Beyond respiratory distress: The impact of H1N1 influenza on circulatory failure

Abstract

We are writing to discuss the occasionally severe clinical course of patients infected with the H1N1 influenza virus, which can cause respiratory failure and severe acute respiratory distress syndrome (ARDS), requiring venovenous extracorporeal membrane oxygenation (ECMO).¹ However, it can also result in severe cardiovascular complications like fulminant myocarditis and secondary circulatory failure. We encountered two cases requiring venoarterial ECMO due to secondary cardiovascular complications. Informed consent was obtained from the patients' families.

A 74-year-old woman with diabetes and valvular heart disease presented in early December 2024 with fever, followed by chest pain. She was diagnosed with influenza A (H1N1) pdm09 and type 2 myocardial infarction due to an ischemic supply–demand mismatch triggered by influenza infection. On admission, her Glasgow Coma Scale (GCS) score was E3V4M6, temperature 37.9°C, heart rate 117 beats/min, blood pressure 121/72 mmHg, respiratory rate 24 breaths/min, and oxygen saturation (SpO₂) 93% on 6 L of oxygen. She reported moderate chest pain, with no other significant abnormalities. Electrocardiography showed extensive ischemic patterns, and echocardiography revealed mild wall motion abnormalities in the anterior septum and apex. Antiviral therapy was initiated, and percutaneous coronary intervention (PCI) was planned. On Day 2, she developed ventricular fibrillation and underwent emergency extracorporeal cardiopulmonary resuscitation. PCI for triple vessel disease improved circulation, but worsening respiratory status necessitated venovenous ECMO. However, her respiratory condition did not improve due to secondary bacterial pneumonia, making ECMO weaning difficult. Despite prolonged ECMO support, she passed away on Day 53.

A 49-year-old woman with no significant medical history experienced fever and dyspnea 3 days before admission. Symptoms worsened on the admission day, leading to severe mobility difficulties and an emergency call. On admission, GCS score was E1V1M4, temperature 39.0°C, heart rate 180 beats/min (atrial fibrillation), blood pressure 100/70 mmHg, respiratory rate 32 breaths/min, and SpO₂ 90% on 10 L of oxygen. Tests showed severe metabolic acidosis (pH, 7.19; base excess, −1.7 mmol/L), elevated thyroid stimulating hormone levels (<0.01 μIU/mL), free triiodothyronine (16.2 pg/mL), and free thyroxine (5.28 ng/dL). Echocardiography showed diffuse severe wall motion abnormalities with a left ventricular ejection fraction of 10%. The patient was diagnosed with acute heart failure (AHF) due to thyroid storm triggered by influenza A (H1N1) pdm09 infection, and venoarterial ECMO was initiated for circulatory failure. Treatments included antivirals, methimazole, and potassium iodide. On Day 2, diuresis improved and cardiac function gradually recovered. The patient was successfully weaned from VA-ECMO on Day 7 and subsequently discharged in a stable condition.

H1N1 influenza infection can trigger acute cardiovascular events, including acute coronary syndrome (ACS) and AHF, particularly in individuals with pre-existing conditions.^{2, 3} Inflammation and hypoxia from H1N1 infection can exacerbate endothelial dysfunction and promote thrombogenesis. Additionally, physiological stress induced by H1N1 infection can exacerbate underlying conditions, as demonstrated in our thyroid storm case.⁴ This severe hypermetabolic state strains the cardiovascular system and may cause AHF. During the H1N1 pandemic, recognizing the risk of dual-organ failure, such as respiratory failure, including ARDS, and circulatory failure from fulminant myocarditis or secondary ACS, is critical. Given the severity and complexity of these complications, nationwide surveys are urgently needed to clarify and address the full impact of H1N1 on the respiratory and cardiovascular systems.

The authors declare no conflicts of interest.

Approval of the research protocol: N/A.

Informed consent: Informed consent was obtained from the patients' family members to report the cases.

Registry and the registration no. of the study/trial: N/A.

Animal studies: N/A.