Pulmonary embolism location is associated with the co-existence of the deep venous thrombosis.

: Multiple studies have shown that in approximately half of individuals with pulmonary embolism (PE), the deep venous thrombosis (DVT) is not evident at the moment of PE diagnosis. The underlying factors and the origin of PE in these patients are not completely understood: missed DVT, embolization of DVT in its entirety, or de-novo PE being possible explanations. The aim of this study was to evaluate the differences in PE patient with or without co-existing DVT. Sixty-three consecutive PE patients were included. Whole leg bilateral Doppler compression ultrasound was performed to all patients. The PE location and extension, C-reactive protein, platelet count, hemostatic markers FV, FVIII, FXIIIa, Fibrinogen, von Willebrand factor antigen, thrombomodulin were assessed. Thorough clinical assessment including echocardiography and pulmonary function tests were performed upon arrival and seven months later. The mean age of the patients was 57 years (SD 17.3) and 33 (52%) were women. Thirty-one patients (49.2%) had co-existing DVT. The presence of DVT was associated with the proximal location of the PE (100%), whereas none of the patients (n = 10) with exclusively peripheral PE had co-existing DVT. The PE extension, the measured hemostatic and inflammatory markers or the patient characteristics did not statistically differ between patients with isolated PE and PE with co-existing DVT. In roughly half of the PE patients no DVT could be detected. The location of the PE was associated with the presence of co-existing DVT. There were no differences in the PE extension, hemostatic markers or in the patient characteristic between patients with isolated PE or PE with co-existing DVT.

Characterization of different fat depots in NAFLD using inflammation-associated proteome, lipidome and metabolome.

Non-alcoholic fatty liver disease (NAFLD) is recognized as a liver manifestation of metabolic syndrome, accompanied with excessive fat accumulation in the liver and other vital organs. Ectopic fat accumulation was previously associated with negative effects at the systemic and local level in the human body. Thus, we aimed to identify and assess the predictive capability of novel potential metabolic biomarkers for ectopic fat depots in non-diabetic men with NAFLD, using the inflammation-associated proteome, lipidome and metabolome. Myocardial and hepatic triglycerides were measured with magnetic spectroscopy while function of left ventricle, pericardial and epicardial fat, subcutaneous and visceral adipose tissue were measured with magnetic resonance imaging. Measured ectopic fat depots were profiled and predicted using a Random Forest algorithm, and by estimating the Area Under the Receiver Operating Characteristic curves. We have identified distinct metabolic signatures of fat depots in the liver (TAG50:1, glutamate, diSM18:0 and CE20:3), pericardium (N-palmitoyl-sphinganine, HGF, diSM18:0, glutamate, and TNFSF14), epicardium (sphingomyelin, CE20:3, PC38:3 and TNFSF14), and myocardium (CE20:3, LAPTGF-ß1, glutamate and glucose). Our analyses highlighted non-invasive biomarkers that accurately predict ectopic fat depots, and reflect their distinct metabolic signatures in subjects with NAFLD.

An Integrated Understanding of the Rapid Metabolic Benefits of a Carbohydrate-Restricted Diet on Hepatic Steatosis in Humans.

A carbohydrate-restricted diet is a widely recommended intervention for non-alcoholic fatty liver disease (NAFLD), but a systematic perspective on the multiple benefits of this diet is lacking. Here, we performed a short-term intervention with an isocaloric low-carbohydrate diet with increased protein content in obese subjects with NAFLD and characterized the resulting alterations in metabolism and the gut microbiota using a multi-omics approach. We observed rapid and dramatic reductions of liver fat and other cardiometabolic risk factors paralleled by (1) marked decreases in hepatic de novo lipogenesis; (2) large increases in serum ß-hydroxybutyrate concentrations, reflecting increased mitochondrial ß-oxidation; and (3) rapid increases in folate-producing Streptococcus and serum folate concentrations. Liver transcriptomic analysis on biopsy samples from a second cohort revealed downregulation of the fatty acid synthesis pathway and upregulation of folate-mediated one-carbon metabolism and fatty acid oxidation pathways. Our results highlight the potential of exploring diet-microbiota interactions for treating NAFLD.

N-terminal Pro-brain Natriuretic Peptide, High-sensitivity Troponin and Pulmonary Artery Clot Score as Predictors of Right Ventricular Dysfunction in Echocardiography.

BACKGROUND: We investigated the ability of cardiac biomarkers and total pulmonary artery (PA) clot score to predict right ventricular dysfunction (RVD) on admission and at seven-month follow-up in subjects with acute pulmonary embolism (APE). METHODS: Sixty-three normotensive patients with APE were divided into two groups: patients with (n= 32, age 58±19 years) and without (n=31, age 55±16 years) echocardiographic RVD. Transthoracic echocardiography (TTE), N-terminal pro-brain natriuretic peptide (NT-proBNP), and high-sensitivity troponin T (hsTnT) were assessed upon arrival and repeated at seven months. Total PA clot score was determined on admission. RESULTS: The age- and sex dependent NT-proBNP on admission, on day 5, and at seven months exhibited the best sensitivity (admission 94%, day 5 100%, seven months 100%) and negative predictive value (NPV) (89%, 100%, 100%) for detecting RVD. Six patients (10%) had persistent RVD at seven months. Total PA clot score showed only low to moderate sensitivity (77%) and PPV (7%) for detection of RVD at seven months. CONCLUSIONS: Normal age- and sex dependent NT-proBNP on admission or measured five days later seems to be useful in exclusion of RVD at follow up. Total PA clot score shows only to be of modest benefit for predicting persistent RVD.

Ectopic fat depots and left ventricular function in nondiabetic men with nonalcoholic fatty liver disease.

BACKGROUND: Nonalcoholic fatty liver disease has emerged as a novel cardiovascular risk factor. The aim of the study was to assess the effect of different ectopic fat depots on left ventricular (LV) function in subjects with nonalcoholic fatty liver disease. METHODS AND RESULTS: Myocardial and hepatic triglyceride contents were measured with 1.5 T magnetic resonance spectroscopy and LV function, visceral adipose tissue (VAT) and subcutaneous adipose tissue, epicardial and pericardial fat by MRI in 75 nondiabetic men. Subjects were stratified by hepatic triglyceride content into low, moderate, and high liver fat groups. Myocardial triglyceride, epicardial and pericardial fat, VAT, and subcutaneous adipose tissue increased stepwise from low to high liver fat group. Parameters of LV diastolic function showed a stepwise decrease over tertiles of liver fat and VAT, and they were inversely correlated with hepatic triglyceride, VAT, and VAT/subcutaneous adipose tissue ratio. In multivariable analyses, hepatic triglyceride and VAT were independent predictors of LV diastolic function, whereas myocardial triglyceride was not associated with measures of diastolic function. CONCLUSIONS: Myocardial triglyceride, epicardial and pericardial fat increased with increasing amount of liver fat and VAT. Hepatic steatosis and VAT associated with significant changes in LV structure and function. The association of LV diastolic function with hepatic triglyceride and VAT may be because of toxic systemic effects. The effects of myocardial triglyceride on LV structure and function seem to be more complex than previously thought and merit further study.

Cardiac steatosis in patients with dilated cardiomyopathy.

OBJECTIVE: Ectopic fat accumulation within and around the heart has been related to increased risk of heart disease. Limited data exist on cardiac adiposity in subjects with dilated cardiomyopathy (DCM). The aim of the study was to examine the components of cardiac steatosis and their relationship to LV structure and function in non-diabetic DCM patients. METHODS: Myocardial and hepatic triglyceride (TG) contents were measured with 1.5 T magnetic resonance spectroscopy (MRS), and LV function, visceral adipose (VAT) and abdominal subcutaneous tissue (SAT), epicardial and pericardial fat by MRI in 10 non-diabetic men with DCM and in 20 controls. RESULTS: In face of comparable intra-abdominal fat depots, myocardial TG [0.41% (0.21-2.19) vs. 0.86% (0.31-2.24), p=0.038] was markedly lower and epicardial (895 mm2±110 vs. 664 mm2±180, p=0.002) and pericardial fat [2173 mm2 (616-3673) vs 1168 mm2 (266-2319), p=0.039] depots were larger in patients with DCM compared with controls. In subjects with DCM, the LV global function index was decreased to a greater extent than the LV EF [21%±6 vs. 34% (16-40)]. CONCLUSIONS: Myocardial TG content decreased and epicardial and pericardial fat depots increased in non-diabetic subjects with DCM. Although recognised as a site of ectopic fat accumulation, the derangement of myocardial TG seems to play a specific role in the myocardial energy metabolism in congestive heart failure.

Cardiac steatosis and left ventricular function in men with metabolic syndrome.

BACKGROUND: Ectopic accumulation of fat accompanies visceral obesity with detrimental effects. Lipid oversupply to cardiomyocytes leads to cardiac steatosis, and in animal studies lipotoxicity has been associated with impaired left ventricular (LV) function. In humans, studies have yielded inconclusive results. The aim of the study was to evaluate the role of epicardial, pericardial and myocardial fat depots on LV structure and function in male subjects with metabolic syndrome (MetS). METHODS: A study population of 37 men with MetS and 38 men without MetS underwent cardiovascular magnetic resonance and proton magnetic spectroscopy at 1.5 T to assess LV function, epicardial and pericardial fat area and myocardial triglyceride (TG) content. RESULTS: All three fat deposits were greater in the MetS than in the control group (p <0.001). LV diastolic dysfunction was associated with MetS as measured by absolute (471 mL/s vs. 667 mL/s, p = 0.002) and normalized (3.37 s⁻¹ vs. 3.75 s⁻¹, p = 0.02) LV early diastolic peak filling rate and the ratio of early diastole (68% vs. 78%, p = 0.001). The amount of epicardial and pericardial fat correlated inversely with LV diastolic function. However, myocardial TG content was not independently associated with LV diastolic dysfunction. CONCLUSIONS: In MetS, accumulation of epicardial and pericardial fat is linked to the severity of structural and functional alterations of the heart. The role of increased intramyocardial TG in MetS is more complex and merits further study.

Diagnostic efficacy of myeloperoxidase to identify acute coronary syndrome in subjects with chest pain.

BACKGROUND: Early diagnosis of acute coronary syndrome (ACS) is frequently a challenging task. AIMS: To assess the role of novel biomarkers to identify ACS. METHODS: Concentrations of lipids, lipoproteins, oxidized LDL (oxLDL), high-sensitivity C-reactive protein (hsCRP), paraoxonase-1 (PON1), secretory phospholipase A2 (sPLA2), and myeloperoxidase (MPO) were measured in 703 patients (mean age 65.5 ± 11.2 years; 422 men, 281 women) without diabetes mellitus assigned to coronary angiogram. The subjects were divided into three groups: ACS (n = 242), stable angina pectoris (SAP) (n = 242), and normal coronary artery (NCA) (n = 219). RESULTS: HDL-cholesterol (HDL-C) (P < 0.001) and apolipoproteinA-I concentrations (P < 0.0001) were lowest in subjects with ACS. LDL-C (P = 0.008) and non-HDL (P < 0.0001) were higher in the ACS group than in the SAP group. Leukocyte count (P < 0.0001), oxLDL (P < 0.05), hsCRP (P < 0.001), sPLA2 (P < 0.05), and MPO (P < 0.0001) were highest in the ACS group. In multivariate models, comprising all biomarkers, elevated level of MPO had the best discriminatory power to identify patients with ACS. Receiver-operating characteristic curve with and without MPO comparison differed significantly (P = 0.03 for both ACS versus NCA and ACS versus SAP). CONCLUSION: Our study shows that ACS associates with low HDL-C and biomarkers of oxidative stress and inflammation. The addition of MPO in biomarker panels might improve diagnostic accuracy for ACS.

Cardiac steatosis associates with visceral obesity in nondiabetic obese men.

BACKGROUND: Liver fat and visceral adiposity are involved in the development of the metabolic syndrome (MetS). Ectopic fat accumulation within and around the heart has been related to increased risk of heart disease. The aim of this study was to explore components of cardiac steatosis and their relationship to intra-abdominal ectopic fat deposits and cardiometabolic risk factors in nondiabetic obese men. METHODS: Myocardial and hepatic triglyceride (TG) contents were measured with 1.5 T magnetic resonance spectroscopy, and visceral adipose (VAT), abdominal subcutaneous tissue (SAT), epicardial and pericardial fat by magnetic resonance imaging in 37 men with the MetS and in 40 men without the MetS. RESULTS: Myocardial and hepatic TG contents, VAT, SAT, epicardial fat volumes, and pericardial fat volumes were higher in men with the MetS compared with subjects without the MetS (P < .001). All components of cardiac steatosis correlated with SAT, VAT, and hepatic TG content and the correlations seemed to be strongest with VAT. Myocardial TG content, epicardial fat, pericardial fat, VAT, and hepatic TG content correlated with waist circumference, body mass index, high-density lipoprotein cholesterol TGs, very low-density lipoprotein-1 TGs, and the insulin-resistance homeostasis model assessment index. VAT was a predictor of TGs, high-density lipoprotein cholesterol, and measures of glucose metabolism, whereas age and SAT were determinants of blood pressure parameters. CONCLUSIONS: We suggest that visceral obesity is the best predictor of epicardial and pericardial fat in abdominally obese subjects. Myocardial TG content may present a separate entity that is influenced by factors beyond visceral adiposity.

Helical computerized tomography and NT-proBNP for screening of right ventricular overload on admission and at long term follow-up of acute pulmonary embolism.

BACKGROUND: Right ventricular dysfunction (RVD) in acute pulmonary embolism (APE) can be assessed with helical computerized tomography (CT) and transthoracic echocardiography (TTE). Signs of RVD and elevated natriuretic peptides like NT-proBNP and cardiac troponin (TnT) are associated with increased risk of mortality. However, the prognostic role of both initial diagnostic strategy and the use of NT-proBNP and TnT for screening for long-term probability of RVD remains unknown. The aim of the study was to determine the role of helical CT and NT-proBNP in detection of RVD in the acute phase. In addition, the value of NT-proBNP for ruling out RVD at long-term follow-up was assessed. METHODS: Sixty-three non-high risk APE patients were studied. RVD was assessed at admission in the emergency department by CT and TTE, and both NT-proBNP and TnT samples were taken. These, excepting CT, were repeated seven months later. RESULTS: At admission RVD was detected by CT in 37 (59 %) patients. RVD in CT correlated strongly with RVD in TTE (p < 0.0001). NT-proBNP was elevated (≥ 350 ng/l) in 32 (86 %) patients with RVD but in only seven (27 %) patients without RVD (p < 0.0001). All the patients survived until the 7-month follow-up. TTE showed persistent RVD in 6 of 63 (10 %) patients who all had RVD in CT at admission. All of them had elevated NT-proBNP levels in the follow-up compared with 5 (9 %) of patients without RVD (p < 0.0001). CONCLUSIONS: TTE does not confer further benefit when helical CT is used for screening for RVD in non-high risk APE. All the patients who were found to have RVD in TTE at seven months follow-up had had RVD in the acute phase CT as well. Thus, patients without RVD in diagnostic CT do not seem to require further routine follow-up to screen for RVD later. On the other hand, persistent RVD and thus need for TTE control can be ruled out by assessment of NT-proBNP at follow-up. A follow-up protocol based on these findings is suggested.

Epicardial fat, cardiac dimensions, and low-grade inflammation in young adult monozygotic twins discordant for obesity.

Epicardial fat with its close proximity to coronary arteries has been suggested to be a significant predictor of cardiovascular disease. We studied the relations among acquired obesity, low-grade inflammation, and genetic factors in the accumulation of epicardial fat. A rare sample (n = 15) of healthy monozygotic (MZ) twin pairs discordant for obesity (intrapair difference in body mass index ≥3 kg/m(2)) and 9 concordant MZ pairs 23 to 33 years old were examined for cardiac structure, function, epicardial fat thickness (echocardiography), abdominal subcutaneous tissue, and visceral adipose tissue (VAT), liver fat (magnetic resonance imaging/spectroscopy), and serum high-sensitivity C-reactive protein. In the entire sample, MZ cotwins were remarkably similar in most echocardiographic measurements including epicardial fat (intraclass correlation 0.63, p = 0.0004). However, in the discordant pairs, the obese cotwins (16.5 kg, 23% heavier) had 26% more epicardial fat (p = 0.0029) than nonobese cotwins. They also had significantly larger atrial and left ventricular dimensions. Epicardial fat correlated with VAT (r = 0.49, p = 0.02) in individual twins and when using intrapair differences of measurements within pairs (r = 0.39, p = 0.06). In multiple regression analyses including abdominal subcutaneous tissue, VAT, and liver fat, high-sensitivity C-reactive protein was the only factor that remained significantly associated with epicardial fat in individual twins and within pairs. In conclusion, subjects who share the same genes seem to have similar cardiac dimensions. However, acquired obesity increases epicardial fat independent of genetic factors. The close relation between epicardial fat and low-grade inflammation is likely to contribute to the development of cardiovascular disease in obesity.

Reduction in membrane component of diffusing capacity is associated with the extent of acute pulmonary embolism.

Acute pulmonary embolism (PE) often decreases pulmonary diffusing capacity for carbon monoxide (DL,CO), but data on the mechanisms involved are inconsistent. We wanted to investigate whether reduction in diffusing capacity of alveolo-capillary membrane (DM) and pulmonary capillary blood volume (Vc) is associated with the extent of PE or the presence and severity of right ventricular dysfunction (RVD) induced by PE and how the possible changes are corrected after 7-month follow-up. Forty-seven patients with acute non-massive PE in spiral computed tomography (CT) were included. The extent of PE was assessed by scoring mass of embolism. DL,CO, Vc, DM and alveolar volume (VA) were measured by using a single breath method with carbon monoxide and oxygen both at the acute phase and 7 months later. RVD was evaluated with transthoracic echocardiography and electrocardiogram. Fifteen healthy subjects were included as controls. DL,CO, DL, CO/VA, DM, vital capacity (VC) and VA were significantly lower in the patients with acute PE than in healthy controls (P < 0.001). DM/Vc relation was significantly lower in patients with RVD than in healthy controls (P = 0.004). DM correlated inversely with central mass of embolism (r = -0.312; P = 0.047) whereas Vc did not. DM, DL,CO, VC and VA improved significantly within 7 months. In all patients (P = 0.001, P = 0.001) and persistent RVD (P = 0.020, P = 0.012), DM and DL,CO remained significantly lower than in healthy controls in the follow-up. DM was inversely related to central mass of embolism. Reduction in DM mainly explains the sustained decrease in DL,CO in PE after 7 months despite modern treatment of PE.

[Cardiac sarcoidosis]. / Sydänsarkoidoosi.

Cardiac sarcoidosis is a severe inflammatory disease of the cardiac muscle, manifesting itself as atrioventricular block, ventricular tachycardias, cardiac insufficiency and combinations thereof. Approximately half of cardiac sarcoidosis patients exhibit no clinical signs of sarcoidosis outside the heart. The diagnosis is based on cardiac muscle imaging and myocardial biopsy. High dose corticosteroid medication is utilized for treatment. A life-threatening cardiac event occurred in more than one third of cardiac sarcoidosis patients at Meilahti hospital.

Apolipoprotein E polymorphism is associated with both carotid and coronary atherosclerosis in patients with coronary artery disease.

BACKGROUND AND AIMS: Apolipoprotein E (apoE) polymorphism plays a significant role in the development of atherosclerosis and cardiovascular disease. Therefore, the aim of the present study was to examine the association between apoE polymorphism and carotid intima-media thickness (IMT), and severity and extent of coronary artery disease (CAD). METHODS AND RESULTS: B-mode ultrasound and quantitative coronary angiography (QCA) were used to assess carotid, and coronary artery atherosclerosis in 91 patients with clinically suspected CAD referred for cardiac catheterization. Two apoE phenotype groups were defined: apoE3 (E3/E3) and apoE4 (including E4/E3, E4/E4 phenotypes). Maximum IMT was higher in the apoE4 group than in the apoE3 group (p=0.022). The global atheroma burden index was similarly higher in the apoE4 group than in the apoE3 group (p=0.033). ApoE4 subjects had higher levels of apolipoprotein B (apoB) (p=0.008), triglycerides (p=0.006), remnant lipoprotein-cholesterol (RLP-C) (p=0.023), and lipoprotein(a) [(Lp(a)] (p=0.041) than apoE3 subjects. The mean LDL particle size was smaller in the apoE4 group than in the apoE3 group (p=0.041). CONCLUSIONS: ApoE polymorphism was associated with both carotid and coronary atherosclerosis. Patients with the apoE4 isoform had an increased carotid IMT and a more severe and extensive CAD than patients with the apoE3 isoform.

Rosiglitazone reduces liver fat and insulin requirements and improves hepatic insulin sensitivity and glycemic control in patients with type 2 diabetes requiring high insulin doses.

BACKGROUND: Liver fat is an important determinant of insulin requirements during insulin therapy. Peroxisome proliferator-activated receptor (PPAR)-gamma agonists reduce liver fat. We therefore hypothesized that type 2 diabetic patients using exceptionally high doses of insulin might respond well to addition of a PPARgamma agonist. METHODS: We determined the effect of the PPARgamma agonist rosiglitazone on liver fat and directly measured hepatic insulin sensitivity in 14 patients with type 2 diabetes (aged 51 +/- 3 yr, body mass index 36.7 +/- 1.1 kg/m2), who were poorly controlled (glycosylated hemoglobin A 1c (HbA 1c) 8.9 +/- 0.4%) despite using high doses of insulin (218 +/- 22 IU/d) in combination with metformin. Liver fat content (1H-magnetic resonance spectroscopy), hepatic insulin sensitivity [6 h hyperinsulinemic euglycemic clamp (insulin 0.3 mU/kg.min) combined with [3-3H]glucose], body composition (magnetic resonance imaging), substrate oxidation rates (indirect calorimetry), clinical parameters, and liver enzymes were measured before and after rosiglitazone treatment (8 mg/d) for 8 months. RESULTS: During rosiglitazone, HbA(1c) decreased from 8.9 +/- 0.4% to 7.8 +/- 0.3% (P = 0.007) and insulin requirements from 218 +/- 22 to 129 +/- 20 IU/d (P = 0.002). Liver fat content decreased by 46 +/- 9% from 20 +/- 3% to 11 +/- 3% (P = 0.0002). Hepatic insulin sensitivity, measured from the percent suppression of endogenous glucose production by insulin, increased from -40 +/- 7% to -89 +/- 12% (P = 0.001). The percent change in liver fat correlated with the percent decrease in HbA 1c (r = 0.53, P = 0.06), insulin dose (r = 0.66, P = 0.014), and suppression of endogenous glucose production (r = 0.76, P = 0.003). CONCLUSIONS: Our results suggest that rosiglitazone may be particularly effective in type 2 diabetic patients who are poorly controlled despite using high insulin doses. The mechanism is likely to involve reduced liver fat and enhanced hepatic insulin sensitivity.

Insulin resistance as predictor of the angiographic severity and extent of coronary artery disease.

BACKGROUND: Insulin resistance (IR) is frequently observed in patients with coronary artery disease (CAD). Aim. To examine the association between IR and severity and extent of CAD. METHODS: Quantitative coronary angiography (QCA) was used to assess coronary atherosclerosis in 107 patients with clinically suspected CAD. QCA-derived indexes reflecting CAD severity, extent, and overall atheroma burden were calculated for the entire coronary tree, and separately for different coronary segments. IR was quantified using the homeostasis model assessment insulin resistance index (HOMA IR). Nondiabetic subjects (n = 83) were divided into group 1 (n = 41) with HOMA IR <1.8 (the median value), and group 2 (n = 42) with HOMA IR >or=1.8. Group 3 comprised diabetic subjects (n = 24). RESULTS: Global age- and gender-adjusted indexes for severity (P = 0.007), extent (P = 0.038), and atheroma burden (P = 0.035) of CAD were higher in group 2 than in group 1. Similarly, the global severity (P = 0.027), extent (P = 0.090), and global atheroma burden (P = 0.024) indexes were higher in group 3 compared with group 1. IR was correlated with quantitative angiographic indexes for distal segments only, but not for proximal or mid segments of coronary vessels. CONCLUSIONS: Patients with more severe degree of IR have a more severe, extensive, and distal type of CAD than patients with lower degree of IR.

Association of paraoxonase-1 activity and concentration with angiographic severity and extent of coronary artery disease.

OBJECTIVES: The goal of this study was to examine the association between paraoxonase-1 (PON1) activity and concentration and the severity and extent of coronary artery disease (CAD). BACKGROUND: Paraoxonase-1, a high-density lipoprotein-associated enzyme, is proposed to have an antiatherogenic effect by protecting low-density lipoproteins against oxidation. METHODS: We studied PON1 activity and concentration in 107 patients with known or suspected CAD referred for cardiac catheterization. Based on visual estimation of coronary angiograms, subjects were classified as having no or mild CAD (<50% stenosis) and significant CAD (> or =50% stenosis). Quantitative coronary angiography (QCA) was used to estimate the indexes of severity, extent, and overall atheroma burden of CAD. RESULTS: We found lower values of PON1 activity and concentration (p = 0.003 and p = 0.016, respectively) in the group with significant CAD as compared with the group with no or mild CAD. The PON1 activity was significantly inversely correlated with CAD severity (r = -0.364, p < 0.001), extent (r = -0.221, p = 0.022), and atheroma burden (r = -0.277, p = 0.004). Similarly, PON1 concentration correlated with CAD severity (r = -0.306, p = 0.001) and atheroma burden (r = -0.229, p = 0.017). In multiple regression analysis, gender and PON1 activity were significant determinants of the severity of CAD independently of age, hypertension, smoking, abnormal glucose regulation, and high-density lipoprotein cholesterol. CONCLUSIONS: Our results indicate that PON1 activity and concentration are lower in subjects with significant CAD, and that there is a significant relationship between PON1 activity and concentration and CAD assessed by QCA.

Association of carotid intima-media thickness with angiographic severity and extent of coronary artery disease.

The present study examined the association between carotid intima-media thickness (IMT) and severity and extent of coronary artery disease (CAD). B-mode ultrasound and quantitative coronary angiography were used to assess carotid and coronary artery atherosclerosis in 108 patients with known or suspected CAD who had been referred for cardiac catheterization. Maximum and mean IMT values of carotid arteries were measured and expressed as mean aggregate values. To evaluate anatomic severity and extent of CAD, several quantitative coronary angiographically derived parameters were incorporated into indexes. These quantitative coronary angiographic measurements reflected CAD severity, extent, and overall "atheroma burden" and were calculated for the entire coronary tree and separately for different coronary segments (i.e., left main, proximal, mid, and distal segments). Maximum and mean IMT values were significantly correlated with CAD severity (p = 0.004 and 0.005, respectively), extent (p = 0.022 and 0.016, respectively), and atheroma burden (p = 0.008 for the 2 values). Further, carotid IMT was correlated with quantitative angiographic indexes for mid and distal segments but not with the proximal segments of coronary vessels. In conclusion, our study shows an association between carotid IMT and severity and extent of CAD as assessed by quantitative coronary angiography. Carotid IMT seems to be a weaker predictor of coronary atherosclerosis in the proximal parts of the coronary tree than in the mid and distal parts.