The role of distal myocardial protection devices during percutaneous coronary interventions.
ABSTRACT The success of intervention and clinical outcome is markedly reduced in patients who sustain distal embolization during percutaneous coronary intervention (PCI). Such embolization occurs in up to 15% of patients with acute myocardial infarction (AMI) undergoing PCI, and angiographic indicators of embolization are highly predictive of clinical and functional outcome. Saphenous vein graft (SVG) interventions carry a 20% risk of major adverse cardiac events (MACE), predominantly AMI, and significant risk of no-reflow. There are four types of embolic protection: distal occlusion/aspiration systems, filters, proximal occlusion/aspiration devices, and thrombectomy catheters. There seem to be no data to suggest that routine use of any embolic protection system is beneficial in patients with ST-elevation myocardial infarction (STEMI) undergoing PCI. The message from both the EMERALD and PROMISE trials is that embolic protection does not improve perfusion in the setting of AMI. Although pretreatment with thrombus aspiration before PCI improves angiographic reperfusion rates compared with standard PCI, enzymatic release and early clinical outcomes are not improved. Although the clinical implications of routine thrombus aspiration have yet to be established, selective use may be justified in patients with the highest thrombus burden. In addition, it should be considered in those with acute stent thrombosis and elective use of filter-based protection considered in very high risk vessel PCI (eg, last remaining conduit). There is no easy way to anticipate which SVG intervention will result in embolization. In SVG intervention, both balloon occlusion/aspiration and filter-based distal protection devices have significantly reduced the incidence of 30-day MACE, driven by AMI and should, I believe, be used routinely. Risk of complications is low with all the established devices. The profile and deliverability are continuing to improve with newer devices. Cost-effectiveness of selective use in high-risk graft cases has only recently been demonstrated.
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ABSTRACT: Riassunto La rapida riapertura, farmacologica o meccanica, dell'arteria epicardica rappresenta il gold standard nel trattamento del-l'infarto miocardico acuto. Nonostante la ricanalizzazione del vaso, alterazioni del microcircolo possono ridurre significa-tivamente il flusso miocardico in una proporzione variabile di pazienti. Tale fenomeno è conosciuto come no-reflow mio-cardico. Esso si associa ad una ridotta frazione di eiezione del ventricolo sinistro, ad un rimodellamento ventricolare nega-tivo e ad una prognosi non buona. Il fenomeno del no-reflow presenta un'eziopatogenesi multifattoriale, comprendendo l'embolizzazione distale di materiale aterotrombotico, il danno da ischemia-riperfusione e la suscettibilità individuale al danno del microcircolo. Diversi indici angiografici e tecniche di immagine non invasive consentono una rapida e sensibi-le identificazione del fenomeno. Infine, vari sistemi meccanici ed approcci farmacologici sono stati proposti nel tentativo di prevenire e trattare il no-reflow. Questa rassegna discute i meccanismi patogenetici del fenomeno, esamina le tecni-che per la sua corretta diagnosi ed analizza le principali opzioni terapeutiche. Summary The rapid restoration of coronary flow has become the gold standard therapy for patients with acute myocardial infarc-tion. Despite an open infarct-related artery, alterations in the microvasculature can significantly reduce antegrade myo-cardial blood flow in a variable proportion of patients. This phenomenon is known as myocardial no-reflow. Of note, no-reflow is associated with reduced left ventricular ejection fraction, adverse left ventricular remodelling and poor clinical outcomes. The phenomenon has a multifactorial pathogenesis, including: distal embolization, ischemia-reperfusion injury, and individual predisposition of coronary microcirculation to injury. In addition, no-reflow can be evaluated by several methods, including angiographic indexes and non invasive imaging modalities. Various mechanical devices and pharma-cological approaches have been proposed to prevent and treat the phenomenon. This review will discuss the postulated mechanisms of the phenomenon, examine the modalities for the correct diagnosis, and address the main treatment options.