Primary and secondary prevention of cardiovascular diseases: a practical evidence-based approach

Abstract

Despite the fact that we possess highly effective tools for the primary and secondary prevention of myocardial infarction and other complications of atherosclerosis, coronary heart disease remains the most common cause of death in our society. Arterial inflammation and endothelial dysfunction play central roles in the pathogenesis of atherosclerosis and adverse cardiovascular (CV) events. Therapeutic lifestyle changes in conjunction with an aggressive multidrug regimen targeted toward the normalization of the major CV risk factors will neutralize the atherogenic milieu, reduce vascular inflammation, and markedly decrease the risk of adverse CV events and need for revascularization procedures. Specific CV risk factors and optimal therapies for primary and secondary prevention are discussed.

FIGURE 1.

Patients randomly assigned to optimal medical therapy (OMT) did equally well during follow-up as those assigned to percutaneous coronary intervention (PCI) plus OMT with respect to the primary end point (nonfatal myocardial infarction or death from any cause). CI = confidence interval; HR = hazard ratio. From N Engl J Med, with permission. ©2007 Massachusetts Medical Society. All rights reserved.

FIGURE 2.

Kaplan-Meier curves for time to first adverse cardiovascular event for patients treated with benazepril plus amlodipine (calcium channel blocker [CCB]/angiotensin-converting enzyme inhibitor [ACEI]) compared with benazepril plus hydrochlorothiazide (HCTZ). CI = confidence interval; HR = hazard ratio. From N Engl J Med, with permission. ©2008 Massachusetts Medical Society. All rights reserved.

FIGURE 3.

Cumulative incidence of adverse cardiovascular events of rosuvastatin compared with placebo. CI = confidence interval; HR = hazard ratio. From N Engl J Med, with permission. ©2008 Massachusetts Medical Society. All rights reserved.

FIGURE 4.

Highly significant association between atherosclerotic progression and on-treatment low-density lipoprotein cholesterol (LDL-C). ASTEROID = A Study to Evaluate the Effect of Rosuvastatin on Intravascular Ultrasound-Derived Coronary Atheroma Burden; CCAIT = Canadian Coronary Atherosclerosis Intervention Study; LCAS = Lipoprotein and Coronary Atherosclerosis Study; MAAS = Multicentre Anti Atheroma Study; MARS = Monitored Atherosclerosis Regression Study; MLD = minimum lumen diameter; PLAC I = Pravastatin Limitation of Atherosclerosis in the Coronary Arteries; REGRESS = Regression Growth Evaluation Statin Study. SI conversion factor: To convert LDL-C values to mmol/L, multiply by 0.0259. From Circulation, with permission from Wolters Kluwer Health.

FIGURE 5.

The immediate deleterious effects of 700 kcal/m² consumed as a beverage containing 75 g of glucose mixed with whipping cream on glucose, triglycerides, oxidant stress (nitrotyrosine), inflammation (C-reactive protein [CRP]), and arterial flow-mediated dilation (FMD). From J Am Coll Cardiol, with permission from Elsevier.

FIGURE 6.

Cumulative incidence of major coronary events in patients treated with eicosapentaenoic acid (EPA) plus statin compared with statin alone. CI = confidence interval; HR = hazard ratio. From Lancet, with permission from Elsevier.

FIGURE 7.

Kaplan-Meier curve showing the probability of major adverse cardiovascular events in participants with 25 hydroxyvitamin D (25-[OH] D) levels ≥15 ng/mL vs 25-(OH) D levels <15 ng/mL. SI conversion factor: To convert 25-(OH) D values to nmol/L, multiply by 2.496. From J Am Coll Cardiol, with permission from Elsevier.