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C-reactive protein in acute myocardial infarction: association with heart failure

BACKGROUND High C-reactive protein (CRP) levels have been associated with higher mortality rate in patients with acute myocardial infarction (AMI). However, it is not known whether inflammation plays a role in the time-course of heart failure (HF) in this clinical setting. Our aim was to study the nature of the relationship between CRP and HF during AMI. METHODS This prospective study was carried out in 269 subjects admitted to the hospital for suspected AMI. Of these, 220 had evidence of AMI. The other 49 subjects were studied as controls. CRP was assessed on the first, third, and seventh day after admission. RESULTS CRP was significantly higher in the patients with AMI than in the control patients (P =.001) and peaked on the third day. Among the patients with AMI, CRP was higher in patients with HF than in patients without HF (adjusted P =.008, P =.02 and P =.03 on 1st, 3rd, and 7th day, respectively). Prevalence of HF on admission was slightly higher in the subjects with first-day CRP >or=15 mg/L than in those with CRP <15 mg/L, and the between-group difference progressively increased from the first to the seventh day (P <.0001). At multivariable regression analysis, first-day log-CRP was shown to be a strong independent predictor of both HF progression (P <.0001) and left ventricular ejection fraction (P <.0001). One-year total mortality and HF-mortality rates turned out to be higher in the patients with CRP >or=85 mg/L than in those with CRP below that level (P <.0001), and log-third-day CRP was independently associated with 1-year mortality at multivariable analysis (P =.0001). CONCLUSIONS CRP on admission to hospital is suitable for predicting the time-course of HF in patients with AMI. Peak CRP value is a strong independent predictor of global and HF-mortality during the following year.

Factors Underlying the Increase in Carotid Intima-Media Thickness in Borderline Hypertensives

To define the role played by various risk and behavioral factors in the increase of carotid intima-media thickness (IMT) observed in borderline hypertensives. Using B-mode ultrasonography, we compared 97 borderline hypertensives enrolled in the HARVEST study to 27 normotensive controls. Intima-media thickness was measured in the right and left common carotid artery, bulb, and internal carotid artery. Mean IMT (m-IMT), maximum IMT (M-IMT), the mean of M-IMT (M-MAX), and the prevalence of raised lesions (IMT>1 mm) were established. Compared to the controls, higher systolic BP, diastolic BP, mean arterial blood pressure levels and body mass index (BMI) were present in the borderline hypertensives, whereas age, smoking, physical activity, serum cholesterol, and triglycerides were similar. After adjusting for age, sex, heart rate, BMI, smoking, serum cholesterol, triglycerides, and physical activity, higher values of m-IMT and M-IMT were present in most carotid segments of borderline hypertensives compared with controls. After further adjustment for systolic BP and diastolic BP, differences were no longer significant. The adjusted M-MAX was 0.59+/-0.12 in borderline hypertensives compared with 0.50+/-0.10 in controls (P<0.001). After adjustment for systolic BP and diastolic BP it was 0.58+/-0.11 in borderline hypertensives compared with 0.50+/-0.12 in controls (P<0.005). In the various carotid segments, the prevalence of raised lesions was 1. 2% in borderline hypertensives compared with 0.3% in controls (P<0. 001). In the multivariate analysis m-IMT, M-IMT, and M-MAX were related to ambulatory mean arterial pressure, systolic BP and diastolic BP, serum cholesterol and triglycerides, BMI, age, and physical activity. Higher IMT values were found in subjects who were physically active than in those who were sedentary. In borderline hypertensives, an increase in IMT takes place not only in the common carotid artery but also in the bulb and the internal carotid segment. Blood pressure levels are a main determinant of m-IMT while the interaction of BP with other risk factors such as age and plasma lipids is more relevant for advanced intima-media thickening such as M-MAX.

Specific Cellular Features of Atheroma Associated With Development of Neointima After Carotid Endarterectomy The Carotid Atherosclerosis and Restenosis Study

BACKGROUND The purpose of this study was to investigate whether some cellular and molecular features of tissue retrieved at carotid endarterectomy are associated with the extent of neointima formation at ultrasound follow-up. METHODS AND RESULTS One hundred fifty patients were studied. Endarterectomy specimens were tested by immunocytochemistry with the use of (1) monoclonal antibodies that identify smooth muscle cells (SMCs) and fetal-type SMCs on the basis of smooth muscle and nonmuscle myosin content, (2) the anti-macrophage HAM 56, and (3) the anti-lymphocyte CD45RO. The maximum intima-media thickness (M-IMT) of the revascularized vessel was assessed by the use of B-mode ultrasonography 6 months after surgery. The M-IMT values were related positively to the number of SMCs (r=0.534, P<0.0005) and negatively to that of macrophages and lymphocytes (r=-0.428, P<0.0005, and -0.538, P=0.001, respectively). Patients were classified as class 1 (M-IMT </=1.0 mm), class 2 (1. 01.3 mm). An abundance of SMCs, mostly of fetal type, was found in the plaque of class 3 patients, whereas lesions from class 1 patients were rich in macrophages and lymphocytes. In the multivariate analysis, factors related to M-IMT were the number of SMCs and the percentage of fetal-type SMCs present in the plaque. CONCLUSIONS Although the classic risk factors did not play a role, an abundance of SMCs and a scarcity of macrophages characterized the primary lesion of patients in whom neointima developed after surgery. In patients in whom neointima did not develop, lesions were rich in macrophages and lymphocytes. This approach can be useful in defining patients at risk of restenosis.

Effect of blood pressure and physical activity on carotid artery intima–media thickness in stage 1 hypertensives and controls

The aim of the study was to investigate whether hypertension and physical training induce parallel changes in the arterial wall. Ninety-seven never-treated stage 1 hypertensive patients (HT) (systolic blood pressure 140 to 159 mm Hg or diastolic blood pressure 90 to 99 mm Hg) aged 18 to 45 years taking part in the Hypertension and Ambulatory Recording Venetia Study and 27 normotensive volunteers (NT) aged 30 +/- 9 years were studied. Data on physical or sports activity were collected and scored, and target organ involvement was investigated by assessing microalbuminuria, echocardiography, and carotid ultrasound study. The carotid arteries were examined according to the Atherosclerosis Risk in Communities protocol. Mean (m-IMT) and maximal (M-IMT) carotid intima-media thickness were measured at end-diastole in the far wall common carotid artery, in the bulb and internal carotid artery, in the lateral and posterior projection, averaging the left and right sides. A comparable level of physical activity was present in HT patients and NT subjects. Twenty-four-hour blood pressure and blood lipid levels, as well as target organ damage, were similar in physically active and sedentary HT. The m-IMT of the common carotid was greater in sedentary HT than in sedentary NT, as well as in active than in sedentary NT. The m-IMT of the internal carotid artery was also greater in active HT than in active NT, as well as in active than in sedentary HT. In logistic regression, comparing the first and fourth quartile of m-IMT, scored physical activity was a predictor of m-IMT in the internal carotid artery. No statistical interaction was found between physical activity and hypertension, indicating that these two items have a cumulative effect and act independently of each other. Sedentary HT had significantly greater levels of M-IMT than sedentary NT in all sites but the bulbs; in the internal and common carotid arteries, HT exercisers had significantly greater M-IMT than NT exercisers. Therefore, physical activity appears to be an early independent predictor of carotid wall thickness. This factor should be taken into consideration in population-based studies aimed at investigating supraortic vessels as it can act as a confounder.

Low CD34(+) cells, high neutrophils and the metabolic syndrome are associated with an increased risk of venous thromboembolism.

The relationship between MetS (metabolic syndrome), levels of circulating progenitor/immune cells and the risk of VTE (venous thromboembolism) has not yet been investigated. We studied 240 patients with previous VTE and 240 controls. The presence of MetS was identified according to NCEP ATP III guidelines and flow cytometry was used to quantify circulating CD34(+) cells. VTE patients showed higher BMI (body mass index), waist circumference, triacylglycerol (triglyceride) levels, blood glucose, hs-CRP (high-sensitivity C-reactive protein) and lower HDL-C (high-density lipoprotein cholesterol) levels. The prevalence of MetS was significantly higher in VTE (38.3%) than in control individuals (21.3%) with an adjusted OR (odds ratio) for VTE of 1.96 (P=0.002). VTE patients had higher circulating neutrophils (P<0.0001), while the CD34(+) cell count was significantly lower among patients with unprovoked VTE compared with both provoked VTE (P=0.004) and controls (P=0.003). Subjects were also grouped according to the presence/absence of MetS (MetS(+) or MetS(-)) and the level (high/low) of both CD34(+) cells and neutrophils. Very high adjusted ORs for VTE were observed among neutrophils_high/MetS(+) (OR, 3.58; P<0.0001) and CD34(+)_low/MetS(+) (OR, 3.98; P<0.0001) subjects as compared with the neutrophils_low/MetS(-) and CD34(+)_high/MetS(-) groups respectively. In conclusion, low CD34(+) blood cell count and high circulating neutrophils interplay with MetS in raising the risk for venous thromboembolic events.

Visceral obesity, but not metabolic syndrome, is associated with the presence of post-thrombotic syndrome

INTRODUCTION The relationship between metabolic syndrome (MetS), and the development of post-thrombotic syndrome (PTS) is currently unknown. MATERIALS AND METHODS We enrolled 120 patients with a previous episode of deep venous thrombosis (DVT) diagnosed more than 2years apart from the enrollment. Presence of MetS was identified according to NCEP ATP III criteria and Villalta Score (VS) was used to establish the presence of PTS (VS≥5). RESULTS We identified 49 (40.8%) subjects with clinical diagnosed of PTS. Patients with or without PTS showed comparable age and temporal distance from DVT event. We observed higher BMI (p=0.005) and waist circumference (p=0.006) among subjects with VS≥5 as compared to patients without PTS. No differences between the two groups were found in terms of lipid profile, blood pressure, diabetes, hs-CRP level and ongoing medications. The prevalence of MetS was equally distributed among patients with or without PTS (20% vs 26% respectively, p=0.64). Among the individual components of MetS only the prevalence of visceral adiposity was significantly increased in subjects affected by PTS (OR 2.81, p=0.008). Moreover, a significant linear correlation was found between VS and waist circumference in the entire cohort (r=0,354, p<0.0001). CONCLUSION There is no evidence of association between MetS and PTS. However, the degree of visceral adiposity is strongly correlated with the presence and severity of post-thrombotic disease.

Chronic kidney disease is associated with increased risk of venous thromboembolism recurrence

INTRODUCTION It is currently unclear whether chronic kidney disease (CKD) and the decrease in renal function can influence the risk of venous thromboembolism (VTE) recurrence. MATERIALS AND METHODS We performed an ambispective observational study on 409 patients with a previous episode of VTE. All the patients were included in the retrospective analysis whereas a subgroup of 260 individuals, without history of recurrence and that stopped oral anticoagulation, were then followed-up for a mean of 52.3±20.7months. RESULTS At the enrollment, subjects with history of recurrent VTE were prevalently male with higher blood pressure and lower eGFR. Prevalence of CKD (defined as eGFR<60ml/min/1.73m2) was higher in patients with previous VTE recurrence with an adjusted OR of 5.69 (IC95% 2.17-14.90, p<0.001) compared to patients with normal eGFR. Similar findings were obtained from the prospective study where an adjusted 5.32 HR for VTE recurrence was seen in patients with CKD compared to subjects with normal renal function (IC95% 1.49-18.95, p=0.010). An increase in the risk of recurrent VTE was also observed in patients with mild decrease in renal function (eGFR 60-90 vs ≥90ml/min/1.73m2 adjusted HR 2.84, IC95% 1.13-7.11, p=0.025). Moreover, a multivariate Cox regression analysis including eGFR as continuous variable showed that renal function decrease was independently associated with the risk of VTE recurrence (p=0.001). CONCLUSIONS CKD and mild decrease in renal function are associated with a significant increase in the risk of recurrent VTE.

[BP.12.08] CHRONIC KIDNEY DISEASE IS ASSOCIATED WITH INCREASED RISK OF VENOUS THROMBOEMBOLISM RECURRENCE

Objective: Chronic kidney disease (CKD) has been associated with increased risk of venous thromboembolism (VTE), but it is unclear whether the decline in renal function can also influence the risk of VTE recurrence. Design and method: We enrolled 396 patients who had a previous diagnosed episode of VTE. In this population we identified a group of 68 (17.7%) individuals, which also experienced at least one episode of VTE recurrence. Data collected from each patient were: age, sex, height, weight, BMI, blood pressure levels, history of atherosclerotic cerebro-cardiovascular events, known diabetes, and ongoing medications. Creatinine blood levels were measured in each patient at the enrollment and used to estimate GFR by using the 2009 CKD-EPI creatinine equation. The same cohort of patients was then followed for an average time of 44.3 ± 17.5 months (range 1–65 months) and reliable follow-up clinical data were obtained in 367 patients. During this time period 32 subjects (8.7%) had symptomatic recurrence of VTE. Results: Subjects with history of VTE recurrence were prevalently male with higher blood pressure levels and lower estimated glomerular filtration rate (GFR) as compared to patients without recurrent VTE. At baseline, the prevalence of CKD (GFR < 60 ml/min/1.73 m2) was significantly higher in patients with history of VTE recurrence (22.1% vs 6.4%), with an adjusted odds ratio for recurrence of 4.45 (95% CI 2.05–10.06, p < 0.001). The longitudinal study confirmed baseline data as we found a significant 3.75 hazard ratio for VTE recurrence among patients with CKD (95% CI 1.57–8.94) as compared to subjects with normal renal function. A sizeable increase in the risk of recurrent VTE was also observed in patients with mild-to-moderate decline in renal function. In fact, the adjusted hazard ratio for recurrence was 3.72 (95% CI 1.26–10.97, p = 0.017) for patients in CKD stage 2 compared to patients with GFR > 90 ml/min/1.73 m2. Conclusions: Our study demonstrated that the presence of CKD is associated with a significant increase in the risk of recurrent VTE.

History of hypertension and 5-year global mortality and causes of death after acute myocardial infarction

Abstract OR-9 Key Words: Myocardial Infarction, History of Hypertension, Causes of Death