Cardiovascular Stress Hyperreactivity in Babies of Smokers and in Babies Born Preterm

Abstract

Background-Being born preterm, small, and to a mother who smokes are common perinatal complications with major public health implications. Evidence suggests that each affects the body's structure and function in ways that could increase susceptibility to cardiovascular dysfunction later in life. Here, we used 2 routine stress reactivity tests to identify incipient "silent" programming of cardiovascular dysfunction associated with adverse perinatal events. Methods and Results-We studied 29 control babies born at term to nonsmokers, 18 term-born babies of mothers who smoked throughout pregnancy (mean, 15 cigarettes a day), and 31 babies born preterm to nonsmokers. All infants were compared at the same age after conception (ie, at 40 to 42 weeks), during sleep. We analyzed blood pressure (BP) and heart rate responses to breathing 4% CO 2 for 4 minutes or to passive head-up tilt to 60°. BP was measured continuously from a wrist cuff. CO 2 exposure raised heart rate and BP in controls by 10%, and tilt increased their BP by 5%. CO 2 elicited the expected BP but no heart rate response from preterm infants but a much-greater-than-expected BP and heart rate response from babies of smokers. Tilt elicited a 3-to 4-fold greater rise in BP from preterm and tobacco-exposed babies. Conclusions-Vascular, cardiac, and blood pressure reactivity is heightened in babies born preterm or to smokers. The findings are consistent with in utero and early postnatal "programming" of human cardiovascular dysfunction by adverse circumstances. This incipient dysfunction may be an early manifestation of processes that lead to other problems or complications later on (eg, higher BP or sudden infant death syndrome).

Early life exposure to air pollution induces adult cardiac dysfunction

“…This was confirmed in controlled animal studies where exposure to PAH altered placental vasculature, increased apoptotic markers during gestation, and reduced survival of resultant adult mice (11). Prenatal exposure to environmental sidestream tobacco smoke has also been shown to increase atherogenesis, superoxide dismutase activity, and mitochondrial damage in the heart tissue of mice (48), as well as increase blood pressure reactivity in humans (8).…”

Long-Term Reprogramming of Cardiovascular Function in Infants of Active Smokers

“…1 Because sympathetic overreactivity and autonomic dysfunction more generally are involved in the initiation and progression of disease, [2][3][4][5] we undertook a 1-year follow-up study to track the natural history and to assess the likely impact of the incipient hyperreactivity seen in a smoker's newborn infant.…”

Relationship of Maternal Snuff Use and Cigarette Smoking With Neonatal Apnea

“…[23][24][25] Preterm infants and infants prenatally exposed to nicotine reveal similar disturbances in the neural control of the cardiorespiratory system, with a heightened vascular, cardiac, and blood pressure reactivity. 26 This finding represents an effect of immaturity in the premature infant and a developmental programming effect of a neurotoxic substance, nicotine, in the nicotine-exposed infant. Activation of nicotinic acetylcholine receptors during vulnerable periods of prenatal development may lead to changes in the cellular programming.…”

“…Both epidemiologic studies and animal studies indicate different early and long-term effects of prenatal nicotine exposure. 26,31 In our study, however, we were only assessing the early effects of prenatal nicotine exposure on the infant.…”