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Biomedical subjects

J D Swales

Publications and source records attributed to J D Swales.

At least 19 recordsLinked to original sources
PubMed1995

Insertion/deletion polymorphism in the angiotensin-converting enzyme gene and risk of restenosis after coronary angioplasty.

Early restenosis in over 30% of cases limits the benefits of percutaneous transluminal coronary angioplasty (PTCA). The mechanisms that underlie restenosis are uncertain, although experimental evidence suggests that the renin-angiotensin system is involved in the vascular response to angioplasty. An insertion(I)/deletion(D) polymorphism in the angiotensin-converting enzyme (ACE) gene, which influences plasma ACE level, has been associated with an increased risk of myocardial infarction in those with the DD genotype. To investigate whether this polymorphism influences the risk of restenosis after PTCA, 233 patients who underwent single-vessel angioplasty in the Subcutaneous Heparin and Angioplasty Restenosis Prevention (SHARP) study were genotyped for the I/D polymorphism and pre-PTCA, post-PTCA, and 4-month clinical and quantitative angiographic data were compared in the three genotype groups. The groups, (II 53, ID 117, and DD 63) were well matched for baseline clinical and both pre- and post-PTCA angiographic features. At 4-month follow-up there was no significant difference between the genotype groups with respect to any of the quantitative angiographic criteria of restenosis: minimal luminal diameter at the site of the angioplasty (DD 1.35 [SE 0.10] mm, ID/II 1.43 [0.05] mm, difference -0.08 [95% CI -0.30 to 0.14]), numbers of subjects with more than 50% diameter stenosis (DD 49%, ID/II 46%, relative risk 1.06 [0.79 to 1.43]), or the number of subjects with more than 50% loss of the acute diameter gain after PTCA (DD 54%, ID/II 43%, 1.26 [0.94 to 1.67]). Likewise, there was no difference in the number of subjects with angina or a positive exercise stress test. We conclude that, in patients undergoing elective PTCA, the I/D polymorphism in the ACE gene does not influence the extent of restenosis, and typing for the polymorphism will not be a useful predictor of risk before the procedure.

Adult↗
PubMed1995

Pulse pressure and resistance artery structure in the elderly.

There has been recent interest in the possibility that resistance vessel structural adaptation in hypertension may be more closely related to pulse pressure than to other blood pressure parameters. We investigated the relation between blood pressure and resistance vessel structure in a group of subjects from an age group (older than 60 years) in which a widening of pulse pressure is a typical finding and characterized blood pressure parameters using 24-hour ambulatory blood pressure monitoring. We studied resistance vessels retrieved from biopsies of skin and subcutaneous fat taken from the gluteal region of 32 subjects under local anesthesia (age, 70 +/- 1 years [mean +/- SEM], 21 of whom were hypertensive and 11 normotensive. Media-lumen ratio was higher in the hypertensive than the normotensive subjects (18.6 +/- 1.6% versus 12.8 +/- 1.2%, P < .01) and correlated with age (r = .44, P < .05), clinic systolic pressure (r = .35, P < .05), 24-hour systolic pressure (r = .40, P < .05), and 24-hour pulse pressure (r = .56, P < .001). Stepwise multivariate regression analysis identified clinic and 24-hour pulse pressure as the only significant predictors of media-lumen ratio independent of age, other parameters of clinic blood pressure, and blood pressure variability (R2 = 41%, P < .05). These findings confirm those from animal models of hypertension in demonstrating the importance of pulse pressure in relation to cardiovascular structural adaptation and have important implications for the goals of treatment of hypertension in the elderly.

Aged↗
PubMed1995

Salt and blood pressure revisited.

Modern attempts to link intake of salt with population blood pressure (BP) show striking similarity to early 19th century attitudes which attributed human disease and premature death to inappropriate diet. Under these circumstances there is a danger that conviction of the truth of a hypothesis may lead to selection of evidence. A pooled meta-analysis of rigorously conducted studies of the effect of salt restriction on BP has been carried out. This indicates small but real effects in hypertensive patients although the degree of heterogeneity cannot be assessed. The effect in normotensive subjects is minimal and throws doubt on the value of general reduction in salt intake in lowering population BP.

Blood Pressure↗
PubMed1995

Management guidelines for hypertension: is anyone taking notice?

A number of national bodies and the World Health Organisation/International Society of Hypertension have published guidelines on the treatment of hypertension, and there is reasonable consensus between them. Repeated and accurate BP measurements are an essential starting point in the clinical management of hypertension. In mild-to-moderate hypertension, non-pharmacological treatments should always be instituted and their impact evaluated before drugs are considered. The recommended diastolic threshold for initiation of drug therapy varies between 90 and 100 mmHg and the systolic threshold lies between 140 and 160 mmHg. There is also agreement that this threshold should be reduced to 140/90 mmHg when multiple risk factors co-exist. The generally accepted aim of treatment is to reduce DBP to < 90 mmHg, but there is controversy about lowering it further to < 80 mmHg. There is convincing evidence that elderly patients benefit most from treatment. It is also clear that treated patients with inadequately controlled BP remain at high risk of premature cardiovascular death. This highlights the need for guidelines that are suitable for routine use in clinical practice.

Age Factors↗
PubMed1994

Guidelines for treating hypertension: improved care or retarded progress?

A number of national and international bodies have published guidelines for the management of hypertension. Although there is general agreement on certain aspects of treatment, there are also significant differences (for instance, in the threshold blood pressure for drug treatment, the target blood pressure, and selection of drugs for initial monotherapy). Apparent consensus has been reached despite absence of definitive evidence and despite overlapping membership of some groups responsible for the guidelines. The composition of guidelines for nonexperts is a valuable exercise but its limitations and potential dangers should be clearly defined.

Humans↗
PubMed1994

Growth areas in hypertension.

Essential hypertension is an arbitrarily defined disorder to which both environmental and genetic factors contribute. Identifying these factors is a difficult task because individually their contribution is relatively small and apparent causality may be the result of secondary changes or genetic drift. Associations between elevated blood pressure and genetic or phenotypic characteristics are insufficient therefore to demonstrate a cause and effect relationship. This conclusion requires that stringent criteria are met including the presence of the abnormality at or before the first manifestation of hypertension, co-segregation of the relevant gene, reversibility of hypertension when the abnormality is removed (at least during the early phases of hypertension) and failure of the abnormality to resolve with the correction of hypertension. It is proposed that these conditions constitute 'Koch's postulates' for defining the causes of elevated blood pressure.

Causality↗
PubMed1994

The renin-angiotensin system as a target for therapeutic intervention.

Experimental studies have identified local renin-angiotensin systems in a variety of tissues. The importance of these systems is indicated by the evidence that, in genetic models of hypertension in the rat, blood pressure is elevated by the renin gene independently of changes in plasma levels of renin. Trials of angiotensin-converting enzyme (ACE) inhibitors in human left ventricular dysfunction indicate that they improve the mortality from myocardial infarction (MI); high plasma renin activity is associated with increased risk for myocardial infarction (MI), and an ACE gene allele increases the risk for death from MI. These data point to the importance of the renin-angiotensin system in both ischemic heart disease and hypertension, even without increased circulating levels of plasma renin. The degree to which ACE inhibitors are beneficial as a result of hemodynamic actions on the heart and coronary tree and the extent to which they affect local tissue systems independently of their hemodynamic effect still remains to be clarified.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

Meta-analysis as a guide to clinical practice.

BACKGROUND: Meta-analysis is now widely used in order to increase the power of individual clinical studies. Important far-reaching conclusions have been derived by pooling the results of studies which in isolation would not be large enough to reach definitive conclusions. While the statistical power is thereby amplified, so is the potential for error. OBJECTIVE: To assess the potential and the pitfalls of meta-analysis as a guide to clinical practice. CONCLUSIONS: Conclusions derived from meta-analysis may be influenced by unrecognized selection bias and heterogeneity of studies included. Publication of the results may be in a form which does not lend itself readily to critical analysis and misleading results may therefore be accepted.

Antihypertensive Agents↗
PubMed1993

Vascular RAA system.

Biochemical and bioassay evidence has proved the existence of tissue RAA systems although their function has not been satisfactorily defined. There are two sources of tissue renin: uptake from plasma and local synthesis. The uptake system has been demonstrated in arterial tissue. Retention of renin can be demonstrated in the aortic wall and the presence of renin at this site is closely correlated with the persistent elevation of blood pressure. Renin gene expression can be demonstrated in several organs such as the liver, brain and arterial wall, although the function of renin or pro-renin at these sites is unknown. Intracellular angiotensin II receptors have been identified that play a role in regulating gene expression. In addition to raising vascular tone, angiotensin II generated in this way could have a trophic action upon cardiac and vascular structures. There is now very strong evidence in favour of the extrarenal RAA system having a pathogenetic role in some forms of hypertension. Renin gene polymorphisms co-segregate with blood pressure in some genetic models, despite normal or low plasma renin and incorporation of an additional mouse renin gene construct into the rat genome produces severe hypertension despite suppression of renal renin.

Biological Assay↗