Triglyceride-Glucose Index and Homeostasis Model Assessment-Insulin Resistance in Young Adulthood and Risk of Incident Congestive Heart Failure in Midlife: The Coronary Artery Risk Development in Young Adults Study.

Objective: This study aimed to assess the association between triglyceride-glucose (TyG) index/homeostasis model assessment-insulin resistance (HOMA-IR) within young adults and congestive heart failure (CHF), and to explore whether TyG index can replace HOMA-IR as a surrogate marker for IR in predicting the risk of CHF. Methods: A total of 4,992 participants between the ages of 18 and 30 years were enrolled from the Coronary Artery Risk Development in Young Adults (CARDIA) investigation [from 1985 to 1986 (year 0)]. A Cox proportional hazard regression analysis was conducted for assessing correlations between baseline TyG index/HOMA-IR and CHF events, together with the receiver operating characteristic (ROC) curve employed for scrutinizing TyG index/HOMA-IR and the risk of CHF. Results: During the 31-year follow-up period, 64 (1.3%) of the 4,992 participants developed CHF. In multivariable Cox proportional hazards models, adjusted for confounding factors for CHF, an increased risk of CHF was associated with a per-unit increase in the TyG index [hazard ratio (HR) 2.8; 95% confidence interval (CI), 1.7-4.7] and HOMA-IR (HR 1.2; 95% CI, 1.1-1.3). A Kaplan-Meier curve analysis showed that participants in the TyG index and HOMA-IR index Q4 group had a higher risk of CHF than those in the Q1 group. The area under curve (AUC) for the TyG index and HOMA-IR consisted of 0.67 (95% CI, 0.6-0.742) and 0.675 (95% CI, 0.604-0.746), respectively. There were no significant differences between the TyG index and HOMA-IR for AUC (p = 0.986). Conclusion: The higher TyG index and HOMA-IR are independent risk factors for CHF. The TyG index can replace HOMA-IR in young adulthood as a surrogate marker for IR to predict the risk of CHF.

Iron deficiency is an independent risk factor of increased myocardial energy expenditure in chronic heart failure patients.

BACKGROUND: Chronic heart failure (CHF) is a major public health burden and is associated with high morbidity, mortality, and cost. Recent studies demonstrated iron metabolism and myocardial energy metabolism were altered in CHF patients. In this study, we aimed to analyze the effects and correlations of iron metabolism on myocardial energy metabolism in CHF. METHODS: One hundred and thirty patients with CHF [age: 66.2±11.5 years, males: 58.5% and New York Heart Association (NYHA) class (II/III/IV): 67/43/20] were included. Serum concentrations of ferritin, transferrin saturation (Tsat), and soluble transferrin receptor (sTfR) were quantified as the indexes of iron metabolism, and echocardiography was used to assess myocardial energy expenditure (MEE) levels. Iron deficiency (ID) was defined as ferritin <100 or 100-300 µg/L with Tsat <20%. RESULTS: Patients with CHF were divided into two groups based on iron status. The prevalence of ID in CHF was 36.9%, and increased with the severity of CHF, reaching 80.0% in those with NYHA class IV (NYHA class II/III/IV: 17.9% vs. 46.5% vs. 80.0%, P=0.000). The demographic characteristics [age, sex, body mass index (BMI), blood pressure, and heart rate] and hemoglobin (HGB) concentrations in two groups were similar (all P>0.05). MEE was significantly higher in the ID group (92.7±23.0 vs. 65.6±20.8 cal/min, P=0.000), while NYHA classes II and III was significantly higher in the ID group (71.6±16.4 vs. 60.3±14.8 cal/min, P=0.022; 88.9±10.4 vs. 69.1±20.1 cal/min, P=0.000). In univariable linear regression models, the presence of ID, higher NYHA class, increased N-terminal pro-B-type natriuretic peptide (NT-proBNP), sTfR, left ventricular internal diastolic diameter (LVIDd), as well as reduced ferritin, Tsat levels, and lower left ventricular ejection fraction (LVEF) were associated with elevated MEE levels (all P<0.05). In multivariable regression models, the presence of ID, reduced Tsat. and increased sTfR remained independent predictors of elevated MEE levels after adjustment for all variables that showed a significant association with MEE (all P<0.05). CONCLUSIONS: The prevalence of ID is high in CHF and is associated with the severity of cardiac dysfunction. The presence of ID as well as reduced Tsat and increased sTfR concentrations are associated with elevated MEE levels in CHF.

Serum Peroxisome Proliferator-activated Receptor Gamma Coactivator-1α Related to Myocardial Energy Expenditure in Patients With Chronic Heart Failure.

BACKGROUND: Peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) plays key roles in controlling cardiac metabolism and function. Myocardial energy expenditure (MEE) can reflect myocardial energy metabolism and cardiac function. Whether the variation of PGC-1α can influence MEE levels in chronic heart failure (CHF) is unclear. Therefore, we investigated the relationship between PGC-1α and MEE. MATERIAL AND METHODS: We studied 219 patients with CHF and 66 healthy controls. MEE was measured according to echocardiographic parameters. Serum PGC-1α, N-terminal pro-B-type natriuretic peptide and other parameters were detected. Patients with CHF were divided into different groups according to the left ventricular ejection fraction (LVEF) and the tertile range of MEE. RESULTS: Serum PGC-1α was lower in the MEE 2 and 3 groups compared with controls (both P < 0.05). Patients in the MEE 2 (1.73 ± 0.83 versus 2.16 ± 0.82 ng/mL, P = 0.001) and 3 groups (1.65 ± 0.73 versus 2.16 ± 0.82 ng/mL, P < 0.001) possessed lower levels of PGC-1α than those in the MEE 1 group. Compared with high LVEF, patients with low LVEF had higher MEE (median, 167 versus 73 cal/minute, P < 0.05) and lower PGC-1α (1.71 ± 0.65 versus 1.95 ± 0.91 ng/mL, P = 0.032). Multivariate logistic regression analysis showed that MEE (OR = 0.517, 95% CI = 0.267-0.998, P = 0.049) and creatinine (OR = 2.704, 95% CI = 1.144-6.391, P = 0.023) were independently associated with increased PGC-1α. CONCLUSIONS: Serum PGC-1α was related to MEE and LVEF in patients with CHF and can reflect the degree of MEE and the systolic function of the left ventricle.

Catheter radiofrequency ablation for arrhythmias under the guidance of the Carto 3 three-dimensional mapping system in an operating room without digital subtraction angiography.

Several studies have reported the efficacy of a zero-fluoroscopy approach for catheter radiofrequency ablation of arrhythmias in a digital subtraction angiography (DSA) room. However, no reports are available on the ablation of arrhythmias in the absence of DSA in the operating room. To investigate the efficacy and safety of catheter radiofrequency ablation for arrhythmias under the guidance of a Carto 3 three-dimensional (3D) mapping system in an operating room without DSA. Patients were enrolled according to the type of arrhythmia. The Carto 3 mapping system was used to reconstruct heart models and guide the electrophysiologic examination, mapping, and ablation. The total procedure, reconstruction, electrophysiologic examination, and mapping times were recorded. Furthermore, immediate success rates and complications were also recorded. A total of 20 patients were enrolled, including 12 males. The average age was 51.3 ±â€Š17.2 (19-76) years. Nine cases of atrioventricular nodal re-entrant tachycardia, 7 cases of frequent ventricular premature contractions, 3 cases of Wolff-Parkinson-White syndrome, and 1 case of typical atrial flutter were included. All arrhythmias were successfully ablated. The procedure time was 127.0 ±â€Š21.0 (99-177) minutes, the reconstruction time was 6.5 ±â€Š2.9 (3-14) minutes, the electrophysiologic study time was 10.4 ±â€Š3.4 (6-20) minutes, and the mapping time was 11.7 ±â€Š8.3 (3-36) minutes. No complications occurred. Radiofrequency ablation of arrhythmias without DSA is effective and feasible under the guidance of the Carto 3 mapping system. However, the electrophysiology physician must have sufficient experience, and related emergency measures must be present to ensure safety.

Increased serum 2-oxoglutarate associated with high myocardial energy expenditure and poor prognosis in chronic heart failure patients.

Myocardial energy expenditure (MEE) and 2-oxoglutarate are elevated in chronic heart failure (CHF) patients compared with healthy controls. To explore whether 2-oxoglutarate could reflect the levels of MEE and predict the prognosis of CHF, 219 CHF patients and 66 healthy controls were enrolled. 2-Oxoglutarate was assayed with Liquid Chromatography-Mass Spectrometry/Mass Spectrometry (LC/MS/MS). CHF patients were divided into 4 groups according to interquartile range of MEE and followed for death or recurrent hospital admission due to CHF for the mean follow-up time 6.64±0.16months. 2-Oxoglutarate was increased in CHF patients compared with controls (P<0.01) and correlated with estimated glomerular filtration rate (r=0.142, P=0.036), age (r=-0.269, P<0.01) and MEE levels (r=0.307, P<0.01) in a multiple linear correlation analysis in CHF patients. Furthermore, 2-oxoglutarate (OR=3.470, 95% CI=1.557 to 7.730, P=0.002), N-terminal pro-B-type natriuretic peptide (OR=4.013, 95% CI=1.553 to 10.365, P=0.004), age (OR=1.611, 95% CI=1.136 to 2.283, P=0.007) and left ventricular ejection fraction (OR=7.272, 95% CI=3.110 to 17.000, P<0.001) were independently associated with MEE on multiple logistic regression analysis. Kaplan-Meier event curves showed that high 2-oxoglutarate levels were associated with adverse outcomes (Log Rank, Chi(2)=4.026, P=0.045). This study showed that serum 2-oxoglutarate is associated with MEE levels, which can be used as potential biomarkers for MEE, and it can reflect the clinical severity and short-term outcome of CHF.

1H-NMR-based metabolic analysis of human serum reveals novel markers of myocardial energy expenditure in heart failure patients.

OBJECTIVE: Elevated myocardial energy expenditure (MEE) is related with reduced left ventricular ejection fraction, and has also been documented as an independent predictor of cardiovascular mortality. However, the serum small-molecule metabolite profiles and pathophysiological mechanisms of elevated MEE in heart failure (HF) are still lacking. Herein, we used 1H-NMR-based metabolomics analysis to screen for potential biomarkers of MEE in HF. METHODS: A total of 61 subjects were enrolled, including 46 patients with heart failure and 15 age-matched controls. Venous serum samples were collected from subjects after an 8-hour fast. An INOVA 600 MHz nuclear magnetic resonance spectrometer with Carr-Purcell-Melboom-Gill (CPMG) pulse sequence was employed for the metabolomics analysis and MEE was calculated using colored Doppler echocardiography. Metabolomics data were processed using orthogonal signal correction and regression analysis was performed using the partial least squares method. RESULTS: The mean MEE levels of HF patients and controls were 139.61±58.18 cal/min and 61.09±23.54 cal/min, respectively. Serum metabolomics varied with MEE changed, and 3-hydroxybutyrate, acetone and succinate were significantly elevated with the increasing MEE. Importantly, these three metabolites were independent of administration of angiotensin converting enzyme inhibitor, ß-receptor blockers, diuretics and statins (P>0.05). CONCLUSIONS: These results suggested that in patients with heart failure, MEE elevation was associated with significant changes in serum metabolomics profiles, especially the concentration of 3-hydroxybutyrate, acetone and succinate. These compounds could be used as potential serum biomarkers to study myocardial energy mechanism in HF patients.

[Effect of different doses of perindopril on myocardial energy expenditure in patients with heart failure following myocardial infarction].

OBJECTIVE: To investigate the changes of myocardial energy expenditure in patients with heart failure following myocardial infarction after treatment with different doses of perindopril. METHODS: Sixty-three patients with heart failure after myocardial infarction were treated with perindopril for 12 months at the doses of 4 mg (group N) and 8 mg (group H). Doppler imaging was used to measure the structural and systolic functional parameters before and after the treatment, and the circumferential end-systolic wall stress (cESS) and myocardial energy expenditure (MEE) were calculated. The biochemical indicators including serum creatinine and plasma NT-proBNP were detected before and after the treatment. RESULTS: The two groups had similar measurements before treatment. After 12 months of perindopril treatment, the patients in group N showed higher LA, LV, RA, RV, LVIDs, AD, cESS, lgNT-proBNP, and MEE with lower LVFS and LVEF than those in group H. Compared to those before treatment, LVFS and LVEF were increased and LA, LV, RA, RV, AD, LVIDs, LVMI, lgNT-proBNP and MEEm lowered after the 12-month treatment in group H. Significant changes were also found in the measured parameters except for PWTs, LVET, LVSV and LVFS in group N after the treatment. Bivariate analysis showed a significant positive correlation between MEE and lgNT-proBNP (r=0.513, P<0.01). CONCLUSION: A 12-month treatment with perindopril can suppress myocardial remodeling, improve left ventricular systolic function, and lower NT-proBNP and myocardial energy expenditure in patients with heart failure after myocardial infarction, and a higher dose can produce better results.

[Value of Doppler echocardiography derived myocardial energy expenditure measurements in chronic heart failure patients].

OBJECTIVE: To evaluate the relationship between myocardial energy expenditure (MEE) level and cardiac function in chronic heart failure (CHF) patients. METHODS: A total of 99 CHF patients were divided into 3 groups according to the LVEF (HFNEF > or = 50%, n = 37; HFREF1 35.1% - 49.9%, n = 30; HFREF2 < or = 35%, n = 32) or the New York Heart Association (NYHA II, n = 26; III, n = 42; IV, n = 31) criteria. Thirty patients with cardiovascular disease and without CHF served as controls. Routine examinations including serum CRP (ELISA) and plasma NT-proBNP (chemiluminescence sandwich ELISA) were made on the next morning after admission; echocardiography was performed on the third day after admission. LVMW, LVMWI, RWT, LVIDd, LA, LV, LVEF, LVFS, E/A, EDT, IVRT, Tei index and MEE were measured or calculated. RESULTS: MEE was significantly higher in HFREF patients than in controls (P < 0.01) and similar between HFNEF patients and controls (P > 0.05). MEE increased in proportion to decrease of LVEF and increase of NYHA grades in CHF patients (all P < 0.05). Bivariate analysis confirmed that MEE was significant correlated with LVMW, LVMWI, RWT, LVIDd, LA, LV, LVEF (r = -0.540, P < 0.01), LVFS (r = -0.454, P < 0.01), E/A, EDT, IVRT, Tei index, NYHA grades, CRP and NT-proBNP. CONCLUSION: MEE derived from standard echocardiographic measurements is an effective indicator for myocardial bioenergetics and significantly correlated with cardiac function in CHF patients, especially in CHF patients with reduced LVEF.