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2.  Adiponectin is associated with abnormal lipid profile and coronary microvascular dysfunction in patients with dilated cardiomyopathy without overt heart failure 
Reduced plasma adiponectin has been associated with abnormal lipid profile, reduced left ventricle (LV) function, and the extent of coronary atherosclerosis in coronary artery disease. The aim of this study was to assess these relationships in patients with dilated cardiomyopathy (DCM) without overt heart failure. Plasma adiponectin was measured in 55 DCM patients (age, 59 ± 12 years; male, 36; body mass index [BMI], 26.9 ± 0.49 kg/m2; LV ejection fraction, 39.8% ± 1.3%; New York Heart Association class I-II) and in 40 age- and BMI-matched healthy controls. In a subset of 25 patients, myocardial blood flow (MBF) was measured at rest and during intravenous dipyridamole (0.56 mg/kg in 4 minutes) by positron emission tomography and 13N-ammonia as a flow tracer. Adiponectin was 6.6 ± 0.34 μg/mL in controls and 10.9 ± 0.85 μg/mL in DCM patients (P < .001), where it was related inversely with BMI (P = .009) and directly with brain natriuretic peptide (P = .017), high-density lipoprotein (HDL) cholesterol (P = .002), and MBF dipyridamole (P = .020). Adiponectin lesser than median value in patients was associated with higher total to HDL cholesterol ratio (4.8 ± 0.24 vs 3.9 ± 0.18, P = .009) and lower MBF reserve (1.76 ± 0.16 vs 2.43 ± 0.19, P = .01). These results could suggest that down-regulation of the adiponectin levels and reduced HDL cholesterol have a key role in causing impaired coronary function and myocardial perfusion in DCM.
PMCID: PMC3706193  PMID: 20199784
3.  T−786→C polymorphism of the endothelial nitric oxide synthase gene is associated with insulin resistance in patients with ischemic or non ischemic cardiomyopathy 
BMC Medical Genetics  2012;13:92.
Insulin resistance (IR) and endothelial dysfunction are frequently associated in cardiac disease. The T−786→C variant in the promoter region of the endothelial nitric oxide synthase (eNOS) gene has been associated with IR in both non-diabetic and diabetic subjects. Aim of the study was to assess the reciprocal relationships between T−786→C eNOS polymorphism and IR in ischemic and non-ischemic cardiomyopathy.
A group of 132 patients (108 males, median age 65 years) with global left ventricular (LV) dysfunction secondary to ischemic or non-ischemic heart disease was enrolled. Genotyping of T−786→C eNOS gene promoter, fasting glucose, insulin, and insulin resistance (defined as HOMA-IR index > 2.5) were determined in all patients.
Genotyping analysis yielded 37 patients homozygous for the T allele (TT), 70 heterozygotes (TC) and 25 homozygous for C (CC). Patients with CC genotype had significantly higher systemic arterial pressure, blood glucose, plasma insulin and HOMA index levels than TT. At multivariate logistic analysis, the history of hypertension and the genotype were the only predictors of IR. In particular, CC genotype increased the risk of IR (CI% 1.4-15.0, p < 0.01) 4.5-fold. The only parameter independently associated with the extent of LV dysfunction and the presence of heart failure (HF) was the HOMA index (2.4 CI% 1.1-5.6, p < 0.04).
T−786→C eNOS polymorphism was the major independent determinant of IR in a population of patients with ischemic and non-ischemic cardiomyopathy. The results suggest that a condition of primitive eNOS lower expression can predispose to an impairment of glucose homeostasis, which in turn is able to affect the severity of heart disease.
PMCID: PMC3495192  PMID: 23031426
eNOS polymorphism; Insulin resistance; Heart failure
4.  Cobalt-Protoporphyrin Improves Heart Function by Blunting Oxidative Stress and Restoring NO Synthase Equilibrium in an Animal Model of Experimental Diabetes 
Myocardial dysfunction and coronary macro/microvascular alterations are the hallmarks of diabetic cardiomyopathy and are ascribed to increased oxidative stress and altered nitric oxide synthase (NOS) activity. We hypothesize that pre-treatment by cobalt-protoporphyrin IX (CoPP) ameliorates both myocardial function and coronary circulation in streptozotocin (STZ)-induced diabetic rats. Isolated hearts from diabetic rats in Langendorff configuration displayed lower left ventricular function and higher coronary resistance (CR) compared to hearts from control animals. CoPP treatment of diabetic animals (0.3 mg/100 g body weight i.p., once a week for 3 weeks) significantly increased all the contractile/relaxation indexes (p < 0.01), while decreasing CR (p < 0.01). CoPP enhanced HO-1 protein levels and reduced oxidative stress in diabetic animals, as indicated by the significant (p < 0.05) decrease in heart % GSSG, O2− and malondialdehyde (MDA) levels. CoPP increased adiponectin levels and phosphorylation of AKT and AMPK and reversed the eNOS/iNOS expression imbalance observed in the untreated diabetic heart. Furthermore, after CoPP treatment, a rise in malonyl-CoA as well as a decrease in acetyl-CoA was observed in diabetic hearts. In this experimental model of diabetic cardiomyopathy, CoPP treatment improved both cardiac function and coronary flow by blunting oxidative stress, restoring eNOS/iNOS expression balance and increasing HO-1 levels, thereby favoring improvement in both endothelial function and insulin sensitivity.
PMCID: PMC3366474  PMID: 22675305
diabetes; cardiac contractility; AMPK; nitric oxide; coronary microcirculation
5.  Automatic PET-CT Image Registration Method Based on Mutual Information and Genetic Algorithms 
The Scientific World Journal  2012;2012:567067.
Hybrid PET/CT scanners can simultaneously visualize coronary artery disease as revealed by computed tomography (CT) and myocardial perfusion as measured by positron emission tomography (PET). Manual registration is usually required in clinical practice to compensate spatial mismatch between datasets. In this paper, we present a registration algorithm that is able to automatically align PET/CT cardiac images. The algorithm bases on mutual information (MI) as registration metric and on genetic algorithm as optimization method. A multiresolution approach was used to optimize the processing time. The algorithm was tested on computerized models of volumetric PET/CT cardiac data and on real PET/CT datasets. The proposed automatic registration algorithm smoothes the pattern of the MI and allows it to reach the global maximum of the similarity function. The implemented method also allows the definition of the correct spatial transformation that matches both synthetic and real PET and CT volumetric datasets.
PMCID: PMC3349214  PMID: 22593696
6.  Effects of long‐term treatment with carvedilol on myocardial blood flow in idiopathic dilated cardiomyopathy 
Heart  2007;93(7):808-813.
To assess whether chronic treatment with carvedilol can increase myocardial blood flow (MBF) and MBF reserve in idiopathic dilated cardiomyopathy (IDC).
Study design
In a double‐blind, placebo‐controlled trial, 16 consecutive patients with IDC were randomised to treatment with either carvedilol up to 25 mg twice a day (n = 8, 7 men, mean (SD) age 60 (9) years, mean (SD) left ventricular ejection fraction (LVEF) 30% (5%)), or placebo (n = 8 , 6 men, mean (SD) age 62 (9) years, mean (SD) LVEF 28% (6%), NS vs carvedilol group). Before and 6 months after treatment, regional MBF was measured at rest and after intravenous injection of dipyridamole (Dip; 0.56 mg/kg in 4 min) by positron emission tomography and using 13N‐ammonia as a flow tracer. Exercise capacity was assessed as the time duration in a maximal bicycle exercise stress test.
Carvedilol induced a significant decrease in heart rate at rest and during maximal exercise, and an increase in exercise capacity. Absolute MBF values did not significantly change after carvedilol or placebo treatment, either at rest or during Dip injection, although Dip‐MBF tended to improve after treatment. Coronary flow reserve significantly increased following carvedilol treatment (from 1.67 (0.63) to 2.58 (1.04), p<0.001), whereas it remained unchanged following the placebo treatment (from 1.80 (0.84) to 1.77 (0.60), NS). Stress‐induced regional perfusion defects decreased after carvedilol treatment (from 38% to 15%).
Long‐term treatment with carvedilol can significantly increase coronary flow reserve and reduce the occurrence of stress‐induced perfusion defects, suggesting a favourable effect of the drug on coronary microvascular function in patients with IDC.
PMCID: PMC1994449  PMID: 17237134
7.  Circulating heat shock proteins and inflammatory markers in patients with idiopathic left ventricular dysfunction: their relationships with myocardial and microvascular impairment 
Cell Stress & Chaperones  2007;12(3):265-274.
Little information is available on peripheral levels of Hsp72, Hsp60, and anti-Hsp60 antibodies in patients with left ventricular (LV) dysfunction due to non-atherosclerotic cardiac disease. In this study, serum Hsp72, Hsp60 and anti-Hsp60 antibodies, IL-6, and C-reactive protein (CRP) were measured in 44 healthy controls and in 82 patients with angiographically normal coronary arteries (LV ejection fraction [EF] ≥ 50%, n = 22; ≥35% to <50%, n = 32; <35%, n = 28). Patients with more severe disease (more depressed myocardial blood flow at rest and during dipyridamole, indicative of coronary microvascular impairment) showed more elevated circulating Hsp60 and auto-antibodies, Hsp72, and CRP levels. IL-6 was increased progressively as a function of severity of LV dysfunction. Anti-Hsp60 antibodies, Hsp72, and IL-6 were significantly correlated with brain natriuretic peptide (BNP) levels and LV end-diastolic dimensions (LVEDD) values. IL-6 tended to be related with Hsp72 in particular in patients with more severe disease (r = 0.45, P = 0.021). Hsp60 and Hsp72 activation and inflammatory markers were correlated with the extent of cardiac and microvascular dysfunction in patients with angiographycally normal coronary arteries. These results suggest a pathogenic role of infective-metabolic insult and inflammatory reaction in the development of vascular and myocardial damage in patients with heart failure even in the absence of overt coronary artery disease.
PMCID: PMC1971236  PMID: 17915559

Results 1-7 (7)