| Background:Coronary heart disease (CHD) is multifactorial and has an important hereditary component. Its complex pathophysiologic characteristics are not completely clear. And now percutaneous coronary intervention (PCI) is one of the most widely utilized treatment modalities for patients with coronary artery disease. However, PCI is a traumatic procedure from the perspective of the arterial wall. The consequence is a locally pro-thrombotic and inflammatory state that puts patients at increased risk for restenosis and cardiac events following successful PCI. It is reported that paracrine / autocrine dysfunction of cardiology vasculature system has been shown in the progressive nature of CHD and the complication of them after PCI. Nitric oxide (NO) and carbon monoxide (CO), as the important members of paracrine / autocrine system, are endogenous gasotransmitter involved in many aspects of cardiology function in health and disease. The data indicate that the protective effect of NO and CO relies on its ability to relax the vascular smooth muscle cells, block platelet infiltration as well as smooth muscle cell proliferation and transference. And now, Inhalation ofL-arginine, which is the donor of nitric oxide, has been a promising treatment in patients with coronary atherogenesis and the restenosis after PCI. That tells us not only understanding the role of endogenous gastransmitter in the pathophysiological process of CHD and complication after PCI is important, but it is useful for the protection and treatment of patients with CHD and the complication after PCI.Recently, H2S which is generated by mammalian tissue from two pyridoxal-5-dependent enzymes, cystathionin- P -synthasem (CBS) and cystathionine-Y -lyase (CSE) has been found to be endogenous generated that play many cardiovascular effects such as relax the vascular smooth muscle cells, reduce the arterial pressure and inhibited the proliferation of vascular smooth muscle cells (VSCM) as well as model the constriction of myocardial. More and more studies showed that the endogenous CSE/H2S pathway impacted the pathophysiological process of many vascular disorders such as hypoxia-induced pulmonary hypertension, hypertension, septic and endotoxin shock. So endogenous H2S has been proposed to be a new gaseous transmitter similar to two other vasoactive gases, NO and CO. Recently, people found that impaired endogenous CSE/ H2S pathway take part in the pathophysiological process of isoproterenol-induced rat myocardial injury. Administration of exogenous H2S effectively protected rat myocardium against ischemic injury. However, the changes in endogenous CSE/ H2S pathway and the role of endogenous H2S in the pathophysiological process of human coronary heart disease (CHD) are not clear. In order to clarify the role of endogenous H2S in human CHD and after PCI pathophysiological process, we investigated the vary of plasma H2S and NO levels in forty CHD patients and seventeen control subjects and the influence of PCI on plasma H2S and NO levels, and discuss whether any changes of H2S might be related to the extent of the CHD disease and PCI, through that we hope to show a new research field about prevention and treatment of CHD and bad results of PCI.Objective:1. We have studied the variation of H2S and NO in the blood circulation of patients with CHD or with normal angiography, besides; we also studied the variation of them on patients with different clinical subtype of CHD. And the aim of this study was to evaluate clinical signification and action of H2S and NO in the process of CHD progression.2. Among the CHD patients, we have studied the relationship between plasma H2S, NO levels and risk factors of CHD, we evaluated the rule of CHD risk factors influencing on paracrine/autocrine function of endogenous H2S and NO.3. By studying the relationship between plasma H2S, NO levels and angipgraphic morphology as well as severity of coronary lesion in patients with CHD, we valuated the association this pair of vasoactive substances interactional mechanism in the severity of coronary lesion.4. By monitoring the variation of H2S and NO in the blood circulation before and after PCI and studying the relationship of them with restenosis, we evaluated the influence of them on bad results after PCI.Methods:1. The study group comprises 40 CHD patients who underwent coronary angioplasty, at the same time 17 angiographically normal patients as controls. Among the CHD patients, 33 patients received PCI. age, gender, hypertension, diabetes, smoking, blood glucose, TC, TG, LDL-C, HDL-C, BMI and LVEF were recoded in every patient in detail.2. Peripheral blood samples were obtained before and after angiography in CHD patients and control subjects. Among the 40 CHD patients, 33 patients who received the PCI, their blood samples were obtained from the femoral artery before and afterangiography, immediately after PCI and from the arm vein 24hour and 72hour after the procedure. After centrifugation at 3000rpm at 4°C for 15 min, the plasma was decanted and stored at -70 °C until analysis. Plasma H2S levels were measured by sensible sulfide node and the Plasma NO levels were measured by Griess method.3. Angiographic and PCI characteristics of patients were recoded in detail. Results:1. There were no significant differences in baseline clinical characteristics between patients with or without CHD such as sex, ages, diabetes, hypertension, smoking, blood lipid and LVEF. The comparison of baseline clinical and coronary lesion characteristics among different CHD clinical subtypes of stable angina pectoris patients (SAP), unstable angina pectoris patients (UAP) and acute myocardial infarction patients (AMI) showed no significance.2. The varying of plasma H2S and NO between the CHD patients and control subjects and among different clinical subtypes of CHD patients.The plasma H2S levels were significantly decreased 49.56% in CHD patients in comparison with that in the control subjects (26.10±14.27umol/L vs 51.74±11.94 umol/L, P<0.01) , and the plasma NO levels were decreased 17.30% in the CHD group than that in control group (44.25±9.71 umol/L vs 53.51±4.33 umol/L, PO.01); Among the CHD patients, There was significantly decreased of the H2S levels in the UAP patients (23.60±14.41 umol/L) and AMI patients (19.98±7.52 umol/L) than that of SAP patients (38.41±14.53umol/L).The H2S levels was significantly decreased by 38.56% (p<0.05) and by 47.98% (PO.05) than that in the SAP patients, respectively. And the plasma NO levels in the AMI patients (39.71±6.03umol/L) were lower than that in the SAP patients (44.25±9.71 umol/L) and UAP (45.91±10.90umol/L), but there was no significant different between them (p>0.05).3. The relationship between CHD risk factors of CHD and the plasma H2S and NO levels.Among the patients of CHD, Plasma H2S levels were significantly lower in smokers than in no-smokers(20.60±7.53umol/Lvs32.24±16.79umol/L, PO.05) and in patients with hypertension than that without hypertension respectively (21.89±10.54 umol/Lvs31.17±15.69umol/L, PO.01) ; but the plasma NO levels showed no significant changes in CHD patients between smokers and no-smokers, with hyperten -sion and without hypertension. Plasma H2S levels showed a significant negative correlation with blood glucose(r=-0.4939, p=0.0016), but it had no significant relation -ship with ages, TG, TC, LDL, HDL, and BMI, respectively.4. The varying of plasma H2S and NO among different type changes of coronary artery.The plasma H2S levels were no significantly different between CHD patients with double-vessel and multi-vessel changes (P>0.05). But the plasma H2S levels were significantly lower in CHD patients with double-vessel or multi-vessel lesion than that with single-vessel lesion (16.91±7.98umol/L vs 33.04±15.01umol/L, PO.05 or 18.39±7.78umol/L vs 33.04±15.01umol/L, PO.01). And the plasma H2S levels were decreased 32.65% in CHD patients with coronary artery occlusion than that with simple stenosis subjects (19.04±9.55umol/L vs 28.24±14.85umol/L, PO.05). The plasma H2S levels were lower in CHD patients with restenosis than that with no-restenosis after stent planting (27.64±14.85 vs34.21±16.84umol/L),but there was no significantly difference between them (p>0.05). the results showed that there was no significant changes of the plasma NO levels in patients with different vessel lesions, but the NO levels fell 13.87% in patients with coronary artery occlusion than that with simple stenosis (41.03±7.27umol/L vs 47.64±11.07umol/L, PO.05), and it decreased by 21.96% in the patients with resteosis than that without restenosis afterstenting (38.63±5.99umol/Lvs 49.50±11.16umol/L, P<0.05). 5. The influence of PCI on plasma H2S and NO levels There were no difference of plasma H2S and NO levels before and after CAQ but the plasma H2S and NO levels were significantly decreased after PCI compared with the levels before the procedure [ (16.51±9.33umol/L vs 26.01±14.08umol/L, PO.05) and (38.06±8.67umol/L vs 44.25 + 9.7lumol/L, P<0.05)]. PlasmaH2S levels recovered to baseline 24h past PCI, however, the plasma NO levels fell to the least levels 24h after PCI(35.74± 7.42 n mol/L) and didn't recover to baseline 72h after the procedures.Conclusion:1. Plasma H2S levels in CHD patients group were lower than that in control group and the Plasma H2S levels of CHD patients decreased in proportion with clinical severity. It shows that decreased plasma H2S maybe take part in the occurrence and development of CHD, and plasma H2S levels may become a clinical prognostic indicator of estimating CHD degree.2. Among the patients of CHD, plasma H2S levels were significantly lower in smokers than that in no-smokers or with hypertension than that without hypertension, respectively, and the plasma H2S levels showed a significant negative correlation with blood glucose. These tell us the falling of plasma H2S level maybe has corrected with the CHD risk factors such as high blood glucose, smoking, and hypertension.3. The results of our study showed the Plasma H2S levels in CHD patients with double-vessel or multi-vessel lesions were lower than that with single vessel lesion, and plasma H2S levels were significantly lower in CHD patients with coronary artery occlusion than that with simple stenosis subjects. So, blood circulation level of plasmaH2S was strongly associated with the severity of coronary lesion.
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