Effect of Afterload Reduction on Vena Contracta Width in Mitral Regurgitation

Objective: Osteopontin (OPN), a sialoprotein present within atherosclerotic lesions, especially in calcified plaques, is linked to the progression of coronary artery disease and heart failure. We assessed the impact of valve surgery on serum OPN and left ventricular (LV) function in patients with mitral regurgitation (MR). Methods: Thirty-two patients with severe MR scheduled for surgery were included in the study. Echocardiography markers were assessed preoperatively and at 3 months following the surgery and matched with the serum OPN levels. Results: Valve surgery was associated with a reduction of the ejection fraction (EF) from 55.2 ± 6.3 to 48.8 ± 7.1% after surgery, p < 0.001. Following surgery, the OPN level was significantly higher than preoperatively (mean 245, range 36-2,284 ng/ml vs. 76, 6-486 ng/ml, p = 0.007). Preoperative OPN exhibited a slight negative correlation with the EF (r = -0.35, p = 0.04), and a moderate correlation with vena contracta (r = -0.38, p = 0.02). There were no other meaningful correlations between conventional echocardiographic parameters and OPN. Conclusion: Following valve surgery due to severe MR, patients exhibited a decrease in EF and an increase in OPN levels. The assessment of preoperative OPN failed to strongly predict probable LV dysfunction.

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Abstract 15934: Refractory Cardiogenic Shock in a Patient With Hypertrophic Obstructive Cardiomyopathy and Mitral Regurgitation Necessitating Intra-Aortic Balloon Pump Use

Circulation ◽

10.1161/circ.130.suppl_2.15934 ◽

2014 ◽

Vol 130 (suppl_2) ◽

Author(s):

Indrajeet Mahata ◽

Michael Faulx ◽

Snigdha kola ◽

Sweta Singh

Keyword(s):

Mitral Valve ◽

Mitral Regurgitation ◽

Cardiogenic Shock ◽

Pulmonary Edema ◽

Muscle Protein ◽

Hypertrophic Obstructive Cardiomyopathy ◽

Left Ventricular ◽

Afterload Reduction ◽

Intra Aortic Balloon Pump ◽

Refractory Cardiogenic Shock

Introduction: Hypertrophic obstructive cardiomyopathy (HOCM) is a genetic disease due to a mutation in cardiac muscle protein resulting in left ventricular wall and septal hypertrophy. The presence of systolic anterior motion (SAM) of the mitral valve leads to dynamic left ventricular outflow tract (LVOT) obstruction. With increasing SAM of the anterior mitral leaflet there is resultant loss of coaptation leading to mitral regurgitation (MR). MR has been associated with HOCM but severe MR physiology causing refractory cardiogenic shock and requiring the use of afterload reduction through intra-aortic balloon pump (IABP) is rare and seems paradoxical to the conventional therapy for HOCM. Case summary: This is a case of 71year old female with HOCM, presenting with worsening shortness of breath. She had pulmonary vascular congestion on Chest X-ray and her Transthoracic Echocardiography demonstrated significant LVOT obstruction with moderate MR. She was being evaluated for myomectomy while being treated medically with beta blocker therapy for HOCM. She decompensated with acute respiratory failure from pulmonary edema, her blood pressure and oxygen saturation dropped. She was intubated. Swan- ganz catheter reading suggested wedge pressures of 22 and elevated pulmonary pressures. MvO2 was 32% and this was suggestive of cardiogenic shock. The Trans-esophageal echocardiogram (TEE) showed normal EF with severe concentric LVH and a moderate to severe (3+) MR due to restricted leaflet motion with regurgitant orifice area being 2.5cm2. At that point her MR was the dominant physiology behind her acute decompensation and cardiogenic shock and hence an IABP was placed for reducing afterload that helped in stabilizing her. Subsequently her wedge pressure and MvO2 improved, she was weaned off the IABP and extubated. The patient is being evaluated for myomectomy and mitral valve repair. Conclusion: This case illustrates complex hemodynamics and a challenging management due to competing MR and HOCM physiologies, too much central volume to offset HOCM may worsen MR and pulmonary edema while too much afterload reduction might worsen the HOCM. The use of IABP in a HOCM patient though seems paradoxical but was necessary in this setting to deal with complex physiologies.

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