| Objective: Observe and analyse the role and effect of the individually largesimvastatin drug to cure pulmonary arterial hypertension in clinical.Pulmonary arterial hypertension (PAH) is a malignant complication mergedin some cardiovascular diseases such as congenital heart disease, rheumaticheart disease, coronary heart disease and chronic obstructive pulmonarydisease (COPD), etc. About70%of the patients focus on young people anddied of the hardly corrected right heart failure finally. Especially the patientsof cardiac disease merged pulmonary hypertension who need the surgicaltreatment, the mortality of the peroperative and hospital is obviously higherthan the non pulmonary hypertension patients. The pathology mechanism ofthe PAH is complex, involve the change of molecylar and cellular mechanismincluding the Bone state kind protein receptors-II (BMPR-II), the Activinsample kinase type-1,5-serotonin transporter factor (5-HTT) geneticmechanism and Prostacyclin, Endothelin, Endothelial function abnormal,Nitric oxide access,5-Hydroxytryptamine(5-HT), inflammation, blood clots orelse. After years' research, there have been significant progress abouttreatment of the PAH in recent years, including basic therapy, new drugstherapy according to the pathogenesis, intervention cure,surgery and others.The drugs and methods for clinical therapy of the pulmonary arterialhypertension include nitric oxide (NO) of inhaled, Prostacycline (Epopros-tenol, Prostaglandin E1, Beraprost), Phosphodiesterase inhibitors (SildenafilCitrate), Endothelin receptor antagonists (Bosentan),etc. The latest researchesinclude vascular active bowel peptide which could inhibite platelet activationand smooth muscle cells' proliferation and show a significantly expandfunction to the pulmonary vascular. At the same time, the growth factors' inhibitory factor is a new research direction which resists the pulmonaryarterial hypertension. The Gene therapy still at the research of enlighteningstage, it may become an effective treatment which could control the PAH andbring an extensive prospect. Meanwhile the endothelin of progenitor cells ofthe PAH mouse model transfects nitric oxide synthase, made the PAH mices'right ventricular pressure reduced and the survival time to extend. In a word,the research development of treatment of the pulmonary arterial hypertensionis faster. The clinical doctors should consider various factors in the drugs'treatment include the cardiopulmonary hemodynamics, with or without heartfailure, drugs interactions and adverse reactions. The patient's heart-lungfunction classification is important to choose drugs and evaluate the effect ofmedicines. But these drugs and treatment methods have more serious sideeffects and obvious economic factors. Statins is a HMG-CoA reductaseinhibitors. It through to endogenous cholesterol synthesis speed limit enzyme(HMG-CoA) reduction enzyme inhibition of competitive to block cell methyleacid is metabolism, so that the synthesis of cholesterol in cells reduce, also thestimulation of feedback on the cell membrane surface which of mainly for theliver cell, low density lipoprotein (low density lipoprotein, LDL) receptornumber and activity increase, make serum cholesterol levels drop, increase ofclear. Statins can also hold-up the liver cell synthesis apolipoprotein B-100,reduce the rich in triglyceride and lipoprotein synthesis and secretion, it is themost effective and most classic cholesterol drugs and widely used in clinicalhyperlipidemia treatment. In recent years, about the statins's researches foundthat the drugs are more independent of cholesterol in the role of the multiplecardiovascular protective effect, it could inhibite smooth muscle cellproliferation and migration and platelet sex thrombosis with dose dependent. Itcould activate the nitric oxide synthase (NOS) with concentration dependenceand down-regulate reversal pulmonary vascular reconstruction, but also it hasanti-inflammatory, resistance to oxidation stability, patch, reduceneuroendocrine activation, anticoagulation, antiplatelet, improve endothelialfunction and inhibit endothelial function inflammation. At home and abroad clinical studies have showed statins with multiple cardiovascular protectiveeffect in recent years, include statins and sildenafil united clinical observations.It has advantages on side effects which to cure and price compared tocurrently existed clinical treatments. The experiment get the new researchresults and the treatment method to cure the PAH from clinical observations ofthe statins on pulmonary hypertension alone.Methods: The research objects were50cases diagnosed congenital heartdisease with pulmonary hypertension in clinical, older than17years, not usedstatins preoperative. Simvastatin (comfortable drop, Merck company,40mg/specification of)80mg/day application for a week, mean PulmonaryArtery Pressure (mPAP), Artery blood oxygen partial pressure (PaO2), Bloodoxygen saturation (SaO2), Right ventricular end systolic diameter (RVSD),Right ventricular anterior wall (RVAW) and Pulmonary artery diameter(PA)were observed before and after processing. At the same time the change of theliver function was monitored. The Pulmonary artery pressure use heartultrasound measurement, the arterial blood gas analysis apply the large bloodgas analyze measurement. The statistical software SPSS13.0, each sets' resultsshowed by xˉ±s. Need the independent sample t-test to contrast betweengroups which of the disease types. Before and after test result applies thematching t test, when the P＜0.05is the discrepancy which shows thestatistical significance. But in the experimental stage, we make the observationwhich are the right ventricular end-diastolic inner diameter(RVSD), the rightventricular wall (RVAW) and the main pulmonary artery (PA) diameter tohave no change. So it has not further statistics in later of the clinical trialobservation. These may have a direct correlation about the time that the drugaffect. We need more time of the clinical trial observation if we want to takethe correlation between the simvastatin and the RVSD, RVAW and PAwhether or not. On the analysis of the disease types in patients, because theyhave obviously different factors which cause the pulmonary hypertension inthe haemodynamics between the atrial septal defect (ASD) and ventricularseptal defect(VSD). The experiment of us only made the comparative of the disease variety itself, we did't have the consequence of the drug's effectcontrast between the twoes.Results: From the overall data,changes of mean Pulmonary Artery Pressure(mPAP), Artery blood oxygen partial pressure (PaO2), and Blood oxygensaturation (SaO2) were smaller range after a week drug used before and aftertreatment.The primary outcome of the participants'(50cases) mPAP(33.63±7.924mmHg) before treatment and (33.35±7.851mmHg) after cure,PaO2(91.75±8.126mmHg) before and after is (92.53±6.762mmHg), SaO2(96.10±2.587mmHg) before cure and after is (92.53±2.082mmHg), there wasno dramatical change. While values about26%of patients' mPAP had almostno change actually. More than14%of patients' mPAP did not reduce but risedsmall. About20%of patients' PaO2also had not change, and that was morefor SaO2about30%. But matching t test results before and after processingshowed that the observation index of four groups P-value was less than0.05,and there was statistical significance (The result detailed to see the forms).Conclusion: Simvastatin separated to the clinical congenital heart diseasecombined of pulmonary hypertension treatment exists certain effect. Becauseobservation was in a relatively short time test, the outcome part of subjectswas no perfect. Another proof could't advocate applications of simvastatin inpatients who need to be reduced pulmonary hypertension quickly. Andsimvastatin can be used to patients with mild-moderate donor pulmonaryarterial hypertension as a long-term treatment, or a more effective lowpulmonary artery pressure drug as an auxiliary one. |
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