Associazione Nazionale Medici Cardiologi Ospedalieri



“Finding of myocardial crypts in sudden cardiac arrest patients: two case report”

Caraffini Andrea Parma (Parma) – Azienda Ospedalier Universitaria Parma | Bricoli Serena Piacenza (Piacenza) – Ospedale G. Da Saliceto Piacenza | Canu Eleonora Parma (Parma) – Azienda Ospedaliero Universitaria Parma | De Santis Nicola Parma (Parma) – Azienda Ospedaliero Universitaria Parma | Pelizzoni Valentina Piacenza (Piacenza) – Ospedale G Da Saliceto | Binno Simone Piacenza (Piacenza) – Ospedale G Da Saliceto | Vermi Annachiara Piacenza (Piacenza) – Ospedale G Da Saliceto | Di Spigno Francesco Piacenza (Piacenza) – Ospedale G Da Saliceto | Perrino Felice Piacenza (Piacenza) – Ospedale G Da Saliceto | Ferraro Stefano Piacenza (Piacenza) – Ospedale G Da Saliceto | Aschieri Daniela Piacenza (Piacenza) – Ospedale G Da Saliceto

Left ventricular myocardial crypts are definined as deep blood-filled invaginations trasversing > 50% of the myocardial wall and are located predominantly at the mid-basal segment of inferoseptal wall or at the apical segment. To date the incidence of crypts is 9.1% of patients undergoing cardiac CT and are not associated with intermediate-term major adverse cardiovascular events. However several studies have suggested that the presence of crypts is a marker of myocardial disease that should warrant clinical follow-up prior to the potential development of left ventricular hypertrophy and occurrence of serious cardiovascular events, such as heart failure or death. A lot of publications demonstrate that ventricular crypts could be a pre-phenotypic marker of hypertrophic cardiomyopathy (HCM). HCM is a genetic ereditary cardiomyopathy which is associated with fatal ventricular arrhytmias.


We present the case of two patients who had a sudden cardiac arrest resuscitated with cardiac defibrillation. These are two males, 59 and 53 years old respectively, without cardiovascular risk factor and with familiarity for HCM. The first patient had a sudden cardiac arrest during exercise and was resuscitated with early cardiac defibrillation. The second patient had ventricular fibrillation after otolaryngology surgery treated with single defibrillator shock. Coronary arteries were free from atherosclerotic lesions at the angiografy study and no other reversible causes of cardiac arrest were identified. CMR showed normal biventricular funtion and ruled out signs of myocardial oedema or fibrosis. The only morphological finding was the detection of single left ventricular myocardial crypt at the CMR study in both patients: in one patient the crypt was located at the inferior wall while in the other at the level of the septum in the mid-apical segment. Ultimately both patients underwent genetic testing for cardiomyopathy.


These findings may be a pre-phenotypic markers of HCM in patients who don’t present a clear expression of the pathology but may be a correlation with sudden cardiac arrest. The rarity of their finding in patient who have had sudden cardiac arrest can be explained by the small survival rate in patients with sudden cardiac arrest. Future studies and the increasingly simple access to advanced imaging methods like CMR and CT will allow us to clarify the role of these myocardial anomalies in the risk of developing fatal arrhythmic events.