Number 16-04: Cardiovascular magnetic resonance imaging in ventricular tachycardia: in search of...
Share |

Cardiovascular magnetic resonance imaging in ventricular tachycardia:in search of the culprit

Authors - 

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

# Both authors contributed equally

Institution: Department of Cardiology, Onze Lieve Vrouwe Gasthuis, Amsterdam, The Netherlands. 


A 55-year old female patient was presented after an episode of syncope based on polymorphic ventricular tachycardia (pVT). Her medical history included impaired glucose tolerance and a deep venous thrombosis 17 years ago. She did not use any medication. Retrospectively she experienced four to ten days before presentation typical complaints of angina pectoris – duration up to six hours – with radiation to the left arm and vegetative symptoms. On general examination, vital signs were normal and only raccoon eyes as a result of her syncope were observed. CT-cerebrum excluded intracranial pathology. During the hospital stay she experienced six episodes of pVT (Figure 1a) without prolongation of the QT interval or short-long-short sequention, which was treated by defibrillation or converted spontaneously to sinus rhythm. 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%.

The ECG showed a sinus rhythm of 78 bpm with a normal axis, normal conduction intervals and normal repolarisation (Figure 1b). Upon admission, troponin level was 0.226 ug/L (normal: up to 0.014 ug/L) with a CK-MB level of 3.3 ug/L (normal: up to 4.7 ug/L), and LDH and ASAT levels of 197 IU/L (normal: up to 247 IU/L) and 18 IU/L (normal: up to 31 IU/L), respectively. Transthoracic echocardiography showed normal systolic left ventricular function and dimensions with mild septal wall motion abnormalities, and no valve insufficiencies (Figure 2). Our initial conclusion was a non-ST-elevated myocardial infarction with polymorphic VT due to cardiac ischemia (Grace risk score 112). A coronary angiogram revealed, unexpectedly, no epicardial coronary artery disease. There was only a non-significant stenosis in the septal branch of the left anterior descending artery (Figure 3a and 3b).

The differentiation between ischemic, inflammatory or other entities was challenging because the expected typical signs and findings by noninvasive and invasive investigations were lacking. In this case there was uncertainty about the ischemic origin of the complaints and subsequently the pVT’s despite the typical angina and mildly elevated cardiac biomarkers. The discussion arose when the coronary angiogram showed no significant stenosis in the epicardial vessels to explain the sequel of events. The classical differential diagnosis was inflammatory disease, (peri)myocarditis or due to 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 by being pause depended, short-long-short sequence and proceeded by documented long QTc. However, myocarditis could not be excluded by the laboratory findings and echocardiography.


Since our differential diagnosis changed to a possible myocarditis [2], a cardiac magnetic resonance imaging scan was made as investigation modality of choice to differentiate between ischemic and inflammatory cardiac syndromes [3]. Cardiac magnetic resonance (CMR) is a reliable modal­ity due to the combination of accurate tissue characterization and excellent safety profile [4]. For example, edema is typically localized 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. Especially when malignant arrhythmias are present, a quick diagnosis is essential to start the right therapy. Few studies describe the incidence of malignant arrhythmias in patients with non-ST segment elevation myocardial infarction. It seems low (6-7%), especially after successful revascularization [1,7,8]. However, this patient group is globally increasing.

The diagnostic tool of choice was CMR [9] with a myocarditis protocol due to the unparalleled ability in tissue characterization. CMR showed a normal anatomy of the heart and great vessels. The axial T2 weighted ‘short tau inversion recovery’ STIR images showed localized high signal intensity mid-septal, suggestive for edema. There was a good cardiac contractility. Late enhancement showed a transmural mid-septal defect (Figure 4a-d). The CMR scan in our patient did not meet the criteria for myocarditis according to the Lake Louise Consensus Criteria for myocarditis (Table 1). However, CMR imaging had shown the evidence of ischemic changes at the mid-septal region of the left ventricle, corresponding to the septal branch with “non-significant stenosis” on the coronary angiogram. The transmural late Gadolinium enhancement in that region, made it necessary to reassess the coronary angiogram. Upon reassessment an intermediate stenosis of the septal branch was identified explaining the ischemic origin of the symptoms and the polymorphic ventricular tachycardia.



Our conclusion was a non-ST-elevated myocardial infarction with pVT due to cardiac ischemia, and ACS (‘golden five’) medication was prescribed according to current guidelines. Moreover, the pVT was treated with amiodaron intravenously [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 ventricular tachycardia was observed. The discussion arose concerning implantable cardioverter defibrillator (ICD) indication. The patient did not receive an ICD because of the biochemical and imaging evidence of ischemia at the time of VT and the good left ventricle function. 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]. 

The patient was clinically observed with telemetry, and discharged after 8 days without arrhythmias with optimal ACS medication. The echocardiogram was repeated showing similar results except for a dilated left atrium and a mild mitral valve insufficiency. Exercise stress test showed no arrhythmias. 48 hour Holter monitoring was performed showing sporadic multiform premature atrial and ventricular complexes.

After a few weeks, the patient was seen at our outpatient department and experienced no cardiac complaints since discharge. A follow-up magnetic resonance imaging scan showed in the axial T2 STIR images a signal increase mid-septal with hypokinetic wall motion at that point and thinning of the wall without edema (Figure 5a-d). A Holter showed normal sinus rhythm, with eight times a premature ventricular complex without VT’s.



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 the prognostic value of CMR due the presence, burden and the distribution of Late Gadolinum Enhancement (LGE) in the left ventricle.

This has also been demonstrated by Dawson et al. [10], analyzing patients presenting with pVT or even non-sustaind ventricular tachycardia. 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, parallels has been drawn with similar interventions and experiences in 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.



  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.
  1. Pozo E and Sanz J. Differentiating infarction from myocarditis. Heart Metab. 2014;62:13-7.
  2. Friedrich MG. Tissue characterization of acute myocardial infarction and myocarditis by cardiac magnetic resonance. J Am Coll Cardiol Cardiovasc Imag. 2008;1:652-62.
  3. 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.
  4. 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.
  5. 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.
  6. 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.
  7. 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.
  8. 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.
  9. 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.

Mailing Address
19 Mantua Rd
Mt. Royal, NJ 08061
Contact Us
Connect With Us