Patients with severe allergic asthma demonstrate subclinical systolic heart dysfunction of both the left and right ventricles on ultrasound-based speckle-tracking analysis, according to a new study published in the Journal of Asthma.
“In our work, severe asthma was characterized by a relevant airway obstruction measured in the pulmonary function test compared to control,” wrote the authors, led by Izabela Tuleta, MD, PhD, Department of Internal Medicine II—Cardiology, Pulmonology and Angiology, University of Bonn, Germany. The team used results from lung function and sensitization tests to confirm allergic asthma.
Experts know little about the relationship between asthma and heart disease, and researchers have yet to identify the relationship between allergy and heart disease. In the current study, Dr. Tuleta and colleagues assessed heart function in patients with allergic asthma using the following tools:
- Standard echocardiography for measures such as left ventricular ejection fraction (LVEF)
- Tricuspid annular plane systolic excursion (TAPSE) for right ventricle systolic function
- Ultrasound-based speckle-tracking analysis for early, subclinical signs of heart failure
In addition, the investigators looked at inflammation-associated serum biomarkers including NT-pro-brain natriuretic peptide (NT-pro-BNP), immunoglobulin E (IgE), C-reactive protein (CRP), and blood count.
The team assessed these measures in 72 adult patients with either mild-to-moderate allergic asthma or severe asthma, as well as 20 controls matched for age, sex, BMI, cardiovascular risk factors, and cardiovascular disease.
The researchers divided patients into the following four therapeutic subgroups:
- Subgroup 1a: long-acting beta2-agonists (LABA) and inhaled cortisone without oral cortisone treatment with additional omalizumab therapy (n=27);
- Subgroup 1b: LABA and inhaled cortisone without oral cortisone treatment without additional omalizumab therapy (n=21);
- Subgroup 2a: LABA, inhaled cortisone, and omalizumab treatment with oral cortisone (n=12);
- Subgroup 2b: LABA, inhaled cortisone, and omalizumab treatment without oral cortisone (n=27).
Patients in subgroups 1a, 2a, and 2b had severe asthma, whereas patients in subgroup 1b had mild-to-moderate asthma.
The authors found that longitudinal left ventricular strain values were significantly decreased in patients with severe asthma (–12.91 ± 0.84%) and mild-to-moderate asthma (–13.92 ± 1.55%). Moreover, patients with severe asthma experienced decreased longitudinal right ventricular strain compared with the controls.
Subgroups 1a and 1b exhibited comparable cardiac strains. Furthermore, patients in subgroup 2a exhibited decreased heart strains and reduced lung function compared with those measures of patients in subgroup 2b.
Finally, patients with asthma were found to have higher levels of CRP, IgE, and eosinophils when compared with controls.
“The reason for higher coexistence of asthma and heart dysfunction is probably multifactorial,” the investigators wrote. “In our study, we have detected an elevated inflammatory level in blood with increased CRP, IgE, and eosinophils in asthma individuals and a higher absolute leukocyte number in severe asthma patients compared to the control ones.”
Dr. Tuleta and colleagues were unable to ascertain the effect of antiasthmatic treatment on heart function, which has yet to be identified in the literature.
“Severe allergic asthma was associated with an increased occurrence of subclinical biventricular heart dysfunction measured by reduced cardiac strain,” the researchers concluded. “Decreased lung function, enhanced systemic inflammation, and possibly administration of oral cortisone seem to be the underlying pathomechanisms.”
Consequently, they suggest that screening with echocardiography—including utilization of the speck-tracking method—could identify asthma patients who are predisposed to developing heart failure.
To read more about this study, click here.