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Abstract
IntroductionLittle is known on the pulmonary gradients of oxyhemoglobin, carboxyhemoglobin and methemoglobin in pulmonary arterial hypertension (PAH). We sought to determine these gradients in group 1 PAH and assess their association with disease severity and survival.MethodsDuring right heart catheterization (RHC) we obtained blood from pulmonary artery (PA) and pulmonary artery wedge (PAW) positions and used co-oximetry to test their gasometric differences.ResultsWe included a total of 130 patients, 65 had group 1 PAH, 40 had pulmonary hypertension (PH) from groups 2–5 and 25 had no PH during RHC. In all groups, PAW blood had higher pH, carboxyhemoglobin and lactate as well as lower pCO2 than PA blood. In group 1 PAH (age 58 ± 15 years, 72% females), methemoglobin in the PAW was lower than in the PA blood (0.83% ± 0.43 vs 0.95% ± 0.50, p = 0.03) and was directly associated with the degree of change in pulmonary vascular resistance (R = 0.35, p = 0.02) during inhaled nitric oxide test. Oxyhemoglobin in PA (HR (95%CI): 0.90 (0.82–0.99), p = 0.04) and PAW (HR (95%CI): 0.91 (0.84–0.98), p = 0.003) blood was associated with adjusted survival in PAH.ConclusionsMarked differences were observed in the gasometric determinations between PAW and PA blood. The pulmonary gradient of methemoglobin was lower in PAH patients compared to controls and a higher PAW blood methemoglobin was associated with a more pronounced pulmonary vascular response to inhaled nitric oxide. Pulmonary artery and PAW oxyhemoglobin tracked with disease severity and survival in PAH.
Highlights
Little is known on the pulmonary gradients of oxyhemoglobin, carboxyhemoglobin and methemoglobin in pulmonary arterial hypertension (PAH)
(2019) 20:6 oxidation of the hemoglobin iron to a ferric (Fe+++) state, a reaction that occurs when oxyhemoglobin reacts with nitric oxide (NO) [11]; levels of metHb may track with levels of NO, a potent vasodilator implicated in the pathogenesis of PAH [12]
Baseline characteristics We included a total of 130 patients, of whom 65 had group 1 PAH, 40 had pulmonary hypertension (PH) from groups 2–5 and 25 had no PH during right heart catheterization (RHC)
Summary
Little is known on the pulmonary gradients of oxyhemoglobin, carboxyhemoglobin and methemoglobin in pulmonary arterial hypertension (PAH). Pulmonary arterial hypertension (PAH) is a condition characterized by progressive narrowing of the small pulmonary arteries that if left untreated leads to right heart failure and death [1]. This pre-capillary involvement results in a distinct hemodynamic profile characterized by a mean pulmonary artery pressure (mPAP) ≥ 25 mmHg, pulmonary artery wedge pressure (PAWP) ≤ 15 mmHg and pulmonary vascular resistance (PVR) > 3 Wood units [2]. The lungs oxygenate the blood and remove the carbon dioxide (CO2) generated by metabolic processes It remains unknown how the lungs of patients with PAH process carboxyhemoglobin (COHb) and methemoglobin (metHb); which are compounds potentially involved in the pathogenesis of the disease [3,4,5,6]. Methemoglobin results from the (2019) 20:6 oxidation of the hemoglobin iron to a ferric (Fe+++) state, a reaction that occurs when oxyhemoglobin reacts with nitric oxide (NO) [11]; levels of metHb may track with levels of NO, a potent vasodilator implicated in the pathogenesis of PAH [12]
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