Effective Cibenzoline Treatment in a Patient With Midventricular Obstruction After Transcatheter Aortic Valve Implantation

Abstract

A n 80-year-old woman with severe aortic stenosis was admitted to our hospital for transcatheter aortic valve implantation (TAVI). She had New York Heart Association functional class III congestive heart failure. Her comorbidities included multiple myeloma, idiopathic thrombocytopenic purpura treated with chronic steroids, hypertension, diabetes mellitus, and persistent atrial fibrillation. Echocardiography demonstrated a calcified tricuspid aortic valve with leaflet restriction consistent with severe aortic stenosis ( Figure 1A; Movie I in the Data Supplement). The instantaneous peak velocity across the aortic valve on Doppler imaging was 5.0 m/s, and the mean pressure gradient was 53 mm Hg ( Figure 1B). The aortic valve area calculated by using the continuity equation was 0.49 cm 2 . A concentric left ventricular (LV) hypertrophy was observed in the septum, measuring 13 mm, and in the posterior wall, measuring 14 mm. The LV cavity was small, with an LV internal dimension of 39 mm at end diastole. LV ejection fraction was 80%. Late peaking of the midcavitary LV pressure gradient of 25 mm Hg at rest was observed, without LV outflow tract obstruction and systolic anterior motion of the mitral valve leaflet ( Figure 1C). Coronary angiography revealed no significant coronary artery stenosis. Given her severe aortic stenosis and heart failure symptoms with comorbidities of severe thrombocytopenia (platelet count: 15 000 per μL), the patient underwent TAVI via the transfemoral approach. A 23-mm Sapien valve (Edwards Lifesciences, Irvine, CA) was successfully implanted. The hemodynamic profile of the patient throughout and after the procedure was stable. Her symptoms improved, and she was discharged and prescribed with a β-blocker, vasodilators, and diuretics as outpatient treatments.Two months later, she was admitted to our hospital for recurrent exertional dyspnea. Her physical examination revealed jugular venous distension, bilateral legs edema, and a 3 of 6 systolic ejection murmur at the lower left sternal border.Electrocardiography showed atrial fibrillation with bradycardia (heart rate: 30-50 beats per minute). Given her conditions of heart failure with volume overload and bradycardia, intravenous furosemide was administered and the dose of the β-blocker was reduced. However, her symptoms worsened with hypotension and renal dysfunction. Echocardiography revealed that the Edwards Sapien valve prosthesis was functioning properly with minimal paravalvular regurgitation. LV systolic function was hyperdynamic, and significant midventricular obstruction was observed with concentric LV hypertrophy during systole, with a peak pressure gradient of 69 mm Hg at rest (Figure 2A and 2B). No significant LV outflow tract obstruction and systolic anterior motion of the mitral valve were observed. Given the above-mentioned findings, the patient's deterioration was attributed to hypertrophic obstructive cardiomyopathic physiology with the development of midventricular obstruction after the removal of the LV pressure overload. Th...