P318 a lethal spasm

Abstract S.F.E.G., a 52–year–old woman of Filipino origin, with no previous cardiology except arterial hypertension under therapy, came to our attention for a witnessed episode of cardiac arrest at home. Rescued by the emergency medical team, who found ventricular fibrillation at presentation, and performed ACLS with ROSC obtained after 3 DC shocks. The first ECG was unremarkable (sinus rhythm, diffuse ST depression). Total body CT was negative. Admitted to the Coronary Unit, the echocardiogram was normal for cavity dimensions and kinetics, as well was coronary angiography except for “short intramyocardial course in the second segment of LAD with slight systolic "milking". In the following days, however, there was a significant rise in HsTnI (1,000 → 47,000 ng/L), with concomitant sudden ventricular bigeminy and negative anterior T waves, akinesia of the anterior apical segments of the LV at cardiac ultrasound (not present at admission), in a patient still intubated and therefore with a non–evaluable clinic. Coronary angiography was repeated, which highlighted this time significant vasospasm affecting the middle segment of the LAD, that regressed after intracoronary nitrates. She was extubated without neurological sequelae, and subjected to ICD implantation by secondary prevention. To treat the vasospastic angina she was discharged with calcium channel blockers at the maximum tolerated dosage, as per guidelines (diltiazem 120mg TID + nifedipine 60mg BID). One month later the patient returned to our attention due to worsening dyspnoea, abdominal pain and anasarca (ascites, bilateral pleural effusion, peripheral oedemas). Hospitalized in a medical setting and treated with diuretics for suspected heart failure, despite the echocardiogram showing preserved biventricular systolic function, normal diastolic function, no valve disease, no pericardial effusion. BNP was 359 pg/mL, subsequently decreasing to 148 pg/mL. After excluding every other possible causes even with total body CT, our hypothesis was that of calcium channel blocker collateral effect (vasodilatory edema). We tapered the dosage until only diltiazem 60mg TID was mainteined, obtaining a significant clinical improvement (weight loss by 10 kg), without further recurrence of coronary vasospasm. This clinical case demonstrates the potential lethality of coronary vasospasm, and a rare complication during therapy with high doses of calcium channel blockers, with very few cases described in the literature.