The comparative pathobiology of atherosclerosis and restenosis.

Percutaneous coronary interventions (PCIs) play an increasingly important role in the management of patients with coronary artery disease. However, these important procedures are complicated by restenosis in a sizeable number of patients. The pathobiology of atherosclerosis comprises a complex interaction among lipids, the endothelium, circulating and tissue inflammatory cells, platelets, and vascular smooth muscle cells. The superimposition of the mechanical and cellular consequences of PCIs on the abnormal substrate of atherosclerosis leads to a characteristic and distinct pathobiology that initiates and perpetuates restenosis. A clear understanding of the significant differences between atherosclerosis and restenosis will provide a rational basis for developing treatment plans that always address both problems. This article reviews and contrasts the pathobiology of atherosclerosis and restenosis and compares the mechanisms and time-course of these distinct entities.

Rescue percutaneous coronary intervention immediately following coronary artery bypass grafting.

Perioperative graft failure after coronary artery bypass graft (CABG) can result in acute myocardial infarction with dire clinical consequences. We report a case of rescue percutaneous coronary intervention immediately after unsuccessful CABG. This approach salvaged the patient from cardiogenic shock and should be recognized as a viable alternative to immediate reoperation for certain patients.

Sphincter of Oddi dysfunction: two case reports and a review of the literature.

Sphincter of Oddi dysfunction is an underdiagnosed but important clinical condition. It should be considered in the differential diagnosis of biliary pain when the gallbladder sonogram shows no evidence of gallbladder disease. Hepatobiliary scanning (Tc-99m dimethyl iminodiacetic acid) may provide valuable information in the evaluation of these patients and may be helpful in monitoring response to treatment.

Treating ambulatory ischemia in coronary disease by manipulating the cell biology of atherosclerosis.

Obstructive coronary artery disease is the most common cause of morbidity and mortality in the developed world. Our understanding of the pathobiology of coronary atherosclerosis provides us with new opportunities to reduce myocardial ischemia by interventions that address these mechanisms directly. These interventions include lipid-lowering therapies that improve local coronary vasomotion, inflammation, and the procoagulant state. These interventions have also been shown to result in important reductions in clinical events, including angina pectoris, myocardial ischemia and infarction, and death. Ambulatory electrocardiography provides a versatile and quantifiable measure of regional myocardial ischemia. Reductions in ischemia, as quantified by this diagnostic modality, are associated with improved clinical outcomes that may reflect improvements in the cellular pathophysiology of coronary atherosclerosis. This review discusses new information regarding the interactions between low-density lipoprotein cholesterol, the cell biology of atherosclerosis, and the activity of ischemia in patients with coronary artery disease.

Pathophysiology of atherosclerosis: development, regression, restenosis.

There is now a very large number of patients with coronary artery disease who have also undergone percutaneous interventions such as coronary angioplasty. Atherosclerosis and restenosis are two distinct pathologic processes with different underlying pathophysiologic mechanisms, different natural histories, different clinical presentations, and treatment strategies. Management strategies to target both processes are currently poorly applied in clinical practice. The development of integrated management strategies to target atherosclerosis, as well as restenosis in the postprocedural period remains a priority.

Atherogenic lipids and endothelial dysfunction: mechanisms in the genesis of ischemic syndromes.

Atherogenic lipids, particularly oxidized low-density lipoprotein, are responsible for a wide range of cellular dysfunctions within the vessel wall. The effects on endothelial cells disrupt normal control of vasomotion, with a reduction of effective nitric oxide activity, the development of a procoagulant surface, chronic low-grade inflammation, and abnormal cell growth. These changes are central not only in the development of atherosclerosis but also in the evolution of both stable and unstable ischemic syndromes. There is growing evidence that these abnormal changes in cell function respond rapidly to changes in the atherogenic lipids. Certain cell functions can improve within hours or days of cholesterol lowering.