Biomedical subjects
Publications and source records attributed to Ngai-Shing Mok.
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SARS is a new infection in human. Patients recovering from SARS had palpitation in the form of sinus tachycardia. This study to identify the possible causes for the tachycardia excluded active disease, thyroid dysfunction, haematological, cardiac, autonomic and significant pulmonary defect at 2 months from onset of disease. The symptomatology was attributed to physical deconditioning and anxiety state. Physical and psychological fitness should be restored with rehabilitation.
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The typical arrhythmias found in patients with the Brugada syndrome is either ventricular fibrillation or polymorphic ventricular tachycardia. We report the case of a patient who presented with supraventricular tachycardia accompanied by ECG features of the Brugada syndrome (BrS) during both tachyarrhythmia and sinus rhythm. This case lends support to the recently reported association between supraventricular tachyarrhythmia and BrS and the hypothesis that the arrhythmogenic substrate in BrS is not limited to the ventricular level.
Ketoconazole is not known to be proarrhythmic without concomitant use of QT interval-prolonging drugs. We report a woman with coronary artery disease who developed a markedly prolonged QT interval and torsades de pointes (TdP) after taking ketoconazole for treatment of fungal infection. Her QT interval returned to normal upon withdrawal of ketoconazole. Genetic study did not find any mutation in her genes that encode cardiac IKr channel proteins. We postulate that by virtue of its direct blocking action on IKr, ketoconazole alone may prolong QT interval and induce TdP. This calls for attention when ketoconazole is administered to patients with risk factors for acquired long QT syndrome.
Typically Brugada syndrome presents with either ventricular fibrillation or polymorphic ventricular tachycardia that may result in sudden death or syncope in patients without any structural heart disease. We report the case of a patient with Brugada syndrome who presented atypically with recurrent presyncope following physical exertion due to sustained monomorphic ventricular tachycardia, which appeared to be sensitive to both adenosine and catecholamine. He refused ICD implantation but remained asymptomatic on treatment with a beta-blocker.
We report an adolescent with a malignant form of Brugada syndrome who presented with 15 episodes of ventricular fibrillation (VF) over 10 days, shortly after implantation of an implantable cardioverter defibrillator. Oral quinidine bisulphate at a dose of 1000 mg/day successfully suppressed the electrical storm and recurrence of VF over 18-month follow-up. It also normalized the ST-segment elevation in his right precordial leads, suppressed all ambient unifocal ventricular extrasystoles and induction of VF on programmed electrical stimulation. This case suggests that quinidine, by virtue of its blocking action on Ito, may be useful as adjunctive therapy in Brugada syndrome.
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BACKGROUND AND OBJECTIVES: Biventricular pacing is a new modality of treatment for patients with drug-refractory heart failure and ECG evidence of dyssynchronous ventricular contraction. A third lead is required to be placed in a coronary vein through the coronary sinus for left ventricular pacing, in addition to the atrial and right ventricular leads. Subclavian crush phenomenon is associated with lead placement using subclavian puncture. Cephalic venous cutdown, free of this complication, provides vascular access which is probably too small for multiple leads placement in biventricular pacing. Contrast venography guided axillary vein puncture (AP) is an alternative approach. This study reports on clinical experience of this technique in biventricular pacing. METHODS: AP is the method of choice for biventricular pacing in Princess Margaret Hospital and Stanford University Medical Center. Patients' clinical characteristics, effectiveness and safety of the technique were analysed. RESULTS: AP was performed in 35 patients, 29 male and six female with mean age 57.1 +/- 14.7 years from 1 January 2000 to 30 June 2001. Six patients had biventricular pacing alone and 29 patients had biventricular implantable cardioverter defibrillator (ICD) implanted. Twelve (34.3%) patients have ischaemic cardiomyopathy, 22 (62.9%) patients have dilated cardiomyopathy and one (2.9%) patient has hypertrophic cardiomyopathy. Six (17.1%) patients were in NYHA Class II heart failure, 21 (60.0%) patients were in Class III and eight (22.9%) patients were in Class IV. The mean EF was 23.1 +/- 7.6%. AP was attempted for placement of all three leads in all patients. AP was successful in 34 (97.1%) patients. The single failure was due to small size of the axillary vein. There were no AP, lead or contrast-related complications with a follow up of 12 months. CONCLUSIONS: AP is both effective and safe for biventricular pacing. It may be the method of choice in biventricular pacing.
Febrile illness has been rarely reported to modulate ST segment elevation in right precordial leads on ECG or even precipitate ventricular fibrillation in patients with Brugada syndrome. We report the case of a patient whose Brugada ECG pattern was unmasked by hyperthermia secondary to acute cholangitis. Serial ECGs showed progressive attenuation of ST segment elevation as body temperature gradually returned to normal. Structural heart disease was ruled out. Intravenous flecainide injection reproduced a less remarkable ST segment elevation. Genetic screening demonstrated a single amino acid substitution (H681P) in the SCN5A gene, thus confirming the diagnosis of Brugada syndrome. In vitro expression of this newly characterized genetic defect revealed novel biophysical abnormalities consisting of a shift in both steady-state activation and inactivation, resulting in a 60% reduction of sodium window current. Thus, SCN5A-H681P mutation induces a significant loss of transmembrane current and is clinically associated with a pathologic phenotype that is elicited by hyperthermia. Overall the observed clinical features are in agreement with previous observations and strongly suggest that fever may be an environmental modifier among Brugada syndrome patients with a detrimental (and possibly arrhythmogenic) effect on cardiac repolarization.
BACKGROUND: Arterial desaturation is a commonly accepted clinical basis for discontinuing physical activity in people with chronic obstructive pulmonary disease. OBJECTIVE: The purpose of this exploratory study was to examine the electrocardiograms of people with severe chronic obstructive pulmonary disease recovering from exercise-induced arterial desaturation. SUBJECTS: Subjects (n = 25) walked for 6 minutes while oxygen saturation was monitored. METHODS: When the Spo2 decreased below 90%, subjects were asked to sit and rest while the electrocardiograms were recorded. For all patients, Spo2 decreased 11.6% on average below baseline during walking. Four patients developed dysrhythmias during desaturation, with a mean lowest Spo2 of 85%. The Spo2 in six other patients continued to decrease below 80% despite rest, yet these patients did not develop new dysrhythmias. CONCLUSIONS: Our findings suggest that a decrease in Spo2 during exercise does not necessarily correlate with cardiac rhythm.