Journal of Clinical and Preventive Cardiology

: 2016  |  Volume : 5  |  Issue : 4  |  Page : 146--148

An unusual cause of ST elevation: Coronary vasospasm complicating acute myocarditis - A case report and review of the literature

Matthew K Rowe1, Matthew Rutherford2, Karam Kostner1,  
1 Department of Cardiology, Mater Adults Hospital; School of Medicine, The University of Queensland, Brisbane, QLD, Australia
2 Department of Cardiology, Mater Adults Hospital, Brisbane, QLD, Australia

Correspondence Address:
Matthew K Rowe
Mater Adults Hospital, Brisbane, QLD


Coronary vasospasm and myocarditis are both recognized mimics of ST elevation myocardial infarction with normal coronary arteries. The occurrence of both pathologies in the same patient has rarely been described. We report a case of a 27-year-old man initially presenting with history and electrocardiogram (ECG) findings consistent with acute myocarditis who subsequently developed severe chest pain and new ST elevation, mimicking a myocardial infarction. Subsequent coronary angiography was normal, indicative of coronary vasospasm being the cause of ECG changes and symptoms. Previous case reports with a similar presentation are reviewed and potential mechanisms causing this association discussed.

How to cite this article:
Rowe MK, Rutherford M, Kostner K. An unusual cause of ST elevation: Coronary vasospasm complicating acute myocarditis - A case report and review of the literature.J Clin Prev Cardiol 2016;5:146-148

How to cite this URL:
Rowe MK, Rutherford M, Kostner K. An unusual cause of ST elevation: Coronary vasospasm complicating acute myocarditis - A case report and review of the literature. J Clin Prev Cardiol [serial online] 2016 [cited 2022 May 26 ];5:146-148
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Coronary vasospasm and myocarditis are both recognised mimics of ST elevation myocardial infarction with normal coronary arteries. We report a case of a 27 year old man with symptoms mimicking a ST-elevation myocardial infarction where both myocarditis and vasospasm appear to occur concurrently. We then present a review of previous literature and discuss potential mechanisms leading to this association.

 Case Report

A 27-year-old male presented to the emergency department complaining of chest pain. For the preceding 3 days, he had experienced fevers, vomiting, and myalgia. The pain was described as radiating across the chest, worse on inspiration, but unchanged with positioning. He had experienced two episodes of the pain before presentation lasting for approximately 1 h. His children and work colleagues had also been unwell with a flu-like illness.

His only medical history was anxiety, controlled with desvenlafaxine 50 mg. He was a nonsmoker and only consumed alcohol occasionally. He denied any illicit drug use. There was a family history of coronary artery disease before age 50, but no hypertension, hypercholesterolemia, or diabetes.

On admission, he was afebrile, normotensive, and in sinus rhythm at 80 bpm. Examination did not reveal any cardiac rub or murmur. The electrocardiogram (ECG) on presentation is shown in [Figure 1]. Initial high-sensitivity troponin was 8753 ng/L (reference range <26 ng/L). C-reactive protein (CRP) was 96 mg/L. Other laboratory parameters were hemoglobin: 140 g/L, white cell count: 8.9 × 10 9 /L, creatinine: 80 μmol/L, aspartate aminotransferase: 104 U/L, alanine aminotransferase: 86 U/L, alkaline phosphatase and gamma glutamyl transferase were normal. Nasopharyngeal swab for respiratory virus polymerase chain reaction (PCR) was negative and anti-streptolysin O titer was normal.{Figure 1}

Given the presentation being consistent with myopericarditis, initial management consisted of ibuprofen 400 mg t.d.s, colchicine 500 mcg b.d, and prophylactic heparin, and he was admitted to the coronary care unit. The following afternoon, the patient experienced a recurrence of severe chest pain associated with tachypnea. A repeat ECG [Figure 2] demonstrated new ST elevation in the inferior and lateral leads as well as ST depression in V1-V3 suggesting ischemia. Due to these new findings, urgent coronary angiography was undertaken which revealed normal coronary arteries [Figure 3] and left ventricular ejection fraction (LVEF) of 57% by angiography. Considering the ECG findings, which subsequently resolved typical pain and absence of coronary artery disease, a diagnosis of coronary vasospasm was made.{Figure 2}{Figure 3}

The patient returned to the ward and did not have further episodes of pain. A transthoracic echocardiogram showed mildly reduced systolic function (LVEF 50%) without regional wall motion abnormalities. He was discharged home on day 3 after admission on ibuprofen, colchicine, and atenolol. Serology for viral causes of myocarditis was negative. He returned to the outpatient clinic for review 1 month later, at which time his symptoms had resolved and he had returned to usual work duties. CRP had normalized (<0.5 mg/L) and left ventricular function had returned to the normal range. On exercise stress echocardiography, his baseline ejection fraction was normal (60%-65%) with improvement on exercise to 75% and no wall motion abnormalities were observed.


Coronary vasospasm and myocarditis are both well-known causes of ST-segment elevation mimicking acute myocardial infarction. The combination of both these events has been rarely described in the literature. [1],[2] Other potential causes of this presentation are transient thrombosis due to localized plaque rupture or paradoxical embolus from a distal source. We feel that the presence of normal, smooth coronary arteries made plaque rupture less likely and no evidence thrombus was seen when urgent angiography was performed. In addition, the fact that he had experienced two episodes of the pain before presentation lasting for approximately 1 h, and his children and work colleagues had also been unwell with a flu-like illness making myocarditis with coronary vasospasm more likely.

We conducted a MEDLINE search for similar case reports and were only able to identify five such cases. In each of these cases, the patient was young (mean age = 35 years, range 17-59 years, M:F 4:1), and in three, there was a viral prodrome reported. Two patients were smokers; however, smoking status was not reported in two cases. A history of typical, intermittent, chest pain correlating with ST-segment elevation indistinguishable from myocardial infarction is reported similar to our case above. All patients had left ventricular systolic dysfunction, and in the most severe case, the patient developed ventricular fibrillation and cardiogenic shock requiring intra-aortic balloon pump support. [1] On initial angiography, normal coronary arteries were found in all cases; however, two patients with recurrent pain had repeat catheterization showing coronary vasospasm. [1] Use of oral calcium channel blockers (nifedipine, diltiazem) has been described along with treatment of heart failure with β-blockers and angiotensin-converting enzyme inhibitors in some patients.

There are several mechanisms proposed by which myocarditis could provoke coronary vasospasm. Myocarditis-induced endothelial dysfunction may be caused by uptake of viral pathogens or by specific targeting of endothelial cells as has been shown with parvovirus B19. [3] Alternately, smooth muscle hyperreactivity has been demonstrated in models of coronary inflammation due to cytokines such as interleukin-1 and Rho-specific kinase. [2] In addition, high sensitivity CRP itself has been independently associated with vasospasm. [4]

Yilmaz et al. attempted to study this association further by identifying 85 patients with a history consistent with myocarditis and performing provocation testing for vasospasm with acetylcholine. [5] All patients had endomyocardial biopsies with viral PCR and underwent cardiac magnetic resonance imaging (MRI). They found a significantly higher incidence of inducible vasospasm (70% vs. 40%) in patients with positive biopsy findings. Parvovirus B19 found on biopsy was predictive of vasospasm in regression analysis. They propose a coronary vasculitis due to infection of endothelial cells as a potential mechanism to unify the two disease processes.

The degree to which vasospasm might contribute to systolic dysfunction or arrhythmia in myocarditis is currently unknown. Interestingly, when cardiac MRI is undertaken, late gadolinium enhancement has been reported not only subepicardially, as might be expected, but also subendocardially and transmurally suggesting myocardial infarction, potentially caused by vasospasm. [5]


Coronary vasospasm is reported rarely during acute myocarditis. The case we report here shows features consistent with these two conditions occurring concurrently. Smooth muscle hyperreactivity and endothelial dysfunction are proposed mechanisms but are not yet fully understood. Parvovirus B19 seems to have a particular association with vasospasm compared to other viral pathogens. The precise incidence and significance of vasospasm during myocarditis remains unknown and is worthy of further study.

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Conflicts of interest

There are no conflicts of interest.


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