Cardiovascular disease (CVD) is often associated with asthma, and asthma patients have an increased risk of CVD mortality. Our understanding of the bidirectional risk of CVD and asthma has been based on several observational studies. However, the specific pathogenetic mechanisms underlying the development of cardiovascular comorbidities in patients with asthma have not yet been fully determined.  Such cardiovascular complications in patients with asthma have been attributed to airway and system inflammation present in both asthma and CVD. Indeed, there is evidence that mast cells, eosinophils, inflammatory cytokines, and immunoglobulin E increase in both lungs of patients with asthma, and in injured heart and vessels of CVD patients. These findings suggest that allergic asthma and CVD may share pathogenic pathways. Understanding these pathways is critical to the choice of pharmacological interventions. Currently, the most appropriate therapeutic approach lies in using the best available evidence to optimize the management of both asthma and CVD. Therapy should be optimized to take advantage of the favorable benefits that each medication may have on both organs while minimizing the likelihood of adverse effects on the lungs and heart. It is noteworthy that inhaled β₂-agonists induce benefit in patients with acute decompensated heart failure. Furthermore, ICSs may reduce the risk of atherosclerosis. On the other side, asthma is not an absolute contraindication to use cardio-selective β₁-blockers, but these medications should be prescribed with caution especially if are necessary for acute cardiovascular events and alternative treatment options are unavailable. In addition, when aspirin intake causes the onset of hypersensitivity, P2Y₁₂ inhibitors (e.g., clopidogrel, prasugrel, and ticagrelor) are effective and safe treatment alternatives.