Should Diabetes Be Considered a Coronary Heart Disease Risk Equivalent? Results from 25 years of follow-up in the Renfrew and Paisley Survey
ABSTRACT The purpose of our study was to confirm or refute the view that diabetes be regarded as a coronary heart disease (CHD) risk equivalent and to test for sex differences in mortality.
This was a prospective cohort study of 7,052 men and 8,354 women aged 45-64 years from Renfrew and Paisley, Scotland, who were first screened in 1972-1976 and followed for 25 years. All-cause mortality was calculated as death per 1,000 person-years. A Cox proportional hazards model was used to adjust survival for age, smoking habit, blood pressure, serum cholesterol, BMI, and social class.
There were 192 deaths in 228 subjects with diabetes and 2,016 deaths in 3,076 subjects with CHD. The highest mortality was in the group with both diabetes and CHD (100.2 deaths/1,000 person-years in men, 93.6 in women) and the lowest in the group with neither (29.2 deaths/1,000 person-years in men, 19.4 in women). Men and women with diabetes only and CHD only formed an intermediate risk group. The adjusted hazard ratio (HR) for CHD mortality in men with diabetes only compared with men with CHD only was 1.17 (95% CI 0.78-1.74; P = 0.56). Corresponding HR for women was 1.97 (1.27-3.08; P = 0.003).
Diabetes without previous CHD carries a lifetime risk of vascular death as high as that for CHD alone. Women may be at particular risk. Our data support the view that cardiovascular risk factors in diabetes should be treated as aggressively as in people with CHD.
Full-textDOI: · Available from: Chris Isles, Aug 31, 2015
- SourceAvailable from: Igor Kizub
[Show abstract] [Hide abstract]
- "DM is a prominent healthcare burden because both type 1 and type 2 of DM are associated with the development of circulatory disorders which account for up to 80% of premature excess mortality in diabetic patients . The macrovascular manifestations of DM include angiopathy, atherosclerosis, medial calcification, and arterial hypertension mostly located in coronary and carotid arteries  , cerebral vessels , and large peripheral arteries of the lower extremities . The microvascular complications of DM, also known as microangiopathy , include retinopathy , nephropathy , and peripheral neuropathy . "
ABSTRACT: Diabetes mellitus (DM) is a complex syndrome which leads to multiple dysfunctions including vascular disorders. Hyperglycemia is considered to be a key factor responsible for the development of diabetic vascular complications and can mediate their adverse effects through multiple pathways. One of those mechanisms is the activation of protein kinase C (PKC). This important regulatory enzyme is involved in a signal transduction of several vascular functions including vascular smooth muscle contractility. Many studies have shown that hyperglycemia in DM results in oxidative stress. Overproduction of reactive oxygen species (ROS) by different oxidases and the mitochondrial electron transport chain (ETC), advanced glycation end products, polyol pathway flux, and hyperglicemia-induced rising in diacylglycerol (DAG) contribute to the activation of PKC. Activation of endothelial PKC in DM leads to endothelium-dependent vasodilator dysfunction. The main manifestations of this are inhibition of vasodilatation mediated by nitric oxide (NO), endothelium-derived hyperpolarizing factor (EDHF) and prostacyclin, and activation of vasoconstriction mediated by endothelin-1 (ET-1), prostaglandin E2 (PGE2) and thromboxane A2 (TXA2). Activated PKC in DM also increases vascular endothelial growth factor (VEGF) expression and activates NADPH oxidases leading to raised ROS production. On the other hand, PKC in DM is involved in enhancement of vascular contractility in an endothelium-independent manner by inactivation of K(+) channels and Ca(2+) sensitization of myofilaments in vascular smooth muscle cells. This shows that PKC is a potential therapeutic target for treating vascular diabetic complications.International journal of cardiology 04/2014; 174:230-242. DOI:10.1016/j.ijcard.2014.04.117 · 6.18 Impact Factor
[Show abstract] [Hide abstract]
- "In addition, evidence suggests that post-AMI patients who develop DM are at high risk of adverse events . As these findings indicate that diabetic individuals with CHD have worse morbidity and mortality than non-diabetic CHD patients  , risk stratification in the clinical setting for the development of de novo DM (dn-DM) is expected to improve mortality in post-AMI patients. To date, however, few predictive markers for the development of dn-DM after AMI have been identified. "
ABSTRACT: Acute hyperglycemia (AH) after the onset of acute myocardial infarction (AMI) is a manifestation of transient abnormal glucose metabolism that may reflect AMI severity, and thus be a predictor of poor prognosis. However, it remains unknown whether AH may predict development of de novo diabetes mellitus (dn-DM) in non-diabetic AMI patients. Among AMI patients registered in the Osaka Acute Coronary Insufficiency Study between 1998 and 2007, we investigated hospital records of 1493 patients who had an admission glycated hemoglobin A1c (HbA1c) level of ≤6.0% and were subjected to glycometabolic profiling after survival discharge. dn-DM was defined as initiation of diabetic medication or documentation of an HbA1c level of ≥6.5% during the 5-year follow-up period. AH, defined as an admission serum glucose level of ≥200mg/dl, was observed in 133 (8.9%) patients. dn-DM development was more frequent in post-AMI patients with AH than those without [24.8% vs 12.0%, adjusted hazard ratio (HR) 1.776, p=0.021], particularly among patients with an HbA1c of <5.6% on admission. Treatment with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers was associated with a reduced incidence of dn-DM in patients with AH (adjusted HR 0.397, p=0.031). Admission AH was a predictor of dn-DM in non-diabetic post-AMI patients. Renin-angiotensin system inhibitors were associated with reduced incidence of dn-DM in post-AMI patients with AH.Journal of Cardiology 10/2013; 63(3-4). DOI:10.1016/j.jjcc.2013.08.012 · 2.57 Impact Factor
[Show abstract] [Hide abstract]
- "The global prevalence of T2DM has been estimated at 171 million people and is projected to more than double by 2030 . The epidemiological establishment of T2DM as a coronary artery disease equivalent has been confirmed in several investigations [2–4]. Type 2 diabetes mellitus (T2DM) is a progressive multisystemic disease accompanied by endothelial dysfunction [5–7] and an increased cardiovascular mortality [3, 8]. "
ABSTRACT: Type 2 diabetes mellitus (T2DM) is a progressive multisystemic disease accompanied by vascular dysfunction and a tremendous increase in cardiovascular mortality. Numerous adipose-tissue-derived factors and beta cell dysfunction contribute to the increased cardiovascular risk in patients with T2DM. Nowadays, numerous pharmacological interventions are available to lower blood glucose levels in patients with type 2 diabetes. Beside more or less comparable glucose lowering efficacy, some of them have shown limited or probably even unfavorable effects on the cardiovascular system and overall mortality. Recently, incretin-based therapies (GLP-1 receptor agonists and DPP-IV inhibitors) have been introduced in the treatment of T2DM. Beside the effects of GLP-1 on insulin secretion, glucagon secretion, and gastrointestinal motility, recent studies suggested a couple of direct cardiovascular effects of GLP-1-based therapies. The goal of this paper is to provide an overview about the current knowledge of direct GLP-1 effects on endothelial and vascular function and potential consequences on the cardiovascular outcome in patients with T2DM treated with GLP-1 receptor agonists or DPP-IV inhibitors.Experimental Diabetes Research 04/2012; 2012(1687-5214):635472. DOI:10.1155/2012/635472 · 3.54 Impact Factor