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Objectives: There is growing evidence that myocardial segments with reverse redistribution are viable in patients with chronic coronary artery disease. The aim of this study was to assess the effects of myocardial revascularization on systolic function and thallium-201 uptake in such segments.Methods: Rest-redistribution thallium-201 tomography before and after myocardial revascularization was performed in 47 patients with chronic coronary artery disease. Regional function was evaluated by two-dimensional echocardiography before and after revascularization according to a 3-point scale (1 = normal, 2 = hypokinetic, 3 = a/dyskinetic). Improvement of dysfunctional segments was defined when systolic function score decreased > or =1 after revascularization. Reverse redistribution was defined as >8% decrease in relative thallium-201 uptake between rest and redistribution images.Results: Reverse redistribution was found in 27 (57%) of 47 patients, corresponding to 60 (11%) of 564 myocardial segments. Of such segments, 24 (40%) had normal systolic function, 19 (32%) were hypokinetic, and 17 (28%) were a/dyskinetic. Thirty-six segments underwent myocardial revascularization, and reverse redistribution was no longer present in 86% of them subsequent to the procedure. Of 26 dyssynergic segments with reverse redistribution subjected to revascularization, 18 (69%) improved at follow-up.Conclusions: The findings of the present study indicate that reverse redistribution is a reversible phenomenon and is often associated with improvement of systolic function following revascularization in patients with chronic coronary artery disease. [ABSTRACT FROM AUTHOR]

The impact of the duration of atrioventricular (AV) delay on obstruction in hypertrophic cardiomyopathy was evaluated in 12 patients by cardiac catheterization, and in 8 of them also by Doppler echocardiography. The AV delay was programmed in random order at 125, 100 and 75 ms in the invasive study and at 120, 100 and 80 ms after pacemaker implantation. The arterial pressure did not changed throughout the studies, whereas the gradient decreased significantly by reducing the AV delay value; the greater gradient reduction was obtained, in both studies, with the AV delay set between 75 or 80 and 100 ms. QRS duration increased significantly by reducing the AV delay during both studies. The widest QRS was not associated with the smallest gradient in all patients. Changes in gradients were similar during the invasive and noninvasive protocols. [ABSTRACT FROM AUTHOR]

Heart Failure (HF) is a syndrome, which implies the existence of different phenotypes. The new categorization includes patients with preserved ejection fraction (HFpEF), mid-range EF (HFmrEF), and reduced EF (HFrEF) but the molecular mechanisms involved in these HF phenotypes have not yet been exhaustively investigated. Sirt1 plays a crucial role in biological processes strongly related to HF. This study aimed to evaluate whether Sirt1 activity was correlated with EF and other parameters in HFpEF, HFmrEF, and HFrEF. Seventy patients, HFpEF (n = 23), HFmrEF (n = 23) and HFrEF (n = 24), were enrolled at the Cardiology Unit of the University Hospital of Salerno. Sirt1 activity was measured in peripheral blood mononuclear cells (PBMCs). Angiotensin-Converting Enzyme 2 (ACE2) activity, Tumor Necrosis Factor-alpha (TNF-α) and Brain Natriuretic Peptide (BNP) levels were quantified in plasma. HFpEF showed lower Sirt1 and ACE2 activities than both HFmrEF and HFrEF (p < 0.0001), without difference compared to No HF controls. In HFmrEF and HFrEF a very strong correlation was found between Sirt1 activity and EF (r2 = 0.899 and r2 = 0.909, respectively), and between ACE2 activity and Sirt1 (r2 = 0.801 and r2 = 0.802, respectively). HFrEF showed the highest TNF-α levels without reaching statistical significance. Significant differences in BNP were found among the groups, with the highest levels in the HFrEF. Determining Sirt1 activity in PBMCs is useful to distinguish the HF patients' phenotypes from each other, especially HFmrEF/HFrEF from HFpEF. [ABSTRACT FROM AUTHOR]

Objective: To assess immediate and mid-term clinical and angiographic outcomes of the dexamethasone drug-eluting stent (D-DES) in patients with acute coronary syndrome (ACS). Patients and methods: A prospective, nationwide, controlled, registry. Inflammation plays a key role in ACS, and the anti-inflammatory effects of local elution of dexamethasone in unstable plaques may represent a valid therapeutic approach. All patients had ACS on admission (n = 332). 81.5% of the patients had unstable angina and 18.5% had non-ST elevation myocardial infarction (MI). 47% had ST·T segment changes, 59% had troponin elevation, 77% had elevated C-reactive protein levels and 48% had intermediate-high Thrombolysis in Myocardial Infarction risk score. Patients were treated according to an early invasive approach with 420 D-DES in 387 coronary lesions. Primary end point was the cumulative incidence of death, MI and ischaemia-driven target vessel revascularisation (TVR) at 6 months. Results: At 30 days, 2 (0.6%l patients died, and sub-acute stent thrombosis occurred in 2 patients. At 6 months, 328 (98.8%) patients were controlled, 3 (0.9%) patients had died, 7 (2.1%) had MI and 28 (8.5%) underwent ischaemia-driven TVR. Therefore, the primary end point occurred in 11 .5% of patients. At multivariate analysis, multi-vessel coronary artery disease (odds ratio (OR) = 2.16, 95% CI = 1 .47 to 3.17, p=0.0001) and vessel diameter ⩽2.75 mm (OR = 1.64, 95% CI = 1.08 to 2.49, p=0.02) were independent predictors of 6-month clinical events. Global angiographic restenosis rate was 33.3%. Conclusion: This is the first large, multicentre analysis of the clinical and angiographic outcomes obtained with D-DES implanted in ACS. D-DES offers a low rate of clinical events at 6 months, but has no anti-restenosis effect. [ABSTRACT FROM AUTHOR]

Background: In patients with Normal Glucose Tolerance (NGT) some causes of ischemic heart disease (IHD) were not completely investigated. The role both of metabolic milieu and adipokines in IHD progression was not fully investigated. Our aim was to assess the link between adipokines plasma levels, insulin resistance (IR) and IHD in NGT patients undergoing Percutaneous Coronary Intervention (PCI). Methods: AIRE is a single-center prospective longitudinal observational study investigating the IHD outcome of NGT subjects who underwent coronary revascularization by PCI in a third level cardiology center at A.O. dei Colli Hospital, University of Campania "Luigi Vanvitelli". Six hundred seventy-nine subjects hospitalized in 2015 for coronary arteriography not suffering from Acute Coronary Syndrome (ACS) in the previous 4 weeks, as well as from all conditions could affect glycemic plasma levels and IR status, were assessed for eligibility. Fifty-four patients with neither history of diabetes nor Altered Fasting Glucose (AFG)/Impaired Fasting Glucose (IGT) after Oral Glucose Tolerance Test (OGTT) were finally enrolled. Primary endpoint was the assessment of the relationship of adipokines and HOMA-IR with the occurrence of restenosis in NGT subjects. As secondary endpoint we assessed the association of the same adipokines and IR with overall ACS events after PCI in NGT subjects. Results: The 54 NGT patients enrolled were mainly males (85%), with a median age of 60 years [IQR 58–63 years]. Only 4 patients (7.4%) experimented restenosis. Median follow-up was equal to 29.5 months [IQR 14.7–34 months]. Adiponectin levels were independently associated to restenosis (OR 0.206; 95% CI 0.053–0.796; p = 0.000). Instead HOMA-IR and adiponectin appeared independently associated both to de novo IHD (OR 9.6*1013; 95% CI 3.026–3.08*1027; p = 0.042 and OR 0.206; 95% CI 0.053–0.796; p = 0.000, respectively) and overall new PCI (OR 1.5*1011; 95% CI 2.593–8.68*1021; p = 0.042 and OR 0.206; 95% CI 0.053–0.796; p = 0.000, respectively). Moreover, we fixed a potential cut-off for adiponectin for risk of restenosis (≤ 8.5 µg/mL) and overall new PCI (≤ 9.5 µg/mL). Conclusion: IR and cytokines play a role in progression of any stage of IHD also in NGT subjects. Our results in this setting of patients, though the relatively small sample size, represent a novelty. Future studies on larger populations are needed to analyze more in depth adipokines and insulin resistance role on IHD progression in non-diabetic people. [ABSTRACT FROM AUTHOR]