Temperature heterogeneity due to inflammatory activity may have a pivotal role in predicting plaque composition and allow differentiation between stable and unstable atherosclerotic plaques. Plaques prone to rupture¹ are associated with greater macrophage accumulation than are stable plaques, which have less intense inflammatory activity.^2,3 Characterizing atherosclerotic plaque’s propensity for rupture may further our understanding of how pharmacological treatments alter clinical outcomes.^4–7

The majority of acute coronary syndromes are the result of nonobstructive coronary plaque rupture and subsequent thrombosis. The structure of these plaques, rather than their size, is the major determinant of plaque vulnerability. Identifying vulnerable from stable plaque remains an elusive goal, but one which could have a significant impact on the primary prevention of myocardial infarction in the future. In a recent editorial in the New York Times, this concept of identifying which patients are prone to plaque rupture was described as the “Holy Grail of cardiology”.¹

No-reflow is a common complication during percutaneous coronary intervention in degenerated saphenous vein grafts (SVGs), and is associated with serious adverse clinical outcomes.^1–6 The important role of microvascular vasoconstriction as a predominant mechanism of no-reflow has been demonstrated by the successful reversal of no-reflow events using a variety of microvascular vasodilators (verapamil, diltiazem, adenosine, nitroprusside, etc.).^6–11

Nicardipine is a highly potent arteriolar vasodilator with a longer duration of action than either diltiazem or verapamil when given by intracoronary administration.^11–13 Nicardipine has relatively greater coronary vasoselectivity, greater microcirculatory vasodilating activity and is associated with minimal myocardial depression or atrioventricular nodal disruption.^14–16 Thus nicardipine has many attractive properties when considering the best agent to prevent or reverse no-reflow.

Bare-metal stents (BMS) lower the risk of restenosis and the need for repeat coronary revascularization compared to balloon angioplasty alone.¹ The introduction of drug-eluting stents (DES) has further markedly decreased angiographic restenosis rates to approximately 3–4% at 6 months.^2–4 DES were developed to reduce the risk of major adverse cardiac events (MACE) after percutaneous coronary interventions (PCI) by inhibiting neointimal proliferation and reducing the risk of restenosis.

The choice of anticoagulant in patients undergoing percutaneous coronary intervention (PCI) has been the subject of intense investigation over the past decade. Ever since anticoagulation with heparin was observed to be an essential treatment in patients undergoing balloon angioplasty, unfractionated heparin (UFH) has been the mainstay of procedural anticoagulation. However, use of this therapy is not without side effects, including a high incidence of bleeding when used at standard dose in conjunction with glycoprotein IIb/IIIa inhibitors (GPI).¹ Moreover, activation of platelets occurs with use of UFH, necessitating additional treatment with antiplatelet agents. Two newer anticoagulants, low-molecular weight heparin (LMWH) and bivalirudin have both been extensively studied in the PCI setting. LMWH has greater anti-Xa activity than does UFH, making it a potentially more potent anticoagulant. It also does not activate platelets.

Coronary stenting has demonstrated a consistent ability to reduce restenosis rates compared with percutaneous “plain old” balloon catheter angioplasty. However, in-stent restenosis has long remained the major limitation of coronary stenting. Recent randomized trials have shown that the use of both paclitaxel- and sirolimus-eluting stents (Taxus^®, Boston Scientific, Natick, Massachusetts and Cypher™, Cordis Corp., Miami, Florida, respectively) by polymer-regulated delivery appears to markedly reduce the risk of in-stent restenosis following treatment of de novo lesions^1–4 and even lesions at high risk for in-stent restenosis.^5,6 Although drug-eluting stents (DES) are effective for restenosis reduction, there are concerns regarding long-term safety and efficacy.

Left main (LM) trifurcation coronary stenting is a challenging and complex percutaneous procedure that has been reported in small series and case reports.^1–5 Typically, this disease is treated surgically, but with the advent of drug-eluting stents (DES), interventionalists are increasingly tackling more complex coronary artery disease (CAD), including trifurcation disease. The outcome of DES in the treatment of LM trifurcation disease remains unknown. In this study, we report on our experience with patients who underwent trifurcation LM stenting using paclitaxel-eluting stents and present their long-term outcomes. To our knowledge, this is the largest reported experience in the literature describing in-hospital and long-term outcomes for LM trifurcation treatment using paclitaxel-eluting stents.

Methods

Percutaneous coronary intervention and coronary angiography are increasingly performed via radial artery access after resurrection of this route by Campeau in 1989.¹ The reasons for this are reduced local complication rates compared to procedures using other access sites such as the femoral and brachial arteries,^2-4 as well as reduced procedural costs and early patient mobilization.⁵ However, radial access is not always successful, and there are recent reports of ulnar artery cannulation in such cases. This article reviews the literature relating to ulnar artery access for coronary angiography and percutaneous coronary intervention.

Methods

Case Report. A 57-year-old white female school teacher had undergone mitral valve replacement 8 months earlier for streptococcal endocarditis and had required subsequent repair of a paravalvular leak 2 months later. The patient recently fell and fractured her right tibia bone and presented to the clinic for preoperative cardiac evaluation and clearance prior to orthopedic surgery. The patient denied chest discomfort or shortness of breath and reported mild intermittent palpitations without syncope or near-syncope. On physical exam, her blood pressure was 78/54 mmHg and her heart rate was 92 beats/minute and regular. The patient’s jugular venous pressure appeared normal and her chest was clear. The left ventricular apex impulse was diffuse on palpation. Heart sounds were distant and a 2/6 soft systolic murmur was best heard at the left ventricular apex.