Is Altered Oxygen-Transport The Mechanism For Increased Left-Ventricular Thickness In Passive Smoking Children

Active smoking, a risk factor for ischemic heart disease, causes marked changes in systemic oxygen transport. To determine the effects of chronic passive smoking (PS) on oxygen transport and myocardial oxygen demand, we examined the relationship of PS to both left ventricular (LV) wall thickness and red cell 2, 3 diphosphoglycerate (DPG). We studied 168 nonsmoking(NS) and 40 PS preadolescent twins (11.6 years old) by supine m-mode echocardiography and measured blood levels of DPG and thiocyanate (SCN). PS twins had a thicker ventricular septum(VS) (.67±.08 vs .64±.08 cm, p<.05) and LV posterior wall (LVPW) (.66±.09 vs .64±.07 cm, p<.05). M-mode increases occurred mainly in male PS twins (p<.001). LV radius/LVPW was lower in PS twins (3.36±.45 vs 3.56±.45, p<.05) and correlated with SCN, r=(−).37, p<.01. LV wall stress index was higher in PS twins (32.8±4.8 vs 31.0±5.2 torr, p<.05) and correlated with SCN, r=(+).31, p<.05. DPG was increased in twins whose mothers smoked >10 cigarettes/d (2.34±.25 vs 2.06±.26umol/ml, rp<.05). DPG correlated positively with VS(p<.005) and with LVPW(p<.001) and correlated negatively with LV radius/LVPW (p=.0001). We conclude that chronic PS twins have both increased LV wall thickness and wall stress which increase myocardial oxygen requirements. These changes occur mainly in males. Since twin DPG is increased in chronic PS, altered oxygen supply/demand may be the mechanism for the increased LV thickness and the subsequent development of ischemic heart disease.