61-year-old woman with a history of high blood pressure and smoking. Family history: a sister who "suffers from heart disease", with no other relevant data.

History, current disease and physical examination
Her medical history includes a transthoracic echocardiography in 2010 with the following data: Obstructive hypertrophic cardiomyopathy. Moderate MI. Normal LV systolic function. Slightly dilated LA (LA volume: 30 ml/m2). LV hypertrophy mainly at the level of the interventricular septum. Mitral valve function with incomplete SAM and dynamic gradient in LVOT (Baseline: 40 mmHg, which after Valsalva manoeuvres reaches up to 57 mmHg). The patient had not undergone subsequent follow-up. She came to the emergency department in November 2012, reporting a progressive increase in dyspnoea for about four months, which in recent weeks has evolved rapidly to the point of becoming resting, and which is accompanied by intense asthenia. He denies other associated cardiological or infectious symptoms. She denies a history of palpitations or syncope.
Examination revealed the presence of an intense systolic murmur on cardiac auscultation, predominantly in the left parasternal border, which increased with Valsalva manoeuvres and did not clear the second tone. There was also a loud regurgitation murmur in the mitral focus radiating to the axilla. Pulmonary auscultation showed crackles up to the apex and generalised wheezing. A symmetrical magnus and celer pulse was palpated. Otherwise he is haemodynamically stable with basal saturation of 90% and blood pressure of 183/89. Heart rate: 73 bpm.

Complementary tests
- ECG: On admission with sinus rhythm at 76 bpm. Doubtful ST elevation, 1mm in V1, similar to previous ECG. Criteria for left ventricular hypertrophy.
- Chest X-ray: shows borderline CTI and bilateral centrifugal alveolar infiltrate. Laboratory tests showed BNP of 3,000 with no other relevant alterations.
- Transthoracic echocardiogram: Performed during his admission to the Cardiology Department of our hospital. It reflected the following findings: LVH data with interventricular septum of 27 mm, LV posterior wall of 20 mm. Gradient across the LVOT reaching 120 mmHg. Presence of systolic anterior motion of the anterior leaflet of the mitral valve contributing to the mechanism of moderate-severe MI.
- 24-hour Holter-ECG: Showing sinus rhythm throughout the recording, with high-density polymorphic ventricular extrasystoles, isolated, sparsely bigeminy and in pairs, as well as several bouts of ventricular tachycardia, the most prolonged of eight beats. No pathological pauses.
- Haemodynamic study: hypertrophic cardiomyopathy with a dynamic gradient of 130 to 140 mmHg, accompanied by severe mitral insufficiency (III/IV). Coronary angiography showed no significant lesions and evidenced the existence of an anatomically adequate septal branch for septal ablation.

Clinical evolution
With this information, the existing therapeutic possibilities were discussed with the patient, who opted to undergo percutaneous septal ablation. The patient was transferred to the haemodynamics room where, under sedation, the intervention was performed. The MCP cable was placed in the right ventricle with access through the right femoral vein. A balloon catheter was introduced via the arterial route through the left coronary artery until it reached the first septal branch.
Subsequently, the expected response to ischaemia induced by occluding the first septal branch by inflating the balloon at that level, together with the injection of echocardiographic contrast, is assessed by echocardiographic support.
Induction of ischaemia in the desired proximal septal region is verified, as well as a fall in the gradient across the LVOT, so alcohol is infused in this area. At this point the patient becomes dependent on MCP pacing. After a few minutes, a significant drop in the gradient to 70 mmHg and a decrease in mitral regurgitation was observed. Angiographically, a small sub-branch of the aforementioned septal branch was observed to be permeable, so an additional 1cc of absolute alcohol was infused, bringing the gradient down a further 10 mmHg.
The patient was transferred to the Coronary Unit with alternating pacing and pacemaker pacing, and in a stable haemodynamic condition. Enzyme seriation showed a peak troponin level of 90 ng/dL. No malignant ventricular arrhythmias were recorded in the monitoring and given the good evolution of the patient, it was decided to transfer her to the ward after 72 hours.
On admission, the woman presented with severe acute pulmonary oedema in the context of heart failure due to severe obstruction of the left ventricular outflow tract and associated mitral insufficiency. Symptomatic treatment was initiated with careful use of diuretics and lusotopics, and after reaching the diagnosis by careful examination and imaging techniques, the patient was offered the available treatment options.
At discharge, there was still a high gradient, around 60 mmHg, and moderate mitral regurgitation, but the patient showed a marked symptomatic improvement, being eupneic in decubitus, with good tolerance to the onset of physical activity and in a clinical situation that she described as excellent. She was discharged with generous doses of lusotopic treatment and was soon to be reviewed by the Cardiology Department.

Diagnosis
- Heart failure with acute pulmonary oedema.
- Hypertrophic obstructive cardiomyopathy with severe LVOT obstruction. Treated by percutaneous alcohol ablation of the first septal branch.
- Complete AV block during the procedure resolved at discharge.
- Moderate mitral insufficiency.
