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Biomedical subjects

T R Downes

Publications and source records attributed to T R Downes.

18 recordsLinked to original sources
PubMed1999

The heart is not necessarily empty at syncope.

BACKGROUND: Although extensively investigated, the mechanism(s) of post-spaceflight orthostatic intolerance has not been elucidated. Several researchers have proposed that the "trigger" for syncope is an empty ventricle, initiated when a hypercontractile state, possibly due to a sudden surge in epinephrine, causes the walls of the left ventricle to touch leading to a profound sympatho-inhibition and intense vagal stimulation. HYPOTHESIS: A markedly reduced left ventricular end systolic volume (LVESV) achieved during progressive, presyncopal-limited lower body negative pressure (LBNP) is the trigger for syncope. METHODS: Eight healthy men, age 25.1+/-1.3 yr, volunteered for the study. Changes in left ventricular end-diastolic volume and LVESV were measured, using two-dimensional echocardiography, at each stage of LBNP from rest up to presyncope (PS). Plasma venous catecholamine concentrations were measured at the end of each stage by high performance liquid chromatography (HPLC) with electrochemical detection. RESULTS: All subjects reached PS. Three men became bradycardic at presyncope while five remained tachycardic. LVESV decreased by 28% at PS with no evidence of ventricular cavity obliteration. Norepinephrine increased by 44% from rest to PS, but no epinephrine surge was detected (35% increase from rest to PS). CONCLUSION: These data indicate that it is possible to initiate syncope with only a 28% decrease in LVESV, and that sympatho-inhibition and bradycardia are not required elements for syncope to occur.

Adult↗
PubMed1999

Moderate sodium restriction does not alter lower body negative pressure tolerance.

HYPOTHESIS: Space travel with exposure to microgravity leads to a significant reduction in orthostatic tolerance on return to Earth, for which countermeasures are only partially successful. The purpose of this study was to examine the effect of moderate dietary sodium restriction on tolerance to LBNP. METHODS: Eight healthy men, age 25.1+/-1.3 yr, volunteered for the study. Subjects were exposed to presyncopal LBNP after consuming their "typical" diet (C) for 5 d and after consuming a sodium restricted (SR) diet for 5 d. Diet sequence was randomized and adherence was verified by 24-h urine collection on the 4th and 5th days of each diet. RESULTS: All subjects reached presyncope during the LBNP, regardless of diet. Urinary sodium excretion was 3390+/-950 mg on the C diet and 1174+/-560 mg on the SR diet. Urinary potassium was not different between the diets. Cumulative stress index scores were 655+/-460 (mm Hg x min) on the C diet and 639+/-388 (mm Hg x min) during SR. Cardiac volumes, BP and total peripheral resistance were not different at any stage of the LBNP between the diets, nor were catecholamines. Plasma renin activity, determined by radioimmunoassay, was significantly higher during SR at rest, and during all stages of LBNP in comparison with the control diet. CONCLUSION: Moderate dietary sodium restriction is not detrimental to orthostatic tolerance.

Adult↗
PubMed1999

Immediate angioplasty for acute myocardial infarction: a community hospital's experience.

This study describes prospective outcome data from 100 consecutive patients presenting with acute myocardial infarction and treated with immediate angioplasty in a community hospital setting. Successful angioplasty was achieved in 86% of patients with a mean reperfusion time of 77.5 minutes. Only 4 patients did not survive initial hospitalization; three of these initially presented with cardiogenic shock. The survival rate in noncardiogenic shock patients was 98.9%. Four patients underwent repeat angioplasty of the infarct-related artery and 6 patients were referred for coronary artery bypass surgery during initial hospitalization. During the 6 month follow-up, nine patients required repeat hospitalization. Seven of these patients presented with recurrent ischemia; four underwent repeat angioplasty and 3 coronary artery bypass surgery. There were no subsequent deaths or reinfarctions during the 6 month follow-up. The angioplasty success rate and clinical outcomes in this study compare favorably to previous trials performed in select interventional centers and suggest that immediate angioplasty can be the preferred reperfusion therapy in a community hospital setting.

Acute Disease↗
PubMed1999

Validation of impedance cardiography during lower body negative pressure.

BACKGROUND: Both echocardiographic and impedance cardiographic techniques have been used individually for the determination of stroke volume (SV) during lower body negative pressure (LBNP). Impedance cardiography has not been validated during LBNP. HYPOTHESIS: The purpose of this study was to determine both the absolute values for SV and the change in SV for each stage of LBNP using both impedance and echocardiographic techniques during staged LBNP to presyncope. The hypothesis was that there would be no difference between the two techniques for either the absolute values of SV or for the change in SV with each stage of LBNP. METHODS: There were 16 men who volunteered to undergo LBNP. LBNP was lowered in 10 mmHg stages for 5 min per stage until presyncope was reached. Left ventricular SV was determined by two-dimensional echocardiography and impedance cardiography. Both the absolute values for SV and the change in SV from baseline at each stage of LBNP were compared for the two methods. RESULTS: There were no significant differences between the two techniques for the measurement of either the absolute SV or the change in SV with LBNP. The two methods correlated highly with r = 0.89 for the absolute SV values and r = 0.93 for the change in SV. Graphical analysis with the Bland-Altman analysis showed little bias in the impedance measurement for SV (-0.031 ml) and the change in SV (-2.7 ml). CONCLUSIONS: Impedance cardiography was a reliable measure of SV, as well as the change in SV, during LBNP stress to presyncope.

Adult↗
PubMed1994

Qualitative and quantitative contrasts in the mechanisms of lumen enlargement by coronary balloon angioplasty and directional coronary atherectomy.

OBJECTIVES: This study was designed to define and contrast the mechanisms of lumen enlargement from coronary balloon angioplasty and directional coronary atherectomy using intracoronary ultrasound imaging in vivo. BACKGROUND: The mechanisms of lumen enlargement produced by percutaneous transluminal coronary balloon angioplasty and directional coronary atherectomy are not known because the coronary artery wall has not previously been studied both before and after dilation. METHODS: We used intracoronary ultrasound to quantitate coronary lumen, vessel and plaque area both before and immediately after successful coronary angioplasty (n = 30) and directional coronary atherectomy (n = 25) at the site of most severe stenosis. RESULTS: Angioplasty increased lumen area by 2.80 +/- 0.25 mm2 (mean +/- SE, p < 0.0001). Eighty-one percent of this lumen gain resulted from an increase in vessel area and the remaining 19% from a reduction in plaque area. Lumen gain of individual lesions was separated into three groups: 67% had an increase in vessel area (vessel expansion), 13% had a decrease in plaque area and 20% had a combination of both. In contrast, vessel expansion contributed only 22% of the lumen gain with directional coronary atherectomy, with the majority (78%) of increase in lumen size coming from a reduction in plaque area. Directional coronary atherectomy increased lumen area from 2.36 +/- 0.05 to 7.00 +/- 0.28 mm2 (p < 0.0001). Plaque reduction was the sole mechanism in 60% of lesions, vessel expansion was the sole mechanism in 12% and a combination of both mechanisms occurred in 28%. Lumen enlargement of eccentric lesions treated with directional coronary atherectomy was more commonly associated with plaque reduction (p < 0.02), whereas eccentricity did not affect the mechanism of lumen enlargement with coronary angioplasty. CONCLUSIONS: This is the first study to systematically examine the coronary artery wall in vivo at the site of a severe stenosis both before and after catheter-based interventions in humans. Lumen enlargement from coronary angioplasty occurs predominantly from vessel expansion or stretching, although a reduction in plaque area contributes to the lumen gain in many patients and is the sole mechanism in a few. Lumen gain from directional coronary atherectomy is predominantly from reduction in plaque area (probably owing to tissue removal), although vessel stretching (balloon effect) occurs and is the sole mechanism in a small minority of vessels. Plaque reduction is more common in directional coronary atherectomy of eccentric lesions.

Adult↗
PubMed1993

Candida endocarditis. A treatable form of pacemaker infection.

Fungal endocarditis is a rare complication of permanent pacemaker implantation. In all reports we have identified, this infection has been fatal, diagnosed postmortem. We present a patient in whom early echocardiographic diagnosis resulted in curative surgical and antimicrobial therapy. Fungal endocarditis is an unusual, but treatable complication of permanent pacemakers.

Candidiasis↗
PubMed1992

Magnetic resonance imaging evaluation of recipient for cryopreserved aortic allograft.

Aortic valve replacement with a cryopreserved aortic allograft is the procedure of choice for many patients with aortic valvular heart disease. We have used magnetic resonance imaging preoperatively to determine annular size and coronary artery orientation in the recipient, which not only has enabled us to select an allograft of appropriate size from a distant tissue bank, but also has helped us to identify preoperatively the recipient with a truly bicuspid valve in which the coronary arteries are oriented 180 degrees apart. Sixteen consecutive patients were evaluated preoperatively, the aortic annulus being measured with both magnetic resonance imaging and echocardiography. Cryopreserved aortic allografts were ordered on the basis of the magnetic resonance imaging measurement. Annular size was then measured intraoperatively with calibrated sizers. Magnetic resonance imaging annular measurements correlated highly with those found at operation (r = 0.92), whereas echocardiographic measurements correlated less well (r = 0.69). Coronary orientation was accurately predicted in every case (r = 1.0). Therefore, we have found magnetic resonance imaging to be useful in the preoperative evaluation of patients for aortic valve replacement with a cryopreserved aortic allograft.

Adolescent↗
PubMed1991

The underlying coronary lesion in myocardial infarction: implications for coronary angiography.

Myocardial infarction is usually caused by sudden thrombotic occlusion of a coronary artery at the site of a fissured atherosclerotic plaque. Recent evidence suggests that coronary angiography may be insensitive in detecting and quantitating atherosclerosis. Serial angiographic studies demonstrate that the majority of myocardial infarctions occur due to occlusion of arteries that previously did not contain angiographically significant (greater than 50%) stenoses. Similarly, quantitative angiography performed after thrombolytic therapy indicates that the coronary lesion underlying the clot is frequently not severely stenotic. Thus, an angiographically apparent stenosis is not necessary for the development of a thrombotic occlusion resulting in an MI. These observations suggest that coronary angiography does not accurately predict the site of a subsequent occlusion that will produce a myocardial infarction.

Autopsy↗
PubMed1991

Thrombosis and the heart.

The heart is an important site for thrombus formation and cardioembolic events are a frequent cause of stroke. Many cardiac factors may contribute to the risk of cardioembolism. Clinicians must be mindful that those cardiac disorders most likely to cause cardioembolic events include atrial fibrillation, left ventricular dysfunction, valvular heart disease, and structural cardiac abnormalities. The presence of many such conditions mandates the use of specific preventive therapies. Improved diagnostic methods, particularly TEE, now allow more accurate identification and follow-up of potential cardiac sources. Embolus detection monitoring has the potential to allow in vivo identification of embolic events and offers the possibility of objective longitudinal assessment of the impact of therapy. Intravascular ultrasound is an invasive test, but it may eventually allow the most accurate evaluation of the cardiac chambers. New therapies, and new combinations of currently available compounds, may ultimately offer more specific and efficacious alternatives to prevent formation of cardiac thrombus and subsequent cardioembolism. The importance of the heart-brain relationship in stroke has finally been appreciated. Improved understanding of this complex interrelationship will have great impact on clinical practice in the future.

Heart Diseases↗
PubMed1990

Effect of alteration in loading conditions on both normal and abnormal patterns of left ventricular filling in healthy individuals.

Doppler analysis of mitral flow provides a means of analyzing left ventricular (LV) diastolic function. While experimental studies have suggested that changes in left atrial pressure may affect the normal pattern of early diastolic filling, the effect of such changes on abnormal patterns of filling is unknown. Accordingly, the Doppler pattern of LV filling was analyzed in 20 subjects with LV hypertrophy (mean age 59 +/- 13 years, +/- standard deviation), in 25 healthy normal subjects (29 +/- 6 years) and in 11 elderly subjects (68 +/- 5 years). All underwent Doppler examination of LV inflow at rest and immediately after postural changes. In all 3 groups, head-down positioning increased early diastolic flow velocity (E) (p less than 0.001), and raised the E to late diastolic flow velocity (A) ratio (p less than 0.01). However, an abnormal E/A ratio never approached a normal resting value. Likewise, although E and the E/A ratio decreased significantly in normal subjects with head-up positioning, it did not become abnormal. The magnitude of change in E, A and E/A ratio did not differ among the 3 groups in response to postural changes. Thus, alterations of LV loading conditions alter the pattern of LV filling, whether normal or abnormal at baseline. The magnitude of change appears to be independent of the resting flow pattern. Although loading conditions may affect the Doppler pattern of filling, simple changes in venous return do not "normalize" an abnormal pattern, nor do they "abnormalize" a normal pattern.

Adult↗
PubMed1990

Invasive evaluation of left ventricular diastolic performance.

Diastole can be divided into four phases: 1. isovolumic relaxation; 2. early filling; 3. diastasis; and 4. atrial systole. The amount of left ventricular (LV) filling that occurs during each of these phases depends on: 1. myocardial relaxation; 2. the passive characteristics of the LV; 3. the characteristics of the left atrium, pulmonary veins and mitral valve; and 4. the heart rate. When diastolic function is normal, the net effect of these factors results in LV filling sufficient to produce an adequate cardiac output, while mean pulmonary venous pressure is maintained below 12 mm Hg. Diastolic dysfunction is normally manifest as pulmonary congestion. In the absence of systolic dysfunction, abnormal diastolic performance is usually due to abnormal relaxation and/or changes in the passive LV characteristics, external compression or disease of the mitral valve and left atrium. Invasive studies can quantify the rate of myocardial relaxation from the time course of the fall of LV pressure during isovolumic relaxation and the passive LV properties from the LV diastolic pressure-volume relation. In addition, frame-by-frame analysis of contrast ventriculography and conductance determination of LV volume can quantify the pattern of LV diastolic filling. Normally, at rest, most LV filling occurs early in diastole. Conditions that produce diastolic dysfunction, such as LV hypertrophy and ischemia, are associated with reduced early diastolic filling and an augmented importance of atrial systole. It is important to recognize that such patterns can occur in patients without clinically apparent diastolic dysfunction and in normals if left atrial pressure is sufficiently elevated. Furthermore, a normal pattern can occur in patients with severe diastolic dysfunction. Reduced early diastolic filling in the absence of pulmonary congestion indicates the loss of diastolic reserve, since the left atrium is being used as a booster-pump. This pattern of diastolic filling in a patient with symptoms of pulmonary congestion suggests diastolic dysfunction, even if systolic LV performance is normal.

Atrial Function↗
PubMed1989

Mechanism of altered pattern of left ventricular filling with aging in subjects without cardiac disease.

The mechanism whereby aging, in the absence of cardiac disease, may alter the pattern of left ventricular (LV) diastolic filling is unknown. Accordingly, this study was designed to examine the factors that may be in part responsible for aging's effect on the pattern of LV diastolic filling. The LV end-diastolic pressure-volume relation was analyzed in 11 elderly subjects (68 +/- 5 years, mean +/- standard deviation) and 15 normal young adults (31 +/- 7 years) without coronary artery disease, systemic hypertension, LV hypertrophy or abnormality of LV systolic function. After catheterization, the subjects underwent pulsed Doppler analysis of mitral flow. All had normal 2-dimensional echocardiograms without LV or valvular dysfunction. Peak early filling velocity in the elderly subjects was decreased in comparison with that in young adults (61 +/- 14 vs 83 +/- 8 cm/s, p less than 0.001) and the ratio of early and late diastolic filling velocity was reduced (0.81 +/- 0.26 vs 1.88 +/- 0.40, p less than 0.001). The isovolumic relaxation time did not differ between the elderly and young subjects (158 +/- 20 vs 146 +/- 22 ms, difference not significant). In the elderly, LV end-diastolic pressure was increased (15 +/- 7 vs 11 +/- 4 mm Hg, p less than 0.05) despite a smaller end-diastolic volume index (60 +/- 16 vs 74 +/- 18 ml/m2, p less than 0.05), indicating a shift of the passive diastolic pressure-volume relation. It was concluded that early diastolic filling is reduced in normal aged subjects, even in the absence of coronary artery disease and systolic dysfunction. This altered pattern of diastolic filling may result from a shift of the passive LV diastolic pressure-volume relation.

Aged↗
PubMed1989

Diastolic mitral regurgitation in acute but not chronic aortic regurgitation: implications regarding the mechanism of mitral closure.

In acute aortic regurgitation, left ventricular pressure rises rapidly during diastole, which produces presystolic mitral valve closure. This does not occur in chronic aortic regurgitation. Since normal, nonregurgitant mitral valve closure may depend on properly coordinated atrial and ventricular contractions, we hypothesized that abnormal mitral valve closure occurring before systole in acute aortic regurgitation may produce diastolic mitral regurgitation detectable by Doppler echocardiography. Accordingly, we performed ultrasonic Doppler examination of seven patients with acute aortic regurgitation and 12 patients with chronic aortic regurgitation. Regurgitant aortic flow was severe in all cases. Doppler sampling within the left atrium demonstrated regurgitant mitral flow in late diastole in all patients with acute aortic regurgitation. The onset of diastolic mitral regurgitation coincided with mitral valve preclosure in patients with acute aortic regurgitation and occurred regardless of the position of the mitral leaflets at the initiation of closure. In contrast, none of the 12 patients with chronic aortic regurgitation had mitral valve preclosure or diastolic mitral regurgitation (p less than 0.05 versus acute aortic regurgitation). We conclude that diastolic mitral regurgitation accompanies mitral valve preclosure, which occurs in acute but not chronic aortic regurgitation. Thus diastolic mitral regurgitation may be a Doppler sign of acute aortic regurgitation, in the absence of a markedly prolonged PR interval. Furthermore, this observation suggests that normal, nonregurgitant mitral closure requires more than an increase in left ventricular pressure above left atrial pressure, regardless of the position of the mitral leaflets before closure.

Acute Disease↗
PubMedDate not supplied

Clinical evaluation of left ventricular diastolic performance.

Diastole can be divided into four phases: isovolumic relaxation, early filling, diastasis, and atrial systole. The amount of LV filling that occurs during each of these phases depends on myocardial relaxation, the passive characteristics of the LV, the characteristics of the left atrium, pulmonary veins, and mitral valve, and the heart rate. When diastolic function is normal, the net effect of these factors results in an LV filling sufficient to produce an adequate cardiac output, while mean pulmonary venous pressure is maintained below 12 mm Hg. In the absence of systolic dysfunction, abnormal diastolic performance is usually due to abnormal relaxation and/or changes in the passive LV characteristics. Invasive studies can quantitate the rate of myocardial relaxation and the LV diastolic pressure-volume relation. More recently, RNA and Doppler echocardiography have been used to noninvasively evaluate diastolic performance by determining the pattern of LV diastolic filling. At rest, most LV filling occurs early in diastole. Conditions that produce diastolic dysfunction, such as LV hypertrophy and ischemia, are associated with reduced early diastolic filling and an augmented importance of atrial systole. It is important to recognize that such patterns can occur in patients who do not have clinically apparent diastolic dysfunction and in normals. Furthermore, a normal pattern can occur in patients who have severe diastolic dysfunction. A reduced early diastolic filling, in the absence of pulmonary congestion, indicates the loss of diastolic reserve, since the left atrium is being used as a booster pump. This pattern of diastolic filling in a patient who has symptoms of pulmonary congestion may suggest diastolic dysfunction, even if the systolic LV performance is normal. Since diastolic filling of the LV results from a complex interplay of factors, it is unlikely that a single, easily interpreted index of LV diastolic performance will ever be developed. However, the recent development of a noninvasive evaluation of the pattern of LV diastolic filling by RNA or Doppler echocardiography is an important advance. When interpreted with an understanding of the determinants of LV filling and the patient's clinical status, these noninvasive tests can contribute to the rational assessment of LV diastolic performance.

Animals↗
PubMedDate not supplied

Mechanism of physiologic and pathologic S3 gallop sounds.

Although the S3 gallop sound has long been used clinically as an indicator of left ventricular systolic dysfunction, the mechanism responsible for its production remains controversial. The same sound is often found in young healthy individuals, and whether a similar mechanism is responsible is also unknown. The relationship of the S3 gallop sound to the dynamics of left ventricular filling was compared in 18 healthy young triathletes and 15 older subjects with cardiac disease. Twenty healthy normal subjects without an S3 were included as controls. Phonocardiographic, two-dimensional echocardiographic, and Doppler echocardiographic analysis of left ventricular inflow were evaluated. The S3 in both groups always occurred close to peak early filling velocity (E), during early flow deceleration. Mean E deceleration rate was higher in the subjects with S3 (726 +/- 153 cm/sec2 in the triathletes and 819 +/- 274 cm/sec2 in those with cardiac disease) than in control subjects (563 +/- 131 cm/sec2, p less than 0.001 in both cases). Ten triathletes underwent examination both before and immediately after 30 degrees head-up tilt. E deceleration rate dropped significantly with head-up tilt (720 +/- 137 vs 590 +/- 174 cm/sec2, p less than 0.01), while concurrently the S3 disappeared or was diminished in amplitude. Similar changes were seen in subjects with cardiac disease. We conclude that both the "pathologic" and "physiologic" S3 are related to abnormally rapid deceleration of early diastolic left ventricular inflow. Although the presence of the S3 is not dependent on the state of left ventricular systolic function, diastolic filling is characterized by a predominance of early inflow with a rapid flow deceleration rate.

Adult↗
PubMedDate not supplied

Perforation of the anterior mitral leaflet caused by aortic valve endocarditis: diagnosis by two-dimensional, transesophageal echocardiography and color flow Doppler.

Perforation of the mitral valve as a result of aortic valve endocarditis is rare. Recognition of such abnormality is very important before surgical intervention. Diagnosis is very difficult by either invasive or noninvasive techniques. This report stresses the role of echocardiography in evaluating this rare abnormality. Perforation of the anterior mitral valve leaflet developed in our patient as a complication of aortic valve endocarditis. The perforation was suggested by the surface echocardiogram (as an interruption of the leaflet continuity) and by the color flow Doppler (which suggested turbulent flow at the area of suspected interruption). The perforation was confirmed during surgery by transesophageal echocardiography and alerted the surgeon to repair, rather than replace, the valve.

Adult↗