An 83 yr old male with history of HLD & prior tobacco use presented with worsening dyspnea for the last 6 month and PND. Physical examination revealed BP 150/100 mmHg, holosystolic murmur in left 2nd intercostal space, diastolic murmur at the apex, decreased bibasilar lung sound & left leg swelling. CXR demonstrated cardiomegaly without evidence of pulmonary edema. ECG showed sinus rhythm with left atrial enlargement. Labs were remarkable for proBNP: 6,886 pg/mL and D dimer: 1.99 mg/L. Echocardiogram showed LV EF of 61%, dilated left atrium, severe mitral regurgitation (MR) with P2 focal cord rupture and moderate pulmonary hypertension (pHTN). He underwent a CT scan of his chest which revealed small right pulmonary embolism. He underwent cardiac catheterization which revealed mild CAD, increased left ventricular filling pressures (20 mmHg) severe pHTN without response to inhaled nitric oxide, PVR: 14 woods units, SVR: 2575 dynes/seconds/cm5, transpulmonary gradient: 41 mmHg & cardiogenic shock with cardiac output (CO) 2.77 and Cardiac Index (CI) 1.4. He was diuresed, started on milrinone, endothelin receptor antagonist (macitentan) and later guanylate cyclase stimulator (riociguat). Days later he underwent insertion of an IABP for afterload optimization & repeat hemodynamics showed normalized intracardiac filling pressures & improvement of cardiac index and SVR. The next day the patient underwent successful transcatheter mitral edge-to-edge repair (TEER). Echocardiogram showed mild MR with mean trans-mitral gradient of 5mmHg & RVSP of 47 mmHg. IABP was removed the next day and he returned home within a week of TEER. There is a paucity of data for the use of IABP in acute MR in the setting of mixed precapillary and post capillary pHTN which necessitates the use of endothelin receptor antagonist and guanylate cyclase stimulator as a bridge to TEER. Our case demonstrates the importance and success of a multidisciplinary strategy in this complex valvular cardiac condition.