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Allan D Struthers

Publications and source records attributed to Allan D Struthers.

63 records · Page 4Linked to original sources
PubMed2002

The neurohormonal natural history of essential hypertension: towards primary or tertiary aldosteronism?

Use of the aldosterone-to-renin ratio has controversially suggested that approximately 10% of hypertensives have primary aldosteronism, and most of these individuals are thought to have idiopathic hyperaldosteronism. The usual renin-angiotensin system control is intact in these individuals and is similar to that in low renin and essential hypertensives, differing only in the degree of sensitivity. There is recent evidence suggesting that hyperaldosteronism relates to aldosterone synthase genetic polymorphism, and also that increased angiotensin II stimulation of the adrenal glands appears to paradoxically upregulate the receptors increasing angiotensin II sensitivity. Taken together, the possibility arises that, in susceptible hypertensives, hyperaldosteronism could be acquired. Indeed, it is well known that renin-driven renovascular hypertension is associated with the development of hyperaldosteronism. Hypothetically, within the wider hypertensive population, these findings set the scene that angiotensin II adrenal sensitivity increases over time until the secretion of aldosterone becomes "autonomous" and hence "tertiary" aldosteronism in a significant proportion of hypertensives.

Aldosterone↗
PubMed2002

Exercise capacity and brain natruiretic peptide in hypertension.

Brain natriuretic peptide (BNP) is increased and it is also released during exercise in hypertension, but its biologic role is unclear. However, since BNP is released from the left ventricule and it is known to reduce left ventricular filling pressure, it is possible that it exerts a favorable effect on exercise performance. We studied the relationship between endogenous BNP release and exercise capacity in hypertension with reference to left ventricular hypertrophy (LVH). Cardiopulmonary exercise study was carried out in 2 groups of hypertensives, 24 [16 men, aged 50 (SD 11) years] of whom had echocardiographic LVH and 25 [16 men, aged 41 ( 12)] who did not have LVH. In multiple regression analyses, the major determinants of peak oxygen uptake (VO max) were age (-), sex (male), peak exercise systolic BP (+) and post-exercise BNP (-). For the predicted adjusted %VO max as a measure of individualised exercise capacity, the significant predictors were the exercise-induced BNP rise (-) (p = 0.0003) and peak exercise systolic BP (+) (p = 0.001). In other words, subjects with greater myocardial dysfunction had a greater rise in BNP during exercise. LVH did not however relate to exercise capacity. The baseline, post-exercise and the % rise in BNP (pmol/L) with exercise were not statistically different in those with LVH compared with those without (median values of 11.2, 14.6 and 133% versus 10.6, 11.5 and 120% respectively). Similarly, there were no significant differences in exercise capacity between the groups: exercise time, oxygen uptakes at ventilatory threshold and at peak exercise (VO max) were 10.8 (2.5) min, 15.8 (4.6) and 33.6 (7.6) ml/min/kg in the LVH group against 11.4 (2.9) min, 18.6 (5.2) and 36 (11.1) ml/min/kg in the non-LVH group respectively. The estimated VO max was not different from that predicted from age, sex, weight and height in either group suggesting preserved exercise capacity in these subjects as a whole. In Conclusion, BNP may potentially act as a homeostatic mechanism that helps to limit exercise incapacity in hypertension irrespective of LVH.

Adult↗
PubMed2002

Vasopeptidase inhibitors in heart failure.

Considerable attention has recently focused on the vasopeptidase inhibitors (VPI), a new class of drug that combines angiotensin-converting enzyme (ACE) inhibitor activity with inhibition of natriuretic peptide breakdown. In theory, a drug with these properties may be beneficial both in hypertension and in heart failure. Whilst the efficacy of VPIs in hypertension has been consistently demonstrated in pre-clinical and clinical studies, the role of VPIs, if any, in heart failure is less clear, since numerous small studies have produced conflicting results. Furthermore, preliminary results from the recently completed Omapatrilat Versus Enalapril Randomised Trial of Utility in Reducing Events (OVERTURE) study have failed to establish the VPI, omapatrilat, as a first line therapy in the treatment of chronic heart failure. We review the literature on VPIs in heart failure and discuss possible reasons for the reported lack of benefit over ACE inhibitors.

Angiotensin-Converting Enzyme Inhibitors↗
PubMedDate not supplied

Impact of aldosterone on vascular pathophysiology.

The fact that spironolactone reduces deaths in cardiac failure suggests that aldosterone promotes cardiac death in heart failure, which begs the question: What are the mechanisms whereby it does this? The mechanisms whereby aldosterone promotes cardiac death are likely to be a combination of its production of endothelial dysfunction, myocardial fibrosis, and autonomic imbalance. It is quite possible that all three of these mechanisms actually stem from aldosterone's adverse effects on the endothelium. The term "aldosterone vasculopathy" has been coined to describe that the fundamentally adverse effect of aldosterone may well be on endothelial nitric oxide.

Aldosterone↗
PubMedDate not supplied

Prevalence of symptomatic diastolic heart failure in patients hospitalized with cerebral or peripheral vascular disease.

The authors sought to determine the prevalence of diastolic heart failure (DHF) in patients hospitalized with their first stroke, transient ischemic attack, or new onset of peripheral vascular disease. A total of 216 prospective consecutive stroke, transient ischemic attack, and peripheral vascular disease patients (vascular group) were identified at their first noncardiac presentation to a hospital and compared with 164 age-matched control patients (nonvascular group). DHF was clinically defined as the presence of left ventricular ejection fraction>or=45% on echocardiography. DHF occurred in 40% and 73% of vascular and control patients, respectively, with symptomatic heart failure. Overall, it was found in 12% of vascular (10% of stroke/transient ischemic attack, 16% of peripheral vascular disease) and 11% of control patients. Advancing age and female gender were independently associated with the presence of DHF in vascular patients (p<0.05). DHF is found in a similar percentage of vascular and nonvascular patients. Symptomatic DHF is less common than systolic heart failure among vascular disease patients with heart failure. In contrast, symptomatic DHF is found in three times as many age-matched control heart failure patients without clinical vascular disease.

Aged↗