NEW ORLEANS, LA — An analysis from the Bogalusa Heart Study suggests childhood asthma is independently associated with increased left ventricular (LV) mass in adulthood, a well-established predictor of major CV events and death[1].
“The most important implication of this finding is that prevention and treatment of asthma in the early stages of life is very important to reduce the risk of heart disease in adulthood; that is the take-home message,” senior author Dr Lu Qi (Tulane University, New Orleans, LA and Harvard University School of Public Health, Boston, MA) told theheart.org|Medscape Cardiology.
The study was published online June 26, 2017 in the JACC: Heart Failure.
In an accompanying editorial[2], Dr John Gottdiener (University of Maryland Medical Center, Baltimore) observed that the difference in LV mass index between adults with a history of childhood asthma and nonasthmatics was only about 8%.
“Although this difference would by itself confer a relatively small incremental risk of incident CVD (about 1.08-fold increase) based on Framingham Heart Study data, in large populations with major comorbidities, the public-health implications could be substantial,” he said.
The incidence of asthma in children has nearly doubled since 1980, and its prevalence is estimated at nearly one in 10 children and 7% in adults, Gottdiener noted.
Despite this, the investigators point out that the number of studies specifically examining the relationship between asthma and LV hypertrophy or heart failure (HF) can be counted on one hand. The team was interested in examining HF but because of too few cases in the Bogalusa Heart Study, LV mass was used as a surrogate marker, Qi said.
The analysis, led by Dr Dianjianyi Sun (Tulane University), included 1118 asymptomatic individuals, of whom 104 self-reported childhood asthma and 1014 did not. The mean age at baseline was 27.5 and 32 years, respectively. LV measurements were performed using 2-D echocardiography during follow-up only (mean 10.4 years).
Childhood asthmatics compared with nonasthmatics had a significantly higher body-mass index (BMI) at last follow-up (31.5 vs 29.9 kg/m2), although smoking rates were similar (27.9% vs 30.4%).
Participants with a history of asthma compared with those without had a higher mean LV mass (169.0 g vs 157.5 g; P=0.01) and LV mass index (41.1 g/m2.7 vs 37.9 g/m2.7; P<0.01), even after adjustment for age, sex, race, smoking status, antihypertensive medication use, and heart rate.
Notably, a 1-unit increase in high-sensitivity C-reactive protein (hs-CRP) was significantly associated with a 1.40 and 0.40 increase in LV mass and LV mass index, respectively.
In the final model, however, that further adjusted for BMI, systolic blood pressure (SBP), and CRP, the difference between those with and without childhood asthma persisted for LV mass index (38.4 g/m2.7 vs 36.6 g/m2.7; P=0.04) but not LV mass.
“Inflammation is the primary potential mechanism that links these two diseases, but even after we adjusted for CRP, an inflammatory marker, it didn’t completely eliminate the association, which suggests that other mechanisms could be involved,” Qi said.
In addition, the investigators observed a significant interaction between SBP and asthma on both LV outcomes in stratified analyses (P for interaction <0.01). The association was stronger among participants with prehypertension or hypertension (>130 mm Hg) than those with normal SBP (regression coefficient [ß]: 39.5 vs 2.2 for LV mass and 9.0 vs 0.9 for LV mass index).
“High blood pressure is a well-known risk factor for heart failure and high left ventricular mass, and our study suggests that asthma and high blood pressure may walk together to increase the risk of heart failure,” Qi said.
Gottdiener noted that “targeting individuals with asthma and hypertension or prehypertension for intensified risk reduction could have important benefits.”
Still, the study leaves several questions unanswered, he said. Because of the lack of baseline echocardiograms, it’s possible participants could have had increasing LV mass prior to asthma onset. The current data also do not “exclude the possibility that asthma is a comorbidity of CVD and perhaps is a fellow traveler with CVD severity rather than being a cause of CVD.”
Finally, it is unknown whether LV mass was associated with asthma severity and the frequency of corticosteroid or beta-agonist use, “important information for selecting individuals who are at the highest risk,” Gottdiener added.
The study was supported by grants from the National Heart, Lung, and Blood Institute, National Institute of Diabetes and Digestive and Kidney Diseases, the Boston Obesity Nutrition Research Center, and United States-Israel Binational Science Foundation. Qi reports receiving the American Heart Association Scientist Development Award. The coauthors have no relevant financial relationships, nor does Gottdiener.
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