Increased aortic stiffness and elevated blood pressure in response to exercise in adult survivors of prematurity.

OBJECTIVES: Adults born prematurely have an increased risk of early heart failure. The impact of prematurity on left and right ventricular function has been well documented, but little is known about the impact on the systemic vasculature. The goals of this study were to measure aortic stiffness and the blood pressure response to physiological stressors; in particular, normoxic and hypoxic exercise. METHODS: Preterm participants (n = 10) were recruited from the Newborn Lung Project Cohort and matched with term-born, age-matched subjects (n = 12). Aortic pulse wave velocity was derived from the brachial arterial waveform and the heart rate and blood pressure responses to incremental exercise in normoxia (21% O2 ) or hypoxia (12% O2 ) were evaluated. RESULTS: Aortic pulse wave velocity was higher in the preterm groups. Additionally, heart rate, systolic blood pressure, and pulse pressure were higher throughout the normoxic exercise bout, consistent with higher conduit artery stiffness. Hypoxic exercise caused a decline in diastolic pressure in this group, but not in term-born controls. CONCLUSIONS: In this first report of the blood pressure response to exercise in adults born prematurely, we found exercise-induced hypertension relative to a term-born control group that is associated with increased large artery stiffness. These experiments performed in hypoxia reveal abnormalities in vascular function in adult survivors of prematurity that may further deteriorate as this population ages.

Inspiratory and expiratory resistance cause right-to-left bubble passage through the foramen ovale.

A patent foramen ovale (PFO) is linked to increased risk of decompression illness in divers. One theory is that venous gas emboli crossing the PFO can be minimized by avoiding lifting, straining and Valsalva maneuvers. Alternatively, we hypothesized that mild increases in external inspiratory and expiratory resistance, similar to that provided by a SCUBA regulator, recruit the PFO. Nine healthy adults with a Valsalva-proven PFO completed three randomized trials (inspiratory, expiratory, and combined external loading) with six levels of increasing external resistance (2-20 cmH2 O/L/sec). An agitated saline contrast echocardiogram was performed at each level to determine foramen ovale patency. Contrary to our hypothesis, there was no relationship between the number of subjects recruiting their PFO and the level of external resistance. In fact, at least 50% of participants recruited their PFO during 14 of 18 trials and there was no difference between the combined inspiratory, expiratory, or combined external resistance trials (P > 0.05). We further examined the relationship between PFO recruitment and intrathoracic pressure, estimated from esophageal pressure. Esophageal pressure was not different between participants with and without a recruited PFO. Intrasubject variability was the most important predictor of PFO patency, suggesting that some individuals are more likely to recruit their PFO in the face of even mild external resistance. Right-to-left bubble passage through the PFO occurs in conditions that are physiologically relevant to divers. Transthoracic echocardiography with mild external breathing resistance may be a tool to identify divers that are at risk of PFO-related decompression illness.

Effect of body position and oxygen tension on foramen ovale recruitment.

While there is an increased prevalence of stroke at altitude in individuals who are considered to be low risk for thrombotic events, it is uncertain how venous thrombi reach the brain. The patent foramen ovale (PFO) is a recruitable intracardiac shunt between the right and left atrium. We aimed to determine whether body position and oxygen tension affect blood flow through the PFO in healthy adults. We hypothesized that hypoxia and body positions that promote right atrial filling would independently recruit the PFO. Subjects with a PFO (n = 11) performed 11 trials, combining four different fractions of inhaled oxygen (FiO2) (1.0, 0.21, 0.15, and 0.10) and three positions (upright, supine, and 45° head down), with the exception of FiO2 = 0.10, while 45° head down. After 5 min in each position, breathing the prescribed oxygen tension, saline bubbles were injected into an antecubital vein and a four-chamber echocardiogram was obtained to evaluate PFO recruitment. We observed a high incidence of PFO recruitment in all conditions, with increased recruitment in response to severe hypoxia and some contribution of body position at moderate levels of hypoxia. We suspect that increased pulmonary vascular pressure, secondary to hypoxia-induced pulmonary vasoconstriction, increased right atrial pressure enough to recruit the PFO. Additionally, we hypothesize that the minor increase in breathing resistance that was added by the mouthpiece, used during experimental trials, affected intrathoracic pressure and venous return sufficiently to recruit the PFO.