Abstract
Myocarditis is a disease with variable clinical presentation, ranging from an uncomplicated febrile illness to cardiogenic shock. Herein, we report a case of fulminant myocarditis secondary to murine typhus in a 52-year-old male that initially mimicked an acute coronary syndrome. Emergent coronary angiography showed angiographically normal coronary arteries. Left ventriculography showed global hypokinesis with an ejection fraction of 10%. The patient required mechanical support with an intra-aortic balloon pump and fully recovered.
<Learning objective:Fulminant myocarditis secondary to murine typhus may occur in urban areas. Clinical complications such as cardiogenic shock and acute heart failure can be overcome with supportive therapy such as an intra-aortic balloon pump and guideline-directed medical therapy.>
Keywords: Chest pain, Acute coronary syndrome, Acute heart failure, Ejection fraction, Beta-blockers, Angiotensin-converting enzyme inhibitor
Introduction
Most cases of myocarditis are presumed idiopathic given the wide range of possible etiologies. Few cases of fulminant myocarditis secondary to Rickettsia typhi have been reported [1]. This case highlights a patient who developed a rare, life-threatening complication of murine typhus, fulminant myocarditis, with subsequent recovery after initiation of antibiotic therapy and guideline-directed medical therapy for heart failure.
Case report
A 52-year-old Hispanic male in his usual state of health presented with a 4-day history of fevers, left-sided substernal chest pain, shortness of breath, and dyspnea on exertion. He also reported accompanying fevers, chills, fatigue, headaches, and productive cough. Vital signs on admission included: temperature 39.1 °C, heart rate 140 bpm, blood pressure 90/68 mmHg, respiratory rate 26 breaths/min, oxygen saturation 94% with 10 L/min supplemental oxygen.
Medical history was significant for non-insulin dependent diabetes. Family history was not significant for coronary artery disease, myocardial infarction, heart failure, or cerebrovascular disease. He did not use alcohol, tobacco, or illicit drugs.
Chest radiograph showed pulmonary congestion (Fig. 1). Electrocardiogram (ECG) showed ST segment elevation in the inferior leads (Fig. 2), consistent with an acute inferior wall ST segment elevation myocardial infarction (STEMI). Troponin-T was elevated at 3.46 ng/mL (normal <0.01 ng/mL), and N-terminal-prohormone brain natriuretic peptide was elevated at 17,549 pg/mL (normal <125 pg/mL). Other notable laboratory values on admission included: white blood cell count 12.3 K/mm3, hemoglobin 14.5 g/dL, platelet 196 K/mm3, sodium 134 mmol/L, potassium 4.5 mmol/L, chloride 98 mmol/L, bicarbonate 21 mmol/L, blood urea nitrogen 21 mg/dL, creatinine 0.89 mg/dL, aspartate aminotransferase 94 U/L, alanine transaminase 78 U/L, magnesium 2.1 mg/dL, phosphorus 2.5 mg/dL, d-dimer 1.66 mcg/mL (normal <0.49 mcg/mL), C-reactive protein 341.6 mg/L (normal <4.9 mg/L).
Fig. 1.
Chest radiograph on admission showed pulmonary congestion.
Fig. 2.
Electrocardiogram showed ST segment elevation in the inferior leads, consistent with an acute inferior wall ST segment elevation myocardial infarction.
The patient was brought immediately to the cardiac catheterization laboratory, where coronary angiography (Online Video 1) showed no obstructive coronary artery disease. Left ventriculography (Online Video 1) showed an ejection fraction (EF) of 10% with global hypokinesis. An intra-aortic balloon pump (IABP) and Swan-Ganz catheter were placed for hemodynamic support and monitoring, and he was admitted to the coronary care unit. Initial Swan-Ganz catheter measurements with the IABP in place showed: right atrial pressure 15 mmHg, pulmonary capillary wedge pressure (PCWP) 31 mmHg, cardiac index (thermodilution) 2.3 L/min/m2. Baseline cardiac power output (CPO) was 0.65 Watts. He was aggressively diuresed with intravenous furosemide. The PCWP peaked at 36 mmHg and then decreased to 13 mmHg with aggressive diuresis and continued IABP support. Transthoracic echocardiography (Online Video 2) on hospital day #1 showed a left ventricular EF of 25–30% and moderate global hypokinesis as well as mild-to-moderately reduced right ventricular systolic function. His-overall clinical condition improved, CPO increased to 0.99 Watts on hospital day #3, and the IABP was removed. Despite a 3-day course of ceftriaxone and vancomycin, fevers persisted. Rickettsia typhi was subsequently detected with an IgM titer of 1:64, indicating ongoing infection. Doxycycline was given and fevers resolved within 24 h. He was started on lisinopril 5 mg daily and carvedilol 6.25 mg twice daily, weaned off supplemental oxygen, and discharged on hospital day #6.
A repeat R. typhi IgM titer 2 weeks after the initial titer showed a 4-fold increase (1:256), which confirmed diagnosis of murine typhus and likely etiology of fulminant myocarditis. The patient later reported that there were several feral cats around his home. Repeat ECG 3 weeks post-hospitalization (Fig. 3) showed resolution of prior ST segment elevation in the inferior leads. Repeat transthoracic echocardiography 3 months post-hospitalization (Online Video 3) showed improvement in EF to 50–55%. The patient remains asymptomatic and continues on guideline-directed medical therapy including: lisinopril 5 mg daily, metoprolol succinate 25 mg daily, spironolactone 12.5 mg daily, and furosemide 20 mg daily.
Fig. 3.
Repeat electrocardiogram 3 weeks post-hospitalization showed sinus bradycardia and resolution of prior ST segment elevation in the inferior leads.
Discussion
Fulminant myocarditis should be suspected in patients with a febrile prodrome, heart failure, elevated troponins, and electrocardiographic changes suggestive of an acute coronary syndrome, in the absence of obstructive coronary artery disease. Patients with fulminant myocarditis have lower in-hospital survival compared to those with non-fulminant myocarditis [2].
Patients with cardiogenic shock secondary to fulminant myocarditis may benefit from inotropes and/or mechanical circulatory support. CPO provides an objective assessment of cardiac efficiency and is the strongest independent hemodynamic correlate of in-hospital mortality in patients with cardiogenic shock [3]. CPO <0.6 Watts is associated with increased mortality and should trigger an escalation of care with additional mechanical circulatory support, vasopressors, and/or inotropes. Beta-blockers and angiotensin-converting enzyme inhibitors should be initiated once cardiogenic shock resolves to improve survival and promote recovery of left ventricular function [4,5].
Myocarditis can be caused by a variety of infectious and noninfectious etiologies. Recognition of murine typhus as a potential cause of myocarditis in endemic areas allows for directed antibiotic therapy. The number of murine typhus cases in Los Angeles County increased three-fold from 2010 to 2018 [6]. Additionally, Ctenocephalides felis, a cat flea, has been identified as the principal vector [7].
Hispanics have the highest average annual incidence of murine typhus among ethnic groups [1]. While cough is the predominant symptom in murine typhus, another common finding is a fine erythematous papular rash. Rashes are most prevalent among White patients with murine typhus, with an incidence of more than 80%. In contrast, rashes occurred in only 20% of black patients [8]. Mildly elevated hepatic enzymes may also correlate with rickettsial infection of hepatic sinusoids [1]. Ultimately, timely diagnosis and treatment of murine typhus may reduce morbidity and prevent sequalae of infection, including fulminant myocarditis. Patients with fulminant myocarditis who survive acute illness frequently have dramatic improvement in systolic function within several months [9].
Declaration of Competing Interest
The authors declare that there is no conflict of interest.
Acknowledgments
Funding
None.
Disclosures
All authors have no relationships with industry.
Footnotes
Supplementary material associated with this article can be found, in the online version, at doi:10.1016/j.jccase.2021.02.007.
Appendix. Supplementary materials
Online Video 1 Coronary angiography showed no obstructive coronary artery disease. Left ventriculography showed an ejection fraction of 10% with global hypokinesis.
Online Video 2 Transthoracic echocardiography on hospital day #1 showed an ejection fraction of 25–30%, moderate global hypokinesis.
Online Video 3 Repeat transthoracic echocardiography 3 months post-hospitalization showed improvement in ejection fraction to 50–55%.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Online Video 1 Coronary angiography showed no obstructive coronary artery disease. Left ventriculography showed an ejection fraction of 10% with global hypokinesis.
Online Video 2 Transthoracic echocardiography on hospital day #1 showed an ejection fraction of 25–30%, moderate global hypokinesis.
Online Video 3 Repeat transthoracic echocardiography 3 months post-hospitalization showed improvement in ejection fraction to 50–55%.