Coronary No Reflow Phenomenon: A Case Study

Background: The phenomenon of coronary no reflow is defined as inadequate myocardial perfusion through without angiographic evidence of epicardial obstruction. After percutaneous coronary intervention (PCI), coronary filling is assessed using the Thrombolysis in Myocardial Infarction (TIMI) grading system. Coronary no reflow is defined when TIMI flow grades are 0. The mechanism is likely multifactorial and consists of causes including distal embolization of thrombus fragments during PCI, microvascular dysfunction, coronary dissection, and vasospasm. Therapy is dependent upon the underlying etiology. In this case report we discuss a patient scenario in which coronary no reflow occurred after elective PCI and was managed in the catheterization laboratory.

Case Presentation: A 50-year-old gentleman with a past medical history of insulin dependent diabetes and essential hypertension who presented for typical chest pain. Prior to presentation, the patient had recently had an echocardiogram that revealed an ejection fraction of 50-55%.

Upon presentation to our facility, the patient had lab work that was significant for a troponin level within normal limits and an electrocardiogram that did not reveal any evidence of acute ischemia. Ultimately a decision was made to pursue additional ischemic evaluation with coronary angiogram.

The patient underwent coronary angiogram which revealed 80% disease of the mid right coronary artery in which PCI was performed. The patient subsequently had ST segment elevations in the inferior leads and concurrent chest pain. Upon repeat coronary angiogram poor blood flow distal to the lesion was appreciated and acute dissection was suspected. Subsequently, a drug eluting stent was deployed to the mid and distal right coronary artery which did not improve blood flow to the artery. A second drug-eluting stent was deployed proximal to the stent in an overlapping fashion. Subsequent angiography revealed continued no reflow.

Intravascular Ultrasound (IVUS) was utilized which did not reveal any evidence of coronary artery dissection and good stent apposition was appreciated. Multiple doses of vasodilator medications, including nitroprusside and nicardipine, were administered with ultimate improvement of blood flow to the coronary artery with TIMI III flow.

Discussion: Coronary no reflow phenomenon is recognized in less than 2% of elective PCI cases. Risk factors of no reflow include age, smoking, diabetes mellitus, and depressed left ventricular ejection fraction. Our patient did display risk factors including smoking and diabetes, placing him at increased risk. IVUS has become an invaluable tool in helping to define underlying etiology of no reflow and ruling out coronary dissection. During our patient case, after no reflow was appreciated IVUS was incorporated to help discern the etiology. Pharmacotherapy for the treatment of no reflow is targeted towards local vasodilator or antiplatelet therapy. Our patient responded well to vasodilator therapy with eventual improved coronary flow. Although more research is needed for appropriate prevention of no reflow, early studies indicate that factors such as reducing time to intervention and administration of pre-procedural medications such as aspirin, beta-blocker, and heparin may improve microvascular integrity and reduce risk of subsequent no reflow.