Early pacing-induced systolic dyssynchrony is a strong predictor of left ventricular adverse remodeling: Analysis from the Pacing to Avoid Cardiac Enlargement (PACE) trial

Background

Right ventricular apical (RVA) pacing is associated with adverse left ventricular (LV) remodeling and biventricular (BiV) pacing may prevent it although the mechanisms remain unclear. The current study aimed to assess the role of early pacing-induced systolic dyssynchrony (DYS) to predict adverse LV remodeling.

Methods

Patients with standard pacing indications and normal LV ejection fraction were randomized either to BiV (n = 89) or RVA pacing (n = 88). Pacing-induced DYS, defined as the standard deviation of the time to peak systolic velocity (Dyssynchrony Index) > 33 ms in a 12-segmental model of LV, was measured by tissue Doppler echocardiography at 1 month.

Results

At 1 month, 59 patients (33%) had DYS which was more prevalent in RVA than BiV pacing group (52% vs. 15%, χ² = 28.3, p < 0.001), though Dyssynchrony Index was similar at baseline (30 ± 14 vs. 26 ± 11 ms, p = 0.06). At 12 months, those developing DYS had significantly lower LV ejection fraction (55.1 ± 9.7 vs. 62.2 ± 7.9%, p < 0.001) and larger LV end-systolic volume (35.3 ± 14.3 vs. 27.0 ± 10.4 ml, p < 0.001) when compared to those without DYS. Reduction of ejection fraction ≥ 5% occurred in 67% (39 out of 58) of patients with DYS, but only in 18% (21 out of 115) in those without DYS (χ² = 40.8, p < 0.001). Both DYS at 1 month (odds ratio [OR]: 4.725, p = 0.001) and RVA pacing (OR: 3.427, p = 0.009) were independent predictors for reduction of ejection fraction at 12 months.

Conclusion

Early pacing-induced DYS is a significant predictor of LV adverse remodeling and the observed benefit of BiV pacing may be related to the prevention of DYS.

Clinical trial registration

Centre for Clinical Trials number, CUHK_CCT00037 (URL: http://www.cct.cuhk.edu.hk/Registry/publictrialrecord.aspx?trialid=CUHK_CCT00037).     

Plasma osteopontin reveals left ventricular reverse remodelling following cardiac resynchronization therapy in heart failure

Background

Cardiac resynchronization therapy (CRT) promotes left ventricular (LV) reverse remodelling and affects myocardial collagen turnover in heart failure (HF) patients. Osteopontin (OPN) is a matrix glycoprotein required for the activation of fibroblasts upon TGF-β1 stimulation. In humans, plasma OPN and OPN-expressing lymphocytes correlate with the severity of HF. We sought to evaluate whether plasma OPN and TGF-β1 reflect LV reverse remodelling following CRT.

Methods

Eighteen patients (12 men, mean age 65 ± 11 years) undergoing CRT were studied. Patients underwent baseline clinical and echocardiographic evaluation, and assessment of plasma OPN and TGF-β1. The evaluation was repeated 8.5 ± 4 months after device implantation. Eight healthy age- and sex-matched subjects served as controls.

Results

In HF patients, baseline plasma OPN and TGF-β1 were higher as compared to control subjects (OPN: 99 ± 48 vs 59 ± 22 ng/ml; p < 0.05; TGF-β1: 15.9 ± 8.0 vs 9.3 ± 5.6 ng/ml; p < 0.05). At follow-up, 12 patients responded to CRT and showed LV reverse remodelling, whereas 6 did not. Plasma OPN decreased in CRT responders (108 ± 47 vs 84 ± 37 ng/ml; p = 0.03) and increased in non-responders (79 ± 58 vs 115 ± 63 ng/ml; p < 0.01). TGF-β1 showed a trend towards reduction in responders (17.5 ± 8.7 vs 10.2 ± 8.9 ng/ml; p = 0.08) and was unchanged in non-responders. A significant correlation (r = − 0.56; p = 0.01) was found between relative changes of LVESV and plasma OPN.

Conclusions

CRT-induced LV reverse remodelling is reflected by changes in plasma OPN. Circulating OPN may represent a marker of LV dilation/impairment and an indicator of the response to HF therapies promoting LV reverse remodelling.     

Quantification of left ventricular performance in different heart failure phenotypes by comprehensive ergometry stress echocardiography

Background

We evaluated the left ventricular (LV) performance in patients with heart failure and preserved ejection fraction (HFPEF) during exercise as compared to those with heart failure and reduced ejection fraction (HFREF) and healthy subjects.

Methods

All subjects received echocardiographic (Vivid7, GE Healthcare) examination with symptom-limited exercise testing on a semi-recumbent and tilting bicycle ergometer (Lode BV, Netherlands). The exercise images for 2-dimensional (2D) speckle tracking were acquired with heart rate of 90–100 bpm, while exercise images for tissue Doppler imaging (TDI) and M-mode echocardiography were stored with attainment of > 85% of maximal age-predicted heart rate.

Results

Stress echocardiographic examinations were performed in 40 HFPEF (aged 65 ± 9 years; 53% male), 40 HFREF (aged 62 ± 9 years; 90% male) and 30 normal controls (aged 56 ± 5 years; 33% male). Trends of progressive decline in 2D global longitudinal, circumferential and radial strains (GLS, GCS and GRS); TDI septal s′ and Sm; and M-mode mitral annular plane systolic excursion (MAPSE) were observed from control, HFPEF to HFREF groups (p < 0.05 for all). LV twist was preserved in HFPEF but reduced in HFREF patients as compared to normal controls (p < 0.05). Diastolic function measured by TDI septal e′, Em and septal E/e′ progressively decreased from controls, HFPEF to HFREF patients (all p < 0.05). Stroke volumes and cardiac indices (LVSI & LVCI) were preserved in HFPEF but deteriorated in HFREF than controls.

Conclusions

This study provides the reference values of LV performance during exercise in HFPEF and knowledge about these changes provide important insights for future clinical studies.     

Underestimation of duration of ventricular activation by 12-lead ECG compared with direct measurement of activation duration derived from implanted pacemaker leads

Aim

To determine extent to which 12-lead ECG QRS duration (QRSd) reflects ventricular activation duration compared with time relations from unpaced ventricular myograms in cardiac resynchronisation therapy (CRT) patients.

Methods

Left (LV) and right ventricular (RV) myograms were recorded during spontaneous rhythm from in-situ pacemaker leads in 77 patients receiving CRT; 14 ‘normal activation’ (unpaced QRSd < 120 ms), 10 ‘simple left bundle branch block’ (LBBB, QRSd 120-149 ms), 40 ‘advanced LBBB’ (QRS ≥ 150 ms) and 13 right bundle branch block. Delay in onset (Q-LV, Q-RV) and duration (dur-LV, dur-RV) of activation were measured. Interventricular delay (ΔT: Q-LV minus Q-RV) and ‘LV-overrun’ (time between end 12-lead QRS and Q-end LV myogram) were calculated.

Results

‘Normal activation’: Neither Q-LV, Q-RV (38 ± 6 ms, 39 ± 11 ms), nor dur-LV, dur-RV (66 ± 9 ms, 81 ± 25 ms) differed. ΔT (− 1 ± 11 ms) was not different from zero, nor was Q-end LV (104 ± 10 ms) different from QRSd (p = 0.09).‘Simple LBBB’: Q-LV (102 ± 28 ms) was longer than ‘normal activation’ (p < 0.001), but Q-RV, dur-LV, and dur-RV were no different. ΔT (54 ± 23 ms) was increased (p < 0.001) and Q-end LV (187 ± 48 ms) was longer than QRSd (p = 0.005).‘Advanced LBBB’: Q-LV (115 ± 52 ms) was longer than ‘normal activation’ (p < 0.001) but Q-RV was no different, so ΔT (72 ± 47 ms) was increased (p < 0.001 compared to normal, p = 0.04 compared to simple LBBB). Dur-LV (102 ± 27 ms) was also prolonged, so Q-end LV (218 ± 48 ms) was longer than QRSd (p < 0.001). Longer LV-overrun was associated with longer ΔT (p < 0.001).

Conclusions

Prolonged LV myopotential duration, associated with interventricular delay, is electrically silent on 12-lead QRSd. Unpaced surface QRSd underestimates true duration of native LV activation in CRT patients.     

Relation of flow-mediated dilation to global arterial load: Impact of hypertension and additional cardiovascular risk factors

Background

Endothelial dysfunction may be related to increased left ventricular (LV) mass due to an association between endothelial dysfunction with increased arterial load. Therefore, we evaluated whether brachial artery flow-mediated dilation (FMD) is related to global arterial load.

Methods

Pulse pressure/stroke index (PP/SVi, global arterial stiffness, prognostically validated), stroke volume/PP (SV/PP, global arterial compliance), and % of the predicted SV/PP by heart rate, age and body weight (confounder-adjusted global compliance, prognostically validated) were used as LV geometry-related indices of global arterial load.

Results

Compared to normotensive participants (NT, n = 50), those with hypertension (HTN, n = 51) had lower FMD (8.3% ± 5.4 vs. 12.8% ± 6.5), higher PP/SVi (1.24 ± 0.34 vs. 1.04 ± 0.28 mm Hg m²/ml), higher LV mass and higher relative wall thickness (all p < 0.01); in contrast, SV/PP and % of predicted SV/PP did not differ between NT and HTN (all p > 0.1). Impaired FMD was 3-4-fold more prevalent than LV hypertrophy or increased arterial load both in NT and in HTN. Within NT and HTN separately, PP/SVi, SV/PP and % of predicted SV/PP were comparable among tertiles of FMD. Only in NT, lower FMD was associated with higher peak exercise systolic BP (p < 0.05). In multivariable regression models, FMD was not associated with indices of arterial load independently (all p > 0.1).

Conclusions

In young-to-middle-age subjects with cardiovascular risk factors, impaired FMD is more prevalent than traditional preclinical manifestation of cardiovascular disease, and may exist independent to increased arterial load. Thus, endothelial dysfunction assessment may refine cardiovascular risk profile and risk-reduction strategies based on detection of traditional target organ damage.     

Histological regression of liver fibrosis with immunosuppressive therapy in autoimmune hepatitis

Reversibility of liver fibrosis with immunosuppressive therapy (IT) has been described in autoimmune hepatitis (AIH)

Objective

To compare initial fibrosis and fibrosis after IT in patients with AIH.

Methods

A total of 54 patients were admitted with positive ANA or AML antibodies, or both, elevated IgG immunoglobulins and who met international criteria for a diagnosis of AIH. The mean age was 39 years (range 13-65) and there were 47 women (87%). Two liver biopsies were taken: one at diagnosis and another at a mean of 28 ± 8 months after initiation of IT with prednisone and azathioprine. The degree of inflammation (0-18) and fibrosis (0-6) according to Ishak score was compared between the initial and the follow-up biopsy.

Results

Fibrosis decreased from 2.9 ± 0.3 to 2.2 ± 0.3 (p = 0.005) and histological activity index from 6.8 ± 0.45 to 2.6 ± 0.2 (P < .001). In subgroups, fibrosis decreased from 3.6 ± 0.4 to 1.4 ± 0.3 (P < .001) in 22 patients (41%), was unchanged in 27 (50%) and increased in five (9%). There were seven patients with histological cirrhosis at IT initiation. After IT, four showed a reduction in Ishak score (achieving scores of 0-3). Transaminase values were not associated with histological improvement.

Conclusion

Fibrosis in patients with AIH significantly improved with IT, emphasizing the importance of studying the prognostic factors associated with this favorable response.     

Distal protection device aggravated microvascular obstruction evaluated by cardiac MR after primary percutaneous intervention for ST-elevation myocardial infarction

Background

Protection of distal embolization by balloon occlusion and thrombus aspiration has not improved microvascular circulation nor decreased myocardial injury during primary percutaneous intervention (PCI) for ST-elevation myocardial infarction (STEMI) in randomized trials. In a prospective randomized trial, we investigated the mechanism of the poor effect of distal protection and thrombus aspiration (DP–TA) in 126 patients with STEMI.

Methods

Patients with first-diagnosed STEMI were randomly assigned to DP–TA pretreatment or conventional PCI (c-PCI). Primary endpoint was reduced left ventricular end-diastolic volume (LVEDV) measured by MRI at post-PCI and 6 months after PCI. Secondary end points were infarct ratio (infarct size to entire LV size) by delayed enhancement (DE), area at risk (AAR) ratio (AAR to entire LV size) by T2 high signal, microvascular occlusion index (MVO) ratio (MVO to entire LV size) by DE, and myocardial salvage index (MSI: (AAR − infarct size) ∗ 100 / AAR) using cardiac magnetic resonance imaging (MRI) within 3 days after PCI.

Results

Baseline characteristics of the patients including cardiovascular risk factors and lesion characteristics were similar between the two groups. DT–PA failed to improve LV remodeling at 6 months (LVEDV 140 ± 39 vs 133 ± 37 in c-PCI group, p = 0.418). Infarct ratio, AAR ratio and MSI were not statistically different between DP–TA group and c-PCI group. However, MVO ratio was significantly larger in DP–TA group than in c-PCI group (2.4 ± 2.7 vs 1.1 ± 1.9, p = 0.045).

Conclusion

DP–TA was potentially hazardous in primary PCI for STEMI by increasing MVO. DP–TA should not be used in STEMI.     

Intravenous immunoglobulin does not reduce left ventricular remodeling in patients with myocardial dysfunction during hospitalization after acute myocardial infarction

Background

Left ventricular (LV) remodeling takes place after acute myocardial infarction (MI), potentially leading to overt heart failure (HF). Enhanced inflammation may contribute to LV remodeling. Our hypothesis was that the immunomodulating effects of intravenous immunoglobulin (IVIg) would be beneficial in patients with impaired myocardial function after MI by reducing myocardial remodeling and improving myocardial function.

Methods

Sixty-two patients with acute MI treated by percutaneous coronary intervention, with depressed LV ejection fraction (LVEF) were randomized in a double-blinded fashion to IVIg as induction therapy and thereafter as monthly infusions or placebo for 26 weeks. The primary end point was changes in LVEF from baseline to 6 months as assessed by MRI.

Results

Our main findings were: (i) LVEF increased significantly from 38 ± 10 (mean ± SD) to 45 ± 13% after IVIg and from 42 ± 9 to 49 ± 12% after placebo with no difference between the groups. (ii) The scar area decreased significantly by 3% and 5% in the IVIg and placebo group, respectively, with no difference between the groups. (iii) During the induction therapy (baseline to day 5), IVIg induced both inflammatory (e.g., increase in tumor necrosis factor α and monocyte chemoattractant protein-1) and anti-inflammatory (e.g., increase in interleukin-10 and decrease in leukocyte counts) variables, but during maintenance therapy there were no differences in changes of inflammatory mediators between IVIg and placebo.

Conclusions

IVIg therapy after ST elevation MI managed by primary PCI does not affect LV remodeling or function. This illustrates the challenges of therapeutic intervention directed against the cytokine network, to prevent post-MI remodeling.     

Increased temporal dispersion of myocardial repolarization in myotonic dystrophy type 1: beyond the cardiac conduction system

Objectives

To assess ventricular dysfunction and ventricular interaction after repair of Tetralogy of Fallot (ToF) employing echocardiography speckle-tracking and cardiac magnetic resonance imaging (CMR).

Background

Severe pulmonary regurgitation and right ventricular (RV) dysfunction are common after repair of ToF and may also affect the shape and function of the left ventricle (LV). Recent studies suggest that LV dysfunction may be of particular prognostic value.

Methods and results

Twenty-one consecutive adults with repaired ToF (15 male, mean age 38 ± 11 years, 7 with severe PR) underwent a comprehensive echocardiographic exam including speckle-tracking analysis, CMR and cardiopulmonary exercise testing. Twenty-one subjects without relevant heart disease served as controls. Echocardiographically measured RV diameters correlated with RV volumes obtained from CMR (r = 0.63; p = 0.006). In addition, a close correlation was found between RV and LV function on CMR (r = 0.74, p = 0.002), speckle-tracking LV and RV peak longitudinal 2D strain (r = 0.66, p = 0.003) and mitral and tricuspid annular plain systolic excursion (r = 0.71, p = 0.0003). While LV ejection fraction was normal in the majority of patients and not different from controls, LV longitudinal strain was significantly reduced in ToF patients (− 16.5 ± 3.3 vs. -20.5 ± 2.7%, p = 0.0001).

Conclusion

Left and right ventricular function both by CMR and speckle-tracking is interrelated in adults with repaired ToF. Despite normal LV ejection fraction, 2D longitudinal strain is significantly reduced in ToF patients, suggesting subclinical LV myocardial damage. Considering the potential prognostic value of LV dysfunction in ToF, this measurement may gain importance and should be included in future outcome studies.     

Vascular function is impaired early after the initiation of chronic cigarette smoking

Background

The aim of this study was to assess resistance artery function in short-term chronic cigarette smokers and non-smoking control subjects.

Methods

Reactive hyperemia was assessed in 19 cigarette smokers (age 23 ± 1 years) and 19 non-smokers (age 23 ± 1 years).

Results

Cigarette smokers demonstrated a 23% lower peak forearm blood flow response compared with non-smokers (15.81 ± 0.66 vs. 20.58 ± 1.26 mL/min/100 mL, p < 0.05) and a 22% lower area under the curve of the reactive hyperemia response (607 ± 51.57 vs. 775 ± 53.51 mL/min/100 mL × 3 min, p < 0.05).

Conclusions

These results indicate that smoking-induced impairments of vascular function occur early after the initiation of chronic cigarette smoking.     

Mortality rates and modes of death in heart failure patients with reduced versus preserved systolic function

Background

There are conflicting reports regarding the characteristics and mortality rates of heart failure patients with preserved (HFPSF) vs. reduced systolic left ventricular function (SHF).

Methods

We evaluated the clinical profiles, mortality rates and modes of death in 481 consecutive symptomatic heart failure patients. In 317(66%) patients LVEF was < 40% (SHF), and in 164(34%) LVEF ≥ 40% (HFPSF).

Results

Compared to the HFPSF group, SHF patients were predominantly younger males with ischemic etiology and less cardiovascular comorbidities such as obesity, hypertension, diabetes mellitus and atrial fibrillation. Over a mean follow-up period of 2 years, 148(31%) patients died. Overall mortality was similar between the two groups: 53(32%) HFPSF patients and 95(30%) SHF patients died (p = 0.6), even after adjusting for baseline variables, including age, gender and comorbidities (hazard ratio 1.09; 95% confidence interval 0.74-1.61; p = 0.67). In contrast to the similar mortality rates, the modes of death were different. SHF patients had higher death rates due to pump failure compared to the HFPSF group {32/95(34%) vs. 9/53(17%) patients, p = 0.03}. A trend towards higher rate of non-cardiac death was observed in HFPSF group {33/53(62%) patients vs. 45/95(47%) patients, respectively, p = 0.08}. The prevalence of arrhythmic death was similar in both groups {17/95(18%) vs. 10/53(19%) patients, p = 0.9}.

Conclusions

Although the characteristics of HFPSF and SHF patients are distinctively different, the mortality rates are similar. The mode of death is different among the two groups of patients, as pump failure death is significantly higher in SHF patients, while non-cardiac mortality is more prevalent in HFPSF patients.     

Diastolic ventricular interaction in patients after atrial switch for transposition of the great arteries: A speckle tracking echocardiographic study

Background

We tested the hypothesis that diastolic ventricular interaction occurs after atrial switch operation for transposition of the great arteries (TGA) and that subpulmonary LV diastolic function is influenced by septal geometry.

Methods

Twenty-nine patients (male 19) after atrial switch operation for TGA aged 20.8 ± 4.1 years and 27 healthy controls were studied. Two-dimensional longitudinal systolic strain, systolic (SRs), early diastolic (SRe), and late diastolic (SRa) strain rates of both ventricles were determined using speckle tracking echocardiography. Early diastolic trans-atrioventricular velocity (E) and myocardial early diastolic myocardial velocity (e) at the ventricular free wall-annular junction were measured. Geometry of the morphologic left ventricle was quantified by the diastolic eccentricity index (EI).

Results

In both systemic and subpulmonary ventricles, SRe and SRa were significantly lower and trans-atrioventricular E/e ratios higher in patients than controls (all p < 0.001). In patients, RV SRe correlated with left ventricular (LV) SRe (r = 0.49, p = 0.008), and RV SRa correlated with LV SRa (r = 0.46, p = 0.01). Significant leftward shifting of the septum in patients was reflected by the greater LV EI (p < 0.001). In patients, LV EI correlated with age- and sex-adjusted z score of LV end-diastolic volume. As a group, LV EI correlated negatively with LV SRe (r =−0.62, p < 0.001) and LV SRa (r = − 0.51, p < 0.001), and positively with mitral E/e ratio (r = 0.33, p = 0.02).

Conclusions

Systemic RV diastolic dysfunction occurs after atrial switch operation and correlates with subpulmonary LV diastolic dysfunction. The observed diastolic ventricular interaction may potentially be mediated through alteration of septal geometry.     

Contemporary clinical outcomes of patients treated with or without rotational coronary atherectomy — An analysis of the UK central cardiac audit database

Introduction

Rotational atherectomy (RA) is widely used for treating calcified coronary lesions. Clinical data however remain limited.

Methods

We assessed outcome and survival among patients undergoing percutaneous coronary intervention (PCI) with or without RA in the UK between September 2007 and March 2011.

Results

Data from 221,669 percutaneous coronary intervention (PCI) procedures were analysed; 2152 patients (0.97%) underwent RA (RA +); the remainder underwent conventional PCI (RA −). RA + patients were older (71.7 ± 9.6 vs. 64.1 ± 12.8 year; p < 0.001), and had a higher incidence of diabetes (26.4% vs. 18.0%; p < 0.001), hypertension, (61.9% vs. 49.4%; p < 0.001), peripheral vascular disease (9.9% vs. 4.2%, p < 0.001), cerebrovascular disease (5.5% vs. 3.4%, p < 0.001), renal impairment (3.4% vs. 1.5%, p < 0.001) and poor left ventricular function (11.4% vs. 4.3%,p < 0.001). Procedural success was lower among RA + patients (90.3% vs 94.6%; p < 0.001) and procedural complications were more frequent (9.7% vs 5.4%; p < 0.001). After 2.4 ± 1.2 years follow-up, unadjusted Cox proportional hazard modeling demonstrated poorer survival for RA + patients (HR 2.21, 95%CI 1.97–2.49; p < 0.0001). This disadvantage remained after adjustment for adverse variables (HR 1.26, 95%CI 1.11–1.44; p = 0.0004) and following propensity analysis. There was evidence however of improved survival for RA + patients with left main stem disease (HR 0.52, 95%CI 0.35–0.75, p < 0.0001), and peripheral vascular disease (HR 0.65, 95%CI 0.43–0.98, p < 0.0005).

Conclusions

Rotational atherectomy was undertaken in patients with higher pre-procedural risk. Medium term survival was worse among patients undergoing rotational atherectomy, and this survival disadvantage remained after correction for available adverse factors. Rotational atherectomy however remains clinically useful for patients with calcified coronary lesions.     

Facilitation of left ventricular function recovery post percutaneous coronary intervention by levosimendan

Background

Efficiency of percutaneous revascularization and the utility of levosimendan for advanced ischemic heart failure (HF) is unclear. We examined the efficacy of revascularization and levosimendan on left ventricular ejection fraction (LVEF) and mortality of patients admitted with acute decompensated HF and severe left ventricular dysfunction.

Methods

A prospective case control study that enrolled 84 patients with ischemic decompensated HF with LVEF < 35% and preserved LV wall thickness. Group A: 42 patients whose LVEF improved post percutaneous coronary intervention (PCI). Group B1: 22 patients whose LVEF did not improve post-PCI alone but improved after levosimendan. Group B2: 20 patients whose LVEF did not improve neither post-PCI nor post levosimendan.

Results

LVEF increased in group A from 22 ± 5 to 29 ± 5% post PCI and continued to improve at the 6 month follow-up (36 ± 4%). In group B1 LVEF did not improve after PCI, but increased after levosimendan from 23 ± 4% to 32 ± 4% and remained constant at 6 months. In group B2 LVEF 26 ± 4% did not change following both interventions.Reverse remodeling with a decrease in end-diastolic and end-systolic diameters was observed only in groups A and B1.Group B2 had a dismal prognosis with 36% in-hospital and 43% six month mortality. Groups A and B1 had a lower in hospital (4.7%, 4.5%) and mid term (11%, 11%) mortality.

Conclusion

Improvement of LV size and function with better prognosis can be expected in the majority of patients undergoing PCI for decompensated ischemic HF. Levosimendan enhanced the recovery of LV function post PCI.     

Spontaneous visits to the emergency service and hepatology day hospital by patients with liver cirrhosis

Introduction

Because of the current overload of emergency services, new units, such as day units, have had to be created. Liver cirrhosis (LC) is a chronic disease with frequent decompensations requiring medical attention. The aim of this study was to compare differences between emergency consultations in a hepatology day hospital (HDH) and in an emergency service (ES) among patients with LC.

Methods and material

We performed an observational prospective study. All patients with LC attending the HDH or ES from September 2007 to August 2008 were asked to complete a questionnaire. Demographic, clinical, and radiological variables were collected.

Results

There were 743 consultations, of which 62% involved the HDH. The mean age was 65 ± 12 years, and the male/female ratio was 2:3. The most frequent diagnosis in the ES was hepatic encephalopathy (26.2% ES versus 6% HDH, p < 0.001) followed by upper gastrointestinal hemorrhage (17.7% ES versus 0.6% HDH, p < 0.001), while the most frequent diagnosis in the HDH was ascites (66.2% HDH versus 22.7% ES, p < 0.001). The tests performed were as follows: blood analysis: 95% ES versus 60% HDH (p < 0.01); radiology: 71% ES versus 11% HDH (p < 0.01) and paracentesis: 51% ES versus 74% HDH (p < 0.01). The mean length of stay in the ES was 21.3 ± 121.5 hours compared with 3.3 ± 2.4 hours in the HDH (p < 0.001). A total of 53% of patients attended in the ES were hospitalized compared with 12% of those attended in the HDH (p < 0.05).

Conclusion

Patients with LC preferentially attend the HDH, where fewer tests are performed and the length of stay is shorter. The care provided in the HDH is appropriate and efficient.     

Increased epicardial adipose tissue in type 1 diabetes is associated with central obesity and metabolic syndrome

Aims

The present study evaluated the relationship between metabolic syndrome (MS), body fat composition and epicardial adipose tissue (EAT) in type 1 diabetes. Epicardial adipose tissue is a new independent marker of coronary artery disease (CAD).

Methods

Forty-five type 1 diabetic women were evaluated (age 36 ± 9 years; body mass index 24.6 ± 4.4 kg/m²). Metabolic syndrome was defined by the World Health Organization criteria. Body fat composition and EAT were analyzed by dual-energy-X-ray absorptiometry and echocardiogram, respectively.

Results

Twenty patients (45%) had MS. Patients with MS had greater android (central) fat deposition than patients without MS (41.9 ± 2.0% vs. 33.7 ± 1.8%, p = 0.004). Total body fat and gynoid (peripheric) fat distribution were similar between the groups. Mean EAT was higher in patients with MS (6.15 ± 0.34 mm vs. 4.96 ± 0.25 mm; p = 0.006) and EAT was positively correlated with android (central) fat distribution (r = 0.44; p = 0.002), however no correlation was found with gynoid (peripheric) fat distribution.

Conclusions

There was a high incidence of MS in type 1 diabetes related to increased central adiposity, despite the absence of obesity. Metabolic syndrome and central obesity were associated with increased EAT. Thus, young non-obese type 1 diabetic women with central adiposity and/or MS may have increased EAT, what may predict CAD risk.     

Exercise at ventilatory threshold aggravates left ventricular remodeling in patients with extensive anterior acute myocardial infarction

Background

The effects of physical training on ventricular remodeling after extensive anterior acute myocardial infarction (AMI) have not yet been defined. This randomized controlled study examines whether exercise aggravates left ventricular (LV) remodeling in patients with extensive anterior AMI.

Methods

Forty-eight consecutive patients with a first extensive anterior AMI and an LV ejection fraction (EF) of <45% assessed with left ventriculography (LVG) within 3 days of onset were randomly allocated to a training group (n = 24) or a control group (n = 24). Exercise intensity was determined by the heart rate of each patient at ventilatory threshold (VT). Three weeks after onset, a second LVG was performed, followed by a supervised exercise program at VT for 12 weeks. The LVG was reassessed after the exercise program. We then calculated the global LV volume (end-diastolic volume index [EDVI], end-systolic volume index [ESVI]) and systolic expansion volume index (SEVI), a new parameter for measuring the infarction site expansion at the end-systolic phase.

Results

Both EDVI and ESVI significantly decreased in the control group from 1 to 4 months after onset (91.2 ± 26.1 to 83.3 ± 24.0 mL/m², P <.05; 52.4 ± 22.5 to 45.7 ± 18.8mL/m², P <.01, respectively), but not in the exercise group. The SEVI also significantly decreased in the control group from 1 to 4 months (33.1 ± 16.9 to 25.7 ± 13.9 mL/m², P <.05), but not in the training group (34.2 ± 12.9 to 36.5 ± 15.5 mL/m², P = not significant).

Conclusion

Exercise while healing in patients with extensive anterior AMI, even at the VT level, induces LV enlargement and thus might aggravate LV remodeling. Therefore, in these patients, clinicians should consider withholding exercise training for at least 8 weeks, versus the 3-week period used in this trial.     

Effects of losartan and captopril on left ventricular systolic and diastolic function after acute myocardial infarction: results of the Optimal Trial in Myocardial Infarction with Angiotensin II Antagonist Losartan (OPTIMAAL) echocardiographic substudy

Background

Angiotensin-converting enzyme inhibitors have been shown to attenuate adverse remodeling after acute myocardial infarction (AMI), and the same has been suggested for angiotensin II type 1 receptor antagonists in animal models. Therefore the aim of the study was to compare the effects of losartan and captopril on regional systolic, diastolic, and overall left ventricular (LV) function after AMI.

Methods

Two hundred twenty-five patients aged ≥50 years with documented AMI and heart failure and/or LV dysfunction were randomly assigned treatment with either losartan (50 mg/d) or captopril (50 mg 3 times/d). Echocardiography was performed at randomization and after 3 months; echocardiograms were analyzed blinded at the core laboratory. Main outcome measures were changes in wall motion score index (WMSI), E-wave deceleration time (E-DT), and Tei index of overall LV function.

Results

WMSI decreased in both groups (losartan 1.58 ± 0.23 to 1.52 ± 0.26, P = .009, captopril 1.60 ± 0.24 to 1.48 ± 0.22, P < .001), although the decrease was greater in patients allocated to captopril (captopril −0.12 ± 0.17 vs losartan −0.05 ± 0.19, P = .007). In both groups E-DT increased, although the increase was significant only in patients treated with captoril (193 ± 61 ms to 208 ± 70 ms, P = .05). The change in E-DT was not different between treatment groups (captopril 14 ± 74 ms vs losartan 7 ± 80 ms, P = .52). Tei index decreased in both groups (losartan 0.59 ± 0.13 to 0.55 ± 0.15, P = .04, captopril 0.62 ± 0.15 to 0.55 ± 0.13, P < .001). However, the reduction was significantly greater in patients treated with captopril (captopril −0.08 ± 0.14 vs losartan −0.03 ± 0.14, P = .01).

Conclusion

Losartan and captopril improve systolic and overall LV function after AMI, but the benefit is greater for patients treated with captopril.     

Left ventricular twist in clinically stable heart transplantation recipients: A speckle tracking echocardiography study

Background and aim

Cavity twist is an integral part of LV function and its pattern in transplanted hearts is not well known. This study aimed at exploring LV twist in clinically stable heart transplant (HT) recipients with no evidence for rejection.

Methods

We studied 32 HT patients (54 ± 24 months after HT), 34 other cardiac surgery (CS) patients and compared them with 35 health controls using speckle tracking echocardiography, measuring peak twist angle, time-to-peak twist, and untwist rate.

Results

LV twist angle was smaller in the HT group (6.2 ± 3.3°) in comparison with the CS group and controls (13.2 ± 3.5° and 13.1 ± 4.5°, respectively; p < 0.0001 for all) and untwist rate was reduced (HT group: − 74 ± 30°/s; CS group: − 118 ± 43°/s; controls: − 116 ± 39°/s; p < 0.0001 for all). Time-to-peak twist was not different between groups. Time after HT was the main independent predictor of both LV twist angle and untwist rate (β = 0.8, p < 0.0001).

Conclusion

Though clinically stable, LV twist dynamics are significantly impaired in HT recipients, even in comparison with patients who underwent other cardiac surgery.     

Effect of metformin on oxidative stress, nitrosative stress and inflammatory biomarkers in type 2 diabetes patients

Aim

Advanced research has radically changed both diagnosis and treatment of diabetes during last three decades; a number of classes of oral antidiabetic agents are currently available for better glycemic control. Present study aims to evaluate the effect of metformin on different stress and inflammatory parameters in diabetic subjects.

Methods

208 type 2 diabetes patients were randomly assigned for metformin and placebo.

Results

Reactive oxygen species generation, advanced oxidation protein products (179.65 ± 13.6, 120.65 ± 10.5 μmol/l) and pentosidine (107 ± 10.4, 78 ± 7.6 pmol/ml) were found to be reduced by metformin treatment compared to placebo. On the other hand metformin administration enhanced total thiol and nitric oxide level (p < 0.05). But nutrient level (Mg⁺², Ca⁺²) in plasma was not altered by the treatment. Significant restoration of C reactive protein (p < 0.05) was noticed after metformin therapy. Metformin administration also improved Na⁺K⁺ATPase activity (0.28 ± 0.08, 0.41 ± 0.07 μmol Pi/mg/h) in erythrocyte membrane.

Conclusions

This study explores that metformin treatment restores the antioxidant status, enzymatic activity and inflammatory parameters in type 2 diabetic patients. Metformin therapy improves the status of oxidative and nitrosative stress altered in type 2 diabetes. This study unfolds the cardio protective role of metformin as an oral hypoglycemic agent.