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Ilovi, C, LULE GN, Obel AO, Irimu HM.  2011.  Correlation of WHO Clinical Staging with CD4 cell count in adult HIV patient at Kenyatta National Hospital. East African Medical Journal. 88(2):67-70.


Nesbitt, WH, Lampe C, Lustgarten D, Obel OA.  2007.  Supraventricular tachycardia with two VA intervals: what is the mechanism?


Obel, OA, d'Avila A, Neuzil P, Saad EB, Ruskin JN, Reddy VY.  2006.  Ablation of left ventricular epicardial outflow tract tachycardia from the distal great cardiac vein. AbstractWebsite

The purpose of this study was to examine the feasibility and safety of ablation of idiopathic outflow tract ventricular tachycardia (OTVT) from the distal ramifications of the coronary sinus (CS).
A significant minority of patients presenting with idiopathic OTVT have an epicardial focus, the standard approach to which involves ablation from within one of the aortic valve cusps (AVCs). We describe the successful ablation of idiopathic epicardial OTVT from within the CS in the distal great cardiac vein (GCV).

Ablation from the distal GCV was performed in 5 patients with idiopathic OTVT who had unfavorable mapping, in some cases unsuccessful ablation from various endocardial and epicardial sites including the AVCs, and in 1 patient via the direct epicardial approach. An electroanatomic mapping system (Carto) was used in 3 patients, and conventional mapping was performed in 2 patients, and in 3 patients cryothermal ablation was performed.
In all patients, the first ablation lesion in the GCV successfully eliminated the arrhythmia. All patients have remained free of VT after a mean follow-up of 24 (7 to 44) months. There were no immediate or long-term complications.
Idiopathic epicardial OTVT can be successfully ablated from the distal GCV, and should be seen as an alternative to ablation from the aortic valve cusps.




Obel, OA, Camm AJ.  1998.  Accessory pathway reciprocating tachycardia. AbstractWebsite

Patients who have an accessory pathway (AP) of atrioventricular (AV) conduction may develop circus movement tachycardia otherwise known as atrioventricular re-entrant tachycardia (AVRT). Orthodromic AVRT is the most common form. It occurs as a result of antegrade conduction through the normal AV conduction system and retrograde conduction to the atria via the AP. Less commonly, conduction occurs in the opposite direction resulting in antidromic AVRT. Tachycardia may also involve multiple APs which may provide both antegrade and retrograde conduction and may alternate antegradely or retrogradely. Tachycardia may occur in which the AP simply acts as a bystander, and does not participate in the tachycardia mechanism. When atrial fibrillation is conducted to the ventricles via and AP, the resultant ventricular rate may be extremely rapid, placing the patient at risk of developing ventricular fibrillation and cardiac arrest. This paper reviews the anatomical and physiological substrates involved in the pathogenesis of AVRT. The acute and long-term management of patients who suffer from these arrhythmias will then be discussed. The normal AV annulus is composed exclusively of electrically inert fibrous tissue. The AV node and His bundle normally act as the sole route of electrical conduction. Accessory pathways occur at all points along the AV ring, and usually occur as isolated abnormalities, although a proportion of patients have associated congenital abnormalities. This is particularly true of right-sided APs. Most APs exhibit non-decremental conduction properties, and conduct faster than normal AV conduction tissue. In many patients with APs the surface ECG reveals clear evidence of pre-excitation, and a good idea of pathway localization is possible using one or more of several algorithms which have been developed. Patients with latent pre-excitation, intermittent pre-excitation, and patients with concealed APs have not evidence of pre-excitation on a proportion or all of Their surface ECGs. Patients present with a history of paroxysmal palpitations, often with associated symptoms such as chest discomfort Syncope is a rare presenting symptom. Unless bundle branch block is present, patients with orthodromic AVRT exhibit a narrow complex tachycardia on the surface ECG. Patients with pre-excited tachycardia including antidromic AVRT, and other forms of SVT in which the AP conducts to the ventricles as a bystander but does not participate in the tachycardias mechanism, present as broad complex tachycardias on the surface ECG which may be difficult to distinguish from ventricular tachycardia. Adenosine is increasingly used for this purpose since it is highly efficacious and has an extremely short half-life. Adenosine is also very useful in the diagnosis of broad-complex tachycardia, and in unmasking latent pre-excitation during sinus rhythm. Electrophysiology study in these patients is frequently performed at the same time as an attempt at catheter ablation; it aims to diagnose, localize and determine the functional characteristics of an AP, and to characterize the role of the pathway in tachycardia. AVRT can be reliably terminated by effective AV nodal blockade. Drug therapy for the prevention of AVRT is useful for temporary control whilst awaiting more definitive measures and in certain cases as long-term management. No class of drug stands out as 'therapy of choice', and physician preference, pro-arrhythmic effects and associated conditions need to be taken into account such that an individual choice can be made in each patient. The management of patients with AVRT has been revolutionized in recent years with the advent of catheter-based techniques for their cure. Whilst this method of treatment is highly effective and has low complication rates, pathways in particular locations such as the septal region remain challenging.

Obel, OA, Camm AJ.  1998.  The use of drugs for cardioversion of recent onset atrial fibrillation and flutter. Focus on ibutilide. Abstract

Atrial fibrillation (AF) is the most common sustained arrhythmia, particularly in the elderly population. It is well recognised that AF is a major cause of stroke, even in the absence of underlying heart disease. Although AF and atrial flutter share many causes and may be seen in the same patient, there are differences between these arrhythmias: atrial flutter is less common, and the risk of stroke associated with it is less than that with AF. In addition to stroke, both AF and atrial flutter may cause cardiomyopathy, which may be fully reversible with effective treatment of the arrhythmia. Both AF and atrial flutter can result in severe symptoms and may precipitate heart failure, ischaemia and syncope. Recent research indicates that AF is a self-perpetuating arrhythmia, and that the longer it is left untreated the less likely it is that effective cardioversion will be possible. Drugs are an attractive option for the cardioversion of AF and atrial flutter because their use does not require anaesthesia. Antiarrhythmic drugs in class III of the Vaughan-Williams classification are effective in the treatment of AF, but they have adverse effects; several new 'pure' class III agents are under development. The first of these to be made available is ibutilide, a methanesulphonamide derivative. Initial results are encouraging, particularly for atrial flutter. However, the drug has the potential for proarrhythmic effects and physicians who use it will need to be aware of these.


Obel, OA.  1997.  Cardiological examinations. Website
Obel, OA, Camm AJ.  1997.  Supraventricular tachycardia. ECG diagnosis and anatomy. Abstract

This paper reviews the anatomical substrates responsible for the induction and maintenance of supraventricular tachycardia and discusses the ECG findings associated with these tachycardias. The normal anatomy of the supraventricular conducting system, particularly within the atria, is complex with conduction proceeding along preferential pathway, which are in turn determined in part by the anisotropic properties of the atrial myocardium. There appear to be at least dual inputs to the atrioventricular node, a posteriorly situated slow pathway and an anterior fast pathway. It is sometimes possible to relate ECG findings directly to anatomical substrates; for example, in some cases of atrial tachycardia the site of the atrial focus (left or right, superior or inferior) can be determined by the polarity of the P wave. The anatomical substrates responsible for intra-atrial re-entry, atrial flutter and atrial fibrillation relate to anatomical barriers to impulse propagation and areas of slow conduction. In atrial flutter the crista terminalis, Eustachian valve, inferior vena cava, coronary sinus os, and tricuspid annulus have been identified as anatomical barriers to conduction around which a macro re-entrant circuit within the right atrium may conduct, usually in a counter-clockwise direction. Clockwise direction of conduction, and other mechanisms of tachycardia, occur in some of the less typical forms of atrial fluter. Atrial fibrillation is caused by multiple wavelets which randomly conduct through the atrial myocardium and are responsible for the irregular 'fibrillation waves' on the ECG. Supraventricular tachycardia presents as a narrow complex tachycardia unless pre-existing or rate-related bundle branch block is present. Less common causes for a broad complex tachycardia occurring in supraventricular tachycardia include an accessory atrioventricular or atriofascicular pathway conducting antegradely during tachycardia, or accessory pathway participation as a bystander during supraventricular tachycardia. ECG features which can help to distinguish between atrioventricular nodal re-entrant tachycardia and atrioventricular re-entrant tachycardia include: (1) the presence of a delta wave during sinus rhythm which is highly suggestive of atrioventricular re-entrant tachycardia as the mechanism of supraventricular tachycardia; (2) the finding of a pseudo s (lead II) or pseudo r' (lead V1) during tachycardia in atrioventricular nodal re-entrant tachycardia; (3) lengthening of the tachycardia cycle length in cases of atrioventricular re-entrant tachycardia when bundle branch block occurs ipsilateral to the accessory pathway and (4) the finding of QRS alternans during tachycardia which is suggestive of atrioventricular re-entrant tachycardia. "Long RP' tachycardia may be caused by an atrial tachycardia due to an inferiorly situated area of abnormal automaticity, atypical atrioventricular nodal re-entrant tachycardia with slow retrograde conduction, or atrioventricular re-entrant tachycardia with an accessory pathway conducting slowly from ventricle to atrium during tachycardia.

Gallagher, MM, Obel OA, Camm JA.  1997.  Tachycardia-induced atrial myopathy: an important mechanism in the pathophysiology of atrial fibrillation? Abstract

The atrial myocardium of patients with chronic atrial fibrillation (AF) is often abnormal in its histologic features and in its electrophysiologic properties. These abnormalities have been interpreted in some cases as the cause of AF and in others as a consequence of AF. We believe that both are the case. We will review the features of this atrial myopathy and discuss the likely mechanisms and consequences of the process.


Obel, AO.  1993.  Pharmacology of beta adrenoreceptor blocking agents. East African Medical Journal.. 70(7):401.
Obel, AO.  1993.  Anti - mycotic agents and their relevance to HIV – infected patients. Medicine in Africa. (2):6-8..


Koech D.K, Obel AO.  1991.  Potassium supplementation versus bendrofluazide in mildly to mo derately hypertensive Kenyans. Journal of Cardiovascular Pharmacology. (17):504-507.


Koech D.K, Obel AO.  1990.  Treatment of HIV infections and AIDS: New Horizons. East African Medical. (67):77-81. Abstract

Treatment of HIV infections has involved the use of antiviral drugs as well as those drugs that act against opportunistic infections. Immune modulators have also been used. A review of these drugs is reported emphasizing on those which have great promise in the clinical management of HIV infections in the light of our present knowledge on immunopathology of the disease.


Obel, AO.  1989.  Placebo - controlled trial of potassium supplements in black patients with mild essential hypertension. ournal of Cardiovascular Pharmacology. 14(2):294-296.


Obel, AO.  1988.  Body mass index in Non - Insulin Dependent Diabetes in K enya. Tropical and Geographical Medicine . 40(2):93-96.


Obel, AO, W.M KT-, Ellison R.H MM.  1985.  Dietary sodium/potassium ratios in salt substitute and its putative significance in essential hypertension. East African Medical Journal. ( 62):507-514.


AO, O, SK S, SO ML, Gitonga E, Shah MV, Gitau W.  1984.  Acquired immunodeficiency syndrome in an African. Website
Obel, AO, L G, J W.  1984.  Comparison of slow - release frusemide (Lasic Retard) and bendrofluazide in the trea tment of moderate hypertension in Kenya Negroes. Clinical Trial Journal. (21):443-50. AbstractWebsite

The relative efficacy and the risk of producing biochemical disturbances by bendrofluazide, 10 mg once daily and slow-release frusemide (Lasix Retard) 60 mg once daily, during treatment of moderate hypertension in Kenyan negroes were compared in a double-blind randomized control study. Fifty newly diagnosed hypertensive patients entered the study which lasted for 36 wk. There were 7 drop-outs at the end of the trial. Both slow-release frusemide and bendrofluazide significantly decreased both supine and standing diastolic pressures and standing systolic pressure (P < 0.05). Bendrofluazide also showed a significant effect on supine systolic pressure (P < 0.01), which was greater than that of slow-release frusemide. Biochemical disturbances were more pronounced in patients receiving bendrofluazide than in those on slow-release frusemide. Bendrofluazide treatment resulted in significant hyperuricemia (P < 0.02), hypokalemia (P < 0.01) and a rise in blood glucose which was not statistically significant (t [test of significance] = 0.26). Slow-release frusemide produced no significant alterations in blood uric acid, K and blood glucose. Both treatment modalities produced no significant change in other biochemical and hematological indices. Compared with slow-release frusemide, bendrofluazide produced potentially serious adverse biochemical changes. The drugs were equally effective in controlling moderate hypertension although the hypotensive effect on systolic blood pressure was more pronounced with bendrofluazide.


Obel, AO.  1983.  Poisons information and treatment.
Obel, AO.  1983.  A comparison of timolol plus hydrochlorothiazide plus amiloride and methyldopa in essential hypertension in black Africans. ropical and Geographical Medicine. (35):285-91. AbstractWebsite

The antihypertensive effect of the fixed combination of timolol, a beta-blocking agent, hydrochlorothiazide, a thiazide diuretic, and amiloride, a potassium sparing agent, was compared against that of methyldopa in an open study lasting 16 weeks in 32 ambulatory African patients with previously untreated diastolic blood pressure of 95-120 mm Hg. A significant fall in mean diastolic and systolic blood pressure was achieved in both groups up to 8 weeks of treatment and was sustained in the timolol-hydrochlorothiazide-amiloride group during the entire follow-up. In the methyldopa group, mean diastolic and systolic blood pressure rose during follow-up. At 16 weeks the fall in mean diastolic and systolic blood pressure was significantly greater in the timolol-hydrochlorothiazide-amiloride treated patients than in the methyldopa group. Adverse reactions were more frequent and severe in the methyldopa group than in timolol-hydrochlorothiazide-amiloride treated patients. It is concluded that the fixed drug combination of timolol-hydrochlorothiazide-amiloride (Moducren) is effective in controlling mild to moderate hypertension in Africans and is better tolerated than methyldopa in these patients. It is further noted that hypertensive patients can be treated with a combination tablet once a day. This is of crucial significance as it would promote better compliance and, hence, minimize the sequelae of poorly controlled hypertension.

Obel, AO.  1983.  Epidemiology and diabetes mellitus in referral hospital in a tropical developing country. . Tohoku Journal of Experimental Medicine. (14):207-10.


Obel, AO.  1982.  Pharmacokinetics in medicine.

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