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Biomedical subjects

R P Steeds

Publications and source records attributed to R P Steeds.

At least 19 recordsLinked to original sources
PubMed2006

The treatment of coronary artery disease in patients with chronic kidney disease.

Premature cardiovascular disease is the largest cause of mortality, and a major cause of morbidity, in patients with chronic kidney disease (CKD). Patients with end-stage kidney disease (ESKD) are at extreme risk, but cardiovascular event rates are increased even in early CKD. There is little controlled trial evidence on which to base treatment, as most therapeutic trials have excluded CKD patients. Current treatment strategies are therefore based upon small prospective studies or retrospective analyses of controlled trials and registry data. It is thus unclear whether CKD patients benefit from modern secondary preventive treatments in the same manner as patients with normal renal function. There is a need for randomized trials to identify effective drugs to prevent and treat coronary artery disease in CKD. Revascularization by CABG in CKD has been widely reported in registry data to provide better results than medical treatment or angioplasty. Recent angioplasty data in patients with CKD, however, show improving results, and the risks of CABG in CKD remain high. It is not clear which revascularization technique has a better outcome in patients 'equally suitable' on angiographic criteria for either procedure. The high rate of late adverse cardiovascular events after both CABG and angioplasty accentuates the need for effective secondary preventive therapy disease in these high-risk patients.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2006

Comparison of transthoracic echocardiography with harmonic imaging with transoesophageal echocardiography for the diagnosis of patent foramen ovale.

The optimal diagnostic method for patent foramen ovale is currently unclear. This study compared bubble contrast second harmonic transthoracic (TTE) and transoesophageal echocardiography (TOE) on 87 consecutive patients referred for TOE for all indications. A right left shunt was diagnosed in 34 cases (39%), with TTE positive in 26 cases (sensitivity 76.5%), TOE positive in 27 cases (sensitivity 79.4%). Pitfalls of TTE included quality of echo and left sided valve lesions, and for TOE the ability to perform an adequate Valsalva manoeuvre. In conclusion, both tests have similar sensitivity and should be viewed as complementary modalities.

Adult↗
PubMed2005

Takayasu arteritis: role of cardiovascular magnetic imaging.

Takayasu arteritis (TA) is a primary arteritis of unknown cause that commonly affects the aorta and its main branches. Traditionally, X-ray contrast angiography has been the gold standard for diagnosis and review of this chronic disease but recent developments suggest that non-invasive imaging with multiplanar cardiovascular magnetic resonance imaging (CMR) and magnetic resonance angiography (MRA) have a number of advantages for use in routine care. This review utilises a series of cases referred for imaging at the Royal Brompton Hospital, London to illustrate these points of development.

Adult↗
PubMed2004

Predicting late sudden death from ventricular arrhythmia in adults following surgical repair of tetralogy of Fallot.

Tetralogy of Fallot was the first complex congenital cardiac defect to undergo open repair. The life expectancy and quality of life of those surviving surgery is now good, although late survival is compromised by the occurrence of sudden death. The emergence of successful methods for both the prevention of arrhythmias (including valve replacements and electrophysiological ablation) and the treatment of arrhythmias when they occur (including implantable defibrillators), has meant the identification of those at risk is of even greater importance. This paper reviews the predictive methods currently available to the practising physician caring for these increasingly common patients.

Adult↗
PubMed2001

Novel platelet membrane glycoprotein VI dimorphism is a risk factor for myocardial infarction.

BACKGROUND: Glycoprotein (GP) VI plays a crucial role in platelet activation and aggregation. We investigated whether polymorphic variation at the GP VI locus confers an increased risk of myocardial infarction (MI). METHODS AND RESULTS: Coding and 5' and 3' non-coding regions of the GP VI gene were analyzed by polymerase chain reaction and conformation sensitive gel electrophoresis in 21 healthy subjects. Ten dimorphisms, 5 of which predicted amino acid substitutions (T13254C, A19871G, A21908G, A22630T, C22644A), were identified. Two core haplotypes involving 7 dimorphisms (C10781A and G10873A and all those predicting amino acid substitutions) were apparent. The contribution of the T13254C dimorphism, which predicted the substitution of serine 219 by proline, to risk of MI was assessed in 525 patients with acute MI and 474 controls, all aged <75 years. The allelic odds ratio (OR) for MI associated with the 13254C allele was 1.16 (95% CI, 0.91 to 1.46; P=0.23). Compared with corresponding control subgroups, the 13254CC genotype was more common among cases who were female (OR, 4.52; 95% CI, 1.23 to 16.64; P=0.029), nonsmokers (OR, 2.50; 95% CI, 0.98 to 6.38; P=0.048), aged >/=60 years (OR, 6.48; 95% CI, 1.47 to 28.45; P=0.009) or carried the beta-fibrinogen -148T allele associated with increased fibrinogen levels (OR, 10.49; 95% CI, 1.32 to 83.42; P=0.02). In logistic regression analysis that took other cardiovascular risk factors into account, the interactions of GP VI genotype with age (P=0.005) and beta-fibrinogen genotype (P=0.035) remained significant. CONCLUSIONS: The GP VI 13254CC genotype increases the risk of MI, particularly in older individuals, and the interaction of the GP VI 13254C allele with other candidate risk alleles may accentuate this risk.

Aged↗
PubMed2001

Analysis of the postulated interaction between the angiotensin II sub-type 1 receptor gene A1166C polymorphism and the insertion/deletion polymorphism of the angiotensin converting enzyme gene on risk of myocardial infarction.

A synergistic interaction between the insertion/deletion (I/D) polymorphism within the angiotensin-converting enzyme (ACE) gene and an A/C transversion at nucleotide position 1166 within the angiotensin II sub-type 1 receptor (AT1R) gene on risk of myocardial infarction has been reported. The risk associated with the ACE DD genotype increased with the number of AT1R C alleles present. To investigate this further, ACE I/D and AT1R A1166C genotypes were determined in 541 cases recruited at the time of infarction and 507 population-based controls. There was no difference in either the genotype distribution or allele frequencies between cases and controls for either the ACE polymorphism (P=0.48 and 0.35 respectively) or the AT1R polymorphism (P=0.35 and 0.21 respectively). Odds ratios for risk of MI associated with the ACE DD and AT1R CC genotypes were 1.09 (95% CI, 0.82-1.45) and 1.06 (0.67-1.68) respectively. 3.1% of cases versus 3.6% of controls were homozygous for both the D and C alleles (P=0.71). There was no increase in risk associated with the DD genotype in the presence of either one or two AT1R C alleles in the whole cohorts (OR 0.99, 95% CI 0.65-1.51 and 0.76, 95% CI 0.30-1.88, respectively) nor in sub-groups defined by specific risk factors. In conclusion, no evidence was found to support any interaction between the ACE gene I/D polymorphism and the ATIR gene A1166C transversion in determining the risk of myocardial infarction in the population studied.

Aged↗
PubMed2001

The -1185 A/G and -1051 G/A dimorphisms in the von Willebrand factor gene promoter and risk of myocardial infarction.

Elevated plasma von Willebrand factor (VWF) levels are associated with coronary artery disease, although the precise mechanism for this is unclear. Recently, four linked dimorphisms in the VWF gene promoter were demonstrated to influence plasma VWF level. We conducted a case-control study of 525 acute myocardial infarction (MI) cases and 451 control subjects, all aged < or = 75 years, to assess the potential contribution of two of these dimorphisms (-1185 G/A and -1051 A/G) to the risk of MI. The frequency of the -1185A/-1051G haplotype, associated with elevated VWF levels, was similar in the case and control groups, yielding a haplotypic odds ratio for MI of 0.93 (95% CI 0.77, 1.12, P = 0.43), and there was no significant association between the -1185A/-1051G haplotype and the risk of MI in any subgroup analysed. We therefore conclude that possession of the -1185A/-1051G haplotype does not confer an increased risk for MI.

Aged↗
PubMed2000

Low-dose transdermal testosterone therapy improves angina threshold in men with chronic stable angina: A randomized, double-blind, placebo-controlled study.

BACKGROUND: Experimental studies suggest that androgens induce coronary vasodilatation. We performed this pilot project to examine the clinical effects of long-term low-dose androgens in men with angina. METHODS AND RESULTS: Forty-six men with stable angina completed a 2-week, single-blind placebo run-in, followed by double-blind randomization to 5 mg testosterone daily by transdermal patch or matching placebo for 12 weeks, in addition to their current medication. Time to 1-mm ST-segment depression on treadmill exercise testing and hormone levels were measured and quality of life was assessed by SF-36 at baseline and after 4 and 12 weeks of treatment. Active treatment resulted in a 2-fold increase in androgen levels and an increase in time to 1-mm ST-segment depression from (mean+/-SEM) 309+/-27 seconds at baseline to 343+/-26 seconds after 4 weeks and to 361+/-22 seconds after 12 weeks. This change was statistically significant compared with that seen in the placebo group (from 266+/-25 seconds at baseline to 284+/-23 seconds after 4 weeks and to 292+/-24 seconds after 12 weeks; P:=0.02 between the 2 groups by ANCOVA). The magnitude of the response was greater in those with lower baseline levels of bioavailable testosterone (r=-0. 455, P:<0.05). There were no significant changes in prostate specific antigen, hemoglobin, lipids, or coagulation profiles during the study. There were significant improvements in pain perception (P:=0.026) and role limitation resulting from physical problems (P:=0.024) in the testosterone-treated group. CONCLUSIONS: Low-dose supplemental testosterone treatment in men with chronic stable angina reduces exercise-induced myocardial ischemia.

Administration, Cutaneous↗
PubMed2000

Men with coronary artery disease have lower levels of androgens than men with normal coronary angiograms.

AIMS: High androgen levels are presumed by many to explain the male predisposition to coronary artery disease. However, natural androgens inhibit male atherosclerosis(1). Our aim was to determine whether levels of androgens differ between men with and without coronary artery disease. METHODS AND RESULTS: Ninety male subjects (60 with positive, and 30 with negative coronary angiograms) were recruited. Early morning, fasting blood samples were taken from each patient and free, total and bioavailable testosterone, sex hormone binding globulin, oestradiol, and lipids were measured. Bioavailable testosterone was assayed using a modified technique. Free androgen index was calculated. Men with coronary artery disease had significantly lower levels of free testosterone (mean (standard deviation)); 47.95 (13.77) vs 59.87 (26. 05) pmol. l(-1), P=0.027), bioavailable testosterone; 2.55 (0.77) vs 3.26 (1.18) nmol. l(-1), P=0.005 and free androgen index; 37.8 (10. 4) vs 48.47 (18.3), P=0.005, than controls. After controlling for differences in age and body mass index the differences in free androgen index and bioavailable testosterone remained statistically significant (P=0.008 and P=0.013, respectively). CONCLUSION: Men with coronary artery disease have significantly lower levels of androgens than normal controls, challenging the preconception that physiologically high levels of androgens in men account for their increased relative risk for coronary artery disease.

Adult↗
PubMed1999

The GPIa C807T dimorphism associated with platelet collagen receptor density is not a risk factor for myocardial infarction.

The platelet collagen receptor, GPIa/IIa, is an important mediator of platelet adhesion to fibrillar collagens at sites of vascular injury. Recently, a dimorphism at nucleotide 807 of the GPIa cDNA (TTC/TTT in codon 224) was shown to be associated with variation in GPIa/IIa receptor density on the platelet surface. We conducted a case-control study to determine if the 807T allele, linked with increased GPIa/IIa density, contributed to risk of myocardial infarction (MI). DNA from 546 acute MI cases and 507 controls, all aged <75 years, was genotyped for the C807T dimorphism using the TaqManTM system of allelic discrimination. The allelic odds ratio (OR) for MI in the complete cohort was 0.88 (95% CI 0.74-1.05, P = 0.17), indicating that the 807T allele was not associated with an increased risk of MI. There was also no increased risk of MI associated with the homozygous 807TT (P = 0.22) or heterozygous 807CT (P = 0.24) genotypes or for carriers of the 807T allele in any cohort subgroup analysed. We conclude that the GPIa 807T allele is not a risk factor for MI in our population either alone or in combination with other major cardiovascular risk factors.

Adult↗
PubMed1999

An open label, randomised, crossover study comparing sotalol and atenolol in the treatment of symptomatic paroxysmal atrial fibrillation.

OBJECTIVE: To compare sotalol and atenolol in the treatment of symptomatic paroxysmal atrial fibrillation. DESIGN: Prospective, randomised, open label, crossover study. SETTING: University hospital. PATIENTS: 47 subjects aged over 50 years were recruited from the hospital outpatient department following ECG documentation of paroxysmal atrial fibrillation that coincided with symptoms. Six patients withdrew and 41 completed the trial. INTERVENTIONS: Patients were randomised to one month's treatment with sotalol 80 mg twice daily or atenolol 50 mg once daily. Treatment arms were then crossed over. Patients underwent 72 hour Holter monitoring before randomisation and repeat studies were carried out at the end of both treatment periods. Symptom assessments were completed using linear analogue scales and the Nottingham health profile. MAIN OUTCOME MEASURE: Frequency of paroxysmal atrial fibrillation; secondary outcome measures included average and total duration of paroxysmal atrial fibrillation, total ectopic count, and symptom assessments. RESULTS: A reduction in the number and duration of episodes of paroxysmal atrial fibrillation was noted following treatment with sotalol and atenolol. There was no difference in frequency of paroxysmal atrial fibrillation during treatment with sotalol or atenolol (median difference 0; 95% confidence interval (CI) 0 to 1; p = 0.47). There was no difference in total duration of paroxysmal atrial fibrillation (median difference 0 min; 95% CI -1 to 2; p = 0. 51) or in average duration (median difference 0 min; 95% CI 0 to 1; p = 0.31). No difference was found in total ectopic count between sotalol and atenolol (median difference -123; 95% CI -362 to 135; p = 0.14). Treatments were equally tolerated with no difference in linear analogue scores for symptoms of paroxysmal atrial fibrillation (median difference -5; 95% CI -20 to 5; p = 0.26) or in all categories of the Nottingham health profile. CONCLUSIONS: No difference was found in terms of ECG or symptomatic control of paroxysmal atrial fibrillation between prescribing sotalol 80 mg twice daily and atenolol 50 mg once daily. There was an improvement in paroxysmal atrial fibrillation from baseline following treatment with either sotalol or atenolol.

Adrenergic beta-Antagonists↗