No Reflow – Case 2
- 65-year-old male who presented with chest pain (CCS Class II). Underwent cardiac catheterization showing 3-Vessel CAD. Patient was referred for surgical evaluation but refused surgical revascularization, and was referred for Impella assisted PCI of the RCA.
Past Medical History
- HTN, HLD, DM, Former Tobacco Use, CAD s/p PCI
- LVEF 35%
- Prior Cardiac Catheterization: Mid RCA 70-80% stenosis, distal RCA 80-90% stenosis, AV Continuation subtotal occlusion, D1 80-90% stenosis, OM1 CTO and fills via collaterals from the LAD, LPL CTO and fills via collaterals from the LAD, RI CTO.
- Home Medications: Aspirin, Clopidogrel, Simvastatin, Carvedilol, Valsartan, furosemide, dorzolamide-timolol (eye drops)
- Adjunct Pharmacotherapy: Clopidogrel, Bivalirudin
- no significant disease in the left anterior descending (LAD) and left circumflex (LCx) coronary arteries
- totally occluded first obtuse marginal (OM1) and left posterolateral (LPL1) branches.
- Underwent Impella supported intervention of the RCA.
- Procedure was complicated no-reflow after serial balloon inflations.
- Intracoronray vasodilators administered through the guide catheter without improvement in flow.
- Concern for dissection and a two stents were placed in the RCA without improvement in flow.
- At the conclusion of the procedure, the patient was having ongoing chest pain. Therefore, decision was made to remove the Impella support device, and insert an IABP.
- Patient was given IV integrillin bolus and admitted to the CCU.
- Troponin-I peaked at 15.85 ng/mL and CK-MB peaked at 68.5 ng/mL.
- Patient was discharged home 3 days later without further sequelae.
- What is the likely explanation or reason why the complication occurred?
- No-reflow following PTCA – likely due to distal embolization of debris.
- How could the complication have been prevented?
- Vasodilators should always be given prophylactically and for treatment of slow flow/no-reflow.
- Assure patient is given adequate periprocedure antithrombotic therapy (antiplatelets and anticoagulants).
- Pay close attention to the ACT during the procedure and dose anticoagulation accordingly to maintain ACT >300 prior to performing an intervention (Hemochron machine).
- We recommend using a intra-coronary imaging (OCT/IVUS) when performing an intervention involving an ectatic vessel.
- Intra-coronary imaging would have been helpful in delineating the composition of the plaque. If there was high burden of necrosis within the core of the plaque, this would have suggested the lesion is more prone to embolization if intervened on.
- Intra-coronary imaging helps determine the optimal stent length and diameter. This is important because in severely diffused ectatic vessels, the diameter and lesion length can be overestimated or underestimated.
- High pressure inflation should be avoided to prevent a “cheese-grater” effect in lesions which are prone to result in distal embolization.
- Is there an alternate strategy that could have been used to manage the complication?
- The initial step in management of slow flow/no-reflow involves administration of intra-coronary vasodilators through the guide catheter. If this fails, recommended using a dual-lumen microcatheter (Twinpass is the only dual lumen microcatheter available in the USA) to deliver intra-coronary medications to the distal vessel and microvasculature. Next, perform angiography with delivery of contrast through the microcatheter to determine if there is distal coronary flow. If distal vessel flow is not preserved the likely etiology of abrupt vessel closure (AVC) is no-reflow due to distal embolization of debris or thrombus, and IC vasodilators should be administered through the microcatheter targeted to the distal vessel and microvasculature. If flow is preserved, then the likely etiology of AVC is dissection (proximal to the point of microcatheter injection), and treatment involves placement of a stent. It is reasonable to perform aspiration thrombectomy prior to microcatheter based angiography injection (depending on the clinical context/presence of thrombus).
- Intravascular imaging of the coronaries with IVUS would have helped with determining the etiology of AVC, and guide further management.
- What are the important learning points?
- The best treatment for slow flow/no-reflow is to prevent it from happening.
- The exact mechanism of the no-reflow phenomenon is unclear, but it is thought to be associated with endothelial swelling, neutrophil infiltration, and platelet aggregation causing obstruction and spasm in the microvasculature.
- When AVC occurs after PTCA or stent placement you have to consider a broad differential which includes the possibility of a coronary spasm, thrombus or debris with distal embolization, and dissection.
- Important to have multiple vasodilators readily available during a procedure. We use the following agents and administer them intra-coronary:
- Nitroprusside 50-200 mcg, Adenosine 30-40 mcg, Verapamil 100-200 mcg, Nicardipine 100-200 mcg
- Nitroglycerin 100-200 mcg (we use NTG for slow flow/no-reflow when it involved the epicardial vessels and not the coronary microvasculature)
- If the patient is hypotensive and this impedes the administration of intra-coronary vasodilators to treat slow flow/no-reflow, we recommend administration of IV phenylephrine 100-200 mcg as needed (may result in reflex bradycardia) to increase blood pressure, and then administer intra-coronary vasodilators.
- If there is refractory slow flow/no reflow then consider placement of an IABP. This helps with reduction in afterload, and improves coronary perfusion pressure by increasing coronary blood flow during diastole, and reduction in LVEDP.
- Depending on the size and function of the LV (LVEF <30%), consider using upfront LV support as it can help improve coronary perfusion pressure.
- Distal flow should always be established before placing a stent, unless dissection is considered as an etiology. In this case, AVC was thought to be due to dissection and a stent was immediately placed. However, absence of distal flow after stenting in this case argues against dissection as the etiology of AVC.