• Experimental Cardiology
• Cardiac Electrophysiology and Pharmacology
• Electrophysiological and pathophysiological basis of
  cardiac arrhythmias
• Pharmacology of antiarrhythmic agents
• Pharmacology of non-antiarrhythmic agents with
  cardiac actions
• Sudden cardiac death
• Long QT Syndrome
• Brugada Syndrome
• Electrocardiographic (ECG) manifestations of electrical heterogeneity
• Mechanisms underlying QT dispersion
• Electrical heterogeneity as the basis for pharmacologic distinctions in the heart

My principal interests are in the area of cardiac electrophysiology and pharmacology. I have been involved in a number of investigations designed to assess the role of electrical heterogeneity in the genesis of cardiac arrhythmias using microelectrode techniques applied to cardiac tissues and the arterially perfused wedge preparation developed at our institute.

This preparation permits simultaneous recordings of a pseudo-electrocardiogram together with the recordings of the electrical activity (action potentials) of the different cell-type (endocardial, epicardial and M cell) present across the ventricular wall of the heart. This model allows us to evaluate the effects of compounds on the electrical activity of the heart. The compound tested can be agents with a potential antiarrhythmic effect, designed to prevent, reduce or eliminate cardiac arrhythmias, or a compound whose primary effect is not on the heart (antidepressant, antibiotic, antihistaminic etc.), but one that can have a secondary effect on the electrical activity of the heart. This secondary effect can be beneficial or harmful, particularly if it has the potential to induce an abnormal rhythm of the heart or arrhythmia.

A good deal of my time is devoted to assessing the action of new pharmacological agents on electrophysiological parameters using the canine left ventricular wedge preparation. Our primary focus is the ability of drugs to prolong the action potential and the QT interval of the ECG and accentuate transmural dispersion of action potential duration (TD-APD), thus setting the stage for the development of life-threatening cardiac arrhythmias.

I am also involved in studies designed to evaluate the effects of drugs or pathophysiological conditions on the electrical activity of pulmonary vein (PV) sleeves preparations. The rationale of this experimental work is that recent studies have shown that atrial fibrillation, the most common arrhythmia requiring medical treatment is commonly triggered by extra beats originating in the PV sleeves. This work involves isolation of PV sleeves, electrical stimulation and recording of the electrical activity using microelectrode techniques.

Sicouri S, Antzelevitch C. A subpopulation of cells with unique electrophysiologic properties in the deep subepicardium of the canine ventricle. The M Cell. Cir. Res., 68: 1729-1741, 1991.
PubMed ID: 2036721

Antzelevitch C, Sicouri S. Clinical relevance of cardiac arrhythmias generated by afterdepolarizations. The role of M cells in the generation of U waves, triggered activity and Torsade de Pointes. J Am Coll. Cardiol 23:259-277, 1994.
PubMed ID: 8277090

Sicouri S, Moro S, Litovsky SH, Elizari MV, Antzelevitch C. Chronic amiodarone reduces transmural dispersion of repolarization in the canine heart. J Cardiovasc Electrophysiol. 1997;8:1269-1279.
PubMed ID: 9395170