Abstract Funding Acknowledgements This work was supported by CREDO Project - ID: 49182, financed through the SOP IEC -A2-0.2.2.1-2013-1 cofinanced by the ERDF Background Echocardiographic assessment of diastolic dysfunction and left ventricular (LV) filling pressures is a complex and challenging process, requiring a multiparameter analysis. In recent years strain imaging has been emerging as a promising method for evaluation of left atrium (LA) function, being correlated with LV systolic dysfunction. Purpose We sought to evaluate LA mechanics in a cohort of patients with ischemic heart failure (HF) at one month after ST elevation myocardial infarction (STEMI) Material and methods 40 patients were enrolled in this study: 30 consecutive patients with ischemic HF after STEMI, with LVEF < 50% and 10 healthy age- and sex-matched controls. All patients had standard echocardiographic examination; also LA strain curves were obtained using speckle tracking with measurement of peak LA systolic strain. Categorization of diastolic dysfunction severity into 3 grades was realized according to 2016 guidelines. Results 2D and 3D LVEF (33% vs 55%, p = 0.00), LV global strain (-10 vs -19, p = 0.00) and peak LA systolic strain (16 vs 33, p = 0.00) were significantly reduced in HF patients compared to controls. In both groups LA strain correlated with the following parameters: 2D EF (p = 0.024), 3D EF (p = 0.02), LV global strain (p = 0.00), E/A (p = 0.05), septal e’ (p = 0.00), lateral e’ (p = 0.00), E/septal e’ (p = 0.006), E/lateral e’ (p = 0.003), E/mean e’ (p = 0.014), LA volume (p = 0.014) and LV filling pressures (p = 0.001). Peak LA systolic strain (PALS) values progressively decreased with worsening of diastolic function showing significant differences between all diastolic dysfunction grades. Using ROC analysis we identified 3 PALS thresholds to distinguish between normal diastolic function and the 3 diastolic dysfunction grades. The optimal cut off values were as follows: between normal diastolic function and grades 1-3 with PALS cut off value of 26.5 (Sb 90%, Sp 87%), AUC 0.963, CI 95%, p = 0.00; between grades 0-1 and grades 2-3 with peak LA strain cut off value of 17.2 (Sb 75%, Sp 93%) AUC = 0.828, CI 95%, p = 0.002; between grade 0-2 and grade 3 with peak LA strain cut off value of 11 (Sb 85%, Sp 93%), AUC 0.942, CI 95%, p = 0.00. Also, PALS value differed significantly between patients with normal vs high LV filling pressures. Using ROC analysis we determined a cut off value for LA of 15.1 to differentiate between the two subgroups with excellent discrimination power AUC 0.902, CI 95%, p = 0.00, Sb 88.9%, Sp 83% thus making LA strain an accurate surrogate estimate of LV filling pressures. Conclusions Global peak LA systolic strain is significantly correlated with LV systolic and diastolic function. PALS is a feasible option for detection and categorization of diastolic dysfunction in patients with HF and depressed LVEF after STEMI. Incorporating LA strain into noninvasive assessment of LV diastolic dysfunction may improve the detection of elevated LV filling pressures. Further large scale studies are needed to validate this data.

Background Apical hyperthrophic cardiomyopathy (AHCM) is an uncommon form of hyperthrophic cardiomyopathy (HCM) with less prevalent detection of gene mutations and sudden cardiac death compared with other types of HCM. We present the case of a 76 years old patient with multiple cardiovascular risk factors (hypertension, dyslipidemia, obesity, former smoker) with history of unprovoked pulmonary embolism - PE (2018), without evidence of deep venous thrombosis, in treatment with rivaroxaban, who presented with worsening severe dyspnea at effort and peripheral edemas, symptoms started a few days before admission. He denied angina or palpitations. On clinical examination we identified obesity grade II and bilateral leg edema and routine laboratory tests revealed controlled dyslipidemia. The electrocardiogram (ECG) showed atrial flutter (AF) with block 5:1, heart rate 50/min, with negative T waves in DI, aVL and V2-V6. Transthoracic echocardiography with contrast was performed showing no wall motion abnormalities otherwise with a mild concentric left ventricle hypertrophy (LVH) except for the apex where there was severe LVH suggestive for AHCM; there was an increased aortic velocity with an aortic valve with degenerative changes. We thought that the changes on the ECG were most likely due to AHCM. A thoracic tomography scan with contrast was also performed because of associated dyspnea which excluded an acute recurrence of PE. The next day the T waves on ECG normalized, putting forward for consideration an acute coronary syndrome. We performed a coronarography which confirmed a 80% stenosis of proximal left anterior descending (LAD) artery with subsequent placement of a drug eluting stent. We also did a transesophageal echocardiography (noncompliant patient) for exclusion of intracardiac thrombi (which also showed bicuspid aortic valve) and then we performed radiofrequency ablation of the cavotricuspid isthmus followed by atrial overdrive pacing for typical AF, but unsuccessful, with degeneration into atrial fibrillation. Sometimes heart failure might occur due to multiple etiological factors and mechanisms of decompensation. We had a patient with AHCM with an ECG that could be interpreted as typical for this pathology but with concomitent severely affected LAD coronary artery, with AF and high grade atrioventricular block plus mild aortic stenosis with a bicuspid aortic valve with indication for strict follow up. AHCM was first described in Japan where has the highest prevalence, but is also documented in other countries (rare in Caucasian population). Note that AHCM often mimic acute coronary syndromes through clinical manifestations and electrocardiographic aspects. Our case report showed a Caucasian patient with AHCM with concomitent severe atherosclerotic desease and aortic stenosis on a bicuspid valve.

Acute aortic dissection is a relative rare disease which can sometimes mimic acute myocardial infarction, usually inferior, secondary to right coronary artery involvement. Accurate rapid diagnosis is mandatory for successful treatment and usually implies cardiac surgery with the correction of arterial wall. We present a case of spontaneous limited aortic dissection of the left Valsalva sinus, complicated by non-ST elevation MI (non-STEMI) presented to the emergency room as cardiogenic shock and successfully treated by emergent angioplasty of the left main, therapy which proved lifesaving as a bridge to surgery. The case highlights that even in front of a well-defined clinical, ECG and biological presentation suggestive for acute MI, one should always be mindful for the differential diagnosis of acute aortic dissection. The interventional treatment in this critical situation was effective due to the pathological peculiarity of the dissection, which was strictly focal and limited and could be stabilized by left main stenting. This case also underlines that treatment should always be adapted to the patient’s disease, and that sometimes therapies with an absolute contraindication may be a lifesaving solution in a specific context.