Myocardial Crypts and Ventricular Fibrillation: Two Case Reports

Abstract

Background Left ventricular myocardial crypts are defined as invaginations traversing >50% of the myocardial wall, with an incidence of 9.1% in the general population. Several studies have suggested that these morphological findings could be a marker of myocardial disease. The authors present two cases of cardiac arrest (CA) due to ventricular fibrillation (VF) and incidental findings on cardiac magnetic resonance (CMR) of myocardial crypts, discuss the diagnosis, the possible correlation with hypertrophic cardiomyopathy, and hypothesise the significance of this entity. Case Presentation Case 1 discusses a 58-year-old male affected by arterial hypertension, with a family history of hypertrophic cardiomyopathy (HCM), who presented to the emergency department for a CA due to VF. The 12-lead electrocardiogram was negative for ST-elevation myocardial infarction, Bragada’s pattern, or QT time elongation. Blood gas analysis showed no ionic abnormalities and no hypoxia. Coronary arteries were free from stenosing atheromatous lesions at coronary angiography. CMR showed isolated left ventricular crypt with mild hypertrophy of myocardial wall, preserved ejection fraction, no hyperintensity in the short tau inversion recovery sequences compatible with oedema, and no sign of fibro-adipose tissue substitution at postcontrast sequences. An implantable defibrillator for secondary prevention was implanted and genetic testing was carried out for HCM. Case 2 discusses a 59-year-old Peruvian male, with a family history of cardiovascular diseases, who suffered from CA due to VF while under elective ear surgical intervention. A defibrillation with a single DC shock was sufficient to restore sinus rhythm. The 12 lead electrocardiogram was negative for ST-elevation myocardial infarction, Bragada’s pattern, or QT time elongation. Transthoracic echocardiography showed mild ventricular hypertrophy and normal global and regional biventricular kinetics (60%), along with mild mitral regurgitation. Coronary arteries were free from stenosing atheromatous lesions at coronary angiography. At CMR, an isolated left ventricular crypt in the inferior basal wall with an extension of 7 mm LL was detected; there wasn’t hyperintensity in the short tau inversion recovery sequences compatible with oedema and no sign of fibro-adipose tissue substitution at postcontrast sequences was seen. The authors performed genetics testing for HCM, still ongoing. An implantable defibrillator for secondary prevention was implanted. Discussion These cases suggest that the presence of crypt could be a marker of myocardial disease. This should warrant clinical follow-up prior to the potential development of left ventricular hypertrophy and the occurrence of serious cardiovascular events, such as heart failure or death. With the evolution of new imaging techniques such as CMR and CT, the detection of these myocardial defects is more accurate. Genetic testing is useful to identify carriers of pathological mutation of HCM that need close follow-up.