Applicability of percutaneous transluminal coronary angioplasty to patients with recombinant tissue plasminogen activator mediated thrombolysis

To test the utility and safety of percutaneous transluminal coronary angioplasty (PTCA) after recombinant tissue plasminogen activator (t-PA), we performed the procedure in all suitable candidates with acute myocardial infarction (MI) who had successful t-PA mediated coronary thrombolysis. Twenty consecutive patients with MI received t-PA after coronary angiographic conformation of total occlusion. Successful recanalization with t-PA was achieved in 13 patients, leaving a residual obstruction of 84 ± 6% in the nine patients for whom PTCA was attempted at a mean of 21.6 h. Success was achieved in seven patients, leading to a residual lesion of 29 ± 7%. In the two patients for whom PTCA was unsuccessful, total reocclusion occurred prior to the attempt despite therapy with heparin, aspirin, dipyridamole, and nifedipine. All PTCA procedures were uncomplicated. Serial two-dimensional echocardiography at 10 days, compared to admission, demonstrated infarct zone wall motion index improvement in the patients with successful PTCA (group A, 0.83 ± 0.36 to 1.46 ± 0.49) as compared to the 13 patients without thrombolysis or successful PTCA (group B, 0.61 ± 0.26 to 0.66 ± 0.39), (P < 0.05). One patient of group A sustained a massive stroke at 2 weeks after hospital discharge. In the remaining six patients, follow-up exercise testing and/or coronary arteriography demonstrated a negative treadmill test and/or patent infarct vessel, respectively. After successful PTCA, no patient had clinical signs of reocclusion, reinfarction, postinfarction angina, or congestive heart failure. At 9.4 ± 2 months, all six patients are asymptomatic and have returned to work. Thus, sequential PTCA after t-PA can be performed safely and successfully in patients with MI and this approach may be associated with improved regional function and a favorable post-MI course.     

Recurrence of coronary artery spasm after successful percutaneous transluminal coronary angioplasty

A 47-year-old man presented with angina, and coronary angiograms showed a significant organic stenosis with spasm in the left anterior descending coronary artery. Percutaneous transluminal coronary angioplasty was successfully performed for the organic lesion in the left anterior descending coronary artery. Symptom of angina due to coronary artery spasm recurred, even without restenosis at the site of successful angioplasty.     

The resolution of coronary collaterals after successful percutaneous transluminal coronary angioplasty

It has been shown that collaterals can develop rapidly during acute coronary occlusion, either due to thrombosis or during angioplasty (PTCA). However, the fate of well-developed collaterals immediately after a successful PTCA is unknown. Accordingly, 15 patients with Rentrop class 2 or 3 collaterals as visualized angiographically were studied immediately after successful single-vessel PTCA. The left anterior descending artery contained the stenosis in nine patients and the right coronary contained the stenosis in six patients. There was total occlusion of six vessels and subtotal occlusions of nine vessels pre PTCA. Immediately after PTCA, flow through the collaterals to the stenosed artery could no longer be visualized angiographically in eight patients (group 1), but remained faintly visible in seven patients (group 2). There was no difference between these two groups with regard to pre PTCA transstenotic pressure gradient (46 +/- 12 vs 42 +/- 14 mm Hg), post PTCA pressure gradient (13 +/- 7 vs 11 +/- 10 mm Hg), or post PTCA percent luminal diameter narrowing (26 +/- 18% vs 24 +/- 13%). These findings suggest that despite similar hemodynamic and angiographic improvement, the resolution of collaterals immediately after PTCA is variable.     

Disappearance of mitral valve regurgitation after successful percutaneous transluminal coronary angioplasty

Percutaneous transluminal coronary angioplasty has been reported to improve several clinical parameters. Functional papillary muscle dysfunction, which is also known to induce mitral valve regurgitation, is reversible after revascularization. We described a patient, with a 95% stenosis of proximal right coronary artery, whose mitral valve regurgitation disappeared after successful percutaneous transluminal coronary angioplasty.     

Coronary revascularization after intravenous tissue plasminogen activator for unstable angina pectoris: results of a randomized, double-blind, placebo-controlled trial

To determine the role of intravenous tissue plasminogen activator (t-PA) in unstable angina, it was compared with placebo in a randomized, double-blind trial. Forty patients with angina at rest and provocable ischemia (pacing induced) had baseline coronary angiography, study drug infusion and then repeat angiography at 20 +/- 9 hours. All patients received diltiazem, nitrates, beta blockers, aspirin and intravenous heparin. During study drug infusion (150 mg over 8 hours), refractory ischemia necessitating emergency bypass surgery (CABG) or coronary angioplasty (PTCA) occurred in 4 of 20 t-PA patients compared with 1 of 20 placebo patients (p = 0.21). Before discharge, revascularization for persistent, provocable ischemia and a residual stenosis greater than or equal to 60% was as follows: t-PA patients, 8 PTCA and 7 CABG; placebo patients, 11 PTCA and 8 CABG (p = 0.39). Quantitative angiographic percent diameter stenosis of the culprit artery at baseline and follow-up was: t-PA 71 +/- 17 and 63 +/- 22; placebo 70 +/- 19 and 67 +/- 22 (difference not significant). However, 3 t-PA patients compared with no placebo patients demonstrated an insignificant (less than 60% diameter) residual stenosis and averted PTCA (p = 0.14). There were no complications of PTCA in the 8 t-PA patients; in contrast, 3 of 11 placebo patients had abrupt closure, necessitating emergency CABG in 2 (p = 0.23). Thus, intravenous t-PA in unstable angina can eliminate the need for PTCA in a few patients, does not appear to decrease the overall or emergency rate of revascularization procedures and may facilitate the safety of PTCA.     

Restenosis after successful percutaneous transluminal coronary angioplasty: the Montreal Heart Institute experience

Repeat coronary angiography was performed within 6 months after successful percutaneous transluminal coronary angioplasty (PTCA) in 178 of our first 181 patients (98%). The remaining 3 patients were symptom free, had negative treadmill exercise test results and were considered not to have had restenosis. A second follow-up angiogram was performed in 107 patients (59%), including all patients with persistent or recurrent anginal symptoms, between 7 and 18 months after PTCA. Fifty-one of the 181 patients (28%) had restenosis on 51 of 205 successfully dilated segments (25%). The stenosis was greater than or equal to 70% in 49 of these 51 segments; it was 65% and 55%, respectively, in the 2 remaining patients. Restenosis was documented angiographically at a median time of 4.7 +/- 4 months. However, 47 patients (92%) had restenosis documented within 6 months, 2 between 7 and 12 months and 2 between 13 and 18 months after PTCA. Stepwise logistic regression analysis selected the following factors as independent predictors of restenosis after PTCA: variant angina, multivessel disease, severity of residual stenosis and less reduction in the diameter of the stenosis on the angiogram immediately after PTCA. Of these 4 factors, the degree of residual stenosis immediately after PTCA was by far the most significant. It is concluded that restenosis occurs in approximately 25% of patients, almost always within the first 6 months, after successful PTCA. The degree of residual stenosis after PTCA is the most important predictor of restenosis. Increased experience and improved instrumentation may eventually lead to less residual stenosis and better late results after PTCA.     

Early detection of restenosis after successful percutaneous transluminal coronary angioplasty by exercise-redistribution thallium scintigraphy

The value of exercise testing and thallium scintigraphy in predicting recurrence of angina pectoris and restenosis after a primary successful transluminal coronary angioplasty (PTCA) was prospectively evaluated. In 89 patients, a symptom-limited exercise electrocardiogram (ECG) and thallium scintigraphy were performed 4 weeks after they had undergone successful PTCA. Thereafter, the patients were followed for 6.4 ± 2.5 months (mean ± standard deviation) or until recurrence of angina. They all underwent a repeat coronary angiography at 6 months or earlier if symptoms recurred. PTCA was considered successful if the patients had no symptoms and if the stenosis was reduced to less than 50% of the luminal diameter. Restenosis was defined as an increase of the stenosis to more than 50% luminal diameter. The ability of the thallium scintigram (presence of a reversible defect) to predict recurrence of angina was 66%, vs 38% for the exercise ECG (ST-segment depression or angina at peak workload). Restenosis was predicted in 74% of patients by thallium scintigraphy, but only in 50% of patients by the exercise ECG. Thus, thallium scintigraphy was highly predictive but the exercise ECG was not (p < 0.005). These results suggest that restenosis had occurred to some extent already at 4 weeks after the PTCA in most patients in whom it was going to occur.     

放射治疗预防血管成形术后再狭窄的研究现状

经皮冠状动脉球囊成形术(FICA)后有30％～40％的患者在半年内发生再狭窄,严重限制了其远期疗效。血管成形术后再狭窄的发生主要是由于内膜的增生和血管的重塑。冠状动脉支架植入的应用抵消了血管的病理性重塑,使再狭窄率下降了10％,但是支架内的内膜增生程度反而加重。目前国内外对预防再狭窄的研究包括药物治疗、基因治疗、新的成形术和放射疗法等。前三者均未得满意的效果,而放射线辐射具有特定的生物学效应,致再狭窄的防治获得良好的效果。本文对放射治疗预防再狭窄的现状和进展进行归纳和分     

Angiographic de novo appearance of a myocardial bridge after successful percutaneous transluminal coronary angioplasty

Background: NT-proBNP has prognostic implications in heart failure. In acute coronary syndromes (ACS) setting, the prognostic significance of NT-proBNP is being sought. We studied short-term prognostic impact of admission NT-proBNP in patients admitted for ACS and in association with GRACE risk score (GRS). Methods and Results: We studied 1035 patients admitted with ACS. Patients were divided in quartiles according to NT-proBNP levels on admission: Q1 <180 pg/ml; Q2 180–691 pg/ml; Q3 696–2664 pg/ml; Q4 2698–35 000 pg/ml. Groups were compared in terms of short-term all-cause mortality. Patients with higher NT-proBNP had worst GRS on admission. They also received less aggressive treatment. In-hospital mortality was 0.8%, 3.0%, 5.8% and 12.8% (P<0.001) and 30-day mortality 1.6%, 4.6%, 6.5% and 16.7% (P<0.001) respectively. In multivariate logistic regression analysis, NT-proBNP is an independent predictor of in-hospital (OR 2.35; 95% CI: 1.12–4.93, P=0.022) and 30-day mortality (OR 2.20; 95% CI: 1.17–4.12, P=0.014). However, NT-proBNP does not add any incremental benefit to GRS for prediction of outcome by ROC curve analysis. Conclusions: NT-proBNP is an independent predictor of in-hospital and 30-day mortality after ACS, independently of left ventricular function, but does not increase the prognostic accuracy of GRS.     

Prediction of coronary artery reperfusion after tissue plasminogen activator infusion

We investigated whether clinical and laboratory variables can predict perfusion status after t-PA administration, by using the data from 138 patients who received t-PA during the Thrombolysis in Myocardial Infarction (TIMI) I study. All clinical and laboratory variables that were collected at baseline or during perfusion for TIMI I were evaluated by the current study. Via stepwise discriminant analysis, 7 variables were closely associated with perfusion status at 90 minutes (listed in the order of their discriminant effect): baseline grade of stenosis in the infarct-related coronary artery, whether nausea was present during the infusion, baseline aspartate aminotransferase (SGOT) concentration, whether arrhythmias were present during the infusion, baseline fibrinogen concentration, baseline partial thromboplastin time, and baseline diastolic blood pressure. Baseline severity of stenosis and the likelihood of there being reperfusion were inversely related. Eighty-four percent of patients with adequate perfusion after 90 minutes of t-PA infusion were classified correctly, but only 50% of those without perfusion at 90 minutes were classified correctly. In addition, since 70% of the TIMI I patients, on average, did achieve perfusion, the use of these 7 variables added little predictive information. Our findings suggest that 1) there is as yet no practical way to predict reperfusion after t-PA therapy and 2) the severity of coronary stenoses, if known ahead of time, should be considered when selecting patients for thrombolytic therapy.     

Restenosis after successful percutaneous transluminal coronary angioplasty: serial angiographic follow-up of 229 patients

To further understand the temporal mode and mechanisms of coronary restenosis, 229 patients were studied by prospective angiographic follow-up on day 1 and at 1, 3 and 6 months and 1 year after successful percutaneous transluminal coronary angioplasty. Quantitative measurement of coronary stenosis was achieved by cinevideodensitometric analysis. Actuarial restenosis rate was 12.7% at 1 month, 43.0% at 3 months, 49.4% at 6 months and 52.5% at 1 year. In 219 patients followed up for greater than or equal to 3 months, mean stenosis diameter was 1.91 +/- 0.53 mm immediately after coronary angioplasty, 1.72 +/- 0.52 mm on day 1, 1.86 +/- 0.58 mm at 1 month and 1.43 +/- 0.67 mm at 3 months. In 149 patients followed up for greater than or equal to 6 months, mean stenosis diameter was 1.66 +/- 0.58 mm at 3 months and 1.66 +/- 0.62 mm at 6 months. In 73 patients followed up for 1 year, mean stenosis diameter was 1.65 +/- 0.56 mm at 6 months and 1.66 +/- 0.57 mm at 1 year. Thus, stenosis diameter decreased markedly between 1 month and 3 months after coronary angioplasty and reached a plateau thereafter. In conclusion, restenosis is most prevalent between 1 and 3 months and rarely occurs beyond 3 months after coronary angioplasty.     

Three year anatomic, functional and clinical follow-up after successful percutaneous transluminal coronary angioplasty

Because the long-term anatomic effects of percutaneous transluminal coronary angioplasty are unknown, follow-up evaluations including coronary angiography, treadmill exercise testing and rest and bicycle exercise radionuclide angiography were performed in 46 patients 6.3 +/- 2.0 and 37.6 +/- 3.6 (mean +/- SD) months after they had undergone successful single lesion angioplasty. The severity of the coronary stenosis decreased significantly at each evaluation; the mean diameter stenosis was 66 +/- 13% before angioplasty, 30 +/- 13% immediately after and 26 +/- 16% and 19 +/- 13% at 6 months and 3 years, respectively. Exercise time increased from 9.8 +/- 4.4 minutes before angioplasty to 18.3 +/- 4.5 minutes immediately after the procedure and remained at that level at 6 months (20.3 +/- 4.6 minutes) and 3 years (18.2 +/- 4.5 minutes). Left ventricular ejection fraction during exercise decreased 4 +/- 6% compared with rest before angioplasty, but increased 7 +/- 7% immediately after angioplasty and this increase was maintained at 6 months (+/- 6 +/- 7%) and 3 years (+/- 4 +/- 6%). Before angioplasty, 1 patient was in Canadian Heart Association functional class 0, 15 were in class II, 24 in class III and 6 in class IV. Three years later, 25 were in class 0, 10 in class I, 7 in class II and 4 in class III. These results indicate that the short-term anatomic and functional success of coronary angioplasty is maintained for at least 3 years.     

Coronary arterial rupture during percutaneous transluminal coronary angioplasty: a case report

A case who developed rupture in a diagonal branch of the left anterior descending coronary artery (LAD) during percutaneous transluminal coronary angioplasty (PTCA) is reported here. The present case was 80-year-old man with severe focal stenosis of the LAD at its junction with a diagonal branch. PTCA for the LAD lesion was successfully performed, but occlusion of the diagonal branch developed later. A subsequent ECG showed elevation of an ST segment in a VL, and PTCA for the diagonal branch was attempted. A 018 Hi-torque floppy guide wire was introduced into the occluded diagonal branch, and its dilatation was attempted using a 2 mm Simpson-Robert catheter. During a maximal pressure of 120 psi, a deformity was found at the distal end of the balloon. Post-PTCA angiograms showed rupture of the diagonal arterial branch, and mild to moderate pericardial effusion was observed by echocardiography. The patient experienced transient hypotension (60 mmHg at systolic), but his condition gradually stabilized after the administration of only a pressor medication. Neither pericardiocentesis nor emergency surgery was performed. The next day, follow-up angiograms showed diagonal branch occlusion at the proximal portion of the rupture site. His clinical course was satisfactory with spontaneous resolution of pericardial effusion and mild elevation of his cardiac enzymes (CPK = 243IU). In this case, it was concluded that the cause of coronary arterial rupture was the difference in diameters of the coronary artery (1 mm) and the balloon catheter (2 mm). This was the first rupture case experienced among 750 PTCA sites (0.13%).(ABSTRACT TRUNCATED AT 250 WORDS)     

Buccal nitroglycerin decreases ischemic pain during coronary angioplasty: a double-blind, randomized, placebo-controlled study.

Nitroglycerin (NTG) has the potential to reduce myocardial ischemia during percutaneous transluminal coronary angioplasty (PTCA). Buccal administration of NTG offers practical advantages compared to intravenous or intracoronary administration. In a double-blind, randomized, placebo-controlled study, 100 patients were given 5 mg of buccal NTG or placebo during PTCA. A scoring system for ischemic pain during balloon inflation was defined as pain intensity (0 to 5) multiplied by duration of pain after balloon deflation (1 = 0 to 30 seconds, 2 = 30 to 60 seconds, 3 = 60 to 120 seconds, 4 = greater than 120 seconds but subsiding, and 5 = until next inflation). Fourteen patients were excluded: 12 for vagal reaction (eight NTG and four placebo; p greater than 0.05) requiring atropine, making buccal absorption unreliable, and two for inability to dilate. Eighteen patients (nine NTG and nine placebo) had no pain during balloon inflation. Sixty-eight patients (32 NTG and 36 placebo) had ischemic pain with a pain score (mean +/- SD) of 4.8 +/- 3.8 for the NTG group versus 7.1 +/- 4.8 for the placebo group (p = 0.03). We conclude that buccal NTG significantly decreases myocardial ischemia during PTCA.