P391 A ‘FAKE’ PERIPARTUM CARDIOMYOPATHY: THE KEY ROLE OF CARDIAC MRI

Abstract

Abstract K.M. Woman, 47 years old; Moroccan–born, she doesn’t speak Italian. History limited by the language barrier Medical histroy: caesarean section two months prior to admission (pluriparae with 6 births) In home therapy with estrogen–progestin pill Access to the emergency room for thoraco–abdominal pain of not exactly onset with dyspnoea (Killip II) EKG: sinus tachycardia, poor progression of the R wave in the precordial leads with mild ST–elevation in the same leads TTS echocardiographic: slightly dilated left ventricle, hypo / akinesia of the apex in its entirity with LVEF 38%; mild mitral regurgitation. Normal size and fuction of RV, PAPS slightly elevated; no pericardial effusion. Coronarography: mild non–critical atheroma of the main vessels. Occlusion of a small branch of division of OM Ventriculography (suspected Tako–Tsubo): reduced contractile function of the LV in relation to akinesia of the apex in its entirety Chest CT without contrast: diffuse areas of parenchymal nodular thickening >> lower lobes, thickening of interlobular and intralobular septa, mild pericardial effusion Blood sampling: elevated cardiac troponin hs in the absence of a typical curve for ACS; high inflammation markers Admission to cardiology with diagnosis of acute heart failure in PPCM (vs myocarditis.) Pneumonia. Slow and progressive improvement of the hemodynamic status and of the septic status with diuretic and antibiotic therapy. Prolactin antagonist (cabergoline) therapy and therapy for heart failure was started. During the hospital stay the patient was asymptomatic, not more angor, no arrhythmias on the EKG monitor, hemodynamic stability. Upon completion of the diagnosis, cardiac MRI was performed which modifies the diagnosis: dilated eccentric remodeling of the left ventricle with moderate reduction of global systolic function; akinesia of the lateral segments on the mid–basal, septal and lower apical planes and of the apex which corresponds to LGE ischemic–type enhancement for MI– outcomes. No evident endoventricular thrombi. Faded reactive signs of the pericardium with a slight fluid share Acute heart failure in hypokinetic heart disease with ischemic etiopathogenesis due to undated anterior silent MI (likely due to spontaneous coronary dissection)