Myocardial deformation to determine transmurality of myocardial infarction.
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Biomedical subjects
Publications and source records attributed to John E Sanderson.
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This study was performed to determine whether the N-terminal pro-brain natriuretic peptide (NT-pro-BNP) is a useful biomarker in predicting cardiovascular congestion, mortality, and cardiovascular death and event in chronic peritoneal dialysis (PD) patients. A prospective cohort study was conducted in 230 chronic PD patients in a dialysis unit of a university teaching hospital. Serum NT-pro-BNP was measured at baseline together with echocardiography and dialysis indices. Each patient was followed for 3 yr from the day of enrollment or until death. Time to develop first episode of cardiovascular congestion and other cardiovascular event and time to mortality and cardiovascular death were studied in relation to NT-pro-BNP. NT-pro-BNP showed the strongest correlation with residual GFR, followed by left ventricular ejection fraction and left ventricular mass index. In the univariate Cox regression model, NT-pro-BNP was a significant predictor of cardiovascular congestion, mortality, and cardiovascular death and event. In the fully adjusted multivariable Cox regression analysis that included residual GFR, left ventricular ejection fraction, and left ventricular mass index, the hazard ratios for cardiovascular congestion, mortality, composite end point of mortality and cardiovascular congestion, and cardiovascular death and event for patients of the fourth quartile were 4.25 (95% confidence interval [CI] 1.56 to 11.62; P = 0.005), 4.97 (95% CI 1.35 to 18.28; P = 0.016), 5.03 (95% CI 2.07 to 12.26; P < 0.001), 7.50 (95% CI 1.36 to 41.39; P = 0.021), and 9.10 (95% CI 2.46 to 33.67; P = 0.001), respectively, compared with the first quartile. These data showed that NT-pro-BNP is an important risk predictor of cardiovascular congestion, mortality, and adverse cardiovascular outcomes in chronic PD patients and adds important prognostic information beyond that contributed by left ventricular hypertrophy, systolic dysfunction, and other conventional risk factors.
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AIMS: The purpose of this study was to assess the feasibility of measuring left atrial dysfunction with tissue Doppler imaging derived strain rate and to explore its role in predicting the maintenance of sinus rhythm after cardioversion for atrial fibrillation. METHODS AND RESULTS: Strain rate (SR) and tissue Doppler imaging (TDI) were performed with offline analysis of the basal left atrial wall (LA). SR detected a systolic (Ssr) and early diastolic (Esr) deformation induced by ventricular motion. LA dimensions and volume were measured. Left atrial appendage emptying (LAA_EV) and filling (LAA_FV) velocities were also obtained by transesophageal echocardiography. 27 healthy age-matched controls and 42 patients with AF before cardioversion were studied. Patients were grouped into (1): those who remained in sinus rhythm (group S, n=12) and (2) those who either failed cardioversion or reverted to AF within 4 weeks (group F, n=30). LA dimensions were significantly larger and atrial Esr was significantly lower in group F than group S (all p<0.01). LAA_EV and LAA_FV were not different between groups S and F. Multivariate regression analysis showed that a lower Esr and larger transverse LA diameter (LADtr) were independent predictors of failure of cardioversion (HR, 95% CI: 0.36, 0.14-0.88 and 2.85, 1.33-6.10, respectively). Esr combined with LADtr improved the sensitivity and specificity for predicting successful cardioversion. CONCLUSIONS: SR can be measured in the basal LA wall in atrial fibrillation and the magnitude of the early diastolic SR could predict the success of cardioversion and the likelihood of maintenance of sinus rhythm.
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BACKGROUND: It has become apparent recently that cardiac myocytes can divide after myocardial infarction, a circumstance that challenges the orthodox view that myocytes may be terminally differentiated. Replacement of the necrosed heart tissue by newly regenerated functional myocardium is a therapeutic ideal, but attempts to reconstitute functional myocardia and coronary vessels have been less successful. METHODS: We isolated a fraction containing 5 compounds from the Chinese herb Geum japonicum, which stimulates the processes of angiogenesis and cardiomyogenesis. We investigated these dual properties in both ex vivo and in vivo systems. RESULTS: We observed that this bioactive fraction displayed favorable dual actions on early angiogenesis and cardiomyogenesis in acute myocardial infarction in an animal model. Our results demonstrated that application of this bioactive fraction showed pronounced effects on limiting infarct size by 35%-45%, stimulating early development of new blood vessels in 24 h, and regenerating myocardium, replacing approximately 49% of the total infarction volume after 2 weeks. Echocardiographic studies demonstrated marked improvement of left ventricular function within 2 days after infarction, and the improvement was sustained for >1 month. CONCLUSIONS: The properties of this bioactive fraction appear to be entirely novel and represent a new approach for the treatment of ischemic heart disease.
Muscle repair following severe injury is slow and incomplete due to the limited regenerative capacity of muscles comprising the function. In this study, one pure compound structurally corresponding to triterpenoid, which can directly induce the activation, proliferation and maturation of quiescent satellite cells into myocytes in vitro, was isolated from Geum japonicum. The potential effect of this compound on myogenesis was further tested in repair of severe muscle injury. It was found that this compound could significantly stimulate the regenerative potential of the damaged muscle resulting in regeneration of myotubes and myotube bundles time-dependently replacing the damaged muscle tissues. This compound-mediated active regeneration of new myofibers repairing damaged muscles was probably due to its direct action on activation and proliferation of quiescent myogenic precursor cells and enhancement of their maturation into regenerating myotubes, as was demonstrated in our primary myogenic precursor cells culture experiments. The up-regulated expression of endogenous phospho-Akt1 in compound-treated myogenic precursor cells may also contribute to the process of myofiber regeneration and muscle repair probably via promoting myogenic cell survival capacity.
BACKGROUND: The prevalence of hepatotoxicity after longterm oral amiodarone therapy in Chinese patients with or without elevated liver enzymes at baseline is unknown. HYPOTHESIS: Amiodarone may still be safely prescribed for Chinese patients who have baseline liver dysfunction. METHODS: This is a retrospective cross-sectional study. Significant liver dysfunction (SLD) was defined as alanine aminotransferase (ALT) > 2 times upper limit of normal range. RESULTS: Baseline liver function was checked in 628 of the 720 Chinese patients identified. The mean duration of amiodarone use was 615.9 +/- 703.1 days. Ninety patients (14.3%) had elevated baseline ALT. The prevalence of SLD was 3.7% (confidence interval [CI] 2.1-5.3%) and 4.4% (CI 0.2-8.6%) in patients with normal (n = 538) and elevated (n = 90) baseline ALT, respectively (p = 0.765). Therapy was continued in 42 patients with elevated baseline ALT until final follow-up. Eight of these (19.0%) had elevated ALT upon final follow-up, but the derangement was mild (mean ALT 134.8 +/- 145.9 IU/l, median 76 IU/l). During follow up, 24 patients developed SLD and half of these subsequently withdrew from therapy. The ALT levels at final follow-up had improved over time in both groups, but the mean difference was not significant (255.1 +/- 706.4 vs. 131.0 +/- 207.5 IU/l, p = 0.312). CONCLUSION: The prevalence of SLD in Chinese patients taking oral amiodarone with or without elevated baseline ALT was similar (4.4 vs. 3.7%). It seems that amiodarone may be safely prescribed in patients with elevated baseline ALT.
BACKGROUND: Atrial function is an integral part of cardiac function which is often neglected. The presence of coronary artery disease (CAD) may impair atrial function. This study investigated if atrial mechanical dysfunction was present in patients with CAD by tissue Doppler echocardiography (TDI). METHODS: Echocardiography with TDI was performed in 118 patients with CAD, and compared with 100 normal controls with comparable age and heart rate. Regional atrial function was assessed at the left (LA) and right (RA) atrial free wall and inter-atrial septum (IAS). The peak regional atrial contraction velocity of (V(A)) and the timing of mechanical events were compared. RESULTS: The V(A) in the LA (5.0+/-2.6 Vs 7.7+/-2.6 cm/s), IAS (4.8+/-1.7 Vs 5.7+/-1.5 cm/s) and RA (6.8+/-3.1 Vs 9.2+/-2.9 cm/s) were significantly decreased in patients with CAD when compared with controls (all p<0.001). Patients with impaired systolic function (ejection fraction 50% (both p<0.001); and were lower in those with restrictive filling pattern (RFP) than non-RFP of diastolic dysfunction (both p<0.05). The V(A) in all the subgroups was lower than controls. In contrast, transmitral atrial velocity was unable to reveal any abnormality except in the subgroup with a RFP. The LA dimension, area and volume were increased in the disease groups, but were largely unchanged in the RA despite abnormal V(A). The physiological inter-atrial delay for the onset and peak atrial contraction between the RA and LA were unaffected by CAD. CONCLUSIONS: The atrial contractile function in both atria was impaired in the presence of CAD, especially in the LA. This was detected even in patients with preserved systolic function or mild diastolic dysfunction such as non-RFP. Direct assessment of atrial velocity by TDI may better reflect atrial mechanical function than transmitral atrial velocity.
OBJECTIVES: The aim of this study was to determine if strain rate imaging (SRI) correlates with the transmural extent of myocardial infarction (MI) measured by contrast-enhanced magnetic resonance imaging (Ce-MRI). BACKGROUND: Identification of the transmural extent of myocardial necrosis and degree of non-viability after acute MI is clinically important. METHODS: Tissue Doppler echocardiography with SRI and Ce-MRI were performed in 47 consecutive patients with a first acute MI between days 2 and 6 and compared to 60 age-matched healthy volunteers. Peak myocardial velocities and peak myocardial deformation strain rates were measured. Location and size of the infarct zone was confirmed by Ce-MRI using the delayed enhancement technique with a 16-segment model. RESULTS: Contrast-enhanced MRI identified transmural infarction in 21 patients, non-transmural infarction in 15 (mean transmurality of infarct 72.3 +/- 10.6%), and another 11 patients with subendocardial infarction (<50% transmural extent of the left ventricular wall). Peak systolic strain rate (SRs) of the transmural infarction segments was significantly lower compared to normal myocardium or with non-transmural infarction segments (both p < 0.0005). A cutoff value of SRs >-0.59 s(-1) detected a transmural infarction with high sensitivity (90.9%) and high specificity (96.4%), and -0.98 s(-1) >SRs >-1.26 s(-1) distinguished subendocardial infarction from normal myocardium with a sensitivity of 81.3% and a specificity of 83.3%. CONCLUSIONS: Peak myocardial deformation by SRI can differentiate transmural from non-transmural MI, and it allows noninvasive determination of transmurality of the scar after MI and thereby the extent of non-viable myocardium.
Although the beneficial role of cardiac resynchronization therapy (CRT) in selected patients with heart failure is well proven, its effect on the incidence of atrial fibrillation (AF) is unclear. The present study compared the incidence of AF in 36 consecutive patients with chronic heart failure receiving CRT with its incidence in controls matched for age, gender, and left ventricular ejection fraction but not receiving CRT. The findings suggest that patients with CRT had a significantly lower incidence of AF than controls. Further studies to establish the role of CRT in preventing AF and its mechanisms are warranted.
BACKGROUND: Stents are now widely used in Hong Kong and China and there is a clinical impression that restenosis is less common because of the lower prevalence of coronary artery disease and associated risk factors in the Chinese. However, there are no published data on angiographic stent restenosis rates in Chinese patients. METHOD: In a prospective study of 114 consecutive Chinese patients who underwent coronary stenting, quantitative coronary analyses were made at the time of stent implantation and subsequently at 6 months post-stenting (n = 97). RESULTS: At 6 months, restenosis (> or = 50% diameter stenosis in the dilated segment) was present in 42 (43.3%) of the 97 patients and 54 (33.5%) of the total 161 lesions stented. Vessel reference diameter (VRD) of < 3 mm and stented length of > or = 18 mm were associated with higher restenosis rates (36% and 38%). Compared to those without, those with restenosis had a greater residual stenosis of 16.53+/-11.54% and smaller final minimal luminal diameter (MLD) of 2.41+/-0.49 mm, (p < 0.01 and p < 0.008 respectively). Standard coronary risk factors were not associated with a higher rate of restenosis. Lesion morphology was significantly associated with restenosis. CONCLUSION: Coronary stenting in Hong Kong Chinese patients is associated with a restenosis rate comparable to that demonstrated in previously published trials from populations in the West.
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BACKGROUND: Fetuin-A (alpha2-Heremans Schmid glycoprotein) has recently been identified as a circulating inhibitor of calcification and is regulated as a negative acute phase protein. However, its relationships with cardiac valvular calcification and atherosclerosis and outcome have not been evaluated in peritoneal dialysis (PD) patients. METHOD: We performed a prospective follow-up study in 238 PD patients with echocardiography done at baseline to detect cardiac valvular calcification and biochemical analysis performed for serum fetuin-A, albumin and C-reactive protein (CRP). RESULTS: Baseline serum fetuin-A concentration was (mean+/-SD) 0.309+/-0.068 g/l (normal range 0.4-0.95). Across the three tertiles of increasing serum fetuin-A, a significant trend effect was observed for age (P = 0.023), diabetes (P = 0.008), background atherosclerotic vascular disease (P = 0.010), cardiac valvular calcification (P = 0.002), serum albumin (P<0.001), subjective global assessment (P = 0.005) and CRP (P<0.001). Adjusting for CRP and calcium x phosphorus product, every 0.01 g/l increase in serum fetuin-A remained independently associated with a 6% decrease in the risk of valvular calcification (95% confidence intervals, 0.90-0.99; P = 0.028). Furthermore, serum fetuin-A showed a significant decrease across the four groups of patients with increasing components of the malnutrition, inflammation, atherosclerosis/calcification (MIAC) syndrome (P<0.001) and was the lowest among patients with all components of the MIAC syndrome (0.263+/-0.055 g/l) and highest among those who do not have the MIAC syndrome at all (0.338+/-0.063 g/l). Lower serum fetuin-A was associated with greater all-cause mortality (P = 0.0011) and fatal and non-fatal cardiovascular events (P = 0.0017), but its significance was lost when atherosclerotic vascular disease, valvular calcification, inflammation and malnutrition were included in the model. CONCLUSIONS: Serum fetuin-A showed important associations with valvular calcification, atherosclerosis, malnutrition and inflammation, and was linked to mortality and cardiovascular events in PD patients via its close relationships with the MIAC syndrome.
OBJECTIVES: This study was designed to investigate if tissue synchronization imaging (TSI) is useful to identify regional wall delay and predict left ventricular (LV) reverse remodeling after cardiac resynchronization therapy (CRT). BACKGROUND: Echocardiographic assessment of systolic asynchrony is helpful to predict a positive response to CRT. Tissue synchronization imaging is a new imaging technique that allows quick evaluation of regional systolic delay. METHODS: Tissue synchronization imaging was performed in 56 heart failure patients at baseline and three months after CRT. Regional wall delay was identified on TSI images and the time to regional peak systolic velocity (Ts) in LV was measured by the six-basal-six-mid-segmental model. Eight TSI parameters of systolic asynchrony were computed when Ts was measured in ejection phase or also included postsystolic shortening. RESULTS: Severe lateral wall delay occurred in 17 patients, which predicted LV reverse remodeling (chi-square = 8.13, p = 0.004). Among the eight quantitative parameters of asynchrony, the predictive values were higher for parameters that measured Ts in ejection phase than in postsystolic shortening. The standard deviation of Ts of 12 LV segments in ejection phase (Ts-SD-12-ejection) was most powerful to predict reverse remodeling (r = -0.61, p < 0.001) and gain in ejection fraction (r = 0.53, p < 0.001). The area of the receiver-operating characteristic (ROC) curve was the largest for Ts-SD-12-ejection (0.90, p < 0.001), with a sensitivity of 87% and specificity of 81% at a cutoff of 34.4 ms. The combination of lateral wall delay with Ts-SD-12-ejection gave a sensitivity and specificity of 82% and 87%. CONCLUSIONS: Tissue synchronization imaging allows quick evaluation of regional wall delay, and combined with Ts-SD-12-ejection provides a reliable way of predicting reverse remodeling after CRT.
BACKGROUND: Patients with end-stage renal disease (ESRD) are at increased risk for tissue calcifications as a result of deranged mineral metabolism. We tested the hypothesis that valvular calcification is a marker of atherosclerosis in patients with ESRD. METHODS: Echocardiography was performed in 92 patients undergoing peritoneal dialysis with no background atherosclerotic vascular complications to detect valvular calcification. We used B-mode ultrasonography to determine carotid artery intima-media thickness and the presence of plaque and calcification. RESULTS: Compared with patients without valvular calcification (n=66), those with valvular calcification (n=26) had higher C-reactive protein levels (P=.01) and greater mean +/- SE carotid intima-media thickness (1.12 +/- 0.06 vs 0.88 +/- 0.04 mm; P=.003). Carotid artery calcification was present unilaterally and bilaterally in 4 patients (15%) and 17 patients (65%) with valvular calcification vs 11 (17%) and 14 (21%) without, respectively (P<.001). Carotid artery plaque was present unilaterally and bilaterally in 11 patients (12%) and 16 patients (65%) with valvular calcification vs 3 (17%) and 17 (24%) without, respectively (P=.001). Using multiple logistic regression analysis, every 1-mm increase in carotid intima-media thickness was independently associated with a 6.51-fold (95% confidence interval, 1.58-26.73; P=.009) increased risk of valvular calcification, and calcification and plaque in the carotid arteries were associated with a 7.18-fold (95% confidence interval, 2.39-21.51; P<.001) and a 5.00-fold (95% confidence interval, 1.77-14.13; P=.002) increased risk of valvular calcification, respectively. CONCLUSION: The associations among valvular calcification, inflammation, carotid atherosclerosis, and arterial calcification suggest that valvular calcification is a marker of atherosclerosis and arterial calcification in patients with ESRD.
OBJECTIVES: This study sought to investigate the incremental prognostic value of non-invasive measures of early myocardial relaxation and left ventricular diastolic pressure (LVDP) in patients with impaired left ventricular (LV) systolic function. BACKGROUND: The early diastolic mitral annulus velocity (Em) reflects myocardial relaxation, and the combined ratio of the early transmitral flow velocity (E) to Em (E/Em) >15 correlates well with elevated mean LVDP. It is unknown if these new indexes will predict poorer survival in patients with LV systolic dysfunction. METHODS: Echocardiograms were prospectively obtained in 182 patients with impaired LV systolic function, defined as an LV ejection fraction <0.50. The end point was cardiac mortality. The majority of this patient sample (80%) has been reported on in a previous publication. RESULTS: After a median 48 months' follow-up, Em emerged as an independent predictor of survival (hazard ratio 0.61, 95% confidence interval 0.45 to 0.82). An Em <3 cm/s was associated with a significantly excess mortality (log-rank statistic 9.36, p = 0.002), and this measurement added incremental prognostic value to standard indexes of systolic or diastolic function, including a deceleration time <140 ms and an E/Em >15 (p = 0.038). CONCLUSIONS: Early diastolic mitral annulus velocity is a powerful predictor of cardiac mortality in patients with LV systolic impairment; Em <3 cm/s emerged as the best prognosticator in long-term follow-up, incremental to other clinical or echocardiographic variables, including the ratio E/Em.