[In-hospital management of acute coronary syndrome patients: influence of age, gender and admission department on medical policy and outcome]. / Gestione ospedaliera del paziente con sindrome coronarica acuta: influenza dell'età, del genere e del reparto di ricovero sulle scelte mediche e l'esito.

BACKGROUND: Although the improvement of therapeutic strategies is leading to a dramatic decline of in-hospital acute coronary syndrome (ACS) death rates, differences in care and prognosis of ACS patients exist when age, gender and admission department are considered. METHODS: The national hospital informative system was used. Only data recorded in three Italian Regions from December 1, 2005 to November 30, 2007 were analyzed. This approach allowed to identify 70 413 patients reporting ACS as primary or secondary diagnosis. The ACS cohort was stratified by age (≤64, 65-74 and ≥75 years) and gender. ACS events were divided into two groups: 42 503 patients with non-ST-elevation ACS (NSTE-ACS) and 27 910 patients with ST-elevation ACS (STEMI). The proportion of NSTE-ACS and STEMI patients treated in general medicine or cardiology departments requiring a coronary procedure or extensive investigations, and in-hospital 30-day mortality rates adjusted by age and gender were analyzed. RESULTS: 19% of STEMI and 15% of NSTE-ACS patients are admitted to a general medicine department. For STEMI patients, the proportion increases up to 37.6% when females aged ≥75 years are considered. Patients undergo a coronary procedure or extensive investigations less commonly in general medicine than in cardiology departments; in-hospital 30-day adjusted mortality rates in general medicine departments are approximately 2-fold higher than those recorded in cardiology departments (STEMI: 26.4 vs 16.7%; NSTE-ACS: 7.7 vs 4.2%). CONCLUSIONS: In-hospital mortality rates of ACS patients admitted to cardiology departments are lower than those reported in general medicine departments. Nevertheless, in-hospital management of women and elderly ACS patients does not completely comply with the recommended guidelines and exposes them to unfavorable prognosis.

Gender-specific aspects of treatment of cardiovascular risk factors in primary and secondary prevention.

In men, cardiovascular diseases (CVD) increase steadily by the age of 35 years and reach a plateau in the 7th decade of life, whereas in women few years after the menopause, from about 50 years, the incidence of cardio-cerebro-vascular diseases progressively increases, becoming the leading cause of mortality and morbidity. Because of the greater incidence of CVD in men until the early 1980s, the information on cardiovascular risk factors has been gathered mainly from men and then translated in women. But sex steroid milieu has a different impact on cardiovascular risk profile, as cardiovascular risk factors have a different importance in determining future cardiovascular events in the two sexes and therapeutic strategies have a different impact on reducing cardiovascular risk in the two sexes. Aim of this study is to review the gender-specific aspects influencing the development of cardiovascular risk factors and cardiovascular preventative strategies both in primary and in secondary prevention.

Heart rate control in an unselected consecutive population of outpatients with stable coronary artery disease: Analysis of the CARDIf Study Cohort.

BACKGROUND: Despite increasing pharmacological and mechanical treatment options, coronary artery disease (CAD) continues to be associated with considerable mortality and morbidity. The detrimental effects of elevated heart rate (HR) on cardiac morbidity and mortality are well established. Although ß-blockers represent the mainstay of treatment of patients with CAD and heart failure (HF), according to current guidelines, these drugs are most often undertitrated for various reasons despite the lack of real contraindications. This observational, cross-sectional, multicenter survey was designed to assess which clinical variables influence HR and whether HR is adequately controlled; and the rate of administration of ß-blockers in patients with chronic CAD attending outpatient clinics. METHODS: Over 6 months 2226 (of 2362 screened) outpatients with stable CAD and resting HR > 60 beats/min (bpm) were enrolled. Left ventricular systolic function was not a criterion of inclusion. Each patient had a full clinical examination and the past medical history, angina, or HF-related symptoms were evaluated. In each patient, the demographics and cardiovascular risk factors were assessed; weight, height, and body mass index (BMI) was calculated; sitting blood pressure and a HR by a 12-lead electrocardiogram was obtained. RESULTS: Overall, 45.4% of patients with CAD were not under ß-blocker therapy. Male patients featured a significantly lower HR than females, corrected from ß-blockers use. In multiple regression analysis, which also included the use/nonuse of ß-blockers as independent variable, not using ß-blockers, female sex (OR 2.55), New York Heart Association (NYHA) classes I and II (OR 1.62 vs classes III-IV), smoking (OR 0.89), and increased BMI (OR 0.14) were all independent determinants of resting HR, with the lack of ß-blockade therapy (OR 3.35) being the main determinant of the magnitude of HR increase. Heart rate in patients under ß-blocker therapy was significantly less than in untreated patients (73.6 ± 10.0 vs 77.1 ± 10.4, P < .0001), although it often did not reach target values of <70 bpm. Among patients with HF symptoms, 56.6% were under ß-blocker therapy. In patients free of symptoms of HF, HR was significantly less in those receiving a ß-blocker (72.3 ± 10 vs 76.7 ± 11 bpm, P < .0001). CONCLUSION: This survey demonstrates that HR is poorly controlled in a broadly representative cohort of outpatients with CAD, even in those on ß-blocker therapy, mainly because of undertitration of therapy-almost half of the patients with CAD and elevated resting HR are not on ß-blockers. This might be related to absolute or relative controindications and to haemodynamic and chronotropic intolerance to beta-blockers.

Magnetic resonance imaging of carotid plaque inflammation in acute coronary syndromes: a sign of multisite plaque activation.

Widespread plaque inflammation has been demonstrated in acute coronary syndromes (ACS). We evaluated signs of plaque inflammation in carotid arteries of patients with ACS by contrast-enhanced magnetic resonance imaging (MRI). Carotid MRI was performed in 13 patients with ACS and in 9 controls having at least 1 carotid plaque with a stenosis > or =40%. MRI criteria of plaque inflammation were: increased T2 signal >50% of the plaque areas (tissue oedema) and/or enhancement after gadolinium injection (neo-vascularization). MRI signs of inflammation were found in 95% and in 33% of patients with ACS and controls, respectively (p<0.001). Carotid artery MRI may serve as a window to the entire cardiovascular system, to identify "vulnerable" patients.

Prophylactic aspirin therapy does not increase faecal calprotectin concentrations.

OBJECTIVE: Non-steroidal anti-inflammatory drugs (NSAID) can induce enteropathy. Aspirin ingestion is associated with a lower small-intestinal inflammation than other NSAID. Faecal calprotectin concentrations have recently been proposed as a simple non-invasive test to identify NSAID enteropathy. The aim of our pilot study was to evaluate calprotectin concentrations in patients on treatment with low-dose aspirin. METHODS: Twenty-two patients on prophylactic treatment with aspirin were recruited. Twenty-five healthy volunteers were enrolled as a control group. Faecal calprotectin concentrations were determined by enzyme-linked immunosorbent assay. Statistical analysis was performed by t-test for unpaired data. RESULTS: The mean faecal calprotectin concentration in patients (57.95+/-44.28 microg/g) did not show significant differences compared with controls (45.76+/-26.45 microg/g; P=0.251). CONCLUSIONS: We found that low-dose aspirin does not induce an increase in faecal calprotectin increase.

Mobilization of bone marrow-derived stem cells after myocardial infarction and left ventricular function.

AIMS: Recent data suggest that the administration of bone marrow-derived stem cells (BMSC) might improve myocardial perfusion and left ventricular (LV) function after acute myocardial infarction (AMI). The aim of this study was to assess spontaneous mobilization of BMSC expressing the haematopoietic and endothelial progenitor cell-associated antigen CD34+ after AMI and its relation to post-infarction remodelling. METHODS AND RESULTS: Peripheral blood concentration of CD34+ BMSC was measured by flow cytometry in 54 patients with AMI, 26 patients with chronic stable angina (CSA), and 43 normal healthy subjects. In patients with AMI, LV function was measured by 2D-echocardiography. Eighteen AMI patients were reassessed at 1 year. BMSC concentration was higher in patients with AMI (mean peak value: 7.04+/-6.27 cells/microL), than in patients with CSA (3.80+/-2.12 cells/microL, P=0.036) and in healthy controls (1.87+/-1.52 cells/microL, P<0.001). At multivariable analysis statin use (P<0.001), primary percutaneous intervention (P=0.048) and anterior AMI (P=0.05) were the only independent predictors of increased BMSC mobilization after AMI. In the 28 patients without subsequent acute coronary events reassessed at 1 year follow-up, CD34+ cell concentration was an independent predictor of global and regional improvement of LV function (r=0.52, P=0.004 and r=-0.41, P=0.03, respectively). CONCLUSION: AMI is followed by enhanced spontaneous mobilization of BMSC, in particular, in patients on statin therapy and following a primary percutaneous intervention. More importantly persistent spontaneous mobilization of BMSC might contribute to determine a more favourable post-AMI remodelling.