Robert Roberts, MD, FRSC, FRCPC, MACC, LLD (Hon.), FAHA

CAD has proved to be a highly preventable disease. Reduction in risk for CAD has been accomplished by changes in lifestyle such as cessation of smoking or lowering plasma cholesterol by drug therapy. Multiple randomized placebo-controlled clinical trials since the early 1990s targeting lowering of plasma cholesterol have consistently been associated with a 30% to 40% reduction in cardiac morbidity and mortality. Despite these efforts, CVD remains the most common cause of death in the U.S. and is also the most common cause of death throughout the world. Secondary prevention has been effective, whereas primary prevention offers even greater benefits and is more appropriate, if not necessary, to reduce this pandemic.

The landmark TAILOR-PCI trial showed encouraging evidence for genotype-guided antiplatelet therapy.

CAD, despite the success of secondary prevention, is pandemic and the leading cause of death in high-, middle- and low-income countries throughout the world.

The modern era of the application of molecular biology and recombinant DNA techniques is claimed to be initiated in the early 1970s due to four discoveries.

Much work has been put in to discovering genetic variants predisposing to CAD since the first, 9p21, was discovered in 2007. The CAD phenotype in the original study and subsequent association studies did not differentiate MI and CAD.

Mitral valve prolapse is known to be one of the most common cardiac abnormalities in the general population.

Inherited defects affecting the heart at birth are the most common of all birth defects in the world. About 5% of congenital heart defects are due to atrioventricular septal defects and the prevalence is about 0.4% per 1,000 live births.

Genetic variants associated solely with increased levels of plasma HDL cholesterol are not associated with the expected decrease in risk for MI.

In a large genome-wide association study, a genetic variant predisposing to CAD was identified on the short arm of chromosome 6 (6p21.3).

In an international consortium of 14 genome-wide association studies, 23 genetic risk variants were validated as having an association with coronary artery disease.