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Is myocardial revascularisation for tight coronary stenoses always necessary?
Viewpoint
myocardial revascularisation for tight coronary stenoses always necessary? Is
Over the last 25 years, the rate of development of myocardial revascularisation procedures has been astounding. In particular, coronary angioplasty has increased from a few dozen cases in the late 1970s to several hundred thousand at present, representing a large increase in health expenditure. Without doubt, these procedures have contributed to improvements in the clinical status and well-being of many patients with coronary artery disease. However, such a tremendous growth-particularly when it is very often the same physician who performs the diagnostic angiogram, indicates, and does the revascularisation procedure, and judges its success-invites a reappraisal of the necessity and cost-effectiveness of myocardial revascularisation procedures. To conduct such a reappraisal, it is necessary critically to analyse the intuitive reasoning of a cardiologist who wants to treat a patient, in whom a tight coronary artery stenosis has been discovered, with angioplasty or surgery in order to correct or bypass the narrowing. This reasoning is based on two postulates: that a tight coronary artery stenosis is always dangerous; and that revascularisation procedures are always effective and safe. Is a tight coronary artery stenosis always dangerous? Several retrospective studies suggest that severe stenoses have a higher risk of occlusion. 1,2 Recently, a large prospective study with repeated coronary angiograms demonstrated that 30% of stenoses with more than a 60% reduction in intraluminal diameter on the first coronary angiogram were totally occluded after 5 years, compared with only 3% for stenoses of 60% or less.3 However, a totally occluded coronary artery is not in itself a clinically significant danger. In fact, the danger of an occluded coronary artery can be related either to an acute myocardial infarction and its associated risks, or to a long-term deleterious effect on left-ventricular function, which is likely to alter the long-term outcome. Indeed, although most acute myocardial infarctions are caused by acute thrombotic coronary occlusions,4it is less certain that these complete occlusions always develop at sites of previous tight stenoses. After thrombolysis in the acute stage of myocardial infarction, the residual stenosis documented by coronary angiography is often moderate.6 Moreover, the spontaneous occlusion of severely narrowed coronary arteries, such as those treated by coronary angioplasty, is more often than not well tolerated and usually does not provoke a myocardial infarction or a significant alteration in left-ventricular function. It is clear, therefore, that the occlusion of a tight stenosis is a less severe clinical event with a smaller effect on left ventricular function than that of a normal or only mildly narrowed artery.7 So, although an Service de Cardiologie A, Centre Hospitalier Universitaire, NancyBrabois, 54500 Vandoeuvre-lès-Nancy, France (Prof N Danchin MD)
224
myocardial infarction is nearly always caused by the occlusion of a coronary artery, all coronary occlusions do not cause myocardial infarctions. Even in the absence of myocardial infarction, longstanding, repeated episodes of myocardial ischaemia can lead to structural alterations of the myocardium with an increased amount of interstitial tissue and increased myocyte thickness both within and outside the ischaemic area.8 Nevertheless, these structural alterations seem to be of limited clinical significance because there is no detectable long-term modification of global left-ventricular function in patients with totally occluded coronary arteries without myocardial infarction, despite persistent evidence of signs or symptoms of exercise myocardial ischaemia.9 It seems likely, therefore, that the presence of a severe coronary stenosis promotes the development of collateral channels that prevent or limit the extent of myocardial infarction or ischaemia if acute coronary occlusion occurs.10-12 acute
acute
Are revascularisation procedures totally safe and effective? Although it is well documented that myocardial revascularisation reduces angina, its impact on life prolongation is less clear. Randomised studies have shown that coronary artery bypass grafting may prolong life in limited subsets of patients, such as those with left main stem stenosis or triple vessel coronary artery disease, particularly in cases of altered left-ventricular function or of involvement of the proximal left anterior descending coronary artery,13,14 However, these results were in younger patient populations with a low operative mortality, and cannot be directly extrapolated to the older patients referred for coronary surgery at present, or to centres where experience is less. Very limited data are available on the comparative efficacy of coronary angioplasty. In one randomised tria1,15 angioplasty reduced angina at 6 months and slightly increased exercise tolerance compared with medical therapy in patients with single vessel coronary artery disease," but more patients in the angioplasty group had a myocardial infarction, which was usually peri-procedural, confirming the definite operative risk of the procedure.16 In a recent comparison of coronary angioplasty and coronary artery bypass surgery,I7 the in-hospital mortality rate was 1-2% for coronary surgery and 0-8% for angioplasty, with 2-4% and 35% infarction rates, respectively. However, the outcome after 25 years was similar in the two groups, although coronary bypass grafting led to a lower risk of angina recurrence and fewer subsequent therapeutic interventions. In the long-term, coronary bypass grafting accelerates the progression of coronary artery disease in the proximal segments of the grafted vessels,18,19 while saphenous vein grafts progressively deteriorate ’21 which explains the pro-
gressive increase in annual mortality rates observed after 7 to 10 years in the randomised trials.21 Although improved long-term results are hoped for with internal mammary artery grafts, which have an excellent long-term patency rate,22 complete myocardial revascularisation with arterial grafts alone is often difficult to achieve. For coronary angioplasty, the restenosis rate in the months after the procedure remains high (30-40%) despite all attempts to find a restenosis-reducing medication.23 Furthermore, in previously employed patients, myocardial revascularisation procedures, despite their favourable effect on symptoms, do not improve work resumption, compared with medically treated patients. "1,2-1 As the number of revascularisation procedures increases, the absence of a direct correlation between the angiographic severity of a coronary artery stenosis and its risk needs to be emphasised. Myocardial revascularisation procedures are extremely helpful to alleviate symptoms and should, therefore, be used to treat patients rather than so-called "menacing" angiographic images.
References 1 Danchin N, Oswald T, Voiriot P, Juillière Y, Cherrier F. Significance of spontaneous obstruction of high degree coronary artery stenoses between diagnostic angiography and later percutaneous transluminal coronary angioplasty. Am J Cardiol 1989; 63: 660-62. 2 Moise A, Lespérance J, Théroux P, Tayemans Y, Goulet C, Bourassa MG. Clinical and angiographic predictors of new total coronary occlusion in coronary artery disease: analysis of 313 nonoperated patients. Am J Cardiol 1984; 54: 1176-81. 3 Bissett JK, Ngo WL, Wyeth RP, et al. Angiographic progression to total coronary occlusion in hyperlipidemic patients after acute myocardial infarction. Am J Cardiol 1990; 66: 1293-97. 4 DeWood MA, Spores J, Notske R, et al. Prevalence of total coronary occlusion during the early hours of transmural myocardial infarction.
N Engl J Med 1980; 303: 897-902. 5 Little WC, Constantinescu M, Applegate RJ, et al. Can coronary angiography predict the site of a subsequent myocardial infarction in patients with mild to moderate coronary artery disease? Circulation 1988; 78: 1157-66. 6 Cribier A, Saoudi N, Berland J, Letac B. Régression de la sténose coronaire résiduelle après recanalisation par fibrinolyse dans l’infarctus du myocarde: analyse quantitative de la coronarographie immédiatement après désobstruction, au 15è jour et au 3è mois de l’évolution. Arch Mal Coeur 1985; 78: 353-60. 7 Ambrose JA, Tannenbaum MA, Alexopoulos D, et al. Angiographic progression of coronary artery disease and the development of myocardial infarction. J Am Coll Cardiol 1988; 12: 56-62. 8 Hess OM, Schneider J, Nonogi H, et al. Myocardial structure in patients with exercise-induced ischemia. Circulation 1988; 77: 967-77. 9 Juillière Y, Marie PY, Danchin N, Karcher G, Bertrand A, Cherrier F. Evolution of myocardial ischemia and left ventricular function in
10
11
patients with angina pectoris without myocardial infarction and total occlusion of the left anterior descending coronary artery and collaterals from other coronary arteries. Am J Cardiol 1991; 68: 7-12. Rentrop KP, Thornton JC, Feit F, Van Buskirk M. Determinants and protective potential of coronary arterial collaterals as assessed by an angioplasty model. Am J Cardiol 1988; 61: 677-84. Epstein SE. Influence of stenosis severity on coronary collateral development and importance of collaterals in maintaining left ventricular function during acute coronary occlusion. Am J Cardiol 1988; 61: 866-68.
12
Juillière Y, Danchin N, Grentzinger A, et al. Role of previous angina pectoris and collateral flow to preserve left ventricular function in the presence or absence of myocardial infarction in isolated total occlusion of the left anterior descending coronary artery. Am J Cardiol 1990; 65:
277-81. 13 Alderman EL, Bourassa MG, Cohen LS, et al. Ten-year follow-up of survival and myocardial infarction in the randomized coronary artery surgery study. Circulation 1990; 82: 1629-46. 14 Varnauskas E, European Coronary Surgery Study Group. Twelve-year follow-up of survival in the randomized European Coronary Surgery Study. N Engl J Med 1988; 319: 332-37. 15 Parisi AF, Folland ED, Hartigan P. A comparison of angioplasty with medical therapy in the treatment of single-vessel coronary artery disease. N Engl J Med 1992; 326: 10-16. 16 Hartz AJ, Kuhn EM, Pryor DB, et al. Mortality after coronary angioplasty and coronary artery bypass surgery (the National Medicare experience). Am J Cardiol 1992; 70: 179-85. 17 RITA trial participants. Coronary angioplasty versus coronary artery bypass surgery: the Randomised Intervention Treatment of Angina (RITA) trial. Lancet 1993; 341: 573-80. 18 Kroncke GM, Kosolcharoen P, Clayman JA, Peduzzi PN, Detre K, Takaro T. Five-year changes in coronary arteries of medical and surgical patients of the Veterans Administration randomized study of bypass surgery. Circulation 1988; 78 (suppl I): I144-50. 19 Hwang MH, Meadows WR, Palac RT, et al. Progression of native coronary artery disease at 10 years: insights from a randomized study of medical versus surgical therapy for angina. J Am Coll Cardiol 1990; 16: 1066-70. 20 Campeau L, Enjalbert M, Lespérance J, Vaislic C, Grondin CM, Bourassa MG. Atherosclerosis and late closure of aortocoronary saphenous vein grafts: sequential angiographic studies at 2 weeks, 1 year, 5 to 7 years, and 10 to 12 years after surgery. Circulation 1983; 68
(suppl II): II1-7. Coronary Artery Bypass Surgery Cooperative Study Group. Eighteen-year follow-up in the Veterans Affairs Cooperative study of coronary artery bypass surgery for stable angina. Circulation 1992; 86:
21 The VA
121-30. 22 Grondin CM,
23
24
25
Campeau L, Lespérance J, Enjalbert M, Bourassa MG. Comparison of late changes in internal mammary and saphenous vein grafts in two consecutive series of patients 10 years after operation. Circulation 1984; 70 (suppl I): 1208-12. Hermans WRM, Rensing BJ, Strauss BH, Serruys PW. Prevention of restenosis after percutaneous transluminal coronary angioplasty: the search for a "magic bullet". Am Heart J 1991; 122: 171-87. Danchin N, Juillière Y, Selton-Suty C, et al. Return to work after percutaneous transluminal coronary angioplasty: a continuing problem. Eur Heart J 1989; 10 (suppl G): G54-57. Rogers WJ, Coggin J, Gersh BJ, et al. Ten-year follow-up of quality of life in patients randomized to receive medical therapy or coronary artery bypass graft surgery: the Coronary Artery Surgery Study (CASS). Circulation 1990; 82: 1647-58.
225
myocardial revascularisation for tight coronary stenoses always necessary? Is
Over the last 25 years, the rate of development of myocardial revascularisation procedures has been astounding. In particular, coronary angioplasty has increased from a few dozen cases in the late 1970s to several hundred thousand at present, representing a large increase in health expenditure. Without doubt, these procedures have contributed to improvements in the clinical status and well-being of many patients with coronary artery disease. However, such a tremendous growth-particularly when it is very often the same physician who performs the diagnostic angiogram, indicates, and does the revascularisation procedure, and judges its success-invites a reappraisal of the necessity and cost-effectiveness of myocardial revascularisation procedures. To conduct such a reappraisal, it is necessary critically to analyse the intuitive reasoning of a cardiologist who wants to treat a patient, in whom a tight coronary artery stenosis has been discovered, with angioplasty or surgery in order to correct or bypass the narrowing. This reasoning is based on two postulates: that a tight coronary artery stenosis is always dangerous; and that revascularisation procedures are always effective and safe. Is a tight coronary artery stenosis always dangerous? Several retrospective studies suggest that severe stenoses have a higher risk of occlusion. 1,2 Recently, a large prospective study with repeated coronary angiograms demonstrated that 30% of stenoses with more than a 60% reduction in intraluminal diameter on the first coronary angiogram were totally occluded after 5 years, compared with only 3% for stenoses of 60% or less.3 However, a totally occluded coronary artery is not in itself a clinically significant danger. In fact, the danger of an occluded coronary artery can be related either to an acute myocardial infarction and its associated risks, or to a long-term deleterious effect on left-ventricular function, which is likely to alter the long-term outcome. Indeed, although most acute myocardial infarctions are caused by acute thrombotic coronary occlusions,4it is less certain that these complete occlusions always develop at sites of previous tight stenoses. After thrombolysis in the acute stage of myocardial infarction, the residual stenosis documented by coronary angiography is often moderate.6 Moreover, the spontaneous occlusion of severely narrowed coronary arteries, such as those treated by coronary angioplasty, is more often than not well tolerated and usually does not provoke a myocardial infarction or a significant alteration in left-ventricular function. It is clear, therefore, that the occlusion of a tight stenosis is a less severe clinical event with a smaller effect on left ventricular function than that of a normal or only mildly narrowed artery.7 So, although an Service de Cardiologie A, Centre Hospitalier Universitaire, NancyBrabois, 54500 Vandoeuvre-lès-Nancy, France (Prof N Danchin MD)
224
myocardial infarction is nearly always caused by the occlusion of a coronary artery, all coronary occlusions do not cause myocardial infarctions. Even in the absence of myocardial infarction, longstanding, repeated episodes of myocardial ischaemia can lead to structural alterations of the myocardium with an increased amount of interstitial tissue and increased myocyte thickness both within and outside the ischaemic area.8 Nevertheless, these structural alterations seem to be of limited clinical significance because there is no detectable long-term modification of global left-ventricular function in patients with totally occluded coronary arteries without myocardial infarction, despite persistent evidence of signs or symptoms of exercise myocardial ischaemia.9 It seems likely, therefore, that the presence of a severe coronary stenosis promotes the development of collateral channels that prevent or limit the extent of myocardial infarction or ischaemia if acute coronary occlusion occurs.10-12 acute
acute
Are revascularisation procedures totally safe and effective? Although it is well documented that myocardial revascularisation reduces angina, its impact on life prolongation is less clear. Randomised studies have shown that coronary artery bypass grafting may prolong life in limited subsets of patients, such as those with left main stem stenosis or triple vessel coronary artery disease, particularly in cases of altered left-ventricular function or of involvement of the proximal left anterior descending coronary artery,13,14 However, these results were in younger patient populations with a low operative mortality, and cannot be directly extrapolated to the older patients referred for coronary surgery at present, or to centres where experience is less. Very limited data are available on the comparative efficacy of coronary angioplasty. In one randomised tria1,15 angioplasty reduced angina at 6 months and slightly increased exercise tolerance compared with medical therapy in patients with single vessel coronary artery disease," but more patients in the angioplasty group had a myocardial infarction, which was usually peri-procedural, confirming the definite operative risk of the procedure.16 In a recent comparison of coronary angioplasty and coronary artery bypass surgery,I7 the in-hospital mortality rate was 1-2% for coronary surgery and 0-8% for angioplasty, with 2-4% and 35% infarction rates, respectively. However, the outcome after 25 years was similar in the two groups, although coronary bypass grafting led to a lower risk of angina recurrence and fewer subsequent therapeutic interventions. In the long-term, coronary bypass grafting accelerates the progression of coronary artery disease in the proximal segments of the grafted vessels,18,19 while saphenous vein grafts progressively deteriorate ’21 which explains the pro-
gressive increase in annual mortality rates observed after 7 to 10 years in the randomised trials.21 Although improved long-term results are hoped for with internal mammary artery grafts, which have an excellent long-term patency rate,22 complete myocardial revascularisation with arterial grafts alone is often difficult to achieve. For coronary angioplasty, the restenosis rate in the months after the procedure remains high (30-40%) despite all attempts to find a restenosis-reducing medication.23 Furthermore, in previously employed patients, myocardial revascularisation procedures, despite their favourable effect on symptoms, do not improve work resumption, compared with medically treated patients. "1,2-1 As the number of revascularisation procedures increases, the absence of a direct correlation between the angiographic severity of a coronary artery stenosis and its risk needs to be emphasised. Myocardial revascularisation procedures are extremely helpful to alleviate symptoms and should, therefore, be used to treat patients rather than so-called "menacing" angiographic images.
References 1 Danchin N, Oswald T, Voiriot P, Juillière Y, Cherrier F. Significance of spontaneous obstruction of high degree coronary artery stenoses between diagnostic angiography and later percutaneous transluminal coronary angioplasty. Am J Cardiol 1989; 63: 660-62. 2 Moise A, Lespérance J, Théroux P, Tayemans Y, Goulet C, Bourassa MG. Clinical and angiographic predictors of new total coronary occlusion in coronary artery disease: analysis of 313 nonoperated patients. Am J Cardiol 1984; 54: 1176-81. 3 Bissett JK, Ngo WL, Wyeth RP, et al. Angiographic progression to total coronary occlusion in hyperlipidemic patients after acute myocardial infarction. Am J Cardiol 1990; 66: 1293-97. 4 DeWood MA, Spores J, Notske R, et al. Prevalence of total coronary occlusion during the early hours of transmural myocardial infarction.
N Engl J Med 1980; 303: 897-902. 5 Little WC, Constantinescu M, Applegate RJ, et al. Can coronary angiography predict the site of a subsequent myocardial infarction in patients with mild to moderate coronary artery disease? Circulation 1988; 78: 1157-66. 6 Cribier A, Saoudi N, Berland J, Letac B. Régression de la sténose coronaire résiduelle après recanalisation par fibrinolyse dans l’infarctus du myocarde: analyse quantitative de la coronarographie immédiatement après désobstruction, au 15è jour et au 3è mois de l’évolution. Arch Mal Coeur 1985; 78: 353-60. 7 Ambrose JA, Tannenbaum MA, Alexopoulos D, et al. Angiographic progression of coronary artery disease and the development of myocardial infarction. J Am Coll Cardiol 1988; 12: 56-62. 8 Hess OM, Schneider J, Nonogi H, et al. Myocardial structure in patients with exercise-induced ischemia. Circulation 1988; 77: 967-77. 9 Juillière Y, Marie PY, Danchin N, Karcher G, Bertrand A, Cherrier F. Evolution of myocardial ischemia and left ventricular function in
10
11
patients with angina pectoris without myocardial infarction and total occlusion of the left anterior descending coronary artery and collaterals from other coronary arteries. Am J Cardiol 1991; 68: 7-12. Rentrop KP, Thornton JC, Feit F, Van Buskirk M. Determinants and protective potential of coronary arterial collaterals as assessed by an angioplasty model. Am J Cardiol 1988; 61: 677-84. Epstein SE. Influence of stenosis severity on coronary collateral development and importance of collaterals in maintaining left ventricular function during acute coronary occlusion. Am J Cardiol 1988; 61: 866-68.
12
Juillière Y, Danchin N, Grentzinger A, et al. Role of previous angina pectoris and collateral flow to preserve left ventricular function in the presence or absence of myocardial infarction in isolated total occlusion of the left anterior descending coronary artery. Am J Cardiol 1990; 65:
277-81. 13 Alderman EL, Bourassa MG, Cohen LS, et al. Ten-year follow-up of survival and myocardial infarction in the randomized coronary artery surgery study. Circulation 1990; 82: 1629-46. 14 Varnauskas E, European Coronary Surgery Study Group. Twelve-year follow-up of survival in the randomized European Coronary Surgery Study. N Engl J Med 1988; 319: 332-37. 15 Parisi AF, Folland ED, Hartigan P. A comparison of angioplasty with medical therapy in the treatment of single-vessel coronary artery disease. N Engl J Med 1992; 326: 10-16. 16 Hartz AJ, Kuhn EM, Pryor DB, et al. Mortality after coronary angioplasty and coronary artery bypass surgery (the National Medicare experience). Am J Cardiol 1992; 70: 179-85. 17 RITA trial participants. Coronary angioplasty versus coronary artery bypass surgery: the Randomised Intervention Treatment of Angina (RITA) trial. Lancet 1993; 341: 573-80. 18 Kroncke GM, Kosolcharoen P, Clayman JA, Peduzzi PN, Detre K, Takaro T. Five-year changes in coronary arteries of medical and surgical patients of the Veterans Administration randomized study of bypass surgery. Circulation 1988; 78 (suppl I): I144-50. 19 Hwang MH, Meadows WR, Palac RT, et al. Progression of native coronary artery disease at 10 years: insights from a randomized study of medical versus surgical therapy for angina. J Am Coll Cardiol 1990; 16: 1066-70. 20 Campeau L, Enjalbert M, Lespérance J, Vaislic C, Grondin CM, Bourassa MG. Atherosclerosis and late closure of aortocoronary saphenous vein grafts: sequential angiographic studies at 2 weeks, 1 year, 5 to 7 years, and 10 to 12 years after surgery. Circulation 1983; 68
(suppl II): II1-7. Coronary Artery Bypass Surgery Cooperative Study Group. Eighteen-year follow-up in the Veterans Affairs Cooperative study of coronary artery bypass surgery for stable angina. Circulation 1992; 86:
21 The VA
121-30. 22 Grondin CM,
23
24
25
Campeau L, Lespérance J, Enjalbert M, Bourassa MG. Comparison of late changes in internal mammary and saphenous vein grafts in two consecutive series of patients 10 years after operation. Circulation 1984; 70 (suppl I): 1208-12. Hermans WRM, Rensing BJ, Strauss BH, Serruys PW. Prevention of restenosis after percutaneous transluminal coronary angioplasty: the search for a "magic bullet". Am Heart J 1991; 122: 171-87. Danchin N, Juillière Y, Selton-Suty C, et al. Return to work after percutaneous transluminal coronary angioplasty: a continuing problem. Eur Heart J 1989; 10 (suppl G): G54-57. Rogers WJ, Coggin J, Gersh BJ, et al. Ten-year follow-up of quality of life in patients randomized to receive medical therapy or coronary artery bypass graft surgery: the Coronary Artery Surgery Study (CASS). Circulation 1990; 82: 1647-58.
225