JACC Vol. 16, ND. 3 September 1990576-7
576
The present study. In vivo studies performed in our in 1987by Jain et al. (7) using pressure-v01 curves of data obtained during balloon inflation sugge that different mechanisms predominate in different coronary lesions. In what appears to be th reported in this issue of the Journal (8) have applied a cons rably simpler technique: the pressure-diameter relation. ith the use of the pressure gauge on , an on-line videode~sitometric a routine inflation de program and a balloon made of a m plastic, they determined that 1) most of luminaldiameter occurs at low inflation lesions that were the most easily distensible were also the most elastic. Commendably, the investigators were careful ;o differentiate elasticity from coronary artery spasm by administermg intracoronary nitroglycerin. These investigators chose to examine a relatively homogeneous group of patients. Twenty-four of their 27 patients had either unstable angina or a recent myocardial infarction, whereas only 3 presented with stable angina pectoris. In addition, the nature of the study required that pati s have a focal discrete lesion in a relatively larc:e(23 mm visual estimate) vessel. Despite the clinical homogeneity of their patients, there was a difference in the manner in which dilation occurred that relates to the morphology of the lesion. Lesions were classi ed with a well characterized schema previously published by these investigators (9). Eccentric irregular lesions showed more dilation at low pressures and more elasticity than did noneccentric irregular lesions. This observation is important in that it indicates that the mechanism of coronary angioplasty may be different for lesions having different anatomic and morphologic features. laboratory
NEAL S. KLEIMAN,
MD, FACC,
ALBERT E. RAIZNER,
MD, FACC,
ROBERT ROBERTS, MD, FACC Houston, Texas
ecbanismsof coronaryangioplasty. Thirteen years have elapsed since Grucntzig’soriginal “nonoperative dilatation” of a coronary artery stenosis and, although > 1 million such procedures have been performed, the mechanism by which angioplasty works is still unknown. We have long known that Gruentzig’sinitialtheory that angioplastysimply results in compaction of a soft plaque is incorrect, but we have been unable to define the relative roles of plaque compression (I), plaque fracture (2,3), medial splitting (3,4), distension of normal vessel wall (2) and release of a “splinting” mechanism by the plaque (5). We do know from pathologic studies that the luminal improvement seen on the angiogram does not reflect the true cross-sectional area of the successfully dilated vessel (6). Unfortunately, few of the many studies describing the advantages, limitations and outcomes of coronary angioplasty have been directed to the mechanism of this procedure. Such data will become particularly important as new modifications of the technique are developed. Attempts to provide insight into the mechanisms of angioplasty are limited by two fundamental problems: I) the heterogeneous spectrum of human atherosclerosis and the lack of an animal model to mimic it, and 2) the lack of a valid technique to visualize the luminal topography of a recently dilated artery in viva. In truth, the histologic appearance of coronary arteries after angioplasty represents the result rather than the mechanism of coronary lumen dilation. The actual mechanismof coronary angioplasty can be truly ascertained only by in viva studies in humans as they are undergoing the procedure.
*Editorials published in Journal of rirp Amerimn College of Curdio/ogy reflect the views of the authors and do not necessarily represent the views of JACC or the Ar.lerican College of Cardiology. From the Bayior College of Medicine and The Methodist Hospital. Houston, Texas. v Robert Roberts, MD. 7a!e Methodist Hospital. 6535 Fantin Street. MS F-905, Houston. Texas 77030. 01990 by
the
AmericanCollege of
Cardiology
Thus, this study provides subgroup
of patients
further insight into a key undergoing coronary angioplasty.
Pathologic studies have shown that such patients are likely to have recently disrupted plaques, frequently with adherent thrombus (10-12). These plaques may have different contents and different architecture from those of stable plaques. Perhaps the same property causing the vascular and, l~..e, the clinical instability that led to angioplasty of these lesions was responsible for both their easy distensibility and their greater elasticity. If this is so, then distension of the normal arterial wall opposite an eccentric atheroma is not the only plausible explanation for the phencmena reported by I-Ijemdahl-Monsen et al. (8). It would be a contribution to our rrnderstandingof both angioplasty and pathophysiology to know whether an even different pressure-diameter relation (that is, less distensibility and less elasticity) would be present in patients with a more chronic, stable variety of angina as well as in those undergoing angioplasty of more diffusely narrowed vessels. 0735-1097/90/$3.50
JACC Vol. 16, No. 3 September 1990576-7
ies er-
an
coronary arteries I. Gruentzig AR. Senning A. Siegenthaler WE. Nonoperative dilatation of coronary-artery stenosis. Percutaneous transluminal coronary angioplasty. N Engl J Med 1979:301:61-8.
2. Faxon DP. Weber VJ. Haudenschild C. Gottsman SB. McGovern
WA, cts of transluminal angioplasty in three experimental models of atherosclerosis. Arteriosclerosis 398X: 125-33. ler RK. Stertzer S, Fallon JT. Morphology of transluminal human beings. N Engl J Med 1981;305:382-5.
.3.
vo ~~travasc~la~ult
4. Steele PM. Chesebro JH. Stanson AW. et al. Balloon angioplasty: m&Hal history of the pathophysiological response to injury in a pi8 model. Circ Res 1985357: 105-12.
5.
Ultrasound e~a~n~natio~ of a highly elastic lesiort crffer angioplasty, for exam might allow determination
ock PC. Tbe mechanism of transluminal a terial stenoses that are most amenable to Practice of Coronary t’ngioplasty. New Yor 14.
6. Waller BF. Morphologic correlates of coronary angiographic patterns at the site of percutaneous transluminal coronary angioplasty. Clin Cardiol l988:t 1:817-23. Jain A. Demer LL. Raizner AE. Hartley CJ. Lewis JM, Roberts R. vivo assessment of vascular dilatation during percutaneous transluminal coronary angioplasty. Am J Cardiol 1987:60:988-92. Hjemdahl-Monsen CE. /,nbrose JA. Borrico S, et al. Angiographic patterns of balloon inflation during percutaneous transhuninal coronary angioplasty: role of pressure-diameter curves in studying distensibility and elasticity of the stenotic lesion and the mechanism of dilation. J Am Coil Cardiol 1990:16:569-75.
bad remained corn~~ete~yintact, tion had merely distended the n
Ambrose JA. Winters SL. Stern A, et at. Angiographic morphology and the pathogenesis of unstable angina pectoris. J Am Coll Cardiol 1985:5: 609-16. IQ. Falk E. Unstable angina with fatal outcome: dynamic coronary thrombosis leadine IO infarction sndlor sudden death. Circulation 1985;71:699708. -
balloon, as some lasers are today. The availability of simultaneous pressure and dimensional measurements would enable us to visualize the process by which various plaque components are translocated during balloon inflation, permit us more precise intraluminal measurements and allow us to detail the time course and anatomic changes of elastic recoil. Onepoint is clear: the paucity of in vivo human studies of the mechanism of angioplasty is lamentable. The information that could be gleaned from such investigations may have far-reaching consequences. For instance, it is possible that one could define those patients likely to have abrupt vessel closure or inadequate dilation while the procedure is being performed. It is even remotely possible that we could predict with greater accuracy those patients who are likely *o develop restenosis or to need subsequent dilation.
11. Davies MJ. Thomas AC. Plaque fissuring: the cause of acute myocardial infarction. sudden ischaemic death. and crescendo angina. Br Heart J 1985:53:363-73.
1’ Ri:hard;on 6.
PD. Davies MJ. Born GVR. Influence of plaque configumltion and stress distribution on fissuring of coronary atherosclerotic plaques. Lancet 1989:2:941-4.
13. Linnemeier TJ. Giebel RA. Rothbaum DA, et al. intravascular coronary ultrasound assessment post-elective percutaneous transluminal coronary angioplastt., tabstrt. J Am Coll Cardiol 1990;15(suppl A):106A. 14. Potkin BN. Bartorelli AL, Gessert JM, et al. Coronary artery imaging with intravascular high-frequency ultrasound. Circulation 1990;81:157585. 15. DeJesus S. Roseheld K. Losordo DW, et al. Three-dimensional reconstruction of vascular lumen from images recorded during percutaneous 2-D intravascular ultrasound tabstr). J Am Coll CtHdiOt 19YtJ:l5tsttppt AklO6A. 16. Pandian NG. Kreis A. Weintraub A. el al. Real-time intravasculal ultrasound imaging in humans. Am J Cardiol 1990;65:1392-6.
576
The present study. In vivo studies performed in our in 1987by Jain et al. (7) using pressure-v01 curves of data obtained during balloon inflation sugge that different mechanisms predominate in different coronary lesions. In what appears to be th reported in this issue of the Journal (8) have applied a cons rably simpler technique: the pressure-diameter relation. ith the use of the pressure gauge on , an on-line videode~sitometric a routine inflation de program and a balloon made of a m plastic, they determined that 1) most of luminaldiameter occurs at low inflation lesions that were the most easily distensible were also the most elastic. Commendably, the investigators were careful ;o differentiate elasticity from coronary artery spasm by administermg intracoronary nitroglycerin. These investigators chose to examine a relatively homogeneous group of patients. Twenty-four of their 27 patients had either unstable angina or a recent myocardial infarction, whereas only 3 presented with stable angina pectoris. In addition, the nature of the study required that pati s have a focal discrete lesion in a relatively larc:e(23 mm visual estimate) vessel. Despite the clinical homogeneity of their patients, there was a difference in the manner in which dilation occurred that relates to the morphology of the lesion. Lesions were classi ed with a well characterized schema previously published by these investigators (9). Eccentric irregular lesions showed more dilation at low pressures and more elasticity than did noneccentric irregular lesions. This observation is important in that it indicates that the mechanism of coronary angioplasty may be different for lesions having different anatomic and morphologic features. laboratory
NEAL S. KLEIMAN,
MD, FACC,
ALBERT E. RAIZNER,
MD, FACC,
ROBERT ROBERTS, MD, FACC Houston, Texas
ecbanismsof coronaryangioplasty. Thirteen years have elapsed since Grucntzig’soriginal “nonoperative dilatation” of a coronary artery stenosis and, although > 1 million such procedures have been performed, the mechanism by which angioplasty works is still unknown. We have long known that Gruentzig’sinitialtheory that angioplastysimply results in compaction of a soft plaque is incorrect, but we have been unable to define the relative roles of plaque compression (I), plaque fracture (2,3), medial splitting (3,4), distension of normal vessel wall (2) and release of a “splinting” mechanism by the plaque (5). We do know from pathologic studies that the luminal improvement seen on the angiogram does not reflect the true cross-sectional area of the successfully dilated vessel (6). Unfortunately, few of the many studies describing the advantages, limitations and outcomes of coronary angioplasty have been directed to the mechanism of this procedure. Such data will become particularly important as new modifications of the technique are developed. Attempts to provide insight into the mechanisms of angioplasty are limited by two fundamental problems: I) the heterogeneous spectrum of human atherosclerosis and the lack of an animal model to mimic it, and 2) the lack of a valid technique to visualize the luminal topography of a recently dilated artery in viva. In truth, the histologic appearance of coronary arteries after angioplasty represents the result rather than the mechanism of coronary lumen dilation. The actual mechanismof coronary angioplasty can be truly ascertained only by in viva studies in humans as they are undergoing the procedure.
*Editorials published in Journal of rirp Amerimn College of Curdio/ogy reflect the views of the authors and do not necessarily represent the views of JACC or the Ar.lerican College of Cardiology. From the Bayior College of Medicine and The Methodist Hospital. Houston, Texas. v Robert Roberts, MD. 7a!e Methodist Hospital. 6535 Fantin Street. MS F-905, Houston. Texas 77030. 01990 by
the
AmericanCollege of
Cardiology
Thus, this study provides subgroup
of patients
further insight into a key undergoing coronary angioplasty.
Pathologic studies have shown that such patients are likely to have recently disrupted plaques, frequently with adherent thrombus (10-12). These plaques may have different contents and different architecture from those of stable plaques. Perhaps the same property causing the vascular and, l~..e, the clinical instability that led to angioplasty of these lesions was responsible for both their easy distensibility and their greater elasticity. If this is so, then distension of the normal arterial wall opposite an eccentric atheroma is not the only plausible explanation for the phencmena reported by I-Ijemdahl-Monsen et al. (8). It would be a contribution to our rrnderstandingof both angioplasty and pathophysiology to know whether an even different pressure-diameter relation (that is, less distensibility and less elasticity) would be present in patients with a more chronic, stable variety of angina as well as in those undergoing angioplasty of more diffusely narrowed vessels. 0735-1097/90/$3.50
JACC Vol. 16, No. 3 September 1990576-7
ies er-
an
coronary arteries I. Gruentzig AR. Senning A. Siegenthaler WE. Nonoperative dilatation of coronary-artery stenosis. Percutaneous transluminal coronary angioplasty. N Engl J Med 1979:301:61-8.
2. Faxon DP. Weber VJ. Haudenschild C. Gottsman SB. McGovern
WA, cts of transluminal angioplasty in three experimental models of atherosclerosis. Arteriosclerosis 398X: 125-33. ler RK. Stertzer S, Fallon JT. Morphology of transluminal human beings. N Engl J Med 1981;305:382-5.
.3.
vo ~~travasc~la~ult
4. Steele PM. Chesebro JH. Stanson AW. et al. Balloon angioplasty: m&Hal history of the pathophysiological response to injury in a pi8 model. Circ Res 1985357: 105-12.
5.
Ultrasound e~a~n~natio~ of a highly elastic lesiort crffer angioplasty, for exam might allow determination
ock PC. Tbe mechanism of transluminal a terial stenoses that are most amenable to Practice of Coronary t’ngioplasty. New Yor 14.
6. Waller BF. Morphologic correlates of coronary angiographic patterns at the site of percutaneous transluminal coronary angioplasty. Clin Cardiol l988:t 1:817-23. Jain A. Demer LL. Raizner AE. Hartley CJ. Lewis JM, Roberts R. vivo assessment of vascular dilatation during percutaneous transluminal coronary angioplasty. Am J Cardiol 1987:60:988-92. Hjemdahl-Monsen CE. /,nbrose JA. Borrico S, et al. Angiographic patterns of balloon inflation during percutaneous transhuninal coronary angioplasty: role of pressure-diameter curves in studying distensibility and elasticity of the stenotic lesion and the mechanism of dilation. J Am Coil Cardiol 1990:16:569-75.
bad remained corn~~ete~yintact, tion had merely distended the n
Ambrose JA. Winters SL. Stern A, et at. Angiographic morphology and the pathogenesis of unstable angina pectoris. J Am Coll Cardiol 1985:5: 609-16. IQ. Falk E. Unstable angina with fatal outcome: dynamic coronary thrombosis leadine IO infarction sndlor sudden death. Circulation 1985;71:699708. -
balloon, as some lasers are today. The availability of simultaneous pressure and dimensional measurements would enable us to visualize the process by which various plaque components are translocated during balloon inflation, permit us more precise intraluminal measurements and allow us to detail the time course and anatomic changes of elastic recoil. Onepoint is clear: the paucity of in vivo human studies of the mechanism of angioplasty is lamentable. The information that could be gleaned from such investigations may have far-reaching consequences. For instance, it is possible that one could define those patients likely to have abrupt vessel closure or inadequate dilation while the procedure is being performed. It is even remotely possible that we could predict with greater accuracy those patients who are likely *o develop restenosis or to need subsequent dilation.
11. Davies MJ. Thomas AC. Plaque fissuring: the cause of acute myocardial infarction. sudden ischaemic death. and crescendo angina. Br Heart J 1985:53:363-73.
1’ Ri:hard;on 6.
PD. Davies MJ. Born GVR. Influence of plaque configumltion and stress distribution on fissuring of coronary atherosclerotic plaques. Lancet 1989:2:941-4.
13. Linnemeier TJ. Giebel RA. Rothbaum DA, et al. intravascular coronary ultrasound assessment post-elective percutaneous transluminal coronary angioplastt., tabstrt. J Am Coll Cardiol 1990;15(suppl A):106A. 14. Potkin BN. Bartorelli AL, Gessert JM, et al. Coronary artery imaging with intravascular high-frequency ultrasound. Circulation 1990;81:157585. 15. DeJesus S. Roseheld K. Losordo DW, et al. Three-dimensional reconstruction of vascular lumen from images recorded during percutaneous 2-D intravascular ultrasound tabstr). J Am Coll CtHdiOt 19YtJ:l5tsttppt AklO6A. 16. Pandian NG. Kreis A. Weintraub A. el al. Real-time intravasculal ultrasound imaging in humans. Am J Cardiol 1990;65:1392-6.
