Abstract

Pulmonary hypertension (PH) is a chronic pulmonary vascular disorder that can be caused by a variety of pathophysiological states. Five groups of PH sharing similar hemodynamics, and management were identified: 1) pulmonary arterial hypertension (Group 1); 2) PH due to left heart disease (Group 2); 3) PH due to chronic lung disease (Group 3); 4) chronic thromboembolic PH (Group 4); and 5) miscellaneous mechanisms (Group 5) [1]. Physiologically, PH is defined as mean pulmonary artery pressure (mPAP) ≥ 25 mm Hg at rest or >30 mm Hg with exercise. Clinically, PH leads to right heart ventricular failure and cardiac death [2,3]. Group 2 PH is found commonly and is reported in >60% of heart failure patients [4]. Patients with chronic left heart failure often have other atrial arrhythmias. Atrial fibrillation (AF) is commonly encountered in >3 million people in the United States [5]. Heart failure patients are 5 to 10 times more likely to develop AF than healthy patients [6,7]. AF portends a worse long-term prognosis attributable to the loss of atrial kick, loss of atrioventricular synchrony, and the increased risk of stroke [8,9]. Similarly, the prevalence of Group 2 PH related AF is as high as 57%, and 23% in other forms of PH [10]. The cornerstone of surgical treatment of AF has been AF ablation. Haussaiguarre et al. first reported that AF initiates in the posterior wall of the left atrium near the ostium of pulmonary veins [11]. AF ablation is achieved either radio-frequency (electrocautery) or cryoablation. To date, limited data are available regarding the impact of PH on patients undergoing AF ablation. Therefore, we have demonstrated the effect of PH in patients getting AF ablation in this National Inpatient Sample (NIS) analysis.

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