Limits...
Treatment of diabetic vasculopathy with rosiglitazone and ramipril: Hype or hope?

Rahman S, Ismail AA, Rahman AR - Int J Diabetes Dev Ctries (2009)

Bottom Line: Cardiovascular diseases are responsible for increased morbidity and mortality in people with diabetes.Diabetic macrovasculopathy is associated with structural and functional changes in large arteries, which causes endothelial dysfunction, increased arterial stiffness, or decreased arterial distensability.Treatment goals for patients with type 2 diabetes specify targets for glycemia and other cardiometabolic risk factors, for example, hypertension and dyslipidemia.

View Article: PubMed Central - PubMed

Affiliation: Department of Clinical Sciences, School of Life Sciences, University of Bradford, Bradford, UK.

ABSTRACT
Cardiovascular diseases are responsible for increased morbidity and mortality in people with diabetes. Diabetic macrovasculopathy is associated with structural and functional changes in large arteries, which causes endothelial dysfunction, increased arterial stiffness, or decreased arterial distensability. Diabetic complications can be controlled and avoided by strict glycemic control, maintaining normal lipid profiles, regular physical exercise, adopting a healthy lifestyle and pharmacological interventions. Treatment goals for patients with type 2 diabetes specify targets for glycemia and other cardiometabolic risk factors, for example, hypertension and dyslipidemia. In recent years, special attention has been devoted to both thiazolidindiones (TZDs) and angiotensin converting enzyme (ACE) inhibitors as clinical trials revealed that these drugs may reduce the rate of progression to diabetes or delay the onset of diabetes, regression of impaired glucose tolerance (IGT) to normoglycemia and reduces the composite of all-cause mortality, nonfatal myocardial infarction and stroke in patients with diabetes. This review focuses on the potential roles of rosiglitazone, a member of TZD class of antidiabetic agents, and ramipril, an ACE inhibitor, in preventing the preclinical macrovasculopathy in diabetes and IGT population.

No MeSH data available.


Related in: MedlinePlus

Pathogenesis and pathophysiology of diabetic macrovasculopathy
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC2822214&req=5

Figure 0001: Pathogenesis and pathophysiology of diabetic macrovasculopathy

Mentions: Diabetes mellitus is a multifactorial disease associated with a number of microvascular (retinopathy, neuropathy, and nephropathy) and macrovascular complications.[34] Diabetic macrovasculopathy is associated with structural and functional changes in large arteries that lead to increased stiffness, abnormal pulse wave travel, and systolic hypertension.[4] Structural changes mainly result from glycation of wall components and functional changes originate in endothelial dysfunction, increased arterial stiffness or decreased arterial distensibility [Figure 1]. These changes promote the development of left ventricular hypertrophy, an independent risk factor for cardiovascular (CV) mortality.[5] Apart from the above-mentioned mechanisms, metabolic [advanced glycation end production (AGE), cytokines], humoral (renin-angiotensin system, endothelin, sympathetic nervous system) and hemodynamic (arterial hypertension and mechanical strain) factors contribute to the characteristic dysfunction in diabetic vasculopathy.[6] The initiators of vasculopathy that ultimately develop into long-term diabetic complications can be controlled and avoided by strict glycemic control, maintaining normal lipid profiles, regular physical exercise, adopting a healthy lifestyle and pharmacological interventions.


Treatment of diabetic vasculopathy with rosiglitazone and ramipril: Hype or hope?

Rahman S, Ismail AA, Rahman AR - Int J Diabetes Dev Ctries (2009)

Pathogenesis and pathophysiology of diabetic macrovasculopathy
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2822214&req=5

Figure 0001: Pathogenesis and pathophysiology of diabetic macrovasculopathy
Mentions: Diabetes mellitus is a multifactorial disease associated with a number of microvascular (retinopathy, neuropathy, and nephropathy) and macrovascular complications.[34] Diabetic macrovasculopathy is associated with structural and functional changes in large arteries that lead to increased stiffness, abnormal pulse wave travel, and systolic hypertension.[4] Structural changes mainly result from glycation of wall components and functional changes originate in endothelial dysfunction, increased arterial stiffness or decreased arterial distensibility [Figure 1]. These changes promote the development of left ventricular hypertrophy, an independent risk factor for cardiovascular (CV) mortality.[5] Apart from the above-mentioned mechanisms, metabolic [advanced glycation end production (AGE), cytokines], humoral (renin-angiotensin system, endothelin, sympathetic nervous system) and hemodynamic (arterial hypertension and mechanical strain) factors contribute to the characteristic dysfunction in diabetic vasculopathy.[6] The initiators of vasculopathy that ultimately develop into long-term diabetic complications can be controlled and avoided by strict glycemic control, maintaining normal lipid profiles, regular physical exercise, adopting a healthy lifestyle and pharmacological interventions.

Bottom Line: Cardiovascular diseases are responsible for increased morbidity and mortality in people with diabetes.Diabetic macrovasculopathy is associated with structural and functional changes in large arteries, which causes endothelial dysfunction, increased arterial stiffness, or decreased arterial distensability.Treatment goals for patients with type 2 diabetes specify targets for glycemia and other cardiometabolic risk factors, for example, hypertension and dyslipidemia.

View Article: PubMed Central - PubMed

Affiliation: Department of Clinical Sciences, School of Life Sciences, University of Bradford, Bradford, UK.

ABSTRACT
Cardiovascular diseases are responsible for increased morbidity and mortality in people with diabetes. Diabetic macrovasculopathy is associated with structural and functional changes in large arteries, which causes endothelial dysfunction, increased arterial stiffness, or decreased arterial distensability. Diabetic complications can be controlled and avoided by strict glycemic control, maintaining normal lipid profiles, regular physical exercise, adopting a healthy lifestyle and pharmacological interventions. Treatment goals for patients with type 2 diabetes specify targets for glycemia and other cardiometabolic risk factors, for example, hypertension and dyslipidemia. In recent years, special attention has been devoted to both thiazolidindiones (TZDs) and angiotensin converting enzyme (ACE) inhibitors as clinical trials revealed that these drugs may reduce the rate of progression to diabetes or delay the onset of diabetes, regression of impaired glucose tolerance (IGT) to normoglycemia and reduces the composite of all-cause mortality, nonfatal myocardial infarction and stroke in patients with diabetes. This review focuses on the potential roles of rosiglitazone, a member of TZD class of antidiabetic agents, and ramipril, an ACE inhibitor, in preventing the preclinical macrovasculopathy in diabetes and IGT population.

No MeSH data available.


Related in: MedlinePlus