缺血预处理对体外循环中左心功能的恢复及心肌细胞膜流动性变化的影响

目的:观察缺血预处理(IPC)对体外循环(CPB)中心肌细胞膜流动性变化及心功能恢复的影响,评价IPC的心肌保护作用。方法:将72只健康家猫随机分为3组:单纯并行循环(CPB)组、缺血再灌注(IR)组和IPC组。监测CPB中猫左心室内压峰值(LVSP)、左心室等容收缩期压力升高最大速率(dp/dtmax)、左心室舒张期压力下降最大速率(dp/dtmin)等左心功能指标,并应用荧光偏振法测定心肌细胞膜的微黏度(η),以η的倒数表示心肌细胞膜脂流动性。结果:CPB组体外循环过程中左心功能各指标和心肌细胞膜微黏度均无明显变化;IR组主动脉阻断(ACC)期间η明显上升且于再灌注期间进一步升高,IPC组ACC期间η无明显变化,再灌注期间虽有所升高但明显低于IR组;心功能恢复阶段IPC组猫心LVSP、dp/dtmax和dp/dtmin均明显高于IR组。结论:IPC能够有效维持CPB中缺血再灌注心肌细胞膜脂的流动性,同时可改善左心功能的恢复。     

左心导管与超声心动图检查对比评价冠状动脉病变对左心室舒张功能的影响

目的探讨冠心病患者冠状动脉病变程度对左心室舒张功能的影响。方法应用心导管及超声心动图检查,对75例经选择性冠状动脉造影确诊的冠心病患者进行了研究。根据冠状动脉造影结果 ,将冠心病患者按病变狭窄所累及的动脉支数分为4组:轻度狭窄组、单支病变组、双支病变组及三支病变组。应用导管法测定主动脉内的收缩压、舒张压、心率、左心室舒张末期压(LVEDP),收缩期及舒张期左室压力最大变化率(dp/dtmax,dp/dtmin)及等容舒张期压力衰减时间常数。比较不同的冠状动脉狭窄程度与心室舒张功能的关系。应用心导管法与超声心动图检查分析左心房内径(LAD)、左心室舒张末期容积(EDV)、收缩末期容积(ESV)、舒张期前1/3充盈量(1/3V)及舒张早期充盈分数(1/3FF),并计算左心室射血分数。应用超声应变率显像分别测量左心室各壁不同节段收缩期、快速充盈期及舒张晚期的峰值应变率,对各峰值应变率与导管法所测的相应指标进行相关性分析。结果常规超声心动图指标比较,在不同冠状动脉狭窄病变组,仅LAD在三支病变组〔(38.74±4.57)mm〕较轻度冠脉病变组〔(33.87±3.80)mm〕及单支血管病变组〔(33.77±3.94)mm〕显著增加。左心导管测定的LVEDP、dp/dtmax、dp/dtmin、EDV、ESV各组比较均无显著的统计学差异。而轻度冠脉病变组的等容舒张期压力衰减时间常数〔(30.31±6.50)ms〕低于其他各组。舒张早期充盈的1/3V及1/3FF在冠状动脉显著狭窄组低于轻度冠脉病变组。结论不同程度的冠状动脉病变对心室的舒张功能具有一定的影响,而且随着病变程度的加重影响增大。超声应变率显像技术可以准确判断冠心病患者的心室舒张功能。     

Isradipine (PN 200-110), a new dihydropyridine calcium antagonist with slight negative inotropic properties in comparison with nifedipine

The influence of isradipine (PN 200-110), a new dihydropyridine calcium antagonist, in comparison to nifedipine and placebo on hemodynamics and left ventricular function was investigated in patients with coronary artery disease (10 patients in each group). The drugs were infused intravenously within 30 min in a dosage which led to a comparable afterload reduction (nifedipine [N] 2 mg, isradipine [I] 0.5 mg, AOP mean decrease: N, 14.7%, I, 13.1%). Increase of cardiac output (N +12.5%, I +15%) and decrease of systemic vascular resistance (N -29.2%, I -25%) were equal in both groups. Nifedipine caused a significant reflex increase of heart rate (+9.2%, p less than 0.001), which was not present with isradipine. The consequence was a significant decrease of the rate-pressure product with isradipine only (-12.5%, p less than 0.001) and not with nifedipine. Although afterload reduction was equal in both groups, isradipine caused a more pronounced decrease of LV volumes (EDVI: N -10%, I -16%) and an increase of ejection fraction (N +8%, I +14%). A significant increase of dp/dtmax, as a result of the afterload reduction, occurred after isradipine only (+13.5%, p less than 0.001) with no changes of dp/dtmax after nifedipine. Since changes of parameters (preload, afterload, HR, LVSP), which influence dp/dtmax independent of the inotropic state, were equal in both groups, the increase of dp/dtmax after isradipine should be a result of less negative inotropic properties of isradipine compared to nifedipine.     

Emergency angioplasty in acute anterior myocardial infarction

Ninety-three patients with acute anterior myocardial infarction were treated with emergency percutaneous transluminal coronary angioplasty (PTCA). All were found to have a high-grade obstruction in the left anterior descending (LAD) vessel or the bypass graft to this vessel; 64 patients had a total occlusion. A completely successful PTCA, defined as a residual lesion of less than or equal to 50%, was achieved in 73 (78%) patients. A partially successful PTCA, with a residual lesion of 51% to 99%, was achieved in 12 (13%) patients. PTCA was unsuccessful in eight (9%) patients. Hospital mortality was 14%. Three parameters viewed separately each predicted hospital mortality: presence of shock, a proximal location of the LAD vessel occlusion, and the residual stenosis after PTCA. Reocclusion was found in only 11% of patients but 34% had evidence of restenosis on restudy.     

腺苷对猪急性心肌梗死再灌注后无再流的影响

目的评价腺苷防治猪急性心肌梗死(AMI)再灌注后无再流的作用。方法中华小型猪24只随机分成对照组、腺苷组(100μg·kg-1·min-1持续静点)和假手术组,每组8只。前2组行冠状动脉结扎3h,松解1h建立AMI再灌注模型。AMI前、后和再灌注后均行血流动力学测定和心肌声学造影检查,最终行病理学分析。结果(1)与AMI前相比,对照组AMI后3h主动脉收缩和舒张压、左室收缩压、心排量和左室内压最大收缩和舒张变化速率(±dp/dtmax)均显著下降(P<0.05～0.01),肺毛细血管楔压和左室舒张末压均显著升高(P<0.01);再灌注后1h仅左室舒张末压显著恢复(P<0.05)然而±dp/dtmax继续显著下降(P<0.05);而腺苷组AMI后3h各项指标变化与对照组相同;但再灌注后1h左室收缩压、左室舒张末压、±dp/dtmax和心排量均显著恢复(P均<0.05),且比对照组更显著(P均<0.05)。(2)对照组心肌声学造影和病理染色所测的冠状动脉结扎区心肌范围高度一致,再灌注后无再流面积分别为67.5%和69.3%,心肌坏死面积(NA)占结扎区心肌面积(LA)的98.5%;而腺苷组LA均与对照组相当,但两方法所测无再流面积仅分别为21.5%和20.8%,NA仅为75.2%,均显著小于对照组(P<0.05～0.01)。(3)对照组再灌注即刻和再灌注后1h冠状动脉血流量仅占AMI前的45.8%和50.6%(P均<0.01),而腺苷组冠     

ST segment response to acute coronary occlusion: coronary hemodynamic and angiographic determinants of direction of ST segment shift

To assess the relationship between the direction of ST segment response to transient coronary occlusion and collateral function, we studied 25 patients with diagnostic ST segment changes during transient occlusion of the proximal left anterior descending artery (LAD). Electrocardiographic leads I, II, V2, and V5; left ventricular filling, aortic, and distal coronary pressures; and great cardiac vein flow were measured during percutaneous transluminal coronary angioplasty (PTCA) of the LAD. During a 1 min LAD balloon occlusion, 16 patients had reversible ST elevation (group I) and nine patients had ST depression (group II). The ST responses in individual patients were consistent during repeated occlusions, and ST depression never preceded ST elevation. Angiography before PTCA showed less severe LAD stenosis in group I (69 +/- 15%) than in group II (88 +/- 10%; p less than .01) and collateral filling of the LAD in no group I patient but in six of nine patients in group II (p less than .01). During LAD occlusion, determinants of myocardial oxygen demand (left ventricular filling pressure, aortic pressure, heart rate, and double product) were similar in both groups. Group I patients, however, had lower distal coronary pressure (25 +/- 8 vs 41 +/- 16 mm Hg) and residual great cardiac vein flow (33 +/- 14 vs 51 +/- 22 ml/min) and higher coronary collateral resistance (3.1 +/- 2.1 vs 1.5 +/- 0.8 mm Hg/ml/min) than group II patients (all p less than .05). In patients with ST elevation during LAD occlusion, stenosis before PTCA was less severe, visible collaterals were not present, and hemodynamic variables during LAD occlusion reflected poorer collateral function.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of acute short-term ischemia during PTCA on the function of the right ventricle

To determine whether a transient ischemia of the right ventricle leads to right ventricular impairment and whether RV function can also be influenced by septal ischemia caused by an occlusion of the left anterior descending coronary artery (LAD), RV function before and at the end of 60 s of ischemia during PTCA was assessed in 15 patients with single-vessel disease of either the right coronary artery (RCA, n = 10) or the LAD (n = 5). The RV-enddiastolic pressure and the pulmonary capillary wedge pressure (PCW) were recorded continuously. The RV ejection fraction was determined from ventriculograms performed before and during coronary occlusion. An increase of RVEDP from 3.7 +/- 1.2 to 8.3 +/- 1.8 mm Hg (p less than or equal to 0.001) and a decrease of the RV-ejection fraction from 52 +/- 3 to 33 +/- 8% (p less than or equal to 0.001) occurred during RCA occlusion with a predominant ischemia of the RV free wall only, and not during LAD occlusion with left ventricular and septal ischemia. The extent of the RV dysfunction was independent of an additional increase of RV afterload (PCW increase). Comparable to ischemic effects on left ventricular function, an acute right ventricular myocardial ischemia results in a severe RV contractile failure.     

Effects of diltiazem and nitroglycerin on left ventricular diastolic properties in patients with coronary artery disease

To determine the effects of diltiazem (DTZ) and nitroglycerin (NTG) on left ventricular (LV) diastolic relaxation and filling in patients with cornary artery disease (CADpts), LV graphy and time constant (Tc) of LV isovolumic pressure decay were studied before and 5 min after intravenous DTZ (10 mg) in 16 CADpts and sublingual NTG (0.3 mg) in 11 CADpts. Diastolic regional ventricular filling dynamics were quantitated by segmental area-time curves during early-, mid- and late-filling periods. After NTG, LV systolic pressure (LVSP), end-diastolic pressure (EDP) and end-diastolic volume (EDV) decreased. Early-filling rate (EFR) decreased (165 +/- 82 to 122 +/- 61 ml/sec/m2) due to a decrease in the regional early-filling rate in the normokinetic area and late-filling rate (LFR) increased (95 +/- 38 to 145 +/- 45 ml/sec/m2), while LV peak positive dp/dt, peak LVSP/end-systolic volume (ESV) ratio, Tc and mid-filling rate (MFR) were unchanged. After DTZ, LVSP decreased and EDV increased. EFR increased. EFR increased (127 +/- 54 to 166 +/- 60 ml/sec/m2) due to an enhanced regional early-filling rate in the mildly hypokinetic area, while EDP, LV peak positive dp/dt, peak LVSP/ESV ratio, Tc, MFR and LFR were unchanged. From these results, it was postulated that NTG caused a decrease in LV early filling and an increase in LV late filling, probably due to LV preload reduction. In contrast, DTZ caused significant improvement of LV early filling particularly in the mild hypokinetic area. Thus, DTZ but not NTG was able to relieve local myocardial dysfunction secondary to a stenosed coronary artery during the filling period, resulting in clinical improvement in CADpts.     

Left ventricular diastolic function in PTCA: a Doppler echocardiographic study

The measurement of left ventricular inflow by Doppler echocardiography provides a continuous, non-invasive assessment of parameters of diastolic function. We studied changes in left ventricular diastolic function during percutaneous transluminal coronary angioplasty (PTCA) of the left anterior descending coronary artery (LAD). In ten patients, the diastolic flow velocity profile across the mitral valve was measured by Doppler echocardiography, before and 60 s after inflation and 60 s after deflation of the balloon. The peak velocity of early diastolic filling (VE) significantly decreased during angioplasty, from 68 +/- 12 to 56 +/- 10 cm/s (p less than 0.001), while the peak velocity of late diastolic filling caused by atrial contraction (VA) showed no change. This resulted in a significant decline in the diastolic velocity ratio (VE/VA) from 1.11 +/- 0.47 to 0.92 +/- 0.35 (p less than 0.01). The total area under the diastolic flow velocity profile representing the total filling volume fell from 14.3 +/- 4.1 to 10.9 +/- 3.6 cm (p less than 0.001). The early diastolic filling fraction decreased from 68 +/- 5% to 64 +/- 7%, in favor of the filling fraction due to atrial contraction, which increased from 32 +/- 5%, to 36 +/- 7% (p less than 0.01). 60 s after deflation of the balloon, the parameters of diastolic filling returned to baseline values. We conclude from our results that diastolic dysfunction caused by angioplasty of the LAD results in a decrease in early diastolic left ventricular filling, which is completely reversible after 60 s.     

Transient Increase in ST-segment Changes at Time of Reperfusion in Acute Myocardial Infarction Treated by Coronary Angioplasty

PURPOSE: The clinical significance of early ST-segment re-elevation, a so called òreperfusion peakó in patients with acute myocardial infarction (AMI) treated with thrombolysis is unclear. We examined the incidence and significance of early ST-segment re-elevation immediately upon reperfusion in patients undergoing percutaneous transluminal coronary angioplasty (PTCA) where the time of reperfusion can be precisely established. METHODS: Thirty-two patients (6 women, 26 men, age 61.5 +/- 10.2 years) with an AMI, admitted less than four hours after the onset of chest pain, were included. Twenty-four patients were treated with primary PTCA and eight with rescue PTCA. Computerized on-line vectorcardiography was used for continuous ischemia monitoring. A reperfusion peak was defined as an increase in ST-vector magnitude (ST-VM) of > 50 μV, starting within two minutes after the re-opening of the infarct-related coronary artery and followed by an immediate decrease in the ST segment. RESULTS: Primary success was achieved in all treated patients. Twenty of the patients (63%) developed a reperfusion peak. ST-VM before coronary angiography was significantly larger (p = 0.004) and peak enzyme levels were higher (p = 0.014) in patients who developed a reperfusion peak. Thrombolytic treatment prior to rescue angioplasty, time to reperfusion, target vessel, presence of collaterals or medication on admission did not differ significantly between the groups. CONCLUSION: The occurrence of a reperfusion peak during the minutes after the onset of reperfusion is a common finding in patients with AMI treated at an early stage with angioplasty. There is a relationship with the occurrence of a reperfusion peak and the extent of the initial ST deviation (presumably reflecting the myocardium at risk) and peak enzyme levels. The importance of a reperfusion peak for clinical outcome and prognosis is so far not known.     

Creatine kinase release after successful percutaneous transluminal coronary angioplasty

After successful percutaneous transluminal coronary angioplasty (PTCA), 25 (20%) of 128 patients had elevation of creatine kinase MB isoenzyme (CK-MB). The increase was mild (mean 9% MB with total creatine kinase of 179 U/L). Three variables were significantly related to the enzyme elevation: chest pain, small branch vessel occlusion, and recent myocardial infarction. Of the patients with CK-MB elevation, 60% experienced chest pain and 32% sustained a small branch vessel occlusion during PTCA, compared with 11% and 8%, respectively, of the 103 patients without enzyme elevation (p less than 0.001 and p less than 0.01). Of 16 patients with recent myocardial infarction, seven (44%) had release of CK-MB. Although mild enzyme elevation after successful PTCA is likely due to a small amount of myocardial necrosis, this phenomenon was not associated with increased cardiac morbidity or mortality. Therefore, release of CK-MB without other clinical evidence for myocardial infarction after successful PTCA does not in itself warrant longer hospitalization, and routine serial enzyme determinations are probably unnecessary. By reducing the number of laboratory tests and the duration of hospitalization, the cost effectiveness of PTCA may be increased.     

Myocardial thallium-201 kinetics during coronary occlusion and reperfusion: influence of method of reflow and timing of thallium-201 administration

Thallium-201 (201Tl) uptake and redistribution kinetics were examined in an open-chest canine preparation of occlusion and reperfusion. Seven dogs (group I) underwent 3 hr of sustained occlusion and received 1.5 mCi of 201Tl after 40 min of occlusion of the left anterior descending coronary artery (LAD). Group II (n = 18) underwent 60 min of LAD occlusion followed by sudden and total release of the ligature. Group IIa (n = 8) received intravenous 201Tl during occlusion of the LAD, whereas group IIb (n = 10) received intravenous 201Tl at the time of peak reflow. Group III dogs (n = 26) also underwent 60 min of LAD occlusion that was followed by gradual reflow through a residual critical stenosis. Animals in this group also received 201Tl either before (IIIa; n = 16) or after reflow was established (IIIb; n = 10). In group I, the relative 201Tl gradient (nonischemic minus ischemic activity) decreased from 88 +/- 8% (mean +/- SEM) to 59 +/- 6% during 3 hr of coronary occlusion (p = .034). After rapid and total reperfusion (group IIa), this gradient decreased from 71 +/- 6% during occlusion to 26 +/- 5% after reflow (p less than .001). After slow reperfusion through a residual stenosis (group IIIa), the gradient decreased from 81 +/- 5% to 31 +/- 5% (p less than .001) (p = .56 compared with group IIa). In rapidly reperfused dogs receiving intravenous thallium during peak reflow (IIb), initial 201Tl activity in the ischemic zone was 155 +/- 20% of initial normal activity and fell to 93 +/- 13% of normal after 2 hr of reperfusion. Similarly, in dogs reperfused slowly through a critical stenosis (IIIb), which received 201Tl during reflow, 201Tl activity soon after reflow was 94 +/- 4% of initial normal and decreased to 80 +/- 6% at 2 hr of reperfusion (p = .10). Histochemical evidence of necrosis was present in the biopsy region in 80% of the 20 dogs subjected to triphenyl tetrazolium chloride (TTC) staining. Microsphere-determined transmural blood flow was similar in all groups during LAD occlusion and final flows after 2 hr were comparable in all subgroups undergoing reflow. Ischemic zone flow (% normal) was significantly higher at the time of 201Tl administration in groups IIb (192 +/- 25%) and IIIb (110 +/- 5%), which received 201Tl during reflow, than in groups IIa (31 +/- 9%) and IIIa (22 +/- 5%), which received 201Tl during occlusion.(ABSTRACT TRUNCATED AT 400 WORDS)     

Left ventricular diastolic pressure-volume relations during exercise (author's transl)

Left ventricular diastolic pressure-volume relations (PVR) were analysed from biplane ventriculograms and simultaneous pressure measurements in 33 patients at rest (R) and during ergometer exercise (E) (8 normals [N], 8 patients with coronary artery disease [CAD], 8 patients with congestive cardiomyopathy [COCM], 5 patients with aortic insufficiency [AI] and 5 patients with pressure overload (4 with aortic stenosis [A-St.] and 1 coarctation of the aorta). In N and AI diastolic PVR was essentially unchanged with E, the time constant of isovolumic relaxation (T) decreased significantly (N: delta T = -24.4 +/- 11.6%, p less than 0.001; AI: delta T = -27.3 +/- 6.8%, p less than 0.005). In CAD diastolic PVR was shifted upwards in all cases with angina pectoris during E (7/8), minimal rate of left ventricular pressure change (dp/dtmin) and T did not change significantly. In COCM diastolic PVR was shifted upwards in 4 cases, while dp/dtmin increased significantly (R = -1107 +/- 327, E = -1508 +/- 626 mm Hg-s-1, p less than 0.05), T on the average was unchanged (R = 53 +/- 10.5, E = 51 +/- 14.2 msec). In A-St. in 3 of 4 cases diastolic PVR was significantly shifted upwards with E, dp/dtmin increased (R = -1633 +/- 93, E = -2093 +/- 170 mm Hg-s-1, p less than 0.001), T in contrast to N and AI was prolonged (R = 33.8 +/- 4, E = 39.9 +/- 1.9 msec). Conclusion: In N and AI diastolic ventricular function is not altered with exercise. In COCM and especially in A-St., however, there are similar alterations like in CAD with angina pectoris. Changes in T indicate that shifts of the PVR with exercise in non-ischemic heart disease are related to a disturbed ventricular relaxation.     

Left ventricular function after successful percutaneous transluminal coronary angioplasty for postinfarction angina pectoris

The purpose of this study was to determine if coronary revascularization by balloon angioplasty (PTCA) in patients with postinfarction angina can elicit an improvement of global systolic left ventricular (LV) function. LV function was evaluated in 18 patients with postinfarction angina based on peak aortic blood acceleration measured noninvasively with a continuous wave Doppler velocimeter. Initial Doppler measurements were made 4 +/- 1 days after infarction and just before PTCA and were repeated 24 to 48 hours after PTCA. Patients were divided into 2 groups. Group I (n = 10) had successful PTCA (reperfusion). Group II (n = 8) either had an unsuccessful PTCA or did not undergo PTCA or thrombolytic therapy (no reperfusion). In group I patients, peak acceleration increased from 16 +/- 1 m/s/s just before PTCA to 24 +/- 2 m/s/s 24 to 48 hours after successful PTCA (p less than 0.001). In group II patients, peak acceleration was 17 +/- 2 m/s/s just before PTCA and remained relatively unchanged (18 +/- 2 m/s/s) 24 to 48 hours later. These data indicate that revascularization of coronary arteries in patients with postinfarction angina can elicit considerable improvement of global LV systolic function.     

Primary stenting produces earlier and more efficient myocardial reperfusion than primary PTCA alone in patients with acute ST segment elevation MI

Restoration of blood flow in the infarct-related artery and subsequent myocardial reperfusion are major goals of both thrombolysis and primary percutaneous interventions. Whether percutaneous transluminal coronary angioplasty (PTCA) with immediate stenting (primary stenting) produces reperfusion more rapidly than primary PTCA alone is uncertain. This study determines whether primary stenting produces earlier myocardial reperfusion than primary PTCA alone in patients with acute ST segment elevation myocardial infarction using troponin T release kinetics. Primary stenting was performed on 60 patients and primary PTCA alone on 44 patients with typical ischemic chest pain and greater than 1.5 MV ST segment elevation in more than 2 contiguous electrocardiographic leads. Serum troponin T concentrations were measured before and after intervention; every 6 hours for 24 hours; then at 36, 48 and 72 hours. The mean time from onset of chest pain to peak serum troponin T concentration was 7.8 +/- 2.7 hours after primary stenting and 14.5 +/- 4.4 hours after primary PTCA (p < 0.0005). The mean peak serum troponin T concentration was 9.8 +/- 6.3 ng/dL after primary stenting and 13.6 +/-6.4 ng/dL after primary PTCA (p < 0.012). A significant univariate association with time to peak concentration of serum troponin T was identified for primary stenting (p < 0.0005), time from onset of chest pain to intervention (p < 0.04), and diabetes mellitus (p < 0.01). The only significant univariate marker associated with peak concentration of serum troponin T was primary stenting (p < 0.012). Multivariate analysis indicated that primary stenting (p < 0.0005), time from onset of chest pain to intervention (p < 0.048), and diabetes mellitus (p < 0.022) significantly influenced time to peak serum concentration or troponin T. Primary stenting produces earlier myocardial reperfusion than primary PTCA in patients with acute ST segment elevation myocardial infarction.     

The effect of superoxide dismutase and reduced glutathione on cardiac performance after coronary occlusion and reperfusion--an experimental study in dogs.

To determine the effect of Superoxide Dismutase (SOD) and Reduced Glutathione (GSH) as free-radical scavengers on cardiac performance in the reperfusion period up to 60 minutes after occlusion of the Left Anterior Descending artery (LAD), 16 dogs were selected for study. In the 30th and 60th minutes of LAD occlusion and reperfusion periods Cardiac Output (CO), Heart Rate (HR), Mean Arterial Pressure (MAP), Pulmonary Capillary Wedge Pressure (PCWP), Coronary Perfusion Pressure (CPP), Rate Pressure Product (RPP) and Triple Index (TI) values were determined. Of the 16 dogs, 7 as controls and 7 treated with SOD and GSH could be included in the study, and 2 had to be excluded because of death. In the 30th and 60th minutes of reperfusion period, the treated dogs had higher CO and CPP (p less than 0.05, p less than 0.01 respectively), MAP values were different (p greater than 0.05, p less than 0.05 respectively) from controls, whereas lower HR (p less than 0.05, p greater than 0.05, respectively), RPP and TI values (p less than 0.05) were determined. It was concluded that the combination of SOD and GSH may improve cardiac performance in the reperfusion period.     

Regional differences in postischemic recovery in the stunned canine myocardium

To determine if differences exist in the degree of ischemic damage and in postischemic recovery when different coronary arteries are occluded and reperfused, 40 barbital-anesthetized dogs were subjected to brief 15-minute periods of coronary artery occlusion followed by 3 hours of reperfusion ("stunned" myocardium) of the left anterior descending (LAD) or the left circumflex (LCX) coronary arteries. Myocardial segment shortening (%SS) in the subendocardium of nonischemic and ischemic reperfused areas was measured by sonomicrometry, and regional myocardial blood flow was measured by radioactive microspheres. Transmural tissue biopsies were taken at the end of reperfusion for the measurement of adenine nucleotides and total tissue water content. Arterial and local coronary venous blood samples were collected during preocclusion, during occlusion, and at 30 and 180 minutes of reperfusion for determination of blood oxygen content and oxygen consumption in the ischemic area. During occlusion, subendocardial blood flow (LAD flow = 0.11 +/- 0.02; LCX flow = 0.15 +/- 0.04 ml/min/gm), myocardial oxygen consumption (LAD = 2.4 +/- 0.7; LCX = 2.7 +/- 0.7 ml/min/100 gm), and areas of the left ventricle at risk (LAD = 27.4 +/- 2.3%; LCX = 32.4 +/- 2.4) were similar in both groups, thus indicating equivalent degrees of ischemia. There were no differences between groups in hemodynamics throughout the experiment or in the loss of myocardial high-energy phosphates or increase in total tissue water in the ischemic reperfused area at 3 hours of reperfusion. There was a significantly greater loss (p less than 0.05) of systolic wall function during LAD versus LCX occlusion and a greater recovery of segment function from 5 minutes throughout 1 hour of reperfusion after LCX occlusion (p less than 0.05), with no difference in %SS at 2 and 3 hours following reperfusion. Thus, although similar changes occurred in blood flow, metabolite parameters, tissue edema, wall function, and overall hemodynamics when either the LAD or LCX perfusion territories were occluded and reperfused, the loss of systolic wall function and recovery of segment shortening were more variable after regional stunning of the LCX perfusion bed. These data suggest that evaluation of pharmacologic or surgical interventions to improve postischemic functional recovery may be more reliably performed when the LAD coronary artery is the vessel occluded.     

实验性顿抑心肌微血管结构和功能改变

目的 探讨心肌顿抑时心肌微血管结构和功能改变。方法 制备冠状动脉左前降支（LAD）不同阻断时间（15min和60min)后再灌注犬心肌顿抑模型，在不同观察时间点静脉注射含全氟丙烷声振白蛋白微泡造影剂，采用二次谐波成像和间歇发射技术行心肌声学造影。由主动脉根部分别注射乙酰胆碱（ACH）和硝酸甘油（NG）后重复心肌声学造影，并计算用药后／前二维超声上所示心肌灰阶峰值比值（PVIR）和顿抑区与正常区心肌灰阶峰值比值的比值PVIRR。心肌标本行透射电镜检查。结果 （1）LAD阻断15min组再灌注早期NG－PVIR和ACH－PVIR明显减低，但分别在再灌注60min和120min时恢复至结扎前水平；（2）LAD阻断60min组再灌注早期NG－PVIR减低，至再灌注120min时才恢复到结扎前水平，而再灌注ACH-PVIR明显减低，随着再灌注时间的延长虽有逐渐回升趋势，但至再灌注120min仍未恢复至结扎前水平；（3）两组PVIRR的变化与PVIR一致，唯恢复稍慢；（4）LAD阻断15min组心肌毛细血管和内皮细胞结构未见明显改变，而LAD阻断60min组毛细血管内皮细胞肿胀，内皮细胞间连接间隙稍增宽。结论 顿抑心肌微血管舒张功能受损，缺血时间较长则还有微血管结构改变，其受损的细胞主要是内皮细胞。     

Coronary angioplasty in high-risk patients with left main coronary stenosis: results from the National Registry of Elective Supported Angioplasty.

To assess the outcome of PTCA in circulatory supported patients with left main coronary artery (LMCA) stenosis, the National Registry of Elective Supported Angioplasty data bank was searched. Patients entered in the registry were considered high-risk PTCA and the PTCA was performed using percutaneous cardiopulmonary bypass (PCPB). Criteria for high risk was left ventricular ejection fraction less than or equal to 25% or a target lesion supplying greater than or equal to 50% of functioning myocardium. Of 455 patients entered in the registry, 61 (13.3%) had LMCA stenosis greater than or equal to 60%. There were 42 patients in whom the PTCA target vessel was the LMCA (PTCA-LMCA) and 19 in whom it was vessel(s) other than the LMCA (PTCA-OTHER). The mean age was similar in the 2 groups (65 +/- 10 vs. 68 +/- 9 yrs, p = ns). The left ventricular ejection fraction (LVEF) was higher in PTCA-LMCA than in PTCA-other (38 +/- 16% vs. 27 +/- 16%, p less than 0.05). The number of vessels dilated/patient was higher in PTCA-LMCA than in PTCA-OTHER (2.1 +/- 1.0 vs. 1.1 +/- 0.3, p less than 0.001). There were a total of 10 in-hospital deaths (16%) in patients with LMCA greater than or equal to 60% stenosis. This exceeds the mortality of the patients with less than 60% LMCA stenosis entered in the registry (4.5%, p less than 0.001). There were 6 in-hospital deaths (14%) in PTCA-LMCA and 4 (21%) in PTCA-OTHER (p = ns).(ABSTRACT TRUNCATED AT 250 WORDS)     

Predictors of success in percutaneous transluminal coronary angioplasty of chronic total occlusions

Earlier studies have indicated that percutaneous transluminal coronary angioplasty (PTCA) of chronic total occlusions has a low success rate. To determine success rate and assess clinical and angiographic variables associated with success and complications, 57 total occlusions in 56 patients undergoing PTCA were analyzed. The clinical duration of occlusion was 51 +/- 86 days. Success (less than 50% residual stenosis) was achieved at 40 of 57 (70%) dilatation sites. Of these 57 total occlusions, 5 were attempted within 24 hours of acute myocardial infarction, 35 between 1 day and 8 weeks of clinical occlusion, 13 greater than 8 weeks and 4 were of unknown duration. Success rates were 4 of 5, 25 of 35, 9 of 13 and 2 of 4, respectively, in each group (difference not significant, comparison of all time groups). Of the 9 narrowings with a successful PTCA for an occlusion greater than 8 weeks, the mean duration of occlusion was 93 +/- 41 days (range 60 to 180). None of the attempted dilatations of occlusions with a clinical duration of greater than 180 days (n = 3) was successful. None of the clinical or angiographic variables (including tortuosity, length of occlusion gap, distance of the occlusion from the vessel origin, thrombus, lesion calcium, collaterals, prior myocardial infarction, vessel dilated or diffuse disease) impacted on success rate (difference not significant for all). No patient died, had a Q-wave infarction, required emergency coronary artery bypass grafting or underwent repeat PTCA within 7 days of the procedure. Non-Q-wave infarction occurred in 2 of 56 patients (4%).(ABSTRACT TRUNCATED AT 250 WORDS)