Diffuse Coronary Artery Spasm Induced by Guidewire Insertion

Coronary spasm induced solely by guidewire insertion is very rare. We report a rare case of diffuse coronary spasm secondary to coronary angioplasty guidewire insertion. Although such a significant level of spasm is very rare, lesser degrees of spasm that are not easily recognized might be more common. Therefore, routine use of nitrates after guidewire insertion may be a good option to optimize vessel diameter for the selection of stent size. Case Report. A 67-year-old man presented to the outpatient clinic with recent onset of angina. He had known coronary artery disease and had undergone angioplasty with stent implantation to both the left anterior descending and circumflex arteries 3 years prior. He was also a smoker and dyslipidemic on treatment. His medications included aspirin, clopidogrel, propranolol and simvastatin. His electrocardiogram (ECG) on presentation was normal. He was referred for coronary angiography, which revealed a 70%, long stenotic segment in the proximal right coronary artery (RCA) (Figure 1A) with patent stents in the left coronary artery. Angioplasty to the RCA lesion was started using a 7 French (Fr) JR 4.0 guiding catheter. Following the introduction of a 0.014´´ ACS High Torque Floppy II guidewire (Guidant Corporation, Temecula, California), the RCA developed diffuse spasm with reduction in its lumen diameter from 4.0 mm to 2.5 mm in its proximal segment, from 4.2 mm to 3.0 mm in its middle segment, and from 3.0 mm to 2.0 mm in its distal segment (Figure 1B). The patient was asymptomatic and had no ischemic ECG changes. Following the administration of 200 µg intracoronary nitroglycerine, the spasm resolved and the vessel size returned to baseline (Figure 1C). The lesion was dilated with a 2.5 mm balloon and a 3.5 x 18 mm Multi-Link stent was subsequently deployed at 14 atmospheres with an excellent final angiographic result (Figure 1D). Discussion. Coronary artery spasm is reported to occur in 1–5% of percutaneous coronary interventions.1–3 However, spasm induced solely by guidewire insertion is very rare. Takahashi et al. reported a case of focal spasm in the RCA distal to the dilated lesion that was resistant to intracoronary nitrates and intravenous calcium-channel blocker as well as balloon dilatation, but that subsided completely upon withdrawal of the guidewire.4 In a recent study of 906 patients undergoing intracoronary Doppler flow measurement using 0.014´´ or 0.018´´ Doppler FloWire, 1% of the patients were reported to develop coronary spasm during the passage of the wire.5 Our patient demonstrated diffuse spasm of the RCA following the introduction of the guidewire with significant reduction in the luminal diameter. Although this spasm did not result in any ischemic or hemodynamic changes, prompt recognition and treatment with nitrates were crucial to estimate the real vessel size and therefore to determine the choice of the optimal stent diameter. Although it is common practice to give nitrates at the beginning of percutaneous coronary interventions, they are rarely given after guidewire insertion. Our case showed dramatic diffuse spasm, which was easy to recognize. However, more subtle and frequent spasms might occur secondary to guidewire insertion without recognition. It therefore might be a good option to routinely give nitrates after inserting the guidewire to treat minor spasms that might not be easily recognized and therefore optimize the vessel size for stent selection and deployment. Conclusion. This report demonstrates a rare case of diffuse coronary spasm secondary to coronary angioplasty guidewire insertion. Although such a significant level of spasm is very rare, lesser degrees of spasm that are not easily recognized might be more common; therefore, routine use of nitrates after guidewire insertion may be a good option to optimize vessel diameter for the selection of stent size.

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