Article

Fulminant myocarditis complicated with obstructive ST-elevation myocardial infarction—a rare case report

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Case Report

Fulminant myocarditis complicated with obstructive ST-elevation myocardial infarction–a rare case report

Abstract

acute myocarditis mimicking ST-elevation myocardial infarction has been reported in the literature, and most of the cases had relatively Normal coronary arteries. However, there is no literature mentioning fulminant myocarditis complicated with obstructive myocardial infarction. Herein, we report a 72-year-old male suffering from progressive dyspnea and acute chest pain after recent common cold episode. Electrocardiography revealed ST elevation over inferior leads and emergent coronary angiography showed right coronary artery occlusion, but left ventriculography revealed poor left ventricular (LV) function with global hypokine- sia, different from previously normal echocardiographic finding 3 months previously. After percutaneous coronary intervention, extracorporeal membrane oxygenation was also instituted due to unstable hemodynamic and electrical conduction disturbance. Fulminant myocarditis was highly suspected according to the clinical course and incompatible LV function. This patient finally expired a few days later due to no obvious recovery of LV function and family’s willing. This case reminds physicians that acute coronary occlusion is still a possible but extremely rare complica- tion of fulminant myocarditis. Despite intensive Mechanical support, this kind of patient might have poorer prognosis than other myocarditis cases without coronary occlusion and hence need more attention.

Fulminant myocarditis is a relatively rare diagnosis characterized by heart failure preceded by symptoms of viral infection. The electrocardiographic findings are often variable [1,2]. Myocarditis can frequently mimic myocardial infarction (MI) [1,3-6], and most of these cases were reported to have normal coronary arteries [3-6], and long-term prognosis is generally good [1,3]. Herein, we report a patient of fulminant myocarditis complicated with obstructive MI finally leading to poor prognosis.

A 72-year-old man suffered from severe chest pain and was brought to our Emergent department . Tracing back his history, the patient denied any significant systemic disease before. Echocar- diographic examination about 3 months previously had revealed normal heart function. He had an episode of common cold about 2 weeks before, and had started to have intermittent dyspnea and chest discomfort. However, he did not pay attention to the symptoms. On ED arrival, electrocardiogram(ECG) showed ST elevation over lead II, III, and aVF and right side leads also showed ST elevation over V3R and V4R. Laboratory data initially revealed creatine kinase MB 91.7 U/L, and troponin-I 72.68 ng/mL. Under the impression of ST-elevation

myocardial infarction, emergent coronary angiography was arranged. Right coronary angiogram showed subtotal occlusion over middle right coronary artery (Fig. 1A), and left coronary angiogram showed only diagonal 1 branch of left anterior descending artery with significant lesion. Then coronary angioplasty with stenting was performed over RCA and TIMI 3 flow was restored (Fig. 1B). However, left ventriculography revealed left ventricular (LV) global hypokinesia (LV ejection fraction only 14.1%). After the procedure, he was transferred to our cardiac care unit. During cardiac care unit stay, despite chest pain being relieved initially, ventricular tachycardia occurred a few hours later and the patient lost consciousness with development of profound shock even after spontaneous recovery of sinus rhythm. High-dose vasopressor was used, and follow-up ECG revealed ST elevation over leads III and aVF. Under the impression of possible acute re-occlusion or Stent thrombosis, emergent coronary angiography was performed again but patent RCA was found. Serial ECG follow-up later revealed a variety of conduction disturbances and high degree AV block (Fig. 2A and B), and a Temporary pacemaker was then inserted. Due to highly suspect fulminant myocarditis with ongoing cardiogenic shock, intra-aortic ballooning pump and extra- corporeal membrane oxygenation were instituted. Continuous veno- venous hemodialysis was started for anuria and metabolic acidosis. Further Laboratory workup revealed elevated serum Coxsackie B viral titers. Despite intensive mechanical support, diverse cardiac arrhyth- mias were still noted and there was no recovery of heart function. The patient finally expired after 2 weeks of intensive care.

Myocarditis has a wide spectrum of clinical presentations,

ranging from absence of clinical symptoms to fulminant cardio- genic shock. The diagnosis of myocarditis has been traditionally made by usage of the Dallas criteria, but due to low sensitivity and Interobserver variability, the criteria are considered to be inadequate to reliably make the diagnosis [7]. Because it is difficult to make the diagnosis of myocarditis, the disease should be suspected clinically in patients with an Acute chest pain syndrome, particularly while electrocardiographic abnormalities being found beyond a single vascular territory, or global rather than segmental LV dysfunction noted on echocardiography or ventriculography [3,8]. Most cases of acute myocarditis reported in the literature revealed normal coronary arteries or only non- significant lesions [3-6]. To our knowledge, our case should be the first case of fulminant myocarditis complicated with obstruc- tive myocardial infarction.

In this case, fulminant myocarditis was highly suspected according to the following reasons: First, this patient had a history of virus-like infection two weeks previous to admission

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Fig. 1. A (left) Right coronary angiogram before intervention showed subtotal occlusion over middle right coronary artery. B (right) Right coronary angiogram after intervention showed restored Thrombolysis in Myocardial Infarction 3 flow after angioplasty with stenting.

and laboratory workup later revealed elevated Coxsackie B viral titers. Second, left ventriculography showed global hypokinesia but not inferior hypokinesia, which is not compatible with electrocardiographic and angiographic finding of RCA occlusion.

Third, echocardiography revealed normal segmental wall motion and LV function three months previously, proving there was actually an acute deterioration of heart function. Fourth, serial ECG follow-up showed a variety of conduction disturbances.

Fig. 2. Electrocardiogram revealed intraventricular conduction disturbance (A, upper panel) and high degree AV block (B, lower panel) in our cardiac care unit.

Case Report / American Journal of Emergency Medicine 31 (2013) 635.e1635.e3

The possible mechanism in our case might be as follows: acute myocarditis could cause gradual deterioration of heart function, which decreases coronary perfusion in the case with coronary artery disease, and finally leads to obstructive MI. Furthermore, long-term prognosis of acute myocarditis is generally good [1,3]. Even for the cases of fulminant myocarditis, early mechanical support such as extracorporeal membrane oxygenation was greatly helpful and outcome seemed promising as in recent studies [9,10]. However, in the case of fulminant myocarditis complicated with obstructive MI, such as our patient, prognosis seemed poorer. Owing to limited case reports, further studies will be needed.

In conclusion, this rare case reminds physicians Acute coronary occlusion is still a possible but rare complication of fulminant myocarditis. Despite under intensive mechanical support, this kind of patient might have poorer prognosis than other fulminant myocarditis without coronary occlusion and need more attention.

Wen-Han Feng MD Division of cardiology department of Internal Medicine

Kaohsiung Medical university hospital

College of Medicine Kaohsiung Medical University Kaohsiung 80708, Taiwan

635.e3

Wen-chol Voon MD Wen-Ter Lai MD

Sheng-Hsiung Sheu MD Division of Cardiology Department of Internal Medicine

Kaohsiung Medical University Hospital

College of Medicine Kaohsiung Medical University Kaohsiung 80708, Taiwan Department of Internal Medicine

Faculty of Medicine College of Medicine Kaohsiung Medical University Kaohsiung 80708, Taiwan

Po-Chao Hsu MD Division of Cardiology Department of Internal Medicine

Kaohsiung Medical University Hospital

College of Medicine Kaohsiung Medical University Kaohsiung 80708, Taiwan Graduate Institute of Medicine

College of Medicine Kaohsiung Medical University Kaohsiung 80708, Taiwan

E-mail address: [email protected]

http://dx.doi.org/10.1016/j.ajem.2012.10.022

Tsung-Hsien Lin MD, PHD

Ho-Ming Su MD Division of Cardiology Department of Internal Medicine

Kaohsiung Medical University Hospital

College of Medicine Kaohsiung Medical University Kaohsiung 80708, Taiwan Department of Internal Medicine

Faculty of Medicine College of Medicine Kaohsiung Medical University Kaohsiung 80708, Taiwan

Chong-Chao Hsieh MD Division of Cardiovascular Surgery Kaohsiung Medical University Hospital

College of Medicine Kaohsiung Medical University Kaohsiung 80708, Taiwan

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