Unmasking Effect of Propafenone on the Concealed Form of the Brugada Phenomenon ANTE MATANA, VLADIMIR GOLDNER, KARLO STANIC, ZARKO MAVRIC, LUKA ZAPUTOVIC, and ZRINKA MATANA From the Department of Internal Medicine, Division of Cardiology, Clinical Hospital Center Rijeka, Rijeka, Croatia MATANA, A., ET AL.,: Unmasking Effect of Propafenone on the Concealed Form of the Brugada Phe- nomenon. A case report of a patient with frequent ventricular premature beats but with an otherwise nor- mal ECG and no structural heart disease. Propafenone in therapeutical doses unmasked the ECG picture of the Brugada phenomenon. (PACE 2000; 23:416-418) Brugada syndrome, propafenone Introduction In 1992 the Brugada syndrome was described as a separate clinical entity comprising a persis- tent ST elevation in leads V1-V3 of a 12-lead ECG, right bundle branch block (RBBB) and sudden un- expected death (i.e., idiopathic ventricular fibril- lation [VF] in the absence of a structural heart dis- ease).^ Basically, the syndrome is a disturbance at the level of the sodium channel, and is genetically transmitted as an autosomal dominant trait.^"^ In many affected individuals the ECG occasionally appears normal, and the phenotype can be un- masked by group I antiarrhythmics. '^ The only ef- fective therapy for the protection of patients from sudden death is the implantation of an im- plantable cardioverter defibrillator ^^ Case Report A 64-year-old female patient complained of persistent palpitations during the last month, but without syncope. She had mild hypertension and diabetes that was regulated by diet, but was other- wise healthy. There was no family history of sud- den deaths. Physical examination was normal, but the patient was overweight. Laboratory analyses showed elevated blood levels of glucose, choles- terol, and triglycerides, the others were within normal limits. Chest X ray and echocardiographic findings were normal. The 12-lead ECG showed a sinus rhythm of 60/min and single ventricular premature heats (VPB). PR interval, QRS duration, QTc interval, and the QT interval dispersion were within normal limits (Fig. lA). The ECG exercise stress testing and the stress myocardial scintigra- Address for reprints: Ante Matana, M.D., Department of Inter- nal Medicine, Division of Cardiology, Clinica! Hospital Center Rijeka, HR 51000 Rijeka. T. Stri26a 3. Croatia. Fax: +385-51- 218-059. Received September 13, 1999; accepted October 27, 1999. phy (SPECT) were normal. No late ventricular po- tentials were registered in the sigual-averaged ECG. Holter monitoring registered a total of 40,550 VPB (of which two pairs), 13 supraventricular pre- mature beats (SVPB), and the heart rate variability (HRV) parameters were within normal values (SDNN - 118.2 ms, ASDNN 5 = 68.3 ms, SDANN 5 = 92.0 ms). Coronary arteriography was normal. Since therapy with atenolol followed by sotalol had no effects, the patient finally received propafenone in a daily dose of 150 mg tid. During the propafenoue therapy the patient was well and without palpitations. However, the ECG done dur- ing the propafenone therapy registered a coved- type down-sloping ST segment elevation, ending in a negative deflection in leads V1-V2. a saddle- back ST elevation in V3 and RBBB (QRS = 120 ms), prolongation of the PR interval (220 ms), and a left axis deviation (-50°). (Fig. IB). VPB disap- peared. On repeated Holter monitoring 1 SVPB and no VPB were registered, and the HRV param- eters were shortened (SDNN ^ 51.3 ms. ASDNN 5 - 30.7 ms, SDANN 5 = 41.3 ms). Therapy with propafenone was discontinued and ECG resumed its earlier aspect. (Fig. lC). During the eiectro- physiological study the basic measurements were within normal limits (PQ = 170 ms, QRS up to 90 ms, RR = 770 ms, QT = 370 ms, QTc - 422 ms; AH interval = 100 ms, HV interval = 55 ms). Ven- tricular tachycardia (VT) could not be provoked with programmed stimulation from the right ven- tricular apex and from the right ventricle outflow tract with a 510 and 440 ms basic cycle length, with one and two extrastimuli. Since the patient showed no signs of ischemic or inflammatory heart disease, disorders of the central or peripheral nervous system, pulmonary thromboembolism, and electrolyte or metabolic disorders,^ it was concluded that this was a case of concealed Brugada phenomenon temporarily un- masked by the propafenone therapy. The patient 416 March 2000 PACE. Vol. 23