Cardiovascular magnetic resonance imaging in ventricular tachycardia: Search for the culprit

Kirsten A. Kortekaas MD PhD#, Wisam Yassi MD#, Rene J. van der Schaaf MD PhD, and Gijsbert S. de Ruiter MD

Institution: Department of Cardiology, Onze Lieve Vrouwe Gasthuis, Amsterdam, The Netherlands.
# Both authors contributed equally


A 55-year old female patient presented after an episode of syncope secondary to polymorphic ventricular tachycardia (pVT). Her medical history included impaired glucose tolerance and deep venous thrombosis 17 years ago. She did not use any medication. On examination, vital signs were normal and only raccoon eyes were observed. CT-cerebrum excluded intracranial pathology. During the hospital stay she experienced six episodes of pVT (Figure 1a) with minimal prolongation of the QT interval, which converted to sinus rhythm either spontaneously or with defibrillation. 

Figure 1a:   ECG showing polymorphic VT starting with a premature ventricular complex (not pause dependent), with a slightly prolonged QTc. 

The electrocardiogram showed sinus rhythm with heart rate 78 bpm, normal QRS axis, normal conduction intervals, minimal prolongation of the QT interval and normal repolarisation (Figure 1b). Upon admission, troponin measured 0.226 ug/L (normal: up to 0.014 ug/L) with CK-MB 3.3 ug/L (normal: up to 4.7 ug/L), LDH 197 IU/L (normal: up to 247 IU/L) and ASAT 18 IU/L (normal: up to 31 IU/L). No electrolyte abnormalities were observed. 

Figure 1b:  ECG showing sinus rhythm with heart rate 78 bpm, normal QRS axis, normal conduction intervals, minimal prolongation of the QT interval and normal repolarisation (QTc 479 ms).

Transthoracic echocardiography showed normal systolic global left ventricular function and dimensions with hypokinetic segment 8 (according to the 17 segment model terminology) and no valve insufficiency (Figure 2). 

 Figure 2:  Cardiac echography, four chamber view, showing normal systolic global left ventricular function and dimensions with hypokinetic segment 8 according to the 17-segment model terminology (mid-anteroseptal region). 

Our initial conclusion was non-ST-elevated myocardial infarction with polymorphic VT due to cardiac ischemia (Grace risk score 112). To our surprise, coronary angiogram revealed no significant coronary artery disease. There was ‘non-significant’ stenosis in the septal branch of the left anterior descending artery (Figure 3).

Figure 3a and 3b:  The culprit lesion in the first septal branch. Orthogonal view of the coronary angiogram showing ‘non-significant’ stenosis of the first septal branch with normal LAD and RCx. 


The differentiation between ischemic, inflammatory or other entities was challenging in this case. There was uncertainty about the ischemic origin of the complaints and the pVT’s, despite the typical angina and mildly elevated cardiac biomarkers. According to a risk stratification model [1], there was a low risk of pVT (0.2%) based on a Grace risk score below 140 and a left ventricular ejection fraction above 35%.

When the coronary angiogram showed no significant coronary artery stenosis, the possibilities were narrowed to inflammatory myocarditis or latent long QT-syndrome. The latter was less likely because we did not register a significant increase in QTc interval on admission. Also the pVT did not meet the criteria for Torsade de Pointes. 


Since our differential diagnosis included possible myocarditis [2], cardiac magnetic resonance imaging (CMR) scan was the investigative modality of choice to differentiate between ischemic and inflammatory cardiac syndromes [3]. CMR is a reliable modal­ity due to the combination of accurate tissue characterisation and excellent safety profile [4]. For example, edema is typically localised to the territory of the culprit vessel in patients with ACS whereas the edema may be more diffuse in patients with myocarditis [5,6]. Therefore, by integrating CMR early in the diagnostic process, inappropriate treatment strategy and needless costs can be avoided. When malignant arrhythmias are present, a quick diagnosis is essential to start the right therapy. The incidence of malignant arrhythmias in patients with non-ST segment elevation myocardial infarction is low (6-7%), especially after successful revascularization [1,7,8]. However, this patient group is globally increasing.

CMR with a myocarditis protocol showed normal anatomy of the heart and great vessels. The axial T2 weighted ‘short tau inversion recovery’ STIR images showed localised high signal intensity in the mid-septal region, suggestive of edema. There was normal systolic global ventricular function (ejection fraction of 60%) but hypokinetic segment 8 (mid-anteroseptal region). In addition, mild mitral valve regurgitation and floppy interatrial septum were observed. Late gadolinium enhancement imaging showed almost transmural mid-septal enhancement (Figure 4a-d). The CMR scan in our patient did not meet the criteria for myocarditis according to the Louise Consensus Criteria for myocarditis [9]. Instead, there was evidence of recent ischemic myocardial damage in segment 8 in the mid-septal region of the left ventricle, corresponding to the distribution of the septal branch with “non-significant stenosis” noted on the coronary angiogram. Upon reassessment of the coronary angiogram, intermediate stenosis of the septal branch was identified explaining the ischemic origin of the symptoms and the pVT. 

Figure 4a and 4b: Initial CMR according to myocarditis protocol shows transmural edema on the T2 weighted ‘short tau inversion recovery’ STIR image (4a) and almost transmural late Gadolinium enhancement (4b) in  segment 8 (the septal region) on the short axis view.

Figure 4c and 4d: Initial CMR according to myocarditis protocol shows normal systolic global left ventricular function but hypokinetic segment 8 (mid-anteroseptal region) on the short axis and 4-chamber cine CMR.


To conclude our patient had non-ST-elevated myocardial infarction with pVT due to cardiac ischemia, and ACS (‘golden five’) medication was prescribed according to current guidelines. pVT was treated with intravenous Amiodarone [2]. Since the efficacy of percutaneous coronary intervention (PCI) of intramyocardial segments is poor, no PCI was performed on the non-significant stenosis of the septal branch of the left anterior descending artery. No recurrence of pVT was observed. After discussion and consideration of implantable cardioverter defibrillator, it was decided not to perform an ICD implantation because there was biochemical and imaging evidence of ischemia at the time of VT and the left ventricle function was normal. Furthermore, pVT within 48 hours after an ischemic event or due to a reversible cause is not considered an indication for ICD implantation according to the European guidelines [2]. 

An echocardiogram prior to discharge was unchanged except for a mild increase in left atrial dilatation and mild mitral valve insufficiency. Exercise stress test showed no arrhythmias. 48-hour Holter monitoring showed sporadic multiform premature atrial and ventricular complexes. The patient was clinically observed and discharged after 8 days with optimal ACS medication. After a few weeks, the patient was seen at our outpatient department and had experienced no cardiac complaints since discharge. A follow-up CMR scan showed thinning and hypokinetic wall motion in the mid-septal region with a decreased signal on the T2 STIR images and almost transmural enhancement on LGE imaging in the mid-septal region (Figure 5a-d). Holter showed normal sinus rhythm, with occasional premature ventricular complex and no VT’s.  

Figure 5a and 5b: Follow-up CMR according to myocarditis protocol shows minimal transmural edema on the T2 weighted ‘short tau inversion recovery’ STIR image and almost transmural late Gadolinium enhancement (LGE) in the septal region in the short axis view.

Figure 5cFollow-up CMR according to myocarditis protocol shows thinning of the wall without edema on the short axis and 4-chamber cine CMR.


This report shows the usefulness of CMR in the setting of chest pain, abnormal ECG and/or elevated cardiac enzymes, and normal or inconclusive angiograms. It shows the emerging role of CMR in not only identifying the culprit, but also in prognostication by identifying the presence, burden and the distribution of Late Gadolinum Enhancement in the myocardium. This has also been demonstrated by Dawson et al. [10], analyzing patients presenting with pVT or non-sustained VT. Therefore, we suggest the early integration of CMR in the diagnostic process when the combination of clinical, biochemical and other imaging modalities are unequivocal in differentiating between acute ischemic and inflammatory cardiac syndromes. Due to the scarce evidence for PCI efficacy of a septal branch or intramyocardial coronary segments, we looked at the literature on patients with myocardial bridging. In such cases PCI was associated with poor efficacy and even stent fractures were observed [11]. Optimal medical therapy and adequate follow-up could be a good alternative, as shown in our case.

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  1. Zorzi A, Turri R, Zilio F, et al. At-admission risk stratification for in-hospital life-threatening ventricular arrhythmias and death in non-ST elevation myocardial infarction patients. Eur Heart J Acute Cardiovasc Care 2014;3:304-12.
  2. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death – executive  European Heart Journal (2006);27:2099-2140.
  3. Pozo E and Sanz J. Differentiating infarction from myocarditis. Heart Metab. 2014;62:13-7.
  4. Friedrich MG. Tissue characterization of acute myocardial infarction and myocarditis by cardiac magnetic resonance. J Am Coll Cardiol Cardiovasc Imag. 2008;1:652-62.
  5. Raman SV, Simonetti OP, Winner MW, et al. Cardiac magnetic resonance with edema imaging identifies myocar­dium at risk and predicts worse outcome in patients with non-ST-segment elevation acute coronary syndrome. J Am Coll Cardiol 2010;55:2480-8.
  6. Abdel-Aty H, Boye P, Zagrosek A, et al. Diagnostic performance of cardiovascular magnetic resonance in patients with suspected acute myocarditis: comparison of different approaches. J Am Coll Cardiol 2005;45:1815–22.
  7. Wildi K, Cuculi F, Twerenbold R, et al. Incidence and timing of serious arrhythmias after early revascularization in non ST-elevation myocardial infarction. Eur Heart J Acute Cardiovasc Care 2014;4:359-64.
  8. Gupta S, Pressman GS, Figueredo VM. Incidence of, predictors for, and mortality associated with malignant ventricular arrhythmias in non-ST elevation myocardial infarction patients. Coron Artery Dis 2010;21:460-5.
  9. Friedrich MG, Sechtem U, Schulz-Menger J, et al. Cardiovascular magnetic resonance in myocarditis: A JACC White Paper. J Am Coll Cardiol. 2009;53:1475-87.
  10. Dawson DK, Hawlisch K, Prescott G, et al. Prognostic role of CMR in patients presenting with ventricular arrhythmias. JACC cardiovasular imaging 2013;6:335-44.
  11. Tandar A, Whisenant B, Michaels A. Stent Fracture Following Stenting of a Myocardial Bridge: report of two cases. Catheter Cardiovasc Interv 2008;71:191–6.

 Case prepared by SCMR COTW Associate Editor: Madhusudan Ganigara. 

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