Vicent Bodí

University of Valencia, Valenza, Valencia, Spain

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Publications (162)624.47 Total impact

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    ABSTRACT: Aims: Galectin-3 (Gal-3) and carbohydrate antigen 125 (CA125) have emerged as robust prognostic biomarkers in heart failure. Experimental data have also suggested a potential molecular interaction between CA125 and Gal-3; however, the biological and clinical relevance of this interaction is still uncertain. We sought to evaluate, in patients admitted for acute heart failure, the association between plasma Gal-3 with all-cause mortality and the risk for rehospitalizations among high and low levels of CA125. Methods and results: We included 264 consecutive patients admitted for acute heart failure to the Cardiology Department in a third-level center. Both biomarkers were measured on admission. Negative binomial and Cox regression models were used to evaluate the prognostic effect of the interaction between Gal-3 and CA125 (dichotomized by its median) with hospital readmission and all-cause mortality, respectively. During a median follow-up of 2 years (IQR = 1-2.8), 108 (40.9%) patients deaths and 365 rehospitalizations in 171 (69.5%) patients were registered. In a multivariable setting, the effect of Gal-3 on mortality and rehospitalization was differentially mediated by CA125 (p = 0.007 and p<0.001, respectively). Indeed, in patients with CA125 above median (>67 U/ml), values across the continuum of Gal-3 showed a positive and almost linear relationship with either the risk of death or rehospitalization. Conversely, when CA125 was below median (≤67 U/ml), Gal-3 lacked any prognostic effect on both endpoints. Conclusion: In patients with acute heart failure, Gal-3 was strongly associated with higher risk of long-term mortality and repeated rehospitalizations, but only in those patients exhibiting higher values of CA125 (above 67 U/ml).
    Full-text · Article · Apr 2015 · PLoS ONE
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    ABSTRACT: Tricuspid regurgitation (TR) is a common echocardiographic finding that has been related to adverse outcome under various clinical scenarios. Nevertheless, evidence supporting its prognostic value in heart failure (HF) is scarce, and, in most cases, contradictory. We evaluated the association of TR grade with 1-year all-cause mortality in acute HF (AHF).Methods and Results:We included 1,842 consecutive patients admitted for AHF. Mean age was 72.8±11.3 years, 51% were female and 45.5% had LVEF <50%. The severity of TR was graded in non-TR, mild (1), moderate (2), moderate-severe (3) and severe (4). At 1-year follow-up, 370 patients (20.1%) had died. In patients with LVEF ≥50%, a significant and positive association between TR severity and mortality was noted. Indeed, the HR for mortality for TR 3 and 4 vs. no TR/TR 1 were as follows: hazard ratios (HR), 1.68; 95% confidence intervals (95% CI): 1.08-2.60, P=0.02; and HR, 2.87; 95% CI: 1.61-5.09, P<0.001, respectively. In contrast, no association between TR grade and mortality (P=0.650) was observed in patients with LVEF <50% (P-value for interaction=0.033). A differential prognostic effect of TR severity on 1-year mortality was observed for LVEF HF status. The association was significant only in patients with LVEF ≥50%, with increasing mortality risk as TR became more severe.
    Full-text · Article · Apr 2015 · Circulation Journal
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    ABSTRACT: Background: Traditionally, procalcitonin (PCT) is considered a diagnostic marker of bacterial infections. However, slightly elevated levels of PCT have also been found in patients with heart failure. In this context, it has been suggested that PCT may serve as a proxy for underrecognized infection, endotoxemia, or heightened proinflammatory activity. Nevertheless, the clinical utility of PCT in this setting is scarce. We aimed to evaluate the association between PCT and the risk of long-term outcomes. Methods and results: We measured at admission PCT of 261 consecutive patients admitted for acute heart failure (AHF) after excluding active infection. Cox and negative binomial regression methods were used to evaluate the association between PCT and the risk of death and recurrent rehospitalizations, respectively. At a median follow-up of 2years (IQR: 1.0-2.8), 108 deaths, 170 all-cause rehospitalizations and 96 AHF-rehospitalizations were registered. In an adjusted analysis, including well-established risk factors such as natriuretic peptides and indices of renal function, the logarithm of PCT was associated with a higher risk of death (HR=1.43, CI 95%: 1.12-1.82; p=0.004), all-cause rehospitalizations (IRR=1.22, CI 95% 1.02-1.44; p=0.025) and AHF-rehospitalizations (IRR=1.28, CI 95%: 1.02-1.61; p=0.032). The association with these endpoints persisted after adjustment for other inflammatory biomarkers such as white blood cells, C-reactive protein and interleukins. Conclusion: In patients with AHF and no evidence of infection, PCT was independently and positively associated with the risk of long-term death and recurrent rehospitalizations.
    Full-text · Article · Jan 2015 · European Journal of Internal Medicine

  • No preview · Article · Jan 2015 · Cardiology
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    ABSTRACT: Aims: Fluid overload is a hallmark in acute heart failure (AHF). Bioelectrical impedance vector analysis (BIVA) has emerged as a noninvasive method for quantifying patients' hydration. We aimed to evaluate the effect of BIVA hydration status (BHS) measured before discharge on mortality and rehospitalization for AHF. Methods: We included 369 consecutive patients discharged from the cardiology department from a third-level hospital with a diagnosis of AHF. On the basis of BHS, patients were grouped into three categories: hyper-hydration (>74.3%), normo-hydration (72.7-74.3%) and dehydration (<72.7%). Appropriate survival techniques were used to evaluate the association between BHS and the risk of death and readmission for AHF. Results: At a median follow-up of 12 months (interquartile range, IQR: 5-19), 80 (21.7%) deaths and 93 (25.2%) readmissions for AHF were registered. The mortality and readmission rates for the BHS categories were hyper-hydration (3.28 and 3.83 per 10 persons-years); normo-hydration (1.43 and 2.68 per 10 persons-years); and dehydration (2.24 and 2.53 per 10 persons-years) (P < 0.05 for all comparisons). In an adjusted analysis, BHS displayed a significant association with mortality (P = 0.004), with a higher mortality risk in those with hyperhydration. Likewise, BHS showed to linearly predict AHF-readmission risk [hazard ratio 1.06 (1.03-1.10); P = 0.001 per increase in 1%]. Conclusion: In patients admitted with AHF, BHS assessed before discharge was independently associated with the risk of death and AHF-readmission.
    Full-text · Article · Oct 2014 · Journal of Cardiovascular Medicine
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    ABSTRACT: Background: The changes in renal function that occurred in patients with acute decompensated heart failure (ADHF) are prevalent, and have multifactorial etiology and dissimilar prognosis. To what extent the prognostic role of such changes may vary according to the presence of renal insufficiency at admission is not clear. Accordingly, we sought to determine whether early creatinine changes (ΔCr) (admission to 48-72 hours) had an effect on 1-year mortality relative to the presence of renal insufficiency at admission. Methods: We included 705 consecutive patients admitted with the diagnosis of ADHF. Admission renal insufficiency was defined as serum creatinine ≥1.4mg/dl (A-RIcr) or estimated glomerular filtration rate <60ml/min/1.73m(2) (A-RIGFR). Appropriate survival regression techniques were used. Results: The mean age was 72.9±11.4 years and 51.2% were males. Patients with admission renal insufficiency (24.7% and 42.8% for A-RIcr and A-RIGFR, respectively) had higher prevalence of extreme values in ΔCr in either direction (increasing/decreasing). At 1-year follow-up, 114 (16.2%) deaths were registered. The multivariable analysis showed a significant interaction between admission renal insufficiency and ΔCr (p=0.004 and p=0.019 for A-RIcr and A-RIGFR, respectively). In the presence of renal insufficiency, the continuum of ΔCr followed a positive and almost linear relationship with mortality risk. Conversely, in patients without renal insufficiency, those changes adopted a 'J-shape' trajectory with increased mortality at both ends of the curve distribution. Conclusions: In patients with ADHF the effect of ΔCr on 1-year mortality varied according to its magnitude and the presence of admission renal insufficiency. There was a graded-association with mortality when renal insufficiency was present on admission.
    Full-text · Article · Jul 2014 · European Heart Journal: Acute Cardiovascular Care
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    ABSTRACT: Purpose: Fibrosis plays a key role in the pathophysiology of left ventricular (LV) remodelling after myocardial infarction (MI). The dynamics of this process and whether it is a localized or diffuse phenomenon has not been totally clarified. We aimed to characterize these issues in a swine model of reperfused anterior MI. Methods: Swine were subjected by means of percutaneous balloon inflation to a transient 90-min occlusion of mid left anterior descending artery followed by 72-h (acute MI model) or 1-month (chronic MI model) reperfusion. The extent of fibrosis was macroscopically (triphenyltetrazolium staining, % of LV volume) and microscopically (Sirius red staining, % of field) quantified in the infarct, adjacent and remote areas as well as in controls. TGF-β1, collagen1-A1, A2 and 3A1 gene expression was determined. Results: Macroscopically, necrosis (16±5% in the acute MI model) and fibrosis (16±4% in the chronic MI model) were detected in all cases. Macroscopic fibrosis occurred in the infarct but not in the adjacent or remote areas (Figure). At microscopic level, in comparison with controls, fibrosis was only significantly increased in the chronic MI model at the infarct area (35±4%, p<0.001) but not in the acute MI model or in the adjacent and remote areas in the chronic MI model (<4% in all cases, p=ns, Figure). TGF-β1 (p<0.05, acute and chronic MI models, Figure) and collagen1-A1, A2 and 3A1 (p<0.001, chronic MI model) gene expression were significantly increased in the infarct but not in the adjacent or remote areas (p=ns). Conclusion: In a model of anterior MI, 1-month after reperfusion, at macroscopic, microscopic and molecular levels, myocardial fibrosis appears as a localized process which mainly affects the infarct area but not the adjacent or remote regions.
    Preview · Article · Jul 2014 · Cardiovascular Research
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    ABSTRACT: Purpose: In the context of myocardial infarction (MI) the availability of metabolites is clearly restricted, therefore a fuel metabolic shifts takes place. Previous studies have indicated that peroxisome proliferator activated receptor co-activator alpha (PGC-1α) pathway is a crucial regulator of cardiac metabolism in response to cardiac stress. Here we address the role of PGC-1α in regulating metabolic changes of MI. Methods: We studied a group of 12 common swine in which anterior MI was induced by means of angioplasty balloon inflation. A series of 6 swine were sacrificed at 48h post-infarction (acute infarction group) and another series of 6 swine were sacrificed at 3 weeks (chronic infarction group). Metabolites such as: glucose, pyruvate, ketone bodies, and lipids were analyzed in serum (mmol/L) at baseline, 75 min after balloon inflation, 2 h, 48 h and 3 weeks after reperfusion by means of enzymatic analysis. Results were compared to baseline levels. Genes related to PGC-1α such as: PGC-1α, ERR-α, PPAR-α, and HIF-1α, were analysed (fold change) in infarcted, adjacent and remote areas of porcine hearts 48h or 3 weeks post-infarction by molecular biology. Results were compared to 5 control swine without infarction. Results: In all groups, after 2h of infarction, a striking increase of lactate (3.2 ± 0.6 vs. 0.8 ± 0.3) and non-esterified fatty acids (0.6 ± 0.2 vs. 1.8 ± 0.3) was observed in serum compared to baseline (p<0.001 in both cases). Conversely, a significant decrease of glucose (5.2 ± 0.3 vs. 3.8 ± 0.2) and β-Hydroxybutyrate (1.8 ± 0.5 vs. 0.6 ± 0.2) occurred at the same time (p<0.001 in both cases). All values reverted progressively to baseline after 3 weeks. In comparison with controls, molecular biology analysis of acute infarcted hearts revealed a significant decrease of expression in mRNA and protein levels of transcription factors related to lipid and mitochondrial metabolism: PGC-1α(0.3 ± 0.1 vs. 1.2 ± 0.2 fold), ERR-α(0.8 ± 0.3 vs. 1.6 ± 0.2 fold) and PPAR-α(0.9 ± 0.3 vs. 1.7 ± 0.2 fold) (p<0.01 in all cases). Values didn't change after 3 weeks. However genes related to glucose metabolism were significantly increased in acute infarcts compared to controls: GLUT-1 (3.8 ± 0.4 vs. 1.1 ± 0.3 fold), HIF-1α(4.2 ± 1.3 vs. 1.0 ± 0.2 fold) (p<0.01 in both cases). These values recovered control levels after 3 weeks. Conclusion: A metabolic deregulation mediated by PGC-1α decreased expression takes place in the context of acute MI. This is mediated by a decrease of fatty acid oxidation and an increase of glucose utilization and it reverts after 3 weeks.
    Full-text · Article · Jul 2014 · Cardiovascular Research
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    ABSTRACT: Programmed death-1 (PD-1) and Programmed death-1 ligand (PD-L1) regulate immune response. Previous studies associate an immune deregulation in ST-elevation myocardial infarction STEMI. We recruited 100 patients with a first STEMI treated with reperfusion. In all patients PD-1 and PD-L1 expression was studied 24 h post-reperfusion in peripheral blood mononuclear cells (PBMCs), by means of flow cytometry and molecular biology. PD-1 and PD-L1 expression was serially analyzed in the first 20 patients before reperfusion and 24h, 96h and 30 days afterwards. Results were compared with 30 age- and sex-matched controls. Cardiac Magnetic Resonance was used to quantify infarct size 1-week after infarction. In a series of 8 swine with induced STEMI, PD-1 and PD-L1 expression was analyzed at baseline, 90 min after balloon inflation, 2 h and 24 h after reperfusion in PBMCs, and in swine hearts. Results were compared to 5 controls. In patients, in comparison with controls, a significant decrease of PD-1 expression [mRNA fold change 0.8 ± 0.3 vs. 1.2 ± 0.6] and an increase of PD-L1+ expression [mRNA fold change 2.7 ± 2.1 vs. 0.9 ± 0.5] was observed 24h after infarction in PBMCs (p <0.05). STEMI patients with large infarct size showed decreased PD-1 expression, PD-L1 did not changed (Figure 1). Both in patients and swine, showed a significant increase of PD-1 and PD-L1 expression before reperfusion. Swine hearts revealed a marked infiltration of PMBCs and a significant increase of PD-1 and PD-L1 expression in the infarcted area compared to controls (Figure 2) Acute changes in the PD-1 pathway take place in acute STEMI. A lesser expresion of PD-1 in peripheral blood, which could be due to myocardial infiltration in the infarcted area of PBMCs, associates with a larger infarct size.
    Preview · Article · Jul 2014 · Cardiovascular Research
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    ABSTRACT: Purpose: Using cardiac imaging techniques it has been demonstrated that, after successful coronary revascularization of acute myocardial infarction (MI), microvascular obstruction (MVO) resolves spontaneously. Data on the course of this process in “in vivo” models are scarce. We aimed to characterize the dynamics of MVO in a swine model of reperfused anterior MI. Methods: Swine were subjected, by means of percutaneous balloon inflation, to a transient 90-min occlusion of mid left anterior descending artery followed by 72-h (acute MI model) or 1-month (chronic MI model) reperfusion. Area at risk (thioflavin-S staining) and the extent of MVO (% of area at risk without thioflavin-S staining) were quantified. Microvessel density (using immunohistochemistry by von Willebrand factor antibody, vessels/field) and the expression of Hypoxia Induced Factor-1α (HIF-1α mRNA) were determined in controls and in the acute and chronic MI models. Results: In the acute MI model, MVO (8.4±4.5%) was detected in all cases. MVO significantly decreased in the chronic MI model (0.14±0.09%, p <0.001 vs. acute MI model, Figure). Microvessel density was significantly reduced in the acute MI model in comparison with the chronic MI model and controls (p <0.001, Figure). The expression of HIF-1α mRNA was significantly increased in the acute MI model in the infarct area (p<0.05 vs. controls) and in the chronic MI model in the infarct, adjacent and remote areas (p <0.01 vs. controls, Figure). Conclusion: In an “in vivo” controlled model of reperfused anterior MI, MVO spontaneously improves one month after reperfusion at macroscopic and microscopic levels. HIF could play a role in the molecular control of this process.
    No preview · Article · Jul 2014 · Cardiovascular Research
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    ABSTRACT: Background Tissue Doppler–derived transmitral to mitral annular early diastolic velocity ratio (E/Ea), as a noninvasive estimation of left ventricular (LV) filling pressures, is a strong prognosticator in various cardiac scenarios including chronic heart failure; nevertheless, its utility for risk stratification in the whole spectrum of acute heart failure (AHF) patients remains elusive. Thus, the aim of this study was to determine the association between E/Ea ratio and 1-year mortality in nonselected patients with AHF.Methods The study included 417 consecutive patients admitted for AHF. Twenty-two patients were excluded due to nonaccurate Ea measurements, leaving the final sample to be 395 patients. E-wave, septal, and lateral Ea velocities were measured following initial stabilization and according to current recommendations. The association of mean E/Ea ratio with all-cause mortality was assessed using Cox regression analysis.ResultsAt a median follow-up of 306 days (interquartile range, 118–564), 89 deaths (22.5%) were registered. Mean age and E/Ea ratio were 72 ± 11.5 and 20 ± 3. Proportion of LV ejection fraction ≥50% was 47%. In multivariate analysis, after adjusting for well-known prognostic factors, including natriuretic peptides, E/Ea ratio was linearly associated with an increase risk of all-cause mortality (HR 1.04, 95% CI 1.03–1.05; P < 0.001, per increase in one unit of E/Ea). The threshold of risk was identified above 20. No significant interactions among the most important subgroups were found.Conclusion In AHF patients, tissue Doppler imaging derived E/Ea ratio is independently associated with an increased risk of all-cause mortality.
    No preview · Article · May 2014 · Echocardiography
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    ABSTRACT: The use of loop diuretics in acute heart failure (AHF) is largely empirical and has been associated with renal function impairment by reducing renal perfusion but also renal improvement by decreasing renal venous congestion. Antigen carbohydrate 125 (CA125) has emerged as a proxy for fluid overload. We sought to evaluate whether the early changes in creatinine (ΔCr) induced by intravenous furosemide doses (ivFD) differ among clinical groups defined by overload status (CA125) and creatinine on admission (Cr). We included 526 consecutive patients admitted for AHF. All patients received intravenous furosemide for the first 48hours. CA125 and Cr were dichotomized at 35 U/ml and 1.4mg/dl, respectively, and grouped as follows: C1 [Cr <1.4, CA125 ≤35 (n=151)]; C2 [Cr <1.4, CA125 >35 (n=241)]; C3 [Cr ≥1.4, CA125 ≤35 (n=45)]; and C4 [Cr ≥1.4, CA125 >35 (n=89)]. Clinicians in charge of the management of patients were blind to CA125 values. ΔCr was estimated as the absolute difference in Cr between admission and 48-72 hours. Multivariable linear regression analysis was used for modeling purposes. The adjusted analysis showed a differential effect of ivFD on ΔCr. Per increase in 20mg/day of ivFD, the mean ΔCr was 0.010mg/dl (p=0.464) in C1, 0.002mg/dl (p=0.831) in C2, 0.045mg/dl (p=0.032) in C3, and -0.045mg/dl (p<0.001) in C4 (omnibus p<0.001). A similar pattern of response was observed in a validation cohort. In patients with AHF, the magnitude and direction of ΔCr attributable to ivFD were differentially associated with values of CA125 and Cr on admission.
    Full-text · Article · Apr 2014 · International journal of cardiology
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    Full-text · Article · Apr 2014 · International journal of cardiology
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    ABSTRACT: Background: Red blood cell distribution width (RDW) has been found to be an independent predictor for adverse outcome in patients with heart failure (HF), but there are no data on the association of longitudinal RDW with all-cause mortality and occurrence of anemia. Methods and results: 1,702 patients discharged from a previous admission for acute HF (AHF) were included. RDW was measured during the available longitudinal history of the patient. Joint modeling and Multistate Markov were used for the analysis. The median RDW at baseline was 15.0% (IQR: 14.0-16.5), and 45.6% of patients had anemia. At a median follow-up of 1.5 years (IQR: 0.45-3.25), 713 patients died. The last RDW-trajectory value and cumulative RDW-trajectory mean were predictive of mortality (HR, 1.18; 95% CI: 1.12-1.24; and HR, 1.12; 95% CI: 1.08-1.16, respectively; P<0.001 for both). This effect, however, varied according the anemia status (P for interaction<0.001), being more pronounced in absence of anemia [HR=1.31 (95% CI: 1.22-1.42) and HR=1.48 (95% CI: 1.33-1.64)] compared to those with anemia [HR=1.08 (95% CI: 1.04-1.13), 1.12 (95% CI: 1.06-1.18)]. Longitudinal RDW (per 1% increasing) was also independently associated with incident anemia [HR=1.10 (95% CI: 1.03-1.18) P=0.002]. Conclusions: Following an admission for AHF, higher longitudinal RDW values over time were associated to an increased risk for both developing anemia and dying. The effect on mortality was more pronounced among non-anemic patients.
    Full-text · Article · Nov 2013 · Circulation Journal
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    ABSTRACT: In recent years, there has been a proliferation of new biomarkers with potential prognostic implication in heart failure (HF). Nevertheless, most of them do not fulfill the required criteria for being used in daily clinical practice. Tumor marker antigen carbohydrate 125 (CA125), a glycoprotein widely used for ovarian cancer monitoring, is synthesized by epithelial serous cells in response to fluid accumulation and/or cytokine stimuli. This glycoprotein has been emerged as a potential biomarker in HF. Plasma CA125 correlates with clinical, hemodynamic, and echocardiographic parameters related to the severity of the disease. High levels have shown to be present in the majority of acutely decompensated patients, and in this setting, it has shown to be independently related to mortality or subsequent admission for acute HF. In addition, certain characteristics such as wide availability and the close correlation between plasma changes with disease severity and clinical outcomes have increased the interest of researchers about the potential of this glycoprotein for monitoring and guiding therapy in HF. In this article, we have reviewed the available evidence supporting the potential role of CA125 as a biomarker in HF.
    Full-text · Article · Aug 2013 · Heart Failure Reviews
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    ABSTRACT: -Infarct size (IS) determined by cardiovascular magnetic resonance (CMR) has proven an additional value, on top of left ventricular ejection fraction (LVEF), in prediction of adverse arrhythmic cardiovascular events (AACE) in chronic ischemic heart disease. Its value soon after an acute ST-elevation myocardial infarction (STEMI) remains unknown. Our aim was to determine whether early CMR can improve AACE risk prediction after acute STEMI. -Patients admitted for a first non-complicated STEMI were prospectively followed-up. A total of 440 patients were included. All of them underwent CMR 1 week after admission. CMR-derived LVEF and IS (g/m(2)) were quantified. AACE included post-discharge sudden death, sustained ventricular tachycardia (VT) and/or ventricular fibrillation (VF) either documented on ECG or recorded via an implantable cardiac-defibrillator (ICD). Within 2-years median follow-up, 11 AACE (2.5%) were detected: 5 sudden deaths (1.1%) and 6 spontaneous VT/VF. In the whole group AACE associated with more depressed LVEF (Adjusted HR [95% CI]: 0.90 [0.83-0.97], p< 0.01) and larger IS (adjusted HR [95% CI]: 1.06 [1.01-1.12], p= 0.01). According to the corresponding area under the receiver operating characteristics curve, LVEF ≤36% and IS ≥23.5g/m(2) best predicted AACE. The vast majority of AACE (10/11) occurred in patients with simultaneous depressed LVEF≤36% and IS≥23.5g/m(2) (n=39). -In the era of reperfusion therapies, occurrence of AACE in patients with an in-hospital non-complicated first STEMI is low. In this setting, assessment of an early CMR-derived IS could be useful for further optimization of AACE risk prediction.
    Full-text · Article · Aug 2013 · Circulation Cardiovascular Imaging
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    ABSTRACT: Purpose: Risk stratification in TAVI remains challenging. The use of biomarkers in this setting represents represent a promising tool. We studied the predictive value of tumor marker carbohydrate antigen 125 (CA125) before and after Transcatheter Aortic Valve Implantation (TAVI) for all-cause death and a composite endpoint of death, admission for heart failure, myocardial infarction and stroke (MACE). Methods: CA125 was measured in 228 patients before and after TAVI. The association with outcomes was assessed using parametric Cox regression and joint modeling for baseline and longitudinal analyses, respectively. CA125 was evaluated as logarithm transformation and dichotomized by its median value (M1:≤15.7 vs. M2:>15.7 U/ml). Results: At a median follow-up of 183 days [63-365] and 144 days [56-365], 50 patients (22%) died and 75 patients (33%) experienced MACE. A 3-fold increase in the rates for death (figure 1) and MACE was observed in patients above the median (M2 vs. M1) of CA125 (5.2 vs. 1.6 and 8.3 vs. 3.3 per 10 person-years, respectively; p for both <0.001). In a multivariable analysis adjusted for logistic EuroScore, NYHA class III/IV and device success, baseline values of CA125 (M2 vs. M1) independently predicted death (hazard ratio (HR)=2.18; 95% confidence interval (CI) [1.11-4.26]; p=0.023) and MACE (HR=1.77; 95% CI [1.05-2.98]; p=0.031). In the longitudinal analysis, lnCA125 as a time-varying exposure, was highly associated with both endpoints: HR=1.47; 95% CI (1.01-2.14); p=0.043 and HR=2.26; 95% CI (1.28-3.98); p=0.005, for death and MACE respectively.
    Full-text · Article · Aug 2013 · European Heart Journal
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    ABSTRACT: Purpose: Myocardial fibrosis plays a potential role in left ventricular remodeling and patients' outcome. After myocardial infarction innate immune cells infiltrate infarcted area and replace necrotic tissue by fibrotic tissue. However the role of adaptive immunity, especially T cells, has not yet been investigated in this scenario. Methods: We studied 94 patients with a first STEMI treated with percutaneous revascularization. Leucocyte subsets and a wide variety of lymphocyte subtypes were determined in peripheral blood 24 h after reperfusion by means of flow cytometry. Infarct size and cardiac fibrosis were measured by late enhancement Cardiac Magnetic Resonance (CRM) 1 week and 6 months after infarction. Results: Innate immune cells were significantly increased at 24 h post-reperfusion in patients with extensive infarction, considered as ≥30% of left ventricular mass at first week, with more neutrophils (9440±1980 vs 7910±1570) and monocytes (695±195 vs 549±120) cells/ul (p<0.05 in both cases). However, there were no significantly differences between innate immune cells and extensive cardiac fibrosis, considered as ≥30% of left ventricular mass at 6th month. Lymphocyte subsets did not relate with the extent of infarction (Figure A). But remarkably T cells were significantly decreased at 24 h post-reperfusion in patients with extensive cardiac fibrosis (Figure B). CD4+ cells dropped while CD8 did not change, a reduction of CD4 T cell effector cells occurred (CXCR3 cells and CCR4 cells) and anti-inflammatory CD4 T regulatory cells were also decreased in patients with extensive cardiac fibrosis (p<0.05 in all cases).
    Preview · Article · Aug 2013 · European Heart Journal
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    ABSTRACT: Purpose: Repaired tetralogy of Fallot (rtoF) patients are at risk of atrial or ventricular tachyarrhythmia and sudden cardiac death. We investigated the significance of right atrial (RA) and right ventricular (RV) anatomy and function for arrhythmia prediction by cardiac magnetic resonance imaging (CMR). Methods: One-hundred-and-fifty-four rtoF adults who underwent CMR were studied with the pre-specified endpoint of new-onset atrial or ventricular arrhythmia (sustained ventricular tachycardia/ventricular fibrillation) during a longitudinal follow-up. Results: Median age was 31 (IQR:22-40), median follow-up was 5.6 (IQR:4.6-7.0) years Atrial tachyarrhythmia (n=11) was predicted by maximal right atrial area indexed to body surface area (RAAi) on cine-CMR (Hazard ratio; HR1.17, 95%CI 1.07-1.28 per cm2/m2; P=0.0005, survival ROC curve analysis, area under curve; AUC 0.74[0.66-0.81]; cut-off value 16cm2/m2). Atrial arrhythmia-free survival was reduced in patients with RAAi ≥16cm2/m2 (Logrank; P=0.0001). RV restrictive physiology on echocardiography (n=38) related to higher RAAi (P=0.02) but did not predict atrial tachyarrhythmia (P=0.057). RV restrictive physiology patients had similar RV dilatation and exercise impairment to remaining patients representing a different phenotype from previous reports. Ventricular arrhythmia (n=9) was predicted by CMR RV outflow tract (RVOT) akinetic area length (HR1.05,95%CI 1.01-1.09 per mm; P=0.003, survival ROC analysis, AUC 0.77[0.83-0.61];cut-off value 30mm) and decreased RV ejection fraction (HR0.93 95%CI 0.87-0.99 per %; P=0.03, respectively). Ventricular arrhythmia-free survival was reduced in patients with RVOT akinetic region length >30mm (Logrank; P=0.02). Conclusions: RAAi predicts atrial arrhythmia and RVOT akinetic region length predicts ventricular arrhythmia in late follow-up of rtoF. These are simple, feasible measurements for serial surveillance and risk stratification of rtoF patients.
    Full-text · Article · Dec 2012 · European Heart Journal Cardiovascular Imaging
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    ABSTRACT: El reingreso precoz tras una hospitalización por insuficiencia cardiaca aguda (ICA) es frecuente, sin embargo, los factores asociados a este no están claramente establecidos. Los valores plasmáticos del antígeno carbohidrato 125 (CA125) han mostrado asociarse con la presencia de congestión sistémica y aumento del riesgo de muerte en pacientes con ICA. El objetivo de este trabajo fue determinar la relación entre los valores de CA125 (durante el ingreso, en la primera visita ambulatoria o sus cambios) y el reingreso por ICA a 6 meses de seguimiento.
    No preview · Article · Nov 2012 · Medicina Clínica

Publication Stats

2k Citations
624.47 Total Impact Points

Institutions

  • 2005-2015
    • University of Valencia
      • Department of Pathology
      Valenza, Valencia, Spain
  • 1995-2015
    • Hospital Clínico Universitario de Valencia
      Valenza, Valencia, Spain
  • 2010-2014
    • Fundación de Investigación del Hospital Clínico Universitario de Valencia INCLIVA
      Valenza, Valencia, Spain
  • 1999-2000
    • Hospital Marina Baixa
      Villajoyosa, Valencia, Spain