Key result
Pulmonary artery ablation increases 6MWD by ~200m in refractory PAH.
Why the study?
Pulmonary arterial hypertension remains a life-threatening condition without a cure despite existing therapies, and the effect of pulmonary arterial denervation on this disease is not well established.
Does pulmonary artery ablation improve functional capacity and hemodynamics in a patient with pulmonary arterial hypertension?
Case Report (n=1)
No
Does pulmonary artery ablation improve functional capacity and hemodynamics in a patient with pulmonary arterial hypertension?
Absolute Event Rate: 302% vs 104%
Pulmonary artery ablation (denervation) may be a feasible therapeutic option to improve functional capacity and hemodynamics in patients with pulmonary arterial hypertension.
Pulmonary arterial denervation may improve hemodynamics in refractory IPAH; hypothesis-generating case report leaves open efficacy, safety, and role versus medical therapy.
INTRODUCTION: Idiopathic pulmonary arterial hypertension is defined as a group of diseases characterized by a progressive increase in pulmonary vascular resistance that results in right heart failure and premature death. Although therapies exist to improve hemodynamic instability and symptoms, there is no cure for pulmonary arterial hypertension and it remains a life-threatening condition. A recent study performed in China reported, for the first time, the effect of pulmonary arterial denervation on functional capacity and hemodynamics in patients with refractory idiopathic pulmonary arterial hypertension. CASE PRESENTATION: We report a case of a 60-year-old white Brazilian man, with controlled hypertension and stage 2 obesity who complained of progressive fatigue with moderate to light exertion of approximately 1 year's duration. During this period, he underwent myocardial perfusion scintigraphy without evidence of obstructive ischemic disease. He had no clinical evidence of systolic heart failure. He had undergone biological mitral valve replacement 3 years previously for mitral valve stenosis and ablation of atrioventricular nodal reentry tachycardia 18 months previously. At the time of valve replacement, he had no reported evidence of pulmonary arterial hypertension. His echocardiogram showed normal function of a mitral prosthesis, normal global left ventricular systolic function (left ventricular ejection fraction 62 % measured using the Teichholz method), stage I diastolic dysfunction, and a mean systolic pulmonary arterial blood pressure of 50 mmHg. In the 6-minute walk test, the patient walked 104 meters. Catheterization of his right heart chambers and pulmonary arteries confirmed the diagnosis of pulmonary hypertension. Electroanatomic reconstruction of the right ventricular outflow tract and pulmonary artery was performed under direct fluoroscopic visualization, and a merger was made with a formatted image of cardiac computed tomography angiography. Then we performed irrigated cardiac catheter ablation of the pulmonary trunk. CONCLUSIONS: At the patient's 3-month follow-up, he showed improvement in functional class for fatigue on major exertion, increased distance walked in the 6-minute walk test, and reductions in pressure of both the right cavities and the pulmonary artery. Currently, with 6 months of clinical follow-up, the patient has maintained his functional classification and is pedaling his bicycle.
No takes yet. Share an insight, caveat, or question.
Kiuchi et al. (2015) conducted a case report in Pulmonary arterial hypertension (n=1). Pulmonary artery ablation vs. Baseline was evaluated on 6-minute walk test distance (meters). Pulmonary artery ablation in a patient with refractory pulmonary arterial hypertension increased 6-minute walk test distance from 104 meters to 302 meters and reduced pulmonary pressures at 6 months.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: