Arresting cardiovascular disease progression

• Published in: Postgraduate medicine Vol. 116; no. 2; p. 45
• Main Author: C. Venkata S. Ram, MD Pedro Vergne-Marini, MD
• Format: Journal Article
• Language: English
• Published: Minneapolis JTE Multimedia 01.08.2004
• ISSN: 0032-5481; 1941-9260

Another risk factor is diabetes, which, when combined with the other factors attributed to CVD, creates an even greater cost burden than hypertension.3 (Reference) Since 1990, the prevalence of diabetes has increased 61%.4 (Reference) In 2001, the overall death rate from diabetes was 25.3%.1 (Reference) As a result of increases in the diagnosis and prevalence of diabetes, its estimated cost in 2002 was $132 billion. Of this amount, $91.8 billion was due to direct medical costs, and $39.8 billion was due to indirect costs.5 (Reference) In 2002, 11% of national healthcare expenditures were attributed to diabetes care alone.5 (Reference) In addition, the average medical expenditure per year for a patient with diabetes was $13,243, or 2.4 times the amount spent for a patient without diabetes.5 (Reference) In the pathophysiology of the RAAS, renin catalyzes the breakdown of inactive angiotensinogen to angiotensin I. Angiotensin I is then converted by angiotensin-converting enzyme (ACE) to angiotensin II, a potent vasoconstrictor. Angiotensin II promotes vascular smooth-muscle cell growth and migration and activates adhesion molecules and other inflammatory markers. These actions of angiotensin II are mediated through the angiotensin II type 1 (AT1) receptors.8,11,12 (Reference) ACE inhibitors work by inhibiting not only the conversion of angiotensin I to angiotensin II but also the degradation of bradykinin. Therefore, ACE inhibitors allow the beneficial effects of nitric oxide to be maintained.8 (Reference) On the other hand, angiotensin II receptor blockers (ARBs) block the actions of angiotensin II by binding specifically to the AT1 receptors without a major effect on the degradation of bradykinin.12 (Reference) Traditional antihypertensive therapies have had some positive proven effect in reducing the complication rate in patients with CVD; however, this is not enough to eliminate the disease. Major trials have showed beneficial effects in patients with hypercholesterolemia. For example, the Prospective Pravastatin Pooling Project13 (Reference) showed a 23% reduction in CVD mortality, nonfatal MI, coronary artery bypass grafting, or percutaneous transluminal coronary angioplasty among nearly 20,000 patients in three trials: the Cholesterol and Recurrent Events (CARE) study,14 (Reference) the Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) study,15 (Reference) and the West of Scotland Coronary Prevention Study (WOSCOPS).16 (Reference) In addition, the Scandinavian Simvastatin Survival Study (4S)17 (Reference) showed a 42% relative risk reduction in coronary deaths among 4,444 patients.