Fulminant Myocarditis in a Patient with Severe Coronary Artery Disease

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Journal of Cardiology Cases 9 (2014) 15–17

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Journal of Cardiology Cases

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Case Report

Fulminant myocarditis in a patient with severe coronary artery disease

a a,∗ b

Satoshi Fujita (MD) , Ryuji Okamoto (MD, FJCC) , Takeshi Takamura (MD) ,

a a a

Hiroshi Nakajima (MD) , Masaki Tanabe (MD) , Shiro Nakamori (MD) ,

c a a

Kaoru Dohi (MD, FJCC) , Takashi Tanigawa (MD, FJCC) , Mashio Nakamura (MD, FJCC) ,

Masaaki Ito (MD, FJCC)

Department of Cardiology and Nephrology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu, Mie 514-8507, Japan

Department of Cardiology, Ise Red Cross Hospital, Ise, Japan

Department of Laboratory Medicine, Mie University Graduate School of Medicine, Tsu, Japan

a r a

t i c l e i n f o b s t r a c t

Article history: A 55-year-old man complaining of fever and exertional dyspnea was admitted for coronary angiography

Received 4 December 2012

to differentiate between fulminant myocarditis and acute coronary syndrome. He had been treated for

Received in revised form 20 June 2013

17 years for angina pectoris. His electrocardiogram demonstrated ST segment changes in almost all leads.

Accepted 21 August 2013

Cardiac catheterization demonstrated severe stenosis in the left descending artery, the diagonal branch,

and the right coronary artery. Ultrasonography, however, revealed diffuse hypokinesis of the left ven-

Keywords:

tricle and edematous wall thickening, suggesting fulminant myocarditis. This is the ﬁrst report in which

Fulminant myocarditis

a patient with fulminant myocarditis with severe coronary artery disease was successfully treated with

Coronary artery disease

mechanical cardiopulmonary support, intensive pharmacological therapy, and staged coronary interven-

Differential diagnosis

tion procedures. Complicated coronary artery disease may delay the diagnosis of myocarditis and worsen

Percutaneous coronary intervention

Percutaneous cardiopulmonary support the clinical outcome. Patients having fulminant myocarditis with coronary artery disease need careful

diagnosis, and percutaneous cardiopulmonary support should be considered in the early clinical stage.

worsen the clinical outcome. It is considered safe to use percutaneous cardiopulmonary support for such

patients in the early clinical stage. The present case was rescued with mechanical support in the acute

phase of fulminant myocarditis and elective coronary angioplasty in the recovery phase.>

Introduction Case report

Fulminant myocarditis is characterized by severe hemodynamic A 55-year-old male had a 2-day prodrome of fever and mild

compromise requiring high-dose vasopressor support or mechani- chest pain. He was diagnosed as having effort angina pectoris 17

cal circulatory support. The co-existence of coronary artery disease, years earlier and received medication, although he refused coro-

however, can make the diagnosis of myocarditis more complicated nary angiography. He had three coronary risk factors, hypertension,

and the cardiac function worse, resulting in a poor clinical outcome dyslipidemia, and obesity. Since he developed exertional dyspnea,

[1]. Therefore it is important to exclude the coexistence of coro- he visited a local hospital. Because his electrocardiogram (ECG)

nary artery disease by emergency angiography when necessary. demonstrated 1–2-mm ST elevation in II, III, aVF, aVR, V1–V3, and

We report the case of a 55-year-old male, with severe ventricu- 1–2-mm ST depression in I, aVL, and V4–V6 (Fig. 1A), although

lar dysfunction and heart failure, who was found to have coronary his previous ECG was normal, acute coronary syndrome was sus-

artery disease involving right and left coronary arteries and who pected. Transthoracic echocardiography revealed severe, diffuse,

underwent successful intensive supportive therapy for fulminant left ventricular hypokinesis (ejection fraction 14%) without left

myocarditis and staged percutaneous transluminal coronary angio- ventricular dilation. However, the left ventricular wall was sig-

plasty. niﬁcantly thickened with edema [Fig. 2A, intraventricular septal

wall (IVS) thickness 18 mm, posterior wall (PW) thickness 18 mm].

We could observe also minor pericardial effusion. He was admit-

ted, and emergency cardiac catheterization and myocardial biopsy

∗ were performed. Coronary angiography revealed total occlusion of

Corresponding author. Tel.: +81 59 231 5015; fax: +81 59 231 5201.

E-mail address: [email protected] (R. Okamoto). the distal right coronary artery with collateral ﬂow from the left

16 S. Fujita et al. / Journal of Cardiology Cases 9 (2014) 15–17

Fig. 1. (A) Electrocardiogram on admission showing ST-T changes in almost all leads. (B) Right coronary angiogram on admission showing total occlusion in the distal segment

of the right coronary artery (RCA) with collateral arteries. (C) Left coronary angiogram on admission showing 90% stenosis in the left anterior descending (LAD) artery and

the ﬁrst major diagonal branch (D1).

Fig. 2. (A) Ultrasonography in the acute phase showing severely impaired left ventricular systolic function and edematous wall thickening in the intraventricular septal (IVS)

wall and the left ventricular posterior wall (PW). (B) Ultrasonography before discharge showing recovery of left ventricular systolic function and the disappearance of left

ventricular wall edema. Note the normal pulse-wave Doppler velocity in left ventricular outﬂow.

S. Fujita et al. / Journal of Cardiology Cases 9 (2014) 15–17 17

vasopressor support or mechanical circulatory support. Clinical

presentations of myocarditis range from nonspeciﬁc systemic

symptoms including fever, myalgia, palpitations, and exertional

dyspnea to fulminant hemodynamic collapse and sudden death.

Thus, once fulminant myocarditis is suspected, immediate treat-

ment, including intensive hemodynamic support and aggressive

pharmacological intervention such as vasopressors and positive

inotropic agents should be started, as in other patients with

advanced heart failure due to profound left ventricular dysfunction.

However, the incidence and prevalence of fulminant myocardi-

tis remain unknown because of its rarity. A single-center study

reported that the prevalence of fulminant myocarditis was 10.2%

among patients with biopsy-proven myocarditis and 0.9% among

patients with new-onset heart failure [3].

Fulminant myocarditis masquerading as an acute coronary syn-

drome has been often described [4]. Although the present patient

had severe coronary artery stenosis, the diagnosis was fulminant

myocarditis because of the clinical course, including symptoms of

upper respiratory infection, unexplained new onset heart failure,

Fig. 3. Endomyocardial biopsy specimen on admission showing lymphocytic inﬁl-

and echocardiography ﬁndings including normal left ventricular

trate and myocardial necrosis (hematoxylin and eosin, 200×).

cavity size and reversible left ventricular hypertrophy [2,5]. A

Japanese national survey reported that 8 (18.6%) of 43 cases with

circumﬂex artery (Fig. 1B) and severe stenosis in the proximal seg-

fulminant myocarditis were diagnosed as having an abnormal coro-

ment of the left anterior descending artery and the ﬁrst major

nary artery [6]. However, it has been rarely reported that a patient

diagonal branch (Fig. 1C). Left ventriculography showed severe

with fulminant myocarditis had signiﬁcant stenoses in multiple

diffuse left ventricular hypokinesis with elevated left ventricular

coronary vessels [1]. The co-existence of coronary artery disease

end-diastolic pressure. An intra-aortic balloon pump (IABP) was

can make the diagnosis of myocarditis more complicated and the

inserted due to cardiogenic shock. Although angiographic ﬁndings

cardiac function worse, resulting in a poor clinical outcome [1].

suggested severe coronary artery disease, he was diagnosed as hav-

Furthermore, myocarditis itself can induce coronary vasospasm

ing fulminant myocarditis based on the echocardiographic ﬁndings

even in a normal coronary artery [7], which can worsen myocar-

and clinical course, and he was immediately transferred to our

dial ischemia. Thus, it is important to exclude the coexistence of

hospital for intensive treatment.

coronary artery disease by emergency angiography when neces-

On admission, his blood pressure was 65/40 mmHg under

sary. When patients with myocarditis have severe coronary artery

IABP support, his pulse was 120 beats/min, and his tempera-

◦ disease, such patients must be treated very carefully. The present

ture was 37.5 C. He developed dyspnea and heart failure, which

case was rescued with mechanical support in the acute phase

rapidly progressed to cardiogenic shock and required mechani-

of myocarditis and elective coronary angioplasty in the recovery

cal ventilation, percutaneous cardiopulmonary support (PCPS), and

phase. Unexpectedly, this is, to the best of our knowledge, the

continuous hemodiaﬁltration (CHDF). With mechanical support,

ﬁrst report that coronary atherosclerotic disease complicating ful-

a 2 g/kg dose of immunoglobulin was administered intravenously

minant myocarditis was treated successfully by staged coronary

over 48 h. Right ventricular endomyocardial biopsy revealed mul-

interventions. It is considered safe to use percutaneous cardiopul-

tiple necroses, degeneration of myocardial cells, and extensive

monary support for such patients in the early clinical stage.

inﬁltration of inﬂammatory cells, consistent with acute myocardi-

tis. Creatine kinase and cardiac troponin T on admission were

Conﬂict of interest

938 IU/l (normal < 170 IU/l) and 2.28 (normal ≤ 0.10 ng/ml), respec-

tively. The endomyocardial biopsy showed the inﬁltration of

Authors declare that there is no conﬂict of interest.

lymphocytes and necrosis of myocytes, consistent with lympho-

cytic myocarditis (Fig. 3).

References

The patient’s clinical course was satisfactory: the PCPS was

removed on the 5th day, and he was weaned off IABP and CHDF on

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