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PubMed1991

Thrombolytic therapy: then and now.

Although thrombolytic agents were discovered nearly 60 years ago, it is only within the past decade that the clinical use of these agents has revolutionized the treatment of acute myocardial infarction. There are four currently available agents approved for use in treatment of myocardial infarction: streptokinase, urokinase, tissue plasminogen activator, and anistreplase. Although each of these agents works in a unique fashion, the common end point of therapy is the dissolution of a fibrin clot by the conversion of plasminogen to plasmin. A number of clinically measurable end points have been used to determine the effectiveness of these agents in the treatment of acute myocardial infarction, including mortality, reperfusion, patency, left ventricular function, left ventricular volumes, and quantitative creatine kinase isoenzyme analysis. Secondary end points have included bleeding and stroke, as well as recurrent ischemic events. Numerous clinical studies have demonstrated the effectiveness of all of these agents in achieving the desired end points and comparative studies, including several large-scale trials, have failed to differentiate among these agents with regard to efficacy. Newer dosing regimens for currently available thrombolytic agents, as well as new thrombolytic agents, are currently under active investigation and will be the subject of intense research over the next few years. Despite the lack of consensus as to which agent is superior, it is clear that thrombolytic therapy for acute myocardial infarction is the treatment of choice.

Angioplasty, Balloon, Coronary↗
PubMed1991

Thrombolytic therapy within one hour of the onset of acute myocardial infarction.

Between 1986 and 1988, 239 consecutive patients with acute myocardial infarction received thrombolytic therapy up to 285 minutes after onset of symptoms; in 39 (17 with anterior infarction, 21 inferior, one lateral infarction) recombinant tissue plasminogen activator or anistreplase was administered a mean of 51 minutes (range 20-60 minutes) after the onset of symptoms. The patency rates (26 of 30; 87 per cent), rapid ST segment resolution (36 of 38; 95 per cent) and QRS score of less than or equal to 3 (28 of 38; 74 per cent) were statistically significantly higher for those seen and treated in the first hour in comparison with those seen and treated later. For those treated within the first hour mean peak creatine kinase was 1264 U/l for those with TIMI grade 2 or 3 (partial or complete perfusion) compared with 3005 U/l for those with TIMI grade 0 or 1 (no perfusion or penetration without perfusion) (p = 0.02): mean peak creatine kinase-MB for those with TIMI grade 2 or 3 perfusion was 115 U/l compared with 312 U/l for those with TIMI grade 0 or 1 (p = 0.01). Four of the 39 patients developed ventricular fibrillation following thrombolytic therapy, three within 24 hours of infarction and one following reinfarction on day 15. There were no significant bleeding complications. One patient died. Thrombolytic therapy within 1 hour of the onset of symptoms led to a very high angiographic patency rate, rapid ST segment resolution with preservation of left ventricular function. This therapy is without significant complications.

Anistreplase↗
PubMed1990

[Effect of thrombolytic agents on infarct size and left ventricle systolic function in myocardial infarction].

The early intravenous administration of thrombolytic agents in the acute phase of myocardial infarction induces reperfusion of the artery responsible for the necrosis, thereby limiting the size of the infarct and preserving the left ventricular systolic function with consequent reduction of short- or long-term mortality. With the exception of urokinase, these effects have been demonstrated with all thrombolytic agents used so far, including streptokinase, plasminogen tissue activator and anistreplase. Owing to its special pharmacokinetic properties, the latest thrombolytic agent, formerly known as APSAC (anisoylated plasminogen streptokinase activator complex), provides a high arterial reperfusion rate with a low percentage of reocclusion. As a result, the mean size of the infarct is reduced by 31 per cent (36% in the case of anterior infarct), and the left ventricular systolic function is highly significantly preserved.

Anistreplase↗
PubMed1989

[The new thrombolytic agents].

Among the new thrombolytic agents, two are or will be available in the near future: plasminogen tissue activator and antistreplase or anysoiled plasminogen-streptokinase activator complex (APSAC). The repermeabilization rate provided by these two thrombolytic agents administered intravenously, is practically identical, close to 70 p. cent, i.e. comparable to that obtained by intracoronary administration of streptokinase. The rate of secondary reobstruction is estimated near 17 p. cent for the tissue plasminogen activator and 10 p. cent for APSAC. Secondary reobstruction would be more frequently observed with thrombolytics with a short half-life (5 to 8 minutes of the tissue plasminogen activator whether it has one or two chains, versus 90 minutes with APSAC). Other factors influence it: persistence of a thrombogenic stimulus at the site of the stenosis, presence of thrombin, platelet activation... Both products have been found to be effective in limiting the size of the myocardial infarction and preservation of the left ventricular function. Finally, both have been shown to be effective on the reduction of the immediate and long-term mortality during extensive multicentric trials. The tissue plasminogen activator, although specific for fibrin, results in haemorrhagic complications which are as frequent as those cause by anistreplase which does not present this specificity for fibrin. The fibrin of pathological thrombi and the fibrin of the haemostatic centrifugate are identical. It is therefore lysed in the same fashion by all thrombolytic agents, whether or not specific of fibrin.

Anistreplase↗
PubMed1992

Advances in thrombolytic therapy.

Alteplase and saruplase are more fibrin-specific thrombolytic drugs than anistreplase. These and the thrombolytic drugs of the first generation (streptokinase and urokinase) have shortcomings and limitations. The prolonged intravenous maintenance infusions have been replaced by a bolus injection, accelerated infusions, or the combined intravenous administration of thrombolytic agents. Numerous truncated alteplase or saruplase molecules have been constructed by deletion and domain substitution or hybrids made of the two molecules without gaining in thrombolytic potency. Recombinant staphylokinase and plasminogen activator from bat saliva have some interesting properties and are being investigated. Thrombus-targeted thrombolytic drugs were constructed using monoclonal antibodies against fibrin fragments or against epitopes of activated platelets. Fibrin-specific thrombolytic drugs require the concomitant use of a potent antithrombotic drug to prevent reocclusion. Whether hirudin or synthetic thrombin inhibitors are superior to heparin and whether novel antiplatelet agents, including monoclonal antibodies to platelet receptors and disintegrins, are more effective than aspirin is under clinical investigation. The place of stable analogues of prostacyclin during thrombolytic treatment is still unsettled.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Thrombolytic Therapy for Acute Myocardial Infarction in Patients with Prior Coronary Bypass Surgery: Results from the Thrombolysis in Myocardial Infarction (TIMI) 4 Trial.

Little data exist on the value of intravenous thrombolysis for acute myocardial infarction in patients with previous coronary bypass surgery. The Thrombolysis In Myocardial Infarction (TIMI) 4 trial was a randomized study comparing tissue plasminogen activator, anistreplase, or a combination in patients with evolving myocardial infarction; patients with previous coronary bypass surgery were not excluded. Coronary angiography was performed 90 minutes and 18-36 hours after randomization, a myocardial perfusion scan was performed at 18-36 hours and predischarge, and a radionuclide ventriculogram was obtained predischarge. Angiographic and clinical outcome variables were determined in patients with and without a history of coronary bypass surgery. A total of 416 patients were randomized and 13 of them had previous bypass surgery; of these, 6 had an occluded vein graft as the infarct-related vessel. The incidence of TIMI grade 3 flow at 90 minutes was lower in patients with previous coronary surgery as compared with controls (42% vs. 49%), and overall patency was significantly lower (50% vs. 77%, p = 0.04). This trend persisted at 18-36 hours after randomization. Furthermore, patients with previous coronary surgery had more thrombus in their infarct-related arteries, especially with occlusion of a vein graft (83% vs. 32%, p = 0.04) and higher rates of recurrent ischemia (15% vs. 8%) and recurrent infarction (23% vs. 5%, p = 0.03) than controls. Thus, in patients with previous coronary bypass surgery intravenous thrombolysis yields results that are inferior to those achieved in patients without such a history and alternative methods of reperfusion should be considered.

Journal Article↗
PubMed1997

[Prehospital thrombolytic therapy in acute myocardial infarction].

The extent of myocardial damage occurring during acute myocardial infarction is time dependent, and there is abundant evidence from most clinical trials that mortality reduction is greatest in patients treated early with thrombolytic agents, although beneficial effects have been shown with treatment initiated up to 12 h after onset of symptoms. All studies on prehospital thrombolysis have conclusively shown the practicability and safety of patient selection and administration of the thrombolytic agent. The accuracy of diagnosis in the prehospital setting was comparable to trials of in-hospital thrombolysis, e.g., in the Myocardial Infarction Triage and Intervention Project (MITI) 98% of the patients enrolled had subsequent evidence of acute myocardial infarction. With regard to time savings, all randomized studies showed positive results. The smallest time gain was observed in the MITI trial: prehospital-treated patients received thrombolytic therapy an average of 33 min earlier than those treated in hospital. In the European Myocardial Infarction Project (EMIP) the difference in time between prehospital and hospital treatment was a median of 55 min. However, none of these trials was able to show a significant short-term mortality difference between the two groups. Only a meta analysis of five randomized studies with a combined median time gain of about 60 min showed a significant 17% reduction in short-term mortality for patients who received thrombolytic therapy in the prehospital phase. In the Grampian Region Early Anistreplase Trial (GREAT), a study performed in a more rural area than other studies, the time gain by prehospital initiation of thrombolysis was a median of 130 min. GREAT was the only study to date reporting a significant mortality benefit for prehospital-treated patients after 3 months and 1 year. In conclusion, prehospital thrombolysis is feasible and safe. Patients with acute myocardial infarction can be correctly identified and treated with thrombolytic agents in the prehospital setting with the same rate of complications as expected for in-hospital thrombolysis, provided basic resuscitation equipment including a defibrillator is available. The results of randomized studies comparing the results of prehospital and in-hospital thrombolysis seem to justify the prehospital institution of thrombolytic therapy, especially in rural areas where transport times to the hospital are long and the expected time gain is largest. The choice of the thrombolytic agent seems to be of minor importance and should follow prehospital practicability (bolus injection) and costs. Aspirin should be given to all prehospital patients with suspected myocardial infarction regardless of thrombolytic therapy.

Acute Disease↗
PubMed1991

Overview of patency as an end point of thrombolytic therapy.

Underlying the use of thrombolytic therapy is the hypothesis that reestablishment and maintenance of coronary blood flow (coronary patency) are the primary mechanisms of therapeutic benefit in patients with acute myocardial infarction. Early achievement and maintenance of adequate coronary blood flow (patency) in the infarct-related artery are the primary goals of thrombolytic therapy. One third of patients may achieve spontaneous patency within a few days following acute myocardial infarction. When antithrombotic therapy (i.e., heparin) is administered, this rate increases to greater than 50%, but patency is achieved only gradually and mortality reductions comparable to thrombolytic therapy are not achieved. After administration of a thrombolytic agent, early (90-minute) patency rates are greater with alteplase or anistreplase than with streptokinase. However, patency rates for alteplase decline by 10-30% if intravenous heparin is not given concurrently. When patency is assessed greater than 24 hours following thrombolytic therapy, no significant difference exists among the agents. A single angiographic observation of the artery at 90 minutes, although useful, may be inadequate to distinguish among the beneficial clinical effects of different thrombolytic regimens. The overall reperfusion or patency profile is probably a better basis for assessing relative benefits. Intravenous thrombolytic regimens that are increasingly effective in rapidly achieving and maintaining coronary patency are now available and in further development.

Coronary Vessels↗
PubMed1991

Thrombolysis, anticoagulation, and reocclusion.

Based on apparent higher recanalization rates of the infarct-related artery, preferential use of thrombolytic agents with high clot specificity has been proposed for treating patients with acute myocardial infarction. In the Thrombolysis in Myocardial infarction (TIMI-I) and European Cooperative Group studies, higher reperfusion rates were observed with alteplase compared with streptokinase, causing many to assume that the former would achieve a greater reduction in early hospital mortality. However, the Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico (GISSI-2) and its associated International Study Group failed to show any differences in 15-day mortality between these agents in more than 20,000 patients. This apparent lack of correlation between reperfusion rates and early mortality may be explained in part when one considers that recanalization or patency rates measured at a given point in time, such as 90 minutes after onset of therapy, fail to define the subsequent vessel status. Early reocclusion is the major reason for this and is a major limitation to the clinical efficacy of thrombolytic drugs. Following recanalization, residual fibrin-bound thrombin adherent to the site of arterial injury from plaque rupture strongly promotes rethrombosis. Although antiplatelet and antithrombin agents such as aspirin and heparin help to decrease rethrombosis, these agents are far from ideal. Thrombolytic agents that produce a significantly prolonged systemic thrombolytic state, such as streptokinase and anistreplase, are likely to result in less rethrombosis. Therefore, a systemic fibrinolytic state would appear to be an advantage rather than a disadvantage, particularly because the incidence of intracerebral hemorrhage does not appear to be greater with their use compared with agents producing less systemic fibrinolysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Anticoagulants↗
PubMed1994

A pooled analysis of coronary arterial patency and left ventricular function after intravenous thrombolysis for acute myocardial infarction.

Individual studies of patency rates and left ventricular (LV) function after thrombolysis have generally been limited by small numbers of observations, wide confidence intervals, and limited numbers of time points. To obtain a more reliable estimate of patterns of patency and LV ejection fraction, a systemic overview of angiographic studies was performed after intravenous thrombolytic therapy. A total of 14,124 angiographic observations from 58 studies evaluating patency after no thrombolytic agent, streptokinase, standard dose tissue-type plasminogen activator (t-PA), accelerated dose t-PA, or anistreplase (anisoylated plasminogen streptokinase activator complex [APSAC]) were included. At 60 and 90 minutes, streptokinase had the lowest patency rates of 48% and 51%, respectively, standard dose t-PA and APSAC had similar intermediate rates of approximately 60% and 70%, and accelerated t-PA had the highest patency rates of 74% and 84%. By 2 to 3 hours and longer, the patency rates were similar for the various regimens. Reocclusion rates in studies including 1,172 patients randomized to t-PA versus a nonfibrin-specific agent were higher after t-PA (13.4% vs 8.0%, p = 0.002). Ten studies enrolling 4,088 patients treated with thrombolytic therapy versus control demonstrated a modest improvement in mean LV ejection fraction in the thrombolytic group at each of the times after thrombolytic therapy: hour 4, day 1, day 4, day 7 to 10, and day 10 to 28 after thrombolysis. By 4 days, mean ejection fraction was 53% versus 47% (thrombolytic vs control therapy, p < 0.01); by 10 to 28 days it was 54.1% and 51.5%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Disease↗
PubMed1995

How do smokers differ from nonsmokers in their response to thrombolysis? (the TIMI-4 trial)

Smokers with acute myocardial infarction appear to have a better outcome after thrombolysis than do nonsmokers. To identify factors that could contribute to this curious finding, we analyzed data from the Thrombolysis in Myocardial Infarction (TIMI-4) trial, in which 382 patients with acute myocardial infarction were randomized to tissue plasminogen activator, anistreplase, or both. Coronary angiography was performed 90 minutes and 18 to 36 hours after randomization, a myocardial perfusion scan was performed at 18 to 36 hours and before discharge, and a radionuclide ventriculogram was obtained before discharge. Angiographic and clinical outcome variables were determined in current smokers, ex-smokers, and nonsmokers, and regression analysis was used to correct for differences in baseline characteristics. The in-hospital mortality of current smokers was lower than that of ex-smokers and nonsmokers: 2.3% versus 5.2% versus 7.0%, respectively (p = 0.04 by paired comparison, current vs nonsmokers). Ninety minutes after randomization, the incidence of TIMI grade 3 flow was significantly higher in smokers than in ex-smokers and nonsmokers (55% vs 43% and 45%, p = 0.02); this difference was no longer observed at the second angiogram, nor did smokers differ from nonsmokers with respect to residual stenosis, thrombus grade, infarct size, ejection fraction, or recurrent ischemia. Because a strong inverse relation exists between TIMI grade 3 flow at 90 minutes and mortality, our findings suggest that the lower mortality of current smokers after thrombolytic therapy may be related to a higher incidence of early, complete reperfusion.

Double-Blind Method↗
PubMed1996

Liver rupture after cardiopulmonary resuscitation in a patient receiving thrombolytic therapy.

A patient with an acute myocardial infarction had to be resuscitated due to recurring ventricular fibrillation. After stabilisation, she received thrombolytic treatment with anistreplase. Fourteen hours later, clinical signs of hemoperitoneum developed and the diagnosis of liver rupture was made. After abdominal surgery and coronary revascularisation, the subsequent clinical course was uncomplicated. The literature on liver trauma after CPR as well as thrombolysis in association with CPR is reviewed. This observation suggests that there are no convincing arguments to withhold thrombolytic therapy in acute myocardial infarction after CPR in the absence of gross trauma. We stress that a high degree of clinical alertness is necessary to diagnose this life-threatening condition because of its frequent subacute evolution in patients that are per se hemodynamically unstable.

Adult↗
PubMed1995

Thrombin generation and activity during thrombolysis and concomitant heparin therapy in patients with acute myocardial infarction.

OBJECTIVES: This prospective study investigated the behavior of thrombin generation and activity during thrombolysis and concomitant heparin administration. BACKGROUND: It has been shown that during thrombolytic therapy there is an increase in thrombin generation and activity. Increased thrombin activity is suppressed by concomitant intravenous heparin, but it is unknown whether thrombin generation is also affected. METHODS: Thrombin generation was assessed by measuring prothrombin fragment 1 + 2 and thrombin-antithrombin complex plasma levels and thrombin activity by measuring fibrinopeptide A plasma levels. Serial blood samples were obtained before and at 90 min and 24 and 48 h after the administration of streptokinase (15 patients), recombinant tissue-type plasminogen activator (15 patients) or anistreplase (13 patients). An intravenous bolus of heparin (5,000 IU) was administered before the start of thrombolytic therapy, followed by an infusion of 1,000 U/h to maintain an activated partial thromboplastin time > 1.5 times baseline. RESULTS: During thrombolytic and concomitant heparin therapy, there was an increase in the plasma levels of prothrombin fragment 1 + 2 (baseline 1.08 vs. 2.73 nmol/liter, p < 0.001) and thrombin-antithrombin complex (baseline 6.5 vs. 17.1 micrograms/ml, p < 0.01) at 90 min, whereas no change was observed in fibrinopeptide A at 90 min (baseline 2.8 vs. 3.0 nmol/liter, p = NS). CONCLUSIONS: During thrombolytic therapy with both fibrin-specific and non-fibrin-specific drugs, there is an increase in thrombin generation despite concomitant administration of intravenous heparin.

Aged↗
PubMed1993

Thrombolysis in acute lower limb ischaemia.

For the past three decades balloon embolectomy has been the treatment of choice for acute lower limb occlusion. However, although usually successful in emboli, results are often disappointing in thrombotic atherosclerotic vessels. Attempted dissolution of the clot is accordingly attractive, and has theoretically been possible since the introduction of streptokinase in 1933. This was initially used intravenously, with variable success rates, although intraarterial administration is currently the method of choice. Later thrombolytic drugs such as tissue plasminogen activator, urokinase and anistreplase have been introduced. Lysis time has also been increased by using pharmaco-mechanical methods of administration such as pulsed spray catheters, which could increase the usefulness of thrombolysis in patients with rapidly progressive neurological signs where currently surgical embolectomy would be advocated. Several newer drugs with theoretical advantages over older drugs such as single-chain urokinase-type plasminogen activator or K1K2PU are currently undergoing trials. The role of thrombolysis as an adjunct to surgical embolectomy is also promising, though again requires further trials. There is still no consensus as to which patients are best suited to thrombolysis, nor an optimum drug or method of administration. However, there seems no doubt that thrombolysis will be increasingly used in the management of peripheral limb ischaemia, though requiring a team approach between surgeons, radiologists and haematologists.

Acute Disease↗
PubMed1993

Repeat thrombolysis.

Since 20% of patients with myocardial infarction (MI) have had a previous infarction, and reinfarction within one year after infarction occurs in 9% of cases, it is important to clarify the role of repeat thrombolysis. After streptokinase (SK) administration, IgG antibodies rise to a peak at two weeks and slowly fall over the next 12 months, but 50% of patients still have antibody levels sufficient to neutralise a standard dose of SK up to four years after initial SK administration. On this evidence, SK or anistreplase should not be readministered, except perhaps in the first two to three days after initial treatment. The efficacy of tissue plasminogen activator (t-PA) and urokinase is not affected by prior treatment with SK.

Antibodies↗
PubMed1994

Attitudes of general practitioners to prehospital thrombolysis.

OBJECTIVE: To investigate reasons for general practitioners not giving thrombolytic treatment to eligible patients with acute myocardial infarction. DESIGN: Postal questionnaires were sent to 424 general practitioners. SUBJECTS: 97 general practitioners who had taken part in the Grampian region early anistreplase trial, 185 whose practices in Scotland were at least 24 km from a district general hospital, and 142 who had attended postgraduate conferences at which thrombolysis had been discussed; 87, 158, and 125 respectively responded. MAIN OUTCOME MEASURES: Answers to questions about readiness to use thrombolytic treatment. RESULTS: Response rate was 87% (370/424). Almost all respondents (350) were convinced of benefits of thrombolysis for acute myocardial infarction, and 277 were convinced that there were additional benefits from its administration in the community at first opportunity. Most doctors working 16 km or more from hospital thought that giving treatment at home would appreciably save time (200/274). Most doctors agreed that they could make time to give thrombolytic treatment (278), and would be willing to record an electrocardiogram (284), and would be able to interpret it (280). Sixty four respondents (17%) reported using thrombolytic treatment in previous year. Among non-users, 150 (49%) were unwilling to use thrombolytic treatment without further training. While many non-users (210 (69%)) were willing to use thrombolytic treatment without encouragement from Department of Health, 184 (60%) were unwilling to use it unless encouraged to do so by their local cardiologist. CONCLUSIONS: The need to become better informed about thrombolysis and lack of encouragement from local cardiologists were important factors preventing wider use of thrombolytic treatment in the community by general practitioners.

Attitude of Health Personnel↗
PubMed1994

Reduction in QT interval dispersion by successful thrombolytic therapy in acute myocardial infarction. TEAM-2 Study Investigators.

BACKGROUND: QT dispersion (QTd, equals maximal minus minimal QT interval) on a standard ECG has been shown to reflect regional variations in ventricular repolarization and is significantly greater in patients with than in those without arrhythmic events. METHODS AND RESULTS: To assess the effect of thrombolytic therapy on QTd, we studied 244 patients (196 men; mean age, 57 +/- 10 years) with acute myocardial infarction (AMI) who were treated with streptokinase (n = 115) or anistreplase (n = 129) at an average of 2.6 hours after symptom onset. Angiograms at 2.4 +/- 1 hours after thrombolytic therapy showed reperfusion (TIMI grade > or = 2) in 75% of patients. QT was measured in 10 +/- 2 leads at 9 +/- 5 days after AMI by using a computerized analysis program interfaced with a digitizer. QTd, QRSd, JT (QT minus QRS), and JT dispersion (JTd, equals maximal minus minimal JT interval) were calculated with a computer. There were significant differences in QTd (96 +/- 31, 88 +/- 25, 60 +/- 22, and 52 +/- 19 milliseconds; P < or = .0001) and in JTd (97 +/- 32, 88 +/- 31, 63 +/- 23, and 58 +/- 21 milliseconds; P = .0001) but not in QRSd (25 +/- 10, 22 +/- 7, 28 +/- 9, and 24 +/- 9 milliseconds; P = .24) among perfusion grades 0, 1, 2, and 3, respectively. Similar results were obtained comparing TIMI grades 0/1 with 2/3 and 0/1/2 with 3. Patients with left anterior descending (versus right and left circumflex) coronary artery occlusion showed significantly greater QTd (70 +/- 29 versus 59 +/- 27 milliseconds, P = .003) and JTd (74 +/- 30 versus 63 +/- 27 milliseconds, P = .004). Similarly, patients with anterior (versus inferior/lateral) AMI showed significantly greater QTd (69 +/- 30 versus 59 +/- 27 milliseconds, P = .006) and JTd (73 +/- 30 versus 63 +/- 27 milliseconds, P = .007). Results did not change when Bazett's QTc or JTc was substituted for QT or JT or when ANOVA included adjustments for age, sex, drug assignment, infarct site, infarct vessel, and number of measurable leads. On ANCOVA, the relation of QTd or JTd and perfusion grade was not influenced by heart rate. CONCLUSIONS: Successful thrombolysis is associated with less QTd and JTd in post-AMI patients. The results are equally significant when either QT or JT is used for analysis. These data support the hypothesis that QTd after AMI depends on reperfusion status as well as infarct site and size. Reduction in QTd and its corresponding risk of ventricular arrhythmia may be mechanisms of benefit of thrombolytic therapy.

Adult↗