Should Diabetes Be Considered a Coronary Heart Disease Risk Equivalent? Results from 25 years of follow-up in the Renfrew and Paisley Survey

University of Glasgow, Glasgow, Scotland, United Kingdom
Diabetes Care (Impact Factor: 8.42). 08/2005; 28(7):1588-93. DOI: 10.2337/diacare.28.7.1588
Source: PubMed

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.

Download full-text

Full-text

Available from: Chris Isles
    • "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 [2]. The macrovascular manifestations of DM include angiopathy, atherosclerosis, medial calcification, and arterial hypertension mostly located in coronary and carotid arteries [4] [5], cerebral vessels [6], and large peripheral arteries of the lower extremities [6]. The microvascular complications of DM, also known as microangiopathy , include retinopathy [7], nephropathy [8], and peripheral neuropathy [9]. "
    [Show abstract] [Hide abstract]
    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 Ca2 + sensitization of myofilaments in vascular smooth muscle cells. This shows that PKC is a potential therapeutic target for treating vascular diabetic complications.
    No preview · Article · Jun 2014
  • Source
    • "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 [2]. The macrovascular manifestations of DM include angiopathy, atherosclerosis, medial calcification, and arterial hypertension mostly located in coronary and carotid arteries [4] [5], cerebral vessels [6], and large peripheral arteries of the lower extremities [6]. The microvascular complications of DM, also known as microangiopathy , include retinopathy [7], nephropathy [8], and peripheral neuropathy [9]. "
    [Show abstract] [Hide abstract]
    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.
    Full-text · Article · Apr 2014 · International journal of cardiology
  • Source
    • "In addition, evidence suggests that post-AMI patients who develop DM are at high risk of adverse events [10]. As these findings indicate that diabetic individuals with CHD have worse morbidity and mortality than non-diabetic CHD patients [11] [12], 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. "
    [Show abstract] [Hide abstract]
    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.
    Full-text · Article · Oct 2013 · Journal of Cardiology
Show more