Associazione Nazionale Medici Cardiologi Ospedalieri

CONGRESS ABSTRACT

CONGRESS ABSTRACT

AN UNUSUAL CASE SYNCOPE DUE TO SILENT CORONARY VASOSPASM

Somaschini Alberto Savona (Savona) – Sc Cardiologia E Utic, Ospedale San Paolo | Astuti Matteo Savona (Savona) – Sc Cardiologia E Utic, Ospedale San Paolo | Cordone Stefano Savona (Savona) – Sc Cardiologia E Utic, Ospedale San Paolo | Botta Marco Savona (Savona) – Sc Cardiologia E Utic, Ospedale San Paolo | Ghione Matteo Savona (Savona) – Sc Cardiologia E Utic, Ospedale San Paolo | Buscaglia Elisa Savona (Savona) – Sc Cardiologia E Utic, Ospedale San Paolo | Cornara Stefano Savona (Savona) – Sc Cardiologia E Utic, Ospedale San Paolo | Bellone Pietro Savona (Savona) – Sc Cardiologia E Utic, Ospedale San Paolo

Background. Variant angina is a condition due to a transient vasospasm of the epicardial coronary arteries, which usually causes chest pain episodes and may be associated with dangerous arrhythmias. A non-negligible subset of patients can also experience silent myocardial ischemia, defined as objective documentation of myocardial ischemia in the absence of angina or equivalents. This condition is associated with increased cardiac mortality and incidence of acute cardiac events.

Description of the case. A 65-years-old man was admitted to our Emergency Department for syncope. He reported palpitations before the event without chest pain. ECG showed biphasic T waves in V2-V6 (Fig 1A), troponin values were normal. Immediately after admission in our coronary care unit for monitoring, he developed dynamic ST segment elevation with signs of inferior and posterior transmural ischemia (Fig 1B) and non-sustained polymorphic ventricular tachycardias (Fig 2), being symptomatic only for palpitations. ECG abnormalities and symptoms quickly resolved after intra-venous nitrates administration. Coronary angiography was performed showing a critical non-occlusive (85%) fixed stenosis at the proximal right coronary artery (Fig 3 A). The lesion was treated by angioplasty and stenting (Fig 3 B) and the patients was discharged on dual anti-platelet therapy, statins and oral high-dose calcium-channel antagonist.

Discussion. This case underlines first the importance of searching for high-risk features in patients with syncope of non-obvious origin: our patient reported palpitations and ECG changes consistent with myocardial ischemia (even with normal troponin values and echocardiographic findings). A peculiarity of our case is that the patient did not complaint any chest pain despite the presence of ST elevation, a condition known as silent ischemia. The transient nature of ECG modification and ventricular arrhythmias, their dramatic response to nitrates and coronary angiography findings were suggestive of silent vasospasm. Coronary vasospasm induces transient myocardial ischemia and may cause ventricular arrhythmias which in turn can cause syncope due to transient cerebral hypoperfusion or, when sustained, even cardiac arrest and sudden death. We did not perform provocative test with acetylcholine or ergonovine due to the likely vasospastic origin of myocardial ischemia and to their potential risks, especially in the presence of non-sustained plymorphic ventricular tachycardias.