Reliability of transfer functions in determining central pulse pressure and augmentation index.
Explore the source record for details and available documents.
Central Venous Pressure↗
Biomedical subjects
Ian T Meredith
Publications and source records attributed to Ian T Meredith.
Prostanoids do not affect endothelium-dependent vasodilation in healthy humans.
Explore the source record for details and available documents.
Acetylcholine↗
Six-month angiographic and 12-month clinical follow-up of MultiLink long (25 to 35 mm) stents for long coronary narrowings in patients with angina pectoris.
There are limited prospective angiographic data on stent deployment for long coronary lesions. This multicenter prospective study enrolled 120 patients with a single de novo stenosis >20 mm in length, in a native vessel > or =3 mm diameter, suitable for a MultiLink stent 25 to 35 mm in length with additional stent deployment if required. Quantitative angiography before and immediately after stenting and at 6-month follow-up assessed restenosis for the complete lesion and for 5-mm segments of the stented and adjacent nonstented vessel. By 1 year, myocardial infarction had occurred in 3% and target vessel repeat revascularization in 12% of patients. The mean stented length (35.8 +/- 14.6 mm) closely matched mean lesion length (30.1 +/- 13.5 mm). Restenosis to > or =50% diameter loss occurred in 32% of patients, but to > or =70% in only 8%. Of the 147 segments (5 mm in length) with baseline stenosis <25%, only 3 patients (2%) developed restenosis of > or =50%, and only in 1 of these was it > or =70%. Stenting of long narrowings is associated with good clinical outcome and a low rate of severe restenosis. Mildly diseased segments of long lesions covered by a stent rarely became severely narrowed and had negligible influence on the overall restenosis rate. These data support a strategy of full lesion coverage by stent deployment.
Adult↗
Effect of ATP-sensitive potassium channel inhibition on resting coronary vascular responses in humans.
Experimental data suggest that vascular ATP-sensitive potassium (K(ATP)) channels regulate coronary blood flow (CBF), but their role in regulating human CBF is unclear. We sought to determine the contribution of K(ATP) channels to resting conduit vessel and microvascular function in the human coronary circulation. Twenty-five patients (19 male/6 female, aged 56 +/- 12 years) were recruited. Systemic and coronary hemodynamics were assessed in 20 patients before and after K(ATP) channel inhibition with graded intracoronary glibenclamide infusions (4, 16, and 40 microg/min), in an angiographically smooth or mildly stenosed coronary artery following successful elective percutaneous coronary intervention to another vessel. Coronary blood velocity was measured with a Doppler guidewire and CBF calculated. Adenosine-induced hyperemia was determined following bolus intracoronary adenosine injection (24 microg). Time control studies were undertaken in 5 patients. Compared with vehicle infusion (0.9% saline), glibenclamide reduced resting conduit vessel diameter from 2.5 +/- 0.1 to 2.3 +/- 0.1 mm (P<0.01), resting CBF by 17% (P=0.05), and resting CBF corrected for rate pressure-product by 18% (P=0.01) in a dose-dependent manner. A corresponding 24% increase in coronary vascular resistance was noted at the highest dose (P<0.01). No alteration to resting CBF was noted in the time control studies. Glibenclamide reduced peak adenosine-induced hyperemia (P=0.01) but did not alter coronary flow reserve. Plasma insulin increased from 5.6 +/- 1.2 to 7.6 +/- 1.3 mU/L (P=0.02); however, plasma glucose was unchanged. Vascular K(ATP) channels are involved in the maintenance of basal coronary tone but may not be essential to adenosine-induced coronary hyperemia in humans.
Adenosine↗
Complexities in ETS-domain transcription factor function and regulation: lessons from the TCF (ternary complex factor) subfamily. The Colworth Medal Lecture.
The ETS-domain transcription factor family can be divided into a series of subfamilies. Elk-1 represents the founding member of the ternary complex factor (TCF) subfamily. By focusing on the TCF subfamily, we can demonstrate the complexities that exist in the function and regulation of ETS-domain transcription factors. This article focuses on Elk-1 in detail and summarizes the functions of other TCFs. The key themes covered include the domain structure of the TCFs, the mechanisms of complex formation with serum response factor, regulation of TCFs by mitogen-activated protein kinase cascades, and transcriptional regulatory properties of the TCFs. Finally, the emerging role of the TCFs in vivo is discussed. A picture is developing indicating that, while these proteins exhibit significant sequence and functional conservation, key differences in their structure and regulation are being identified which may relate to unique functions of these proteins in vivo.
Amino Acid Sequence↗
Coronary artery imaging in the new millennium.
Atherosclerotic disease and its thrombotic complications remain the leading causes of mortality and morbidity in Western society. In Australia, cardiovascular disease is responsible for one in every 2.4 (41%) deaths and is the leading single cause of mortality. The crucial final common process for the conversion of a non-occlusive, often clinically silent, atherosclerotic lesion to a potentially fatal condition is plaque disruption. The mortality associated with atherosclerotic disease relates to the acute coronary syndromes, including acute myocardial infarction, unstable angina pectoris and sudden cardiac death. There is substantial clinical, experimental and postmortem evidence demonstrating the role acute thrombosis upon a disrupted atherosclerotic plaque plays in the onset of acute coronary syndromes. Atherosclerotic plaque composition, rather than the stenotic severity, appears to be central in determining risk of both plaque rupture and subsequent thrombogenicity. In particular, a large lipid core and a thin fibrous cap render an atherosclerotic lesion susceptible or vulnerable to these complications. We are currently limited in our ability to accurately identify patients at risk for an acute coronary event. The armamentarium of diagnostic investigations, both non-invasive and invasive, currently clinically available is only able to provide us with data related to the stenotic severity of a coronary artery. The non-invasive testing includes stress-induced (exercise or pharmacological) ischaemic changes in electrical repolarisation, wall motion or myocardial radioactive-tracer uptake. The invasive test of coronary angiography, although the current 'gold standard' for the detection of coronary atherosclerotic disease, provides us with no data about the composition of the atherosclerotic lesion. However, the vast majority of acute coronary events involve a non-critically stenosed atherosclerotic lesion, and thus with currently available means of identification, these lesions would be undetected by stress testing/imaging techniques. Given the critical role that atherosclerotic lesion composition has been shown to play in the risk of both plaque rupture and subsequent thrombogenicity and, consequently, an acute coronary event, new detection techniques need to be investigated for the task of documenting atherosclerotic lesion composition. In the present review we will focus on the status of imaging modalities available for coronary artery imaging and how they may advance our understanding and management of patients with and at risk of coronary artery disease in the new millennium.
Journal Article↗
Time course of plasma adhesion molecules in acute coronary syndromes.
BACKGROUND: Atherosclerosis is an inflammatory process in which adhesion molecules play an intimate role in both the initiation and progression of lesions. It is postulated that they also play a role in the presentation of acute coronary syndromes and that plasma levels thereafter may be of potential prognostic significance. The stability of sample levels under different laboratory conditions is unknown. METHODS: Stability of plasma levels was assessed in six healthy subjects under four different laboratory conditions. The time course of levels was studied in 57 patients with acute chest pain, 21 of non-cardiac aetiology, 23 unstable angina and 13 acute myocardial infarction, at mean times of 2.3, 8.2 and 17.3 h after the onset of pain. Samples were assayed for intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), P-selectin, E-selectin and C-reactive protein (CRP). RESULTS: ICAM-1, VCAM-1, P-selectin and E-selectin levels did not differ under different laboratory conditions. Levels were similar at presentation in patients with acute chest pain of non-cardiac aetiology, unstable angina or acute myocardial infarction (median levels ICAM-1 269 microg/l, VCAM-1 379 microg/l, P-selectin 167 microg/l and E-selectin 53 microg/l). Levels did not change in the 24 h following the onset of pain. CRP levels did not differ at presentation between groups (median level 2.1 mg/l), but rose more than 12 h after the onset of pain in the group with acute myocardial infarction (P < 0.05). CONCLUSION: Adhesion molecule levels are stable under normal laboratory sample handling conditions. Levels do not change in the 24 h following the onset of chest pain of non-cardiac or acute ischaemic aetiology.
Acute Disease↗
Comparison of generalized and gender-specific transfer functions for the derivation of aortic waveforms.
Arterial transfer functions have been promoted for the derivation of central aortic waveform characteristics not usually accessible noninvasively, but possibly of prognostic significance. The utility of generalized rather than gender-specific transfer functions has not been assessed. Invasive central aortic and noninvasive radial (Millar Mikro-tip tonometer) blood pressure waveforms were recorded simultaneously in 78 subjects (61 male and 17 female). Average transfer functions were obtained for the whole group and for each gender by two methods. Reverse transformation was performed with the use of each transfer function. Measured aortic waveform parameters were compared with those derived using average, gender-appropriate, and gender-inappropriate transfer functions. Differences in central waveform characteristics were demonstrated between men and women. Derived waveform parameters were significantly different from measured values [e.g., subendocardial viability index and augmentation index (P < 0.001)]. A gender-appropriate transfer function significantly improved the derivation of some parameters, including systolic pressure and systolic and diastolic pressure time integrals (P < 0.05). Generalized arterial transfer functions may not be universally applicable across all waveform parameters of potential interest, and gender-specific transfer functions may be more appropriate.
Aorta↗