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Gerard M London

Publications and source records attributed to Gerard M London.

3 recordsLinked to original sources

Clinical utility of aortic pulses and pressures calculated from applanated radial-artery pulses.

Brachial artery cuff blood pressures are but approximations of central aortic pressures. The actual pressures against which the left ventricle must pump would be useful clinical information if obtained noninvasively. Our aim was to determine the clinical utility of aortic pulses and pressures calculated from noninvasively obtained radial-artery pulses. Radial-arterial pulses were recorded by applanation and calibrated with arm/cuff oscillometric pressures. Aortic pulses and pressures were calculated from the radial pulses by Fourier analysis and transfer functions. These calculated aortic pulses were compared with directly recorded aortic pulses by a transducer-tip catheter in a series of 50 patients undergoing cardiac catheterization. The correlation coefficient (r) of the measured versus the calculated aortic systolic blood pressure was +0.89, but the scatter was large (standard deviation of the differences=+/-11.3 mm Hg). The pulse pressure correlations were less good (r=+0.79) and also had a large scatter (+/-13.6 mm Hg). The average calculated pulse pressure was 11.5 mm Hg lower than the measured value because the cuff diastolic blood pressures, used to calibrate the radial pulses, were systematically higher than those in the aorta (8.9 mm Hg). Multivariable analysis incorporating height, age, heart rate, and ejection fraction as additional, independent variables eliminated mean differences between the new "predicted" and measured pressures, significantly improved correlation coefficients, and reduced the scatter. However, the improvements were small. The inaccuracy of the oscillometric cuff method for measuring arm blood pressure appears to be the limiting factor in the prediction of clinically useful, noninvasive aortic pressures.

Adult↗

Left ventricular hypertrophy: why does it happen?

Patients with end-stage renal disease (ESRD) have much higher rates of cardiovascular disease than the healthy population. Left ventricular hypertrophy (LVH), in particular, is common in this patient group. The impact of a decline in haemoglobin concentration on left ventricular mass index has been well documented. Partial correction of anaemia with recombinant human erythropoietin (epoetin) treatment has been recognized as a significant step forward in decreasing left ventricular mass and improving cardiovascular morbidity and mortality. However, LVH and cardiac failure in patients with ESRD comprise a complex condition, which is influenced by a number of factors in addition to anaemia. This article examines some of the pathophysiological aspects of LVH in patients with ESRD.

Anemia↗

Left ventricular alterations and end-stage renal disease.

The prevalence of left ventricular (LV) changes, especially LV hypertrophy (LVH), is high among patients with chronic kidney disease and end-stage renal disease (ESRD). Ventricular enlargement usually is associated with normal systolic function and increased stroke and cardiac index. In the absence of intrinsic heart disease, LV enlargement is most probably attributable to chronic volume/flow overload associated with anaemia, the presence of arteriovenous shunts, and sodium and water retention. In ESRD patients, hypertension is also a leading cause of LVH, but structural LV changes and myocardial fibrosis may also be due to non-haemodynamic factors such as angiotensin II, parathyroid hormone, endothelin, aldosterone, increased sympathetic nerve discharge and increased plasma catecholamines. To improve the clinical outcomes in ESRD, it is essential to prevent LVH and its complications by correcting the factors that contribute to flow and pressure overload, including anaemia.

Hemodynamics↗