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Resting arterial hypoxaemia in subjects with chronic heart failure, pulmonary hypertension and patent foramen ovale (CROSBI ID 299887)

Prilog u časopisu | ostalo | međunarodna recenzija

Lovering, Andrew T. ; Lozo, Mislav ; Barak, Otto ; Davis, James T. ; Lojpur, Mihajlo ; Lozo, Petar ; Čaljkušić, Krešimir ; Dujić, Željko Resting arterial hypoxaemia in subjects with chronic heart failure, pulmonary hypertension and patent foramen ovale // Experimental physiology, 101 (2016), 5; 657-670. doi: 10.1113/ep085657

Podaci o odgovornosti

Lovering, Andrew T. ; Lozo, Mislav ; Barak, Otto ; Davis, James T. ; Lojpur, Mihajlo ; Lozo, Petar ; Čaljkušić, Krešimir ; Dujić, Željko

engleski

Resting arterial hypoxaemia in subjects with chronic heart failure, pulmonary hypertension and patent foramen ovale

Therolesof intrapulmonary andintracardiac shunt in contributing toarterialhypoxaemia at rest in subjects with chronic heart failure (CHF) have not been well investigated. We hypothesized that blood flow through intrapulmonary arteriovenous anastomoses ( ˙Q IPAVA) and/or patent foramen ovale ( ˙Q PFO) could potentially contribute to arterial hypoxaemia and, with pulmonary hypertension (PH) secondary to CHF, this contribution may be exacerbated. Fifty-six subjects with CHF (New York Heart Association Classes I– III), with (+) or without (−) PH [defined as peak tricuspid regurgitation velocity 2.9 m s−1 (CHF PH+, n = 32) and peak tricuspid regurgitation velocity 2.8 m s−1 (CHF PH−, n = 24)], underwent arterial blood gas analysis and transthoracic saline contrast echocardiography concomitant with transcranial Doppler to detect ˙Q IPAVA and ˙Q PFO. Seventeen of 56 subjects with CHF (30%) had ˙Q PFO, but only four of 56 subjects with CHF had ˙Q IPAVA (7%), both similar to age- and sex-matched control subjects. Mean arterial oxygen saturation (SaO2 ) was lower in subjects with ˙Q PFO. Only CHF PH+ subjects with ˙Q PFO had arterial hypoxaemia (mean SaO2 <95%). Bubble scores assessed using transthoracic saline contrast echocardiography were correlatedwith microembolic signals detected with transcranial Doppler in subjects with ˙Q PFO. Significant ˙Q IPAVA was not present in either CHF PH+ or PH− subjects, suggesting that ˙Q IPAVA is not dependent on increased pulmonary pressure and does not contribute significantly to arterial hypoxaemia in older subjects with CHF. Given that SaO2 was lower in all subjects with CHF who had ˙Q PFO compared with those without ˙Q PFO, a patent foramen ovale should be considered when determining potential causes of arterial hypoxaemia, because ˙Q PFO was present in 30% of these subjects.

chronic heart failure ; pulmonary hypertension and patent foramen ovale

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Podaci o izdanju

101 (5)

2016.

657-670

objavljeno

0958-0670

10.1113/ep085657

Povezanost rada

Kliničke medicinske znanosti, Temeljne medicinske znanosti

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