Abraham Kenney, Key Phillip, Pelletier Matthew C, Heslin Ryan
Internal Medicine, Stony Brook University Hospital, Stony Brook, USA.
Cardiology, Stony Brook University Hospital, Stony Brook, USA.
Cureus. 2025 Apr 29;17(4):e83183. doi: 10.7759/cureus.83183. eCollection 2025 Apr.
Viral infections may lead to myocarditis, which is inflammation of the myocardium. This inflammation, when severe enough, can result in left ventricular dysfunction and potentially reduce the left ventricular ejection fraction (LVEF). In rare cases, the effects of this inflammation lead to hemodynamic changes that can be life-threatening. We discuss a case of a 38-year-old female recently diagnosed with influenza A (H3 subtype) who presented to our institution's emergency department for evaluation after an episode of syncope, as well as intermittent chest pressure and dyspnea on exertion. Initial vitals displayed a heart rate of 87 bpm and blood pressure of 105/66 mmHg. The physical examination demonstrated a regular rhythm, no lower extremity edema, and lungs that were clear to auscultation. She was found to have an elevated pro-B-type natriuretic peptide level of 6152 pg/mL and a positive influenza A polymerase chain reaction (PCR) test. A transthoracic echocardiogram (TTE) was obtained and demonstrated globally reduced left ventricular systolic function with an estimated ejection fraction of 28%, as well as reduced right ventricular systolic function. Over the next six hours, the patient became progressively tachycardic and hypotensive, with a heart rate of 135 bpm and a blood pressure measured at 46/28 mmHg. She was initially admitted to the cardiovascular ICU and started on dobutamine and vasopressin. Pulmonary artery catheterization was completed for better evaluation of cardiogenic shock, and it demonstrated a severely reduced cardiac index of 0.9 L/min/m. Due to concerns of worsening cardiogenic shock and impending circulatory collapse, mechanical circulatory support was initiated via veno-arterial extracorporeal membrane oxygenation (VA-ECMO), and she was admitted to the cardiothoracic surgery ICU. Several days later, a biventricular assist device (BiVAD) was implanted with the goal of discontinuing ECMO as a bridge to transplant. Shortly afterwards, a repeat echocardiogram demonstrated a normalized left and right ventricular systolic function, and the BiVAD was removed. Ten days after the initiation of ECMO, it was able to be discontinued, and the patient was decannulated. The patient was discharged home in stable condition. This case exemplifies how fulminant myocarditis (FM) can have positive outcomes, even in critically ill patients, when the timing of intervention is early and aggressive.
病毒感染可能导致心肌炎，即心肌的炎症。这种炎症如果严重到一定程度，可导致左心室功能障碍，并可能降低左心室射血分数（LVEF）。在罕见情况下，这种炎症的影响会导致危及生命的血流动力学变化。我们讨论一例38岁女性病例，该患者最近被诊断为甲型流感（H3亚型），在一次晕厥发作以及间歇性胸痛和劳力性呼吸困难后到我院急诊科就诊。初始生命体征显示心率87次/分，血压105/66 mmHg。体格检查显示心律规整，无下肢水肿，肺部听诊清晰。发现她的B型利钠肽前体水平升高至6152 pg/mL，甲型流感聚合酶链反应（PCR）检测呈阳性。进行了经胸超声心动图（TTE）检查，结果显示左心室整体收缩功能降低，估计射血分数为28%，右心室收缩功能也降低。在接下来的6小时内，患者心率逐渐加快且血压降低，心率达135次/分，血压测量为46/28 mmHg。她最初被收入心血管重症监护病房，并开始使用多巴酚丁胺和血管加压素。为更好地评估心源性休克完成了肺动脉导管插入术，结果显示心脏指数严重降低至0.9 L/（min·m）。由于担心心源性休克恶化和即将发生循环衰竭，通过静脉-动脉体外膜肺氧合（VA-ECMO）启动了机械循环支持，并将她收入心胸外科重症监护病房。几天后，植入了双心室辅助装置（BiVAD），目的是停用ECMO作为移植的桥梁。此后不久，复查超声心动图显示左、右心室收缩功能恢复正常，BiVAD被移除。ECMO启动10天后，能够停用，患者拔除插管。患者病情稳定后出院回家。该病例表明，即使是危重症患者，暴发性心肌炎（FM）如果干预时机早且积极，也可获得良好预后。
