# Cardiovascular Complications of Seasonal Influenza in the Pre- and Post-COVID-19 Era: Epidemiology, Mechanisms, and Clinical Implications

**Authors:** Chikodili Nora Nebuwa, Chukwudi Kingsley Orjichukwu, Rita Ogochukwu Orjichukwu, Peter Kanayochukwu Akpunonu, Paul Chikwado Ugwu, Somtochukwu Godfrey Nnabuife

PMC · DOI: 10.3390/medsci14010057 · Medical Sciences · 2026-01-23

## TL;DR

This paper reviews how seasonal influenza affects heart health before and after the COVID-19 pandemic, highlighting shared risks and the need for better prevention strategies.

## Contribution

The paper introduces a comparative analysis of influenza-related cardiovascular complications in the pre- and post-COVID-19 eras.

## Key findings

- Both influenza and COVID-19 worsen endothelial dysfunction and increase cardiovascular risk.
- The pandemic altered influenza transmission and cardiac complication trends.
- Integrated vaccination strategies may reduce virus-triggered heart disease.

## Abstract

Influenza has long been a well-documented contributor to cardiovascular morbidity and mortality, particularly among high-risk groups. COVID-19 has notably altered the seasonality and natural history of pandemic influenza, with broad implications for related cardiac complications. This review examines the interaction between influenza and cardiovascular illness, especially myocardial infarction, congestive heart failure, stroke, and other acute cardiac events. We review the impact of the COVID-19 pandemic on influenza transmission dynamics, public health policy, and the evolving burden of cardiovascular complications. New evidence indicates that both diseases exacerbate endothelial dysfunction, systemic inflammation, and prothrombotic states, thereby increasing cardiovascular risk. A comparative analysis of pre- and post-COVID-19 influenza-related cardiac complications clarifies evolving trends and guides future preventive strategies. In light of the recent resurgence of influenza following the relaxation of COVID-19 mitigation measures, maximizing vaccine coverage and collaborating to manage viral infections in patients with cardiovascular disease are critical. This review focuses on key research needs to understand long-term cardiac consequences and the urgent requirement for targeted public health strategies to counter viral-mediated cardiovascular threats. In the post-COVID era, integrating influenza and COVID-19 vaccination strategies into cardiovascular risk management may represent a critical opportunity to reduce virus-triggered cardiovascular morbidity and mortality.

## Linked entities

- **Diseases:** influenza (MONDO:0005812), myocardial infarction (MONDO:0005068), congestive heart failure (MONDO:0005009), stroke (MONDO:0005098), COVID-19 (MONDO:0100096)

## Full-text entities

- **Genes:** ACE2 (angiotensin converting enzyme 2) [NCBI Gene 59272] {aka ACEH}, F2 (coagulation factor II, thrombin) [NCBI Gene 2147] {aka PT, RPRGL2, THPH1}, GP6 (glycoprotein VI platelet) [NCBI Gene 51206] {aka BDPLT11, GPIV, GPVI}, PROC (protein C, inactivator of coagulation factors Va and VIIIa) [NCBI Gene 5624] {aka APC, PC, PROC1, THPH3, THPH4}, VWF (von Willebrand factor) [NCBI Gene 7450] {aka F8VWF, VWD}, KLK4 (kallikrein related peptidase 4) [NCBI Gene 9622] {aka AI2A1, ARM1, EMSP, EMSP1, KLK-L1, PRSS17}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, SERPINC1 (serpin family C member 1) [NCBI Gene 462] {aka AT3, AT3D, ATIII, ATIII-R2, ATIII-T1, ATIII-T2}, GP1BA (glycoprotein Ib platelet subunit alpha) [NCBI Gene 2811] {aka BDPLT1, BDPLT3, BSS, CD42B, CD42b-alpha, DBPLT3}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, FGB (fibrinogen beta chain) [NCBI Gene 2244] {aka HEL-S-78p}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207] {aka AKT, PKB, PKB-ALPHA, PRKBA, RAC, RAC-ALPHA}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}
- **Diseases:** myocardial tissue damage (MESH:D017695), long-term effects of the illness (MESH:D000069451), endothelial (MESH:D005642), damage (MESH:D020263), hypoxia (MESH:D000860), autonomic (MESH:D001342), infectious disease (MESH:D003141), anaphylaxis (MESH:D000707), SARS (MESH:D045169), COVID-19 long-term (MESH:D000094024), cardiovascular abnormalities (MESH:D018376), micro- and macrovascular thrombosis (MESH:C536681), immune dysregulation (OMIM:614878), PE (MESH:D011655), necrosis (MESH:D009336), acute illness (MESH:D000208), coronary thrombosis (MESH:D003328), fever (MESH:D005334), myopathy (MESH:D009135), fatigue (MESH:D005221), Thromboembolic Events (MESH:D013923), chest pain (MESH:D002637), Myocardial Injury (MESH:D009202), sudden cardiac death (MESH:D016757), Heart Disease (MESH:D006331), coronary artery blockade (MESH:D003324), Hypercoagulable States (MESH:D019851), cerebral thrombosis (MESH:D020767), Myocarditis (MESH:D009205), systemic (MESH:D015619), Stroke (MESH:D020521), cytokine storm (MESH:D000080424), left ventricular dysfunction (MESH:D018487), respiratory deaths (MESH:D012131), immunothrombosis (MESH:D000090882), obesity (MESH:D009765), hypoxic (MESH:D002534), calcium (MESH:D002128), tachycardia (MESH:D013610), arrhythmia (MESH:D001145), congestive heart failure (MESH:D006333), multi-organ injury (MESH:D009102), infarct (MESH:D007238), cough (MESH:D003371), endothelial injury (MESH:D057772), myocardial involvement (MESH:C564676), DVT (MESH:D020246), myocardial invasion (MESH:D060585), coronary artery occlusion (MESH:D054059), Health (OMIM:603663), ventricular dysfunction (MESH:D018754), dilated cardiomyopathy (MESH:D002311), and arterial (MESH:D012078), infected (MESH:D007239), cardiogenic shock (MESH:D012770), Cardiovascular sequelae (MESH:D002318), coagulation (MESH:D001778), dyspnea (MESH:D004417), AMI (MESH:D009203), oedema (MESH:C536897)
- **Chemicals:** nitric oxide (MESH:D009569), calcium (MESH:D002118), water (MESH:D014867), aspirin (MESH:D001241), oseltamivir (MESH:D053139), ticagrelor (MESH:D000077486), oxygen (MESH:D010100), neuraminidase inhibitors (-), clopidogrel (MESH:D000077144)
- **Species:** H1N1 subtype (serotype) [taxon 114727], H5N1 subtype (serotype) [taxon 102793], Gammacoronavirus (genus) [taxon 694013], Severe acute respiratory syndrome coronavirus 2 (no rank) [taxon 2697049], Homo sapiens (human, species) [taxon 9606], Orthomyxoviridae (family) [taxon 11308], Respiratory syncytial virus (no rank) [taxon 12814]

## Full text

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## Figures

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## References

99 references — full list in the complete paper: https://tomesphere.com/paper/PMC12921884/full.md

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Source: https://tomesphere.com/paper/PMC12921884