Cazzola Mario, Hanania Nicola A, Rogliani Paola, Matera Maria Griella
Chair of Respiratory Medicine, Department of Experimental Medicine, University of Rome Tor Vergata, Rome, Italy.
Section of Pulmonary and Critical Care Medicine, Baylor College of Medicine, Houston, Texas, United States.
Kardiol Pol. 2023;81(3):232-241. doi: 10.33963/KP.a2023.0038. Epub 2023 Feb 5.
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, 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 systemic 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 provide benefits in patients with acute decompensated heart failure. Furthermore, inhaled corticosteroids may reduce the risk of atherosclerosis. On the other hand, asthma is not an absolute contraindication to using cardio-selective β1-blockers, but these medications should be prescribed with caution, especially if they are necessary to prevent 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.
心血管疾病（CVD）常与哮喘相关，哮喘患者发生CVD死亡的风险增加。我们对CVD和哮喘双向风险的理解基于多项观察性研究。然而，哮喘患者发生心血管合并症的具体发病机制尚未完全明确。哮喘患者的此类心血管并发症归因于哮喘和CVD中均存在的气道和全身炎症。事实上，有证据表明，哮喘患者的肺部以及CVD患者受损的心脏和血管中，肥大细胞、嗜酸性粒细胞、炎性细胞因子和免疫球蛋白E均会增加。这些发现表明，过敏性哮喘和CVD可能共享致病途径。了解这些途径对于药物干预的选择至关重要。目前，最合适的治疗方法是利用现有最佳证据优化哮喘和CVD的管理。应优化治疗，以利用每种药物对两个器官可能产生的有益作用，同时将对肺和心脏产生不良反应的可能性降至最低。值得注意的是，吸入性β2受体激动剂对急性失代偿性心力衰竭患者有益。此外，吸入性糖皮质激素可能降低动脉粥样硬化风险。另一方面，哮喘并非使用心脏选择性β1受体阻滞剂的绝对禁忌证，但开具这些药物时应谨慎，尤其是在预防急性心血管事件必要且没有其他替代治疗选择时。此外，当阿司匹林摄入引发超敏反应时，P2Y12抑制剂（如氯吡格雷、普拉格雷和替格瑞洛）是有效且安全的替代治疗药物。
