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Allan D Struthers

Publications and source records attributed to Allan D Struthers.

At least 55 records · Page 3Linked to original sources
PubMed2003

Pulse wave analysis and pulse wave velocity: a critical review of their strengths and weaknesses.

The study of the pulse using the technique of applanation tonometry is undergoing a resurgence with the development of new computerized equipment. We aim here to present a critical review of the uses, potential uses, strengths and weaknesses of the technique of applanation tonometry for the assessment of augmentation index and pulse wave velocity. We will review the technique of applanation tonometry, the physiological factors affecting pulse wave velocity and pulse wave analysis, the changes in pulse wave velocity and pulse wave analysis with pharmacological interventions, and the use of the technique of applanation tonometry as a prognostic tool. We conclude that, although the technique of applanation tonometry initially seems promising, several pertinent issues need to be addressed before it can be used reliably as a clinical or research tool. Importantly, use of the technique of applanation tonometry to derive the central waveform from non-invasively acquired peripheral data needs to be validated prospectively.

Aging↗
PubMed2003

Peripheral blood pressure measurement is as good as applanation tonometry at predicting ascending aortic blood pressure.

BACKGROUND: The Sphygmocor system purports to be able to assess ascending aortic blood pressure using a transfer function. It has been shown to be accurate when data obtained invasively are used, but has not been tested prospectively using data obtained non-invasively. OBJECTIVE: To investigate the accuracy of this equipment when measurements are obtained non-invasively, as would normally be the case in the clinic setting. DESIGN AND METHODS: The study was observational. Ascending aortic pressure measurements were taken simultaneously with radial artery pressure wave recordings for estimation of ascending aortic blood pressure, in 28 patients undergoing diagnostic cardiac catheterization. RESULTS: The transfer function in the Sphygmocor system significantly underestimated invasively measured systolic blood pressure [mean -7.23 +/- 10.07 mmHg; 95% confidence interval (CI) -3.3 to -11.14 mmHg, P = 0.001] and significantly overestimated invasively measured diastolic blood pressure (mean 12.20 +/- 7.14 mmHg; 95% CI 9.43 to 14.97 mmHg, P <0.001). Oscillometrically measured brachial systolic blood pressure was not significantly different from that measured invasively in the ascending aorta (mean 3.36 +/- 10.47 mmHg; 95% CI -0.69 to 7.43 mmHg, P = 0.1), but oscillometric measurement of brachial diastolic blood pressure gave a significant overestimation of that measured invasively (mean 11.70 +/- 7.18 mmHg; 95% CI 8.91 to 14.49 mmHg, P <0.001). CONCLUSIONS The transfer function in the Sphygmocor system is no better at estimating ascending aortic blood pressure than are standard peripheral blood pressure measurements. It may be necessary to derive a new transfer system that is based on data that are acquired entirely non-invasively.

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PubMed2003

Screening for treatable left ventricular abnormalities in diabetic patients.

Cardiovascular disease is the leading cause of death in patients with diabetes mellitus. Attempts to improve this statistic tend to focus primarily on the prevention of coronary artery disease. However, coronary artery disease is not the sole cause of cardiac death in diabetic patients; left ventricular dysfunction (LVD) and left ventricular hypertrophy (LVH) are also implicated and, unlike coronary artery disease, are ideal targets for screening. The treatment of left ventricular abnormalities, even when these are asymptomatic, is associated with prognostic benefit. Prescreening diabetic patients with plasma B-type natriuretic peptide (BNP) may permit identification of those who are likely to have left ventricular abnormalities, so that they may be put forward for echocardiography and receive targeted therapy.

Diabetes Complications↗
PubMed2003

Hyperuricemia and adverse outcomes in cardiovascular disease: potential for therapeutic intervention.

High uric acid levels are associated with increased morbidity and mortality rates in cardiovascular disease. In this article we explore the relationship between cardiovascular disease and xanthine oxidase activity. We look at the evidence that uric acid and its production via the xanthine oxidase pathway, may directly contribute to this increased cardiovascular risk. We examine the relationship between uric acid and other established cardiovascular risk factors and look at the evidence that reducing uric acid production may have a beneficial impact on cardiovascular morbidity and mortality. We conclude that although there is currently insufficient evidence to recommend the routine use of xanthine oxidase inhibitors in those with cardiovascular disease and asymptomatic hyperuricemia, there is sufficient evidence to warrant a large scale morbidity and mortality trial.

Allopurinol↗
PubMed2002

Relation of QT interval dispersion to the number of different cardiac abnormalities in diabetes mellitus.

Three studies have clearly shown that a prolonged QT dispersion (QTD) is the best predictor of cardiac death in patients with type 2 diabetes mellitus (DM). This was originally believed to be because QTD identified electrical inhomogeneity, but recent data suggests that this is unlikely. The alternative possibility is that QTD is a convenient identifier of hidden but lethal cardiac abnormalities. We explored whether the latter possibility is true by examining exactly what spectrum of cardiac abnormalities, if any, are over-represented in diabetics with a prolonged QTD. Two hundred nineteen patients with type 2 DM who had been first diagnosed with DM 3 to 6 years previously underwent intensive cardiac examinations. Patients with prolonged QTD had a significantly increased incidence of myocardial ischemia and left ventricular (LV) hypertrophy, and to a lesser extent, autonomic dysfunction. The main independent determinant of a prolonged QTD was ischemia, as seen on both ambulatory ST-segment monitoring (p <0.001) and Duke score on treadmill testing (p <0.001). It was also observed that QTD increased progressively as the number of different cardiac abnormalities increased (p <0.001). These studies suggest that QTD is a useful, general prescreening test to select diabetics for more detailed cardiac examinations (especially for ischemia and LV hypertrophy), and that if cardiac examinations were targeted by way of QTD screening, then a high incidence of hidden but treatable cardiac abnormalities could be found.

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PubMed2002

Allopurinol improves endothelial dysfunction in chronic heart failure.

BACKGROUND: Increased oxidative stress in chronic heart failure is thought to contribute to endothelial dysfunction. Xanthine oxidase produces oxidative stress and therefore we examined whether allopurinol improved endothelial dysfunction in chronic heart failure. METHODS AND RESULTS: We performed a randomized, placebo-controlled, double-blind crossover study on 11 patients with New York Heart Association class II-III chronic heart failure, comparing 300 mg allopurinol daily (1 month) versus placebo. Endothelial function was assessed by standard forearm venous occlusion plethysmography with acetylcholine, nitroprusside, and verapamil. Plasma malondialdehyde levels were also compared to assess significant changes in oxidative stress. Allopurinol significantly increased the forearm blood flow response to acetylcholine (percentage change in forearm blood flow [mean+/-SEM]: 181+/-19% versus 120+/-22% allopurinol versus placebo; P=0.003). There were no significant differences in the forearm blood flow changes between the placebo and allopurinol treatment arms with regard to sodium nitroprusside or verapamil. Plasma malondialdehyde was significantly reduced with allopurinol treatment (346+/-128 nmol/L versus 461+/-101 nmol/L, allopurinol versus placebo; P=0.03), consistent with reduced oxidative stress with allopurinol therapy. CONCLUSIONS: We have shown that allopurinol improves endothelial dysfunction in chronic heart failure. This raises the distinct possibility that allopurinol might reduce cardiovascular events and even improve exercise capacity in chronic heart failure.

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PubMed2002

Gradual reactivation over time of vascular tissue angiotensin I to angiotensin II conversion during chronic lisinopril therapy in chronic heart failure.

OBJECTIVES: This study was designed to fully characterize vascular tissue angiotensin I (AI)/angiotensin II (AII) conversion changes over time in vivo in humans during chronic angiotensin-converting enzyme (ACE) inhibitor therapy. BACKGROUND: Plasma AII does not remain fully suppressed during chronic ACE inhibitor therapy. However, the plasma renin angiotensin system (RAS) might be dissociated from the vascular tissue RAS. We therefore set out to characterize the time course of vascular RAS reactivation during chronic ACE inhibitor therapy. METHODS: Vascular AI/AII conversion was studied in patients with chronic heart failure (CHF) taking chronic lisinopril therapy by the differential infusion of AI and AII into the brachial artery. A cross-sectional study was done to see whether there were differences in vascular AI/AII conversion according to New York Heart Association (NYHA) class. A second longitudinal study followed 28 patients with NYHA I to II CHF serially over 18 months to see whether vascular ACE inhibition was progressively lost with time despite ACE inhibitor therapy. A third study examined whether increasing the dose of lisinopril affected subsequent vascular ACE inhibition. RESULTS: In the cross-sectional study, vascular AI-to-AII conversion was significantly reduced in NYHA class III compared with class I/II (p < 0.05). In the longitudinal study, vascular ACE inhibition was significantly reduced at 18 months as compared with baseline (p < 0.001), suggesting gradual reactivation of vascular ACE in CHF over time. In the third study, tissue ACE inhibition could be restored by increasing the ACE inhibitor dose. CONCLUSIONS: Vascular AI/AII conversion reactivates over time during chronic ACE inhibitor therapy even if the CHF disease process is clinically stable. It also occurs as the CHF disease process progresses. Even if vascular AI/AII conversion has reactivated, it can be suppressed by increasing the dose of the ACE inhibitor.

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PubMed2002

The prevalence of treatable left ventricular systolic dysfunction in patients who present with noncardiac vascular episodes: a case-control study.

OBJECTIVES: We sought to determine the prevalence of treatable left ventricular (LV) systolic dysfunction (LVSD) in patients who present with their first noncardiac vascular episode. BACKGROUND: Screening for LV dysfunction in patients who present with their first stroke (cerebrovascular accident), their first transient ischemic attack (TIA) or their first manifestation of peripheral vascular disease (PVD) may represent a golden opportunity to identify treatable LV dysfunction, and so their known high incidence of sudden cardiac death may be reduced. METHODS: Participating in this study were 522 (75%) of 700 consecutive patients (302 patients with stroke, TIA or PVD and 220 age- and gender-matched control subjects). Each underwent a full clinical assessment, 12-lead electrocardiography and two-dimensional echocardiography. Left ventricular dysfunction was defined as LV ejection fraction < or = 40%. RESULTS: Seventy-two (28%) patients with vascular disease and 11 (5.5%) control subjects were found to have LVSD. Twenty-six (28%) stroke patients, 22 (26%) patients with TIA and 24 (31%) patients with PVD had LVSD. Left ventricular systolic dysfunction was symptomatic in 44% of patients and in 35% of control subjects. CONCLUSIONS: Left ventricular systolic dysfunction is five times more common among patients with stroke, TIA and PVD than among age- and gender-matched control subjects. Asymptomatic LVSD is more common than symptomatic LVSD in these patients. These findings suggest that routine screening of all patients with noncardiac vascular episodes for LVSD should now be considered. Future studies should investigate whether identifying and treating LVSD in these patients would reduce their known high rate of cardiac death.

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PubMed2002

Heart failure in frail elderly patients: diagnostic difficulties, co-morbidities, polypharmacy and treatment dilemmas.

BACKGROUND: Heart failure (HF) is difficult to diagnose and treat in older patients. Symptoms may be non-specific and the presence of co-morbidities and polypharmacy complicate treatment strategies. There are, however, few data to quantify the extent of these problems in the very elderly. METHODS: A retrospective study of 116 patients (median age 86; range 65-98) with an established diagnosis of HF during their hospital admission. MAIN OUTCOME MEASURES: the accuracy of diagnosis of heart failure according to the European Society of Cardiology (ESC) definition. The aetiology and frequency of associated co-morbidities and the nature of drug treatment. RESULTS: The specificities of clinical signs, chest X-rays and abnormal ECGs for heart failure (ESC definition) were 50%, 20% and 9%, respectively. Only 28% of patients were admitted for worsening symptoms which could be attributed to HF. None of the patients had HF as their only medical problem. Co-morbidities included chest disease (30%), incontinence (29%), cerebrovascular disease (26%), musculoskeletal problems (41%). Barthel (activities of daily living) score was < or = 16/20 in 35%. Mental state questionnaire (MSQ) score was < or =7/10 in 38%. Ninety percent were taking four or more different medications. Thirty-nine percent were on psychotropic drugs. On discharge, a total of 88% of patients returned home to live independently and 35% were monitored by regular day hospital attendance. CONCLUSION: Heart failure in frail elderly patients is often compounded by other major illnesses and polypharmacy which have a profound impact on their functional status. This has implications for the most effective targeting of evidence based treatment.

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PubMed2002

Aldosterone induces acute endothelial dysfunction in vivo in humans: evidence for an aldosterone-induced vasculopathy.

Experimental studies have suggested a role for aldosterone and glucocorticoids in the pathogenesis of endothelial dysfunction. We therefore set out to characterize the acute effects of these hormones on vascular function in vivo in normal humans. A randomized, placebo-controlled, double-blind crossover study was performed on 16 healthy male volunteers (aged 19-29 years), examining the vascular effects of acute intravenous aldosterone infusion (12 pmol.min(-1).kg(-1) for 4 h) and of oral prednisolone (single 50 mg dose). Peripheral arterial vascular function was assessed by bilateral forearm venous occlusion plethysmography using two parallel study protocols. In the first protocol, eight subjects received, successively, acetylcholine, sodium nitroprusside, noradrenaline, angiotensin I and angiotensin II. The remaining eight subjects received, successively, acetylcholine, sodium nitroprusside, verapamil and noradrenaline. Aldosterone attenuated endothelium-dependent vasodilatation to acetylcholine as compared with either prednisolone or placebo (maximum vasodilatation: placebo, 357+/-38%; aldosterone, 257+/-21%; P <0.05). However, background endothelium-independent vasodilatation was not affected by either aldosterone or prednisolone. There were also no significant changes in vasoconstriction induced by angiotensin or noradrenaline following aldosterone or prednisolone treatment compared with placebo. Blood pressure and baseline blood flow did not differ between any of the study phases. Thus acute short-term systemic administration of aldosterone results in endothelial vasodilator dysfunction in normal men, providing evidence for an aldosterone-induced vasculopathy, which may be particularly relevant not only in heart failure but also in hypertensive patients with high aldosterone/renin ratios.

Adult↗
PubMed2002

Aldosterone: cardiovascular assault.

BACKGROUND: Blocking the renin-angiotensin-aldosterone system with angiotensin-converting enzyme inhibitors has improved cardiovascular morbidity and mortality rates. However, because of aldosterone "escape," the effectiveness of this blockade decreases over time. METHODS: Various in vitro and in vivo studies were evaluated to determine the mechanisms by which aldosterone contributes to morbidity and mortality. RESULTS: Aldosterone has several deleterious properties. It causes a vasculopathy with both endothelial dysfunction and a reduction in fibrinolysis, leading to heart, brain, and kidney damage. Aldosterone causes myocardial hypertrophy and fibrosis, autonomic imbalance, and electrolyte abnormalities, contributing to myocardial dysfunction, arrhythmias, and sudden cardiac death. Studies have shown that all of these deleterious effects can, at least in part, be reversed by aldosterone receptor blockade. This may explain why adding an aldosterone blocker to standard heart failure therapy, including angiotensin-converting enzyme inhibitors, reduces morbidity and mortality rates by an additional 30% compared with standard therapy alone. CONCLUSIONS: Eplerenone is a selective aldosterone blocker whose role in reducing morbidity and mortality rates in patients with cardiovascular disease is being investigated.

Aldosterone↗
PubMed2002

B-type natriuretic peptide in the diagnosis of cardiac disease in elderly day hospital patients.

OBJECTIVES: heart failure is primarily a disease of elderly people. Current guidelines suggest all patients with suspected heart failure should undergo objective assessment, usually by echocardiography. In the UK resources are limited and not all patients have access to echocardiography. The electrocardiogram is widely used as a pre-screening investigation. Recently the natriuretic peptides have been shown to correlate well with left ventricular function, and evidence is accumulating which suggests that B-type natriuretic peptide may have a role in detecting cardiovascular disease. Elderly patients attending day hospital often have non-specific cardiovascular symptoms. B-type natriuretic peptide measurement in parallel with conventional electrocardiogram, may offer a novel method of identifying those with significant cardiac disease, which may warrant treatment. This study assessed the role of B-type natriuretic peptide and electrocardiogram in the detection of cardiac disease in patients attending Day Hospital. DESIGN: prospective cohort study of patients referred to Day Hospital with suspected cardiovascular disease. METHODS: this study prospectively evaluated 299 consecutive patients attending day hospital over a period of 13 months. Patients underwent clinical assessment, electrocardiography, echocardiography and natriuretic peptide measurement. Objective evidence of cardiac disease was based on electrocardiogram and echocardiographic findings. SETTING: Medicine for the Elderly Day Hospital, Royal Victoria Hospital, Dundee. MAIN OUTCOME MEASURES: sensitivity, specificity, positive and negative predictive values of screening tests for left ventricular systolic dysfunction. Receiver-Operating-Characteristic curves for ability of B-type natriuretic peptide to detect cardiac disease (including left ventricular systolic dysfunction, valvular disease, atrial fibrillation and left ventricular hypertrophy). Mean B-type natriuretic peptide levels with 'incremental' levels of cardiovascular disease. RESULTS: 299 patients (mean age 79; 65% female) completed the assessment. Ten percent of patients had left ventricular systolic dysfunction but 50% had objective evidence of cardiac disease. B-type natriuretic peptide was significantly elevated in patients with left ventricular systolic dysfunction, atrial fibrillation, left ventricular hypertrophy and valvular disease. Both B-type natriuretic peptide and the electrocardiogram were sensitive in detecting left ventricular systolic dysfunction but lacked specificity. Combining B-type natriuretic peptide with the electrocardiogram improved detection of left ventricular systolic dysfunction. B-type natriuretic peptide levels increased progressively as the number of different cardiac abnormalities increased. CONCLUSIONS: B-type natriuretic peptide may be a useful marker for cardiac disease in patients attending Day Hospital. Half of the patients assessed had cardiac disease detected. Both the electrocardiogram and B-type natriuretic peptide were sensitive in the detection of left ventricular systolic dysfunction but lacked specificity. B-type natriuretic peptide was superior to the electrocardiogram in the detection of valvular disease. If used to pre-screen cardiovascular disease in Day Hospital patients, B-type natriuretic peptide and the electrocardiogram could reduce the need for echocardiography in some patients before implementing evidence-based treatments. B-type natriuretic peptide increases progressively as the number of different cardiac abnormalities increases and this may explain why B-type natriuretic peptide is of such prognostic value in older patients.

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