Shaping ability of ProTaper NEXT and BT-RaCe nickel-titanium instruments in severely curved root canals.

AIM: To compare the shaping ability of four different nickel-titanium rotary instruments during the preparation of curved root canals in extracted teeth. METHODOLOGY: A total of 80 root canals with curvatures ranging between 25° and 39° were divided into four groups of 20 canals. Based on radiographs taken prior to instrumentation, the groups were balanced with respect to the angle and the radius of canal curvature. Canals were prepared to a final apical size of 40 using Mtwo, ProTaper Universal, ProTaper NEXT and BT-RaCe. Using pre- and post-instrumentation radiographs, straightening of the canal curvatures and canal transportation were determined with a computer image analysis programme. Preparation time and instrument failures were also recorded. The data were analysed statistically using anova and Student-Newman-Keuls test. RESULTS: The use of BT-RaCe files resulted in significantly more straightening during instrumentation compared to Mtwo (P < 0.05), whilst the differences between all other instruments were not significant (P > 0.05). No significant differences were obtained between all four instruments regarding canal transportation (P = 0.429). Instrumentation with ProTaper NEXT files was significantly faster than with all other instruments (P < 0.05). During the preparation of the curved canals, one BT2 instrument fractured, whilst no fracture occurred when using the other instruments (P > 0.05). CONCLUSIONS: Within the parameters of this study, all instruments maintained root canal curvature well and were safe. However, care should be taken when using the BT2 instrument due to its unique cylindrical design.

Scintigraphic evidence of the "no reflow" phenomenon in human beings after coronary thrombolysis.

To assess whether the absence of new thallium-201 uptake after successful intracoronary thrombolysis reflects a disturbance of myocardial cell function or lack of capillary reperfusion, dual isotope scintigraphic studies with thallium-201 and technetium-99m micro-albumin aggregates were performed in 16 patients with acute anterior myocardial infarction. Intracoronary thallium-201 and technetium-99m scintigraphy performed before intracoronary thrombolysis in 12 of the 16 patients resulted in identical thallium-201 and technetium-99m defect sizes. Immediately after intracoronary thrombolysis, thallium-201 and technetium-99m scintigraphy was repeated in 11 of the 12 patients. In 4 of the 11, the initial thallium and technetium scintigraphic defects were significantly reduced, and in 6 of the 11, they were only slightly reduced; there was no difference in the size of the residual defect as assessed with both radionuclides in all 10 of the 11 patients. In the eleventh patient, there was a significant reduction of the initial technetium-99m scintigraphic defect but no change in the size of the thallium-201 defect. In four other patients, scintigrams were obtained only after intracoronary thrombolysis; these revealed no difference in thallium-201 and technetium-99m defect size. In seven of eight patients restudied 2 to 4 weeks after intracoronary thrombolysis, thallium-201 and technetium-99m defect sizes were identical with those immediately after intracoronary thrombolysis; in the eighth patient there was no difference in thallium-201 and technetium-99m defect size, although such a difference had been present immediately after intracoronary thrombolysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Short-term results and intermediate-term follow-up of laser wire recanalization of chronic coronary artery occlusions: a single-center experience.

OBJECTIVES: This study sought to elucidate the short-term efficacy and intermediate-term outcome of excimer laser recanalization of chronic coronary artery occlusions in patients in whom attempts at mechanical revascularization had failed. BACKGROUND: Recanalization of chronic coronary occlusions with the use of a mechanical guide wire fails in 30% to 50% of cases, mostly because of inability to pass the wire through the lesion. The value of using excimer laser energy in this setting has not yet been determined. METHODS: The study group comprised 66 consecutive patients with 68 chronic coronary occlusions. Patients were eligible for inclusion in the study if a previous attempt at mechanical revascularization had failed and if their angiographic status was such that 1) the vessel segment distal to the occlusion could be visualized by way of collateral vessels, 2) the entry point of the occlusion was clearly outlined, and 3) not more than one anatomic bend was expected within the occlusion. Excimer laser energy was applied to the lesion through a 0.018-in. (0.046 cm) fiber-optic guide wire. Adjunctive balloon angioplasty and stenting were performed in all successfully treated patients but one. RESULTS: Thirty-four occlusions (50%) in 32 patients (48%) could be crossed with the laser wire. Location and age of the occlusion had no adverse influence on the outcome of laser wire recanalization, nor did the presence of bridging collateral vessels, a major side branch at the site of the lesion or a blunt stump of the occlusion. An inverse relation was found between the success rate and the length of the occlusion, such that a 19% reduction of the success rate accompanied each 10-mm increment of the mean occlusion length. Thus, the success rate was 68% for lesions < or = 10 mm but only 25% for lesions > 30 to < or = 40 mm. The presence of a bend in the lesion exceeding 60 degrees was strongly related to procedural failure. During a median angiographic follow-up period of 18 weeks, restenosis > 50% (n = 6) or reocclusion (n = 4) was found in 10 of the 32 successfully treated patients, for an intermediate-term success rate of 33% (22 of 66). Clinical follow-up revealed improved anginal status in 21 patients (66%) after a median of 24 weeks. Major complications (death, myocardial infarction, emergency operation) were not encountered. CONCLUSIONS: Successful recanalization of a chronic coronary occlusion by using currently available laser wires can be expected in 50% of selected patients in whom attempts at mechanical revascularization fail. Restenosis or reocclusion accounts for an overall 6-month success rate of 35%.

Time from onset of symptoms to thrombolytic therapy: a major determinant of myocardial salvage in patients with acute transmural infarction.

To determine whether myocardial salvage after successful intracoronary or intravenous thrombolysis is time dependent, the relation between left ventricular wall motion and the time to treatment was studied in 69 patients admitted less than 3 hours after onset of acute transmural myocardial infarction (42 patients with reperfusion by intracoronary streptokinase, 27 by intravenous urokinase). A similar significant relation between the time to treatment and the severity of regional hypokinesia at follow-up was found in the intracoronary and intravenous groups. To better define this relation, particularly during the early phase of infarction, the groups were combined. In patients in whom thrombolytic treatment was initiated within 2 hours after symptom onset, wall motion at follow-up was within 2 standard deviations of the normal mean in 82% (14 of 17 patients). If treatment was started 2 to 5 hours after symptom onset, the probability of improved wall motion decreased to 46% (24 of 52 patients, p less than 0.025). The time/wall motion relation appeared to be independent of infarct location, angiographically visible collateral vessels and the presence of subtotal coronary artery occlusion. The severity of hypokinesia at follow-up study correlated with the magnitude of peak serum creatine kinase (r = -0.71), indicating that thrombolytic therapy initiated within 2 hours after the onset of symptoms improves regional left ventricular function and reduces infarct size more than later therapy does.

Influence of treatment modality on angiographic outcome after coronary stenting in diabetic patients: a controlled study.

OBJECTIVES: This retrospective study was designed to determine the six-month angiographic outcome after stenting of native coronary arteries in insulin-treated (ITDM) and non-ITDM patients with diabetes mellitus (DM) and compare the results with those in non-DM patients. BACKGROUND: The influence of the treatment modality for DM on restenosis in patients undergoing coronary artery stenting has not been elucidated sufficiently. METHODS: A total of 1,439 (70%) of 2,061 patients underwent repeated angiography within six months of coronary stenting. The ITDM and non-ITDM (oral hypoglycemic drugs or diet) were documented in 48 (3.3%) and 177 patients (12.3%), respectively, leaving 1,214 non-DM patients. RESULTS: Baseline reference vessel diameter tended to be smaller in ITDM patients (mean, 2.73 mm) than in non-DM and non-ITDM patients (2.88 mm and 2.85 mm, respectively). However, percent diameter stenosis was not different. The median number of stents deployed was 1; median stent length was 15 mm. Statistically significant differences were present after stenting for the means of minimal lumen diameter (MLD) and acute gain between ITDM patients (MLD: 2.67 mm, acute gain: 1.98 mm) and non-DM patients (MLD: 2.81 mm, acute gain: 2.16 mm). At follow-up, percent diameter stenosis, late lumen loss and loss index were significantly higher in both non-ITDM lesions (42%, 1.14 mm and 0.56, respectively) and ITDM lesions (48%, 1.26 mm and 0.65, respectively) than in non-DM lesions (35%, 0.96 mm and 0.45, respectively). The corresponding differences between non-ITDM and ITDM lesions did not reach statistical significance. Restenosis rates in non-DM, non-ITDM and ITDM lesions were 23.8%, 32.8% (p = 0.013 vs. non-DM) and 39.6% (p = 0.02 vs. non-DM, p = 0.477 vs. non-ITDM), respectively. CONCLUSIONS: This study showed that compared with stenting in non-DM patients, stenting of native coronary arteries in DM patients is associated with significantly increased lumen renarrowing, regardless of the treatment modality for DM.

Stenting of nonacute total coronary occlusions: predictors of late angiographic outcome.

OBJECTIVES: This study was designed to determine and assess factors predictive of the intermediate-term outcome of stenting of nonacute total coronary occlusions. BACKGROUND: Balloon angioplasty of recanalized coronary occlusions is associated with a combined restenosis/reocclusion rate of up to 65%. Adjunctive stenting holds the potential to reduce this rate significantly. However, variables affecting the late angiographic outcome of coronary stenting in the setting of a total occlusion have not been elucidated sufficiently. METHODS: Coronary stenting was performed in 143 consecutive patients with a nonacute total occlusion; 120 of these patients (84%), with a total of 121 occlusions, underwent repeat angiography within 6 months and comprised the study group. High pressure stent implantation aimed to cover the site of the occlusion as well as adjacent diameter stenoses > or = 70% and all possibly induced dissections. Pertinent angiographic and procedural variables obtained at the time of the intervention were entered into a multivariate logistic regression analysis model to assess their influence on the angiographic outcome at follow-up. RESULTS: Mean preinterventional reference lumen diameter for the 121 vessels was 2.99 +/- 0.53 mm (mean +/- SD); occlusion length ranged from 4 to 44 mm (median of 7.7). After balloon angioplasty, dissections were found in 80% of patients. Lesions were covered with stents a median of 16 mm in length (range 8 to 53). The minimal lumen diameter (MLD) achieved after stenting was 2.89 +/- 0.48 mm. After a median follow-up period of 4.5 months, mean MLD was assessed at 1.91 +/- 0.90 mm, corresponding to a loss index of 0.34 +/- 0.31. There were 27 vessels with a nonocclusive restenosis > or = 50% and 8 with a reocclusion, for a combined restenosis/reocclusion rate of 29%. Factors found to adversely influence angiographic outcome were a post-stenting MLD < or = 2.54 mm, a stented vessel segment length > 16 mm, a balloon/vessel diameter ratio for final stent expansion < or = 1.00 and the presence of a dissection after balloon angioplasty. CONCLUSIONS: Compared with previous reports on stand-alone balloon angioplasty, stenting of nonacute total coronary occlusions lowers the 6-month restenosis/reocclusion rate to approximately 30%. The late procedural outcome is independently and statistically significantly influenced by the MLD after stenting, the length of the stented vessel segment, the balloon/vessel diameter ratio for final stent expansion and the incidence of dissections after balloon angioplasty.

Clinical use of ultrashort-lived radionuclide krypton-81m for noninvasive analysis of right ventricular performance in normal subjects and patients with right ventricular dysfunction.

The ultrashort-lived radionuclide krypton-81m, eluted in 5% dextrose from a bedside rubidium-81m generator, was intravenously infused for rapid imaging of the right-sided heart chambers in the right anterior oblique projection adjusted for optimal right atrioventricular separation. Left-sided heart and lung background was minimized by rapid decay and efficient exhalation of krypton-81m, requiring no algorithm for background correction. A double region of interest method decreased the variability in the assessment of ejection fraction to 5%. In 10 normal subjects, 11 patients with pulmonary hypertension, 4 patients with right ventricular outflow tract obstruction and 4 patients with right ventricular infarction, right ventricular ejection fraction determined by krypton-81m equilibrium blood pool imaging ranged from 14 to 76%. The correlation between these values and those determined by cineangiography according to Simpson's rule was close: r = 0.93 for all data points (p less than 0.001), r = 0.92 for studies at rest (p less than 0.001) and r = 0.93 for exercise studies (p less than 0.001). Exercise-related changes in right ventricular function revealed a disturbed functional reserve with pulmonary hypertension and right ventricular infarction, whereas in compensated right ventricular outflow tract obstruction there was a physiologic increase in ejection fraction with exercise (p less than 0.001). Thus, equilibrium-gated right ventricular imaging using ultrashort-lived krypton-81m is a simple, accurate and reproducible method with potential for serial assessment of right ventricular ejection fraction in a variety of right ventricular anatomic and functional abnormalities, both at rest and during exercise. Advantages of this method include an extremely low radiation dose to patients and clear right atrioventricular separation without the need to correct for background activity.

Effects of streptokinase, urokinase, and recombinant tissue plasminogen activator on platelet aggregability and stability of platelet aggregates.

STUDY OBJECTIVE: The aim of the study was to evaluate the effects of streptokinase, urokinase and recombinant tissue plasminogen activator (TPA) on platelet aggregability and metabolism and the stability of preformed platelet aggregates. DESIGN: The experiments (n = 15 for each condition) were performed on citrated plasma or on platelet suspensions in phosphate buffered saline, both with a standardised platelet count of 250 x 10(9).litre-1. SUBJECTS: were healthy volunteers. MEASUREMENTS AND MAIN RESULTS: With both ADP (1 mumol.litre-1) and collagen (1 mg.litre-1) as aggregating agents, streptokinase at greater than or equal to 10(5) units.litre-1 led to reduction in the rate of platelet aggregation. With collagen and in most instances with ADP, this was associated with a decreased extent of aggregation, though in five out of 30 cases with ADP as aggregating agent, a conversion from reversible to irreversible aggregation occurred with streptokinase. Urokinase inhibited platelet aggregation at greater than or equal to 3 x 10(5) units.litre-1 with both aggregating agents. TPA inhibited aggregation at greater than or equal to 1 mg.litre-1 with ADP and at greater than or equal to 3.3 mg.litre-1 with collagen as aggregating agent. The inhibitory effect was still present when the platelets were suspended in saline. Platelet synthesis of thromboxane on stimulation with collagen, and of c-AMP on stimulation with prostaglandin E1, was markedly reduced by either agent. The stability of platelet aggregates, as assessed photometrically during a 90 min exposure to stirring stress, increased when streptokinase or urokinase was added to platelet rich plasma, but remained uninfluenced with TPA. CONCLUSIONS: Urokinase and TPA inhibited platelet aggregability uniformly and in a dose dependent manner. Streptokinase inhibited platelet aggregation in most instances, but led to a stimulation of aggregation in a minority of cases. These effects of the thrombolytic agents on platelets might have an influence on the occurrence of bleeding and of reocclusion after thrombolytic therapy.

Influence of the terminal complement-complex on reperfusion injury, no-reflow and arrhythmias: a comparison between C6-competent and C6-deficient rabbits.

OBJECTIVE: The complement system has been suggested to play a role in reperfusion injury which may result from an enhanced destruction of myocardial tissue or from an impairment of reflow. We investigated the influence of the C5b-9 complement complex on infarct size, reflow and arrhythmogenesis. METHODS: Twenty-eight C6-competent rabbits and 18 rabbits with congenital C6 deficiency were subjected to either 30 min or 2 h of coronary artery occlusion followed by reperfusion. C6 deficiency was confirmed by the complement titration test and immunohistology. The triphenyl tetrazolium chloride method was used to delineate infarct size. Reflow into infarcted areas was evaluated histologically after an in vivo injection of propidium iodide which served as an early fluorescence microscopic marker of damaged myocardium subjected to reflow. Continuous ECG monitoring allowed the recording of arrhythmias. RESULTS: After 30 min of coronary artery occlusion infarct size was significantly smaller in C6-deficient rabbits (5.0 +/- 2% of the risk region) as compared to C6-competent rabbits (28.4 +/- 8.5%, P = 0.0371). The extent of reflow into damaged myocardium was nearly the same in both animal groups at this time (38 +/- 9 vs. 39 +/- 7% of the risk region). After 2 h of coronary artery occlusion, infarct size was not different between both animal groups, but the extent of reflow into damaged myocardium was significantly smaller in C6-competent rabbits than in C6-deficient rabbits (25 +/- 4 vs. 40 +/- 4%; P = 0.0185). Two of the 18 C6-deficient rabbits had ventricular arrhythmias (Lown II-IV), none of which was fatal. Eleven of the 28 C6-competent animals had major ventricular arrhythmias which were fatal in 6 rabbits. CONCLUSIONS: These results suggest that the lytic C5b-9 complement complex leads to reperfusion injury in the early phase (30 min) of ischaemia, resulting in a larger infarct. After 2 h of ischaemia, complement activation enhances the no-reflow phenomenon but does not affect infarct size. Finally, the C6 status seems to influence the susceptibility to ventricular arrhythmias after coronary artery occlusion, independent of reperfusion.

Coronary thrombolysis with intravenous urokinase in patients with acute myocardial infarction.

Regional left ventricular wall motion, about two to three weeks after acute myocardial infarction (MI), is perhaps the best clinical measure of myocardial salvage and limitation of infarct size by thrombolytic therapy. Normal or only slightly depressed wall motion at the site of infarction indicates significant limitation of infarct size, whereas markedly abnormal wall motion indicates irreversible myocardial damage. Early studies found significant improvement in regional wall motion in only 40 percent of patients undergoing successful intracoronary thrombolytic therapy after the onset of symptoms of acute MI. Why only 40 percent of these reperfused patients demonstrated salvage of ischemic myocardium could not be answered at that time. Animal experiments show that the duration of coronary occlusion is an important factor in determining myocardial salvage after reperfusion. To study whether this time dependency also exists under clinical circumstances in patients with coronary artery disease, the relationship between regional wall motion (as an index of infarct size) and the time to thrombolytic therapy after the onset of symptoms (as an index of duration of coronary occlusion) was examined. After showing that such time dependency does indeed exist in patients with acute MI, the efficacy and safety of intravenous bolus injections of urokinase were then demonstrated.

Left ventricular hemodynamics and function in acute myocardial infarction: studies during the acute phase, convalescence and late recovery.

The left ventricular hemodynamics of 70 patients with acute myocardial infarction were determined from measurements of pulmonary arterial end-diastolic pressure, cardiac index, mean arterial pressure and heart rate during the acute phase(first study, 5 hours after admission), 4 to 6 weeks later (second study, during convalescence) and in 35 percent of all subjects 6 to 12 months after the acute infarction (third study). Serial analysis of serum creatine kinase was carried out during the acute phase. The peak CK value normalized for body surface area was used as a rough index of the extent of the acute myocardial necrosis. The condition of all survivors of the acute stage improved. Patients with only slightly reduced left ventricular performance during the acute stage recovered to nearly normal during convalescence. The condition of patients with greatly reduced left ventricular function also improved but remained impaired during convalescence. In all patients the main changes in left ventricular hemodynamics occurred within the first 4 to 6 weeks; there was almost no further alteration during the following 9 months.

Limitations in the interpretation of rest-exercise ejection fraction changes after early thrombolytic therapy during acute myocardial infarction.

The effect of exercise on left ventricular wall motion in the infarct and noninfarct regions, and their contribution to the global ejection fraction response to exercise was evaluated in 24 patients studied at least 2 weeks following thrombolytic therapy for acute myocardial infarction. To achieve this goal, a nonstandard protocol was used: contrast ventriculography was performed at rest and immediately following 3 minutes of supine bicycle exercise at 50 watts. Wall motion in the infarct and noninfarct regions was measured using the centerline method. The global ejection fraction response to exercise correlated poorly with the exercise response of motion in the infarct region (r = 0.38). In 15 of the 24 patients, the function of the infarct and noninfarct regions changed in opposing directions, and in only 8 (53%) of these did the global ejection fraction response follow the exercise response of motion in the infarct region. The motion of the noninfarct region was the predominant influence on the ejection fraction response in the other 7 patients. Subgroup analysis revealed that the global ejection fraction response was more dependent on the response of motion in the anterior wall (r = 0.71, p less than 0.001) than in the inferior wall (r = 0.16), regardless of infarct location. The regional wall motion response to exercise also better distinguished reperfused from nonreperfused patients than did the ejection fraction response. These results indicate that the global ejection fraction response to exercise may be an unreliable indicator of the functional status of the infarct region.(ABSTRACT TRUNCATED AT 250 WORDS)

Recanalization of chronic coronary artery occlusions using laser followed by balloon angioplasty.

Excimer laser angioplasty with adjunctive percutaneous transluminal coronary angioplasty of chronic coronary artery occlusions was performed using the Litvack 1.3 Z laser catheter in 80 patients in whom the occlusion could be passed by a guidewire; success rate was 89%. Angiographic follow-up revealed a restenosis rate of 33% and a reocclusion rate of 20%, and clinical follow-up showed a significant symptomatic improvement. It is concluded that laser angioplasty is a promising method for the treatment of chronic coronary artery occlusions.

Effect of interventions in salvaging left ventricular function in acute myocardial infarction: a study of intracoronary streptokinase.

The ability of intracoronary streptokinase (STK) infused early in acute myocardial infarction (MI) to salvage left ventricular (LV) function was studied in 52 patients who underwent contrast angiography immediately after STK and 6 +/- 7 weeks later. Ten nonrevascularized patients had no lysis or reocclusion. Of 42 patients with thrombolysis, 22 with optimal reperfusion underwent coronary artery bypass grafting (CABG) to prevent rethrombosis (STK + CABG group) and 20 did not (STK group). Motion was measured at 100 chords around the left ventricle and expressed in standard deviations (SD) from the normal mean. Hypokinesia was computed as the mean motion of chords in the infarct artery territory and hyperkinesia on the opposite wall was similarly computed. Hypokinesia improved greater than or equal to 1 SD/chord in 9 STK + CABG patients (41%), 8 STK patients (30%) (p = not significant versus STK + CABG) and 0 nonrevascularized patients. However, the ejection fraction did not change because it was normal in acute MI despite severe hypokinesia due to hyperkinesia on the opposite wall, and a subsequent decrease in hyperkinesia masked significant improvement in hypokinesia. It is concluded that regional wall motion must be measured to adequately assess the effect of therapeutic interventions on LV function. Early thrombolysis in acute MI results in improved LV function. The main benefit of CABG is to prevent rethrombosis.

Intravenous urokinase in acute myocardial infarction.

To achieve reperfusion early, an intravenous bolus of 2 million units of urokinase was administered in 50 patients with transmural acute myocardial infarction (AMI) 1.8 +/- 2.5 hours after the onset of symptoms. Coronary angiography performed 1.1 +/- 0.6 hours after urokinase therapy revealed patent coronary arteries in 30 patients (60%), with no significant difference between those with anterior and those with inferior AMI. Reocclusion occurred in only 1 of 24 patients restudied. Failure to achieve reperfusion was not related to the degree of systemic fibrinolytic activity, which was equally high in patients who did and those who did not achieve reperfusion, as evident from serially obtained fibrinogen measurements (77 +/- 52 vs 84 +/- 24 mg/dl, difference not significant). Plasmin activity, measured serially from 15 minutes to 24 hours after urokinase in 7 patients, was maximal at 15 minutes and undetectable after 3 hours. Wall motion at the infarct site measured from contrast ventriculograms was significantly better at follow-up only in patients in whom reperfusion was achieved and who received urokinase within 2 hours after the onset of symptoms as compared with patients in whom reperfusion was not achieved (-1.2 +/- 1.4 vs -2.4 +/- 0.9 standard deviations from normal, p less than 0.05). Peak serum creatine kinase level was significantly lower in patients in whom reperfusion was achieved than in those in whom it was not or those who had rethrombosis (802 +/- 763 vs 1,973 +/- 1,071 U/liter, p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Usefulness of recanalization to luminal diameter of 0.6 millimeter or more with intracoronary streptokinase during acute myocardial infarction in predicting "normal" perfusion status, continued arterial patency and survival at one year.

To determine whether arteriographic dimensions of the acutely recanalized coronary lumen provide information about regional perfusion or clinical outcome, quantitative arteriography was used to measure minimum luminal diameter achieved with intracoronary streptokinase administration in 44 patients with acute myocardial infarction (AMI). Degree of coronary reperfusion was independently assessed visually using the criteria applied in the multicenter Thrombolysis in Myocardial Infarction study. Minimum diameter and qualitative reperfusion grade were both assessed from 172 coronary injections during thrombolysis. Partial perfusion (grade 1 or 2) was seen in 95 of 135 injections (70%) in which the minimum diameter was less than 0.6 mm and complete perfusion (grade 3) was seen in 35 of 37 injections (95%) in which it was 0.6 mm or more (p less than 0.001). Repeat cardiac catheterization was performed at 5.5 +/- 4.9 weeks after AMI (n = 20). When vessels were opened acutely to a minimum diameter of less than 0.6 mm, 5 of 12 vessels (42%) were reoccluded at the time of restudy and 8 of 29 patients (28%) died within 12 months. By contrast, 0 of 8 vessels (0%) were reoccluded when the artery was opened to a diameter of at least 0.6 mm (difference not significant), and only 1 of 15 patients (7%) died (p less than 0.05). Of the patients with grade 1 o r 2 perfusion at the end of the thrombolytic infusion, 7 of 19 (37%) died within 12 months and 2 of 4 vessels (50%) reoccluded; of the patients with grade 3 perfusion, 2 of 25 (8%) died (p less than 0.05) and 2 of 16 vessels (13%) reoccluded (difference not significant).(ABSTRACT TRUNCATED AT 250 WORDS)

Improved survival up to four years after early coronary thrombolysis.

The long-term prognosis after thrombolytic therapy in patients with acute myocardial infarction (AMI) is unknown. This question was investigated in a 4-year follow-up study of 227 patients. According to the status of reperfusion at the end of the acute catheterization, the patients were divided into a patent (n = 171) and an occluded (n = 56) group. Both hospital and 4-year mortality rates were significantly reduced in the patent group by 13 and 14%, respectively (p less than or equal to 0.005 for both). Baseline variables known to be important for prognosis did not differ between the 2 groups. Patients with a patent infarct artery who underwent early acute coronary artery bypass grafting (CABG) had a greater survival (p less than 0.10) and better left ventricular function (p less than 0.01) than did patients with a patent infarct artery who did not undergo CABG. This difference was associated with a lower frequency of fatal reinfarction and cardiogenic shock in the CABG group. Thus, survival is improved up to 4 years after successful thrombolysis and appears to be further enhanced by early CABG.

Recombinant single-chain urokinase-type plasminogen activator during acute myocardial infarction.

Recombinant single-chain urokinase-type plasminogen activator was intravenously administered in 2 different doses in 24 patients with acute myocardial infarction and angiographically proved occlusion of the infarct-related artery. Patients with first infarction without contraindications of thrombolysis were treated within the first 4 hours after the onset of symptoms. Group A (12 patients) received 20 mg of rscu-PA as a bolus followed by 60 mg infused over 1 hour and group B received 10 mg as a bolus and 30 mg as infusion. The 2 groups showed no significant difference in age, sex, height, weight, time between onset of symptoms and start of therapy, peak values and course of infarct-related enzymes. Time to reperfusion was 43 minutes in group A versus 67 minutes in group B (p less than 0.005). The rate of reperfusion 90 minutes after start of treatment was 91% in group A and 50% in group B (p less than 0.001). Plasma levels of fibrinogen, plasminogen and alpha-2-antiplasmin did not differ significantly in both groups. Systemic lytic state (fibrinogen less than 100 mg/dl) occurred in 33% of group A and in 9% of group B. Intravenous infusion of 80 mg (but not 40 mg) of rscu-PA led to reperfusion of the occluded coronary artery in nearly all patients. Approximately one-third of the patients treated with this dose demonstrated systemic lysis.

Prehospital thrombolysis in acute myocardial infarction.

The benefit and risk of prehospital thrombolysis for acute myocardial infarction (AMI) were evaluated in a double-blind randomized trial. Patients presenting less than 4 hours after symptom onset received 2 million units of urokinase as an intravenous bolus either before (group A, n = 40) or after (group B, n = 38) hospital admission. The mean time interval from onset of symptoms to thrombolytic therapy was 85 +/- 51 minutes in group A and 137 +/- 50 minutes in group B (p less than 0.0005). In 91% of the patients, thrombolytic therapy was administered less than 3 hours after symptom onset. Complication rates during the pre- and in-hospital period were low and did not differ between groups. Three patients died (1 in group A, 2 in group B) from reinfarction 7 to 14 days after admission. Left-sided cardiac catheterization before discharge revealed a patency rate in the infarct-related artery of 61% in group A and 67% in group B (difference not significant). Global left ventricular function and regional wall motion at the infarct site did not differ significantly between group A and B (ejection fraction 51 +/- 10%, n = 28 vs 53 +/- 14%, n = 28; wall motion -2.3 +/- 1.3 vs -2.2 +/- 1.1 standard deviation, respectively). Also, peak creatine kinase did not differ significantly (838 +/- 634 U/liter in group A vs 924 +/- 595 U/liter in group B). Prehospital thrombolysis using a bolus injection of urokinase has a low risk when performed by a trained physician with a mobile care unit. The saving of 45 minutes in the early stage of an acute infarction through prehospital thrombolysis did not appear to be important for salvage of myocardial function.