
Vol 17 ◽  
Author(s):  
Michal Kulecki ◽  
Aleksandra Uruska ◽  
Dariusz Naskret ◽  
Dorota Zozulinska-Ziolkiewicz

: The most common cause of mortality among people with type 1 diabetes is cardiovascular diseases. Arterial stiffness allows predicting cardiovascular complications, cardiovascular mortality, and all-cause mortality. There are different ways to measure arterial stiffness; the gold standard is pulse wave velocity. Arterial stiffness is increased in people with type 1 diabetes compared to healthy controls. It increases with age and duration of type 1 diabetes. Arterial stiffness among people with type 1 diabetes has a positive association with systolic blood pressure, obesity, glycated hemoglobin, waist circumference, and waist to hip ratio. It has a negative correlation with estimated glomerular filtration rate, high-density lipoprotein, and the absence of carotid plaques. The increased arterial stiffness could be the result of insulin resistance, collagen increase due to inadequate enzymatic glycation, endothelial and autonomic dysfunction. The insulin-induced decrease in arterial stiffness is impaired in type 1 diabetes. There are not enough proofs to use pharmacotherapy in the prevention of arterial stiffness, but some of the medicaments have obtained promising results in single studies, for example, renin-angiotensin-aldosterone system inhibitors, statins, and SGLT2 inhibitors. The main form of prevention of arterial stiffness progression remains glycemic control and a healthy lifestyle.

Diabetes Care ◽  
2022 ◽  
Author(s):  
Bruce A. Perkins ◽  
Ionut Bebu ◽  
Xiaoyu Gao ◽  
Amy B. Karger ◽  
Irl B. Hirsch ◽  
...  

OBJECTIVE Rapid loss of estimated glomerular filtration rate (eGFR) within its normal range has been proposed as a strong predictor of future kidney disease. We investigated this association of eGFR slope early in the course of type 1 diabetes with long-term incidence of kidney and cardiovascular complications. RESEARCH DESIGN AND METHODS The annual percentage change in eGFR (slope) was calculated during the Diabetes Control and Complications Trial (DCCT) for each of 1,441 participants over a mean of 6.5 years and dichotomized by the presence or absence of early rapid eGFR loss (slope ≤−3% per year) as the exposure of interest. Outcomes were incident reduced eGFR (eGFR <60 mL/min/1.73 m2), composite cardiovascular events, or major adverse cardiovascular events (MACE) during the subsequent 24 years post-DCCT closeout follow-up. RESULTS At DCCT closeout (the baseline for this analysis), diabetes duration was 12 ± 4.8 years, most participants (85.9%) had normoalbuminuria, mean eGFR was 117.0 ± 13.4 mL/min/1.73 m2, and 149 (10.4%) had experienced early rapid eGFR loss over the preceding trial phase. Over the 24-year subsequent follow-up, there were 187 reduced eGFR (6.3 per 1,000 person-years) and 113 MACE (3.6 per 1,000 person-years) events. Early rapid eGFR loss was associated with risk of reduced eGFR (hazard ratio [HR] 1.81, 95% CI 1.18–2.79, P = 0.0064), but not after adjustment for baseline eGFR level (HR 0.94, 95% CI 0.53–1.66, P = 0.84). There was no association with composite cardiovascular events or MACE. CONCLUSIONS In people with type 1 diabetes primarily with normal eGFR and normoalbuminuria, the preceding slope of eGFR confers no additional association with kidney or cardiovascular outcomes beyond knowledge of an individual’s current level.


2021 ◽  
Vol 30 (2) ◽  
pp. 17-21
Author(s):  
A.E. Petrosyan ◽  
M.L. Diane ◽  
E.O. Kotova

The authors review approaches to the early prediction of cardiovascular diseases in patients with type 1 diabetes mellitus, e.g. using central arterial pressure, arterial stiffness, and a loss of arterial stiffness gradient. The bulk of data was presented either on diabetes mellitus in general or on type 2 diabetes mellitus, while there is a clear gap in information on type 1 diabetes mellitus. The study of the elastic properties of the vascular bed in these patients can become the basis for the early prevention of cardiovascular complications.


2019 ◽  
Author(s):  
Karina Sarkisova ◽  
Iwona-Renata Jarek-Martynowa ◽  
Marina Shestakova ◽  
Minara Shamkhalova ◽  
Alexander Parfenov

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 1695-P
Author(s):  
STUART MCGURNAGHAN ◽  
ATHINA SPILIOPOULOU ◽  
HELEN M. COLHOUN ◽  
PAUL M. MCKEIGUE

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 618-P
Author(s):  
GIUSEPPE PENNO ◽  
MONIA GAROFOLO ◽  
ROSA GIANNARELLI ◽  
FABRIZIO CAMPI ◽  
DANIELA LUCCHESI ◽  
...  

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1694-P
Author(s):  
MONIA GAROFOLO ◽  
ALESSANDRA BERTOLOTTO ◽  
FABRIZIO CAMPI ◽  
DANIELA LUCCHESI ◽  
LAURA GIUSTI ◽  
...  

Science ◽  
2021 ◽  
Vol 373 (6554) ◽  
pp. 510-516
Author(s):  
Jeffrey A. Bluestone ◽  
Jane H. Buckner ◽  
Kevan C. Herold

Type 1 diabetes (T1D) is an autoimmune disease in which T cells attack and destroy the insulin-producing β cells in the pancreatic islets. Genetic and environmental factors increase T1D risk by compromising immune homeostasis. Although the discovery and use of insulin have transformed T1D treatment, insulin therapy does not change the underlying disease or fully prevent complications. Over the past two decades, research has identified multiple immune cell types and soluble factors that destroy insulin-producing β cells. These insights into disease pathogenesis have enabled the development of therapies to prevent and modify T1D. In this review, we highlight the key events that initiate and sustain pancreatic islet inflammation in T1D, the current state of the immunological therapies, and their advantages for the treatment of T1D.


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