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Background: Early cardiovascular impairment in obstructive sleep apnea (OSA) patients is often overlooked, leading to irreversible outcome. Left ventricular (LV) global longitudinal strain (GLS) derived from automated function imaging (AFI) echocardiography provides a fast tool to assess global longitudinal function. We therefore aimed to compare the feasibility and reproducibility of AFI with mitral annulus plane systolic excursion (MAPSE) as obesity is common in OSA. Methods: A comprehensive echocardiographic examination was done in 186 consecutive patients having polysomnography for suspected OSA in this prospective study. MAPSE was measured by using M-mode. AFI was derived by offline analysis of three long-axis views that semi-automatically detects LV endocardial boundary, which is adjusted manually as necessary. Variability of AFI and MAPSE were compared among the different subgroups and further tested in BMI subgroups. Results: Despite a relatively high obesity rate (42.9%), AFI was feasible in 94% (175/186) patients and MAPSE could be recorded in all patients. Although more segments were measured with AFI it showed excellent correlation (r=0.882) superior to MAPSE (r=0.819) between the expert and beginner. Intra- and inter- observer variability of AFI were comparable with MAPSE in Bland-Altman analysis, 5.5% and 6.5% for AFI, 6.2% and 8.8% for MAPSE, respectively. In repeated measurements, AFI showed higher intra-class correlation (ICC=0.95) than MAPSE (ICC=0.87). Furthermore, analysis showed that AFI was feasible even in more obese patients (BMI≥28kg/m2). Conclusions: Even in obese patients with OSA, AFI-GLS is feasible and more reliable for less expert operators than MAPSE for detecting LV longitudinal dysfunction.

Background Limited evidence is available regarding the association between OSA and coronary plaque assessed by using quantitative coronary CT angiography. Research Question Are there any associations between OSA severity-related indexes and the presence and burden of coronary plaque? Study Design and Methods Cross-sectional data from 692 patients who underwent sleep monitoring and coronary CT angiography were used for this study. Of these patients, 120 (17.3%) underwent polysomnography, and 572 (82.7%) underwent respiratory polygraphy. Multivariable logistic and linear regression analyses were used to investigate the associations of OSA severity-related indexes with the presence, volume, and composition of plaque. Results In multivariable analyses, patients with moderate to severe OSA were more likely to have coronary plaques (P = .037), and plaques were more likely to contain a noncalcified plaque (NCP) component (P = .032) and a low-density NCP (LD NCP) component (P = .030). Furthermore, the apnea-hypopnea index and oxygen desaturation index as continuous variables were both associated with the presence of plaque, NCP, and LD NCP (all, P Interpretation OSA was independently associated with the presence and burden of coronary plaque, which suggests an increased risk of coronary events. Clinical Trial Registration Chinese Clinical Trial Registry; No. ChiCTR-ROC-17011027; http://chictr.org.cn .

Purpose: The diagnosis of obstructive sleep apnea (OSA) relies on time-consuming and complicated procedures which are not always readily available and may delay the diagnosis. With the widespread use of Artificial Intelligence, quick identification with simple clinical information and image recognition pointing at craniofacial features might be a useful tool for self-helped screening of OSA. Methods: The subjects suspected of OSA receiving sleep examination and frontal photographing were consecutively recruited. Sixty-eight points were labelled with automated identification. An optimized model with facial features and basic clinical information was established and ten-folds cross-validation was performed. Area under the receiver operating characteristic curve (AUC) was calculated to evaluate the model’s performance using sleep monitoring as the reference standard. Results: A total of 653 subjects (77.2% males, 55.3% OSA) were analyzed. CATBOOST was the most suitable algorithm for OSA classification with a sensitivity, specificity, accuracy and AUC of 0.75, 0.66, 0.71 and 0.76 respectively (PConclusion: OSA could be identified by a machine-learning derived model with automatic recognition of facial photo for Chinese adults, which may facilitate screening of suspected subjects in a simple and quick manner by mobile application. Clinical trial registration Chinese Clinical Trial Registry: No. ChiCTR-ROC-17011027 (http://chictr.org.cn.)

Obstructive sleep apnoea (OSA) is recognised to be a potent risk factor for hypertension, coronary heart disease, strokes and heart failure with a reduced ejection fraction. However, the association between OSA and heart failure with a preserved ejection fraction (HFpEF) is less well recognised. Both conditions are very common globally.It appears that there are many similarities between the pathological effects of OSA and other known aetiologies of HFpEF and its postulated pathophysiology. Intermittent hypoxia induced by OSA leads to widespread stimulation of the sympathetic nervous system, renin–angiotensin–aldosterone system and more importantly a systemic inflammatory state associated with oxidative stress. This is similar to the consequences of hypertension, diabetes, obesity and ageing that are the common precursors to HFpEF. The final common pathway is probably via the development of myocardial fibrosis and structural changes in collagen and myocardial titin that cause myocardial stiffening. Thus, considering the pathophysiology of OSA and HFpEF, OSA is likely to be a significant risk factor for HFpEF and further trials of preventive treatment should be considered.

We aimed to evaluate the validity of the cardiopulmonary coupling (CPC) device, a limited-channel portable monitoring device for obstructive sleep apnea (OSA) screening in one single-center cohort, in particular in those with some cardiovascular diseases since the cardiopulmonary coupling might be different from those without. Consecutive patients referred to the sleep medical center for assessment of possible OSA were enrolled in this study. Patients were examined with standard polysomnography (PSG) and CPC evaluation simultaneously. The results of the two examinations were compared in all subjects and in those with or without cardiovascular abnormalities. A total of 179 subjects suspected with OSA were finally analyzed. According to OSA severity degree based on AHI, the area under ROC curve for the CPC device in the whole cohort patients was 0.79 (mild), 0.79 (moderate), and 0.86 (severe OSA), respectively (all p

Introduction Dialysis patients are frequently advised to restrict fruit and vegetable intake due to their high potassium content. This study aimed to evaluate the association between dietary fiber intake and major adverse cardiovascular events (MACE) among dialysis patients. Methods A total of 219 prevalent dialysis patients were prospectively recruited from a major university teaching hospital and regional dialysis center in Hong Kong. Dietary fiber intake estimated using a 7-day locally validated food frequency questionnaire was examined in relation to a primary composite outcome of MACE over a follow-up period of 4 years. Results A total of 127 patients were complicated with 1 or more MACE. In the multivariable Cox regression analysis, every 1 g higher fiber intake, and every 1 g/d per 1000 kcal higher fiber intake density were associated with an 11% (95% confidence interval [CI]: 0.81–0.97) and a 13% lower risk of MACE (95% CI: 0.77–0.99), respectively, independent of clinical, demographic, biochemical, hemodynamic, adequacy parameters, dietary protein, energy intake, inflammatory, and cardiac markers. Patients in the lower tertile of fiber intake density showed an increased hazard for MACE (adjusted hazard ratio: 1.78; 95% CI: 1.13–2.80) than those in the upper tertile. Conclusion Higher fiber intake and higher fiber intake density may be associated with less inflammation, less myocardial hypertrophy, injury, and lower risk of MACE in dialysis patients. These data form an important basis for a randomized controlled trial to examine fiber supplementation on cardiovascular outcomes in the dialysis population., Graphical abstract

Secondary prevention therapy reduces death and reinfarction after acute myocardial infarction (AMI), but it is underutilized in clinical practice. Mechanisms for this therapeutic gap are not well established. In this study, we have explored and evaluated the impact of passive continuation compared to active initiation of secondary prevention therapy for AMI during the index hospitalization. For this purpose, we have analyzed 1083 consecutive patients with AMI to a tertiary referral hospital in Hong Kong and assessed discharge prescription rates of secondary prevention therapies (aspirin, beta-blockers, statins, and ACEI/ARBs). Multivariate analysis was used to identify independent predictors of discharge medication, and Kaplan–Meier survival curve was used to evaluate 12-month survival. Overall, prescription rates of aspirin, beta-blocker, statin, and ACEI/ARBs on discharge were 94.8%, 64.5%, 83.5%, and 61.4%, respectively. Multivariate analysis showed that prior use of each therapy was an independent predictor of prescription of the same therapy on discharge: aspirin (odds ratio (OR) = 4.8, 95% CI = 1.9–12.3, P < 0.01 ), beta-blocker (OR = 2.5, 95% CI = 1.8–3.4, P < 0.01 ); statin (OR = 8.3, 95% CI = 0.4–15.7, P < 0.01 ), and ACEI/ARBs (OR = 2.9, 95% CI = 2.0–4.3, P < 0.01 ). Passive continuation of prior medication was associated with higher 1-year mortality rates than active initiation in treatment-naïve patients (aspirin (13.7% vs. 5.7%), beta-blockers (12.9% vs. 5.6%), and statins (11.0% vs. 4.6%); all P < 0.01 ). Overall, the use of secondary prevention medication for AMI was suboptimal. Our findings suggested that the practice of passive continuation of prior medication was prevalent and associated with adverse clinical outcomes compared to active initiation of secondary preventive therapies for acute myocardial infarction during the index hospitalization.

Limited evidence is available regarding the association between OSA and coronary plaque assessed by using quantitative coronary CT angiography.Are there any associations between OSA severity-related indexes and the presence and burden of coronary plaque?Cross-sectional data from 692 patients who underwent sleep monitoring and coronary CT angiography were used for this study. Of these patients, 120 (17.3%) underwent polysomnography, and 572 (82.7%) underwent respiratory polygraphy. Multivariable logistic and linear regression analyses were used to investigate the associations of OSA severity-related indexes with the presence, volume, and composition of plaque.In multivariable analyses, patients with moderate to severe OSA were more likely to have coronary plaques (P = .037), and plaques were more likely to contain a noncalcified plaque (NCP) component (P = .032) and a low-density NCP (LD NCP) component (P = .030). Furthermore, the apnea-hypopnea index and oxygen desaturation index as continuous variables were both associated with the presence of plaque, NCP, and LD NCP (all, P .05). Multivariable linear regression models showed that moderate to severe OSA was associated with NCP volume (β = 50.328; P = .042) and LD NCP volume (β = 15.707; P = .011). Moreover, the apnea-hypopnea index (P = .015), oxygen desaturation index (P = .005), and percentage of nighttime with oxygen saturation 90% (P = .017) were all significant predictors of LD NCP volume. Compared with those with no or mild OSA, patients with severe OSA had a significantly higher total plaque volume (P = .036), NCP volume (P = .036), and LD NCP volume (P = .013).OSA was independently associated with the presence and burden of coronary plaque, which suggests an increased risk of coronary events.Chinese Clinical Trial Registry; No. ChiCTR-ROC-17011027; http://chictr.org.cn.

Early detection of left ventricular (LV) dysfunction is crucial in obstructive sleep apnea (OSA) due to its close relationship with cardiovascular diseases. Global longitudinal strain (GLS) derived from automated function imaging (AFI) can precisely assess global longitudinal function. The aim of this study was to determine if LV GLS was reduced in patients with OSA and a normal LV ejection fraction (LVEF) and to assess any associated determinants. Polysomnography (PSG) and echocardiography were done in consecutive patients with suspected OSA and normal LVEF in this prospective study. Patients were divided into two groups according to apnea-hypopnea index (AHI) (Group 1, normal or mild OSA: AHI < 15/h; Group 2, moderate-to-severe OSA: AHI ≥ 15/h). Clinical, PSG, and echocardiographic parameters were compared between the two groups and the associated factors were investigated. Of 425 consecutive patients, 244 were analyzed after exclusions. Patients in Group 2 had significantly worse GLS than those in Group 1 (p < 0.001). The prevalence of GLS reduction (defined as < − 19.7%) was 25% and 76%, respectively (χ2 = 34.19, p < 0.001). Nocturnal lowest pulse oxygen saturation (SpO2), AHI, body mass index (BMI), and gender were associated with GLS reduction (all p < 0.05). Further multivariate analysis showed that the lowest SpO2 (OR: 2.15), gender (OR: 2.45), and BMI (OR: 2.66) remained independent (all p < 0.05), and the lowest SpO2 was the most powerful determinant (χ2 = 33.0, p < 0.001) in forward regression analysis. The intra- and inter-operator variability for AFI and coefficient of repeatability was low even in those with relatively poor images. In patients with normal LVEF, more severe OSA was associated with a worse GLS. The major determinants were lowest nocturnal SpO2, gender, and obesity, but not AHI. GLS can be rapidly and reliably assessed using AFI.

Background: Secondary prevention therapy reduces death and re-infarction after acute myocardial infarction (AMI) but is under-utilized in clinical practice. Mechanisms for this therapeutic gap are not well established. We aimed to evaluate the impact of passive continuation compared to active initiation of secondary prevention therapy for AMI patients during index hospitalization. Methods: We analyzed 1083 consecutive patients with AMI to a tertiary referral hospital in Hong Kong and assessed discharge prescription rates of secondary prevention therapies (aspirin, clopidogrel, beta-blockers, statins, angiotensin-converting enzyme inhibitor or angiotensin II receptor blockers (ACEI/ARBs)). Multivariate analysis was used to identify independent predictors of discharge and 6-month medication, Kaplan-Meier survival curve was used to evaluate 12-month survival. Results: Overall prescription rates of aspirin, clopidogrel, beta-blockers, statins, ACEI/ARBs on discharge was 94.8%, 54.2%, 64.5%, 83.5% and 61.4%, respectively. Multivariate analysis showed that prior use of each therapy, except clopidogrel, was an independent predictor of prescription of the same therapy on discharge: aspirin [Odds ratio (OR) =4.8, 95% CI =1.9-12.3, PConclusions: Overall use of secondary prevention medication for AMI was suboptimal compared to guideline recommendations. Our findings suggested the practice of passive continuation of prior medication was prevalent and associated with adverse clinical outcomes compared to those who received secondary preventive medication for the first time during index hospitalization. Failure to start additional medication and possible inadequate dose titration in the passive continuation group may be in part the reason for the poorer clinical outcome in this group.

Impact of percutaneous coronary interventions (PCI) on health-related quality of life (HRQOL) is important but under-reported in elderly patients.To evaluate long-term health status in elderly patients who underwent PCI.Consecutive patients who underwent PCI at a university-affiliated hospital from September 2009 to June 2012 were prospectively enrolled with HRQOL assessment at baseline (up to 2 weeks before PCI) and at 6-, 12-, and 36-month follow-up using the EuroQol five-dimensional questionnaire descriptive profile and visual analogue scale (VAS). Minimally important benefit (MIB) in HRQOL was defined as greater than half an SD improvement in the baseline VAS score.Of 1957 patients, 49.9%, 29.1%, and 21.0% were aged younger than 65 years, 65 to 74 years, and 75 years and older, respectively. Mean VAS scores at baseline (50.1 ± 20.5 vs. 51.6 ± 20.5 vs. 52.6 ± 21.8; P = 0.09) and at 36 months (72.9 ± 14.0 vs. 72.8 ± 16.1 vs. 72.0 ± 14.8; P = 0.77) were similar between the three age groups, respectively. MIB at 36 months was observed in 65.7%, 61.9%, and 61.2% of patients in each age group, respectively. Proportion of patients aged 75 years and older reporting problems in pain/discomfort and self-care reduced from 91.2% and 24.8% at baseline to 41.4% and 10.1% at 36 months, respectively (both P0.01). Independent predictors of MIB in HRQOL at 36 months in patients 75 years and older included poor baseline HRQOL, MIB at 6 months, and presentation with myocardial infarction (all P0.01).Elderly patients experienced sustained long-term improvement in quality of life comparable with younger patients after PCI. Our findings suggest that age per se should not deter against revascularization because of sustained benefit in HRQOL.

Funding Acknowledgements OSA & Subclinical myocardial impairment Background Early detection of left ventricular (LV) systolic dysfunction is crucial for patients with obstructive sleep apnea (OSA) . LV longitudinal strain (GLS), derived from automated function imaging (AFI) based on 2D echocardiography, provides a new tool to detect subclinical impairment of both global and regional myocardium. Its value in OSA remains unclear compared to traditional parameters since obesity is not uncommon in OSA, which may compromise the accuracy of AFI. We aimed to investigate the feasibility of AFI in OSA and further to explore the impact of OSA severity and degree of hypoxia on LV function. Methods Comprehensive transthoracic echocardiography was done in those receiving polysomnography (PSG) suspected as OSA consecutively (n = 322). All subjects were divided into 3 groups by apnea-hyponea index (AHI) by PSG (Control: AHI＜5; mild-to-moderate AHI 5-30; severe: AHI≥30) and GLS and mitral annular plane systolic excursion (MAPSE) were compared among the 3 groups. Results 322 patients with normal LVEF (≥50%) were finally analyzed. Though more segments were measured, inter- and intra- observer variability of GLS were comparable with MAPSE in a Bland-Altman analysis. For group comparison, GLS was reduced compared to the other 2 groups in the severe OSA category (p ≤ 0.001) while MAPSE showed no differences. Further analysis showed the feasibility of AFI was acceptable even in obese patients. In multivariable analysis of GLS, only maximum desaturation was an independent associated factor (p = 0.027). Conclusions Even in OSA patients with obesity, AFI-derived GLS is feasible. GLS is more sensitive than MAPSE or TDI for detection of reduced LV systolic function in OSA. Control(n = 27) Mild-Mod OSA(n = 145) Severe OSA(n = 160) P-value Age(years) 43 ± 13 47 ± 12 46 ± 11 0.218 Males, n(%) 17(63.0%) 118(81.4%) 154(96.3%) ＜0.001 BSA(m2) 1.82 ± 0.18 1.88 ± 0.18 1.97 ± 0.17*† ＜0.001 BMI(kg/ m2) 24.7 ± 4.4 26.8 ± 3.7* 28.6 ± 4.2*† ＜0.001 LVEF(%) 66.5 ± 6.4 67.0 ± 5.0 66.7 ± 4.6 0.813 Sep S’(cm/s) 8.3 ± 1.7 8.4 ± 1.5 8.7 ± 1.9 0.256 Sep E’(cm/s) 9.5 ± 3.0 9.0 ± 2.4 8.2 ± 2.0*† 0.003 E/ E’ 9.2 ± 2.9 9.1 ± 2.9 9.8 ± 2.9 0.145 GLS(%) 19.1 ± 2.7 19.0 ± 2.5 17.9 ± 2.4*† ＜0.001 MAPSE(mm) 15.1 ± 2.5 14.7 ± 2.3 14.3 ± 2.2 0.302 *p＜0.05 compared with mild OSA patients, †p＜0.05 compared with moderate OSA patients Echo Comparison between 3 OSA Groups

Heart failure with a preserved ejection faction (HFpEF) is a growing and expensive cause of heart failure (HF) affecting particularly the elderly. It differs in substantial ways in addition to the normal left ventricular ejection fraction, from the more easily recognized form of heart failure with a reduced ejection fraction (HFrEF or 'systolic heart failure') and unlike HFrEF there have been little advances in treatment. In part, this relates to the complexity of the pathophysiology and identifying the correct targets. In HFpEF, there appears to be widespread stiffening of the vasculature and the myocardium affecting ventricular function (both systolic and diastolic), impeding ventricular suction, and thus early diastolic filling leading to breathlessness on exertion and later atrial failure and fibrillation. Left ventricular ejection fraction tends to gradually decline and some evolve into HFrEF. Most patients also have a mixture of several co-morbidities including hypertension, diabetes, obesity, poor renal function, lack of fitness, and often poor social conditions. Therefore, many factors may influence outcome in an individual patient. In this review, the epidemiology, possible causation, pathophysiology, the influence of co-morbidities and some of the many potential predictors of outcome will be considered.

The Authors' reply We thank Larissa Albuquerque and her colleagues for their interest in our paper on the relationship of obstructive sleep apnoea (OSA) and heart failure with a preserved (or normal) ejection fraction (HFpEF).1 We are happy that they agree that OSA is likely to be a significant cause of HFpEF given the overlapping pathophysiology of both conditions, which we …

We evaluated the relationship between the degree of chronotropic incompetence and left ventricular (LV) impairment during exercise with severity of exercise intolerance in patients with heart failure and preserved ejection fraction (HFPEF).All patients underwent exercise echocardiography during bicycle Ergometer exercise with the acquisition of long-axis tissue Doppler imaging (TDI). Peak heart rates during exercise were also recorded and the percentages of maximal age-predicted heart rate (%MPHR) and heart rate reserve (%HRR) were calculated thereby. Besides, cardiopulmonary exercise testing was performed with peak oxygen consumption (VO2) measuring averaged at the highest 30-second during exercise.Forty HFPEF patients (aged 65±9 years; 75% male) were divided into two groups according to the median of peak VO2: patients with peak VO216.5 and ≥16.5 ml/kg/min, respectively. Patients with lower peak VO2 had decreased peak heart rates, %MPHR, %HRR, stroke volume and cardiac indices (LVSI and LVCI) than those with higher peak VO2 (all p0.05). The LV long-axis functions (TDI Sm, Em, s' and e') were reduced in patients with lower peak VO2 (all p0.05). Moreover, peak VO2 correlated with the following parameters: peak heart rates, %MPHR, %HRR, LVSI, LVCI, TDI Sm, Em, s' and e'(all p0.05).The degree of blunted chronotropic response and impaired LV long-axis function were more profound in HFPEF patients with poor exercise performance.

Conventional right ventricular (RV) pacing can cause left ventricular (LV) dysfunction and even heart failure (HF) particularly if ventricular pacing is frequent.1 New onset HF has been observed in approximately one third of patients receiving RV pacing for acquired second- or third-degree atrioventricular block (AVB) after a median follow-up of nearly 8 years.2 An elegant study has shown recently that apparent pacing induced cardiomyopathy could occur even if the accumulative pacing percentage was

It is known that oesophageal pain can imitate angina and also that non specific ECG changes, probably catecholamine mediated, can be similar to those due to true myocardial ischaemia. Both of these can therefore pose a problem for the diagnosis of angina pain due to cardiac ischaemia. We report a patient who had both of these conditions simultaneously, pain on exertion appearing as angina but due to oesophagitis, and "ischaemic" ECG changes due to catecholamines—a double mimic of myocardial ischaemia.

Right ventricular (RV) pacing may affect myocardial perfusion and coronary blood flow; however, it remains unknown whether this is related to systolic dyssynchrony induced by RV pacing. This prospective study was aimed to assess the relationship between dyssynchrony and the changes of coronary blood flow.Seventy patients with sinus node dysfunction were prospectively enrolled. Coronary flow was evaluated by measuring diastolic velocity time integral (VTI) and duration at the distal-portion of left anterior descending coronary artery (LAD) with transthoracic echocardiography at baseline and follow-up. Systolic dyssynchrony was assessed with tissue Doppler imaging by time standard deviation to peak systolic velocity of 12 left ventricular segments (Ts-SD, cutoff value ≥ 33 ms).Adequate data for analysis was available from 65 patients. At follow-up (mean follow up time: 127 ± 45 days), LAD velocity-time integral (LAD-VTI: 12.1 ± 4.2 vs. 10.7 ± 4.6 cm, p0.001) was decreased and there was deterioration of left ventricular systolic function (left ventricular ejection fraction: 65 ± 7% vs. 62 ± 7%). However, these changes were only detected in those with RV pacing induced systolic dyssynchrony. Significant reduction of LAD-VTI (defined as ≥ 5%) occurred in 34 (52%) patients which was more prevalent in those with pacing-induced systolic dyssynchrony than those without (85.3% versus 16.1%, χ(2)=31.1, p0.001). Though similar at baseline, LAD-VTI was significantly lower in the dyssynchrony group at follow up (p0.001). Cox-regression analysis showed that pacing-inducing systolic dyssynchrony [hazard ratio (HR): 3.62, p=0.009] and higher accumulative pacing percentage (HR: 1.02, p=0.002) were independently associated with reduction of LAD-VTI. ROC curve demonstrated that accumulative pacing percentage ≥ 35% was 97% sensitive and 84% specific in revealing significant reduction (area under the curve: 0.961, p0.001).RV pacing induced dyssynchrony is associated with reduced coronary flow and this may account for, in part, the deleterious effect of RV pacing on ventricular function over time.

Three-dimensional speckle-tracking echocardiography (3D-STE) is a newly developed technique to evaluate left ventricular (LV) deformation by measuring the area strain (AS) of endocardial surface that combines information from both longitudinal (LS) and circumferential strain (CS). We performed a study to examine myocardial deformation in patients with heart failure (HF) using 3D-STE.A total of 149 subjects including 58 patients with HF and preserved ejection fraction (HFPEF), 45 patients with HF and reduced ejection fraction (HFREF), and 46 normal subjects were prospectively studied by 3D-STE.After adjusting for age, gender and BSA, global CS, LS, radial strain (RS) and AS derived from 3D-STE in patients with HFPEF were significantly higher than their counterparts in patients with HFREF (all p0.001), but lower than that in normal subjects (all p0.05). In addition, among all the strain parameters, global AS exhibited the highest correlation with LV ejection fraction (y=1.243x+6.332, r=0.982, p0.001) and the best intra- (ICCs: 0.986, p0.001) and inter-observer variability (ICCs: 0.978, p0.001) than other parameters of 3D strain (CS: 0.981 and 0.974; LS: 0.908 and 0.841; RS: 0.946 and 0.915; all p0.001).Measurement of endocardial surface AS based on 3D-STE technique is reproducible and proves to be accurate and comprehensive in assessing the global LV performance and multidirectional deformation of the LV myocardium in HF patients.

Cardiovascular disease is the most common cause of death in patients with psoriatic arthritis (PsA) [(1)][1]. An overactive immune response in PsA together with traditional cardiovascular risk factors accelerates early atherosclerosis via a shared inflammatory pathway [(2)][2]. Inflammation may also

Coronary blood flow (CBF) is improved by cardiac resynchronization therapy (CRT) and impaired by right ventricular apical (RVA) pacing in patients with heart failure. However, the underlying mechanism remains unclear.Twenty-nine non-ischemic heart failure patients who responded to CRT underwent transthoracic echocardiography examination including both left anterior descending (LAD) CBF and tissue Doppler imaging in 3 pacing modes: intrinsic conduction, RVA pacing and biventricular (BiV) pacing. LAD velocity-temporal integral (LAD-VTI) and duration were measured. Systolic dyssynchrony was assessed with the standard deviation of a 12-left ventricular segmental model (Ts-SD).BiV pacing improved while RVA pacing reduced CBF compared to intrinsic conduction (all p0.05). Both Ts-SD and ventricular septal velocity deteriorated during RVA pacing but improved during BiV pacing (all p0.05). When systolic dyssynchrony was induced, lower LAD-VTI (9.5 ± 3.4 versus 12.7 ± 5.1cm, p=0.001) and shorter LAD diastolic duration (483 ± 92 versus 542 ± 106 ms, p=0.010) were detected than synchronous status. Systolic dyssynchrony was inversely related to septal velocity (r=-0.41), p0.001 and LAD-VTI (r=-0.30, p=0.007), with the latter found to be moderately correlated to septal velocity (r=0.30, p=0.007).Regional LAD flow was improved in patients subjected to BiV but worsened in those treated with RVA pacing in non-ischemic heart failure CRT responders. Systolic dyssynchrony was more commonly observed in patients subjected to RVA pacing. Reduction of septal velocity with dyssynchrony may directly lead to reduced LAD flow. Improvement of septal velocity by CRT and hence LAD flow may be an important mechanism in determining the response to CRT.

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.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.At 1 month, 59 patients (33%) had DYS which was more prevalent in RVA than BiV pacing group (52% vs. 15%, χ(2)=28.3, p0.001), 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%, p0.001) and larger LV end-systolic volume (35.3 ± 14.3 vs. 27.0 ± 10.4 ml, p0.001) 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 (χ(2)=40.8, p0.001). 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.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.Centre for Clinical Trials number, CUHK_CCT00037 (URL: http://www.cct.cuhk.edu.hk/Registry/publictrialrecord.aspx?trialid=CUHK_CCT00037).

The prevalence of heart failure (HF) is increasing as the population ages, but its rapid diagnosis and phenotype identification remain challenging. We sought to determine whether acoustic cardiography can accurately identify HF and its phenotypes.Three cohorts of patients were studied [94 with hypertension, 109 with HF and normal ejection fraction (HFNEF, EF ≥ 50%) and 89 with HF and reduced ejection fraction (HFREF, EF50%)]. All participants received acoustic cardiography and echocardiography examinations. Acoustic cardiographic parameters included S3 score (probability that the third heart sound exists), electromechanical activation time (EMAT, interval from Q wave to the first heart sound; EMAT/RR is EMAT normalized by heart rate), and systolic dysfunction index (SDI, a combination of EMAT/RR, S3 score, QRS duration and QR interval). Receiver operative characteristic curves were used to determine diagnostic utility of acoustic cardiography.EMAT/RR significantly differentiated HFNEF from hypertension (area under curve [AUC], 0.83; 95% confidence interval [CI], 0.77-0.89) with an EMAT/RR11.54% yielded 55% sensitivity and 90% specificity. Similarly, an echo-measured E/e'15 yielded 55% sensitivity, 90% specificity and 0.84 AUC in detecting HFNEF. Whereas SDI out-performed the other acoustic cardiographic parameters in differentiating HFREF from HFNEF (AUC, 0.81; 95% CI, 0.75-0.87), and an SDI5.43 yielded 53% sensitivity and 91% specificity. The E/e' ratio had a similar diagnostic performance.Our study demonstrates that this bedside technology may be helpful in identifying HF and its phenotypes, especially when echocardiography is not immediately available.

Heart failure is one of the most frequent complications in dialysis patients. However, little is known of the significance of the entity "heart failure with preserved ejection fraction" (HFPEF) in this population. This study aimed to determine the prevalence, clinical profiles, and long-term outcomes of peritoneal dialysis patients with HFPEF.Prospective cohort study.220 patients treated with peritoneal dialysis were recruited from a university teaching hospital in Hong Kong.Heart failure was defined clinically based on the presence of: (1) symptoms and signs, including dyspnea, increased jugular venous pressure, and basal crepitations; (2) radiographic evidence of pulmonary venous congestion or interstitial edema; and (3) resolution of symptoms, signs, and radiographic changes with hypertonic peritoneal dialysis exchanges. Based on a combination of clinical history of heart failure and echocardiography-derived ejection fraction, patients were classified as having no heart failure, HFPEF, and heart failure with reduced ejection fraction (HFREF).All-cause mortality, cardiac death, heart failure, and fatal or nonfatal cardiovascular events.All patients underwent 2-dimensional echocardiography and tissue Doppler imaging at baseline and were followed up prospectively for clinical events for 4 years.86 (39%) patients had heart failure, of whom 54.7% had preserved ejection fraction ≥50% and 45.3% had reduced ejection fraction50%. Patients with HFPEF were intermediate between those with no heart failure and those with HFREF in terms of blood pressure, prevalence of coronary artery disease, diabetes, cardiac biomarkers, left ventricular mass, volume, and ratio of early mitral inflow velocity to peak mitral annulus velocity. In the multivariable Cox regression analysis, patients with HFPEF showed an increased adjusted HR for cardiac death (2.57; 95% CI, 1.20-5.50), heart failure (HR, 2.25; 95% CI, 1.28-3.96), and fatal or nonfatal cardiovascular event (HR, 2.01; 95% CI, 1.26-3.21) compared with those with no heart failure, but the risk was lower compared with those with HFREF.The study included prevalent peritoneal dialysis patients and may introduce survival bias.HFPEF is common in peritoneal dialysis patients (∼55% of all heart failure) and is associated with increased risk of mortality and adverse cardiovascular outcomes compared with those with no heart failure, although the risk was lower than in patients with HFREF. This entity needs to be more recognized in peritoneal dialysis patients.

Background Connective tissue growth factor (CTGF) and vascular endothelial cell growth factor (VEGF) have been implicated as important effectors during cardiac remodeling. This study tested the hypothesis that norepinephrine (NE) induces CTGF and VEGF gene and protein expression in cardiac fibroblasts (CF) and the CTGF/VEGF complex will have an effect on angiogenesis. Methods and results Rats CF were cultured in NE (0.01 to 100 μM) for 24 h. CTGF and VEGF gene expression were measured by quantitative-PCR. CTGF protein and CTGF/VEGF complex were detected by Western blot. The effect of CTGF/VEGF complex on angiogenesis was detected by endothelial cell tube formation assay. VEGF antigen level, reactive oxygen species (ROS) production were measured by ELISA and DCFH-DiOxyQ assay respectively. NE at 0.01 μM up-regulated CTGF mRNA and secretory protein expression significantly whereas at 100 μM both gene and protein were down-regulated significantly when compared with controls. At 0.01 to 0.1 μM of NE, there was no change in VEGF gene and protein level. NE at 100 μM increased VEGF gene and antigen level and ROS production significantly when compared with controls. CTGF/VEGF complex was found to inhibit the angiogenesis of endothelial cells. Conclusions NE regulates CTGF and VEGF expression in a dose-dependent manner and via VEGF can induce angiogenesis. This work suggests NE may have an important role in ventricular remodeling.

Cardiac resynchronization therapy (CRT) is an effective therapy for advanced heart failure (HF) patients. The indications are well defined in recent guidelines and broadly indicate that CRT is suitable for chronic HF patients with left ventricular ejection fraction (EF) ≤35% and in NYHA class III or IV (Class I), and those with prolonged QRS duration ≥120ms with left bundle branch block (LBBB) QRS morphology, or QRS duration ≥150ms irrespective of QRS morphology (Class IIa). For patients with NYHA class II symptoms, CRT is recommended for patients with EF ≤30% and QRS duration ≥130ms with LBBB QRS morphology (Class I, level of evidence: A), or QRS duration ≥150ms irrespective of QRS morphology (Class IIa, level of evidence: A). However, CRT may benefit additional patients outside these criteria. In this review, we summarize the role of CRT in some subgroups, including patients with mild and moderate HF, upgrading to CRT from right ventricular (RV) pacing, bradycardia patients with routine pacing indications, congenital heart disease and specific cardiomyopathies. It is possible that CRT can give symptomatic and mortality benefits in some of these subgroups in the future and further clinical trials are warranted. (Circ J 2013; 77: 1364–1369)

Background Left ventricular (LV) systole and diastole are intimately dependent on myocardial torsion, which involves coupling between myocardial rotation (twisting in systole and untwisting in diastole) and longitudinal motion. Heart failure with normal ejection fraction (HFNEF) is known to involve exercise-induced wall motion abnormalities, but torsion on exercise has not been explored. We hypothesised that torsional dyssynchrony may also be involved and be exaggerated by exercise. Methods and Results 67 patients (age 73±7 years, 45 female) with HFNEF and 38 controls underwent cardiopulmonary exercise testing and echocardiography at rest and on supine exercise. Analysis of three plane motions was performed using speckle tracking and tissue Doppler imaging. Torsional dyssynchrony was quantified as the SD of the time to peak systolic motion (SDSM) (basal and apical rotation, longitudinal and radial displacement); the time difference between peak twist and peak longitudinal displacement (twist-longitudinal motion delay, TLMD) and the ratio of untwist to longitudinal extension (UT:LE). At rest, HFNEF patients had similar SDSM, TLMD and UT:LE compared with controls. Exercise was associated with significantly more dyssynchrony in the HFNEF patients (SDSM 38.8±27.6 ms vs 25.9±15.5 ms, p=0.02; TLMD 28.4±46.2 ms vs 2.9±31.2 ms, p=0.005 and UT:LE 10.4±15.3 vs 3.3±3.8, p=0.022). The SDSM correlated positively with LV wall thickness (r=0.31, p=0.015) and negatively with peak oxygen consumption (r=−0.299, p=0.01) and changes in stroke volume on exercise (r=−0.371, p=0.001). Conclusions HFNEF involves exercise-induced torsional dyssynchrony in systole and diastole, which relates to LV hypertrophy as well as exercise capacity.

Ventricular and arterial stiffness is an accepted cause of myocardial diastolic dysfunction. The aim of this study is to determine whether there is increased ventricular and arterial stiffness in patients with PsA and any relationship with disease-related risk factors.Seventy-three patients with PsA were divided into two subgroups based on the absence or presence of hypertension and/or left ventricular (LV) hypertrophy. Fifty healthy controls were enrolled for comparison. All participants underwent non-invasive assessments including conventional echocardiography with tissue Doppler imaging and pulse wave analysis. Ventricular stiffness was measured by ventricular end-systolic and diastolic elastance, whereas arterial stiffness was measured by total arterial compliance and aortic augmentation index.There was significantly increased ventricular and arterial stiffness in patients with PsA (P0.001), even in those without hypertension and/or LV hypertrophy. Based on the cut-off points derived from the controls, 38.4% of PsA patients had increased LV stiffness including 31.5% in diastole and 17.8% in systole, and 15.1% had increased arterial stiffness. Multivariable logistic regression analysis showed that long PsA disease duration (10 years) (odds ratio = 6.55, P = 0.001) was an independent risk factor for increased LV diastolic elastance after adjusting for age, gender and hypertension.Patients with PsA may have increased ventricular and arterial stiffness even without evidence of LV remodelling, and those with long disease duration may be at a higher risk. Therefore, prolonged inflammatory burden may be an important cause of early cardiovascular disease in patients with PsA.

The pathophysiology of HfpEF is complex. In this review we discuss the molecular aspects of HfpEF as well as the profoundly disturbed haemodynamics with particular focus on exercise haemodynamic abnormalities.

Left ventricular (LV) diastolic dysfunction has been reported in both active and inactive systemic lupus erythematosus (SLE) patients without clinical evidence of cardiovascular disease. However, the relationship between the long-term inflammatory burden reflected by the SLICC/ACR damage index and LV diastolic function has not been studied. Eighty-two SLE patients and 82 controls matched for age, sex, body mass index, blood pressure and heart rate underwent echocardiography with tissue Doppler imaging (TDI). LV diastolic function was estimated by the myocardial early diastolic velocity (E′) at the lateral annulus. There were 51 patients (62.2%) with nephritis, 23 patients (28.0%) with hypertension, 21 patients (25.6%) with vasculitis, 16 patients (19.5%) with pulmonary hypertension, 4 patients (4.9%) with cerebrovascular disease and 2 patients (2.4%) with diabetes mellitus. Sixty-two patients (75.6%) were taking prednisone and 35 patients (42.7%) used a immunosuppressant. Forty-five patients (54.8%) had active disease and suffered from disease-related end-organ damage. Patients with SLICC/ACR damage index ≥1 had more evidence of LV diastolic dysfunction with lower lateral annulus E′ (9.6 ± 3.4 vs 12.9 ± 3.5 cm/s, p 2 = 10.8, p = 0.001) were significantly higher. Multivariate analysis showed that the SLICC/ACR damage index ≥1 was independently associated with LV diastolic dysfunction (OR = 3.80, 95%CI: 1.21–11.95, p = 0.023) after adjusting for hypertension, disease duration and medical therapy. This may suggest that the overall inflammatory burden in SLE, as reflected by SLICC/ACR damage index, is associated with the development of diastolic dysfunction in SLE patients.

Background: The acute effects of right ventricular apical (RVA) pacing on left atrial (LA) function in patients with normal ejection fraction are not clear. Methods: A total of 94 patients (age 68.1 ± 11.1 years, 26 men) with implanted RVA-based dual-chamber pacemakers were recruited into this study. Patients who were pacemaker-dependent, in persistent atrial fibrillation or left ventricular ejection fraction

Health-related quality of life (HRQoL) is an important but often neglected outcome measure in acute coronary syndrome (ACS) management. The prevalence of elderly presenting with ACS and undergoing percutaneous coronary intervention (PCI) is rising. We aimed to explore the impact of PCI on health status in elderly ACS patients.We prospectively enrolled 624 patients admitted to our institution with ACS from February 2006 to May 2008. Short Form (SF)-36 health survey was used to assess HRQoL at baseline and 6 months. Baseline characteristics and HRQoL were compared for patients treated with PCI within 30 days of index ACS admission vs. medical therapy across 3 age groups (60, 60-79 and ≥80 years).PCI was performed in 73.6%, 55.7% and 21.3% in patients aged60, 60-79 and older than 80 years, respectively (p0.01). Elderly patients were more likely to be female (16.9 vs. 35.4 vs. 54.6%, p0.01) and had more co-morbidities (p0.01). Older patients were less likely to undergo angiography (84.8 vs. 65.2 vs. 24.8%, p0.01). Baseline HRQoL decreased with advancing age (p0.01). However, elderly patients who underwent PCI experienced the most improvement in physical health than younger age groups. PCI was an independent predictor (Odds Ratio = 1.79, 95% CI: 1.10-2.92) of better physical health status at 6 months.Elderly ACS patients who underwent PCI experienced the most improvement in physical health compared to younger patients. Our findings suggest that age per se should not deter against revascularization because of potential benefits in HRQOL.

Aims Low serum albumin is common in patients with systolic heart failure and is associated with increased mortality. However, the relationship between albumin and outcome in patients with heart failure and preserved ejection fraction (HFPEF) is not known. The aim of this study was to investigate the effect of serum albumin level on survival in patients with HFPEF. Methods and results We studied 576 consecutive HFPEF patients (left ventricular ejection fraction ≥50%) admitted to our hospital from 2006 to 2009. Standard demographics, transthoracic echocardiography, and routine blood testing including albumin levels were obtained shortly after admission. Outcome was assessed at 1 year after admission. Hypoalbuminaemia (≤34 g/L) was detected in 160 (28%) at admission; and all patients were then divided into hypoalbuminaemia and non-hypoalbuminaemia groups. In the hypoalbuminaemia group, the prevalence of chronic renal failure history, serum creatinine, and urea nitrogen levels were higher when compared with those without hypoalbuminaemia (all P < 0.05). Kaplan–Meier analysis showed that patients with hypoalbuminaemia had a significantly lower survival rate (53% vs. 84%, log-rank χ2 = 53.3, P < 0.001) and a higher rate of cardiovascular death (21.8% vs. 8.9%, log-rank χ2 = 19.7, P < 0.001) when compared with those without hypoalbuminaemia. Cox regression further revealed that hypoalbuminaemia, a history of cerebrovascular disease, and older age were the most powerful independent predictors of all-cause mortality in HFPEF patients at 1 year. Conclusions Hypoalbuminaemia is common in HFPEF patients and is associated with increased risk of death. Renal dysfunction may be the main pathophysiological mechanism underlying hypoalbuminaemia in HFPEF patients.

Atrial Dysfunction and Dyssynchrony Predict Atrial High Rate Episodes. Introduction: Right atrial (RA) appendage pacing may prolong atrial conduction time (ACT). This study aimed to investigate if RA appendage pacing can induce intra- and interatrial dyssynchrony and if atrial dysfunction and dyssynchrony can predict atrial high rate episodes (AHREs) in the first year after pacing. Methods and Results: Patients implanted with dual-chamber pacemakers for symptomatic bradycardia were enrolled. Cumulative percentage of RA appendage pacing (Cum%AP) during 1-year follow-up and AHREs were recorded. Full Doppler echocardiography studies were performed before implantation and 1 year after pacing. ACT and peak atrial velocities (Sm-la, Em-la, Am-la) were measured. One hundred ten patients (age 70.5 ± 11 years; 53 males) were recruited and completed 1-year follow-up. ACT of both RA and left atrial (LA) were more prolonged in patients with Cum%AP > 75% than those with 75% (22.3 ± 12.2 milliseconds vs 9.5 ± 6.2 milliseconds; 53.9 ± 29.7 milliseconds vs 19.7 ± 17.3 milliseconds; both P < 0.001). AHREs occurred in 29% of patients. Atrial pump function and interatrial dyssynchrony independently predicted AHREs in multivariate analysis. Receiver operating characteristic curve provided a cutoff value of Am-la

Although there is little debate over the fact that cardiac resynchronization therapy (CRT) can benefit the majority of patients selected with routine indications, the precise mechanism for improvement may be considered controversial. Among patients selected with New York Heart Association functional class III or IV symptoms, left ventricular ejection fraction ≤ 35% and electrocardiographic QRS widening of at least 120-130 ms, approximately 60-80% of patients improved depending on the definition of response used. Although a reasonable assumption is that electrocardiographic QRS widening is a surrogate for delays in regional ventricular mechanical activation, a large volume of data has demonstrated that there is a subset of patients with widened QRS complexes who have no significant mechanical dyssynchrony. The reason for dissociation of electrical dispersion and mechanical dyssynchrony is unknown presently, but many studies have demonstrated the association of dyssynchrony with favorable outcome following CRT. Perhaps more importantly, several imaging studies (principally by echocardiography) have shown the lack of baseline mechanical dyssynchrony to be as a marker for a less favorable outcome after CRT. Recently, the lack of dyssynchrony before CRT has been shown to be associated with a significantly lower long-term probability of freedom from death, heart transplantation, or left ventricular assist device placement. As further mechanistic evidence for the relationship of mechanical dyssynchrony and LV functional response to CRT, it has been suggested that patients who failed to improve their tissue Doppler measures of dyssynchrony after CRT have a lower chance of reverse remodeling. This topic has been muddled by technical difficulties in measurement of mechanical dyssynchrony by all imaging approaches, the confounding variable of scar in ischemic disease, and the widely variable definitions of response used by different investigators. However, the weight of evidence from a pathophysiological basis to the recent long-term patient outcome data strongly support the notion that resynchronization is the principle mechanism of benefit from CRT.

Whether the relief of chronic right atrial (RA) volume load by device closure of an atrial septal defect (ASD) normalizes RA size is unknown. The present study evaluated the prevalence and determinants of incomplete RA reverse remodeling (RAR) after ASD closure in adults. Transthoracic echocardiography was performed in 44 consecutive patients with secundum ASD (age 43 ± 17 years, 10 men) without a history of atrial arrhythmia shortly before and at 3 months after device closure of ASD. The pulmonary/systemic flow ratio was derived using invasive oximetry. The RA size had significantly decreased at 3 months of follow-up (RA volume index [RAVI] 52 ± 29 to 27 ± 17 ml/m(2), p0.001). Incomplete RAR (defined as a RAVI of ≥21 ml/m(2)) was detected in 25 patients (57%) after closure. They were older, had a larger pulmonary/systemic flow ratio, a higher pulmonary arterial systolic pressure, more tricuspid regurgitation, and larger RA, left atrial, and right ventricular sizes before closure than those with a normalized right atrium. Before closure, RAVI was the only independent determinant for incomplete RAR (odds ratio 1.115, 95% confidence interval 1.019 to 1.220; p = 0.018). A cutoff value of RAVI of ≥40 ml/m(2) has a sensitivity of 84% and specificity of 72% in the receiver operating characteristic curve. The preclosure RAVI correlated moderately with the shunt-duration index, calculated by multiplying the age to pulmonary/systemic flow ratio (r = 0.64, p0.01). In conclusion, incomplete RAR occurred in1/2 of the adult patients at 3 months after ASD device closure and was related to excessive preclosure RA dilation.

Myocardial interstitial fibrosis causes left ventricular stiffness and diastolic dysfunction. Despite its clinical significance, treatment options are limited. The flavonoid baicalein, extracted from roots of a Chinese medicinal plant, Scutellaria baicalensis Georgi was shown to inhibit liver fibrosis. This study sought to investigate whether chronic treatment with baicalein could attenuate myocardial fibrosis in spontaneously hypertensive rats (SHR). SHR were treated daily with baicalein while the control group received vehicle. At the end of study, SHR control group developed significant myocardial fibrosis that was attenuated by baicalein treatment for 4 and 12 weeks. Rats treated with baicalein were protected against an increase in heart to body weight ratio, plasma level of brain natriuretic peptides, intraventricular septum thickness, myocardial collagen volume of left ventricle (all P

Objective.Endothelial dysfunction and early atherosclerosis have been found in patients with psoriatic arthritis (PsA) without cardiovascular disease (CVD) risk factors. Few studies have investigated whether there is any early impairment of myocardial function. The aims of our study were to determine the prevalence of subclinical left ventricular (LV) dysfunction in PsA patients and the disease-related risk factors.Methods.Ninety-four PsA patients without clinical evidence of CVD and 63 healthy subjects were enrolled. All underwent conventional echocardiography and tissue Doppler imaging.Results.Sixty-one (65%) patients with PsA had evidence of subclinical LV dysfunction as defined by mean myocardial peak systolic velocity (Sm) of basal 6 segments < 4.4 cm/s, lateral E’ < 11.5 cm/s, and/or lateral E/E’ > 10. Thirty-six (38%) patients had only diastolic dysfunction, 4 (4%) had only systolic dysfunction, and 21 (22%) had both systolic and diastolic dysfunction. PsA patients with subclinical LV dysfunction were older, had a higher age at diagnosis of PsA and of psoriasis, a longer disease duration, a higher prevalence of hypertension and hyperlipidemia, higher levels of serum creatinine, and more antihypertensive treatment than those with normal LV function. Multivariate regression showed that age at diagnosis of PsA > 40 years (OR 3.388, 95% CI 1.065–10.777, p = 0.039) and hypertension (OR 4.732, 95% CI 1.345–16.639, p = 0.015) were independent predictors of subclinical LV dysfunction.Conclusion.PsA patients without established CVD disease and in the absence of traditional CV risk factors have a high prevalence of subclinical LV dysfunction.

Cardiovascular disease is highly prevalent in patients with chronic kidney failure treated using dialysis. The risk of cardiovascular events is estimated to be at least 2- to 10-fold higher in dialysis patients than in age-, race-, and sex-matched persons with normal kidney function. A significant proportion of cardiovascular events in long-term dialysis patients is caused by heart failure, and the presence of heart failure is predictive of a poor prognosis. Despite the significant morbidity and mortality associated with heart failure, very few therapeutic options are proved to prevent and treat the progression of this complication in dialysis patients. There are several potential reasons for this, chiefly reflecting both challenges with diagnosis due to the coexistence of volume overload and a paucity of adequately powered prospective randomized controlled trials that examine the efficacy of different therapeutic options in dialysis patients with cardiac disease or heart failure. Thus, unlike in the general population, very few advances have been made in managing this severe complication in dialysis patients. In this article, an overview of the prevalence, severity, and risk factors for heart failure in maintenance dialysis patients is provided and the diagnosis of heart failure in these patients is revisited.

Biventricular pacing or cardiac resynchronization therapy (CRT) has been a considerable advance in the therapy of chronic heart failure. However, it is clear that not all patients benefit either in terms of symptoms or cardiac function, and some may be worsened by CRT. In this review, we consider the arguments, both clinical and economical, in favour of improved selection of patients for CRT other than those in current guidelines. It also seems clear that the fundamental mechanism of CRT is correction of dyssynchrony, and we review the various methodologies available to detect dyssynchrony. Other factors are probably also important in determining outcomes such as lead position, the extent and form of myocardial damage, optimizing pacemaker performance, and clinical expertise. The potential costs of inappropriate CRT implantation are high to our patients and to the health economy, and it behooves the cardiology community to develop better selection criteria. The current guidelines can and should be improved.