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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
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
Hypertonic reperfusion preserves endothelial nitric oxide synthase expression after ischemia-reperfusion in isolated working rat hearts
No full textTrimetazidine improves post-ischemic recovery by preserving endothelial nitric oxide synthase expression in isolated working rat hearts.
No full textObjective: Previous investigations have consistently shown that the piperazine derivative trimetazidine (TMZ, 1-[2,3,4-trimethoxybenzil]
piperazine, dihydrocloride) has cardioprotective eVects in the experimental ischemia–reperfusion model. We tested the hypothesis that
cardioprotective eVect of TMZ is partly mediated by preservation of the endothelial barrier of the coronary microcirculation.
Methods: Isolated Wistar rat (250–300 g) hearts were subjected to a 15min period of global ischemia and 180min reperfusion in the
presence or absence of 1 M TMZ. Hemodynamic parameters, heart weight, creatinekinase (CK) release and microvascular permeability
(FITC–albumin extravasation) were evaluated. In addition, eNOS gene expression was estimated by rt-PCR, and eNOS protein levels
were assessed by Western analysis. In order to conWrm the involvement of NO in mediating the cardioprotective eVects of TMZ, 30 M
N-nitro-L-arginine methylester (L-NAME), a speciWc inhibitor of nitric oxide synthase, was used.
Results: After ischemia and reperfusion, TMZ produced a signiWcant improvement of mechanical function associated with a reduction
of CK release and FITC–albumin diVusion (P <0.001); the agent also resulted in improvement in coronary Xow (at 45 min +27% vs
control). The eNOS mRNA and protein levels were signiWcantly higher in TMZ-treated hearts compared to controls. The addition of
L-NAME signiWcantly reduced the beneWcial eVects of TMZ on contractile function, CK release and FITC–albumin diVusion.
Conclusions: in the isolated rat heart, TMZ exerts a relevant, NO-dependent, cardioprotection against ischemia–reperfusion injury
and preserves the endothelial barrier of the coronary circulation. This could contribute to explain the cardioprotective action of TMZ
following ischemia and reperfusio
Regulation of endothelial function in coronary microcirculation by HMG-CoA reductase drugs
No full textTrimetazidine improves post-ischemic recovery by preserving endothelial nitric oxide synthase expression in isolated working rat hearts
No full textObjective: Previous investigations have consistently shown that the piperazine derivative trimetazidine (TMZ, 1-[2,3,4-trimethoxybenzil]
piperazine, dihydrocloride) has cardioprotective eVects in the experimental ischemia–reperfusion model. We tested the hypothesis that
cardioprotective eVect of TMZ is partly mediated by preservation of the endothelial barrier of the coronary microcirculation.
Methods: Isolated Wistar rat (250–300 g) hearts were subjected to a 15min period of global ischemia and 180min reperfusion in the
presence or absence of 1 M TMZ. Hemodynamic parameters, heart weight, creatinekinase (CK) release and microvascular permeability
(FITC–albumin extravasation) were evaluated. In addition, eNOS gene expression was estimated by rt-PCR, and eNOS protein levels
were assessed by Western analysis. In order to conWrm the involvement of NO in mediating the cardioprotective eVects of TMZ, 30 M
N-nitro-L-arginine methylester (L-NAME), a speciWc inhibitor of nitric oxide synthase, was used.
Results: After ischemia and reperfusion, TMZ produced a signiWcant improvement of mechanical function associated with a reduction
of CK release and FITC–albumin diVusion (P <0.001); the agent also resulted in improvement in coronary Xow (at 45 min +27% vs
control). The eNOS mRNA and protein levels were signiWcantly higher in TMZ-treated hearts compared to controls. The addition of
L-NAME signiWcantly reduced the beneWcial eVects of TMZ on contractile function, CK release and FITC–albumin diVusion.
Conclusions: in the isolated rat heart, TMZ exerts a relevant, NO-dependent, cardioprotection against ischemia–reperfusion injury
and preserves the endothelial barrier of the coronary circulation. This could contribute to explain the cardioprotective action of TMZ
following ischemia and reperfusio
Regulation of endothelial function in coronary microcirculation by HMG-CoA reductase drugs
No full text- …
