Epicardial Fat in Nonalcoholic Fatty Liver Disease: Properties and Relationships With Metabolic Factors, Cardiac Structure, and Cardiac Function.

Nonalcoholic fatty liver disease (NAFLD) is closely related to insulin resistance and the metabolic syndrome and might be an important cardiovascular (CV) risk factor. Epicardial adipose tissue (EAT) has been implicated in the pathogenesis of obesity-related CV disease. In an NAFLD population, we investigated EAT thickness and its possible relations to NAFLD and cardiac structure and function. This was an observational study of 57 patients with NAFLD and 48 age-matched controls. Patients with NAFLD had significantly higher body mass index (P < .0001), waist circumference (P < .0001), and high-sensitivity C-reactive protein (P = .005), whereas high-density lipoprotein cholesterol (P = .01) and adiponectin (P = .005) levels were significantly lower. The EAT was not thicker in NAFLD but was positively related to indices of impaired glucose tolerance and inflammation, with diabetes being an independent predictor of EAT thickness (b* = 0.29, P = .04). No relations were found between EAT and cardiac structure and function. In conclusion, this study confirms a pathologic phenotype of NAFLD. Epicardial fat was not significantly related to NAFLD per se, but diabetes, glucose metabolism, and inflammation were closely related to its thickness.

Inflammatory markers and plaque morphology: an optical coherence tomography study.

BACKGROUND: OCT with its unique image resolution is the ideal method to detect culprit lesion characteristics in different clinical presentations. The identification of inflammatory markers related to plaque characteristics may be of clinical importance. METHODS: Thirty-two patients with acute coronary syndromes (ACS) and fourteen patients with stable angina pectoris (SAP) were enrolled in this study. Culprit lesion morphology was assessed by optical coherence tomography (OCT) in patients with ACS and SAP. The possible relations between serum levels of high sensitivity-C reactive protein (hs-CRP) and interleukin-18 (IL-18) with plaque characteristics were investigated in those patients. RESULTS: Plaque rupture and thin-cap fibroatheroma (TCFA) were detected more frequently in ACS patients compared with SAP patients, (78.6% vs. 14.3%, p<0.001, 92.9% vs. 14.3%, p<0.001, respectively). Higher levels of serum hs-CRP and IL-18 were found in patients with plaque rupture vs. those with no plaque rupture (median value: 19.2mg/L vs. 1.6 mg/L, p<0.001 and 219.5 pg/ml vs. 127.5 pg/ml, p=0.001 respectively), and TCFA vs. those without TCFA (median value: 15.2mg/L vs. 1.6 mg/L, p=0.004 and 209.0 pg/ml vs.153.2 pg/ml, p=0.03 respectively). Serum hs-CRP was the only independent predictor of plaque rupture (p=0.02, odds ratio 1.1, 95% confidence interval 1.0 to 1.2). A cut-off value of hs-CRP>4.5mg/L could detect ruptured plaque with a sensitivity of 91.7% and a specificity of 77.8%. CONCLUSIONS: OCT detected plaque rupture and TCFA more frequent in ACS patients compared with SAP. Elevated hs-CRP and IL-18 were positively related to plaque instability and rupture.

Incomplete arterial healing 8 years after the implantation of sirolimus-eluting stent. In vivo visualization by optical coherence tomography.

The time course of complete arterial healing after drug eluting stent implantation is unknown. We present a case of incomplete endothelialization and late stent malapposition identified by optical coherence tomography 8 years after a sirolimus-eluting stent implantation, which was not related with any adverse clinical event.

Visualization of coronary plaque rupture using optical coherence tomography.

Optical coherence tomography (OCT) is an optical analogue of intravascular ultrasound that has recently been proposed as a high-resolution imaging method for plaque characterization. Histology-controlled studies have shown that OCT can evaluate the characteristics of culprit lesions, such as fibrous cap thickness, fibrous cap macrophage density, lipid core and intracoronary thrombus. We describe a case where OCT was used to evaluate the culprit lesion morphology in a patient with acute myocardial infarction. The patient was treated with stent implantation. OCT was also used to confirm good stent apposition.

C-reactive protein, interleukin 6, and N-terminal pro-brain natriuretic peptide following cardioversion of atrial fibrillation: is there a role of biomarkers in arrhythmia recurrence?

AIMS: We investigated the role of high-sensitivity C-reactive protein (hsCRP), interleukin 6 (IL-6), and N-terminal pro-brain natriuretic peptide (NTpro-BNP), in atrial fibrillation (AF) recurrence rate. METHODS: A total of 80 patients with first AF episode were studied prospectively. Echocardiography (ECG), Holter ECG, and measurements of hsCRP, IL-6, and NTproBNP were performed immediately post conversion and at 1 month. RESULTS: Recurrence was positively related to left atrial volume (P < .001), with no difference in NTpro-BNP, hsCRP, and IL-6. Decreased NTpro-BNP was observed in all at 1 month (P < .001, F = 63.4) and was positively related to left atrial volume (P < .01). In the lone AF subgroup, NTpro-BNP was lower and dropped significantly at 1 month (interaction F = 6.53, P < .01). CONCLUSIONS: Atrial volume was related to AF recurrence, whereas hsCRP, IL-6, and NTpro-BNP were not reliable for AF relapse. Relation of NTpro-BNP to left atrial volume could indicate a role in the atrial remodeling process.

DDDR pacing results in left ventricular asynchrony with preservation of ejection fraction and NT-proBNP: a prospective study in sick sinus syndrome and normal ventricular function.

Desynchronization induced by right ventricular pacing may increase the risk for heart failure. We aimed to compare left ventricular (LV) function, synchrony and left atrial size along with NT-proBNP levels, in 2 different modes of pacing: AAIR versus DDDR. This was a prospective study of 60 patients with sick sinus syndrome, preserved LV function and normal atrioventricular conduction. Each pacing mode lasted at least 2 months, in every patient, after which period every patient was switched to the alternate pacing mode. Intraventricular asychrony was assessed by: 1) M-Mode septal-to-posterior wall motion delay (SPWMD), and 2) Tissue Doppler imaging (TDI) septal to lateral delay. NT-proBNP was measured at the end of each pacing mode. LV ejection fraction and left atrial diameter were not different in the 2 pacing modes, although asynchrony was induced in the DDDR arm (p<0.001 for TDI). NT-proBNP was lower in the DDDR compared to the AAIR mode (p=0.003, F=9.64). The NT-proBNP was inversely correlated to LV ejection fraction in the DDDR mode (p=0.0001, R=-0.75), whilst it was significantly correlated to the TDI septal-lateral delay and SPWMD (p=0.007, R=0.4 and p=0.002, R=0.5) in the AAIR mode. In conclusion in sick sinus syndrome with preserved LV function the DDDR mode does not compromise LV systolic function although it causes asynchrony. The NT-proBNP is lower when the right ventricle is paced, is inversely related to LV function and it is related to the degree of LV synchronization in the AAIR mode.

Late acquired stent malapposition detected by optical coherence tomography examination.

Late stent malapposition may play a role in stent thrombosis, but the results of several intravascular ultrasound and few optical coherence tomography (OCT) studies are still controversial. We present a case of late acquired stent malapposition after drug eluting stent implantation, identified by follow-up OCT examination at 12 months, which was not related with any adverse clinical event.

Inverse relation of C-reactive protein levels to heart rate variability in patients after acute myocardial infarction.

INTRODUCTION: Inflammation has a major role in atherosclerosis and the acute phase C-reactive protein (CRP) is elevated after acute myocardial infarction. Inflammation is also implicated in autonomic nervous system control. Heart rate variability (HRV) has been used as a marker of abnormal autonomic activity after myocardial infarction. Our purpose was to investigate the relation between CRP levels and autonomic tone in patients after acute ST-segment elevation myocardial infarction. METHODS: We studied prospectively 98 patients. CRP and the cardiac enzymes CK, CK-MB, and troponin-I were measured for a total of 72 hours and 24-hour Holter ECG recordings for HRV analysis were acquired before hospital discharge. RESULTS: The natural logarithm of CRP levels was inversely correlated with the following logarithmic transformed indices of HRV in the time and in the frequency domain: SDNN, standard deviation of all normal R-R intervals, (r = -0.40, p < 0.001); SDANN index, standard deviation of the average normal R-R intervals for 5-minute segments, (r = -0.46, p < 0.001); SDNN index, mean of the standard deviation of all normal R-R intervals for 5-minute segments (r = -0.41, p < 0.001); total power (TP) (r = -0.38, p < 0.001); high frequency power (HF) (r = -0.31, p < 0.01); low frequency power (LF) (r = -0.45, p < 0.001). The strong inverse relation between CRP and SDNN, SDANN, SDNN index, LF and TP persisted after adjustment for left ventricular function. CONCLUSIONS: Increased levels of circulating CRP after acute myocardial infarction are associated with attenuated HRV indices, suggesting a possible relationship between inflammation and cardiac autonomic balance.

Relation of elevated C-reactive protein and interleukin-6 levels to left atrial size and duration of episodes in patients with atrial fibrillation.

Previous studies have demonstrated inflammation to be a risk factor in patients with atrial fibrillation (AF). In this prospective study of 90 patients with persistent and permanent AF and 46 controls, we found increased C-reactive protein (CRP) and interleukin-6 levels in patients with AF compared with controls (p <0.001). Multivariate analysis revealed CRP to be an independent predictor of AF (p = 0.01). Left atrial diameter was positively related to CRP and interleukin-6 (p <0.001, R = 0.37; p <0.001, R = 0.46, respectively) and negatively related to left ventricular function. Interleukin-6 levels were positively related to AF duration before cardioversion (p = 0.02). Elevation of CRP and interleukin-6 suggest a role of inflammation in AF, and the relation of CRP and interleukin-6 to left atrial size and AF duration before cardioversion indicates that inflammation may participate in the process of atrial remodeling.

Management of inadvertent left ventricular permanent pacing.

Inadvertent implantation of a pacemaker lead in the left ventricle is an uncommon complication. We report a case of a permanent pacemaker lead inadvertently placed through the left subclavian artery, across the aortic valve into the left ventricle. A chest X-ray one month after the procedure showed an unusual course of the lead and a 12-lead ECG and a transthoracic echocardiogram confirmed the diagnosis. The patient refused surgical removal and remained on full anticoagulation. No clinical events were recorded during a 3-year follow-up. In such cases we propose life-long full anticoagulation as an alternative to surgical lead extraction.

Preinfarction angina does not alter infarct size and in hospital outcome after acute myocardial infarction with ST elevation.

BACKGROUND: Preinfarction angina has been reported to limit infarct size, in a manner analogous to experimental preconditioning. However, other studies have reported inconsistent results. We aimed to investigate prospectively the role of preinfarction angina on infarct size and in hospital outcome. METHODS: Ninety-nine patients were divided into three groups according to the timing of angina: the group "< 48 h" reported angina within the last 48 h, the group "> 48 h" earlier than 48 h and the group "acute" no angina before infarction. Myocardial injury was estimated by creatine kinase, creatine kinase-MB, troponin I and C-reactive protein. In hospital events included death, recurrent ischemia, congestive heart failure and atrioventricular block. RESULTS: Clinical characteristics, thrombolysis administration and the magnitude of enzymes released were not statistically different among the three groups: peak creatine kinase was 2139+/-1714 U/l for the >48 h group, vs. 2344+/-1634 U/l for the acute group, vs. 2209+/-1384 U/l for the <48 h group (p=0.88). Peak creatine kinase-MB was 124+/-104 U/l for the >48 h group, vs. 168+/-182 U/l for the acute group, vs. 154+/-108 U/l for the <48 h group (p=0.62). Peak troponin I, peak C-reactive protein and in hospital outcome also did not differ statistically in the three groups; p=0.5, p=0.45. CONCLUSIONS: Infarct size estimated by cardiac enzymes and by the marker of C-reactive protein, as well as in hospital clinical prognosis are not different in patients with and without preinfarction angina. It seems, therefore, that preinfarction angina confers ischemic conditions inadequate to mimic preconditioning.

Myocardial infarction under the age of 36: prevalence of thrombophilic disorders.

It has been suggested that thrombotic tendency increases the risk of myocardial infarction (MI). To investigate the association between the risk of MI at a young age and genetic thrombogenic disorders (G20210A mutation in the prothrombin gene, G1691A mutation in the factor V gene and deficiencies of protein C, protein S and antithrombin III) we conducted a case-control study among 70 survivors of MI who had experienced the event before the age of 36 and 260 healthy subjects. The G20210A mutation in the prothrombin gene was found more often in young patients with MI than among controls (11.4 versus 3.1%). The odds ratio (OR) for MI for carriers versus non-carriers was 4 (95% confidence interval [CI], 1.5 to 11.3). The adjusted OR for major cardiovascular risk factors (smoking, hypecholesterolaemia, diabetes mellitus, hypertension and obesity) was 4.3 (95% CI, 1.3 to 14). The simultaneous presence of both G20210A mutation in the prothrombin gene and smoking further increased the risk of MI compared with nonsmokers and non-carriers (OR, 58; 95% CI, 11.4-294). The G1691A mutation in factor V gene was not associated with an increased relative risk for MI (OR, 0.87; 95% CI, 0.26 to 2.5). Finally, there was no significant difference in the prevalence of deficiencies of protein C, protein S and antithrombin III between cases and controls. In conclusion, our data indicate that the G20210A mutation in the prothrombin gene was the only genetic prothrombotic risk factor associated with the risk of developing MI under the age of 36 years.