Influenza B-Induced Refractory Cardiogenic Shock
During the 1918–1919 influenza pandemic an association between myocarditis and influenza viruses was noted during an autopsy study. While there have been reports of fulminant myocarditis or cardiomyopathy associated with influenza B in children, it has very rarely been reported in adults. In 1958, a group of four patients with pericarditis, subacute myocarditis, and fatal chronic myocarditis associated with influenza B were documented. Ray CG et al. described a 34-year-old healthy woman who presented with acute onset of dilated cardiomyopathy and cardiogenic shock following a few days of flu like syndrome. She had a very complicated course and died 6 weeks after the onset of symptoms. Influenza B virus was isolated from the nasopharynx and the diagnosis of acute myocarditis was confirmed by cardiac autopsy.
McCarthy et al. described fulminant myocarditis as a distinct clinical presentation of abrupt onset of severe heart failure and cardiogenic shock preceded by a viral syndrome similar to our patient. The typical echocardiographic findings in fulminant myocarditis are described as near normal ventricular dimensions, severely depressed LV systolic function, and increased left ventricle wall thickness. Histological diagnosis of fulminant myocarditis can be difficult especially in the early phase of disease. The limited sensitivity of cardiac biopsy for detection of myocarditis is well recognized and negative cardiac biopsies results cannot exclude the diagnosis of myocarditis. Myocarditis usually presents as a focal or patchy infiltration predominantly in the lateral free wall of the left ventricle and often not involving the right ventricle, therefore, biopsies taken from the right ventricle could be falsely negative.
This patient's clinical presentation of refractory cardiogenic shock 6 days after the onset of influenza and severely impaired left ventricular systolic function, and subsequent normalization of ventricular function after recovery of her viral illness; taken together with her typical echocardiogram findings in the setting of normal coronaries supports the clinical diagnosis of viral fulminant myocarditis; regardless of non diagnostic right ventricle biopsies. During influenza infection, severe myocardial dysfunction can be caused not only by direct injury to cardiac myocytes but also by overexpression of cytokines and severe inflammatory response to viral infection resulting cytokine and humoral mediated forms of myocarditis with no cellular infiltrate.
The reason for the unexpected severity of influenza B infection in our patient was not clear. Clinical data about risk factors and complications of influenza B are limited. Her only past medical history was remote myasthenia gravis and thymectomy over 20 years prior. The predominant circulating B strain was B/Wisconsin/1/2010- LIKE when the patient presented to the hospital, which was matched with the B component of the 2012–2013 vaccine. We do not know if the patient had received an influenza vaccine this season. The possible lack of immunologic memory for this infection might have contributed to the severity of influenza B virus infection in our patient. Increasing awareness among patients and physicians about the importance of vaccination as the most important strategy for minimizing the severe complications of influenza infection could help to prevent similar cases in the future.
The treatment of influenza associated fulminant myocarditis still remains supportive. Studies have shown the early use of mechanical circulatory support for patients with fulminant myocarditis and cardiogenic shock who fail aggressive pharmacologic treatment would increase survival rate. Our patient received oseltamivir, standard heart failure treatment but more important early initiation of ECMO support before irreversible organ failure developed.
Discussion
During the 1918–1919 influenza pandemic an association between myocarditis and influenza viruses was noted during an autopsy study. While there have been reports of fulminant myocarditis or cardiomyopathy associated with influenza B in children, it has very rarely been reported in adults. In 1958, a group of four patients with pericarditis, subacute myocarditis, and fatal chronic myocarditis associated with influenza B were documented. Ray CG et al. described a 34-year-old healthy woman who presented with acute onset of dilated cardiomyopathy and cardiogenic shock following a few days of flu like syndrome. She had a very complicated course and died 6 weeks after the onset of symptoms. Influenza B virus was isolated from the nasopharynx and the diagnosis of acute myocarditis was confirmed by cardiac autopsy.
McCarthy et al. described fulminant myocarditis as a distinct clinical presentation of abrupt onset of severe heart failure and cardiogenic shock preceded by a viral syndrome similar to our patient. The typical echocardiographic findings in fulminant myocarditis are described as near normal ventricular dimensions, severely depressed LV systolic function, and increased left ventricle wall thickness. Histological diagnosis of fulminant myocarditis can be difficult especially in the early phase of disease. The limited sensitivity of cardiac biopsy for detection of myocarditis is well recognized and negative cardiac biopsies results cannot exclude the diagnosis of myocarditis. Myocarditis usually presents as a focal or patchy infiltration predominantly in the lateral free wall of the left ventricle and often not involving the right ventricle, therefore, biopsies taken from the right ventricle could be falsely negative.
This patient's clinical presentation of refractory cardiogenic shock 6 days after the onset of influenza and severely impaired left ventricular systolic function, and subsequent normalization of ventricular function after recovery of her viral illness; taken together with her typical echocardiogram findings in the setting of normal coronaries supports the clinical diagnosis of viral fulminant myocarditis; regardless of non diagnostic right ventricle biopsies. During influenza infection, severe myocardial dysfunction can be caused not only by direct injury to cardiac myocytes but also by overexpression of cytokines and severe inflammatory response to viral infection resulting cytokine and humoral mediated forms of myocarditis with no cellular infiltrate.
The reason for the unexpected severity of influenza B infection in our patient was not clear. Clinical data about risk factors and complications of influenza B are limited. Her only past medical history was remote myasthenia gravis and thymectomy over 20 years prior. The predominant circulating B strain was B/Wisconsin/1/2010- LIKE when the patient presented to the hospital, which was matched with the B component of the 2012–2013 vaccine. We do not know if the patient had received an influenza vaccine this season. The possible lack of immunologic memory for this infection might have contributed to the severity of influenza B virus infection in our patient. Increasing awareness among patients and physicians about the importance of vaccination as the most important strategy for minimizing the severe complications of influenza infection could help to prevent similar cases in the future.
The treatment of influenza associated fulminant myocarditis still remains supportive. Studies have shown the early use of mechanical circulatory support for patients with fulminant myocarditis and cardiogenic shock who fail aggressive pharmacologic treatment would increase survival rate. Our patient received oseltamivir, standard heart failure treatment but more important early initiation of ECMO support before irreversible organ failure developed.
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