- Email: [email protected]
Dysglycemia and Cardiovascular Risk
Correspondence
JACC Vol. 60, No. 12, 2012 September 18, 2012:1117–21
CE echocardiography for global left ventricular function when MRI is the reference standard. Johannes Greupner, MD Adrian C. Borges, MD, PhD *Marc Dewey, MD, PhD *Charité, Institut für Radiologie Charitéplatz 1 10117 Berlin Germany E-mail: [email protected] http://dx.doi.org/10.1016/j.jacc.2012.06.020 REFERENCES
1. Hoffmann R, von Bardeleben S, Kasprzak JD, et al. Analysis of regional left ventricular function by cineventriculography, cardiac magnetic resonance imaging, and unenhanced and contrast-enhanced echocardiography: a multicenter comparison of methods. J Am Coll Cardiol 2006; 47:121– 8. 2. Hoffmann R, von Bardeleben S, ten Cate F, et al. Assessment of systolic left ventricular function: a multi-centre comparison of cineventriculography, cardiac magnetic resonance imaging, unenhanced and contrastenhanced echocardiography. Eur Heart J 2005;26:607–16. 3. Arraiza M, Azcarate PM, De Cecco CN, et al. Assessment of left ventricular parameters in orthotopic heart transplant recipients using dual-source CT and contrast-enhanced echocardiography: comparison with MRI. Eur J Radiol 2012 [E-pub ahead of print]. 4. Burianova L, Riedlbauchova L, Lefflerova K, et al. Assessment of left ventricular function in non-dilated and dilated hearts: comparison of contrast-enhanced 2-dimensional echocardiography with multidetector row CT angiography. Acta Cardiol 2009;64:787–94.
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(CV) mortality. The relation between glycemia and CV risk started within the normal blood glucose range, with a linear relationship (4,5). In addition, post-challenge hyperglycemia is strongly associated with future macrovascular events and total mortality in patients with acute myocardial infarction and/or patients with coronary disease who received angiography (6). The results of the STOP-NIDDM (Study to Prevent NonInsulin-Dependent Diabetes Mellitus) trial demonstrated that treating IGT with acarbose, an alpha-glucosidase inhibitor, which specifically reduces postprandial hyperglycemia, significantly reduces the conversion rate of IGT to type 2 diabetes associated with reductions in the development of CV events (by 49%), the incidence of new cases of hypertension (by 34%) (7), and the annual increase of carotid intima–media thickness (by 50%) (8). Moreover, pioglitazone significantly reduces diastolic blood pressure and the rate of the intima–media thickness associated with a reduction in the conversion of IGT to type 2 diabetes (9). Thus, dysglycemia, especially in the case of postprandial hyperglycemia, is related to CV risk and mortality, and a variety of pharmacological and nonpharmacological therapies should be targeted to the management of postprandial blood glucose independent of blood pressure and/or cholesterol. *Katsunori Nonogaki, MD, PhD *Department of Lifestyle Medicine Tohoku University Hospital Sendai, Miyagi 980-8574 Japan E-mail: [email protected] or [email protected] http://dx.doi.org/10.1016/j.jacc.2012.03.078
Dysglycemia and Cardiovascular Risk I read with interest the “state-of-the art” paper by Grundy (1) that was recently published in the Journal. The paper demonstrated that the pre-diabetic range of glucose levels do not directly cause atherosclerosis or its complications, on the basis of a systemic review of the relationship between pre-diabetes and cardiovascular disease (CVD). The paper also indicated that the major targets for the prevention of CVD are elevations of cholesterol and blood pressure, but not elevations of plasma glucose, because certain clinical trials have suggested that the glucose-lowering drugs did not retard atherogenesis. My question is whether it is in fact reasonable to exclude the clinical worth of lowering glucose, especially in postprandial hyperglycemia, for the prevention of CVD in subjects with pre-diabetes. Both epidemiological and interventional studies have shown that pre-diabetes, especially in post-prandial hyperglycemia, is a direct and independent risk factor for CVD (2– 4). In the DECODE (Diabetes Epidemiology: Collaborative Analysis of Diagnostic Criteria in Asia) study, the risk for CVD and stroke increased progressively with the change from impaired fasting glucose to impaired glucose tolerance (IGT) to type 2 diabetes (5), indicating that hyperglycemia is a risk factor for cardiovascular
REFERENCES
1. Grundy SM. Pre-diabetes, metabolic syndrome, and cardiovascular risk. J Am Coll Cardiol 2012;59:635– 43. 2. Ceriello A. Postprandial hyperglycemia and diabetes complications is it time to treat? Diabetes 2005;54:1–7. 3. Gallwitz B. Implications of postprandial glucose and weight control in people with type 2 diabetes. Understanding and implementing the international diabetes federation guidelines. Diabetes Care 2009;32: S322–5. 4. DeFronzo RA, Abdul-Ghani M. Assessment and treatment of cardiovascular risk in prediabetes: impaired glucose tolerance and impaired fasting glucose. Am J Cardiol 2011;108(Suppl):3B–24B. 5. DECODE Study Group. Glucose tolerance and cardiovascular mortality: comparison of fasting and 2-hour diagnostic criteria. Arch Intern Med 2001;161:397– 405. 6. Sourij H, Saely CH, Schmid F, et al. Post-challenge hyperglycaemia is strongly associated with future macrovascular events and total mortality in angiographied coronary patients. Eur Heart J 2010;31:1583–90. 7. Chiasson JL, Josse RG, Gomis R, Hanefeld M, Karasik A, Laakso M. Acarbose treatment and the risk of cardiovascular disease and hypertension in patients with impaired glucose tolerance: the STOPNIDDM trial. JAMA 2003;290:486 –94. 8. Hanefeld M, Chiasson JL, Koehler C, Henkel E, Schaper F, Temelkova-Kurktshiev T. Acarbose slows progression of intima-media thickness of the carotid arteries in subjects with impaired glucose tolerance. Stroke 2004;35:1073– 8. 9. DeFronzo RA, Tripathy D, Schwenke DC, et al. Pioglitazone for diabetes prevention in impaired glucose tolerance. N Engl J Med 2011;364:1104 –15.
JACC Vol. 60, No. 12, 2012 September 18, 2012:1117–21
CE echocardiography for global left ventricular function when MRI is the reference standard. Johannes Greupner, MD Adrian C. Borges, MD, PhD *Marc Dewey, MD, PhD *Charité, Institut für Radiologie Charitéplatz 1 10117 Berlin Germany E-mail: [email protected] http://dx.doi.org/10.1016/j.jacc.2012.06.020 REFERENCES
1. Hoffmann R, von Bardeleben S, Kasprzak JD, et al. Analysis of regional left ventricular function by cineventriculography, cardiac magnetic resonance imaging, and unenhanced and contrast-enhanced echocardiography: a multicenter comparison of methods. J Am Coll Cardiol 2006; 47:121– 8. 2. Hoffmann R, von Bardeleben S, ten Cate F, et al. Assessment of systolic left ventricular function: a multi-centre comparison of cineventriculography, cardiac magnetic resonance imaging, unenhanced and contrastenhanced echocardiography. Eur Heart J 2005;26:607–16. 3. Arraiza M, Azcarate PM, De Cecco CN, et al. Assessment of left ventricular parameters in orthotopic heart transplant recipients using dual-source CT and contrast-enhanced echocardiography: comparison with MRI. Eur J Radiol 2012 [E-pub ahead of print]. 4. Burianova L, Riedlbauchova L, Lefflerova K, et al. Assessment of left ventricular function in non-dilated and dilated hearts: comparison of contrast-enhanced 2-dimensional echocardiography with multidetector row CT angiography. Acta Cardiol 2009;64:787–94.
1121
(CV) mortality. The relation between glycemia and CV risk started within the normal blood glucose range, with a linear relationship (4,5). In addition, post-challenge hyperglycemia is strongly associated with future macrovascular events and total mortality in patients with acute myocardial infarction and/or patients with coronary disease who received angiography (6). The results of the STOP-NIDDM (Study to Prevent NonInsulin-Dependent Diabetes Mellitus) trial demonstrated that treating IGT with acarbose, an alpha-glucosidase inhibitor, which specifically reduces postprandial hyperglycemia, significantly reduces the conversion rate of IGT to type 2 diabetes associated with reductions in the development of CV events (by 49%), the incidence of new cases of hypertension (by 34%) (7), and the annual increase of carotid intima–media thickness (by 50%) (8). Moreover, pioglitazone significantly reduces diastolic blood pressure and the rate of the intima–media thickness associated with a reduction in the conversion of IGT to type 2 diabetes (9). Thus, dysglycemia, especially in the case of postprandial hyperglycemia, is related to CV risk and mortality, and a variety of pharmacological and nonpharmacological therapies should be targeted to the management of postprandial blood glucose independent of blood pressure and/or cholesterol. *Katsunori Nonogaki, MD, PhD *Department of Lifestyle Medicine Tohoku University Hospital Sendai, Miyagi 980-8574 Japan E-mail: [email protected] or [email protected] http://dx.doi.org/10.1016/j.jacc.2012.03.078
Dysglycemia and Cardiovascular Risk I read with interest the “state-of-the art” paper by Grundy (1) that was recently published in the Journal. The paper demonstrated that the pre-diabetic range of glucose levels do not directly cause atherosclerosis or its complications, on the basis of a systemic review of the relationship between pre-diabetes and cardiovascular disease (CVD). The paper also indicated that the major targets for the prevention of CVD are elevations of cholesterol and blood pressure, but not elevations of plasma glucose, because certain clinical trials have suggested that the glucose-lowering drugs did not retard atherogenesis. My question is whether it is in fact reasonable to exclude the clinical worth of lowering glucose, especially in postprandial hyperglycemia, for the prevention of CVD in subjects with pre-diabetes. Both epidemiological and interventional studies have shown that pre-diabetes, especially in post-prandial hyperglycemia, is a direct and independent risk factor for CVD (2– 4). In the DECODE (Diabetes Epidemiology: Collaborative Analysis of Diagnostic Criteria in Asia) study, the risk for CVD and stroke increased progressively with the change from impaired fasting glucose to impaired glucose tolerance (IGT) to type 2 diabetes (5), indicating that hyperglycemia is a risk factor for cardiovascular
REFERENCES
1. Grundy SM. Pre-diabetes, metabolic syndrome, and cardiovascular risk. J Am Coll Cardiol 2012;59:635– 43. 2. Ceriello A. Postprandial hyperglycemia and diabetes complications is it time to treat? Diabetes 2005;54:1–7. 3. Gallwitz B. Implications of postprandial glucose and weight control in people with type 2 diabetes. Understanding and implementing the international diabetes federation guidelines. Diabetes Care 2009;32: S322–5. 4. DeFronzo RA, Abdul-Ghani M. Assessment and treatment of cardiovascular risk in prediabetes: impaired glucose tolerance and impaired fasting glucose. Am J Cardiol 2011;108(Suppl):3B–24B. 5. DECODE Study Group. Glucose tolerance and cardiovascular mortality: comparison of fasting and 2-hour diagnostic criteria. Arch Intern Med 2001;161:397– 405. 6. Sourij H, Saely CH, Schmid F, et al. Post-challenge hyperglycaemia is strongly associated with future macrovascular events and total mortality in angiographied coronary patients. Eur Heart J 2010;31:1583–90. 7. Chiasson JL, Josse RG, Gomis R, Hanefeld M, Karasik A, Laakso M. Acarbose treatment and the risk of cardiovascular disease and hypertension in patients with impaired glucose tolerance: the STOPNIDDM trial. JAMA 2003;290:486 –94. 8. Hanefeld M, Chiasson JL, Koehler C, Henkel E, Schaper F, Temelkova-Kurktshiev T. Acarbose slows progression of intima-media thickness of the carotid arteries in subjects with impaired glucose tolerance. Stroke 2004;35:1073– 8. 9. DeFronzo RA, Tripathy D, Schwenke DC, et al. Pioglitazone for diabetes prevention in impaired glucose tolerance. N Engl J Med 2011;364:1104 –15.