Embolization of thrombi and plaque components liberated by balloon inflation has been speculated1 to cause angiographic no-reflow during percutaneous coronary intervention (PCI) in patients with acute myocardial infarction (AMI). Embolic particles in the cerebral artery can be detected as high-intensity transient signals (HITS) by transcranial Doppler ultrasonography.2,3 Recently it has been reported that coronary emboli can also be detected as HITS with the Doppler guidewire during a PCI procedure,4,5 and an increase in the total number of HITS is associated with minor myocardial injury without coronary flow reduction during the PCI procedure for stable plaque.6 Here, we report a case of AMI in which a cluster of HITS was associated with angiographic no-reflow.
Case Report. A 56-year-old male presented at our hospital with a 1-hour history of sudden chest pain. Electrocardiography on admission showed ST-elevation in leads II, III and aVF.
After administration of 300 mg of aspirin and 100 IU/kg of heparin, the patient underwent emergent catheterization. The mid-portion of the right coronary artery showed complete occlusion (Figure 1A). After thrombectomy, the patient showed residual stenosis of 83% and Thrombolysis in Myocardial Infarction (TIMI) grade 3 flow was achieved (Figure 1B). The onset to recanalization time was only 1.5 hours. We placed the tip of the FloMap Doppler guidewire (Volcano Therapeutics, Inc., Rancho Cordova, California) 3 cm distal to the culprit lesion, and the average peak velocity was 6 cm/second (Figure 2A).
Intravascular ultrasound (IVUS) showed plaque with a large hypoechoic pool (Figure 1C). A 4.0 x 25 mm Duraflex™ stent (Goodman, Nagoya, Japan) was then implanted. Immediately after stent-balloon deflation (Figure 1D), the coronary blood flow velocity waveform showed a series of high-echoic signals during almost 1 beat (Figure 2B), which implied a cluster of HITS. Four beats later, the coronary blood flow disappeared almost completely except for transient antegrade flow associated with left ventricular contraction (Figure 2C), and coronary angiography demonstrated angiographic no-reflow (TIMI grade 0 flow) (Figure 1E). However, IVUS showed full expansion of the stent at the culprit lesion (Figure 1F). After reduction of coronary flow, complete A-V block also occurred and temporal pacing was needed. Twenty minutes after several intracoronary injections of nicorandil and nitroprusside, radio-contrast runoff was improved (TIMI grade 2 flow), and the ECG showed recovery of sinus rhythm. Myocardial perfusion assessed by myocardial contrast echocardiography7,8 was considered to show good reflow. Peak creatine kinase was 2,635 IU/l. The recovery of left ventricular function was good, i.e., wall motion score assessed by echocardiography6 was 11 on admission, and 9 one month later.
Discussion. This is the first report of visualization of a cluster of HITS indicating a large number of embolic particles causing angiographic no-reflow. Recently, distal protection devices have been used for prevention of distal embolization. As distal protection devices can aspirate liberated plaque and thrombotic debris in patients with AMI,1,9,10 embolization of the plaque components and thrombi during PCI has been speculated to cause angiographic no-reflow. In the present case, we detected a series of high-echoic signals immediately after stent-balloon deflation using the Doppler guidewire and then coronary flow reduction occurred, which demonstrated directly that embolic particles during PCI cause angiographic no-reflow.
There are several mechanisms responsible for angiographic no-reflow in patients with AMI.11 In the present case, angiographic no-reflow was caused mainly by embolization, as microvascular damage caused by occlusion of the culprit lesion was minimal because of the early recanalization time, and TIMI grade 3 flow was achieved after recanalization by thrombectomy. The prognosis of angiographic no-reflow caused mainly by embolization is not clear due to a lack of methods to both detect and quantify embolizing particles themselves in vivo except for the Doppler guidewire. Therefore, it is noteworthy that the present case showed goodmyocardial perfusion after injection of nicorandil and nitroprusside, and good recovery of left ventricular function except for temporary deterioration, such as coronary flow reduction and complete A-V block in the acute phase. Coronary flow reduction caused by embolization may be improved to some extent by compensatory vasodilation in the nonembolized zone.12,13 IVUS in the present case showed plaque with a large hypoechoic pool, which was thought to be one of the causes of angiographic no-reflow. The Doppler guidewire can easily detect embolic particles as HITS and allowed us to determine their number. To clarify the prognosis of angiographic no-reflow caused by embolization and the lesion characteristics responsible for production of large numbers of embolic particles during PCI, further Doppler guidewire studies should be performed in a large number of patients with AMI during PCI.
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