1,721,060 research outputs found
Long term cardioprotective action of trimetazidine and potential effect on the inflammatory process in patients with ischaemic dilated cardiomyopathy.
No full textDi Napoli P, Taccardi AA, Barsotti A. Long term cardioprotective action of trimetazidine and potential effect on the inflammatory process in patients with ischaemic dilated cardiomyopathy. Heart. 2005 Feb;91(2):161-5.
Department of Cardiology, Intensive Care Unit, Casa di Cura Villa Pini d'Abruzzo, Chieti, Italy. [email protected]
OBJECTIVE: To investigate the long term effects of trimetazidine in patients with dilated ischaemic cardiomyopathy. The effects of trimetazidine on left
ventricular function as well as its tolerability profile and potential anti-inflammatory effects were studied.
DESIGN: 61 patients were randomly assigned either to receive trimetazidine (20 mg thrice daily) in addition to their conventional treatment or to continue their usual drug treatment for 18 months. Patients were evaluated at baseline and at 6, 12, and 18 months with a clinical examination, echocardiography, and biochemical analysis (C reactive protein). RESULTS: Trimetazidine added to the usual treatment significantly improved the patients' functional status (assessed by New York Heart Association functional
class). The functional improvement of trimetazidine treated patients was associated with a significant increase in left ventricular ejection fraction (30 (6)%, 32 (8)%, 38 (7)%, and 37 (6)% v 31 (8)%, 30 (7)%, 28 (6)%, and 26 (9)% in
control patients at baseline and at 6, 12, and 18 months, respectively) and with a significant effect on ventricular remodelling. C reactive protein plasma concentrations remained stable throughout the study in patients receiving
trimetazidine (2.5 (1.0), 2.7 (2.0), 2.7 (3.0), and 3.0 (2.0) mg/l at baseline and at 6, 12, and 18 months, respectively) but increased significantly in the control group (2.4 (1.0), 3.4 (1.2), 6.0 (4.0), and 7.0 (5.0) mg/l, respectively). No significant adverse event or changes in clinical or biochemical
parameters were detected.
CONCLUSION: Treatment with trimetazidine added to the usual treatment for up to 18 months was well tolerated and induced a functional improvement in patients
with dilated cardiomyopathy. Trimetazidine treatment was associated with a significant improvement of left ventricular function and the remodelling process.
Results also suggest that the inflammatory response was limited in patients treated with trimetazidine
Di Napoli, P A, 5224224
No full textThis record was harvested from a previous catalogue system and will be withdrawn in 2025. Information in this record may be superseded or incomplete. Visit this record in UMA's new catalogue at: https://archives.library.unimelb.edu.au/nodes/view/381697Surname: DI NAPOLI. Given Name(s) or Initials: P A. Military Service Number or Last Known Location: 5224224. Missing, Wounded and Prisoner of War Enquiry Card Index Number: SEA-2743.197763
Item: [2016.0049.13990] "Di Napoli, P A, 5224224
Modeling of a single pulse electric discharge at sphere-flat interface by coupling contact multiphysics and phase transformations
No full textPubblicazione su CDRO
Beneficial effects of trimetazidine treatment on exercise tolerance and B-type natriuretic peptide and troponin T plasma levels in patients with stable ischemic cardiomyopathy.
No full textDi Napoli P, Di Giovanni P, Gaeta MA, D'Apolito G, Barsotti A. Beneficial effects of trimetazidine treatment on exercise tolerance and B-type natriuretic peptide and troponin T plasma levels in patients with stable ischemic cardiomyopathy. Am Heart J. 2007 Sep;154(3):602.e1-5.
Department of Cardiology, Centre for Study and Treatment of Congestive Heart Failure, Villa Pini d'Abruzzo Clinic, Chieti, Italy. [email protected]
BACKGROUND: In patients with ischemic cardiomyopathy, mortality rate and quality of life are unsatisfactory. We investigated the effects of the metabolic agent
trimetazidine (TMZ) on exercise tolerance and prognostic markers B-type natriuretic peptide (BNP) and cardiac troponin T (cTnT) plasma levels.
METHODS: Fifty patients with ischemic cardiomyopathy were randomized either to receive TMZ (20 mg, TID) in addition to their conventional treatment (TMZ group,
n = 25) or to continue their usual drug therapy (control group, n = 25) for 6 months. Patients were evaluated at baseline, at 1 month, and at 6 months (echocardiography and 6-minute walking test). At enrollment and at the end of
follow-up, blood testing was performed for determination of BNP and cTnT plasma levels.
RESULTS: After 6 months, no significant New York Heart Association class changes
occurred in all patients (P = NS). In the TMZ group, a significant increase of
exercise tolerance (P < .01) was detected, whereas left ventricular ejection fraction was unchanged (28% +/- 4%, 29% +/- 5%, and 32% +/- 5% at baseline, at 1
month, and at 6 months, respectively; P = NS). In the TMZ group, BNP was significantly reduced (6 months, 135 +/- 22 vs 252 +/- 44 pg/mL; P < .001), whereas it was significantly increased in controls (6 months, 288 +/- 46 vs 239
+/- 59 pg/mL; P < .02); cTnT significantly (P < .001) reduced during TMZ treatment, whereas it was unchanged in the control group. CONCLUSIONS: Six-month TMZ treatment improves exercise tolerance and reduces plasma levels of BNP and cTnT in patients with compensated ischemic
cardiomyopathy
P. Colletta, Storia del Reame di Napoli, p. p. Nino Cortese.
No full textRomano Ruggiero. P. Colletta, Storia del Reame di Napoli, p. p. Nino Cortese.. In: Annales. Economies, sociétés, civilisations. 19ᵉ année, N. 2, 1964. pp. 408-409
Chronic treatment with rosuvastatin modulates nitric oxide synthase expression and reduces ischemia-reperfusion injury in rat hearts.
No full textDi Napoli P, Taccardi AA, Grilli A, De Lutiis MA, Barsotti A, Felaco M, De Caterina R. Chronic treatment with rosuvastatin modulates nitric oxide synthase expression and reduces ischemia-reperfusion injury in rat hearts. Cardiovasc Res. 2005 Jun 1;66(3):462-71. Epub 2005 Mar 2.
Laboratory of Experimental Cardiology, Department of Clinical Sciences and Bioimaging, and Center of Excellence of Aging, G. d'Annunzio University, Chieti, Italy.
OBJECTIVE: Due to reported modulatory effects of statins on nitric oxide synthase (NOS) expression, we tested the hypothesis of protective effects of in vivo chronic treatment with rosuvastatin, a novel 3-hydroxy-3-methyl-glutaryl coenzyme A-reductase inhibitor, on ischemia-reperfusion injury, and investigated mechanisms involved.
METHODS: After 3 weeks of in vivo treatment with rosuvastatin (0.2-20 mg/kg/day) or placebo, excised hearts from Wistar rats were subjected to 15 min global ischemia and 22-180 min reperfusion. We evaluated creatine-phosphokinase and nitrite levels in the coronary effluent, heart weight changes, microvascular permeability (extravasation of fluoresceine-labeled albumin), ultrastructural alterations, and the expression of endothelial (e) and inducible (i) nitric oxide synthase (NOS) (by reverse-transcription polymerase chain reaction and Western blotting).
RESULTS: Rosuvastatin 0.2 and 2 mg/kg/day significantly reduced myocardial damage and vascular hyperpermeability, concomitant with a reduction in endothelial and cardiomyocyte lesions. At 2 mg/kg/day, rosuvastatin significantly increased eNOS mRNA and protein compared with untreated hearts, and conversely decreased iNOS mRNA and protein, as well as nitrite production after ischemia-reperfusion. The addition of the NOS inhibitor N(omega)-nitro-L-arginine methylester (L-NAME, 30 micromol/L) significantly reduced cardioprotection against ischemia-reperfusion.
CONCLUSIONS: Chronic treatment with rosuvastatin before ischemia reduces ischemia-reperfusion injury and prevents coronary endothelial cell and cardiomyocyte damage by NO-dependent mechanisms
Energy metabolism in the normal and in the diabetic heart
No full textCardiovascular disease is a major health problem all over the world. The prevalence of type 2 diabetes mellitus has been rapidly increasing, together with the risk of cardiovascular events. Patients with diabetes, and/or with insulin resistance as well, have an impaired myocardial metabolism of glucose and free fatty acids (FFA) and accelerated and diffuse atherogenesis, with involvement of coronary artery tree. Significant metabolic alterations at heart level in diabetic patients are the decreased utilization of glucose and the increase in muscular and myocardial FFA uptake and oxidation, occurring as a consequence of the mismatch between blood supply and cardiac metabolic requirements. These metabolic changes are responsible both for the increased susceptibility of the diabetic heart to myocardial ischemia and for a greater decrease of myocardial performance for a given amount of ischemia, compared to non diabetic hearts. A therapeutic approach aimed at an improvement of cardiac metabolism, through manipulations of the utilization of metabolic substrates, may improve myocardial ischemia and left ventricular function. Modulation of myocardial FFA metabolism, in addition to optimal medical therapy, should be the key target for metabolic interventions in patients with coronary artery disease and diabetes. In diabetic patients with ischemic heart disease, the effects of modulation of FFA metabolism could even give greater benefit than in nondiabetic patients. © 2009 Bentham Science Publishers Ltd
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