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A previously healthy 41-year old woman resuscitated from ventricular fibrillation

The patient had been previously quite healthy, with no regular medication.
One evening in November 2008 when she was in the kitchen, she suddenly dropped on the floor unconscious and convulsed.
Myocardial Disease

The patient was resuscitated, the ambulance was called and the patient was defibrillated from ventricular defibrillation (Fig 1.). The return of spontaneous circulation -time was 24 minutes. The patient was transferred to the hospital for intensive care.

Fig. 1.  ECG showing the ventricular arrhythmia before defibrillation

At the arrival at the hospital there was stable sinus rhythm (100/min), with prolonged QT-interval (Fig 2.). The patient was acidotic and hypokalemic.

Fig. 2. ECG taken after resuscitation at the hospital demonstrating sinus rhythm,
normal atrioventricular conduction and prolonged QT-interval.

Thorax X-ray was non-remarkable with some atelectasis. Plasma CK-MBm concentration was 14 ug/l (normal range 0-7 ug/l) and that of troponin T was 0.04 ug/l (normal range < 0.03 ug/l). CRP  was negative.

Bed-side echocardiography showed a slightly increased left ventricular end-diastolic diameter (61mm), diminished ejection fraction and normal ventricular walls (Fig 3). There was mild tricuspid valve regurgitation with a systolic gradient of 25 mmHg.

Fig. 3. In echocardiography there was septal hypokinesia and diminished left ventricular contractility.
No pericardial effusion could be observed.

ECG monitoring demonstrated some episodes of non-sustained ventricular tachycardia (Fig. 4). The patient told that six months earlier she had experienced a tachycardia lasting for about half an hour but it had subsided spontaneously before an ECG could be taken at the local health center.

Fig. 4. After the resuscitation, the patient had episodes of non-sustained ventricular tachycardias

The laboratory results remained negative for infections caused by common viruses, mycoplasma or toxoplasma. There was no evidence of a connective tissue disease (serum ANCA, ENA, PR3AB, MPOAB, ANA titers remained negative). The serum concentrations of lysozyme and calcium and the serum ACE activity were normal as well as the levels of ACTH, aldosterone, renin and cortisol. Cardiac MRI showed a dilated left ventricle with diminished systolic function (LVEF 43%). There was late enhancement in the basal area of the left ventricle anteroseptally, anteriorly and inferoseptally. On the contrary, the right ventricular size and function were normal and there was no late enhancement.


  1. What is your hypothesis?
  2. Which examinations would you recommend?


Possible causes of sudden ventricular fibrillation in this previously healthy patient included coronary artery disease or other coronary artery abnormalities, myocardial disease, inflammatory, infiltrative or neoplastic process, congenital heart disease, primary electrophysiological abnormality, electrolyte disturbance, toxic or metabolic disturbances.
When the patient arrived at the hospital, she was in sinus rhythm with no signs of ischaemia. Her serum potassium was low at 2.6 mmol/l  (3.3-4.9). Soon after the acidosis and hypokalaemia had been treated, the prolonged QT-interval normalized. Later it was found out that the patient used to consume plenty of liquorice. However the aldosterone and renin values were within normal limits and the hypokalaemia was interpreted to relate mainly to the acute event. The results of DNA tests showed that the patient did not carry any of the four most common LQT mutations in Finland, which cover approximately 70 % of the LQT in our country. LQT syndrome was thus considered to be an improbable cause of the ventricular fibrillation. The ECG was not compatible with any other primary electrophysiologic abnormality. Laboratory analyses did not suggest toxic or metabolic disturbances. Congenital heart disease or coronary anomalies were excluded by echocardiography and cardiac MRI. The family history did not suggest any inherited cardiac disease.

The late enhancement in the cardiac MRI raised the suspicion, that the patient had a localized, possibly inflammatory process in the myocardium (Fig. 1.)

Cardic MRI shows late enhancement in the basal area of the left ventricle.


Fig. 1. Cardic MRI shows late enhancement in the basal area of the left ventricle.


Endomyocardial biopsies were taken from the left ventricle. However, the histological findings were non-diagnostic: there was neither sarcoidosis, giant cell myocarditis nor any other type of inflammation or fibrosis to be found. Coronary angiogram demonstrated normal coronary arteries. Thorax X-ray showed transient atelectasis but no enlarged hilar lymphnodes or parenchymal infiltrates.

Due to the cardiac MRI findings cardiac positron emission tomography with FDG (fluorodeoxyglucose)  was performed. The posterobasal area of the septum was 18 F-FDG -positive as well as mediastinal and hilar lymph nodes. The finding was suggestive of inflammation, such as sarcoidosis. High resolution computer tomography (HRCT) of the lungs did not reveal any parenchymal lesions. Bronchoscopy and bronchoalveolar lavation were carried out showing increased relation of CD4+/CD8+ -lymphocytes, suggestive of sarcoidosis, but otherwise the bronchial  biopsies were normal.  Since none of the lymphnodes were easily accessible by other means, biopsies were taken in mediastinoscopy. Finally, histology showed non-necrotizing granulomas consisting of epithelioid cells and individual giant cell confirming the diagnosis of sarcoidosis.

The patient received an ICD. The medical treatment comprised prednisolon for approximately one year and thereafter prednisolon was substituted by azathioprine. There have not been any ICD activations. In follow-up the LVEF and dimensions have been restored. The left ventricle was 59/49 mm and  LVEF was 52 %.

Sarcoidosis is a multisystem disease histologically characterized by non-caseating granulomas. The prevalence varies between populations and it is known to be high in Scandinavia. Sarcoidosis may affect the heart in up to one fourth of cases. Cardiac sarcoidosis typically manifests as conduction defect, or progressive heart failure but also tachyarrhythmias and sudden death are possible. Signs of granulomatous inflammation may be sought using different imaging modalities. Diagnosis is based on showing noncaseating granulomas in a biopsy. Because of the patchy nature of the inflammation, a negative result of a biopsy does not exclude sarcoidosis. Steroid treatment may be useful at the early phase of the disease. Conventional medical is  used for heart failure and in the presence of venricular arrhythmias, an ICD should be considered.


  1. Simon WD, Rodney H Falk. Diagnosis and Management of Cardiac Sarcoidosis. Progree in Cardiovascular Diseases 2010; 52:336-346.

  2. Kim JS, Judson MA, Donnino R et al. Cardiac sarcoidosis. Am Heart J 2009; 157:9-21.

Notes to editor

Presented by Tiina Heliö
Department of Cardiology, Helsinki University Central Hospital, Helsinki, Finland
The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.

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