Seminars in interventional cardiology : SIIC最新文献

Many major clinical trials have been published in the last decade involving a new class of antiplatelet agent-Glycoprotein IIb/IIIa receptor blockers. The largest experience to date with these has been in percutaneous coronary intervention. Seven trials involving three different agents (abciximab, tirofiban, eptifibatide) are discussed. Abciximab is the most widely studied agent and is the only drug licensed for use in this setting. All three agents reduce the incidence of clinically relevant ischaemic events (death, non-fatal myocardial infarction or urgent revascularization). The shorter acting, competitive inhibitors tend to be maximally beneficial during the time of infusion, whereas abciximab has been shown to be effective in the acute and long-term phases. The benefits of treatment are tempered by an increase in the bleeding complications. These can be minimized by changes in heparin dosing and careful management of vascular sheaths. The treatment benefit of abciximab is maintained in those patients with unstable angina, those undergoing atherectomy, vein graft angioplasty or bail out-stenting. Results from the Epistent trial, support the use of abciximab during elective stenting. Nevertheless, rapidly changing interventional techniques and the availability of other potent antiplatelet agents underscore the need for further evaluation of IIb/IIIa inhibition in coronary revascularisation.

The efficacy of GPIIb/IIIa inhibitors has now been evaluated in over 20 000 patients with unstable angina and non-Q MI. These agents have shown great efficacy in patients undergoing percutaneous coronary intervention. They are also effective, even if to a lesser degree, as an addition to medical treatment. The safety profile is satisfactory. Several issues have to be investigated in the future: comparison of agents, use of oral inhibitors, associations with Heparin, consequences on management, and cost efficacy. As of now, it is clear that GPIIb/IIIa inhibitors represent a significant progress in the treatment of patients with acute coronary syndromes.

Achievement of infarct-related artery (IRA) patency with thrombolytic agents has improved the clinical outcome of patients with acute myocardial infarction (MI). Primary angioplasty (PTCA) for direct IRA reperfusion may further improve patient outcome by overcoming several limitations of thrombolytic therapy, e.g. by decreasing the risk of haemorrhagic stroke, increasing the achievement of brisk antegrade flow, decreasing the risk of IRA reocclusion, and allowing early identification of patients who need surgical revascularization. In the PAMI-1 randomized trial, primary PTCA was superior to thrombolytic therapy. The GUSTO-IIb angioplasty substudy supported the same conclusion but with a narrower margin of benefit from PTCA. In order to further improve the outcome of primary mechanical reperfusion, routine intra-aortic balloon pump (IABP) insertion in high-risk MI patients and primary stenting have been evaluated. In PAMI-2, there was no major clinical benefit in routine IABP insertion during primary PTCA in high-risk patients. In contrast, primary stenting appears to offer significant advantages over PTCA, especially by decreasing the need for subsequent IRA revascularization procedures as shown in the recent PAMI Stent Randomized Trial. Adjunctive pharmacotherapy with potent antiplatelet agents in acute MI is being evaluated both in combination with thrombolytic therapy, and with primary PTCA and stenting. Finally, meaningful consideration of cost-effectiveness and health policy guidelines is warranted to optimize the appropriate management of MI patients in the current era, given the increasingly complex and expensive therapeutic strategies available.

From July 1994 to October 1998, 4280 primary PTCA procedures were entered into the registry of the Arbeitsgemeinschaft Leitender Kardiologischer Krankenhausärzte. The success rate of PTCA, as defined by TIMI-3 perfusion of the infarct-related artery was 87.1%, in-hospital mortality was 10.2% and 2.6% had reinfarction. The most powerful predictors of death were cardiogenic shock present in 14.6% of whom 47% died, and failed PTCA with a mortality of 32%. Stents were used in 4.1% in 1994 increasing to 64.5% in 1998 without significant changes in success rates, but associated with a slight decrease in mortality and reinfarction rates.

Growing evidence suggests that primary angioplasty is superior to thrombolysis for the treatment of acute myocardial infarction, in particular in some high-risk subsets. The performance of primary angioplasty in centres without on-site cardiac surgery may extend the availability of this effective reperfusion therapy. This will benefit in particular those patients who would not be treated otherwise. Optimal primary angioplasty requires a high level of logistic organization, operator expertise, and commitment of the whole team. The outcome does not depend on the presence or absence of surgeons on site. In fact, feasibility, safety and efficacy of primary angioplasty are similar in both types of centres when high standards of care are guaranteed.

Timely restoration of antegrade coronary blood flow by primary angioplasty of the infarct-related vessel of a patient with an acute myocardial infarction results in myocardial salvage and improved survival. The main issues pertinent to the delivery of primary angioplasty therapy are discussed, and the 'Zwolle approach' is described with regard to the prehospital phase, the first 15 min in-hospital, pharmacological therapy, angiography and angioplasty, risk stratification, rehabilitation and secondary prevention.

Basic knowledge of the sequence of cellular events that change the relative benign disease coronary atherosclerosis into a life-threatening acute coronary syndrome is of great importance for the interventional cardiologist in order to understand and choose the correct pharmacological and interventional management in patients with acute myocardial infarction. Plaque disruption, or fissuring, with superimposed thrombosis frequently complicates the course of coronary atherosclerosis. Small ruptures often remain clinically silent, whereas more extensive plaque rupture may lead to the development of unstable angina, acute myocardial infarction, and sudden cardiac death. The risk of plaque disruption depends more on plaque composition than on plaque size and stenosis severity. Major determinants of a plaque's vulnerability to rupture are: the size and consistency of the lipid-rich atheromatous core, the thickness of the fibrous cap covering the core, and inflammation and repair within the cap. The elevation of fibrinogen and C-reactive protein in patients with unstable angina may be markers of ongoing plaque inflammation. Both plaque vulnerability and rupture triggers are important for plaque disruption. The resultant thrombotic response, which is important for the clinical presentation and outcome, is in part determined by the reactivity of the circulating platelets and the balance between the fibrinolytic and coagulation systems. New ways of identification and treatment of the dangerous vulnerable plaques responsible for infarction and death and optimization of anti-thrombotic treatment are highly warranted in order to prevent and treat life-threatening coronary thrombosis.