Effects of atrial pacing on arterial and coronary sinus endothelin-1 levels in syndrome X

Syndrome X may be caused by a coronary microvascular dysfunction, possibly due to abnormalities in coronary endothelial function. Previous studies suggested that endothelin-1 (ET-1) might be involved in the pathogenesis of syndrome X. Baseline arterial and coronary sinus ET-1 levels were measured in 13 patients with syndrome X (10 women, 52+/-7 years) and in 8 control patients (5 women, 46+/-11 years). ET-1 was also measured after atrial pacing in 12 patients with syndrome X and all controls. To simultaneously assess the activity of nitric oxide, guanosine 3'-5'-cyclic monophosphate (cGMP) was also measured in 11 patients with syndrome X and 7 controls. Baseline arterial (2.27+/-0.46 vs. 1.90+/-0.22 pg/ml, p<0.05) and coronary sinus (2.03+/-0.43 vs. 1.68+/-0.28 pg/ml, p = 0.06) ET-1 plasma levels were higher in patients than in controls. After pacing, arterial ET-1 levels did not change in either group and coronary sinus ET-1 levels were also unchanged in controls. In contrast, coronary sinus ET-increased significantly in response to atrial pacing in patients with syndrome X (p = 0.023), and differences between coronary sinus ET-1 levels of patients with syndrome X and controls after pacing became highly significant (2.22+/-0.45 vs. 1.69+/-0.20 pg/ml, respectively, p = 0.006). No significant differences in arterial and coronary sinus cGMP concentrations were found between the 2 groups, both at baseline and after pacing. Our findings suggest that an increased vasoconstrictor activity of microvascular endothelium is present in at least some patients with syndrome X and may be involved in the pathogenesis of the syndrome.     

Elevated plasma endothelin-1 levels in coronary sinus during rapid right atrial pacing in patients with slow coronary flow

The aim of the study was to evaluate whether there was an imbalance between endothelin-1 (ET-1) and nitric oxide (NOx) release and diffuse atherosclerotic changes existed in patients with slow coronary flow (SCF). Baseline and post-atrial pacing coronary sinus ET-1 and NOx levels were measured in 19 patients with SCF (11 female, 56 +/- 9 years) and in 14 control subjects (nine female, 54 +/- 7 years). All patients underwent subsequent intravascular ultrasound (IVUS) investigation at the same setting with right atrial pacing. Baseline arterial (12.4 +/- 9.9 vs. 6.3 +/- 5.1 pg/ml, P<0.005) and coronary sinus (12.2 +/- 11.1 vs. 6.4 +/- 6.9 pg/ml, P<0.005) ET-1 plasma levels were higher in patients than in controls. After atrial pacing, concentration of ET-1 level from coronary sinus (24.7 +/- 14.6) significantly increased as compared to baseline (12.4 +/- 9.9, P<0.0001) and control levels (5.3 +/- 6.3, P<0.0001). Additionally, coronary sinus ET-1 level increased significantly with atrial pacing compared to femoral artery ET-1 level (16.3 +/- 8.5, P<0.005) in patients with SCF. After atrial pacing, the femoral artery ET-1 level also increased in patients compared to control level (P<0.0001). No significant differences in arterial and coronary sinus NOx plasma levels were found between the two groups, both at baseline and after pacing. Upon IVUS investigation, the common finding was longitudinally extended massive calcification throughout the epicardial arteries in patients with SCF. Mean intimal thickness was 0.59 +/- 0.18 mm. The data of this study suggest that increased ET-1 levels and insufficient NOx response, as well as the pathological data of IVUS may be associated with coronary microvascular dysfunction and may be the manifestation of early diffuse epicardial atherosclerosis in these patients with SCF.     

Plasma endothelin-1 and thrombomodulin levels in coronary sinus during right atrial pacing and percutaneous transluminal coronary angioplasty

Increases in the levels of plasma endothelins (ETs) have been reported after percutaneous transluminal coronary angioplasty (PTCA). To examine the mechanism of this increase, we measured plasma endothelin-1 (ET-1) and thrombomodulin (TM) levels in both the Valsalva sinus (VAL) and the great cardiac vein (GCV) together with oxygen saturation of the GCV (Sat.GCVO2) during right atrial pacing and PTCA. Thirty patients with stenoses in the left anterior descending coronary arteries were enrolled. A fiberoptic pulmonary artery catheter was placed in GCV for monitoring Sat.GCVO2, and blood sampling was repeated before and after each procedure. ET-1 did not increase during pacing, but after PTCA it significantly increased from basal levels to 24.4+/- 8.3 pg/ml in GCV (P<0.01) and 19.3 +/-7.4 in VAL (P<0.05). Basal TM levels in GCV and VAL were significantly higher in diabetic than in non-diabetic patients, but TM did not change during pacing and PTCA. Sat.GCVO2 significantly decreased from the basal level during pacing and PTCA. We speculate that direct endothelial cell damage is more responsible for the increase of ET-1 during PTCA than myocardial ischemia. Our data indicate that ET-1 may be a useful marker for acute endothelial damage, while TM reflects only chronic and general damage of endothelial cells.     

冠状动脉慢血流患者一氧化氮和内皮素1浓度的变化

目的探讨冠状动脉慢血流(coronary slow flow,CSF)患者的血管内皮功能。方法选择因胸痛行冠状动脉造影的患者40例,根据造影结果分为CSF组20例和对照组20例。2组分别于静息和多巴酚丁胺负荷试验结束时立即抽取血标本,检测血浆内皮素1、血清NO浓度,并进行比较。结果 CSF组静息时血浆内皮素1浓度较对照组升高,但差异无统计学意义(P>0.05),而药物负荷试验后血浆内皮素1浓度较对照组明显升高,差异有统计学意义[(37.60±6.93)ng/L vs(14.16±5.73)ng/L,P<0.01]。CSF组静息时和药物负荷试验后血清NO浓度均明显低于对照组,差异有统计学意义[(42.36±9.72)μmol/L vs(50.39±9.77)μmol/L,(24.88±9.28)μmol/L vs(61.06±8.20)μmol/L,P<0.01)]。结论 CSF患者无论静息或者药物负荷状态下均存在内皮素1及NO平衡失调,负荷状态下这种平衡失调现象更加明显。     

冠状动脉内磁化支架置入术后冠状静脉窦血中NO与ET-1水平的变化

目的 :观察冠心病患者冠状动脉内置入磁化支架后冠状静脉窦血中一氧化氮 （NO）与内皮素 - 1（ET- 1）水平的变化 ,探讨磁化支架防治冠状动脉再狭窄的机制。方法 :经皮腔内冠状动脉成形术及冠状动脉内支架置入术的冠心病患者随机分为磁化支架组 （2 3例 ）及非磁化支架对照组 （16例 ）。经股静脉将 6 F右冠状动脉造影导管置入冠状静脉窦采血 ,采用 Griess法及非平衡法分别测定冠状动脉内支架置入术前及术后 6 h内冠状静脉窦血中 NO及ET- 1的水平。结果 :磁化支架组术后 6 h冠状静脉窦血中 NO含量较对照组相比显著升高 （P<0 .0 1） ;磁化支架组ET- 1水平的改变 ,包括术后即刻降低 P<0 .0 1)与 6 h回升 （P<0 .0 1）都不如对照组明显 ,两组 ET- 1水平在 3h有显著性差异 （P<0 .0 5 ）。结论 :冠状动脉内磁化支架置入术后 NO升高与 ET- 1水平变化趋缓反映了靶区血管局部内皮细胞功能改善 ,磁化支架置入术后急性冠脉痉挛及远期冠脉再狭窄的发生率降低可能与此有关     

冠状静脉窦起搏治疗阵发性心房颤动

心房颤动 (房颤 )的治疗一直是临床难点 ,起搏治疗是临床的选择之一。 1997年 ,Papageorgiou等[1] 的电生理研究表明冠状静脉窦起搏能有效防止房颤发生 ,但冠状静脉窦起搏治疗阵发房颤的长期临床应用尚未见报道。资料和方法患者 6例 ,男性 ,年龄 6 4～ 79(平均 6 9 2 )岁。 6例均为病态窦房结综合征 (病窦 )患者 ,其中 3例合并高血压性心脏病。超声心动图测定左心房直径为 2 7 3～ 37 5 (平均33 7)mm ,其中 3例左心房增大。 6例患者均反复发生阵发性房颤 ,其中 2例合并心房扑动、1例合并二度房室阻滞 ,5例窦性心律时体表心电图P波时限≥ 0 …     

Effects of propranolol on the hemodynamic,coronary sinus blood flow and myocardial metabolic response to atrial pacing

The hemodynamic, coronary sinus blood flow and myocardial metabolic effects of 0.15 mg/kg body weight of intravenously administered propranolol were studied in 19 patients with coronary artery disease and 6 normal patients. Atrial pacing was performed in all patients and produced angina in 15 of the 19 patients with coronary artery disease. In these patients propranolol reduced heart rate from 78 to 69 beats/min, cardiac index from 3.0 to 2.6 liters/min per m² and left ventricular stroke work index from 47 to 43 g-m/m²; it increased total peripheral resistance from 24 to 28 units and lactate extraction from 16.3 to 22.5 percent. There was no significant change in mean arterial pressure, left ventricular end-diastolic pressure, coronary sinus blood flow or myocardial oxygen consumption. During a second pacing stress propranolol produced clinical improvement in 9 of the 15 patients who experienced angina initially. The improvement was associated with less severe abnormalities in S-T depression and left ventricular end-diastolic pressure, increased lactate extraction and no significant change in coronary sinus blood flow or myocardial oxygen consumption. Thus, propranolol appears to be capable of modifying the anginal threshold as determined with atrial pacing, and the clinical response appears to be independent of global changes in coronary sinus blood flow and myocardial oxygen consumption.     

Effect of coronary angiography on plasma endothelin-1 and nitric oxide concentrations

Endothelium takes part in the regulation of vascular tone through the production of endothelium-derived relaxing factor, nitric oxide (NO), and the contracting factor endothelin-(ET-1). Induction of ET-1 and NO is influenced by many stimuli including hypoxia and shear stress. Some of these stimuli may arise during coronary angiography (CAG). In this study, the authors aimed to show endothelial response in patients undergoing CAG by evaluating plasma ET-1 and NO end-products including nitrite and nitrate concentrations. Twenty-four male patients with a mean age of 54.3 years (age range: 37-70) were included in the study. The patients had no coronary atherosclerotic lesions established by CAG. The mean time of the CAG procedures was 24.8 minutes, with a range of 19-33 minutes. Immediately before blood sampling, systolic and diastolic blood pressures were recorded. The mean blood pressures before and after CAG were 140/90 and 150/95, respectively. End products of NO radical, nitrite and nitrate (NOx), in plasma were used as a marker for the production of NO radical. ET-1 concentrations were measured by ELISA method. Significant increases in ET-1 concentrations were observed during CAG while no change observed in NOx concentrations. Duration of the CAG procedure was found to be correlated with the percent increase of the plasma ET-1 concentrations during CAG (r = 0.45, p<0.05, Figure 1), but not with NOx concentrations. Plasma ET-1 concentrations in patients who were cigarette smoking were found higher than those of patients who were nonsmokers (1.26 +/- 0.38 and 2.97 +/- 0.87 fmol/L, respectively). It was concluded that endothelial cells show increased ET-1 production as a response of some mechanical or emotional stimuli during CAG procedure that may play an important role in the regulation of vascular tonicity and some pathological processes. The authors suggest that duration and manipulation of CAG may be an important factor in plasma ET-1 concentrations.     

High-density mapping of left atrial endocardial activation during sinus rhythm and coronary sinus pacing in patients with paroxysmal atrial fibrillation

INTRODUCTION: This study was designed to record global high-density maps of left atrial endocardial activation during sinus rhythm and coronary sinus pacing. METHOD AND RESULTS: Noncontact mapping of the left atrium was performed in nine patients with paroxysmal atrial fibrillation undergoing pulmonary vein ablation procedures. High-density isopotential and isochronal activation maps were superimposed on three-dimensional reconstructions of left atrial geometry. Mapping was repeated during pacing from sites within the coronary sinus. Earliest left atrial endocardial activation occurred anterior to the right pulmonary veins in seven patients and on the anterosuperior septum in two patients. A line of conduction block was seen in the posterior wall and inferior septum in all patients. The direction of activation in the left atrial myocardium overlying the coronary sinus was different from the electrogram sequence in the coronary sinus catheter in 6 of 9 patients. During coronary sinus pacing, activation entered the left atrium a mean (SD) of 41 (13) ms after the pacing stimulus at a site 12 (10) mm from the endocardium overlying the pacing electrode. Lines of conduction block were present in the posterior wall and inferior septum. CONCLUSION: In patients with paroxysmal atrial fibrillation, lines of conduction block are present in the left atrium during sinus rhythm and coronary sinus pacing. Electrograms recorded in the coronary sinus infrequently correspond to the direction of activation in the overlying left atrial myocardium.     

Effect of external counterpulsation on plasma nitric oxide and endothelin-1 levels

Enhanced external counterpulsation (EECP) significantly augments diastolic blood flow and has been postulated to improve endothelial function by increased shear stress. We examined the effects of EECP on plasma nitric oxide and endothelin-1 (ET-1) levels. Plasma nitrate and nitrite (NOx) and ET-1 levels were measured serially in 13 patients with coronary artery disease who received 1-hour daily treatments of EECP over 6 weeks. During the course of EECP therapy, plasma NOx progressively increased and plasma ET-1 progressively decreased. After 36 hours of EECP, there was a 62 +/- 17% increase in plasma NOx compared with baseline (43.6 +/- 4.3 vs 27.1 +/- 2.6 micromol/L, p <0.0001) and a 36 +/- 8% decrease in plasma ET-1 (76.7 +/- 9.5 vs 119.5 +/- 8.5 pg/L, p <0.0001). At 3 months after completion of EECP, NOx remained 12 +/- 11% above baseline (p = 0.002), and ET-1 remained 11 +/- 10% below baseline (p = 0.0068). Our data provides neurohormonal evidence to support the hypothesis that EECP improves endothelial function.     

Seasonal variation in plasma levels of endothelin-1 and nitric oxide.

BACKGROUND: There is a seasonal variation in the incidence of stroke and coronary heart disease with admissions to hospital being higher in the colder months of the year. The mechanism whereby this winter prevalence of vascular disease occurs is still not fully understood. The aim of our study was to measure plasma levels of vasoactive compounds throughout the year to establish whether or not there were any fluctuations which could play a part in the higher winter incidence. METHODS: We measured plasma levels of the vasoconstrictive endothelin-1 (ET) and the vasorelaxant nitric oxide (NO) throughout the year. Blood samples were collected from 176 normal individuals. Samples were collected between 8.00 and 10.00 hours after an overnight fast of at least 12 hours. RESULTS: Results were divided into two-monthly intervals and analysed using a Kruskal-Wallis one-way analysis of variance and Mann-Whitney U tests (SPSS). We found a significant seasonal variation in both parameters. Mean levels of endothelin were highest in January/February (4.0 pg/ml) and lowest in May/June (2.3 pg/ml), whereas plasma 5 nitric oxide levels were lowest in January/February (5.7 microM) and highest in September/October (9.9 microM); p values were <0.0001 (Jan/Feb vs May/June) and 0.049 (Jan/Feb vs Sept/Oct), respectively. CONCLUSIONS: The high levels of the vasoconstrictor endothelin combined with low levels of vasorelaxant nitric oxide may account in part for the increased incidence of stroke and coronary heart disease seen in these months.     

Regional myocardial perfusion during atrial pacing in patients with coronary artery disease.

Regional myocardial perfusion (RMP) was measured with 133xenon and a multiple-crystal scintillation camera at rest and during atrial pacing in 24 patients with normal coronary arteriograms or less than 50% lesions, Group I, and in 24 with significant (greater than 50% lesions) left coronary artery disease (CAD), Group II. Pacing induced increases in the double product (DP) of heart rate and systolic blood pressure, an index of myocardial oxygen consumption, were not different for Groups I and II. In Group I average mean LV perfusion rate was subnormal at rest but rose from 49 to 73 ml/100 g-min during pacing to 150/min without angina. A response index (RI), (deltaMP X 10(3)/deltaDP), averaged 2.93. Twenty patients in Group II developed angina during pacing. The average mean LV perfusion rose less than in Group I, from 48 to 64 ml/100 g-min (P less than 0.05) and the average RI, 1.76, was lower (P less than 0.01). In 19 of these patients, average RMP distal to the major coronary lesion increased from 46 to 58 ml/100 g-min; this increase during pacing was significantly less than in the remainder of the LV of 48 to 66 ml/100 g-min (P less than 0.05). Average regional RIs were 1.39 and 2.18, respectively. In three patients the presence of collaterals termed adequate by radiological criteria was not associated with preferential decreases in the distal regional RI. The data support the hypothesis that in some patients with CAD, angina pectoris results when an obstructive coronary lesion restricts the total or regional myocardial blood flow response to an increased rate of myocardial oxygen consumption.     

N-乙酰半胱氨酸对COPD患者血中血管内皮素、一氧化氮的影响

目的探讨N-乙酰半胱氨酸对慢性阻塞性肺疾病（COPD）患者血清中血管内皮素及一氧化氮水平的影响。方法AECOPD患者60例,随机分为对照组及NAC组,测定两治疗组治疗前、后血浆内皮素-1（ET—1）和一氧化氮（NO）含量的变化。结果两组治疗后ET—1含量均低于治疗前,而NO高于治疗前（P（0．05）;但所有这些变化均以N-乙酰半胱氨酸组的变化程度更明显（P（0．01）。结论N-乙酰半胱氨酸有助于COPD患者维持体内舒血管因子及缩血管因子平衡,可能对肺动脉高压的形成有一定的预防作用。     

冠状动脉粥样硬化患者影像表现与冠状动脉循环血浆内皮素-1和一氧化氮水平的关系

目的　观察冠状动脉粥样硬化影像表现与冠状动脉循环血浆内皮素 - 1( ET- 1)和一氧化氮 ( NO)水平的关系。方法　 5 1例行冠状动脉造影者 ,造影前取血测定冠状静脉窦 ( CS)和冠状动脉开口 ( AO)血浆 ET- 1和 NO水平。冠状动脉腔径狭窄≥ 5 0 %者为严重冠状动脉病变组 ,反之为对照组。分析记录严重冠状动脉病变组病变血管数、狭窄病变数、闭塞病变数和病变范围积分。结果　 1.严重冠状动脉病变组 CS血浆 ET- 1水平 ( ET- 1CS)和 CS与AO的差值 ( ET- 1CS- AO)明显高于对照组 ( P<0 .0 5 ) ;严重冠状动脉病变组 ET- 1CS明显高于 AO血浆 ET- 1水平( ET- 1AO) ( P<0 .0 5 )。 2 .严重冠状动脉病变组 NOCS和 NOCS- AO明显低于对照组 ( P<0 .0 5 ) ;严重冠状动脉病变组NOCS明显低于 NOAO( P<0 .0 5 )。 3 .严重冠状动脉病变组 ,ET- 1CS- AO与冠状动脉病变范围积分呈显著正相关 ( P<0 .0 5 ) ,NOCS- AO与冠状动脉病变范围积分呈显著负相关 ( P<0 .0 5 )。结论　冠状动脉粥样硬化影响冠状动脉循环血浆 ET- 1和 NO水平 ,粥样硬化病变范围与冠状动脉循环血浆 ET- 1和 NO水平有相关关系     

肺血栓栓塞患者血浆ET-1、NO水平与血管内皮依赖性舒张功能的关系

目的探讨肺血栓栓塞症（PTE）患者溶栓和（或）抗凝治疗前后血浆内皮素1（ET-1）、一氧化氮（NO）及血管内皮依赖性舒张功能（EDD）的变化及其临床意义。方法PTE患者82例,分为溶栓组及抗凝组,并选取健康者20例为对照组。应用放射免疫方法检测ET-1,硝酸还原酶法测定血浆NO浓度,同时应用超声测量肱动脉EDD,并比较溶栓和抗凝治疗前及治疗1周时各项指标的变化。结果与对照组相比,溶栓及抗凝治疗组NO、ET-1、EDD差异有统计学意义（P均〈0.01）。两组PTE患者治疗1周后NO、EDD较治疗前明显升高、ET-1明显下降,差异亦有统计学意义（P均〈0.01）。相关分析显示,PTE患者ET与NO、EDD呈负相关（r=-0.508、-0.533,P均〈0.01）;NO与EDD呈正相关（r=0.685,P〈0.01）。结论肺栓塞患者存在血管内皮功能损伤,EDD可以作为评价肺栓塞患者内皮功能损伤的指标。     

Characteristics of right atrial activation during coronary sinus pacing

INTRODUCTION: Anatomic and electrical connections between the left atrium and right atrium (RA) have been described. The relationship between coronary sinus (CS) pacing site and RA activation has not been examined. METHODS AND RESULTS: Fifteen anesthetized swine underwent high-density noncontact mapping of the RA during pacing from up to five different sites within the CS. Isopotential mapping identified the site of earliest RA depolarization and the pattern of subsequent activation. Hearts were excised and endocardial dissection performed. Earliest RA activation occurred at the CS os with proximal CS pacing sites and at Bachmann's bundle at distal pacing sites. The mean depth at which a shift in earliest RA activation site occurred was 46 +/- 13 mm (range 21 to 63 mm). RA activation times following earliest activation at the CS and Bachmann's bundle were 40 +/- 4 msec and 51 +/- 6 msec (P < 0.002). Conduction delay or block was recorded at the lateral cavotricuspid isthmus, terminal crest, and tendon of Todaro. Latest RA activation always occurred in the high anterolateral atrium after ascending the anterolateral wall. The lateral RA was activated by the wavefront that traversed the posterior wall rather than by the wavefront crossing the cavotricuspid isthmus, even with earliest RA activation at the CS os. CONCLUSION: The site of earliest RA activation during CS pacing is dependent upon the pacing depth within the CS. In the porcine heart, areas of conduction delay influence RA activation patterns and timings. These findings may have implications for patients undergoing assessment of radiofrequency ablation of atrial flutter.     

Effects of endothelin-1 and nitric oxide on glucokinase activity in isolated rat hepatocytes

To test the hypothesis that endothelin-1 (ET-1) and nitric oxide (NO) influence glucokinase (GK) activity in an opposite manner, we evaluated the effects of ET-1, L-NAME, an inhibitor of NO synthase, and L-arginine, a substrate for NO synthase, on GK activity and glycogen content in isolated rat hepatocytes. Moreover, to understand the receptor involved in the process, the effects of BQ 788, a specific antagonist of ETB receptor, and PD 142893, an antagonist of ETA-ETB receptors, were also evaluated. GK activity, cyclic guanosine monophosphate (cGMP), and glycogen intracellular content were measured on isolated hepatocytes, while glucose levels and NO as NO2-/NO3- were determined in the medium. High ET-1 levels induced a 20% decrease of NO2-/NO3- levels and cGMP intracellular content, followed by a 49% reduction of GK activity and a 15% decrease of glycogen. In parallel, a 10% increase of glucose in the medium was observed. In the presence of L-NAME, GK activity and glycogen levels showed analogous decrements as observed with ET-1. Also in this case, a significant decrease of the intracellular content of cGMP was observed. No synergistic effects of ET-1 and L-NAME were observed. L-Arginine was able to counteract the inhibitory effect of ET-1 on cGMP and GK activity. Glycogen content was slightly but not significantly reduced, and under those conditions, a significant decrease of glucose in the medium was observed. When hepatocytes were incubated with ET-1 plus BQ 788 or ET-1 plus PD 142893, GK activity was unchanged. Interestingly, no changes were observed in NO2-/NO3- levels and the intracellular content of cGMP was not modified when the antagonists of ET-1 receptors were added to the medium. In conclusion, the present study shows that the NO pathway seems to be an important regulator of GK activity and glycogen content through cGMP activity. In addition, ET-1 seems to be not active per se, but its activity seems mediated by a simultaneous decrease of NO levels.     

冠状静脉窦口起搏对心房激动时间影响及方法学探讨

目的观察冠状静脉窦口起搏对心房激动时间的影响，并探讨该部位起搏的方法学。方法包括两部分，首先对20例射频消融的患者行心内电生理检查，术中分别给予高位右心房（HRA）、冠状静脉窦口（CS9-10）、左心房游离壁（CS1-2）起搏，记录刺激信号至腔内电图最远A波为心房激动时间；HRA至CS1-2的AA间期作为左、右心房间激动时间差，同时测量体表心电图最长P波时限。第二部分研究在可控弯导丝系统的辅助下将心房主动电极导线固定在冠状静脉窦口，比较冠状静脉窦口起搏与HRA起搏的起搏参数及起搏后体表心电图P波时限。结果冠状静脉窦口起搏时P波时限、心房激动时间及左、右心房激动时间差较窦性心律下、高位右心房及左心房游离壁起搏时均明显缩短。两组患者术中及术后起搏参数差异无统计学意义，冠状静脉窦口起搏患者体表心电图P波宽度明显缩短。结论冠状静脉窦口起搏时心房激动时间明显缩短，左、右心房间激动时间差最短。采用可控弯导丝系统的辅助可实现冠状静脉窦口起搏。     

The response of the myocardial metabolism to atrial pacing in patients with coronary slow flow

The pathophysiology of angina pectoris is not precisely known yet in patients who have no coronary lesion but slow coronary flow by angiography. In this study we aim to display metabolic ischemia via atrial pacing to determine the difference of lactate production and arterio-venous O2 content difference (AVO2). Thirty-four patients with slow coronary flow detected by coronary angiography via the TIMI 'frame count' method were included in this study. The resting and stress images from the patients undergoing myocardial perfusion tomography were recorded, pre and postpacing lactate extraction and AVO2 content difference values were calculated. Patients were classified according to their metabolic responses to atrial pacing stress. Group I consisted of 28 patients (18 male, 10 female, mean age 54.42 +/- 9.61) who did not demonstrate metabolic ischemia and group II consisted of six patients (four male, two female, mean age 60 +/- 5.76) who had metabolic ischemia after the procedure. There was no statistically significant difference between prepacing AVO2 content difference in group I (57.38+/-2.05%) and group II (58.23 +/- 2.11%) (P = NS). However postpacing AVO2 content difference of group I and group II was statistically significant (respectively, 57.96+/-2.65 vs. 68.35 +/- 2.15%, P < 0.001). In other words, postpacing AVO2 content difference was unchanged from the basal AVO2 content difference level in group I (respectively, 57.38 +/- 2.05 vs. 57.96 +/- 2.65%; P = NS) in contrast to the postpacing AVO2 content difference which increased significantly in group II (58.23 +/- 2.11 vs. 68.35 +/- 2.15%; P < 0.028). Although basal lactate extraction rates were similar in groups I and II (respectively, 0.24 +/- 0.1 vs. 0.23 +/- 0.18; P = NS), postpacing lactate extraction rates were decreased significantly in the two groups, prominently in group II (0.154 +/- 0.15 vs. -0.471 +/- 0.27; P < 0.0001) which indicated that lactate extraction converted to lactate production. Metabolic ischemia was detected in only 17.6% of patients included in this study and 83.4% of these six patients with proven metabolic ischemia had perfusion defects in scintigraphy. Our data confirmed that angina pectoris was not originated from myocardial ischemia in most of the patients with slow coronary flow. We conclude that perfusion scintigraphy is a reliable and accurate method for detection of true ischemia in this group of patients.