86 years-old man was admitted to our ICCU for chest pain with an ECG diagnosis of atrial fibrillation and inferior STEMI. He had a history of hypertension and ascending aorta aneurysm (48 mm) with no other known cardiovascular risk factor. He reported few episodes of short-duration chest pain in the last days. A fast echocardiogram excluded ascending aorta dissection and pericardial effusion but showed hypokinesia of inferolateral left ventricle wall. Urgent angiography only revealed a moderate stenosis on mid left anterior descending artery associated with slow run-off. No lesions were found on the expected culprit artery. Due to persisting chest pain and patient's history of ascending aorta aneurysm, an urgent Angio CT was performed, but unexpectedly, during the exam, the patient lost consciousness with asistolia. RCP was practised with ROSC. CT scan showed mild pericardial effusion with blushing. A free wall heart rupture was suspected by radiologist. Urgent echocardiogram revealed moderate pericardial effusion with a suggestive colour doppler systolic flow originating from an apparent hole in apical inferolateral left ventricle wall. Rapid hemodynamic failure occurred so pericardiocentesis with amine support and blood transfusions were performed. Heart team excluded urgent surgery due to extremely high operative risk related to patient's age, hemodynamic impairment and poor expected repair durability consequent to acute phase of rupture. ICCU observation was made, with liable hemodynamic stability obtained with norepinephrine infusion. In accordance with patient's family other invasive measurements were not taken. Unfortunately, the patient died the day after. Only few cases of myocardial rupture in myocardial infarction-non obstructive coronary artery disease (MINOCA) are reported in literature. Recurrent chest pain makes plaque complication/embolus resolution a reliable hypothesis. New onset atrial fibrillation might have caused an embolization in coronary artery determining transmural ischaemia, as well as coronary artery plaque rupture/ulceration might have done. Unfortunately, no further exams to exploit the underneath pathological process could be performed: Coronary intravascular ultrasound, optical coherence tomography, Cardiac Magnetic resonance would be a valid help in prognosis and future treatment.

A 65-years old Caucasian woman was referred to the emergency department for chest pain, dyspnoea and high systolic blood pressure. In the previous days she complained a constant state of anxiety and worries due to family troubles. At the admission 12 – lead EKG showed sinus rhythm, ST-T segment depression >1 mm in the lateral and anterior leads (from V2 to V6). Laboratory exams showed elevated values of high sensivity troponin levels (high-sensitive troponin: 41 pg/mL – maximum laboratory cut off value: 12 pg/mL). Bedside echocardiogram showed an LVEF of 40% due to apical hyperkinesis, akynesis of the basal segments and hypokinesis of the mid segments of the left ventricle; a severe double jet MR (Fig.1); a type II diastolic dysfunction (E/A: 1,5; E/e’: 14). Several B lines (> 3) were present in all pulmonary regions assessed by lung POCUS. Cardiac angiography demonstrated non obstructive coronary artery disease. Left ventriculography showed an hyperdynamic apex and severe basal hypokinesis. Clinical and functional status rapidly improved. Daily EKGs were registered with a progressive resolution of the ST-T segment depression. She was discharged on the 7th days and the TTE in pre-discharge showed an LVEF of 60%, without wall motion abnormalities and complete recovery of mitral regurgitation. We report a case of reversible severe mitral regurgitation in a patient with basal ballooning TTS. Mital regurgitation is generally described in the contest of classical apical TTS. The potential mechanisms for severe MR are similar to those of acute myocardial infarction. Admission and daily echocardiographic evaluation is crucial in this subset of patients, with a tailored therapy following the severity of mitral valve disease. Fig. 1

There is an increasing awareness on the association between mitral valve prolapse (MVP) and sudden cardiac death. Mitral annular disjunction (MAD) is a phenotypic risk feature that can help in risk stratification. We present a case of a 58-year-old woman who experienced an out-of-hospital cardiac arrest caused by ventricular fibrillation interrupted by a direct current-shock. No coronary lesions were documented. Echocardiogram showed myxomatous MVP. Nonsustained ventricular tachycardia have been registered during hospital stay. Interestingly, cardiac magnetic resonance revealed MAD and a late gadolinium enhancement area in inferior wall. Finally, a defibrillator has been implanted. For arrhythmic risk stratification of MVP with MAD, multimodality imaging is the diagnostic tool to find out the disease behind many cardiac arrests of unknown cause.

Bicuspid aortic valve (BAV) is a congenital cardiac abnormality, affecting approximately 1%-2% of the general population (male > female). A 33-year-old man was admitted to emergency department (ED) for syncope during exertion. He had a history of cigarette smoking with a known previously discovered BAV with mild stenosis. TTE showed a severely calcified bicuspid aortic valve with severe stenosis and regurgitation. ECGs showed frequent asymptomatic complete hearth block (CHB), unresponsive to isoprenaline infusion. He underwent ministernotomy aortic valve replacement (AVR) with mechanical valve. During hospital stay, the 24h ECG telemetric monitoring did not show any A-V disturbance and TTE demonstrated normal prosthesis function. Pacemaker implantation was delayed, Follow-up was performed at 1, 6 and 10 months after surgery: 24h-ECG recordings were performed showing no A-V conduction disturbances. At 1 year, during routine medical screening, cardiac frequency of 38 bpm was detected (ECG revealed sinus rhythm with CHB and junctional escape rhythm of 38 bpm). ICCU echocardiogram showed good ventricular and prosthesis function. Therefore, a dual-chamber MRI compatible pacemaker was implanted. Few cases are reported in literature of young patients presenting with A-V block having a severely calcified aortic bicuspid valve. Their management is poorly explored, and therapies (medical therapy, aortic valve replacement and pacemaker implantation) are not fully evidence based. In literature, 3 cases of possible reversibility of conducting system disorders after severe stenotic aortic valve surgery are described. Noninvasive strategy was initially successful as demonstrated by both the post-operative absence of any AV conduction disturbance and/or symptoms and the close follow-up monitoring. Despite of previous evidence, our experience demonstrates that a complete heart block can recur following aortic valve surgery, even in young patients. Initial presentation of CHB was intermittent, suggesting that the structural damage to the conducting system could not be irreversible; thus, it could positively respond to valve surgery. Unfortunately, in CHB with calcific aortic stenosis patients should be considered for PM implantation at the time of aortic surgery. When a waiting strategy prevails, especially for young patients, close monitoring and follow-up must be warranted to early detect A-V disturbances recurrence.