Gene therapy remains a daunting task. Table 2 lists the pertinent cardiac conditions. There has been no clinical trial for heart failure or transplantation. Presently impro¬ved oxygen supply to a myocardium deprived of oxygen because of atheromatous coronary artery obstruction is the goal. Success has thus far not been obtained. In addition this goal is fraught with danger, because angiogenesis may increase plaque growth and decrease the thickness of the fibrous plaque which is protective and fragile. New vessels within the plaque are prone to rupture causing ultimate plaque rupture and severe cardiac events, see Section IV.
The most interesting future goal is that gene therapy interventions may be capable of increasing HDL choles¬terol levels and lowering blood triglycerides. This could be a most valuable addition to our therapeutic armamentar¬ium, because the lifesaving statins that lower LDL cholesterol do not significantly increase HDL levels.
The cholesterol ester transfer protein (CETP) mediates the exchange of cholesteryl ester in HDL for triglyceride in very low-density lipoprotein (VLDL). Thus, CETP appears to reduce HDL and cause progression of atheroma formation; a pharmacologic inhibitor supports this hypothesis and gives hope that an anti-gene approach to this target may be possible.