Why the study?
Severe asthma and cardiovascular disease can coexist, mimic one another, and interact through respiratory mechanics and treatment, with important implications for intensive care.
Population
Patients with severe asthma and cardiovascular involvement in intensive care
Design
Narrative review
Answers are grounded in this paper and cite their sources.
May support integrated hemodynamic monitoring in severe asthma ICU care; leaves open prospective validation of outcome benefit.
Background: Severe asthma and cardiovascular disease can coexist, mimic one another, and interact through respiratory mechanics and treatment. This narrative review examines these relationships and their implications for intensive care. Main findings: Conventional and tissue Doppler studies identified cardiac abnormalities in asthma before widespread use of speckle tracking in this field. Subsequent deformation studies include predominantly pediatric or non-ICU populations, alongside limited adult acute severe-asthma evidence. Their findings are heterogeneous and largely observational. During exacerbations, dynamic hyperinflation, intrinsic positive end-expiratory pressure, pleural-pressure swings, right-ventricular loading, ventricular interdependence, gas-exchange abnormalities, adrenergic stimulation, and ventilation may alter filling and forward flow without primary cardiomyopathy. Conversely, heart failure with preserved ejection fraction can present with wheezing, but neither B-lines nor an isolated echocardiographic filling index establishes that diagnosis. Four ICU scenarios illustrate low flow despite high ejection fraction, post-intubation shock, congestion with preserved ejection fraction, and arrhythmia with transient dysfunction. Strain may help characterize serial changes but is load dependent; its incremental clinical value in adult ICU asthma remains unestablished. Systemic inflammatory and catecholaminergic pathways may contribute to myocardial vulnerability. Associations involving allergic inflammation and biologic exposure are hypothesis-generating, and do not demonstrate endotype-specific myocardial injury or cardioprotection. Systemic corticosteroids and biologics require separate consideration of respiratory benefit and cardiovascular effects. Conclusions: Severe asthma can be viewed as an unplanned cardiovascular stress test. Integrated assessment of respiratory mechanics, perfusion, rhythm, congestion, and cardiac function should guide care. Persistent abnormalities warrant reassessment for alternative or coexisting disease rather than an automatic diagnosis of asthma-related cardiomyopathy.
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Hidalgo-Martín et al. (2026) studied this question.
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