Biomedical subjects

J P Sun

Publications and source records attributed to J P Sun.

At least 19 recordsLinked to original sources

PubMed2001

Clinical and echocardiographic characteristics of papillary fibroelastomas: a retrospective and prospective study in 162 patients.

BACKGROUND: Cardiac papillary fibroelastoma (CPF) is a primary cardiac neoplasm that is increasingly detected by echocardiography. The clinical manifestations of this entity are not well described. METHODS AND RESULTS: In a 16-year period, we identified patients with CPF from our pathology and echocardiography databases. A total of 162 patients had pathologically confirmed CPF. Echocardiography was performed in 141 patients with 158 CPFs, and 48 patients had CPFs that were not visible by echocardiography (<0.2 cm), leaving an echocardiographic subgroup of 93 patients with 110 CPFs. An additional 45 patients with a presumed diagnosis of CPF were identified. The mean age of the patients was 60+/-16 years of age, and 46.1% were male. Echocardiographically, the mean size of the CPFs was 9+/-4.6 mm; 82.7% occurred on valves (aortic more than mitral), 43.6% were mobile, and 91.4% were single. During a follow-up period of 11+/-22 months, 23 of 26 patients with a prospective diagnosis of CPF that was confirmed by pathological examination had symptoms that could be attributable to embolization. In the group of 45 patients with a presumed diagnosis of CPF, 3 patients had symptoms that were likely due to embolization (incidence, 6.6%) during a follow-up period of 552+/-706 days. CONCLUSIONS: CPFs are generally small and single, occur most often on valvular surfaces, and may be mobile, resulting in embolization. Because of the potential for embolic events, symptomatic patients, patients undergoing cardiac surgery for other lesions, and those with highly mobile and large CPFs should be considered for surgical excision.

Adolescent↗

PubMed2001

Respiratory variation of mitral and pulmonary venous Doppler flow velocities in constrictive pericarditis before and after pericardiectomy.

The objective of this study was to determine whether Doppler echocardiography is useful in assessing the effects of pericardiectomy in patients with constrictive pericarditis by studying the postoperative change in the respiratory variation of mitral inflow and pulmonary venous Doppler flows. The study population consisted of 35 cases with surgically proven constrictive pericarditis. Thirty-five patients had preoperative Doppler echocardiography, whereas 4 patients died of non-cardiac causes and 1 patient had a heart transplant before follow-up. Postoperative studies were performed at a mean of 1081 +/- 84 days (range 120-2700 days) after pericardiectomy. The mean (+/- SD) respiratory variation changed after surgery from a baseline value of 17% +/- 14% to 8% +/- 8% for peak mitral E velocity (P <.01); from 25% +/- 18% to 7% +/- 13% (P <.001) for pulmonary venous (PV) peak diastolic flow velocity, and from 21% +/- 13% to 11% +/- 13% (P =.009) for PV peak systolic flow velocity. The 23 patients who became asymptomatic after surgery had a significantly lower mean mitral and PV respiratory variation than the 7 patients who were NYHA class II (4% +/- 4% and 6% +/- 4% vs 21% +/- 6% and 19% +/- 10%, respectively, P <.0001 for both). Pulsed Doppler echocardiographic assessment of respiratory variation is useful for evaluating the outcome of pericardiectomy.

Aged↗

PubMed2001

[Effects of fluid percussion injury on intracellular [Ca2+]i and pH in cultured rat neurons].

AIM: To study the change of intracellular [Ca2+]i and pH in cultured neurons after fluid percussion injury, and the therapeutic effect of drugs. METHODS: The neurons of Sprague Dawley rats were cultured for 8-14 days, then treated them with fluid percussion injury (2.5 kPa, 20 ms). Alterations of [Ca2+]i and pH in single neural cells following fluid percussion injury were measured by a laser scanning confocal microscope. After being injured for several hours the cultured neurons were treated with nimodipine or D-(-)-2-amino-5-phosphonovaleric acid (D-AP-5). Two hours later, the effects of drugs on intracellular [Ca2+]i and pH were studied. RESULTS: The Intracellular [Ca2+]i increased quickly after brain injury and reached peak in 12 hours. It then decreased gradually and became normal at 48 hours. The pH decreased slowly, reached minimum in 12 hours, and then kept at a lower level. It did not recover normal at 48 hours. Nimodipine and D-AP-5 decreased significantly the ascension of [Ca2+]i and the descent of pH. But nimodipine and D-AP-5 must be given within 10 hours after injury for a good therapeutic effect. CONCLUSION: According to the change of intracellular [Ca2+]i and pH, early use of nimodipine and D-AP-5, will get a better therapeutic effect.

2-Amino-5-phosphonovalerate↗

PubMed2000

Left ventricular diastolic dysfunction in lone atrial fibrillation determined by Doppler tissue imaging of mitral annular motion.

In this study, we sought evidence for an underlying atrial or ventricular myopathy in patients with paroxysmal lone atrial fibrillation using standard echocardiographic parameters in addition to Doppler tissue imaging of mitral annular motion. No impairment in atrial contractile function was found, but there was evidence for impaired diastolic function in these patients.

Adult↗

PubMed2000

New digital measurement methods for left ventricular volume using real-time three-dimensional echocardiography: comparison with electromagnetic flow method and magnetic resonance imaging.

AIM: The aim of this study was to investigate the feasibility and accuracy of using symmetrically rotated apical long axis planes for the determination of left ventricular (LV) volumes with real-time three-dimensional echocardiography (3DE). METHODS AND RESULTS: Real-time 3DE was performed in six sheep during 24 haemodynamic conditions with electromagnetic flow measurements (EM), and in 29 patients with magnetic resonance imaging measurements (MRI). LV volumes were calculated by Simpson's rule with five 3DE methods (i.e. apical biplane, four-plane, six-plane, nine-plane (in which the angle between each long axis plane was 90 degrees, 45 degrees, 30 degrees or 20 degrees, respectively) and standard short axis views (SAX)). Real-time 3DE correlated well with EM for LV stroke volumes in animals (r=0.68-0.95) and with MRI for absolute volumes in patients (r-values=0.93-0.98). However, agreement between MRI and apical nine-plane, six-plane, and SAX methods in patients was better than those with apical four-plane and bi-plane methods (mean difference = -15, -18, -13, vs. -31 and -48 ml for end-diastolic volume, respectively, P<0.05). CONCLUSION: Apically rotated measurement methods of real-time 3DE correlated well with reference standards for calculating LV volumes. Balancing accuracy and required time for these LV volume measurements, the apical six-plane method is recommended for clinical use.

Adult↗

PubMed2000

Normal values of regional left ventricular endocardial motion: multicenter color kinesis study.

Our goal was to establish normal values for quantitative color kinesis indexes of left ventricular (LV) wall motion over a wide range of ages, which are required for objective diagnosis of regional systolic and diastolic dysfunction. Color-encoded images were obtained in 194 normal subjects (95 males, 99 females, age 2 mo to 79 yr) in four standard views. Quantitative indexes of magnitude and timing of systolic and diastolic function were studied for age- and gender-related differences. Normal limits of all ejection and filling indexes were in a narrow range (< or =25% of the mean), with no major gender-related differences. Despite invariable ejection fractions, both peak filling and ejection rates decreased with age (30 and 20%, correspondingly) with a concomitant increase in mean filling and ejection times, resulting in five- and twofold increases in the late to early filling and ejection ratios, correspondingly. Diastolic asynchrony increased with age (from 4.7 +/- 2.0 to 6.4 +/- 3.2 from the 2nd to 7th decade). The normal values of color kinesis indexes should allow objective detection of regional LV systolic and diastolic dysfunction.

Adolescent↗

PubMed1999

Inferior vena caval masses identified by echocardiography.

The most common cause of an inferior vena caval mass is renal cell carcinoma that extends through the lumen, occurring in 47 of 62 patients (85%). Detection of an inferior vena caval mass affects the surgical approach requiring cardiopulmonary bypass for resection when the mass extends to the heart.

Adolescent↗

PubMed1999

New echocardiographic windows for quantitative determination of aortic regurgitation volume using color Doppler flow convergence and vena contracta.

Color Doppler images of aortic regurgitation (AR) flow acceleration, flow convergence (FC), and the vena contracta (VC) have been reported to be useful for evaluating severity of AR. However, clinical application of these methods has been limited because of the difficulty in clearly imaging the FC and VC. This study aimed to explore new windows for imaging the FC and VC to evaluate AR volumes in patients and to validate this in animals with chronic AR. Forty patients with AR and 17 hemodynamic states in 4 sheep with strictly quantified AR volumes were evaluated. A Toshiba SSH 380A with a 3.75-MHz transducer was used to image the FC and VC. After routine echo Doppler imaging, patients were repositioned in the right lateral decubitus position, and the FC and VC were imaged from high right parasternal windows. In only 15 of the 40 patients was it possible to image clearly and measure accurately the FC and VC from conventional (left decubitus) apical or parasternal views. In contrast, 31 of 40 patients had clearly imaged FC regions and VCs using the new windows. In patients, AR volumes derived from the FC and VC methods combined with continuous velocity agreed well with each other (r = 0.97, mean difference = -7.9 ml +/- 9.9 ml/beat). In chronic animal model studies, AR volumes derived from both the VC and the FC agreed well with the electromagnetically derived AR volumes (r = 0.92, mean difference = -1.3 +/- 4.0 ml/beat). By imaging from high right parasternal windows in the right decubitus position, complementary use of the FC and VC methods can provide clinically valuable information about AR volumes.

Adolescent↗

PubMed1999

Dissociation of chronic vascular cell proliferation and vascular contractility after chronic cigarette smoke exposure.

In guinea pigs, chronic cigarette smoke exposure produces physiological and structural alterations in the pulmonary vasculature via unknown mechanisms. This study aimed to determine whether chronic cigarette smoke exposure can induce altered pulmonary vascular reactivity, and whether chronic smoke exposure would be associated with a continued increase in vascular cell deoxyribonucleic acid (DNA) synthesis, indicative of cell proliferation. Guinea-pigs were therefore exposed to two regimens of smoke. In the first experiment, animals were exposed once to the smoke of seven cigarettes, and sacrificed 24 h post-smoke, while in the second experiment, the guinea-pigs were exposed for 5 days each week for 4 months. Control animals were exposed to air. Lung explant preparations and computer linked image photography were utilized to determine vascular reactivity, and DNA synthesis was assessed using the 5-bromo-2'-deoxyuridine technique. Neither acute nor chronic smoke exposure affected vascular reactivity, although the older animals had lesser reactivity. In the chronically smoked animals, evidence was found of ongoing vascular DNA synthesis, and evidence of structural alterations with increased muscularization of the arterioles (34.7+/-7.6% of arterioles in control versus 62.7+/-5.5% after smoke exposure). Despite evidence of continued deoxyribonucleic acid synthesis in the peribronchiolar vessels, the alterations of vascular physiology previously found in this model cannot be ascribed to increased reactivity at this site. Instead, the chronic deoxyribonucleic acid synthesis in the arterioles adjacent to the alveolar ducts, culminating in an increased number of fully muscularized vessels, would suggest this compartment as the most probable source.

Animals↗

PubMed1999

Assessment of diastolic function by tissue Doppler echocardiography: comparison with standard transmitral and pulmonary venous flow.

The objective of this study was to determine the utility of Doppler tissue echocardiography in the evaluation of diastolic filling and in discriminating between normal subjects and those with various stages of diastolic dysfunction. We measured myocardial velocities in 51 patients with various stages of diastolic dysfunction and in 27 normal volunteers. The discriminating power of each of the standard Doppler indexes of left ventricular filling, pulmonary venous flow, and myocardial velocities was determined with the use of Spearman rank correlation and analysis of variance F statistics. Early diastolic myocardial velocity (E(m)) was higher in normal subjects (16.0 +/- 3.8 cm/s) than in patients with either delayed relaxation (n = 15, 7.5 +/- 2.2 cm/s), pseudonormal filling (n = 26, 7.6 +/- 2.3 cm/s), or restrictive filling (n = 10, 7.4 +/- 2.4 cm/s, P <.0001). E(m ) was the best single discriminator between control subjects and patients with diastolic dysfunction (P =.7, F = 64.5). Myocardial velocities assessed by Doppler tissue echocardiography are useful in differentiating patients with normal from those with abnormal diastolic function. Myocardial velocity remains reduced even in those stages of diastolic dysfunction characterized by increased preload compensation.

Adult↗

PubMed1999

Cigarette smoke exposure causes constriction of rat lung.

Cigarette smoke is known to cause acute increases in airway resistance, but the mechanisms behind this effect are unknown. Lung explants were utilized to examine the constrictive effects of acute cigarette smoke exposure on bronchioles from rats in vitro that had or had not been previously exposed to cigarette smoke in vivo. It was found that smoke induced a small but consistent degree of contraction of the airways in vitro, which could be reduced by an endothelin receptor antagonist in the animals which had had no previous smoke exposure in vivo, and reduced by the oxidant scavengers superoxide dismutase or catalase in the animals with previous smoke exposure. In conclusion, cigarette smoke induces acute small airways constriction through both endothelin release and direct oxidant effects; which mechanisms are operative depends on the prior smoking status.

Animals↗

PubMed1998

Long term cigarette smoke exposure does not increase airway responsiveness in rats.

To ascertain whether chronic cigarette smoke exposure induces increased airway responsiveness, we performed methacholine response tests in Sprague-Dawley rats by calculating pulmonary resistance after nebulization of saline followed by an increasing concentration of methacholine. We also calculated the concentration of methacholine which doubled the baseline resistance (R200). Tests were performed at baseline and after 2, 4, 8, and 12 months of exposure to the smoke of seven cigarettes per day, 5 days each week; control animals were exposed to room air. At the completion of the study, there were 13 rats in the smoke-exposed group and 7 rats remaining in the control group. Airway morphology was assessed using a point counting technique. We found that (1) chronic exposure to cigarette smoke did not alter either the baseline resistance or the R200; (2) the saline baseline resistance decreased over time in the control animals; and (3) at the 12-month time point, smokers with increased baseline airway resistance had greater amounts of airway smooth muscle compared with the smoke-exposed animals without increased resistance. We conclude that in this animal model, long term exposure to cigarette smoke did not alter the response to methacholine but did increase airway smooth muscle and baseline resistance in some but not all animals.

Airway Resistance↗

PubMed1998

Quantification of mitral regurgitation by automated cardiac output measurement: experimental and clinical validation.

OBJECTIVES: To develop and validate an automated noninvasive method to quantify mitral regurgitation. BACKGROUND: Automated cardiac output measurement (ACM), which integrates digital color Doppler velocities in space and in time, has been validated for the left ventricular (LV) outflow tract but has not been tested for the LV inflow tract or to assess mitral regurgitation (MR). METHODS: First, to validate ACM against a gold standard (ultrasonic flow meter), 8 dogs were studied at 40 different stages of cardiac output (CO). Second, to compare ACM to the LV outflow (ACMa) and inflow (ACMm) tracts, 50 normal volunteers without MR or aortic regurgitation (44+/-5 years, 31 male) were studied. Third, to compare ACM with the standard pulsed Doppler-two-dimensional echocardiographic (PD-2D) method for quantification of MR, 51 patients (61+/-14 years, 30 male) with MR were studied. RESULTS: In the canine studies, CO by ACM (1.32+/-0.3 liter/min, y) and flow meter (1.35+/-0.3 liter/min, x) showed good correlation (r=0.95, y=0.89x+0.11) and agreement (deltaCO(y-x)=0.03+/-0.08 [mean+/-SD] liter/min). In the normal subjects, CO measured by ACMm agreed with CO by ACMa (r=0.90, p < 0.0001, deltaCO=-0.09+/-0.42 liter/min), PD (r=0.87, p < 0.0001, deltaCO=0.12+/-0.49 liter/min) and 2D (r=0.84, p < 0.0001, deltaCO=-0.16+/-0.48 liter/min). In the patients, mitral regurgitant volume (MRV) by ACMm-ACMa agreed with PD-2D (r= 0.88, y=0.88x+6.6, p < 0.0001, deltaMRV=2.68+/-9.7 ml). CONCLUSIONS: We determined that ACM is a feasible new method for quantifying LV outflow and inflow volume to measure MRV and that ACM automatically performs calculations that are equivalent to more time-consuming Doppler and 2D measurements. Additionally, ACM should improve MR quantification in routine clinical practice.

Adult↗

PubMed1997

Comparison of mortality rates and progression of left ventricular dysfunction in patients with idiopathic dilated cardiomyopathy and dilated versus nondilated right ventricular cavities.

This study assesses the influence of right ventricular (RV) dilation on the progression of left ventricular (LV) dysfunction and survival in patients with idiopathic dilated cardiomyopathy (IDC). Using transthoracic echocardiography, we studied 100 patients with IDC aged 20 to 80 years (mean 55 +/- 14); 67% were men. In the apical 4-chamber view, diastolic LV and RV chamber area measurements classified patients into 2 groups: group RV enlargement+ (RV area/LV area > 0.5) included 54 patients; group RV enlargement- (no RV enlargement) had RV area/LV area < or = 0.5. Echocardiographic studies were repeated in all patients after a mean of 33 +/- 16 months. At the time of the initial study, the 2 groups did not differ in age, gender, incidence of atrial fibrillation and diabetes, left ventricular mass, and LV ejection fraction, but the RV enlargement+ group had more severe tricuspid regurgitation and less LV enlargement. After 47 +/- 22 months (range 12 to 96), patients in group RV enlargement+ had lower LV ejection fraction (29% vs 34%, p = 0.006) than patients with initial RV enlargement-. At clinical follow-up, mortality was higher (43%) in patients with initial RV enlargement+ than the RV enlargement- patients (15%), p = 0.002. For survivors, the mitral deceleration time averaged 157 +/- 36 ms; for nonsurvivors or patients who required transplant, the mitral deceleration time averaged 97 +/- 12 ms (p < 0.0001). With use of a multivariate Cox model adjusting for LV ejection fraction, LV size, and age, the relative risk ratio of mortality from initial RV enlargement+ was 4.4 (95% confidence limits 1.7 to 11.1) (p = 0.002). Thus, patients with significant RV dilation had nearly triple the mortality over 4 years and more rapidly deteriorating LV function than patients with less initial RV dilation. In IDC, RV enlargement is a strong marker for adverse prognosis that may represent a different morphologic subset.

Adult↗

PubMed1997

Automated cardiac output measurement by spatiotemporal integration of color Doppler data. In vitro and clinical validation.

BACKGROUND: A new Doppler echocardiographic technique has been developed for automated cardiac output measurement (ACOM) that assumes neither a flat flow profile nor collinearity with the scan line, but clinical validation of this method is lacking. METHODS AND RESULTS: In 165 subjects (50 intensive care patients, 10 dobutamine echocardiography patients, and 105 normal volunteers; age, 49.4 +/- 19.3 years; 92 men), ACOM was performed in the left ventricular outflow tract (LVOT), with the color baseline shifted to avoid aliasing. ACOM was also tested in a pulsatile in vitro model. Stroke volume was calculated by double integration of Doppler signals in space (across the LVOT) and in time (through the systolic period), assuming hemiaxial symmetry: integral of integral of pi r v(r,t) dr dt, where v(r,t) is the velocity at a distance r from the center of the LVOT at time t during systole. Stroke volume from ACOM was compared with thermodilution (TD), aortic valve pulsed-wave Doppler (PWAO), and left ventricular echocardiographic (two-dimensional [2D]) methods. There was good correlation between ACOM and PWAO (r = .93). TD (r = .86), and 2D (r = .74), with close agreement seen. ACOM had higher correlation and agreement with TD than did either PWAO (P < .02) or 2D (P < .01). ACOM was also able to track accurately the changes in cardiac output with dobutamine infusion in comparison with PWAO (r = .94). In vitro assessment demonstrated excellent correlation (r = .98, y = 1.0x + 1.94) with little impact of pulse repetition frequency or misalignment up to 30 degrees. Gain dependency was noted but could be optimized by visual inspection of the color image. CONCLUSIONS: Automatic integration of numerical data within color Doppler flow fields is a feasible new method for quantifying flow. It is simpler and faster, requires fewer assumptions, and uses only one apical view. ACOM is a promising new approach to echocardiographic quantification that deserves further study and refinement.

Adolescent↗

PubMed1997

Site of methacholine reactivity in the peripheral airways: analysis using lung explants.

We used a recently developed lung explant technique to investigate the partitioning of airway contractility in the bronchioles of normoresponsive and hyperresponsive rats. Specifically, we addressed the questions 1) whether airway response to methacholine varied with airway size and 2) whether airways from rats known to be innately hyperresponsive to methacholine (Fisher) would have responses different from normoresponsive rats (Sprague-Dawley). We found that, in both strains of rats, contraction to methacholine occurred primarily in the medium- and larger-sized bronchioles (airways of diameter > 0.32 mm) and that, at the higher methacholine concentrations, the Fisher rats had greater degrees of contraction than did the Sprague-Dawley rats. These results suggest that the increased airway responsiveness seen in Fisher rats is due to an intrinsic increase in responsiveness (increased contractility) of their airways, which may be related to amount of smooth muscle, rather than an increase in airway sensitivity to methacholine. They do not, however, completely rule out the possibility of in vivo species-dependent differences in airway-parenchymal interactions.

Airway Resistance↗

PubMed1997

Guinea pig pulmonary hypertension caused by cigarette smoke cannot be explained by capillary bed destruction.

Chronic exposure to cigarette smoke is known to produce pulmonary hypertension in humans and in animal models, but the etiology of this process is controversial. To evaluate whether alterations in the structure of the pulmonary capillary bed or the peribronchiolar arterioles could be correlated with the pulmonary arterial pressure (Ppa), we examined the pulmonary vasculature in guinea pigs that had developed pulmonary hypertension after being exposed to cigarette smoke for 6 mo. The smoke-exposed animals had a significant increased Ppa compared with the control (air-exposed) animals (14.4 +/- 2.4 vs. 9.9 +/- 0.9 cmH2O). In the smoke-exposed animals, there was an increased percentage of muscularized peribronchiolar arterioles (33.5 +/- 5.8% smoke exposed vs. 56.1 +/- 5.8% control), and the capillary diameter and density were significantly decreased in both the center and periphery of the lobule (center diameter 8.8 +/- 1.9, periphery diameter 10.0 +/- 2.0 microns, center density 79 +/- 5, and periphery density 84 +/- 4 in smoked exposed vs. center diameter 7.7 +/- 1.9, periphery diameter 8.6 +/- 2.0 microns, center density 73 +/- 6, and periphery density 77 +/- 6 in controls). Neither group showed any correlation between these values and the Ppa. We conclude that although chronic exposure to cigarette smoke produces alteration of the capillary bed and pulmonary arterioles secondary to emphysematous air-space enlargement, these structural findings cannot explain the increase in Ppa. It appears that pulmonary hypertension due to chronic cigarette smoke exposure is a result of a primary alteration of capillary or muscular arteriolar vascular structure but instead may be secondary to alterations of the dynamic properties of the vascular bed with subsequent increase in vascular resistance.

Animals↗

PubMed1997

A longitudinal analysis of pulmonary function in rats during a 12 month cigarette smoke exposure.

We wanted to examine the longitudinal effects of chronic cigarette smoke exposure, and to determine whether the chronic alterations in pulmonary function induced by long-term cigarette smoke exposure in an animal model could be predicted by initial or early alterations in function. A group of Sprague Dawley rats was exposed to the smoke of 7 cigarettes x day(-1) for 5 days x week(-1) during a total period of 12 months. Lung volume, flow-volume curves and pressure-volume curves were recorded at baseline, and after 2, 4, 8 and 12 months of smoke exposure. A control group of rats was subjected to the same regimen of testing, but was not exposed to smoke. Thirteen rats completed the study in the smoke-exposed group and seven rats in the control group. We found that chronic exposure to cigarette smoke produced early abnormalities in pulmonary function, with the forced expiratory volume in one second/forced vital capacity (FEV1/FVC) ratio showing an acceleration of ageing effect, particularly between 4 and 8 months of exposure. In this model, although the two groups had significantly different airflow after 12 months, the initial values in each group were remarkably similar, and we could not identify any pulmonary function test which had predictive value. We conclude that longitudinal studies of cigarette smoke exposure in this rat model allow better characterization of the nature and time course of the effects of smoking on the lung.

Animals↗