ABSTRACT
The most dangerous form of cardiovascular disease is atherosclerotic coronary artery disease, which leads to narrowing and stiffening of arteries that supply blood to the heart. Atherosclerosis results from repeated injury, subsequent inflammation, and repair of the vascular wall. Endothelial cell injury leads to an inflammatory response and lipid accumulation mostly from low-density lipoprotein cholesterol in the bloodstream. Endothelial cells, along with macrophages, promote rapid accumulation of lipids leading to fatty streaks or foam cells. At this stage, atherosclerosis is considered to be reversible with appropriate changes to risk factors (smoking, exercise, healthy diet, etc.). If atherosclerosis continues, a plaque (atheroma) forms around a lipid core. A stable plaque (fibroatheroma) is characterized by a thick fibrous cap composed of smooth muscle cells and a small lipid core. In contrast, a plaque susceptible to rupture is characterized by a large lipid core and a thin fibrous cap. They are also referred to as vulnerable plaques. Note that the lipid core is highly thrombolytic. Upon rupture, lipids interact with the blood to induce thrombosis (blood clot formation), artery blockage, and ultimately myocardial infarction (heart attack). If the atheroma stabilizes, smooth muscle cell proliferation can prevent rupture but still lead to calcification and severe fibrosis. Continued plaque growth can lead to severe stenosis (vessel occlusion) and ischemia (lack of oxygenated blood). In the past, conventional wisdom in cardiovascular research assumed that most myocardial
infarctions and strokes were caused by artery occlusion due to plaque growth.[2] Recent studies have shown that plaque rupture, not vessel occlusion, is the leading cause of these acute events.[3]
CLINICAL TREATMENTS
To effectively treat atherosclerosis, several interventions have been developed and are currently used in the clinic. The most common interventional procedure is percutaneous transluminal coronary angioplasty (PTCA). In PTCA, a balloon catheter is inserted into the arterial vasculature via the femoral artery over a smaller guide wire. Once the balloon catheter arrives at the coronary lesion to be dilated, the balloon is pressurized with fluid to expand the arterial lumen. The first balloon angioplasty procedure was performed in 1977 by Dr. Gru¨ntzig in Zurich, Switzerland.[4]
The procedure is most effective for softer plaques. Although angioplasty proved effective in many cases, restenosis (subsequent occlusion of the artery lumen after the procedure) rates can still be 20-30%, based on follow-up studies performed about six months after the procedure.[5,6]
Due to the limited success of PTCA procedures, stents were developed to be placed inside the vessel to maintain lumen diameter after the balloon intervention. Stents are meshed scaffold tubes delivered over an angioplasty balloon. As the angioplasty balloon is inflated, the stent expands and is implanted inside the vessel lumen. Since gaining FDA approval in 1994, stents have become the primary interventional procedure accounting for a majority of angioplasty procedures in catheterization laboratories.[7] Stents effectively prop open the occluded vessel by pushing on the plaque and arterial wall to expand the lumen diameter. Clinical complications related to stent deployment are underdeployment and overdeployment. Underdeployment can lead to stent collapse if it is not in complete contact with the vessel lumen. Furthermore, blood can collect in the gap between the arterial tissue and the underdeployed stent leading to thrombosis.
