PubMed Health⌕ Search

Biomedical subjects

Simon R Redwood

Publications and source records attributed to Simon R Redwood.

9 recordsLinked to original sources
PubMed2006

The pressure wire in practice.

Fractional flow reserve (FFR) is increasingly used to evaluate the functional significance of epicardial coronary disease. When compared with non-invasive techniques this index has superior sensitivity and specificity, is largely independent of prevailing haemodynamic conditions and has an unequivocal normal value. Furthermore, it can be used at the time of invasive coronary assessment. FFR measurements are invaluable for evaluation of intermediate coronary lesions but clinical decisions must be based on accurate measurements and an understanding of the limitations of the data supporting its use. This article identifies procedural and clinical issues pertaining to measurement of FFR and identifies potential pitfalls and situations where interpretation can be difficult; for example, the presence of serial stenoses and left main stem disease, its use in specific conditions such as diffuse epicardial disease, microvascular abnormalities, left ventricular dysfunction and acute coronary syndromes.

Blood Pressure↗
PubMed2005

Evaluation of carotid-femoral pulse wave velocity: influence of timing algorithm and heart rate.

Carotid-femoral pulse wave velocity (PWV), a measure of arterial stiffness, is determined from the time taken for the arterial pulse to propagate from the carotid to the femoral artery. Propagation time is measured variously from the foot of the waveform or point of maximum upslope. We investigated whether these methods give comparable values of PWV at rest, during beta-adrenergic stimulation, and pacing-induced tachycardia. In subjects at rest (n=43), values obtained using the foot-to-foot method (SphygmoCor system) were 1.7+/-0.75 m/s (mean+/-SD) greater than those obtained using the maximum slope (Complior system) at a mean value of 12 m/s. Isoprotenerol (0.5 to 1.5 microg/min; n=10), and pacing (in subjects with permanent pacemakers; n=11) increased heart rate but had differential effects on systolic blood pressure and pulse pressure. The increase in heart rate produced by isoprotenerol (18+/-3 bpm) and pacing (40 bpm) was associated with an increase in PWV measured using both systems (increases of 0.7+/-0.2 m/s and 0.9+/-0.2 m/s for SphygmoCor and Complior, respectively, during isoprotenerol and increases of 2.1+/-0.5 m/s and 1.1+/-0.2 m/s for SphygmoCor and Complior, respectively, during pacing, each P<0.001). Reanalysis of waveforms recorded from the Complior system using the foot-to-foot method produced similar values of PWV to those obtained with the SphygmoCor, confirming that the difference between these systems was attributable to the timing algorithm rather than other aspects of signal acquisition. Carotid-femoral PWV is critically dependent on the method used to determine propagation time, but this does not account for variation of PWV with heart rate.

Adrenergic beta-Agonists↗
PubMed2004

The effect of an angiotensin-converting enzyme inhibitor and a K+(ATP) channel opener on warm up angina.

AIMS: In various models, angiotensin-converting enzyme (ACE) inhibitors and K+(ATP) channel openers can potentiate and mimic ischaemic preconditioning, respectively. Our aim was to determine whether these characteristics are shared by the phenomenon of warm up in angina, often regarded as a surrogate of ischaemic preconditioning. METHODS AND RESULTS: Twenty patients with ischaemic heart disease were assigned in a double blind, randomized cross-over design to equivalent pressor doses of nicorandil 20 mg bid, enalapril 10 mg bid, losartan 25 mg bid, or placebo for 3 days. Patients underwent three consecutive exercise tolerance tests on each medication separated by a 1-week interval. Each patient underwent 12 exercise tests in total and 13 patients completed the study. On each medication the second exercise was separated from the first by 15 min of rest and the third exercise was performed 90 min after the second to control for training. The time to 0.1 mV ST depression and rate pressure product at 0.1 mV ST depression increased significantly in all groups during exercise two compared with exercise one. Nicorandil reduced angina but did not attenuate this warm up effect. This benefit of first exercise waned by test three with placebo, losartan, and nicorandil, but not with enalapril. CONCLUSION: In contrast to predictions based on ischaemic preconditioning the magnitude of the warm up was apparently unaltered by nicorandil, losartan, or enalapril, however its duration seemed to be extended by enalapril. Thus ischaemic preconditioning and warm up angina are likely to have differing pharmacological profiles suggesting a diverse underlying mechanism.

Adaptation, Physiological↗
PubMed2004

Circulating humoral factors and endothelial progenitor cells in patients with differing coronary collateral support.

BACKGROUND: The mechanisms underlying the variation in collateral formation between patients, even with similar patterns of coronary artery disease, remain unclear. This study investigates whether circulating humoral or cellular factors can provide an insight into this variation. METHODS AND RESULTS: Thirty patients with isolated left anterior descending coronary artery disease underwent percutaneous coronary intervention with collateral flow index (CFI) determined using a pressure wire. Patients with inadequate (CFI <0.25) compared with those with adequate (CFI > or =0.25) collateral support had, or tended to have, lower concentrations of coronary sinus growth factors and plasma exerting a weaker effect on endothelial cell migration and angiogenesis in vitro. However, there was an inverse correlation between serum mitogenicity and CFI (r=-0.61, P<0.01). No significant differences were detected between the 2 groups in plasma levels of total vascular endothelial growth factor, vascular endothelial growth factor165, or placental growth factor. There was a strong positive correlation between numbers of CD34/CD133-positive circulating hemopoietic precursor cells and CFI (r=0.75, P<0.001). In patients with inadequate, compared with those with adequate, CFI, the numbers of differentiated endothelial progenitor cells (EPCs) appearing in the circulation and in culture were significantly reduced by 75% (P<0.05) and 70% (P<0.05), respectively. CONCLUSIONS: In this study, inadequate coronary collateral development is associated with reduced numbers of circulating EPCs and impaired chemotactic and proangiogenic but not mitogenic activity. These findings are consistent with current efforts to enhance collateral formation by augmentation of circulating EPCs.

Aged↗
PubMed2003

Pressure wave reflection assessed from the peripheral pulse: is a transfer function necessary?

Synthesis of the aortic pressure waveform by application of a transfer function to the radial pulse allows the estimation of aortic systolic blood pressure and aortic augmentation index, an index of pressure wave reflection derived from the early systolic component of the waveform. The accuracy of this approach for determining the aortic augmentation index has been questioned, however, and it may be possible to derive similar information without using a transfer function. We compared aortic systolic blood pressure and the aortic augmentation index obtained from carotid and radial arteries with the use of transfer functions. We examined the correlation between the aortic augmentation index and a radial augmentation index obtained without use of a transfer function. Arterial tonometry (Sphygmocor) was performed in 84 subjects including healthy volunteers (n=30), subjects with essential hypertension (n=30), and patients with coronary artery disease (n=24). Effects of nitroglycerine and norepinephrine on aortic and radial augmentation index were examined in 12 healthy volunteers. Values of aortic systolic pressure obtained from radial and carotid arteries by using transfer functions were in acceptable agreement (R=0.98, difference=-0.9+/-4.6 mm Hg; mean+/-SD, n=84), but those of aortic augmentation index differed especially in control subjects (R=0.47, difference=-3.8+/-12.4%). Aortic augmentation index was, however, closely correlated with radial augmentation index (R=0.96, n=84). Nitroglycerine and norepinephrine produced parallel changes in the aortic and radial augmentation index. Our findings question the use of a transfer function to obtain the aortic augmentation index but suggest that similar information on central pressure wave reflection can be obtained directly from the radial pulse.

Adult↗
PubMed2003

Exercise-induced ischemia initiates the second window of protection in humans independent of collateral recruitment.

OBJECTIVES: This study was designed to examine if exercise-induced ischemia initiated late preconditioning in humans that becomes manifest during subsequent exercise and serial balloon occlusion of the left anterior descending coronary artery (LAD). BACKGROUND: The existence of late preconditioning in humans is controversial. We therefore compared myocardial responses to exercise-induced and intracoronary balloon inflation-induced ischemia in two groups of patients subjected to different temporal patterns of ischemia. METHODS: Thirty patients with stable angina secondary to single-vessel LAD disease underwent percutaneous coronary intervention (PCI) after two separate exercise tolerance test (ETT) protocols designed to investigate isolated early preconditioning (IEP) alone or the second window of protection (SWOP). The IEP subjects underwent three sequential ETTs at least two weeks before PCI. The SWOP subjects underwent five sequential ETTs commencing 24 h before PCI. RESULTS: During PCI there was no significant difference in intracoronary pressure-derived collateral flow index (CFI) between groups (IEP = 0.15 +/- 0.13, SWOP = 0.19 +/- 0.15). In SWOP patients, compared with the initial ETT, the ETT performed 24 h later had a 40% (p < 0.001) increase in time to 0.1-mV ST depression and a 60% (p < 0.05) decrease in ventricular ectopic frequency. During the first balloon inflation, peak ST elevation was reduced by 49% (p < 0.05) in the SWOP versus the IEP group, and the dependence on CFI observed in the IEP group was abolished (analysis of covariance, p < 0.05). The significant attenuation of ST elevation (47%, p < 0.005) seen at the time of the second inflation in the IEP patients was not seen in the SWOP patients. CONCLUSIONS: Exercise-induced ischemia triggers late preconditioning in humans, which becomes manifest during exercise and PCI. This is the first evidence that ischemia induced by coronary occlusion is attenuated in humans by a late preconditioning effect induced by exercise.

Analysis of Variance↗
PubMed2002

Late intervention after anterior myocardial infarction: effects on left ventricular size, function, quality of life, and exercise tolerance: results of the Open Artery Trial (TOAT Study).

OBJECTIVE: We sought to conduct a randomized trial comparing late revascularization with conservative therapy in symptom-free patients after acute myocardial infarction (AMI). BACKGROUND: In the absence of ischemia, the benefits of reperfusion late after AMI remain controversial. However, the possibility exists that an open infarct related artery benefits healing post AMI. METHODS: Of 223 patients enrolled with Q-wave anterior AMI, 66 with isolated persistent occlusion of the left anterior descending coronary artery (LAD) were randomized to the following treatments: 1) medical therapy (closed artery group; n = 34) or 2) late intervention and stent to the LAD + medical therapy (open artery group; n = 32). The study was powered to compare left ventricular (LV) end-systolic volume between the two groups 12 months post AMI. RESULTS: Late intervention 26 +/- 18 days post AMI resulted in significantly greater LV end-systolic and end-diastolic volumes at 12 months than medical therapy alone (106.6 +/- 37.5 ml vs. 79.7 +/- 34.4 ml, p < 0.01 and 162.0 +/- 51.4 ml vs. 130.1 +/- 46.1 ml, p < 0.01, respectively). Exercise duration and peak workload significantly increased in both groups from 6 weeks to 12 months post AMI, although absolute values were greater in the open artery group. Quality of life scores tended to deteriorate during this time interval in the closed artery patients but remained unchanged in the open artery patients. Coronary angiography at 1 year documented a low incidence of intergroup cross-over (spontaneous recanalization in 19% and closure in 11%). CONCLUSIONS: In the present study, recanalization of occluded infarct-related arteries in symptom-free patients approximately 1 month post AMI had an adverse effect on remodeling but tended to increase exercise tolerance and improve quality of life.

Coronary Angiography↗
PubMed2002

Systemic inflammation in unstable angina is the result of myocardial necrosis.

OBJECTIVES: We investigated whether the source of the acute phase response in unstable angina (UA) lay within the culprit coronary plaque or distal myocardium. BACKGROUND: An inflammatory response is an important component of the acute coronary syndromes. However, its origin and mechanism remain unclear. METHODS: In 94 stable patients undergoing coronary angiography, the relationship between systemic levels of tumor necrosis factor (TNF)-alpha, interleukin-6 (IL-6) and C-reactive protein (CRP) and extent of atherosclerosis was studied. The temporal relationship between these markers and troponin T (TnT) was determined in 91 patients with UA. Cytokine levels were measured in the aortic root and coronary sinus of 36 unstable patients. RESULTS: There was no relationship found between stable coronary atherosclerosis and inflammatory marker levels. Compared with this group, admission levels of IL-6 (3.6 +/- 0.3 ng/ml vs. 10.7 +/- 1.7 ng/ml, p < 0.05) and CRP (2.3 +/- 0.1 mg/l vs. 4.6 +/- 0.6 mg/l, p < 0.05) were elevated in patients with UA. In this group, IL-6 and CRP remained elevated in those who subsequently experienced major adverse cardiac events. This inflammatory response occurred in parallel to the appearance of TnT. Both TNF-alpha (19.2 +/- 3.4 ng/ml vs. 17.1 +/- 3.3 ng/ml, p < 0.001) and IL-6 (10.3 +/- 1.4 ng/ml vs. 7.7 +/- 1.1 ng/ml, p < 0.01) were elevated in the coronary sinus compared with aortic root in patients with UA. This was principally observed in those who were TnT positive. There was no cytokine gradient across the culprit plaque. CONCLUSIONS: There is an intracardiac inflammatory response in UA that appears to be the result of low-grade myocardial necrosis. The ruptured plaque does not appear to contribute to the acute phase response.

Aged↗