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Dive into the research topics where James A. Ker is active.

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Featured researches published by James A. Ker.


International Journal of Rheumatic Diseases | 2012

Autonomic impairment in rheumatoid arthritis

Dina Christina Janse van Rensburg; James A. Ker; Catharina C. Grant; Lizelle Fletcher

To determine if there is a difference between autonomic cardiac control as measured by heart rate variability (HRV) in women with rheumatoid arthritis (RA) compared to a healthy control group.


Angiology | 2007

Solitary papillary muscle hypertrophy : a new echo-electrocardiographic syndrome? A case report

James A. Ker

Hypertrophic cardiomyopathy is the term for a heterogeneous group of disorders for which various mutations of genes involving proteins of the cardiac sarcomere lead to hypertrophy of various segments of the left ventricle. The hypertrophy can involve the left and/or right ventricle, be symmetric or asymmetric, involving the septum, free wall, mid-ventricle, or apex. The phenomenon of solitary papillary muscle hypertrophy is rare with only 2 references in the literature. Furthermore, giant negative T and U waves are 2 common electrocardiographic phenomena in hypertrophic cardiomyopathy and have been attributed to hypertrophy of the posterior papillary muscle. Solitary hypertrophy of the anterior papillary muscle might be a new echo-electrocardiographic syndrome.


Inflammation | 2000

Comparison of the Effects of Selective and Non-selective Beta-adrenoreceptor Agonists on the Pro-inflammatory Activities of Human Neutrophils in Vitro

Gregory Ronald Tintinger; Ronald Anderson; Annette J. Theron; Grace Ramafi; James A. Ker

The objective of this study was to measure and compare the effects of 4 selective (fenoterol, formoterol, salbutamol, salmeterol) and 3 non-selective (epinephrine, norepinephrine, isoproterenol), β-adrenoreceptor agonists, at a fixed, final concentration of 1 μM, on intracellular cyclic AMP levels in human neutrophils in vitro and to relate alterations in these to the effects of the test agents on the production of superoxide and release of elastase following activation of the cells with the chemoattractant, FMLP. Intracellular cAMP was measured by radioimmunoassay, while superoxide and elastase were assayed using lucigenin-enhanced chemiluminescence and colorimetric procedures respectively. Of the 7 agents tested, fenoterol, formoterol, epinephrine and isoproterenol caused a substantial increase in neutrophil cAMP levels, which correlated well with the inhibitory effects of these agents on superoxide production and elastase release. The other agents were either inactive (salmeterol), or weakly active (norepinephrine, salbutamol). Pretreatment of neutrophils with the non-selective β-adrenoreceptor blockading agent, propranolol (2 μM), attenuated the cAMP-mediated, anti-inflammatory interactions of formoterol, epinephrine and isoproterenol with neutrophils, while atenolol, a selective β1-blockading agent, as well as α1- and α2-adrenoreceptor antagonists were ineffective. These findings demonstrate that some, but not all, currently used β-agonists suppress the proinflammatory activity of human neutrophils through interaction with β2-adrenoreceptors on these cells and activation of adenylyl cyclase. If operative in vivo, these anti-inflammatory properties may contribute, albeit in a secondary manner, to the therapeutic activity of fenoterol, formoterol, epinephrine and isoproterenol.


South African Medical Journal | 2010

Carboxyhaemoglobin levels in water-pipe and cigarette smokers

Ansa Theron; Cedric Schultz; James A. Ker; Nadia Falzone

UNLABELLED Water-pipe smoking is growing in popularity, especially among young people, because of the social nature of the smoking session and the assumption that the effects are less harmful than those of cigarette smoking. It has however been shown that a single water-pipe smoking session produces a 24-hour urinary cotinine level equivalent to smoking 10 cigarettes per day. AIM We aimed to measure carboxyhaemoglogin (COHb) blood levels before and after water-pipe and cigarette smoking sessions. METHOD Self-confessed smokers older than 18 years (N=30) volunteered to smoke a water-pipe or a cigarette and have their blood COHb levels measured under controlled conditions. RESULTS Mean baseline COHb levels were 2.9% for the 15 cigarette smokers and 1.0% for the 15 water-pipe smokers. Levels increased by a mean of 481.7% in water-pipe smokers as opposed to 39.9% in cigarette smokers. CONCLUSION The study demonstrated that water-pipe smokers had significantly higher increases in blood COHb levels than cigarette smokers during a single smoking session.


Cardiovascular Ultrasound | 2009

Sub aortic tendon induced ST segment elevation – a new echo electrocardiographic phenomenon?

James A. Ker

The causes for ST-segment elevation other than myocardial infarction are numerous.The existence of left ventricular false tendons has been known for more than a century. Currently, the clinical entities associated with these left ventricular false tendons include innocent murmurs and premature ventricular contractions.A case report is presented where such a false tendon, attached to the interventricular septum, is responsible for striking ST-segment elevation in the anterior precordial leads.It is proposed that this is a newly observed entity – that of subaortic tendon-induced ST-segment elevation. This is proposed as a totally benign phenomenon with the clinical importance in that it should not be confused with other pathological processes, such as the Brugada syndrome.


Cardiovascular Ultrasound | 2009

The subaortic tendon as a mimic of hypertrophic cardiomyopathy

James A. Ker

Originally described by Brock and Teare, today hypertrophic cardiomyopathy is clinically defined as left (or right) ventricular hypertrophy without a known cardiac or systemic cause, such as systemic hypertension, Fabrys disease or aortic stenosis.Also appreciated today is the enormous genotypic and phenotypic heterogeneity of this disease with more than 300 mutations over more than 24 genes, encoding various sarcomeric, mitochondrial and calcium-handling proteins, all as genetic causes for hypertrophic cardiomyopathy.Phenotypically, the disease can vary from negligible to extreme hypertrophy, affecting either the left and/or right ventricle in an apical, midventricular or subaortic location.Left ventricular false tendons are thin, fibrous or fibromuscular structures that traverse the left ventricular cavity. Recently, a case report was presented where it was shown that such a false tendon, originating from a subaortic location, was responsible for striking ST-segment elevation on the surface electrocardiogram.In this case report, a case is presented where such a subaortic tendon led to the classic echocardiographic appearance of hypertrophic cardiomyopathy, thus in the assessment of hypertrophic cardiomyopathy, this entity needs to be excluded in order to prevent a false positive diagnosis of hypertrophic cardiomyopathy.


Thyroid Research | 2012

Thyroxine and cardiac electrophysiology - a forgotten physiological duo?

James A. Ker

Thyroid hormone exerts numerous effects on the cardiovascular system. Hypothyroidism can lead to various electrocardiographic and mechanical changes in the heart and blood vessels.The potential risk for sudden cardiac death in patients with hypothyroidism have never been properly explored. However, numerous reports of various electrocardiographic changes indicative of such a risk has been published.In this case report the occurrence of ventricular late potentials in a case of overt hypothyroidism is described and furthermore, the disappearance of these potentials with T4 treatment alone is shown.It is concluded that the concept that undiagnosed and/or untreated hypothyroidism poses a risk for sudden cardiac death is worth exploring.


Current Medical Research and Opinion | 2011

Hypertension and its management in countries in Africa and the Middle East, with special reference to the place of β-blockade

M. Samir Arnaout; Wael Almahmeed; M. Mohsen Ibrahim; James A. Ker; Ma Taher Khalil; Corrie T. Van Wyk; Giuseppe Mancia; Eyas Al Mousa

Abstract Background: The prevalence and clinical consequences of hypertension in countries in Africa and the Middle East have not been studied as well as in other regions. Scope: We have reviewed the literature on the epidemiology and management of hypertension and related cardiovascular complications in countries within Africa and the Middle East. A PubMed search for countries in the region and ‘hypertension’ was supplemented by articles identified from reviews, and by literature suggested by the authors. Findings: The prevalence of hypertension is >20% in some countries in the Middle East and Africa, despite an average population age that is some 10–15 years lower than those of developed countries. Hypertension in these countries is associated with an increased risk of cardiovascular risk factors and cardiovascular disease, as elsewhere. Awareness rates of hypertension are low. Hypertension and its complications are undertreated, and mortality rates from cardiovascular disease are higher than in developed countries. Conclusion: Available resources should be brought to bear on the management of hypertension in these countries. In particular, a recent downgrading of the importance of β-blockers in hypertension management guidelines needs to be reassessed. These agents are as effective as other antihypertensive classes both on blood pressures and on cardiovascular event rates. General concerns over an increased rate of new-onset diabetes with β-blockers have been overstated, although these agents should be avoided in metabolic syndrome.


International Journal of Cardiology | 2010

The “mirror” papillary muscle

James A. Ker

Various structural anomalies of the papillary muscles have been described in a variety of primary and secondary cardiovascular disorders. Some of these lead to intraventricular pressure gradients, while some has no obvious functional consequences at present. A peculiar anterolateral papillary muscle anomaly with an accessory papillary muscle, causing the appearance of a mirror image on transthoracic echocardiography is described.


Cardiovascular Ultrasound | 2010

Bigeminy and the bifid papillary muscle

James A. Ker

Various structural anomalies of the left ventricular papillary muscles have been observed in recent years. Many of these have been linked to electrocardiographic aberrations.Recently two reports have appeared where the base of the posterior papillary muscle was identified as the source of frequent premature ventricular complexes. In some of these patients these frequent premature ventricular complexes have led to left ventricular dysfunction.In this report a newly discovered structural variant of the anterior papillary muscle is described--the bifid papillary muscle. Furthermore, it is proposed that this bifid papillary muscle is the source of frequent ventricular premature complexes, presenting as bigeminy in a patient with normal left ventricular function.

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Ja Ker

University of Pretoria

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M. Samir Arnaout

American University of Beirut

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