A Handbook of Primary PCI: No-Reflow Management

Abstract

Although substantial progress has been made in recent decades in reducing mortality and performing optimal revascularization in patients with acute coronary syndrome (ACS) and stable coronary artery disease (CAD), one of the remaining challenges is to better prevent and treat extended myocardial damage despite "apparent" angiographic optimal percutaneous coronary intervention (PCI). The presence of no-reflow is related to higher risk of major adverse cardiac events (MACE) due to the poor healing of the infarct, adverse left ventricular remodelling, congestive heart failure occurrence and death. Despite optimal epicardial coronary artery reperfusion performed by PCI, distal microembolization into the coronary microcirculation limits myocardial salvage especially during ACS. No-reflow represents the ultimate stage of extended myocardial damage after PCI with absence of contrast medium progression in the coronary artery. This complication occurs mainly during ACS or during PCI of rotational atherectomy and venous graft in stable patients. The objective of this chapter is to describe how to manage a noreflow phenomenon from the pathophysiology to the management in order to help physician to prevent this complication and if no-reflow occurs adapt therapeutics to limit myocardial damage and reduce poor outcomes. DefinitionThe no-reflow phenomenon is defined as inadequate myocardial perfusion through a given segment of the coronary circulation without angiographic evidence of mechanical obstruction [1].

Double trouble in a day!

“…The incidence of acute no reflow phenomenon is approximately 1-3% in overall PCI cases [4]. It is more common in certain conditions such as tobacco use, late presentation of acute coronary syndrome, longer door-to-balloon time, high thrombus burden, venous bypass graft PCI, use of rotational atherectomy, low left ventricular ejection fraction, high Killip classification and also uncontrolled diabetes and hypertension [4,5]. In our cases, both patients were smokers, and had the risks factors of diabetes and hypertension.…”

“…Intensive statin reduces the incidence by 4.2% [6]. Double antiplatelet is also beneficial in reducing complications such as acute stent thrombosis, periprocedural myocardial infarction and acute no-reflow [4]. Intraoperatively, patient should be adequately anticoagulated with unfractionated heparin and monitored with activated clotting time [4].…”

In-Hospital Peak Glycemia in Predicting No-Reflow Phenomenon in Diabetic Patients with STEMI Treated with Primary Percutaneous Coronary Intervention

“…The no-reflow phenomenon is mainly caused by the distal embolization and reperfusion injury, and the patients might complain of chest pain with elevated ST-segment in the electrocardiogram [ 11 , 23 ]. The perfusion of the coronary blood is the most important clinical indicator for the assessment of successful PCI in patients with STEMI.…”

“…However, no-reflow, the major adverse complication of PCI, causes increased mortality due to poor healing of the infarct, adverse left ventricular remodeling and congestive heart failure [ 4 – 6 ]. Tissue perfusion should occur for patients after PCI; however, about 1-3% of the patients encounter a no-reflow in the first 2 hours after PCI [ 6 – 11 ]. Although the occurrence of no-reflow is rare among patients with PCI, the serious complication of reperfusion in patients with STEMI leads to poor prognosis and increased mortality [ 12 – 14 ].…”

The ATRIA and Modified-ATRIA Scores in Evaluating the Risk of No-Reflow in Patients With STEMI Undergoing Primary Percutaneous Coronary Intervention

“…3 Although there are options involving intracoronary nitroglycerine or adenosine administration, there is no definite consensus regarding treatment. 4,5 Studies have shown that age, the presence of diabetes and hypertension (HT), target vessel diameter, length of the lesion, thrombus load, and several laboratory parameters may affect the development of NR. 6–15 Cheng et al 16 demonstrated higher levels of d -dimer and cystatin C in patients with NR in their study consisting of 218 acute anterior myocardial infarction (MI).…”