Cardiovascular magnetic resonance in the diagnosis of acute heart transplant rejection: a review

Background

Left ventricular hypertrophy (LVH) is a hallmark of chronic pressure or volume overload of the left ventricle and is associated with risk of cardiovascular morbidity and mortality. The purpose was to evaluate different electrocardiographic criteria for LVH as determined by cardiovascular magnetic resonance (CMR). Additionally, the effects of concentric and eccentric LVH on depolarization and repolarization were assessed.

Methods

120 patients with aortic valve disease and 30 healthy volunteers were analysed. As ECG criteria for LVH, we assessed the Sokolow-Lyon voltage/product, Gubner-Ungerleider voltage, Cornell voltage/product, Perugia-score and Romhilt-Estes score.

Results

All ECG criteria demonstrated a significant correlation with LV mass and chamber size. The highest predictive values were achieved by the Romhilt-Estes score 4 points with a sensitivity of 86% and specificity of 81%. There was no difference in all ECG criteria between concentric and eccentric LVH. However, the intrinsicoid deflection (V6 37 ± 1.0 ms vs. 43 ± 1.6 ms, p < 0.05) was shorter in concentric LVH than in eccentric LVH and amplitudes of ST-segment (V5 -0.06 ± 0.01 vs. -0.02 ± 0.01) and T-wave (V5 -0.03 ± 0.04 vs. 0.18 ± 0.05) in the anterolateral leads (p < 0.05) were deeper.

Conclusion

By calibration with CMR, a wide range of predictive values was found for the various ECG criteria for LVH with the most favourable results for the Romhilt-Estes score. As electrocardiographic correlate for concentric LVH as compared with eccentric LVH, a shorter intrinsicoid deflection and a significant ST-segment and T-wave depression in the anterolateral leads was noted.     

Electrocardiographic diagnosis of left ventricular hypertrophy in aortic valve disease: evaluation of ECG criteria by cardiovascular magnetic resonance

Background

Left ventricular hypertrophy (LVH) is a hallmark of chronic pressure or volume overload of the left ventricle and is associated with risk of cardiovascular morbidity and mortality. The purpose was to evaluate different electrocardiographic criteria for LVH as determined by cardiovascular magnetic resonance (CMR). Additionally, the effects of concentric and eccentric LVH on depolarization and repolarization were assessed.

Methods

120 patients with aortic valve disease and 30 healthy volunteers were analysed. As ECG criteria for LVH, we assessed the Sokolow-Lyon voltage/product, Gubner-Ungerleider voltage, Cornell voltage/product, Perugia-score and Romhilt-Estes score.

Results

All ECG criteria demonstrated a significant correlation with LV mass and chamber size. The highest predictive values were achieved by the Romhilt-Estes score 4 points with a sensitivity of 86% and specificity of 81%. There was no difference in all ECG criteria between concentric and eccentric LVH. However, the intrinsicoid deflection (V6 37 ± 1.0 ms vs. 43 ± 1.6 ms, p < 0.05) was shorter in concentric LVH than in eccentric LVH and amplitudes of ST-segment (V5 -0.06 ± 0.01 vs. -0.02 ± 0.01) and T-wave (V5 -0.03 ± 0.04 vs. 0.18 ± 0.05) in the anterolateral leads (p < 0.05) were deeper.

Conclusion

By calibration with CMR, a wide range of predictive values was found for the various ECG criteria for LVH with the most favourable results for the Romhilt-Estes score. As electrocardiographic correlate for concentric LVH as compared with eccentric LVH, a shorter intrinsicoid deflection and a significant ST-segment and T-wave depression in the anterolateral leads was noted.     

Left ventricular hypertrophy detection from simple clinical measures combined with electrocardiographic criteria in a group of African ancestry

Background

Whether routine clinical parameters associated with left ventricular mass (LVM) enhance the performance of electrocardiographic (ECG) criteria for LV hypertrophy (LVH) detection and hence modify overall cardiovascular risk stratification is unknown.

Methods

An approach to echocardiographic LVH detection was identified from ECG criteria and clinical variables [age, body mass index (BMI), systolic blood pressure (SBP) and estimated glomerular filtration rate] associated with LVM in 621 participants of African ancestry. Performance (area under the receiver operating curve) and classification accuracy for LVH detection and the impact on cardiovascular risk stratification were determined.

Results

Compared to Cornell criteria alone, the combined use of Cornell criteria and clinical variables increased the performance (p < 0.001) and sensitivity (p < 0.05 to p < 0.0001) for LVH detection. The use of Cornell product together with additional clinical parameters as compared to Cornell product criteria alone increased the proportion of participants with pre-, grade I or grade II hypertension risk stratified as having a high added cardiovascular risk (56.3–67.9 %, p < 0.05).

Conclusions

In individuals of African ancestry, a combination of Cornell product criteria and age, BMI and SBP improves classification accuracy of Cornell criteria for LVH and increases those identified as having a high added as compared to lower cardiovascular risk scores.     

Detection of left ventricular hypertrophy by the R-wave voltage in lead aVL: population-based study

Background

According to hypertension guidelines, the recommended electrocardiographic (ECG) diagnostic criteria for left ventricular hypertrophy (LVH) are the Sokolow–Lyon and Cornel voltage criteria, both with general acceptance by primary care physicians. However, it was recently reported that the R-wave voltage in lead aVL (RaVL) was as good as other more complicated and time-consuming ECG criteria to detect LVH in hypertensive patients. Therefore, our aim was to investigate if the ability of the RaVL to identify echocardiographic left ventricular hypertrophy (ECHO-LVH) could be translated to the general population, a more realistic assessment of its utility in a nonreferral setting.

Methods

682 participants (43.5 % males), aged between 27 and 72 years from the urban population of Vitoria, ES, Brazil, were enrolled. We investigated the association of ECHO-LVH (LV mass >51 g/Ht^2.7) with several ECG voltage measurements: Sokolow–Lyon and Cornel criteria, S-wave voltage in lead V3 (SV3) and RaVL.

Results

The RaVL showed the best positive correlation with LV mass indexed to Ht^2.7, superior to both Cornell and Sokolow–Lyon criteria and was not influenced by gender. Analysis of the ROC curves showed that the RaVL depicted a significant superior performance in relation to all the other measurements in the ability to detect ECHO-LVH. SV3 was not correlated with LV mass. Thus, it seems that most of Cornell’s performance depends on its simplified version, that is, RaVL.

Conclusion

We have shown that the simple and single assessment of RaVL presented a greater diagnostic ability in detecting ECHO-LVH in the general population, signaling its value mainly as a screening tool.     

Differences in left ventricular diastolic dysfunction between eccentric and concentric left ventricular hypertrophy in hypertensive patients with preserved systolic function

Left ventricular (LV) hypertrophy (LVH) may be eccentric or concentric (2 × LV posterior wall thickness relative to LV end-diastolic dimension ≤ 0.42 or > 0.42, respectively). The LV diastolic function between age-matched hypertensive patients with eccentric and concentric LVH was compared in the present study. Echocardiography was used to measure LV mass index (LV mass/body surface area; LVMI) as an index of LVH. LV diastolic function was assessed by measurements of peak early transmitral flow velocity (E)/peak late transmitral flow velocity (A) (the E/A ratio), peak early diastolic mitral annular velocity (e') and the E/e' ratio. Although LVMI, E/A and e' did not differ between the two groups, E/e' was significantly higher (worse) in patients with concentric LVH (13.4 ± 5.4) than in those with eccentric LVH (11.1 ± 3.6). Among hypertensive patients with LVH, those with concentric LVH may, therefore, have more severe LV diastolic dysfunction than those with eccentric LVH even if their LVMIs, which reflect the degree of LVH, are similar.     

Impaired glucose tolerance, but not impaired fasting glucose, underlies left ventricular diastolic dysfunction

OBJECTIVE

Glucose intolerance is recognized as a predictor of congestive heart failure (CHF). However, the association of postprandial hyperglycemia or fasting hyperglycemia with CHF has not been clarified. We determined the impact of the total spectrum of glucose abnormalities on left ventricular (LV) geometry and diastolic function.

RESEARCH DESIGN AND METHODS

Two hundred and eighty-seven Japanese subjects who visited the university hospital to be checked for glucose intolerance or known type 2 diabetes were consecutively recruited. Participants underwent an oral glucose tolerance test if they had no history of diabetes, and LV geometry and LV systolic and diastolic function were analyzed by Doppler echocardiography.

RESULTS

The frequency of LV diastolic dysfunction in subjects with normal glucose tolerance, impaired fasting glucose (IFG), impaired glucose tolerance (IGT), newly detected diabetes, and known diabetes were 13, 22, 50, 51, and 61%, respectively (χ² = 54.2, P < 0.0001). IGT was a predictor for LV diastolic dysfunction after adjusting for age, sex, systolic blood pressure, and heart rate (odds ratio 3.43 [95% CI 1.09–11.2]), but IFG was not (0.49 [0.06–3.08]). IGT was a predictor after adjusting for established CHF risk factors but was no longer significant after adjusting for BMI and homeostasis model assessment of insulin resistance.

CONCLUSIONS

In this hospital-based registry of subjects without CHF, the prevalence of LV diastolic dysfunction was higher in subjects with IGT but not in those with IFG. Results suggest that IGT, as well as newly detected and known diabetes, could be linked to an increased risk of cardiovascular events, partly through LV diastolic dysfunction.Major cardiovascular events or mortality are related to prevailing hyperglycemia, particularly postprandial, but not fasting hyperglycemia (1,2). Abnormalities of the postprandial state are especially hazardous to endothelial function and are important contributing factors to the development of atherosclerosis (3,4). Hyperglycemia also is recognized as a predictor of congestive heart failure (CHF) (5–7), the major cause of cardiovascular morbidity and mortality. However, the association of postprandial hyperglycemia or fasting hyperglycemia with CHF has not been clarified.In patients hospitalized for CHF, 30–40% present only with left ventricular (LV) diastolic dysfunction but not with LV systolic dysfunction (8,9). Patients with LV diastolic dysfunction manifest more subtle symptoms and signs than those with LV systolic dysfunction, and the identification often could be delayed or missed. In a large-scale community study, the prevalence of LV diastolic dysfunction was shown to be strongly associated with diabetes (odds ratio 2.3), as was hypertension (2.8), LV hypertrophy (LVH) (7.6), and having a previous myocardial infarction (4.3) (10). But the association of the total spectrum of glucose abnormalities and LV diastolic function remains unclear.We therefore evaluated the impact of the spectrum of glucose abnormalities, namely, impaired fasting glucose (IFG), impaired glucose tolerance (IGT), newly detected diabetes, and known diabetes, on LV geometry and LV diastolic function in a hospital-based registry.     

Chronic Heart Failure: Contemporary Diagnosis and Management

Chronic heart failure (CHF) remains the only cardiovascular disease with an increasing hospitalization burden and an ongoing drain on health care expenditures. The prevalence of CHF increases with advancing life span, with diastolic heart failure predominating in the elderly population. Primary prevention of coronary artery disease and risk factor management via aggressive blood pressure control are central in preventing new occurrences of left ventricular dysfunction. Optimal therapy for CHF involves identification and correction of potentially reversible precipitants, target-dose titration of medical therapy, and management of hospitalizations for decompensation. The etiological phenotype, absolute decrease in left ventricular ejection fraction and a widening of QRS duration on electrocardiography, is commonly used to identify patients at increased risk of progression of heart failure and sudden death who may benefit from prophylactic implantable cardioverter-defibrillator placement with or without cardiac resynchronization therapy. Patients who transition to advanced stages of disease despite optimal traditional medical and device therapy may be candidates for hemodynamically directed approaches such as a left ventricular assist device; in selected cases, listing for cardiac transplant may be warranted.ACC = American College of Cardiology; ACEI = angiotensin-converting enzyme inhibitor; ADHF = acute decompensated heart failure; AF = atrial fibrillation; AHA = American Heart Association; ARB = angiotensin II receptor blocker; CABG = coronary artery bypass grafting; CAD = coronary artery disease; CHF = chronic heart failure; CRT = cardiac resynchronization therapy; ICD = implantable cardioverter-defibrillator; LV = left ventricular; LVAD = LV assist device; LVEF = LV ejection fraction; MI = myocardial infarction; MR = mitral regurgitation; SCD = sudden cardiac death; UF = ultrafiltrationChronic heart failure (CHF) is a progressive syndrome that results in a poor quality of life for the patient and places an economic burden on the health care system. Despite advances in the control of cardiovascular diseases such as myocardial infarction (MI), the incidence and prevalence of CHF continue to increase.¹ An accurate estimate of disease burden is difficult to gather because of the vast number of patients with asymptomatic left ventricular (LV) dysfunction. As the population ages, there is an epidemiological shift toward a greater prevalence of clinical heart failure with preserved LV function, the so-called stiff-heart syndrome. In fact, heart failure with preserved systolic function may account for up to two-thirds of cases in patients older than 70 years.² Regardless of age, the lifetime risk of developing heart failure is approximately 20% for all patients older than 40 years.³Despite the growing prevalence, novel screening techniques and therapeutic directions have improved the outlook for patients with heart failure by focusing not only on symptom control but also on ameliorating the pathophysiology toward a corrective phenotype. This review discusses accepted and emerging therapeutic directions, with an emphasis on practical implications. In light of the available literature and clinical trials, the primary emphasis will be on systolic dysfunction, with a separate brief discussion of heart failure with preserved systolic function.     

Factors influencing left ventricular diastolic function in elderly patients with chronic heart failure

The purpose of the study was to define factors influencing the diastolic left ventricular (LV) function in elderly patients with chronic heart failure (CHF). Ninety-seven I to IV functional class CHF patients aged 65 to 88 (mean age 76.6+/-5.1 yr), 61 women and 36 men, were examined. CHF was caused by coronary artery disease in 22 (22.7%) patients, by arterial hypertension in 14 (14.4%) patients, and by both in 61 (62.9%) patients. Fourteen (14.4%) patients had type 2 diabetes. Hemoglobin level lower than 130g/l in men or 120g/l in women was considered anemia. Glomerular filtration speed (GFS) was calculated using Cockcroft-Gault formula. EchoCG and Doppler EchoCG were performed in all patients. LV hypertrophy (LVH) was revealed in 90 (92%) of the patients; 52patients had concentric L VH and 38 patients had eccentric LVH. Ejection fraction was less than 45% in 17 (17.5%) patients. Isovolemic relaxation time (IVRT) was over the normal limit in 73 (75.3%) patients; the time of early diastolic flow slowing (DT) changed in different directions and was 211.2+/-55.6 msec. A type of transmitral blood flow with relaxation disorder was found in 58 (59.8%) patients, a pseudonormal type was revealed in 32 (33%), and a restrictive type was found in 7 (7.2%) of patients. The study found a reverse independent correlation between hemoglobin level and the speed of LV filling during atrial systole. An independent correlation between the degree of renal dysfunction (GFS) and disorder of LV relaxation was found: the lower GFS, the longer IVRT and DT. Thus, in addition to age and structural changes in the heart, factors that have adverse effects on diastolic filling parameters are anemia, lowered renal function, and the level of systolic and diastolic pressure.     

Adverse effect of increased left ventricular wall thickness on five year outcomes of patients with negative dobutamine stress

Background

To determine if patients without dobutamine induced left ventricular wall motion abnormalities (WMA) but an increased LV end-diastolic wall thickness (EDWT) exhibit a favorable cardiac prognosis.

Results

Between 1999 and 2001, 175 patients underwent a dobutamine stress cardiovascular magnetic resonance (DCMR) procedure utilizing gradient-echo cines. Participants had a LV ejection fraction >55% without evidence of an inducible WMA during peak dobutamine/atropine stress. After an average of 5.5 years, all participants were contacted and medical records were reviewed to determine the post-DCMR occurrence of cardiac death, myocardial infarction (MI), and unstable angina (USA) or congestive heart failure (CHF) warranting hospitalization.In a multivariate analysis, that took into account Framingham and other risk factors associated with cardiac events, a cine gradient-echo derived LV EDWT ≥12 mm was associated independently with an increase in cardiac death and MI (HR 6.0, p = 0.0016), and the combined end point of MI, cardiac death, and USA or CHF warranting hospitalization (HR 3.0, p = 0.0005).

Conclusion

Similar to echocardiography, CMR measures of increased LV wall thickness should be considered a risk factor for cardiac events in individuals receiving negative reports of inducible ischemia after dobutamine stress. Additional prognostic studies of the importance of LV wall thickness and mass measured with steady-state free precession techniques are warranted.     

Impact of intracoronary reinfusion of bone marrow-derived mononuclear progenitor cells on cardiopulmonary exercise capacity in patients with chronic postinfarction heart failure

Introduction

Intracoronary infusion of bone marrow-derived progenitor cells (BMC) in patients with chronic ischaemic heart failure (CHF) is associated with improvement in left ventricular ejection fraction (LVEF), reduction of NT-proBNP levels and improved prognosis. However, effects of this therapy on cardiopulmonary exercise capacity have not been investigated separately so far.

Patients and methods

One hundred and fifty-four patients with ischaemic heart failure (mean LVEF 40.3 ± 10.9 %, NT-proBNP 1,103 ± 1,436 pg/ml) underwent cardiopulmonary exercise capacity testing (CPX) before and 3 months after intracoronary infusion of autologous BMC. Thirty patients with a potential bias on the CPX course as concomitant coronary intervention, bypass surgery, new onset of arrhythmias or implantation of cardiac resynchronization devices were excluded from further analysis.

Results

The remaining 124 patients showed an increase in exercise time and peak workload by 16.8 and 6 %. Peak oxygen uptake and oxygen uptake efficiency slope also improved by 2.9 and 12.9 %, whereas other parameters like peak oxygen pulse and the slope of minute ventilation versus CO₂ elimination remained unchanged. Analysis of patients with poor, moderate and conserved CPX results prior to cell therapy documented that patients in tertiles with lowest initial exercise capacity showed the largest improvements in CPX after therapy. The differences in response to cell therapy were detectable in all investigated CPX parameters and became significant for exercise time, peak oxygen uptake and peak oxygen pulse.

Summary

These findings indicate that intracoronary BMC therapy improves exercise capacity in CHF patients with more advanced heart failure.     

Renal dysfunction is associated with shorter telomere length in heart failure

Background

Renal dysfunction is a frequent comorbidity associated with high mortality in patients with chronic heart failure (CHF). The intrinsic biological age might affect the ability of the kidney to cope with the challenging environment caused by CHF. We explored the association between leukocyte telomere length, a marker for biological age, and renal function in patients with CHF.

Methods and results

Telomere length was determined by a real-time quantitative polymerase chain reaction in 866 CHF patients. Renal function was estimated with the simplified Modification of Diet in Renal Disease equation. The median age was 74 (interquartile range 64–79) years, 61% male, left ventricular ejection fraction of 30 (23–44)%, and the estimated glomerular filtration rate was 53 (40–68) ml/min/1.73 m². Telomere length was associated with renal function (correlation coefficient 0.123, P < 0.001). This relationship remained significant after adjustment for age, gender, age of CHF onset (standardized-beta 0.091, P = 0.007). Also additionally adjusting for the severity of CHF and baseline differences did not change our findings.

Conclusion

The association between shorter leukocyte telomere length and reduced renal function in heart failure suggests that intrinsic biological aging affects the ability of the kidney to cope with the systemic changes evoked by heart failure.     

Increased serum levels of S100B are related to the severity of cardiac dysfunction, renal insufficiency and major cardiac events in patients with chronic heart failure

Objective

To investigate the correlations between S100B and the severity of cardiac dysfunction, renal insufficiency (RI) and prognosis in chronic heart failure (CHF).

Method

Serum levels of S100B, TNF-α, high sensitivity CRP and NT-proBNP were determined in CHF patients with (n = 96) and without RI (n = 146). Patients with RI only (n = 62) and control subjects (n = 64) served for comparison. Patients were followed up for one year.

Results

S100B levels were higher in CHF patients with a further elevation in those with RI (P < 0.01). Serum S100B levels correlated with left ventricular ejection fraction, left ventricular end-diastolic volume and NT-proBNP in CHF patients, and eGFR in patients with RI (all P < 0.05). Increased S100B levels were associated with major cardiac events (MCE), and were independently associated with the presence of CHF (all P < 0.05).

Conclusion

Increased serum S100B levels were associated with the severity of cardiac dysfunction, RI and an adverse prognosis in CHF patients. It represents an independent risk factor for CHF.     

Low prevalence of fibrosis in thalassemia major assessed by late gadolinium enhancement cardiovascular magnetic resonance

Background

Heart failure remains a major cause of mortality in thalassaemia major. The possible role of cardiac fibrosis in thalassemia major in the genesis of heart failure is not clear. It is also unclear whether cardiac fibrosis might arise as a result of heart failure.

Methods

We studied 45 patients with thalassaemia major who had a wide range of current cardiac iron loading and included patients with prior and current heart failure. Myocardial iron was measured using T2* cardiovascular magnetic resonance (CMR), and following this, late gadolinium enhancement (LGE) was used to determine the presence of macroscopic myocardial fibrosis.

Results

The median myocardial T2* in all patients was 22.6 ms (range 5.3-58.8 ms). Fibrosis was detected in only one patient, whose myocardial T2* was 20.1 ms and left ventricular ejection fraction 57%. No fibrosis was identified in 5 patients with a history of heart failure with full recovery, in 3 patients with current left ventricular dysfunction undergoing treatment, or in 18 patients with myocardial iron loading with cardiacT2* < 20 ms at the time of scan.

Conclusion

This study shows that macroscopic myocardial fibrosis is uncommon in thalassemia major across a broad spectrum of myocardial iron loading. Importantly, there was no macroscopic fibrosis in patients with current or prior heart failure, or in patients with myocardial iron loading without heart failure. Therefore if myocardial fibrosis indeed contributes to myocardial dysfunction in thalassemia, our data combined with the knowledge that the myocardial dysfunction of iron overload can be reversed, indicates that any such fibrosis would need to be both microscopic and reversible.     

Transplantation of progenitor cells and regeneration enhancement in acute myocardial infarction (TOPCARE-AMI): final 5-year results suggest long-term safety and efficacy

Background

Limited data is available for investigating the long-term safety and effects of intracoronary progenitor cell therapy in patients with acute myocardial infarction (AMI).

Objective

To assess the clinical course, NT-proBNP and MRI data as objective markers of cardiac function of the TOPCARE-AMI patients at 5-year follow-up.

Design

The TOPCARE-AMI trial was the first randomized study investigating the effects of intracoronary infusion of circulating (CPC) or bone marrow-derived progenitor cells (BMC) in 59 patients with successfully reperfused AMI.

Results

Five-year follow-up data were completed in 55 patients, 3 patients were lost to follow-up. None of the patients showed any signs of intramyocardial calcification or tumors at 5?years. One patient died during the initial hospitalization, no patient was rehospitalized for heart failure and 16 patients underwent target vessel revascularization (TVR). Only two TVRs occurred later than 1?year after cell administration making it very unlikely that the infused cells accelerate atherosclerotic disease progression. Serum levels of NT-proBNP remained significantly reduced at the 5-year follow-up indicating the absence of heart failure. MRI subgroup analysis in 31 patients documented a persistent improvement of LV ejection fraction (from 46?±?10% at baseline to 57?±?10% at 5?years, p?<?0.001)). Simultaneously, there was a reduction (p?<?0.001) in functional infarct size measured as late enhancement volume normalized to LV mass. However, whereas LV end-systolic volume remained stable, LV end-diastolic volume increased significantly.

Conclusions

The 5-year follow-up of the TOPCARE-AMI trial provides reassurance with respect to the long-term safety of intracoronary cell therapy and suggests favorable effects on LV function.     

Clinical and echocardiographic correlates of serum copper and zinc in acute and chronic heart failure

Aim

Emerging evidence suggests a pathophysiological role of micronutrient dyshomeostasis in heart failure, including promotion of adverse remodeling and clinical deterioration. We sought to evaluate serum copper (Cu) and zinc (Zn) levels in acute (AHF) and chronic (CHF) heart failure.

Methods

We studied 125 patients, 71 % male, aged 69 ± 11 years, 37 % with preserved left ventricular ejection fraction (LVEF ≥40 %) (HFPEF), including 81 with AHF and 44 with CHF; 21 healthy volunteers served as controls. Serum Cu and Zn levels were determined using air–acetylene flame atomic absorption spectrophotometry.

Results

Serum Cu levels were significantly higher in AHF (p = 0.006) and CHF (p = 0.002) patients compared to controls after adjusting for age, gender and comorbidities, whereas they did not differ between AHF and CHF (p = 0.840). Additionally, serum Cu in patients with LVEF <40 % was significantly higher compared to both controls (p < 0.001) and HFPEF patients (p = 0.003). Serum Zn was significantly lower in AHF (p < 0.001) and CHF (p = 0.039) compared to control after adjusting for the above-mentioned variables. Moreover, serum Zn was significantly lower in AHF than in CHF (p = 0.015). In multiple linear regression, LVEF (p = 0.033) and E/e ratio (p = 0.006) were independent predictors of serum Cu in total heart failure population, while NYHA class (p < 0.001) and E/e ratio (p = 0.007) were independent predictors of serum Zn.

Conclusion

Serum Cu was increased both in AHF and CHF and correlated with LV systolic and diastolic function. Serum Zn, in contrast, was decreased both in AHF and CHF and independently predicted by clinical status and LV diastolic function.     

Complement anaphylatoxin C3a as a novel independent prognostic marker in heart failure

Objectives

The purpose of this study was to evaluate complement activation in a heart failure cohort. Based on their powerful biological activity, we hypothesized that the levels of anaphylatoxin C3a are related to pathological signs and outcomes in heart failure.

Design, setting and patients

Complement activation products C3a and SC5b9 were determined in 182 consecutive CHF patients (single centre, prospective cohort study), with a left ventricular ejection fraction <45%. Mortality and re-hospitalisation due to the progression of CHF were assessed after a median follow-up of 14?months.

Interventions

None.

Results

In the univariate analysis, high level of anaphylatoxin C3a was significantly associated with clinical events (p?p?=?0.094). In multivariable Cox analysis, adjusted for age, NT-proBNP, diastolic blood pressure, body mass index (BMI), haemoglobin and creatinine levels, C3a was a significant predictor of HF-related re-hospitalization or death (HR 1.189 per 1-SD increase, 95% CI 1.023–1.383), and of cardiovascular events or death (HR 1.302, CI 1.083–1.566). C3a was strongly associated with the presence of peripheral oedema, inflammatory markers (CRP, prealbumin, IL-6, sTNFRI, sTNFRII), heat-shock protein 70 levels and endothelial activation markers (von-Willebrand factor and endothelin-1).

Conclusions

Results of the present study showed that complement activation is strongly linked to unfavourable outcomes in heart failure. High levels of anaphylatoxin C3a predicted re-hospitalization, cardiovascular events and mortality in adjusted survival model. Increased C3a levels were associated with biomarkers of acute-phase reaction, inflammation, cellular stress response, endothelial-cell activation and oedematous complications independently from disease severity.     

Prevalence of and risk factors for abnormal left ventricular geometrical patterns in hypertensive subjects administered irbesartan

BackgroundDistinct populations differ in LVH prevalence and impaired LV geometry. Currently, the prevalence of and risk factors for LV geometric patterns in Chinese hypertensives administered irbesartan have not been specifically addressed in large studies.MethodsTotally 10,883 patients (6623 men and 4260 women) completed the survey, including 1181 hypertensives administered irbesartan (488 males and 693 females) that were finally enrolled. Based on LVMI and RWT derived from comprehensive echocardiography, the LV geometric patterns of irbesartan‐treated hypertensive individuals were classified into four types, including the normal, concentric remodeling, and concentric and eccentric hypertrophy groups. Logistic regression analysis was applied in males and females, respectively, for determining odds ratios (ORs) and 95% confidence intervals (CIs) for various potential risk factors for abnormal LV geometrical patterns in irbesartan‐treated hypertensives.ResultsThe clinical and echocardiographic data differed significantly between males and females. The prevalence rates of concentric remodeling, concentric hypertrophy, and eccentric hypertrophy were 36.3%, 15.4%, and 6.1% in males, respectively, and 23.5%, 20.3%, and 23.8% in females, accordingly. Gender, daily dose of irbesartan, BMI, SBP, WtHR, and neck‐circumference were significantly associated with LV geometric patterns. After adjustment for confounding factors, risk factors for LVH and impaired LV geometry included SBP, WtHR in males, and MAU‐Cr and WtHR in females.ConclusionsLVH and impaired LV geometric patterns are more prevalent in females (67.7%) compared with that in males (57.8%) among hypertensives upon irbesartan administration. For such population, risk factors beyond elevated blood pressure may be involved in the progression of LVH and impaired LV geometric patterns in both genders.     

Epicardial adipose tissue in patients with heart failure

Purpose

The aim of this study was to evaluate the extent of epicardial adipose tissue (EAT) and its relationship with left ventricular (LV) parameters assessed by cardiovascular magnetic resonance (CMR) in patients with congestive heart failure (CHF) and healthy controls.

Background

EAT is the true visceral fat deposited around the heart which generates various bioactive molecules. Previous studies found that EAT is related to left ventricular mass (LVM) in healthy subjects. Further studies showed a constant EAT to myocardial mass ratio in normal, ischemic and hypertrophied hearts.

Methods

CMR was performed in 66 patients with CHF due to ischemic cardiomyopathy (ICM), or dilated cardiomyopathy (DCM) and 32 healthy controls. Ventricular volumes, dimensions and LV function were assessed. The amount of EAT was determined volumetrically and expressed as mass indexed to body surface area. Additionally, the EAT/LVM and the EAT/left ventricular remodelling index (LVRI) ratios were calculated.

Results

Patients with CHF had less indexed EAT mass than controls (22 ± 5 g/m² versus 34 ± 4 g/m², p < 0.0001). In the subgroup analysis there were no significant differences in indexed EAT mass between patients with ICM and DCM (21 ± 4 g/m² versus 23 ± 6 g/m², p = 0.14). Linear regression analysis showed that with increasing LV end-diastolic diameter (LV-EDD) (r = 0.42, p = 0.0004) and LV end-diastolic mass (LV-EDM) (r = 0.59, p < 0.0001), there was a significantly increased amount of EAT in patients with CHF. However, the ratio of EAT mass/LV-EDM was significantly reduced in patients with CHF compared to healthy controls (0.54 ± 0.1 versus 0.21 ± 0.1, p < 0.0001). In CHF patients higher indexed EAT/LVRI-ratios in CHF patients correlated best with a reduced LV-EF (r = 0.49, p < 0.0001).

Conclusion

Patients with CHF revealed significantly reduced amounts of EAT. An increase in LVM is significantly related to an increase in EAT in both patients with CHF and controls. However, different from previous reports the EAT/LVEDM-ratio in patients with CHF was significantly reduced compared to healthy controls. Furthermore, the LV function correlated best with the indexed EAT/LVRI ratio in CHF patients. Metabolic abnormalities and/or anatomic alterations due to disturbed cardiac function and geometry seem to play a key role and are a possible explanation for these findings.