Radiation damage effects in far-ultraviolet filters, thin films, and substrates.

Advances in vacuum ultraviolet thin-film filter technology have been made through the use of filter designs with multilayers of materials such as Al(2)O(3), BaF(2), CaF(2), HfO(2), LaF(3), MgF(2), and SiO(2). Our immediate application for these filters will be in an imaging system to be flown on a satellite where a 2 × 9 R(E) orbit will expose the instrument to approximately 250 krad of radiation. Because to our knowledge no previous studies have been made on the potential radiation damage of these materials in the thin-film format, we report on such an assessment here. Transmittances and reflectances of BaF(2), CaF(2), HfO(2), MgF(2), and SiO(2) thin films on MgF(2) substrates, Al(2)O(3) thin films on fused-silica substrates, uncoated fused silica and MgF(2), and four multilayer filters made from these materials were measured from 120 to 180 nm beforeand after irradiation by 250 krad from a (60)Co gamma radiation source. No radiation-induced losses in transmittance or reflectance occurred in this wavelength range. Additional postradiation measurements from 160 to 300 nm indicates 2-5% radiation-induced absorption near 260 nm in some of the samples with MgF(2) substrates. From these measurements we conclude that far-ultraviolet filters made from the materials tested should experience less than 5% change from exposure to up to 250 krad of high-energy radiation in space applications.

Response of two-phase droplets to intense electromagnetic radiation.

The response of two-phase droplets to intense radiant heating is studied to determine the incident power that is required for causing explosive boiling in the liquid phase. The droplets studied consist of strongly absorbing coal particles dispersed in a weakly absorbing water medium. Experiments are performed by confining droplets (radii = 37, 55, and 80 microm) electrodynamically and irradiating them from two sides with pulsed laser beams. Emphasis is placed on the transition region from accelerated droplet vaporization to droplet superheating and explosive boiling. The time scale observed for explosive boiling is more than 2 orders of magnitude longer than published values for pure liquids. The delayed response is the result of energy transfer limitations between the absorbing solid phase and the surrounding liquid.

Coronary blood flow in dogs with contractile dysfunction due to experimental volume overload.

BACKGROUND: Abnormalities in coronary blood flow are responsible for stress-induced reductions in contractile function in pressure overload hypertrophy. Less is known about coronary blood flow in volume overload. In this study, we tested the hypothesis that coronary blood flow abnormalities were responsible for contractile abnormalities in experimental volume overload hypertrophy. METHODS AND RESULTS: We examined coronary blood flow at rest and during pacing in seven dogs with contractile dysfunction secondary to chronic experimental mitral regurgitation (average regurgitant fraction at 3 months, 0.58 +/- 0.05). After 3 months of mitral regurgitation, left ventricular mass had increased from 92 +/- 8 g at baseline to 118 +/- 10 g (p less than 0.002). The slope of the end-ejection stress-volume relation, one of our indexes used to estimate contractile function, had fallen from 5.4 +/- 0.3 at baseline to 3.0 +/- 0.3 at 3 months of mitral regurgitation (p less than 0.001). In the mitral regurgitation dogs, coronary blood flow at rest was similar to that of control dogs (endocardial blood flow: control dogs, 1.33 +/- 0.12 ml/min/g; mitral regurgitation dogs, 1.16 ml/min/g, p = NS; epicardial blood flow at rest: control dogs, 1.30 +/- 0.16 ml/min/g; mitral regurgitation dogs 1.13 +/- 0.2 ml/min/g, p = NS). With pacing-induced stress, coronary blood flow increased appropriately in control and mitral regurgitation dogs. Ultrasonic dimension gauges placed in the endocardium and epicardium demonstrated no further deterioration in ventricular function during pacing in the mitral regurgitation dogs. In a separate group of five control dogs and five dogs with mitral regurgitation and left ventricular dysfunction, coronary blood flow was examined in the conscious closed-chest state at rest, during adenosine infusion, and during rapid atrial pacing (240 beats/min). Blood flow increased similarly in both groups during pacing and adenosine infusion. CONCLUSIONS: We conclude that in dogs with mitral regurgitation that have developed contractile dysfunction, abnormalities in coronary blood flow do not explain the resting contractile dysfunction. Furthermore, studies during pacing-induced stress and coronary vasodilation with adenosine demonstrate that substantial coronary blood flow reserve is present in this type of volume overload hypertrophy.

Indications for heart valve replacement.

Proper evaluation of the patient with valvular heart disease begins with a thorough history and physical examination. Today, sophisticated noninvasive tests--especially echocardiography with color flow Doppler imaging--complement the information gained at cardiac catheterization. Information previously available only through cardiac catheterization can now be obtained from these noninvasive techniques. Serial evaluations can be performed, which are important in managing lesions of borderline hemodynamic significance and in avoiding subclinical deterioration of left ventricular contractility. Improvements in surgical expertise and intraoperative myocardial preservation allow postoperative improvement for patients with aortic stenosis and aortic insufficiency despite the presence of left ventricular systolic dysfunction. Many traditional indicators of a poor operative result in aortic insufficiency appear less reliable today. Consequently, these indicators should never be viewed in isolation or be given preeminence over clinical judgment. The long-term results following aortic valvuloplasty have been disappointing. However, mitral valvuloplasty--for technically suitable types of mitral stenosis--is an attractive alternative to surgery. Echocardiography may be helpful in selecting patients best suited for this technique. The timing of valve replacement in mitral insufficiency is made difficult by the altered loading conditions which can mask underlying contractile dysfunction. In this regard, the use of end-systolic measurements (e.g., end-systolic stress-volume ratio) more accurately characterized left ventricular contractility. When mitral insufficiency patients with left ventricular systolic dysfunction require surgery, valve repair appears superior to traditional mitral valve replacement. With valve repair, the postoperative left ventricular ejection fraction is usually higher, as left ventricular contractile reserve is better maintained.

Vacuum ultraviolet thin films. 1: Optical constants of BaF(2), CaF(2), LaF(3), MgF(2), Al(2)O(3), HfO(2), and SiO(2) thin films.

The optical constants of MgF(2) (bulk) and BaF(2), CaF(2), LaF(3), MgF(2), Al(2)O(3), HfO(2), and SiO(2) films deposited on MgF(2) substrates are determined from photometric measurements through an iteration process of matching calculated and measured values of the reflectance and transmittance in the 120-230-nm vacuum ultraviolet wavelength region. The potential use of the listed fluorides and oxides as vacuum ultraviolet coating materials is discussed in part 2 of this paper.

Vacuum ultraviolet thin films. 2: Vacuum ultraviolet all-dielectric narrowband filters.

We report the design and performance of narrowband transmission filters employing the rapidly changing extinction coefficient that is characteristic of BaF(2) and SiO(2) films within certain wavelength intervals in the vacuum ultraviolet. We demonstrate the design concept for two filters centered at 135 nm for BaF(2) and at 141 nm for SiO(2). It is found that these filters provide excellent narrowband spectral performance when combined with narrowband reflection filters. The filter centered at 135 nm has a peak transmittance of 24% and a bandwidth of 4 nm at full width at half-maximum for collimated incident light. The transmittance for lambda(0)

Abnormal subendocardial blood flow in pressure overload hypertrophy is associated with pacing-induced subendocardial dysfunction.

To detect the functional significance of subendocardial hypoperfusion in the pressure-overloaded left ventricle, we studied subendocardial and subepicardial function and subendocardial and subepicardial blood flow simultaneously in seven dogs with left ventricular hypertrophy (left ventricle/body weight ratio, 7.2 g/kg) produced by chronic aortic banding. Seven normal dogs served as controls. Subendocardial and subepicardial segment lengths were measured by ultrasonic dimension gauges, and myocardial blood flow was measured with radioactive microspheres. Atrial pacing (180-200 beats/min for 5 minutes) was used to produce a chronotropic stress. In dogs with left ventricular hypertrophy, the subendocardial blood flow failed to increase during pacing compared with the baseline state (1.21 +/- 0.17 vs. 1.22 +/- 0.17 ml/min/g). Subendocardial shortening fraction deteriorated with pacing stress (before pacing, 30.6 +/- 3.9%; after pacing, 24.2 +/- 3.7%; p less than 0.001). In controls, subendocardial blood flow increased from 1.32 +/- 0.19 to 1.80 +/- 0.19 ml/min/g during pacing, and shortening fraction was preserved (before pacing, 25.5 +/- 3.9%; after pacing, 25.9 +/- 3.3%). Subepicardial blood flow in dogs with hypertrophy increased from 1.54 +/- 0.24 to 2.32 +/- 0.34 ml/min/g, and subepicardial shortening fraction was maintained (before pacing, 10.4 +/- 1.0%; after pacing, 10.5 +/- 1.2%) as it was in controls (subepicardial blood flow, from 1.27 +/- 0.18 to 2.12 +/- 0.17 ml/min/g; shortening fraction, from 16.6 +/- 2.5% to 15.5 +/- 2.2%). We conclude that, with pacing stress in pressure-overload hypertrophy, subendocardial blood flow failed to increase. This abnormality corresponded with a deterioration in subendocardial contractile function.

Supernormal ejection performance is isolated to the ipsilateral congenitally pressure-overloaded ventricle.

Congenital left ventricular pressure overload is associated with "excessive" hypertrophy that leads to subnormal afterload (wall stress), permitting enhanced ventricular ejection performance. Whether congenital right ventricular pressure overload is associated with a similar phenomenon is uncertain. It is also unknown whether supranormal ejection performance affects only the overloaded ventricle or is a general process affecting both ventricles. Conflicting data exist about whether the hypertrophic process associated with pressure overload is induced primarily by local loading conditions or by neuroendocrine influences. If the former postulate is true, the hypertrophic response should be confined to the overloaded ventricle; if the latter is true, one might predict that both ventricles would be affected by a less specific response to circulating catecholamines. To help resolve these issues, both right and left ventricular performance was examined in seven patients with isolated congenital pulmonary stenosis (average pulmonary pressure gradient 78 +/- 13 mm Hg), six patients with isolated congenital aortic stenosis (average gradient 80 +/- 10 mm Hg) and six normal subjects. Right ventricular ejection fraction was increased in patients with pulmonary stenosis (61 +/- 2%) compared with the value in normal subjects (53 +/- 2%, p less than 0.01) and in patients with aortic stenosis (50 +/- 3%, p = 0.007). Left ventricular ejection fraction was increased in patients with congenital aortic stenosis (84 +/- 4%) compared with the value in normal subjects (70 +/- 4%, p less than 0.01) and in patients with congenital pulmonary stenosis (65 +/- 2%, p less than 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)

Left ventricular function in experimental volume overload hypertrophy.

Left ventricular function in volume overload hypertrophy is controversial. In humans, chronic severe volume overload eventually results in left ventricular dysfunction; paradoxically, experimental volume overload hypertrophy has nearly always been associated with normal left ventricular function. However, in most cases, experimental volume overload hypertrophy has either been mild or only present for a short duration. To help resolve the issue of contractile function in volume overload hypertrophy, we examined ventricular function in a recently described model of severe chronic experimental mitral regurgitation. Left ventricular function was measured before and 3 mo after the creation of severe mitral regurgitation (averaged regurgitant fraction 0.64 +/- 0.04). At 3 mo end-diastolic volume had increased from 78 +/- 5 to 114 +/- 7 ml (P less than 0.01). Significant left ventricular hypertrophy had occurred with an increase in the left ventricular weight-to-body weight ratio from 3.84 +/- 0.2 to 5.22 +/- 0.2 (P less than 0.01). All indicators of left ventricular function (ejection fraction, the end ejection stress-volume relationship, this relationship corrected for eccentric hypertrophy, and mean velocity of circumferential fiber shortening at a common stress) were reduced at 3 mo. Our study produced 64% volume overload which was maintained for 3 mo at which time there was a 36% increase in left ventricular mass. This amount of volume overload of this duration produced significant left ventricular dysfunction.

Alterations in left ventricular geometry, wall stress, and ejection performance after correction of congenital aortic stenosis.

Children with congenital aortic stenosis have "excessive" left ventricular hypertrophy with reduced resting systolic wall stress that allows for supernormal ejection performance. If aortic stenosis is uncorrected, this pattern persists until adulthood. The effect of removing the aortic pressure gradient on left ventricular hypertrophy and wall stress in children with congenital aortic stenosis is unknown. To test the hypothesis that removal of the stimulus for hypertrophy by aortic valve replacement or repair would normalize left ventricular mass and wall stress, we measured left ventricular ejection performance, wall stress, and contractile function in seven patients at cardiac catheterization before and 36 +/- 7 months after surgical correction of congenital aortic stenosis. After aortic valve replacement or repair, the aortic valve gradient fell from 87 +/- 12 to 7 +/- 4 mm Hg, and peak left ventricular pressure fell from 187 +/- 14 to 128 +/- 8 mm Hg. Left ventricular ejection fraction decreased postoperatively from 86 +/- 4% to 74 +/- 4% (p less than 0.001), whereas velocity of circumferential fiber shortening decreased from 2.15 +/- 0.15 to 1.6 +/- 0.11 (p less than 0.002). Left ventricular mass remained unchanged preoperatively (121 +/- 14 g/m2) and postoperatively (121 +/- 16 g/m2), but wall thickness (h) decreased in relation to ventricular radius (r) (h/r = 0.55 +/- 0.05 preoperatively, 0.36 +/- 0.02 postoperatively; p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanism of decreased forward stroke volume in children and swine with ventricular septal defect and failure to thrive.

Children with ventricular septal defect (VSD) often demonstrate failure to thrive (FTT). Such patients usually have reduced systemic cardiac output which has been postulated as a cause for their growth retardation. This study was conducted to ascertain the mechanism of the reduced cardiac output in children with VSD and FTT and also in a porcine model of VSD. Forward stroke volume was reduced in VSD-FTT children, 31 +/- 8 ml/m2, compared to normal children, 49 +/- 15 ml/m2 (P less than 0.05), but was not reduced in children with VSD and normal growth and development (41 +/- 16 ml/m2). Forward stroke volume was also reduced in swine with VSD compared to controls. Contractility assessed by mean velocity of circumferential shortening (Vcf) corrected for afterload was similar in normals and VSD-FTT children. Contractile performance was also similar in normal and VSD swine. Afterload assessed as systolic stress was similar in FTT-VSD children and normal subjects. Preload assessed as end-diastolic stress was increased in the VSD-FTT group. End-diastolic volume was not larger in the VSD-FTT group. We conclude that the reduced stroke volume seen in VSD-FTT children and VSD-swine was not due to reduced contractility, increased afterload or reduced preload. The reduced stroke volume may have been due to failure of end-diastolic volume to increase adequately.

Left ventricular diastolic filling abnormalities in left anterior descending disease.

Reduced left ventricular diastolic filling (DF) has been noted in coronary disease (CD) patients with normal left ventricular systolic function (NLVF). However, previous studies have included patients with regional wall disease, hypertension, or left ventricular hypertrophy. In the absence of these factors, only a subgroup of patients who had greater than 75% luminal obstruction of the left anterior descending artery (LAD) demonstrated DF abnormalities. Using 60 frames/sec biplane contrast ventriculography, we evaluated the left ventricular filling curve and its derivative in 21 patients with normal coronary arteries and NLVF (group 1), 17 CD patients with NLVF and no LAD disease (group 2), and 18 patients with LAD disease and NLVF (group 3). The peak filling rate (PFR) as end diastolic volumes/sec (EDV/S) was reduced in group 3 patients (group 3: 3.00 +/- 0.51 EDV/S vs group 1: 3.59 +/- 0.84 EDV/S, p less than .05; and group 2: 3.61 +/- 0.91 EDV/S, p less than .05). There was marked overlap in the PFR's between the normal and LAD group. DF may be normal in CD patients with NLVF in the absence of LAD disease. LAD patients have abnormal DF, but these abnormalities lack predictive valve.

Unexpected persistence into adulthood of low wall stress in patients with congenital aortic stenosis: is there a fundamental difference in the hypertrophic response to a pressure overload present from birth?

Congenital aortic stenosis in children is characterized by low left ventricular systolic wall stress allowing for supernormal ejection performance. In contrast, adults with acquired aortic stenosis have normal or excessive systolic wall stress resulting in either normal or subnormal ejection performance. In this study young children with congenital aortic stenosis, older children and adults with congenital aortic stenosis, and adults with acquired aortic stenosis were evaluated to test the hypothesis that the childhood pattern of low wall stress would convert to the adult pattern with advancing age. Left ventricular end systolic wall stress was lower in both congenital aortic stenosis groups when compared with that in age-matched normal subjects or adults with acquired aortic stenosis. Ejection fraction was higher in both groups of patients with congenital aortic stenosis than in age-matched controls. There was no tendency in the 16 patients with congenital aortic stenosis, some of whom were followed to the age of 33, for the congenital pattern of wall stress and ventricular performance to convert to the adult pattern. These results suggest that there is a fundamental difference in the hypertrophic response to a pressure overload present at birth compared with the response to one acquired later in life.

Incidence of acute myocardial infarction in patients with exercise-induced silent myocardial ischemia.

Fifty-five patients with angiographically proved coronary artery disease (CAD) underwent Bruce protocol exercise stress testing with thallium-201 imaging. Twenty-seven patients (group I) showed myocardial hypoperfusion without angina pectoris during stress, which normalized at rest, and 28 patients (group II) had a similar pattern of reversible myocardial hypoperfusion but also had angina during stress. Patients were followed for at least 30 months. Six patients in group I had an acute myocardial infarction (AMI), 3 of whom died, and only 1 patient in group II had an AMI (p = 0.05), and did not die. Silent myocardial ischemia uncovered during exercise stress thallium testing may predispose to subsequent AMI. The presence of silent myocardial ischemia identified in this manner is of prognostic value, independent of angiographic variables such as extent of CAD and left ventricular ejection fraction.

Hemodynamic predictors of outcome in patients undergoing valve replacement.

The afterload-corrected end-systolic volume index (ratio of end-systolic stress to end-systolic volume index [ESS/ESVI]) was previously useful in predicting outcome in patients with mitral regurgitation undergoing valve replacement. Therefore we tested ESS/ESVI together with standard hemodynamic variables as possible predictors of outcome in 39 patients with various valvular lesions who underwent valve replacement. Thirteen patients had preoperative mitral regurgitation, 16 had aortic stenosis, nine had aortic regurgitation, and one had mitral stenosis. Twenty-seven patients (group S) had a satisfactory outcome as defined by a return to NYHA class I or II together with a normal postoperative ejection fraction. Twelve patients who died, remained in class III or IV, or had a subnormal postoperative ejection fraction were deemed to have an unsatisfactory result (group U). Mean right atrial pressure, pulmonary arterial pressure, pulmonary capillary wedge pressure, end-diastolic volume index, end-systolic volume index (ESVI), and end-systolic wall stress were all greater in group U, whereas ESS/ESVI and ejection fraction were lower in group U. When these and other factors were submitted to stepwise discriminant multivariate analysis, ESS/ESVI and ESVI were the only independent predictors of outcome. However, when patients with mitral regurgitation (who might have biased the study) were excluded, discriminant analysis showed ESVI as the only independent predictive variable. We conclude that end-systolic indicators of ventricular function are superior to other standard hemodynamic variables in predicting outcome of valve replacement.

Cardiac function assessed by attenuation-corrected radionuclide pressure-volume indices.

Using attenuation-corrected radionuclide volumes and arm-cuff peak systolic pressures, we established the mean value for the ratio of left ventricular (LV) peak systolic pressure/end systolic volume at rest for 15 healthy persons. In 43 patients with coronary disease, this ratio was more sensitive as an indicator of abnormal LV function and for predicting coronary artery disease than the resting ejection fraction. The slope of an end systolic pressure-volume line was also calculated from data obtained under three loading conditions: at rest, during isometric handgrip testing, and after the sublingual administration of nitroglycerin. The sensitivity of the slope for predicting the presence of coronary artery disease was not significantly different from the resting peak systolic pressure/end systolic volume ratio but was helpful in identifying patients with coronary artery disease. These results represent an improvement over previous radionuclide pressure-volume measurements that have not used attenuation correction and show the need for accurate, nongeometric measurements of the LV end systolic volume.

Left ventricular wall stress and function in childhood coarctation of the aorta.

Unlike most adults with compensated pressure overload of the left ventricle, children with moderate to severe aortic stenosis exhibit pronounced left ventricular muscle hypertrophy, enhanced ejection performance and diminished wall stress. To determine whether these findings are present in other forms of left ventricular pressure overload in children, left ventricular mechanics were studied by catheterization in 14 children with coarctation of the aorta (average peak gradient 39 +/- 17 mm Hg) and in 10 normal children. Ejection fraction and mean velocity of circumferential fiber shortening in the coarctation group (0.74 +/- 0.09 and 1.71 +/- 0.43 circumferences/s, respectively) were significantly higher than in normal subjects (0.65 +/- 0.05 and 1.27 +/- 0.26 circumferences/s, respectively) (p = 0.008), but the ranges for both groups overlapped. End-systolic stress in children with coarctation (77 +/- 20 dynes X 10(3)/cm2) was less than in normal children (121 +/- 24 dynes X 10(3)/cm2) (p less than 0.001), again with overlap of the ranges for both groups. The ratio of end-systolic stress to end-systolic volume index, an estimate of contractile function, was similar in both groups. Relations between severity of obstruction (left ventricular peak systolic pressure, coarctation gradient) and end-systolic stress and between stress and ejection performance were present within the coarctation group. Comparison of these data with those found in children with moderate to severe aortic stenosis shows a similar but less pronounced response to pressure overload due to coarctation of the aorta.

Long-term efficacy of bepridil in patients with chronic stable angina pectoris: results of a multicenter, placebo-controlled study of extended bepridil use.

To evaluate whether bepridil once a day provides effective antianginal therapy during extended use, a placebo-controlled withdrawal study was conducted in 33 patients with chronic stable angina. Each patient studied had previously had a favorable response to short-term administration of bepridil and had been taking the drug once daily for greater than or equal to 9 months of continuous use. Patients were then randomly assigned to receive either continued bepridil or a placebo substitution once daily during a 4-week, double-blind, parallel-group comparison. Dosage for the bepridil group was constantly maintained for each patient at a level observed to be clinically effective. The study consisted of a comparison of angina frequency and nitroglycerin tablet consumption obtained from patient diaries and results from maximal-graded multistage treadmill tests. Patients randomized to continue receiving bepridil remained stable in terms of angina frequency and exercise performance. Discontinuation of long-term bepridil significantly increased angina frequency and nitroglycerin tablet consumption and reduced exercise capacity. Four patients (24%), all receiving placebo treatment, had increases in angina frequency and had the study terminated. Bepridil was reinstituted in these patients with resolution of symptoms and no untoward effects. The results of this placebo-controlled, double-blind, randomized study confirm that bepridil continues to provide antianginal benefit during long-term administration.