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Articles by J. Hung
Total Records ( 4 ) for J. Hung
  J Solis , D McCarty , R. A Levine , M. D Handschumacher , L Fernandez Friera , A Chen Tournoux , L Mont , B Vidal , J. P Singh , J Brugada , M. H Picard , M Sitges and J. Hung
 

Background— Cardiac resynchronization therapy (CRT) has been shown to reduce functional mitral regurgitation (MR). It has been proposed that the mechanism of MR reduction relates to geometric change or, alternatively, changes in left ventricular (LV) contractile function. Normal mitral valve (MV) function relies on a balance between tethering and closing forces on the MV leaflets. Functional MR results from a derangement of this force–balance relationship, and CRT may be an important modulator of MV function by its ability to enhance the force–balance relationship on the MV. We hypothesized that CRT improves the comprehensive force balance acting on the valve, including favorable changes in both geometry and LV contractile function.

Methods and Results— We examined the effect of CRT on 34 patients with functional MR before and after CRT (209±81 days). MR regurgitant volume, closing forces on MV (derived from Doppler transmitral pressure gradients), including dP/dt and a factor (closing pressure ratio) expressing how long the peak closing gradient is maintained over systole (closing pressure ratio=velocity time integral/MR peak velocityxmitral regurgitation time), and dyssynchrony by tissue Doppler were measured. End-diastolic volume, end-systolic volume, mitral valve annular area (MAA) and contraction (percent change in MAA from end-diastole to midsystole), leaflet closing area (leaflet area during valve closure), and tenting volume (volume under leaflets to annular plane) were measured by 3D echocardiography. After CRT, end-diastolic volume (253±111 versus 221±110 mL, P<0.001) and end-systolic volume (206±97 versus 167±91 mL, P<0.001) decreased and ejection fraction (19±6 versus 27±9%, P<0.001) increased. MR regurgitant volume decreased from 35±17 to 23±14 mL (P<0.001), MAA from 11.6±3.5 to 10.5±3.1 cm2 (P<0.001), leaflet closing area from 15.4±5 to 13.7±3.8 cm2 (P<0.001), and tenting volume from 5.7±2.6 to 4.6±2.2 mL (P<0.001). Peak velocity (and therefore transmitral closing pressure) was more sustained throughout systole, as reflected by the increase in the closing pressure ratio (0.77±0.1 versus 0.84±0.1 before CRT versus after CRT, P=0.01); dP/dt also improved after CRT. There was no change in dyssynchrony or MAA contraction.

Conclusions— Reduction in MR after CRT is associated with favorable changes in MV geometry and closing forces on the MV. It does so by favorably affecting the force balance acting on the MV in 2 ways: reducing tethering through reversal of LV remodeling and increasing the systolic duration of peak transmitral closing pressures.

  J Solis , R. A Levine , B Johnson , J. L Guerrero , M. D Handschumacher , S Sullivan , K Lam , J Berlin , G. J. C Braithwaite , O. K Muratoglu , G. J Vlahakes and J. Hung
  Background—

Ischemic mitral regurgitation (MR) results from displacement of the papillary muscles caused by ischemic ventricular distortion. Progressive left ventricular (LV) remodeling has challenged therapy. Our hypothesis is that repositioning of the papillary muscles can be achieved by injection of polyvinyl-alcohol (PVA) hydrogel polymer into the myocardium in chronic MR despite advanced LV remodeling.

Methods and Results—

Ten sheep underwent ligation of the circumflex branches to produce chronic ischemic MR over 8 weeks. PVA was injected into the myocardium underlying the infarcted papillary muscle. Two-dimensional and 3D echocardiograms and hemodynamic data were obtained before infarct (baseline), before PVA (chronic MR), and after PVA. PVA injection significantly decreased MR from moderate to severe to trace (MR vena contracta, 5.8±1.2 to1.8±1.3 mm; chronic MR to post-PVA stage; P=0.0003). This was associated with a decrease in infarcted papillary muscle–to–mitral annulus tethering distance (30.3±5.7 to 25.9±4.6 mm, P=0.02), tenting volume (1.8±0.7 to 1.4±0.5 mL, P=0.01), and leaflet closure area (8.8±1.3 cm2to 7.6±1.3 cm2, P=0.004) from chronic MR to post-PVA stages. PVA was not associated with significant decreases in LV ejection fraction (41±3% versus 40±3%, P=NS), end-systolic elastance, (82±36 ms to 72±26, P=NS), or LV stiffness coefficient (0.05±0.04 to 0.03±0.01).

Conclusions—

PVA hydrogel injections improve coaptation and reduce remodeling in chronic MR without impairing LV systolic and diastolic function. This new approach offers a potential alternative for relieving tethering and ischemic MR by correcting papillary muscle position.

  T. H. K Teng , J Finn , M Hobbs and J. Hung
 

Background— We examined trends in incidence of first-ever (index) hospitalization for heart failure (HF), hospitalization rates, and 30-day and 1-year all-cause mortality subsequent to index hospitalization for HF.

Methods and Results— The Western Australia Hospital Morbidity Database was used to identify a retrospective population-based cohort with an index hospitalization for HF in Western Australia between 1990 and 2005. Risk-adjusted temporal trends in mortality were examined with the use of multivariable logistic regression models. Baseline period for comparison was 1990–1993. The cohort (n=19 342; mean age, 74.2±13.2 years; 51.3% men) was followed until death or end of 2006. During the period of 1990–2005, age-standardized rates (per 100 000) of index hospitalization for HF as a principal diagnosis decreased from 191.0 to 103.2 in men, with an annual decrease of 3.5%, and from 130.5 to 75.1 in women, with an annual decrease of 3.1%. Risk-adjusted odds ratio of death at 30 days decreased to 0.73 (95% CI, 0.65 to 0.81) based on nonelective admissions. Risk-adjusted odds ratio of 1-year mortality also decreased during the study period in both genders and across all age groups. The total number of HF hospitalizations increased, with nonelective admissions increasing by 14.9% (P for trend, <0.0001) during this period. However, age-standardized rates of nonelective HF hospitalizations decreased during the same period.

Conclusions— During the 16-year period studied, the incidence of index hospitalization for HF in Western Australia decreased steadily in both genders. However, hospitalizations for HF as a measure of health service use increased, despite decreasing rates, partly because of an aging population and improved HF survival.

  J Beilby , M. L Divitini , M. W Knuiman , E Rossi and J. Hung
 

Background: Reduced renal function is an established risk factor for cardiovascular events. We compared 3 measures of renal function—serum cystatin C, serum creatinine, and calculated creatinine clearance—as predictors of subsequent cardiovascular events in a community-based population of elderly individuals.

Methods: Comprehensive cardiovascular risk factor data were available for 1410 surviving participants of previous Busselton health surveys who were ≥60 years old. Hazard ratios for risk of incident coronary heart disease and cardiovascular disease over 10 years of follow-up were derived for each baseline measure of renal function by use of Cox regression.

Results: All measures of renal function were significantly related to risks of morbidity and mortality from coronary heart disease and cardiovascular disease. There were 453 incident cardiovascular disease events; and the age- and sex-adjusted hazard ratios (95% CIs) were 1.34 (1.23–1.46), 1.32 (1.20–1.45), and 1.22 (1.06–1.41) per 1-SD deterioration in cystatin C, creatinine, and creatinine clearance, respectively. All 3 measures gave approximately the same age-adjusted relative risk estimates. After further adjustment for established cardiovascular risk factors, the relative risk estimates were all reduced but remained statistically significant (P < 0.05). Cystatin C was not a significant predictor for cardiovascular disease after adjustment for creatinine clearance.

Conclusions: In relation to predicting risk for coronary heart disease or cardiovascular disease over a 10-year follow-up in a community-based population of elderly subjects, there was no evidence that cystatin C was a better risk predictor than creatinine or creatinine clearance.

 
 
 
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