European Heart Journal (1990) 11 {Supplement F), 56-60
The role of intervention following thrombolysis for acute myocardial infarction W. S. HlLLIS
Department of Medicine and Therapeutics, University of Glasgow, Stobhill General Hospital, Glasgow, Scotland
Introduction
Address for correspondence: Dr W. S. Hilln, Department of Medicine and Therapeutics, University of Glasgow, Stobhill General Hospital, Glasgow G21 3VW. Scotland, U.K.
0195H568X/90/OF056 + 05 $03.00/0
The presence of severe residual stenosis stimulated early investigators to perform immediate coronary angioplasty. This was advocated to reduce residual stenosis and thus improve myocardial blood flow, with subsequent improvement in left ventricular function; this could also reduce the incidence of post-infarct angina and other complications of reocclusion and reinfarction. Serruys et al.{x] showed the feasibility of this approach and advanced the view that early intervention is mandatory to reduce the potential instability of the infarctrelated lesions. Early open studies confirmed that residual stenosis could be reduced in >75% of patients, and confirmed that rescue angioplasty by opening arteries which had not achieved reperfusion by thrombolysis alone could be performed'4-'1. Simoons et a/.'31 examined the effects on mortality of a concerted approach using an invasive strategy to obtain coronary artery reperfusion using intracoronary streptokinase then combining treatment of intravenous and intracoronary streptokinase with the addition of thrombus perforation and angioplasty where appropriate. A patent infarctrelated artery was achieved in 85% and mortality was lower in the intervention group at 28 days (16vs31) and at 8 months (23vs42). In addition, the clinical course in the hospital was more favourable following thrombolysis, reflecting improved left ventricular function. The relative beneficial effects of thrombolysis and angioplasty were not separated. In terms of the risk benefit ratio however, there was a much higher incidence of bleeding in the thrombolytic group (53 vs 7) and associated blood transfusion (48vs22). Hartzler et a/.'6' demonstrated that direct angioplasty in the absence of thrombolysis © 1990 The European Society of Cardiology
Downloaded from http://eurheartj.oxfordjournals.org/ by guest on June 6, 2016
Thrombolytic therapy now has an established role in the treatment of acute myocardial infarction in achieving coronary artery reperfusion, limiting myocardial infarct size and reducing mortality. Controversy remains concerning the role and timing of further interventions such as PTCA. When intracoronary infusion of thrombolytic agents was the route of choice, this allowed visualization of arterial morphology pre- and post-therapy. In addition, with clinical follow-up, serial observations stimulated the development of further pharmacological and interventional approaches to obtain coronary artery reperfusion and to prevent reocclusion. Arteriography confirmed that residual obstruction at the site of previous total coronary occlusion was common, lesions of >70% cross-sectional area being present in the majority, limiting blood flow to the previously totally ischaemic area, and thus influencing recovery of still viable myocardium1'1. Segmental wall motion showed most improvement when the arterial cross-sectional area was >0-4 mm121. Such lesions of >90% were shown to have a high likelihood of early or late reocclusion, with recurrent ischaemia or reinfarction occurring in 15-29% of subjects following intracoronary streptokinase'2'. Reocclusion appeared also to be predisposed by the presence of inadequate anticoagulation or loss of anticoagulant control. Ancillary non-specific therapies were added to intracoronary streptokinase, including intravenous nitrate, antiplatelet therapy, administration of calcium channel blockers as well as anticoagulation with heparin and warfarin'3'.
Angioplasty following intracoronary throrabolysis
The role of intervention might be successful in gaining reperfusion with a reduction in local and distant bleeding complications, and this group has confirmed the efficacy of this technique in large numbers of patients. Remodelling of residual stenosis following i.v. thrombolysis
stenosis decreased from 74 ± 14% to 56 ± 17% independent of the thrombolytic agent. Despite significant change by remodelling, a coronary stenosis of >50% persisted in 82% of patients 3 weeks post-infarct. Kasper et a/.1"1 studied, by angiography performed 4 weeks post-therapy, the remodelling phenomenon in patients treated with APSAC by bolus dose. Residual crosssectional area percentage stenosis was reduced from 85 ± 9 to 74 ± 2 5 % . Where angiographic evidence of residual thrombosis was present, there was a major increase in the cross-sectional area from 1-2 ±0-8 to 2-6 ±2-3 mm2. In five of 37 patients who had reocclusions, neither percentage area of stenosis or minimum cross-sectional area was a predictor of subsequent reocclusion. These observations of remodelling suggest that residual thrombus is dissolved secondary to endogenous thrombolytic activity. A reduction of the atherosclerotic lesion itself following rupture of the 'plaque' and extrusion of material may have occurred, or alternatively subintimal bleeding during the acute phase may be later reabsorbed. Despite remodelling, these studies confirmed that critical stenosis remained in many patients following intravenous thrombolysis, suggesting a continued need to examine the role of angioplasty following intravenous regimes. Angioplasty following intravenous thrombolysis Stack et al.l"] reported the results of immediate angioplasty following intravenous streptokinase (l-5xlO*U) in 216 patients. Persistent coronary perfusion at the end of the combined procedure was 90%, with a low in-hospital reocclusion rate (11%) and a significant improvement in ejection fraction and regional wall motion. This approach was complicated however by a high bleeding rate, with significant groin haematomata in 55% and a drop in haematocrit to
The role of intervention following thrombolysis for acute myocardial infarction W. S. HlLLIS
Department of Medicine and Therapeutics, University of Glasgow, Stobhill General Hospital, Glasgow, Scotland
Introduction
Address for correspondence: Dr W. S. Hilln, Department of Medicine and Therapeutics, University of Glasgow, Stobhill General Hospital, Glasgow G21 3VW. Scotland, U.K.
0195H568X/90/OF056 + 05 $03.00/0
The presence of severe residual stenosis stimulated early investigators to perform immediate coronary angioplasty. This was advocated to reduce residual stenosis and thus improve myocardial blood flow, with subsequent improvement in left ventricular function; this could also reduce the incidence of post-infarct angina and other complications of reocclusion and reinfarction. Serruys et al.{x] showed the feasibility of this approach and advanced the view that early intervention is mandatory to reduce the potential instability of the infarctrelated lesions. Early open studies confirmed that residual stenosis could be reduced in >75% of patients, and confirmed that rescue angioplasty by opening arteries which had not achieved reperfusion by thrombolysis alone could be performed'4-'1. Simoons et a/.'31 examined the effects on mortality of a concerted approach using an invasive strategy to obtain coronary artery reperfusion using intracoronary streptokinase then combining treatment of intravenous and intracoronary streptokinase with the addition of thrombus perforation and angioplasty where appropriate. A patent infarctrelated artery was achieved in 85% and mortality was lower in the intervention group at 28 days (16vs31) and at 8 months (23vs42). In addition, the clinical course in the hospital was more favourable following thrombolysis, reflecting improved left ventricular function. The relative beneficial effects of thrombolysis and angioplasty were not separated. In terms of the risk benefit ratio however, there was a much higher incidence of bleeding in the thrombolytic group (53 vs 7) and associated blood transfusion (48vs22). Hartzler et a/.'6' demonstrated that direct angioplasty in the absence of thrombolysis © 1990 The European Society of Cardiology
Downloaded from http://eurheartj.oxfordjournals.org/ by guest on June 6, 2016
Thrombolytic therapy now has an established role in the treatment of acute myocardial infarction in achieving coronary artery reperfusion, limiting myocardial infarct size and reducing mortality. Controversy remains concerning the role and timing of further interventions such as PTCA. When intracoronary infusion of thrombolytic agents was the route of choice, this allowed visualization of arterial morphology pre- and post-therapy. In addition, with clinical follow-up, serial observations stimulated the development of further pharmacological and interventional approaches to obtain coronary artery reperfusion and to prevent reocclusion. Arteriography confirmed that residual obstruction at the site of previous total coronary occlusion was common, lesions of >70% cross-sectional area being present in the majority, limiting blood flow to the previously totally ischaemic area, and thus influencing recovery of still viable myocardium1'1. Segmental wall motion showed most improvement when the arterial cross-sectional area was >0-4 mm121. Such lesions of >90% were shown to have a high likelihood of early or late reocclusion, with recurrent ischaemia or reinfarction occurring in 15-29% of subjects following intracoronary streptokinase'2'. Reocclusion appeared also to be predisposed by the presence of inadequate anticoagulation or loss of anticoagulant control. Ancillary non-specific therapies were added to intracoronary streptokinase, including intravenous nitrate, antiplatelet therapy, administration of calcium channel blockers as well as anticoagulation with heparin and warfarin'3'.
Angioplasty following intracoronary throrabolysis
The role of intervention might be successful in gaining reperfusion with a reduction in local and distant bleeding complications, and this group has confirmed the efficacy of this technique in large numbers of patients. Remodelling of residual stenosis following i.v. thrombolysis
stenosis decreased from 74 ± 14% to 56 ± 17% independent of the thrombolytic agent. Despite significant change by remodelling, a coronary stenosis of >50% persisted in 82% of patients 3 weeks post-infarct. Kasper et a/.1"1 studied, by angiography performed 4 weeks post-therapy, the remodelling phenomenon in patients treated with APSAC by bolus dose. Residual crosssectional area percentage stenosis was reduced from 85 ± 9 to 74 ± 2 5 % . Where angiographic evidence of residual thrombosis was present, there was a major increase in the cross-sectional area from 1-2 ±0-8 to 2-6 ±2-3 mm2. In five of 37 patients who had reocclusions, neither percentage area of stenosis or minimum cross-sectional area was a predictor of subsequent reocclusion. These observations of remodelling suggest that residual thrombus is dissolved secondary to endogenous thrombolytic activity. A reduction of the atherosclerotic lesion itself following rupture of the 'plaque' and extrusion of material may have occurred, or alternatively subintimal bleeding during the acute phase may be later reabsorbed. Despite remodelling, these studies confirmed that critical stenosis remained in many patients following intravenous thrombolysis, suggesting a continued need to examine the role of angioplasty following intravenous regimes. Angioplasty following intravenous thrombolysis Stack et al.l"] reported the results of immediate angioplasty following intravenous streptokinase (l-5xlO*U) in 216 patients. Persistent coronary perfusion at the end of the combined procedure was 90%, with a low in-hospital reocclusion rate (11%) and a significant improvement in ejection fraction and regional wall motion. This approach was complicated however by a high bleeding rate, with significant groin haematomata in 55% and a drop in haematocrit to
