Vaccination for Respiratory Infections in Patients with Heart Failure

Abstract

Bronchopulmonary infections are a major trigger of cardiac decompensation and are frequently associated with hospitalizations in patients with heart failure (HF). Adverse cardiac effects associated with respiratory infections, more specifically Streptococcus pneumoniae and influenza infections, are the consequence of inflammatory processes and thrombotic events. For both influenza and pneumococcal vaccinations, large multicenter randomized clinical trials are needed to evaluate their efficacy in preventing cardiovascular events, especially in HF patients. No study to date has evaluated the protective effect of the COVID-19 vaccine in patients with HF. Different guidelines recommend annual influenza vaccination for patients with established cardiovascular disease and also recommend pneumococcal vaccination in patients with HF. The Heart Failure group of the French Society of Cardiology recently strongly recommended vaccination against COVID-19 in HF patients. Nevertheless, the implementation of vaccination recommendations against respiratory infections in HF patients remains suboptimal. This suggests that a national health policy is needed to improve vaccination coverage, involving not only the general practitioner, but also other health providers, such as cardiologists, nurses, and pharmacists. This review first summarizes the pathophysiology of the interrelationships between inflammation, infection, and HF. Then, we describe the current clinical knowledge concerning the protective effect of vaccines against respiratory diseases (influenza, pneumococcal infection, and COVID-19) in patients with HF and finally we propose how vaccination coverage could be improved in these patients.

Keywords: COVID-19 vaccine; heart failure; influenza vaccine; pneumococcal vaccine; respiratory infections; review article; vaccination coverage.

Figure 1

The mechanisms of the adverse effects of infection on heart failure.

Figure 2

Schematic representation of thrombosis (adapted from Iba et al. [12]). Tissue factor (TF) is the pivotal initiator of the extrinsic pathway of cascade coagulation. In infection/inflammation, TF is expressed on monocytes, endothelial cells, activated platelets, and leucocytes. TF containing microparticles (MPs), mainly neutrophil- and platelet-derived MPs, represent the major source of circulating TF in plasma. NETosis occurs after stimulation of neutrophils by pathogens, activated platelets, and pro-inflammatory cytokines. NETs (neutrophil extracellular traps) are networks mainly constituted of DNA and histones that bind to pathogens and promote both the intrinsic and extrinsic coagulation pathways through the activity of serine proteases (elastase, cathepsin G) presents on NETs: serine proteases inhibit TFPI (tissue factor pathway Inhibitor), promoting TF and FXII-dependent coagulation. NETs also bind directly FXII and, in cooperation with platelets, support its activation to FXIIa leading to direct activation of the intrinsic pathway of coagulation.