Echocontrastography is an echocardiography method that involves the intravenous administration of a particular contrast medium, formed by microbubbles capable of crossing the pulmonary circulation and distributing themselves in the left sections. These micro bubbles hit by ultrasound break or oscillate emitting ultrasound waves with a different frequency than the beam that hit them, generating a series of harmonic signals that can be processed to observe, for example, the opacification of the left cavities. An 82–year–old diabetic hypertensive man with a strong family history of coronary artery disease underwent routine cardiac evaluation. At the time of the visit, sporadic episodes of non–specific chest pain (localized in the right breast), of an intermittent nature, and not related to physical exertion, were reported. On the ECG, finding of sinus rhythm and q waves in V1–V3 (not present at a previous in 2019). On echocardiography (patient with poor acoustic window): Left ventricle of normal size with mild concentric parietal hypertrophy. Slight reduction in global systolic function due to alterations in district kinetics. Akinesia of the apex and middle segment of the septum and anterior wall. FE 48%. Doubtful apical iso–hyperechoicity (artifact?). Urgent hospitalization for coronary angiography was indicated in the suspicion of subacute anterior AMI. Coronary angiography revealed occlusion of anterior interventricular artery (IVA) in the proximal tract, partially re–inhabited downstream by homocoronary circulation (figure 1). Before proceeding with revascularization, given the absence of movement of the myocardiocitonecrosis indices, it was decided to perform myocardial viability tests. In consideration of the suspected apical thrombotic formation, as well as the patient‘s poor acoustic window, echo contrast was necessary (Figure 2). Once the complete opacification of the left ventricular cavity was highlighted by the contrast agent, suggestive of the absence of apex thrombi, we proceeded to ecostress with dobutamine to evaluate myocardial viability. At the explored dosages (5 – 10 and 20 ug/kg/ min) recovery of the apex kinetics was observed, but not of the mid–apical septum, which remained akinetic. We then proceeded to angioplasty on proximal IVA with a good angiographic result and the patient was discharged on the third day from revascularization in excellent clinical conditions.

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