Fluorescent advanced glycation end products and their soluble receptor: the birth of new plasmatic biomarkers for risk stratification of acute coronary syndrome.

OBJECTIVE: Advanced glycation end products (AGEs) have pathophysiological implications in cardiovascular diseases. The aim of our study was to evaluate the prognostic value of fluorescent AGEs and its soluble receptor (sRAGE) in the context of acute coronary syndrome (ACS), both in-hospital phase and follow-up period. METHODS: A prospective clinical study was performed in patients with debut's ACS. The endpoints were the development of cardiac events (cardiac deaths, re-infarction and new-onset heart failure) during in-hospital phase and follow-up period (366 days, inter-quartile range: 273-519 days). 215 consecutive ACS patients admitted to the coronary care unit (62.7±13.0 years, 24.2% female) were included. 47.4% had a diagnosis of ST segment elevation myocardial infarction. AGEs and sRAGE were analysed by fluorescence spectroscopy and competitive ELISA, respectively. Risk scores (GRACE, TIMI, PURSUIT) were calculated retrospectively using prospective data. The complexity of coronary artery disease was evaluated by SYNTAX score. RESULTS: The mean fluorescent AGEs and sRAGE levels were 57.7±45.1 AU and 1045.4±850.0 pg/mL, respectively. 19 patients presented cardiac events during in-hospital phase and 29 during the follow-up. In-hospital cardiac events were significantly associated with higher sRAGE levels (p = 0.001), but not long-term cardiac events (p = 0.365). Regarding fluorescent AGE the opposite happened. After multivariate analysis correcting by gender, left ventricular ejection fraction, glucose levels, haemoglobin, GRACE and SYNTAX scores, sRAGE was significantly associated with in-hospital prognosis, whereas fluorescent AGEs was significantly associated with long-term prognosis. CONCLUSIONS: We conclude that elevated values of sRAGE are associated with worse in-hospital prognosis, whereas high fluorescent AGE levels are associated with more follow-up events.

Statins modulate feedback regulation mechanisms between advanced glycation end-products and C-reactive protein: evidence in patients with acute myocardial infarction.

OBJECTIVE: High sensitivity C-reactive protein (hsCRP) and advanced glycation end-products (AGEs) have been proposed as mediators in inflammation and atherosclerosis. Therefore, we studied the relation between AGE and hsCRP in patients with acute myocardial infarction (AMI). METHODS: Patients with AMI diagnosis and satisfying our inclusion criteria were included during 2009-2011 in an unicentre registry of AMI patients for a cross-sectional study. The final cohort was composed of 156 patients (46.2% STEMI and 27.6% with type-2 diabetes). AGE and hsCRP were measured in plasma. RESULTS: Diabetic patients were older than non-diabetics (68.6 ± 10.6 vs. 60.4 ± 13.9 years; p<0.05), presented more incidence of hypertension (62.8 vs. 36.3%; p<0.05) and were in a higher Killip class (p<0.05). The mean values of fluorescent AGE and hsCRP levels were 61.3 ± 49.8 AU and 2.4 ± 4.0 mg/L, respectively, and there were no differences in these parameters between diabetic and non-diabetic patients. A direct association between AGE and hsCRP levels was observed, mainly in diabetic patients (r=0.258; p=0.018). Importantly, this association disappeared in patients who had been treated with statins before their AMI (r=-0.055; p=0.845), but it was maintained in non-diabetic patients naïve for statins treatment (r=0.634; p<0.001), independently of other treatments and confounding parameters. CONCLUSIONS: This is the first evidence in humans of a feedback regulation mechanism between CRP and the AGE-RAGE axis modulated by statins.

High-sensitivity C-reactive protein predicts adverse outcomes after non-ST-segment elevation acute coronary syndrome regardless of GRACE risk score, but not after ST-segment elevation myocardial infarction.

INTRODUCTION: Atherosclerosis is an active process and the inflammatory component appears to be particularly correlated with the development of acute coronary syndromes (ACS). C-reactive protein (CRP) is an acute phase protein that appears in the circulation in response to inflammatory cytokines. The present study investigated the association between high-sensitivity C-reactive protein (hsCRP) on admission and follow-up prognosis after an ACS. METHODS: We included 151 consecutive patients admitted to the coronary care unit with a diagnosis of ACS (47% ST-segment elevation myocardial infarction [STEMI]). The primary endpoint was the combination of cardiac death and myocardial reinfarction during the follow-up period (median 19.8 months, interquartile range 16.3-23.7 months). RESULTS: The occurrence of follow-up events was significantly related to admission hsCRP level, which was an excellent predictor of cardiac death and reinfarction during follow-up (HR 1.091, 95% CI 1.014-1.174; p=0.019). Stratifying the population based on type of ACS, adjusted by variables associated with cardiac events in univariate analysis (hsCRP, diabetes, depressed ejection fraction and GRACE risk score), hsCRP proved to be an independent predictor of follow-up outcomes only in non-STEMI patients (HR 1.217, 95% CI: 1.093-1.356, p<0.001), not in STEMI patients. The best cutoff level of hsCRP to predict follow-up outcomes was 1.1mg/dl, with sensitivity of 77.8% and specificity of 63.2%. CONCLUSION: Although the GRACE risk score is routinely used for stratification of patients with ACS, assessment of hsCRP may provide additional prognostic value in the follow-up of non-STEMI patients.

GRACE risk score predicts contrast-induced nephropathy in patients with acute coronary syndrome and normal renal function.

We evaluated the incidence, clinical predictors, and outcomes of contrast-induced nephropathy (CIN) after coronary angiography in patients with myocardial infarction and normal kidney function. We studied 202 consecutive patients with glomerular filtration rate >60 mL/min/1.73 m(2). The CIN was defined according to 3 definitions: increases in serum creatinine (sCr) ≥25%, ≥0.3 mg/dL, and ≥0.5 mg/dL. The CIN occurred in 56 (27.7%), 42 (20.8%), and 13 (6.4%) patients, respectively. In multivariate analysis, the presence of a high Global Registry of Acute Coronary Events (GRACE) risk score (>140) was an independent predictor of CIN in its milder forms (≥25% and ≥0.3 mg/dL of rise in sCr). Increase in sCr ≥0.3 mg/dL was an independent predictor of bleeding. Increase in sCr ≥0.5 mg/dL was an independent predictor of in-hospital cardiac events (mortality, myocardial infraction [MI], and heart failure). As conclusion, the GRACE score is a useful tool to predict CIN in patients with MI and normal renal function.

Predictive value of advanced glycation end products for the development of post-infarction heart failure: a preliminary report.

BACKGROUND: Since post-infarction heart failure (HF) determines a great morbidity and mortality, and given the physiopathology implications of advanced glycation end products (AGE) in the genesis of myocardial dysfunction, it was intended to analyze the prognostic value of these molecules in order to predict post-infarction HF development. METHODS: A prospective clinical study in patients after first acute coronary syndrome was conducted. The follow-up period was consisted in 1 year. In 194 patients consecutively admitted in the coronary unit for myocardial infarct fluorescent AGE levels were measured. The association between glycaemic parameters and the development of post-infarction HF were analyzed in those patients. Finally, we identified the variables with independent predictor value by performing a multivariate analysis of hazard ratio for Cox regression. RESULTS: Eleven out of 194 patients (5.6%) developed HF during follow-up (median: 1.0 years [0.8 - 1.5 years]). Even though basal glucose, fructosamine and glycated haemoglobin were significant predictive factors in the univariate analysis, after being adjusted by confounding variables and AGE they lost their statistical signification. Only AGE (Hazard Ratio 1.016, IC 95%: 1.006-1.026; p<0,001), together with NT-proBNP and the infarct extension were predictors for post-infarction HF development, where AGE levels over the median value 5-fold increased the risk of HF development during follow-up. CONCLUSIONS: AGE are an independent marker of post-infarction HF development risk.

Frequency and predictors of contrast-induced nephropathy after angioplasty for chronic total occlusions.

BACKGROUND: The incidence and predictors of contrast-induced nephropathy (CIN) after percutaneous coronary intervention (PCI) of chronic total occlusions (CTO) have not been specifically reported. METHODS: This retrospective analysis included all consecutive patients referred for PCI of CTO between April 2003 and March 2008, with baseline and 24 h postprocedural available creatinine levels. CIN was defined as 24 h postprocedural increase of baseline creatinine levels > or =0.5 mg/dl (CIN(05)) or > or =25% (CIN(25)). Severe renal dysfunction (SRD) was defined as acute renal failure requiring dialysis, or an increase in baseline creatinine levels > or =2.0 mg/dl (SRD(2)) or > or =50% (SRD%). Patients were classified into risk categories for CIN, according to the validated Mehran risk score. RESULTS: A total of 227 patients were included, mean age of 64+/-10 years, the majority being at low risk for CIN (55% with < or =5 points in the Mehran score). CIN(25) occurred in 6.16% (14/227) patients and CIN(05) in 0.88% (2/227). The incidence of SRD(2) or SDR% was 0% (0/227) and 0.9% (2/227), respectively, with no patient requiring dialysis. Patients who developed CIN(25) received a higher contrast volume than those who did not (312 ml (210-400) vs 260 ml (200-345), p=0.14), but the difference was not statistically significant. CONCLUSIONS: In this consecutive cohort of patients, the incidence of CIN following PCI for CTO was low despite the administration of moderate to large volumes of contrast media. Attempts at revascularization of CTO should not be discouraged or be prematurely interrupted because of the fear of CIN.

Angina crónica estable: fisiopatología y formas de manifestación clínica / Chronic stable angina: pathophysiology and clinical manifestations

La angina de pecho estable es la expresión clínica más común de la cardiopatía isquémica crónica sintomática y la manifestación inicial de la enfermedad coronaria en más de la mitad de los pacientes. La aterotrombosis es el proceso patológico implicado en su génesis y parece que la placa de ateroma estable es el principal sustrato anatómico que origina los síntomas. Se revisan las características histológicas de la placa estable, los diversos factores implicados en el desequilibrio entre el oxígeno aportado por la arteria coronaria y el demandado por el miocardio en riesgo y sus consecuencias en las células. Por último, se comentan las principales escalas de estratificación clínica de la angina crónica estable, sus implicaciones pronósticas y algunas peculiaridades de presentación en subgrupos de pacientes (AU)

Chronic stable angina pectoris is the most common clinical expression of symptomatic chronic ischemic heart disease and is the first manifestation of heart disease in more than half of patients. Atherothrombosis is the pathological process responsible for its development, and stable atheromatous plaque appears to be the principle anatomical substrate responsible for the associated symptoms. This article presents an overview of the histology of stable plaque, of the different factors involved in the imbalance between coronary artery oxygen supply and the oxygen demand of myocardial tissue at risk, and of the consequences of this imbalance at a cellular level. Finally, there is a discussion of the main measurement scales used for the clinical classification of chronic stable angina and their prognostic value, and of the particular forms of presentation in specific subgroup of patients (AU)

Taponamiento cardíaco / Cardiac tamponade

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Génesis de la taquicardia ventricular monomorfa sostenida / Genesis of the monomorphous sustained ventricular tachycardia

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La enfermedad polivascular aterotrombótica: un enemigo común y distintos frentes / Polyvascular atherothrombotic disease: an enemy with many faces

La aterotrombosis es un proceso sistémico, progresivo, con una etiopatogenia común que afecta a diferentes lechos vasculares y cuyas principales manifestaciones clínicas dependen del territorio más gravemente afectado. Sin embargo, la práctica clínica confirma el carácter multisistémico de la enfermedad, y es frecuente encontrar en el mismo sujeto (sintomático o no) manifestaciones clínicas o subclínicas de enfermedad vascular en otro territorio. La cardiopatía isquémica, la enfermedad cerebrovascular y la enfermedad arterial periférica representan los tres frentes de presentación principales y la importante relevancia pronóstica de su coexistencia justifica la valoración vascular integral del paciente. Al tratarse de una enfermedad sistémica con factores de riesgo comunes, el tratamiento con antiagregantes plaquetarios, inhibidores de la enzima de conversión de angiotensina, antagonistas de los receptores de angiotensina II y estatinas ha confirmado sus ventajas pronósticas con independencia del territorio afecto (AU)

Atherothrombosis is a progressive systemic disease with a widespread pathogenetic effect on different vascular beds. Its principal clinical manifestations depend on the vascular territory most seriously affected. However, clinically it is clear that the disease has a multisystemic character since clinical or subclinical manifestations of vascular disease (whether symptomatic or not) are frequently present to a varying degree in the same individual. Ischemic heart disease, cerebrovascular disease and peripheral arterial disease are the three main forms of presentation. The serious prognostic implications of their coexistence justifies requiring patients to undergo a general vascular investigation. Because these conditions all involve a systemic disease with common risk factors, treatment with antiplatelet agents, angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, and statins have been shown to have beneficial effects on prognosis, irrespective of the vascular bed affected (AU)