Introduction
Persistence or recurrence of symptoms early after septal reduction by surgical septal myectomy or alcohol septal ablation (ASA) is most often due to residual or recurrent left ventricular outflow tract obstruction.[1,2] After obtaining written consent from the patient, we describe in the present report that the patient had persistent exertional dyspnea for six months following ASA and was found to have multiple potential cardiac causes for her disability.
Patient presentation and management  
A 71-year-old woman with the previous diagnosis of obstructive HCM presented to our Clinic with complaints of exertional breathlessness and chest fullness for three years.  Because of progressive symptoms that were not relieved with medical therapy, she underwent ASA at another institution. Complete heart block complicated her post-ablation course, and she received a dual-chamber transvenous pacemaker-defibrillator.  Post procedure, she continued to experience persistent limiting symptoms of exertional shortness of breath and chest fullness.
There were several important findings on her clinical examination. She had severe systemic hypertension with blood pressure of 180/90 mmHg. Her jugular venous pressure was markedly elevated with rapid X and Y descents. She had a 2/6 systolic ejection murmur at the left sternal border which increased from the squat to stand position.
Transthoracic echocardiography demonstrated septal hypertrophy and systolic anterior motion of the mitral valve producing severe left ventricular outflow tract (LVOT) obstruction with a peak Doppler gradient of 77 mmHg.  There was, in addition, midventricular obstruction with gradient of 31 mmHg. Extensive calcified plaques in the ascending aorta and aortic arch were seen on CT angiography (Figure 1 ).  Cardiac catheterization demonstrated a large gradient between the LV apex and aorta from combined midventricular and subaortic left ventricular outflow obstruction. The gradient decreased during inspiration (Figure 2A ) with a Brockenborough response after a PVC (Figure 2B ), indicating a dynamic outflow obstruction. There was also elevation and end-equalization of diastolic pressures in all four cardiac chambers to 25 mmHg, and the cardiac index was reduced to 2.3L/min/M2; she had evidence of enhanced ventricular interaction all consistent with the diagnosis of constrictive pericarditis (Figure 2C) . Additional medical problems included systemic hypertension, diabetes, obesity (BMI > 37kg/m2), paroxysmal atrial fibrillation, and chronic obstructive pulmonary disease.
At operation, the pericardium was found to be thickened and intensely constrictive.  Further, severe calcification of the proximal aorta prevented an adequate aortotomy for myectomy. Prior to bypass, the gradient from the left ventricle to the aorta was 80 mm Hg at rest, and this increased to 143 mm Hg following a premature ventricular contraction (PVC).  After myectomy, the gradient was 7 mm Hg at rest and 20 mm Hg following PVC.
After cannulating the proximal aortic arch for arterial inflow, a two-stage cannula was placed in the right atrium. During the initial phase of bypass, a complete pericardiectomy was performed including the anterior portion and the diaphragmatic pericardium. The aorta was cross-clamped, and the calcified midportion of the ascending aorta was excised. We then performed an extended transaortic septal myectomy. A 22-mm Hemashield replacement graft was trimmed to the correct length and sewed to the proximal and distal ends of the aorta. The apex of the heart was elevated into the wound, and through an apical ventriculotomy, we performed an extensive midventricular septal myectomy. The apical ventriculotomy was closed with felt strip reinforcement. Hemodynamics was satisfactory following cardiopulmonary bypass, and intraoperative transesophageal echocardiography demonstrated a good result from myectomy with no residual systolic anterior motion of the mitral valve and a maximum intraventricular gradient of 14 mmHg. Postoperative pathology confirmed a non-calcified fibrous thickening (up to 1 cm) and non-granulomatous lymphoplasmacytic infiltration of the pericardium.  On postoperative TTE, left ventricular ejection fraction was 67% and there was no systolic anterior motion of the mitral valve or residual subaortic obstruction.  She was dismissed home from the hospital 7 days after operation.  At the time of last follow-up three years postoperatively the patient was well and free of cardiac symptoms.