Prevalence of left heart contrast in healthy, young, asymptomatic humans at rest breathing room air

Elliott, Jonathan E.; Nigam, Shishir; Laurie, Steven S.; Beasley, Kara M.; Goodman, Randall D.; Hawn, Jerold A.; Gladstone, Igor M.; Chesnutt, Mark S.; Lovering, Andrew T.

doi:10.1016/j.resp.2013.04.019

Cited by 63 publications

(142 citation statements)

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“…subjects with a PFO and pulmonary hypertension. The prevalence of PFO ranges between 25 and 40% of the general population (Hagen et al 1984;Woods et al 2010;Elliott et al 2013;Marriott et al 2013). In the present study, we found that the prevalence of PFO in subjects with CHF was similar to that of the general population.…”

Section: Patent Foramen Ovale and Arterial Hypoxaemiasupporting

confidence: 77%

“…The echocardiographic technicians were not blinded to the subject's diagnosis (PH+ or PH−). We have previously shown 94-100% agreement among observers using this scoring system (Laurie et al 2010;Elliott et al 2013).…”

Section: Echocardiographic Screening and Saline Contrast Echocardiogrmentioning

confidence: 90%

“…If subjects presented with a PFO, then these subjects breathed 100% O 2 via a rebreathing mask as before (Elliott et al 2013), and we subsequently performed a second injection of saline contrast while imaging the heart to determine the bubble score when breathing 100% O 2 . We have shown previously that breathing 100% O 2 reduces bubble scores in subjects without a PFO, so we performed this second measurement to differentiate betweenQ IPAVA andQ PFO .…”

Section: Echocardiographic Screening and Saline Contrast Echocardiogrmentioning

confidence: 99%

“…Blood flow though a patent foramen ovale (PFO;Q PFO ) is present in at least 30% of the general population (Woods et al 2010;Elliott et al 2013;Marriott et al 2013) and is known to reduce pulmonary gas exchange efficiency in healthy humans Elliott et al 2015) and patient populations (Ilkhanoff et al 2005;Fenster et al 2013). With increased right atrial pressures in subjects with CHF and pulmonary hypertension,Q PFO might be even greater than that in conditions of normal right atrial pressure, and thus,Q PFO could have an even greater potential to worsen pulmonary gas exchange efficiency in these subjects.…”

Section: Introductionmentioning

confidence: 99%

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

Lovering

Lozo

Barak

et al. 2016

Experimental Physiology

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New Findings r What is the central question of this study?Does a patent foramen ovale contribute to resting arterial hypoxaemia, defined as arterial oxygen saturation <95%, in subjects with chronic heart failure with or without pulmonary arterial hypertension? r What is the main finding and its importance?The presence of a patent foramen ovale contributed to resting arterial hypoxaemia only in subjects with chronic heart failure with pulmonary arterial hypertension. These data suggest that the presence of a patent foramen ovale should be considered in chronic heart failure patients with arterial hypoxaemia and pulmonary hypertension.The roles of intrapulmonary and intracardiac shunt in contributing to arterial hypoxaemia 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 detectQ IPAVA andQ PFO . Seventeen of 56 subjects with CHF (30%) hadQ PFO , but only four of 56 subjects with CHF hadQ IPAVA (7%), both similar to age-and sex-matched control subjects. Mean arterial oxygen saturation (S aO 2 ) was lower in subjects withQ PFO . Only CHF PH+ subjects withQ PFO had arterial hypoxaemia (mean S aO 2 <95%). Bubble scores assessed using transthoracic saline contrast echocardiography were correlated with microembolic signals detected with transcranial Doppler in subjects withQ PFO . SignificantQ IPAVA was not present in either CHF PH+ or PH− subjects, suggesting thatQ IPAVA is not dependent on increased A. T. Lovering and others pulmonary pressure and does not contribute significantly to arterial hypoxaemia in older subjects with CHF. Given that S aO 2 was lower in all subjects with CHF who hadQ PFO compared with those withoutQ PFO , a patent foramen ovale should be considered when determining potential causes of arterial hypoxaemia, becauseQ PFO was present in 30% of these subjects.

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Section: Patent Foramen Ovale and Arterial Hypoxaemiasupporting

confidence: 77%

Section: Echocardiographic Screening and Saline Contrast Echocardiogrmentioning

confidence: 90%

Section: Echocardiographic Screening and Saline Contrast Echocardiogrmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Lovering

Lozo

Barak

et al. 2016

Experimental Physiology

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“…TTCE lacks specificity and has a low positive predictive value for the presence of PAVMs. In this study, 23 HHT patients with a grade 2 or 3 RLS had no PAVM on chest CT at the initial screening, which is consistent with the finding that 6-28% of the normal population has a positive TTCE [15][16][17]. This can reflect true false positive results or microscopic PAVMs that are too small to be detected with chest CT.…”

supporting

confidence: 87%

How to follow-up patients with hereditary haemorrhagic telangiectasia and suspected pulmonary arteriovenous malformations

Chinet

2016

Eur Respir J

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@ERSpublications Contrast echocardiography is useful for the follow-up of HHT patients with pulmonary arteriovenous malformations http://ow.ly/YNql5Pulmonary arteriovenous malformations (PAVMs) are abnormal vascular structures that connect one or several pulmonary arteries to one or several pulmonary veins without interposition of a capillary bed, resulting in a right-to-left shunt (RLS) [1]. Over 80% of PAVMs are associated with the genetic disease hereditary haemorrhagic telangiectasia (HHT). The vascular malformations predispose patients to severe complications due to paradoxical systemic emboli of thrombotic or septic origin, such as stroke and brain abscess [2][3][4][5]. The treatment of choice for PAVMs is transcatheter embolotherapy, although concerns are emerging regarding the long-term consequences of this procedure, especially in children [6].Because of the risk of severe complications, international guidelines recommend screening patients with HHT for the presence of PAVMs at the time of initial clinical evaluation and also after puberty, after pregnancy, within 5 years preceding a planned pregnancy, and otherwise every 5-10 years [7]. Transthoracic contrast echocardiography (TTCE) is the first-line screening technique for the detection of PAVMs in HHT [7]. In expert hands, it has excellent sensitivity and negative predictive value for the presence of PAVMs in children and adults. Several grading scales are used in different HHT centres to quantify the pulmonary RLS size [6][7][8]. Microbubbles of air in agitated saline may expose patients with RLS to the risk of cerebral air emboli inducing migraine, blurred vision, numbness and paraesthesia, but these symptoms resolve quickly without residual side effects [9,10]. To minimise this risk, many groups perform a chest radiograph prior to TTCE to detect large-size PAVMs, which are likely to carry the highest risk of complications from air bubbles. TTCE is therefore a safe diagnostic tool and its benefits undoubtedly outweigh its potential minor risks.One must bear in mind that TTCE does not detect PAVMs but rather pulmonary RLS. Chest computed tomography (CT) is considered the gold standard diagnostic tool for PAVMs as it enables visualisation of the vascular malformations (except microscopic ones) and provides essential information on their characteristics (shape, location, size of the feeding arteries, size of the aneurismal sac, etc.). Recent studies have reported that, in patients with HHT, the grade of pulmonary RLS on TTCE predicts the size of PAVMs on chest CT and the feasibility of subsequent transcatheter embolotherapy [7]. The absence of, or a small, pulmonary RLS (i.e. a low grade on TTCE) is associated with no risk of neurological complications and with PAVMs too small for embolisation [5,7].

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Childhood Stroke

Kumar¹,

Governale²,

Lo³

2020

Clinical Child Neurology

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Prevalence of left heart contrast in healthy, young, asymptomatic humans at rest breathing room air

Cited by 63 publications

References 50 publications

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

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

How to follow-up patients with hereditary haemorrhagic telangiectasia and suspected pulmonary arteriovenous malformations

Childhood Stroke

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