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Biomedical subjects

R P Kelly

Publications and source records attributed to R P Kelly.

At least 19 recordsLinked to original sources
PubMed2001

Gender-related differences in left ventricular chamber function.

OBJECTIVES: While women have lower rates of atherosclerotic disease than men, they are more likely to suffer cardiac failure following infarction or cardiac surgery, despite typically having a greater left ventricular (LV) ejection fraction. We hypothesised that gender differences in systolic chamber function and ventriculo-vascular coupling may contribute to these clinical findings. METHODS: LV chamber function was determined in a cohort of 30 patients (16 women) aged 48-75 years with normal LV function using pressure-volume loops obtained by simultaneous conductance catheter volumetry and micromanometer pressure. End-systolic and end-diastolic pressure volume (ESPVR, EDPVR) and preload recruitable stroke work relations (PRSWR) were derived. Results were analysed according to gender, and the effects of body size and chamber dimensions were examined. RESULTS: The groups were closely matched for age (60+/-6 vs. 60+/-8 years) and co-morbid conditions. Women had higher end-systolic blood pressure (139.7+/-21.1 vs. 123.6+/-12.6 mmHg, P=0.001), and smaller LV cavity volume (end-diastolic volume 96.4+/-30.6 vs. 139+/-30.7 ml, P=0.001). Women had significantly higher LV end-systolic elastance (Ees, 2.65+/-0.10 vs. 1.96+/-0.09 mmHg ml(-1), P<0.002), arterial elastance (2.41+/-1.13 vs. 1.54+/-0.55 mmHg ml(-1), P=0.01) and lower passive LV diastolic compliance (slope EDPVR, 6.12+/-0.37 vs. 10.0+/-0.50 ml mmHg(-1), P<0.001). While there was a strong relationship between end-systolic elastance and chamber volume (r=0.69, P<0.001), gender differences in chamber function all persisted after indexing to body size. Higher LV systolic function in women was also shown in PRSWR analysis (slope, M(SW); 101.4+/-3.8 vs. 90.4+/-2.8 mmHg, P<0.05), which is independent of chamber size. After normalising volumes to resting diastolic volume, the greater systolic and diastolic elastance in women was accounted for. The ratio of end-systolic to arterial elastance, a measure of ventriculo-vascular coupling, was similar in women and men (1.19+/-0.40 vs. 1.54+/-0.30, respectively, P=0.23). CONCLUSIONS: This study demonstrates greater systolic chamber function and lower diastolic compliance in women. Within the range of chamber dimensions seen in patients with normal LV function, a strong relationship was found between cardiac size and end-systolic elastance. While these differences were not accounted for by indexing to body size, the greater ventricular elastance in women was removed after normalising to chamber size. Despite differences in resting ventricular elastance, appropriate ventriculo-vascular coupling was maintained in both genders as the greater end-systolic elastance in women was matched by similarly elevated arterial elastance.

Aged↗
PubMed2001

Effect of combination hormone replacement therapy on ambulatory blood pressure and arterial stiffness in diabetic postmenopausal women.

BACKGROUND: Diabetes mellitus negates the premenopausal gender benefit with respect to coronary artery disease. Whether hormone replacement therapy (HRT) offers any cardiovascular advantage to diabetic postmenopausal women is not known. Diabetic subjects have increased vascular load and abnormal 24-h blood pressure (BP) profiles. Hormone replacement therapy has been shown to improve indexes of arterial load in nondiabetic postmenopausal women as well as to restore circadian variation in BP. This aim of this study, therefore, was to determine prospectively whether HRT improved arterial stiffness and 24-h ambulatory BP profile in diabetic postmenopausal women. METHODS: Twelve diabetic postmenopausal women were studied. Six subjects were also hypertensive. Vascular load was characterized by carotid arterial pulse waveform analysis to calculate central augmentation index. All subjects also underwent 24-h BP monitoring. Subjects were studied before commencement of HRT and were then randomized to two groups. The first group was observed for 6 months and then given 2 months of estrogen alone, followed by 4 months of combination estrogen with progestin. The second group received the HRT regimen first, then were restudied after 6 months off HRT. RESULTS: The HRT did not affect either clinic or ambulatory BP. There were no changes in indexes of vascular load or pulse pressure, an indirect measure of arterial stiffness. There was a low rate of circadian variation in 24-h BP at baseline (55%), which was unaltered by HRT. CONCLUSIONS: The HRT was well tolerated. Despite evidence for a beneficial effect of HRT on indexes of arterial load and ambulatory BP previously reported in normal subjects, we found no change in this cohort of diabetic postmenopausal women.

Aged↗
PubMed2001

Vasoactive drugs influence aortic augmentation index independently of pulse-wave velocity in healthy men.

Aortic augmentation index, a measure of central systolic blood pressure augmentation arising mainly from pressure-wave reflection, increases with vascular aging. The augmentation index is influenced by aortic pulse-wave velocity (related to aortic stiffness) and by the site and extent of wave reflection. To clarify the relative influence of pulse-wave velocity and wave reflection on the augmentation index, we studied the association between augmentation index, pulse-wave velocity, and age and examined the effects of vasoactive drugs to determine whether altering vascular tone has differential effects on pulse-wave velocity and the augmentation index. We made simultaneous measurements of the augmentation index and carotid-to-femoral pulse-wave velocity in 50 asymptomatic men aged 19 to 74 years at baseline and, in a subset, during the administration of nitroglycerin, angiotensin II, and saline vehicle. The aortic augmentation index was obtained by radial tonometry (Sphygmocor device, PWV Medical) with the use of an inbuilt radial to aortic transfer function. In multiple regression analysis, the aortic augmentation index was independently correlated only with age (R=0.58, P<0.0001). Nitroglycerin (3 to 300 microg/min IV) reduced the aortic augmentation index from 4.8+/-2.3% to -11.9+/-5.3% (n=10, P<0.002). Angiotensin II (75 to 300 ng/min IV) increased the aortic augmentation index from 9.3+/-2.4% to 18.3+/-2.9% (n=12, P<0.001). These drugs had small effects on aortic pulse-wave velocity, producing mean changes from baseline of <1 m/s (each P<0.05). In healthy men, vasoactive drugs may change aortic augmentation index independently from aortic pulse-wave velocity.

Adult↗
PubMed2000

Acute effects of 17beta-estradiol on ventricular and vascular hemodynamics in postmenopausal women.

Because premenopausal women have lower cardiovascular morbidity than postmenopausal women, it has been proposed that estrogen may have a protective role. Estrogen is involved in smooth muscle relaxation both through its specific receptor as well as through calcium channel blockade. This study examined the acute effect of estradiol on invasive cardiovascular hemodynamics in 18 postmenopausal women (age 62.6 +/- 7.6 years, means +/- SD). The effect of estradiol on left ventricular chamber performance was studied in 9 women using simultaneous left ventricular pressure-volume recordings. In a further group of 9 women, the acute effect of estradiol on arterial function was assessed using input impedance (derived from simultaneous aortic pressure and flow recordings), pressure waveform analysis, and pulse wave velocity. After 2 mg micronized 17beta-estradiol was administered, serum estradiol levels increased from 50.9 +/- 21.9 to 3,190 +/- 2,216 pmol/l, P < 0.0001. There was no effect of estradiol on either left ventricular inotropic or lusitropic function. There was no acute effect of estradiol on arterial impedance, reflection coefficient, augmentation index, or pulse wave velocity. There was a trend to decreased heart rate and cardiac output in both groups of 9 women. Because heart rate and cardiac output were common to both hemodynamic data sets, results for these parameters were pooled. Across all 18 women, there was a small but significant decrease in heart rate (69.2 +/- 10.4 vs. 67.2 +/- 9.9 beats/min, P = 0.02), as well as a significant decrease in cardiac output (4.82 +/- 1.77 vs. 4.17 +/- 1.56 l/min, P = 0.002). Despite achieving supraphysiological serum levels, this study found no significant effect of acute 17beta-estradiol on ventricular or large artery function.

Aorta↗
PubMed2000

Heritability of central systolic pressure augmentation: a twin study.

Less than 50% of the variance in left ventricular mass is explained by conventional factors such as age, blood pressure, and body size. Genetic influences may account for part of the unexplained variance. The central (aortic) pressure augmentation index has been suggested as a noninvasive measure of pulsatile load, which is a likely determinant of left ventricular mass. We quantified the genetic influence on augmentation index and determined the extent to which this influence is dependent on the effects of age, height, heart rate, and blood pressure. We performed a classical twin study composed of 225 monozygotic and 594 dizygotic female white twin pairs aged 18 to 73 years. Augmentation index and mean arterial pressure were based on the central pressure wave derived from the radial waveform as measured by applanation tonometry. Quantitative genetic modeling techniques were used to analyze the data. The heritability of augmentation index was 37%, whereas heritabilities for blood pressure traits varied between 13% and 25%. Most of the variance in augmentation index could be explained by genetic and environmental factors specifically influencing augmentation index. Only a relatively small part of the total variance in augmentation index could be attributed to genes in common with height (3.1%), heart rate (4.6%), and mean arterial pressure (5.6%). Age explained 19% of the total variation in augmentation index. In conclusion, augmentation index has a significant heritable component, which is largely independent of the influence of blood pressure, heart rate, height, and age. Finding genes for the augmentation index could help to unravel pathophysiological mechanisms causing left ventricular hypertrophy and lead to improvements in prevention, diagnosis, and treatment of at-risk populations.

Adolescent↗
PubMed2000

Noninvasive assessment of the digital volume pulse. Comparison with the peripheral pressure pulse.

The digital volume pulse can be recorded simply and noninvasively by photoplethysmography. The objective of the present study was to determine whether a generalized transfer function can be used to relate the digital volume pulse to the peripheral pressure pulse and, hence, to determine whether both volume and pressure pulse waveforms are influenced by the same mechanism. The digital volume pulse was recorded by photoplethysmography in 60 subjects (10 women, aged 24 to 80 years), including 20 subjects with previously diagnosed hypertension. Simultaneous recordings of the peripheral radial pulse and digital artery pulse were obtained by applanation tonometry and a servocontrolled pressure cuff (Finapres), respectively. In 20 normotensive subjects, measurements were obtained after the administration of nitroglycerin (NTG, 500 microgram sublingually). Transfer functions obtained by Fourier analysis of the waveforms were similar in normotensive and hypertensive subjects. In normotensive subjects, transfer functions were similar before and after NTG. By use of a single generalized transfer function for all subjects, the radial and digital artery pressure waveforms could be predicted from the volume pulse with an average root mean square error of 4.4+/-2.0 and 4.3+/-1.9 mm Hg (mean+/-SD) for radial and digital artery waveforms, respectively, similar to the error between the 2 pressure waveforms (4.4+/-1.4 mm Hg). The peripheral pressure pulse is related to the digital volume pulse by a transfer function, which is not influenced by effects of hypertension or NTG. Effects of NTG on the volume pulse and pressure pulse are likely to be determined by a similar mechanism.

Adult↗
PubMed1999

Inhaled nitric oxide in cardiology practice.

Inhaled nitric oxide allows selective pulmonary vasodilatation with rapidity of action. It is effective in the acute post-operative management of pulmonary hypertension in cardiac surgical patients and is also valuable in assessing the pulmonary vasodilator capacity in patients with chronic pulmonary hypertension. This review examines the current role of inhaled nitric oxide in cardiac medicine, discussing issues concerning its administration and toxicity, as well as a summary of clinical studies in cardiac patients. New roles, as a modifier of platelet and leukocyte function, post-thrombolysis and following lung transplantation are described. New agents and alternative therapies, which prolong pulmonary activity, are also discussed.

Cell Adhesion↗
PubMed1999

Photoplethysmographic assessment of pulse wave reflection: blunted response to endothelium-dependent beta2-adrenergic vasodilation in type II diabetes mellitus.

OBJECTIVES: We sought to determine whether a simple index of pressure wave reflection may be derived from the digital volume pulse (DVP) and used to examine endothelium-dependent vasodilation in patients with type II diabetes mellitus. BACKGROUND: The DVP exhibits a characteristic notch or inflection point that can be expressed as percent maximal DVP amplitude (IP(DVP)). Nitrates lower IP(DVP), possibly by reducing pressure wave reflection. Response of IP(DVP) to endothelium-dependent vasodilators may provide a measure of endothelial function. METHODS: The DVP was recorded by photoplethysmography. Albuterol (salbutamol) and glyceryl trinitrate (GTN) were administered locally by brachial artery infusion or systemically. Aortic pulse wave transit time from the root of the subclavian artery to aortic bifurcation (T(Ao)) was measured by simultaneous Doppler velocimetry. RESULTS: Brachial artery infusion of drugs producing a greater than threefold increase in forearm blood flow within the infused limb was without effect on IP(DVP), whereas systemic administration of albuterol and GTN produced dose-dependent reductions in IP(DVP). The time between the first and second peak of the DVP correlated with T(Ao) (r = 0.75, n = 20, p < 0.0001). The effects of albuterol but not GTN on IP(DVP) were attenuated by N(G)-monomethyl-L-arginine. The IP(DVP) response to albuterol (400 microg by inhalation) was blunted in patients with type II diabetes mellitus as compared with control subjects (fall 5.9 +/- 1.8% vs. 11.8 +/- 1.8%, n = 20, p < 0.02), but that to GTN (500 microg sublingually) was preserved (fall 18.3 +/- 1.2% vs. 18.6 +/- 1.9%, p = 0.88). CONCLUSIONS: The IP(DVP) is influenced by pressure wave reflection. The effects of albuterol on IP(DVP) are mediated in part through the nitric oxide pathway and are impaired in patients with type II diabetes.

Adrenergic beta-2 Receptor Agonists↗
PubMed1999

Left ventricular chamber function during inhaled nitric oxide in patients with dilated cardiomyopathy.

Inhaled nitric oxide is a potent and selective pulmonary vasodilator. However, when used in patients with congestive cardiac failure, the decrease in pulmonary vascular resistance is associated with an increase in pulmonary capillary wedge pressure (PCWP). This study examined load-independent indexes of left ventricular chamber function during inhaled nitric oxide in 10 patients with dilated cardiomyopathy (mean ejection fraction, 30.2+/-7.8%, mean +/- SD). Etiology of cardiomyopathy was idiopathic in six and ischemic in four. Pulmonary hemodynamics in seven patients revealed normal resting pulmonary vascular resistance. Chamber function was defined by recording pressure-volume loops at steady state and during inferior vena caval occlusion during inhalation of 20 ppm nitric oxide for 10 min. We found no effect of inhaled nitric oxide on steady-state left ventricular pressures, volumes, contractility (end-systolic elastance or preload recruitable stroke work), contraction duration, or active (tau, dP/dt(min)) or passive (end-diastolic pressure-volume relation) diastolic function. Right heart filling pressures did not change. We therefore conclude that 20 ppm inhaled nitric oxide does not affect left ventricular chamber function in patients with controlled heart failure. Previously described elevations in PCWP during inhaled nitric oxide are most likely due to altered left ventricular loading conditions related to secondary pulmonary hypertension in severe heart failure.

Administration, Inhalation↗
PubMed1999

Effects of postmenopausal hormone replacement therapy on central abdominal fat, glycemic control, lipid metabolism, and vascular factors in type 2 diabetes: a prospective study.

OBJECTIVE: To examine the effects of hormone replacement therapy (HRT) on lipid metabolism, glycemic control, total body and central abdominal fat, blood pressure (BP), and arterial pulse wave velocity (APWV) in overweight postmenopausal females with type 2 diabetes. RESEARCH DESIGN AND METHODS: This was a 12-month prospective study of 14 subjects (mean +/- SD age 57.5+/-5.6 years, BMI 29.5+/-4.8 kg/m2) randomized to 6 months of observation or HRT before crossover. HRT consisted of 2 months of conjugated equine estrogen (CEE) 0.625 mg daily, followed by 4 months CEE and medroxyprogesterone 5 mg daily. Measures included anthropometry, fasting glucose, insulin, HbA1c, total and HDL cholesterol, triglycerides, apolipoprotein B, LDL particle size, nonesterified fatty acids (NEFA), sex hormone-binding globulin, resting energy expenditure (REE), total and central abdominal fat (by dual-energy X-ray absorptiometry), resting BP, APWV (by applanation tonometry), physical activity, well-being, and sexual function. RESULTS: Six months of HRT resulted in significant reductions in waist-to-hip ratio (-0.03+/-0.01 vs. 0.01+/-0.009, P = 0.007), HbA1c (-0.34+/-0.24 vs. 0.6+/-0.4%, P = 0.04), total cholesterol (-0.6+/-0.1 vs. 0.2+/-0.2 mmol/l, P = 0.001), central abdominal fat (-175+/-51 vs. -24+/-56 g, P = 0.05), and improved physical functioning (P = 0.05), compared with observation. There was a minor increase in REE with HRT (33+/-23 vs. -38+/-23 kJ/day, P = 0.04). Total fat mass, fasting glucose, insulin, triglyceride, apolipoprotein B, NEFA, resting BP, APWV, and physical activity were unchanged. CONCLUSIONS: Postmenopausal HRT in these overweight women with type 2 diabetes was associated with a reduction in central adiposity and improvement in lipid metabolism and glycemic control without deterioration in weight status or cardiovascular parameters measured. Whether HRT-induced improvements in these cardiovascular risk factors result in lower long-term cardiovascular morbidity and mortality, as observed in nondiabetic women, awaits further study.

Abdomen↗
PubMed1997

Effect of inhaled nitric oxide on normal human left ventricular function.

OBJECTIVES: This study determined the effects of inhaled nitric oxide (NO) on load-independent indexes of normal human left ventricular (LV) function. BACKGROUND: Inhaled NO is a potent and selective pulmonary vasodilator. However, when it is used in patients with congestive heart failure, the decrease in pulmonary vascular resistance (PVR) is often associated with an increase in pulmonary capillary wedge pressure. NO has been shown to have a negative inotropic action, but it is not known whether it affects LV chamber function when delivered by inhalation. METHODS: Eleven subjects (51 to 69 years old) with normal LV function (mean ejection fraction 72% [range 60% to 80%]) were studied. Four patients had concomitant coronary artery disease. Pressure-volume loop recordings were used to determine end-systolic and end-diastolic pressure-volume and preload recruitable stroke work relations. NO was delivered at 20 ppm for 10 min. In an additional group of patients with normal LV function, PVR (n = 5) and NO metabolites (n = 9) were measured. RESULTS: There was no effect of inhaled NO on steady state LV pressures, volumes, contractility, contraction duration, active relaxation (time constant of relaxation, peak negative first derivative of left ventricular pressure), diastolic compliance or PVR. NO metabolites (methemoglobin and nitrate) were present in the LV cavity at the same concentration as right atrial venous blood, suggesting inactivation of free NO before arrival in the LV chamber. This study had a power of 0.995 to detect a 5% change in contractility (slope of preload recruitable stroke work relation) for alpha = 0.05, based on the multiple linear regression model used. CONCLUSIONS: These results indicate that 20 ppm of inhaled NO does not have significant effects on normal LV function. This lack of effect may be due in part to rapid inactivation of free NO in transit to the heart.

Administration, Inhalation↗
PubMed1997

Gender-related differences in the central arterial pressure waveform.

OBJECTIVES: This study investigated the effect of age and gender on central arterial hemodynamic variables derived from noninvasive tonometric carotid pressure waveforms. BACKGROUND: Women have a greater age-related increase in left ventricular (LV) mass than do men and are more likely to experience symptomatic heart failure after infarction despite their higher ejection fraction. In studies of these changes, ventricular afterload is incompletely defined by brachial blood pressure (BP) measurements. We hypothesized that there exist gender differences in pulsatile vascular load, as revealed by pressure waveform analysis, which may produce suboptimal afterload conditions in women. METHODS: Data from 350 healthy normotensive subjects (187 female) aged 2 to 81 years were analyzed in decade groups. Augmentation index (AIx, the difference between early and late pressure peaks divided by pulse pressure) was used as an index of pulsatile afterload, and the ratio of diastolic to systolic pressure-time integral gave a subendocardial viability index. Heart rate, BP, ejection duration and maximal rate of pressure rise (dP/dt(max)) were also determined. RESULTS: Male subjects had a slightly higher systolic pressure until age 50. Female subjects had higher systolic pressure augmentation after the 1st decade, a difference that was significant after age 30 (p < 0.005 for each decade). In both males and females there was a strong age dependence for AIx (r = 0.77, p < 0.001 for females, r = 0.66, p < 0.001 for males). Although males had a larger body size and higher systolic pressure, systolic pressure-time integral was similar in males and females across all age groups. Diastolic pressure-time integral was consistently lower in females because of their shorter diastolic period. Subendocardial viability index was lower in females across the entire group. Differences in stature and heart rate may contribute to these findings. CONCLUSIONS: These new data may help to explain previous findings in women of an age-related increase in LV mass and excess symptomatic heart failure that are not explained by differences in brachial BP.

Adolescent↗
PubMed1997

Effect of hormone replacement therapy on non-invasive cardiovascular haemodynamics.

OBJECTIVE: To determine the detailed effects of hormone replacement therapy (HRT) on non-invasive haemodynamics, including an assessment of the effect on the pulsatile afterload assessed in terms of the augmentation index and pulse-wave velocity. DESIGN: A cross-sectional study of healthy postmenopausal women using carotid and radial tonometry and pulse-wave velocity measurements. SETTING: Community-based ambulatory women attending the menopause centre at a tertiary hospital. PATIENTS: Seventy postmenopausal women divided into those not currently being administered HRT (n = 38, aged 46-72 years) and those who were being administered a variety of HRT (n = 32, aged 49-67 years). METHODS: Central arterial pressure waveforms were measured using carotid applanation tonometry to derive the augmentation index and ejection duration. The arterial pulse-wave velocity was assessed using paired carotid, radial and dorsalis tonometry waveforms. RESULTS: Women being administered HRT had a significantly lower augmentation index (20.4 +/- 8.6 versus 27.0 +/- 10.2%, P = 0.005) and shorter ejection times (320 +/- 17 versus 329 +/- 18 ms, P = 0.037). There was no significant difference in brachial blood pressure (131/76 versus 129/77 mmHg). Women being administered HRT exhibited a greater reversal in the age-related loss of amplification which occurs owing to arterial stiffening. This amplification between central and peripheral systolic blood pressures was greater among women being administered HRT (5.3 +/- 6.2 versus 2.2 +/- 4.0 mmHg, P = 0.014). There was no difference in pulse-wave velocity between the two groups. CONCLUSIONS: HRT appears to improve the pulsatile vascular afterload by decreasing the augmentation of the late systolic blood pressure. This effect is not apparent from routine brachial cuff measurements, which, as a result, may underestimate haemodynamic benefits. Such effects may help to explain a portion of the improvement in cardiovascular morbidity found in other trials.

Aged↗
PubMed1996

Myocardial ischaemia, infarction and cardiac-related death following carotid endarterectomy: risk assessment by thallium myocardial perfusion scan compared with clinical examination.

Risk factors in 402 patients undergoing 447 carotid endarterectomies were reviewed to see whether the presence of coronary artery disease before operation influenced the likelihood of perioperative cardiac complications. A second aim of the study was to assess whether myocardial thallium scintigraphy was valuable for preoperative assessment. Fourteen patients developed postoperative cardiac complications, six (1.3%) of which were fatal. Four of these deaths occurred in 60 patients undergoing combined carotid-coronary revascularization (6.6%). In 387 carotid endarterectomies without simultaneous coronary revascularization, there were two deaths from myocardial infarcts (0.5%). These fatalities and other cardiac complications occurred in 204 patients with preoperative clinical or ECG evidence of coronary artery disease. In 198 patients with no preoperative evidence of coronary disease there were no fatalities and only one patient with reversible postoperative myocardial ischaemia (0.4%). It is concluded that carotid endarterectomy under general anaesthesia is unlikely to be followed by cardiac complications when there is no preoperative evidence of coronary artery disease. When coronary disease is detected before operation, postoperative cardiac complications occur after 5.6% of operations, including 0.9% fatalities. When coronary artery disease is severe enough to warrant combined carotid-coronary reconstruction, the perioperative mortality rate was 6.6%, all the deaths being cardiac-related. When myocardial thallium scintigraphy was normal, postoperative cardiac complications did not occur.

Carotid Stenosis↗
PubMed1994

Relations between left atrial appendage blood flow velocity, spontaneous echocardiographic contrast and thromboembolic risk in vivo.

OBJECTIVES: The aim of this study was to determine the relations between spontaneous echo contrast, left atrial appendage blood flow velocity and thromboembolism. BACKGROUND: Left atrial thrombus and spontaneous echo contrast, a putative marker of thromboembolic risk, are frequently located in the left atrial appendage. Measurement of left atrial appendage outflow Doppler velocity by transesophageal echocardiography is a recent technique for assessment of left atrial appendage function, which may be important in thrombus formation. METHODS: Transthoracic and transesophageal echocardiographic studies were performed in 140 patients with atrial fibrillation (chronic in 80 patients, paroxysmal in 50 patients, first episode < 2 weeks in 10 patients). The left atrium and appendage were inspected for thrombus and spontaneous echo contrast, which was graded from 0 (none) to 4+ (severe). Outflow velocity profiles were obtained by pulsed wave Doppler at the orifice of the left atrial appendage. RESULTS: Left atrial spontaneous echo contrast was present in 78 patients (56%). In multivariate logistic regression analysis, spontaneous echo contrast was the only significant correlate of left atrial thrombus and was present in 14 (93%) of 15 patients. Spontaneous echo contrast and age were associated positively, and anticoagulant therapy was associated negatively, with previous thromboembolic events. Increasing grades of spontaneous echo contrast were associated with decreasing left atrial appendage blood velocity. The velocity in patients with thrombus was not significantly different from that in patients with 4+ spontaneous echo contrast. In multivariate linear regression analysis, the grade of spontaneous echo contrast was significantly and negatively associated with left atrial appendage velocity (p = -0.0001) and mitral regurgitation (p = -0.0002) and significantly and positively associated with left atrial area (p = 0.0005). The odds ratio for spontaneous echo contrast was 28:1 for low left atrial appendage blood flow velocity (< 35 cm/s) and 96:1 for low velocity and the absence of mitral regurgitation. CONCLUSIONS: Spontaneous echo contrast is the cardiac factor most strongly associated with left atrial appendage thrombus and embolic events. Spontaneous echo contrast formation is promoted by reduced blood flow velocity and increased left atrial size but is diminished by mitral regurgitation.

Adult↗
PubMed1993

An analysis of the relationship between central aortic and peripheral upper limb pressure waves in man.

Amplification of the pressure pulse between central and peripheral arteries renders pressure values in the upper limb an inaccurate measure of ascending aortic (AA) pressure. Accuracy could be improved by allowance for such amplification. Transfer functions (TF) for pressures between AA and brachial artery (BA):(BATF) and between AA and radial artery (RA):(RATF) were derived from high-fidelity pressure recordings obtained at cardiac catheterization in 14 patients under control conditions, and after sublingual nitroglycerine 0.3 mg. There was no significant difference in BATF under control conditions and with nitroglycerine; hence results were pooled. Control and nitroglycerine results were also pooled to obtain a single RATF. BATF and RATF moduli peaked at 5 Hz and 4 Hz, reaching 2.5 and 2.8 times the value at zero frequency respectively. Frequency-dependent changes in modulus and phase of BATF and RATF were attributable to wave travel and reflection in the upper limb. BATF and RATF were compared to published transfer functions and those derived from analysis of aortic and brachial or radial pressure waves in previous publications. Results were similar. Our BATF and RATF were used to synthesize AA pressure waves from published peripheral pulses. Correspondence was close, especially for systolic pressure which differed by 2.4 +/- 1.0 (mean +/- SEM) mmHg, whereas recorded systolic pressure differed by 20.4 +/- 2.6 (mean +/- SEM) mmHg between central and peripheral sites. Results indicate that in adult humans a single generalized TF can be used with acceptable accuracy to determine central from peripheral pressure under different conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗