Case report: Transcatheter edge-to-edge repair with MitraClip for acute mitral regurgitation after myocardial infarction.

INTRODUCTION: Acute mitral regurgitation (MR) due to papillary muscle rupture (PMR) is a rare but lethal mechanical complication of acute myocardial infarction (MI). The treatment of patients with post-MI PMR, especially those with cardiogenic shock, presents great challenges due to the high surgical risk. PATIENT CONCERNS: We report an 80-year-old woman with a history of hypertension and diabetes mellitus, presented with chest pain. Despite an early percutaneous coronary intervention and transfer to the intensive care unit, her general condition and hemodynamic parameters continued to deteriorate rapidly. DIAGNOSIS: Evidenced by electrocardiogram, echocardiogram and coronary angiography, the patient was diagnosed with acute lateral and posterior ST-segment elevation MI, cardiogenic shock, PMR, severe MR, and pulmonary edema. INTERVENTIONS: The patient received percutaneous mitral valve repair with MitraClip (Abbott Vascular, Santa Clara, CA, USA) supported by extracorporeal membranous oxygenation and intra-aortic balloon pump. OUTCOMES: The patient was discharged with relief of heart failure symptoms, reduced MR, and recovery of cardiac function, remaining in a stable condition in New York Heart Association class I after 15-month outpatient follow up. CONCLUSION: Transcatheter edge-to-edge repair with MitraClip can serve as a viable alternative to surgery in reducing MR in post-MI PMR patients at high surgical risk.

Cardiac-Specific Overexpression of Silent Information Regulator 1 Protects Against Heart and Kidney Deterioration in Cardiorenal Syndrome via Inhibition of Endoplasmic Reticulum Stress.

BACKGROUND/AIMS: Increased endoplasmic reticulum (ER) stress contributes to development of cardiorenal syndrome (CRS), and Silent Information Regulator 1 (SIRT1), a class III histone deacetylase, may have protective effects on heart and renal disease, by reducing ER stress. We aimed to determine if SIRT1 alleviates CRS through ER stress reduction. METHODS: Wild type mice (n=37), mice with cardiac-specific SIRT1 knockout (n=29), or overexpression (n=29), and corresponding controls, were randomized into four groups: sham MI (myocardial infarction) +sham STNx (subtotal nephrectomy); MI+sham STNx; sham MI+STNx; and MI+STNx. To establish the CRS model, subtotal nephrectomy (5/6 nephrectomy, SNTx) and myocardial infarction (MI) (induced by ligation of the left anterior descending (LAD) coronary artery) were performed successively to establish CRS model. At week 8, the mice were sacrificed after sequential echocardiographic and hemodynamic studies, and then pathology and Western-blot analysis were performed. RESULTS: Neither MI nor STNx alone significantly influenced the other healthy organ. However, in MI groups, STNx led to more severe cardiac structural and functional deterioration, with increased remodeling, increased BNP levels, and decreased EF, Max +dp/dt, and Max -dp/dt values than in sham MI +STNx groups. Conversely, in STNx groups, MI led to renal structural and functional deterioration, with more severe morphologic changes, augmented desmin and decreased nephrin expression, and increased BUN, SCr and UCAR levels. In MI+STNx groups, SIRT1 knockout led to more severe cardiac structural and functional deterioration, with higher Masson-staining score and BNP levels, and lower EF, FS, Max +dp/dt, and Max -dp/dt values; while SIRT1 overexpression had the opposite attenuating effects. In kidney, SIRT1 knockout resulted in greater structural and functional deterioration, as evidenced by more severe morphologic changes, higher levels of UACR, BUN and SCr, and increased desmin and TGF-ß expression, while SIRT1 overexpression resulted in less severe morphologic changes and increased nephrin expression without significant influence on BUN or SCr levels. The SIRT1 knockout but not overexpression resulted in increased myocardial expression of CHOP and GRP78. Cardiac-specific SIRT1 knockout or overexpression resulted in increased or decreased renal expression of CHOP, Bax, and p53 respectively. CONCLUSIONS: Myocardial SIRT1 activation appears protective to both heart and kidney in CRS models, probably through modulation of ER stress.