Monitoring the effect of heparin by measurement of activated clotting time during and after percutaneous transluminal coronary angioplasty.

The anticoagulant effect of heparin during percutaneous transluminal coronary angioplasty was monitored by measurements of the activated clotting time in two studies that compared the effects of a single bolus of heparin with those of a bolus of heparin combined with a continuous infusion of the drug. In a preliminary study 40 patients received a single heparin bolus of 10,000 units (protocol I) and a further 40 patients received both a heparin bolus of 10,000 and a continuous infusion of heparin at a rate of 2000 units per hour (protocol II). During the first 45 minutes, nine patients (23%) in protocol I but only two patients (5%) in protocol II were found to be inadequately anticoagulated. For 24 hours after angioplasty both groups received an infusion of heparin at the rate of 2000 units per hour which led to consistent anticoagulation in 73 (91%) of patients. In a subsequent randomised study, 40 patients received heparin according to either protocol I or II. Protocol II was again found to lead to a higher rate of adequate anticoagulation. During the first 60 minutes 11 patients (55%) in protocol I but only three patients (15%) in protocol II were inadequately anticoagulated. In addition, the activated clotting time of arterial blood in the first 30 minutes was significantly higher than that of venous blood in 70% of the patients. A bolus of heparin (10,000 units) together with an infusion of 2000 units per hour should be routinely given during coronary angioplasty. The effects of heparin, which can vary considerably from patient to patient, should be monitored by the measurement of the activated clotting time of arterial blood.     

Comparison of activated clotting times to heparin management test for adequacy of heparin anticoagulation in percutaneous transluminal coronary angioplasty

The aim of this study was to compare the activated clotting time (ACT) obtained with the Hemochron device and the Heparin Management Test (HMT) on a new automated whole-blood coagulometer, the Thrombolytic Assessment System, in patients undergoing angioplasty. Fifty patients undergoing balloon angioplasty were prospectively enrolled. The mean ACT after a 10,000 unit bolus of heparin was 283 ± 39 sec at the end of the procedure. The mean HMT after 10,000 units of heparin was 286 ± 31 sec at the end of the procedure in the same patients. The correlation between the two methods was significant (r = 0.6; P < 0.01). The HMT appears to correlate well with standard values obtained with the Hemochron ACT monitor in patients undergoing percutaneous transluminal coronary angioplasty. Cathet. Cardiovasc. Diagn. 45:329–331, 1998. © 1998 Wiley-Liss, Inc.     

Relation between procedural activated coagulation time and outcome after percutaneous transluminal coronary angioplasty

Objectives. The purpose of this study was to determine whether a low procedural activated coagulation time is associated with a high rate of in-hospital complications and to identify whether there is an activated coagulation time range that may be associated with a low rate of complications.Background. In recent years the activated coagulation time has come into widespread use for monitoring anticoagulation in the catheterization laboratory. However, considerable controversy exists as to the standards by which to judge “adequate” anticoagulation for interventional procedures.Methods. From a total of 1,469 consecutive patients with percutaneous transluminal coronary angioplasty, we retrospectively identified 103 (Group I, 7% of the overall population) with major complications of death or emergency or urgent coronary artery bypass graft surgery and compared them with 400 patients without complications (Group II). Group I patients had more high risk clinical characteristics, such as type B and C lesions, class III and IV angina, recent myocardial infarction and recent thrombolytic treatment. Activated coagulation times were compared between Groups I and II at baseline, after administration of 10,000 U of heparin and at the end of the procedure.Results. There were no differences in baseline activated coagulation times between Groups I and II. Group I had significantly lower activated coagulation times after heparin therapy and at the end of the procedure: 61% < 250 s, 20% between 250 and 275 s, 11% between 275 and 300 s and 8% >300 s; 279 of Group II had activated coagulation times 27% <250 s, 17% between 250 and 275 s, 35% between 275 and 300 s and 21% >300 s (p < 0.0001). Complications occurred in all patients with final activated coagulation times < 250 s but in only 0.3% of patients with final activated coagulation times >300 s.Conclusions. A diminished activated coagulation time response to an initial bolus of heparin is associated with major in-hospital complications after coronary angioplasty, although patients with complications did have a higher risk before the procedure. It remains to be determined whether there is an ideal “target” activated coagulation time for interventional procedures.     

Comparison of Hemochron and HemoTec activated coagulation time target values during percutaneous transluminal coronary angioplasty

Objectives. The aim of this study was to determine whether activated coagulation time measurements from Hemochrem and HemoTec machines can be used interchangeably and whether similar activated coagulation time target ranges for adequate anticoagulation can be applied to both machines.Background. Adequate anticoagulation is necessary for the safe performance of intravascular interventions such as percutaneous transluminal coronary angioplasty. In current practice, anticoagulation status is frequently assessed by way of the activated coagulation time one of two commercially available systems, HemoTec and Hemochron. Each one employs a different technique to determine the time of clot formation; however, the same terget activated coagulation time values for adequate anticoagulation have been used interchangeably in published studies.Methods. A total of 311 paired samples were compared in 113 high risk patients undergoing angioplasty enrolled in a randomized trial of a platelet glycoprotein IIb/IIIa receptor antibody. Simultaneous activated coagulation time measurements were obtained before and after administration of heparin, and the difference between the values of both machines was calculated. The relation between the Hemochron and HemoTec values was determined by using linear regression analysis. All activated coagulation time measurements were classified as either therapeutic or subtherapeutic using an arbitrary activated coagulation time target of 300 s.Results. There was a correlation between values from the two machines (r = 0.86), but the Hemochron values were consistently higher than the HemoTec values by a mean value ± SD of 28 ± 29%, with wide individual variation. After heparin administration, there was a signaificant (p < 0.0001) difference between the number of measurements classified as therapeutic by HemoTec (53%) and by Hemochron (94%).Conclusions. HemoTec and Hemochron activated coagulation time measurements cannot be used interchangeably. Appropriate target activated coagulation time ranges to determine adequate anticoagulation during coronary angioplasty need to be established for both machines; the target range for one machine should not be extrapolated to the other.     

冠状动脉腔内心电图在经皮冠状动脉内血管成形术中的监测价值

对84例132支血管行经皮冠状动脉腔内血管成形术(PTCA).术中常规冠状动脉腔内心电图(IC-ECG)进行监测,并与体表心电图(S-ECG)进行对比.发现 IC-ECG 监测心肌缺血的敏感度明显高于 S-ECG(P<0.01).缺血性 ST 段上移幅度也高于 S-ECG。对缺血发生时间,高峰间及减压后缺血变化恢复时间也明显快于 S-ECG。在 PTCA 时,IC-ECG 与 S-ECG 共同监测心肌缺血对判断心肌缺血程度及判断再狭窄有一定指导意义。     

Percutaneous transluminal coronary angioplasty: Comparison of arterial vs. venous activated clotting time

When arterial blood samples for activated clotting time (ACT) are difficult to obtain from the arterial sheath during coronary intervention, venous ACT serves as a substitute. Data are lacking on whether arterial and venous ACT are identical and whether one can serve as an effective substitute for the other. Forty-eight patients undergoing percutaneous transluminal coronary angioplasty (PTCA) were prospectively evaluated to answer this question. Simultaneous arterial and venous ACT samples were drawn from femoral artery and vein vascular sheaths before and during each procedure, and ACT values were determined with a Hemochron automated electronic timer. Porcine heparin dosing was guided by arterial ACT in the first 25 patients and by venous ACT in the last 23 patients. The target ACT value used for continued heparin dosing was 400 sec. At baseline and throughout the study up to 60 min, venous ACT was slightly and significantly greater than arterial ACT. Despite this statistical difference in ACT values, there was no difference in complication rate between the two groups, and the amount of heparin used during either guiding regimen was the same. Therefore, although venous ACT values are slightly higher than arterial, the more convenient venous ACT can be safely used to guide heparin dosing during PTCA when using a target ACT value of 400 sec. © 1996 Wiley-Liss, Inc.     

Activated clotting times in acute coronary syndromes and percutaneous transluminal coronary angioplasty

A discrete fall in the ACT (activated coagulation time) has been observed in patients with known activation of the coagulation cascade. Injury to the coronary artery resulting in thrombin activation, whether spontaneous as in the case of acute myocardial infarction or planned as with percutaneous transluminal coronary angioplasty (PTCA), may there-fore be reflected in a change in ACT values. We reviewed the records of patients under-going PTCA at St. Luke's Episcopal Hospital/Texas Heart Institute from January 1990 through December 1992 for information regarding ACT values and clinical events. A total of 469 patients, whose record contained adequate information for study inclusion, were divided into four separate groups: acute myocardial infarction (group I, n = 62), unstable angina with heparin therapy that was withdrawn at least 4 hr prior to PTCA (group II, n = 102), unstable angina with heparin therapy continued until the time of PTCA (group III, n = 154), and stable angina undergoing elective PTCA (group IV, n = 151). Heparin was discontinued 12–15 hr after the procedure in all but group I where anticoagulation was often maintained up to 72 hr. ACT values were measured prior to the PTCA procedure (baseline), after the initial heparin bolus of 10,000 U (postheparin) and ～ 12–18 hr after the procedure (heparin withdrawal). The “baseline” ACT was significantly lower in patients with unstable angina (93 ± 13 sec) or acute myocardial infarction (78 ± 9 sec) who had their baseline value obtained off of heparin therapy than in patients with stable angina (136 ± 21 sec) or those receiving heparin at the time of baseline measurement (135 ± 14 sec, P < 0.001). All patients with unstable coronary syndromes had a blunted response to heparin (group 1–189 sec, group II-221 sec, group III-248 sec). Although groups I-III were not significantly different compared to one another, each was significantly lower than group IV whose past heparin ACT was 279 sec. Heparin withdrawal ACT values fell within the ranges seen in patients with unstable coronary syndromes untreated with heparin in all but group I (whose heparin therapy was continued through the time of the 12–18-hr postprocedure measurement time). Recurrent ischemic events were seen with increased frequency (16.6%) only in patients with unstable angina whose heparin therapy was interrupted prior to PTCA. In conclusion, low baseline ACT values and a blunted ACT response to heparin are associated with clinical syndromes known to result from thrombus formation. The possibility that the ACT may be of value in reflecting thrombus activity requires prospective evaluation.     

Acute coronary occlusion during percutaneous transluminal coronary angioplasty

Two hundred and forty percutaneous transluminal coronary angioplasty procedures were performed in three centres over a two year period. Acute occlusion of the vessel undergoing angioplasty was seen on 20 (8%) occasions. The cause of occlusion was determined angiographically and in some cases confirmed at the time of emergency open heart surgery. The mechanism of coronary occlusion was arterial dissection in six cases, persisting coronary arterial spasm in seven, and coronary thrombosis in four. In three patients the mechanism could not be determined. Immediate reintroduction of a balloon dilatation catheter was attempted in 10 patients and resulted in restoration of adequate coronary flow in six. The remaining 14 patients underwent open heart surgery as an emergency procedure.     

Distal hemoperfusion during percutaneous transluminal coronary angioplasty

During percutaneous transluminal coronary angioplasty (PTCA), the ability to maintain balloon inflations for 3 to 5 minutes, as opposed to the usual 30 to 60 seconds, may lead to improved early and late results. To determine the feasibility and clarify the advantages of distal hemoperfusion during PTCA, blood from the renal vein was manually sampled and then reinjected through the pressure port of the coronary balloon catheter during sustained balloon inflations in 3 patients. By supplying the periphery of the left anterior descending coronary artery with flows of 30 to 50 ml/min, ischemic manifestations were suppressed in all 3 cases. Hemoperfusion was performed without complications for as long as 5 minutes, using a maximum of 225 ml of blood. This new technique represents a major step toward the long-sought goal of extracorporeal coronary circulation during PTCA.     

Benign coronary perforation during percutaneous transluminal coronary angioplasty

In two patients percutaneous transluminal coronary angioplasty was complicated by coronary perforation. In both cases the complication was managed conservatively.     

Distal coronary hemoperfusion during percutaneous transluminal coronary angioplasty

Distal coronary hemoperfusion during percutaneous transluminal coronary angioplasty (PTCA)—with an autoperfusion balloon or active system—facilitates prolonged balloon inflation. Prolonged inflations may tack up intimal dissections and improve the primary angioplasty result in complex lesions. Additionally, distal perfusion may reduce the likelihood of cardiogenic shock during high-risk PTCA. Autoperfusion balloons are most frequently used to treat acute or threatened closure. There currently is no prospective clinical study showing that stent implantation for this complication is more successful and more cost-effective. The blood flow rates through autoperfusion balloons may not abolish myocardial ischemia, and higher flow rates can often be achieved with pumps. Therefore, during high-risk PTCA, pumps may be preferred to prevent hemodynamic collapse. Clinical application of perfusion pumps is hampered by the risk for mechanical hemolysis during prolonged perfusion and the high velocity of the bloodstream that exits the PTCA catheter, causing distal vessel wall trauma. © 1996 Wiley-Liss, Inc.     

Restenosis after multilesion percutaneous transluminal coronary angioplasty

Experience and new technical advances have resulted in an increasing number of patients with multivessel coronary disease who can be considered for percutaneous transluminal coronary angioplasty (PTCA). In selected patients with multivessel coronary disease, PTCA is a safe and effective procedure for the immediate relief of anginal symptoms. However, many questions remain regarding the long-term therapeutic benefit of the procedure. Few data are available on the incidence and clinical significance of restenosis after multilesion PTCA. Clearly, there is the potential for a higher rate of restenosis in patients who undergo dilatation of more than 1 lesion. Determination of restenosis rates after multilesion PTCA is important in the definition of expanded indications for this procedure. Because of the variations in definitions of restenosis and in patient selection factors, reported recurrence rates after multilesion PTCA are not easily compared between patient series. After multilesion dilatation the risk of developing at least 1 recurrent lesion ranges from 26% to 53% and appears to be greater than that reported for single lesion PTCA. Multilesion restenosis occurs in 7% to 21% of patients who undergo multilesion PTCA and is frequently observed in patients with recurrent symptoms. "Silent" multilesion restenosis (i.e., multiple lesion restenosis without symptoms) is rare. A higher risk of restenosis at one of several dilatation sites in a patient with extensive coronary disease should not be a deterrent in recommending multilesion PTCA to selected patients with multivessel coronary disease because the procedure provides important symptomatic relief to most. Further, recurrent narrowings are usually amenable to a second dilatation attempt if clinically indicated.     

Risk stratification after percutaneous transluminal coronary angioplasty

Summary Approximately 20–30% of patients who undergo elective percutaneous transluminal coronary angioplasty (PTCA) require a second angioplasty within 12 months. A significant proportion of patients develop clinical cardiac events during the first year following the initial procedure. The present investigation was undertaken to establish a statistical model for predicting such events. The study group consisted of 100 patients who underwent elective PTCA at the University of Alberta Hospital. All patients were prescribed nifedipine (10 mg tid) and aspirin (325 mg daily) in addition to other medications determined by the attending cardiologist. The patients were reviewed 10 weeks after the procedure and again at the end of 1 year.The follow-up was completed on 96 patients. Within the first year, forty-five experienced cardiac events (1 death, 5 myocardial infarctions, 4 bypass surgeries, 22 repeat PTCAs). These events occurred in 29 patients. An additional 16 patients experienced significant anginal symptoms. A statistical model based upon the patients' perception of symptoms immediately after the procedure, history of hypertension, vessel subjected to PTCA, ejection fraction pre-PTCA, and occurrence of intimal dissection during PTCA was used to identify patients likely to develop cardiac events. Overall, the model classified 72% of the patients (with and without events). Such a statistical model could be used to identify patients who should be subjected to an enhanced degree of cardiologic surveillance in a rehabilitation program.     

Thromboxane release during percutaneous transluminal coronary angioplasty

The reason for coronary artery occlusion following percutaneous transluminal angioplasty (PTCA) remains an enigma. We postulated that alterations in arachidonic acid metabolism might contribute to coronary artery occlusion, particularly if platelets are perturbed and release thromboxane because of mechanical stimuli during PTCA. We serially monitored coronary sinus and peripheral arterial plasma thromboxane (TX) and prostacyclin (by standard radioimmunoassay of the metabolites TXB2 and 6-keto-PFG1 alpha) during PTCA in 10 patients. TX and prostacyclin were unchanged from control in seven uncomplicated procedures. In one patient with vasospasm, no changes were found. In two patients with occlusion, marked increases were measured in coronary sinus plasma TX. Patient No. 1 increased from 390 to 1375 pg/ml. Patient No. 2 increased from 155 to 1425 pg/ml. Both required emergency bypass grafting. No change in 6-keto-PGF1 alpha was found. Uncomplicated PTCA does not alter arachidonic acid metabolism through cyclooxygenase. Vasospasm need not be associated with TX release, but coronary artery occlusion is. TX may play a role in coronary artery occlusion during PTCA because of (1) increased release and (2) unopposed physiologic effects because increases were not found in the physiologic antagonist prostacyclin.