Non-ST-elevation myocardial infarction following foam ultrasound-guided sclerotherapy

Report

A fit 61-year-old non-smoking female underwent FUGS for treatment of bilateral venous incompetence causing aching and swelling. She had liquid ultrasound-guided sclerotherapy 11 years earlier with no complication and good results. Her medical history included mild hypertension which settled without treatment and hypercholesterolaemia. She had no personal history of heart disease, thrombophilia or migraine. She had known osteoporosis and had two basal cell carcinoma excised. Her father had a cerebellar bleed and possible myocardial infarction, dying aged 61. Medications taken were etridonate and calciferol. Our procedure is to perform several sessions of UGS on consecutive or alternate days until all vessels requiring treatment are closed. Maximum daily volume of foam is 20 mL. A total of 10 mL sodium tetradecyl sulphate (STS) foam (1:4 solution:air, Tessari method using 3-way tap) was directly injected using a 25-gauge needle without local anaesthetic. STS (5 mL, 3%) was injected into the proximal left great saphenous vein (GSV), 2.5 mL of STS 3% into the left small saphenous vein (SSV) and 2.5 mL 1.5% STS (diluted with normal saline) into the proximal right GSV. The procedure was uncomfortable but not painful. The patient assisted in pulling on her compression hose following FUGS. Almost immediately she described feeling disorientated and a sensation of bilateral arm weakness. These symptoms lasted less than five minutes and clinical observations were all normal.

The patient was treated the following day with 6 mL 3% STS foam FUGS, comprising 2.5 mL 3% into the right distal GSV, 1.0 mL into the distal left GSV, 2.5 mL 3% into the right SSV and two days later 2.5 mL 1.5% sclerosant foam into right GSV tributaries. The patient was advised to avoid any straining, in particular her compression hosiery was fitted by the medical assistant.

At her follow-up appointment at five months it was evident that she had a number of unsuccessfully sclerosed vessels. She was treated with a total of 7.5 mL 1.5% polidocanol sclerosant foam, comprising 5 mL to small right distal tributaries and right anterior accessory saphenous vein and 2.5 mL into a small left thigh tributary with no complication. On day two she had 10 mL of sclerosant foam, comprising 2.5 mL 3% STS into the proximal left GSV and left anterior circumflex thigh vein, 5 mL of 1.5% STS into left thigh tributaries and 2.5 mL of 1.5% STS into right medial knee tributaries. Following this treatment she felt ‘light headed’ as she walked through to the changing room and had mild central chest pressure which was also felt in her throat. There was no radiation of discomfort into her arms. She had no cough or shortness of breath. Oxygen was administered immediately. Her blood pressure was 188/95, pulse rate 64 per minute and she had an audible 1/6 soft systolic murmur. She did not look unwell, and was not particularly anxious; however, she remained hypertensive.

Glyceryl trinitrate (GTN) spray was administered on two occasions and she was given aspirin 300 mg. The chest pressure sensation settled after the second GTN spray (15 minutes); however, the throat tightness persisted. On admission to hospital (transferred out of our care) she had minimal chest pain and was otherwise well. Physical examination was unremarkable, blood pressure 140/70, pulse 66, dual heart sounds, soft systolic murmur and chest was clear on auscultation. Relevant positive investigations include Troponin T 155 > 222 ng/L (43% increase); normal <14 ng/L. ECG: T-wave inversion in V2 only, hospital report supplied on discharge summary.

Coronary angiogram showed completely normal coronary arteries. Echocardiogram showed normal left ventricle and right ventricle function; however, an agitated saline study was strongly positive with Mueller movement suggestive of atrial septal defect (ASD) or patent foramen ovale (PFO). Transoesophageal echocardiogram confirmed moderate-sized PFO with left to right shunting and no ASD. The aortic root was mildly dilated with mild central aortic regurgitation. Aortic MRI showed mild eccentric left coronary sinus dilatation.

A diagnosis of small myocardial infarction secondary to paradoxical embolus from known PFO was made.

The patient underwent subsequent uncomplicated closure of PFO nine months later and a follow-up bubble echocardiogram confirmed closure maintained and successful.

Discussion

To our knowledge, this is the first published description of non-ST-elevation myocardial infarction (NSTEMI) post-FUGS. We acknowledge that the NSTEMI could be unrelated to sclerotherapy treatment but in view of the sequence of events and finding of a PFO we believe this occurrence to be caused by FUGS.

Chest pressure has been described alone and associated with visual disturbance following foam sclerotherapy. One series with foam sclerotherapy in 1025 patients had an incidence of chest pressure reported by 12 patients (1.17%) Patients described two different forms, a simple chest pressure or a painful chest tightness, most often disappearing within five minutes. ¹

It would seem reasonable that the mechanism for myocardial injury following UGS is the same as for cerebral events. The possible underlying pathogenic mechanisms are

Paradoxical gas embolism (PGE);

The immediate onset of symptoms after foam sclerotherapy is most likely indicative of PGE or vasospasm. Coronary artery air embolism can present with chest tightness and pain, coronary artery spasm, ischaemia, arrythmias and myocardial infarction. ²

Current suggested preventative measures used to reduce the risk of air embolism include

The use of CO₂ gas in making the sclerosant foam;

A normal angiogram does not exclude gas embolism since the air can be reabsorbed quickly. Current thinking is that the detergent sclerosant is rapidly inactivated by blood cell membranes, ³ albumin and other plasma proteins, ⁴ which makes direct local damage to the myocardium unlikely. Previous studies have shown no abnormality in troponin levels following foam sclerotherapy in asymptomatic patients. ⁵

In vitro studies have shown detergent sclerosants to be biologically active and interfere with the coagulation, antithrombotic and fibrinolytic mechanisms.^4,6,7 Release of cell-derived by-products of sclerosants such s platelet-derived microparticles, inhibitors of fibrinolysis and endothelin possibly play a significant role in the pathogenesis of complications of sclerotherapy. ⁸

Recent studies in rats showed a significant increase in endothelin-1 (ET-1) levels one and five minutes after foam sclerotherapy with STS. Systemic circulation levels of ET-1, measured in a draining vein, have shown a marked increase following polidocanol foam sclerotherapy in 11 humans. ⁸ This evidence of ET-1 release leading to vasospasm could possibly explain the neurological and visual disturbances reported after sclerotherapy. It has also been postulated that the bronchoconstrictor activity of ET-1 could play a role in post-sclerotherapy cough. ⁹

In this case the hypothesis of post-sclerotherapy release of ET-1 (in a patient with a known PFO) leading to sustained coronary artery spasm causing sufficient myocardial damage to be reflected in elevated troponin levels is suggested.

Conclusion

The chest tightness sometimes described by patients following foam sclerotherapy should be taken seriously and considered as possibly cardiac in origin. A patient with persistent symptoms should be hospitalised for monitoring, troponin levels should be measured and ECG taken.