Non-compressible arterial disease and the risk of coronary calcification in type-2 diabetes

Lilly, Scott; Qasim, Atif; Mulvey, Claire K.; Churchill, Timothy W.; Reilly, Muredach P.; Eraso, Luis H.

doi:10.1016/j.atherosclerosis.2013.06.004

Cited by 24 publications

(25 citation statements)

References 38 publications

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“…Noncompressibility is related to the presence of medial arterial calcification which is more common in the elderly and diabetics. 23 This is in contrast to low ABI where atherosclerosis is the primary mechanism. The different underlying pathophysiology may have some bearing on the prognostic significance of ABI <1.0 versus ABI >1.4.…”

Section: Discussionmentioning

confidence: 98%

“…Although the absence of an association in our study is most likely because of a small sample size, there are other explanations to consider. Noncompressibility is related to the presence of medial arterial calcification which is more common in the elderly and diabetics 23. This is in contrast to low ABI where atherosclerosis is the primary mechanism.…”

Section: Discussionmentioning

confidence: 99%

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Association of Peripheral Artery Disease With Incident Atrial Fibrillation: The ARIC (Atherosclerosis Risk in Communities) Study

Bekwelem

Norby

Agarwal

et al. 2018

JAHA

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BackgroundAlthough peripheral artery disease as defined by ankle‐brachial index (ABI) is associated with incident atrial fibrillation (AF), questions remain about the risk of AF in borderline ABI (>0.90 to <1.0) or noncompressible arteries (>1.4). We evaluated the association of borderline ABI and ABI >1.4 in the ARIC (Atherosclerosis Risk in Communities) study, a population‐based prospective cohort study.Methods and ResultsWe included 14 794 participants (age, 54.2±5.8 years, 55% women, 26% blacks) with ABI measured at the baseline (1987–1989) and without AF. AF was identified from hospital records, death certificates, and ECGs. Using Cox proportional hazards, we evaluated the association between ABI and AF. During a median follow‐up of 23.3 years, there were 2288 AF cases. After adjustment for cardiovascular risk factors, hazard ratio (HR) (95% confidence interval) for AF among individuals with ABI <1.0 compared with ABI 1.0 to 1.4, was 1.13 (1.01–1.27). ABI >1.4 was not associated with increased AF risk. ABI ≤0.9 and borderline ABI were associated with a higher risk of AF compared with ABI 1.0 to 1.4. Demographics‐adjusted HRs (95% confidence interval) were 1.43 (1.17–1.75) and 1.32 (1.16–1.50), respectively. However, the associations of ABI ≤0.9 and borderline ABI with AF were attenuated after adjusting for cardiovascular risk factors (HR [95% confidence interval], 1.10 [0.90–1.34] and 1.14 [1.00–1.30]), respectively.ConclusionsPeripheral artery disease indicated by low ABI, including borderline ABI, is a weak risk factor for AF. ABI >1.4 is not associated with an increased AF risk. The relationship between peripheral artery disease and AF appears to be mostly explained by traditional atherosclerotic risk factors.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Association of Peripheral Artery Disease With Incident Atrial Fibrillation: The ARIC (Atherosclerosis Risk in Communities) Study

Bekwelem

Norby

Agarwal

et al. 2018

JAHA

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“…China has the highest number of people with diabetes, which accounts for about one-third of the total number of diabetic patients worldwide [1]. Patients with diabetes commonly manifest vascular calcification, including intima and medial calcification, which are mainly distributed in the coronary artery and lower extremity vessels, respectively [2, 3]. A multi-center epidemiological study demonstrated that the risk of acute cardiovascular events in patients with calcification score >300 is significantly higher than those in patients with calcification score of 1–100 [4, 5].…”

Section: Introductionmentioning

confidence: 99%

CML/RAGE signal induces calcification cascade in diabetes

Wang

et al. 2016

Diabetol Metab Syndr

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ObjectiveVascular calcification is a significant predictor of coronary heart disease events, stroke, and lower-limb amputation. Advanced glycation end-products (AGEs) play a key role in the development of vascular calcification. However, the role of Nε-carboxymethyl-lysine (CML), a major active ingredient of heterogeneous AGEs, in the development of atherosclerotic calcification in diabetic patients and the underlying mechanism remain unclear. Hence, the role and the mechanism of CML in the transmission pathway of diabetic calcification cascade were investigated in the present study.MethodsIn vivo and in vitro investigations were performed. In study I, 45 diabetic patients hospitalized for above-knee amputation in the Department of Orthopedics, Affiliated Hospital of Jiangsu University were recruited from February 2010 to June 2015. The patients were categorized based on the severity of anterior tibial artery stenosis, which was assessed by color Doppler ultrasound, into mild stenosis (0% < stenosis < 50%, n = 15), moderate stenosis (50 ≤ stenosis < 70%, n = 15), and severe stenosis/occlusion groups (70 ≤ stenosis ≤ 100%, n = 15). In study II, the specific mechanism of CML in the transmission pathway of the diabetic calcification cascade signal was investigated in A7r5 aortic smooth muscle cells under high-lipid, apoptosis-coexisting conditions. ELISA (for serum CML concentration of patients), ultrasound (for plaque size, calcification, blood flow filling, vascular stenosis etc.), H&E staining (for plaque morphology), vonKossa staining (for qualitative analysis of calcification), calcium content assay (for quantitative analysis of calcification), and Western blot analyses of CML, receptor for advanced glycation end products (RAGE), NADPH oxidase 4, phosphorylated p38, core-binding factor α1 (cbfα1), alkaline phosphatase (ALP) and β-actin were then performed.ResultsMorphological analysis revealed extensive calcification lesions in the intima and media of the anterior tibial artery. The extent and area of calcium deposition in the intima significantly increased with disease progression. Interestingly, spotty calcification was predominant in the atherosclerotic plaques of diabetic patients with amputation, and macrocalcification was almost invisible. Pearson correlation analysis revealed that serum CML level exhibited a significant positive correlation with calcium content in the arterial wall (R2 = 0.6141, P < 0.0001). Semi-quantitative Western blot analysis suggested that the intensity of CML/RAGE signal increased with progression of atherosclerotic calcification in diabetic patients. In subsequent in vitro study, the related pathway was blocked by anti-RAGE antibody, NADPH oxidase inhibitor DPI, p38MAPK inhibitor SB203580, and anti-cbfa1 antibody in a step-wise manner to observe changes in calcium deposition and molecular signals. Results suggested that CML may play a key role in atherosclerotic calcification mainly through the CML/RAGE- reactive oxygen species (ROS)-p38MAPK-cbfα1-ALP pathway.ConclusionSpotty cal...

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“…In diabetic patients, vascular calcification occurs mainly in coronary and vascular arteries of lower limbs (3,4). This calcification is associated with an increased prevalence of arteriosclerosis vascular disease and cardiovascular morbidity and mortality.…”

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confidence: 99%

Can the NK Family of Osteoblast Homeodomain Transcription Factors Signaling Be a Magic Bullet to Reverse Calcification-Induced Vasculopathy in Diabetes?

Belmadani

Matrougui

2014

Diabetes

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Non-compressible arterial disease and the risk of coronary calcification in type-2 diabetes

Cited by 24 publications

References 38 publications

Association of Peripheral Artery Disease With Incident Atrial Fibrillation: The ARIC (Atherosclerosis Risk in Communities) Study

Association of Peripheral Artery Disease With Incident Atrial Fibrillation: The ARIC (Atherosclerosis Risk in Communities) Study

CML/RAGE signal induces calcification cascade in diabetes

Can the NK Family of Osteoblast Homeodomain Transcription Factors Signaling Be a Magic Bullet to Reverse Calcification-Induced Vasculopathy in Diabetes?

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