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Vicente Climent

Publications and source records attributed to Vicente Climent.

27 records · Page 2Linked to original sources
PubMed2003

Is thrombogenesis in atrial fibrillation related to matrix metalloproteinase-1 and its inhibitor, TIMP-1?

BACKGROUND AND PURPOSE: Decreased matrix metalloproteinase-1 (MMP-1) and increased levels of its inhibitor, tissue inhibitor of matrix metalloproteinase-1 (TIMP-1), reflect impaired matrix degradation with an increase in fibrosis. A prothrombotic state has been described in atrial fibrillation (AF), increasing the risk of stroke and thromboembolism. Because structural abnormalities and remodeling of atria have been observed in AF, we hypothesized that the prothrombotic state in AF may be related to abnormal indexes of matrix degradation. METHODS: We studied 48 consecutive patients (30 men; age, 70.5+/-9.0 years) with chronic nonrheumatic AF who were not on anticoagulation. Plasma levels of MMP-1, TIMP-1, and prothrombin fragment 1+2 (F1+2, an index of thrombogenesis) were measured by enzyme-linked immunosorbent assay. M-mode, 2-dimensional, and Doppler echocardiographic studies were performed in all patients. Research indexes were compared with data from 32 control subjects in sinus rhythm who were of similar age and sex. RESULTS: Patients with AF had lower levels of MMP-1 (P=0.011) but increased levels of TIMP-1 (P=0.033) and F1+2 (P<0.001) and a higher ratio of TIMP-1 to MMP-1 (P=0.009) compared with control subjects. After adjustment for sex, age, hypertension, and diabetes, TIMP-1 levels and the ratio of TIMP-1 to MMP-1 correlated with F1+2 levels (r=0.24, P=0.038; and r=0.26, P=0.023, respectively). In multivariate analysis, there was no independent relationship between MMP-1, TIMP-1, or ratio of TIMP-1 to MMP-1 and the presence of AF. CONCLUSIONS: Patients with AF have evidence of impaired matrix degradation, but this was not independently associated with the presence of AF on multivariate analysis. However, an independent relationship was found between the MMP/TIMP system and prothrombotic state (assessed by F1+2 levels).

Aged↗
PubMed2003

[Assessment of three activity questionnaires in patients with heart failure].

The activity questionnaire most frequently used in heart failure, the New York Heart Association Classification, does not correlate well with peak oxygen uptake. The correlation of this variable with other activity questionnaires was analyzed in 83 patients (69 with heart failure and 14 control patients), 61.5 11 years old, who were interviewed and classified according to the Canadian Cardiovascular Society Classification. The Dyspnea-Fatigue Index and functional capacity according to the Specific Activity Questionnaire were determined for each patient. Subsequently, the treadmill cardiopulmonary exercise test (Naughton) was performed and the following correlations with peak oxygen uptake were found: Canadian Cardiovascular Society, r = 0.39; Dyspnea-Fatigue Index, r = 0.44; Specific Activity Questionnaire, r = 0.38. p < 0.001 for all three. The Dyspnea-Fatigue Index yielded the best correlation, although it was only slightly better than the Canadian Cardiovascular Society Classification, which is easier to obtain.

Adult↗
PubMed2003

[Prognostic value of serum levels of tumor necrosis factor-alpha in patients with heart failure].

INTRODUCTION AND OBJECTIVE: Tumor necrosis factor-alpha is an inflammatory cytokine which rises in heart failure and has prognostic value in severe cases. Its value is less established in moderate cases. Our aim was to determine its prognostic value in cases from a community hospital. PATIENTS: We studied 50 patients, average age 59.5 12.3 years, with dilated cardiomyopathy (72% non-ischemic) and moderate heart failure (59% functional class II). METHODS: Patients were evaluated with an echocardiogram and cardiopulmonary treadmill stress test (Naughton), muscular strength measurements (hand dynamometer), blood tumor necrosis factor levels, and an average follow-up of 17.5 9 months (range, 1-29 months). All causes of mortality, cardiac transplantation, and readmissions for heart failure were recorded. RESULTS: Twenty-three patients experienced events. These patients were older (63 +/- 12.7 vs 55.7 +/- 11.4 years; p = 0.042), had a lower peak VO2 (13.7 +/- 3.9 vs 16 +/- 3.3 ml/kg/min; p = 0.035), and higher peak VE/VCO2 and factor levels [41.9 +/- 10.6 vs 33.2 +/- 5.7; p = 0.001 and 4.3 (3.1-7.9) vs 3.3 (2.4-4.3) pg/ml; p = 0.021, respectively]. In the Cox model, the only variable with independent prognostic value was peak VE/VCO2 [HR 1.13 (1.07-1.19); p < 0.001]. The best cutoff point was 34.5 (sensitivity, 86.4%; specificity, 58.3%; p = 0.0007). The cytokine had no independent prognostic value. CONCLUSIONS: Our patients with events were older, had a lower peak VO2, and higher peak VE/VCO2 and serum tumor necrosis factor levels. However, only peak VE/VCO2 had independent prognostic value.

Body Mass Index↗
PubMed2003

[NT-proBNP and atrioventricular plane displacement. Relationship and diagnostic implications].

INTRODUCTION AND OBJECTIVES: NT-proBNP is useful in the diagnosis of heart failure and ventricular dysfunction. Left atrioventricular plane displacement (AVPD) is a consolidated index of ventricular function. Our objective was to carry out a multicenter population-based study to establish the relationship between plasma NT-proBNP levels with AVPD values. PATIENTS AND METHOD: We studied 215 subjects (age 66 9 years; 57.7% women) chosen from a random sample of 432 people from the Community of Valencia, who previously reported suffering from some degree of dyspnea. Doppler echocardiography was done, AVPD was calculated and plasma NT-proBNP concentrations were determined. All studies were completed in 194 patients. RESULTS: For the whole population NT-proBNP was 88 (0-2,586) pg/ml and AVPD was 11.9 1.6 mm. NT-proBNP concentration correlated well with AVPD (r = 0.44; p < 0.00001), and higher peptide levels were obtained in AVPD quartiles that indicated less displacement (p < 0.05). When NT-proBNP values were grouped according to their association with AVPD lower or higher than the 50th percentile AVPD, the difference was significant at p < 0.01. When AVPD values lower and higher than 10 mm were compared, NT-proBNP values were higher in persons with AVPD lower than 10 mm (p < 0.05). CONCLUSIONS: This population study found higher NT-proBNP concentrations in subjects with lower AVPD, and illustrates the potential diagnostic usefulness of NT-proBNP in clinical practice.

Aged↗
PubMed2002

Induction of cardiogenesis by Hensen's node and fibroblast growth factors.

The earliest events underlying cardiac induction and morphogenesis remain largely unknown. In the present study, we show that Hensen's node, the organizer of the avian embryo, induces cardiogenesis. Specifically, following heterotopic transplantation, Hensen's node induces ectopic host tissue that expresses two early cardiac markers ( cNkx-2.5 and cNkx-2.8), as well as a ventricular marker ( VMHC1), but not an atrial marker ( AMHC1). Moreover, we examine the potential roles of candidate growth factors known to be secreted by Hensen's node. Our results show that fibroblast growth factors (FGF-2 and FGF-4) when ectopically expressed can initiate cardiac development, inducing host tissue to express the two cardiac transcription factors cNkx-2.5 and cNkx-2.8, as well as the cardiac-restricted structural gene VMHC1, but not AMHC1. In contrast to FGFs, TGFbeta family members fail to induce ectopic tissue and expression of cardiac marker genes. We also examined the effects of growth factors on the morphogenesis of the host embryo's heart. Both exogenous FGFs and TGFbeta family members perturb normal morphogenesis of the early cardiac tube and alter patterns of ventricular and atria gene expression in characteristic ways. Namely, exogenous FGFs expand areas expressing the ventricular marker VMHC1 at the expense of areas expressing the atrial marker AMHC1. Conversely, exogenous TGFbeta1 inhibits expression of VMHC1, expanding AMHC1 expression. We show here that Hensen's node and FGFs induce ectopic expression of cardiac lineage markers, and that FGF and TGFbeta family members can modulate early development of the heart. Collectively, these data suggest that the organizer plays a crucial role in cardiac induction and morphogenesis, mediated in part by endogenous members of the FGF and TGFbeta families.

Animals↗
PubMed2002

[Acute myocardial failure in a young man: Q-fever myocarditis].

Coxiella burnetii myocarditis is a rare but severe clinical form of acute Q fever. We report the case of a 40-year-old man hospitalized for acute febrile syndrome. Forty-eight hours later, he presented dyspnea, orthopnea, and paroxysmal nocturnal dyspnea; cardiac auscultation revealed a third sound and echocardiography showed a diffusely hypokinetic and dilated left ventricle (30% ejection fraction). Serological studies showed antibodies against phase-II C. burnetii antigens (IgG titer 1:320 and IgM 1:50). The patient was treated with losartan, furosemide, and clarithromycin, resulting in rapid improvement. Six months after admission, the echocardiographic changes had completely disappeared.

Acute Disease↗
PubMed2002

[Annexin V levels in survivors of early myocardial infarction].

INTRODUCTION AND OBJECTIVES: Annexin V has an anticoagulant effect in vitro that derives from its ability to displace coagulation proteins from phospholipid surfaces, prolonging phospholipid-dependent coagulation reactions. Antiphospholipid antibodies (APL) and annexin V have an affinity for anionic phospholipids, so it has been hypothesized that one of the thrombotic mechanisms of APL may be due to displacement of annexin V from phospholipid surfaces. We studied plasma annexin V levels and analyzed its relationship to risk factors and several blood markers. PATIENTS AND METHOD: We studied 62 patients < 45 years old who had suffered myocardial infarction. The control group comprised 23 healthy subjects of similar age and sex. We analyzed the presence of APL, anti-beta2 glycoprotein I (beta2-GPI), anti-beta2-GPI/phospholipid complexes and anti-annexin V antibodies. We determined plasma annexin V levels. Cholesterol, HDL-cholesterol, triglycerides, antigenic tissue plasminogen activator and its inhibitor, von Willebrand factor, and fibrinogen levels were measured. RESULTS: We detected only 2 patients with positive anti-beta2-GPI/phospholipid complexes and 2 patients with positive anti-annexin V antibodies. We did not detect any positive APL or anti-beta2-GPI antibodies. In the control group there was only 1 patient with positive APL and anti-beta2-GPI antibodies. The myocardial infarction group showed significantly lower levels of annexin V than the control group: 0.640 ng/ml (0.520-0.818 ng/ml) vs 1.570 ng/ml (1.140-2.390 ng/ml), p < 0.01. There were no statistical associations between annexin V levels and other variables. CONCLUSIONS: The low levels of annexin V in young myocardial infarction patients could indicate a procoagulant trend. This hypercoagulable state was unrelated to the presence of APL.

Adult↗