- Email: [email protected]
In vivo assessment by intravascular ultrasound of enlargement in saphenous vein bypass grafts
risk patients have an unexpecteddeath rate of OA%/year. The risk status of these patients was clearly defined at the onset of the study. This involved coronary angiography in 3 of the patients because we had previously found that coronary angiography defined the risk status and management options better than exercise electrocardiography in patients with angina.5Thereafter,the use of investigations was guided by change in the patient’s clinical status; the only test routinely performed was an annual electrocardiogram. Thus, the incidence of coronary angiography after enrollment in the study was 75 patients, and this resulted in revascularization in only 35. The low rate of unexpected death in patients in this study supports an approach to CAD based on clinical risk stratification and the use of angiography
to define risk and management options when there has been a change in symptoms suggestive of unstable or progressive angina or the occurrence of an acute myocardial infarction.‘j 1. Jelinek VM, Krafchek J, McDonald IG. Prognosis of cardiac disease in ambulant patients. Med JAW 1984;141:33+337. 2. Jelinek MV, Chow MO, Santamaria I. The low risk cardiac patient: an opportunity for cost containment. J Clin Epidemiol 1994,47:1013-1020. 3. Breslow N. A generalised Kmskal-Wallis test for comparing K samples subject to unequal patterns of censorship. Biometrika 1970;57:579-594. 4. Mantel N. Evaluation of survival data and two new rank order statistics arising in its consideration. Cancer Chemofher Repotis 1966;50: 163-170. 5. Jelinek MV, Becker NG, Ryan WF, Clemens A. Routine coronary angiography for effort angina. Med J Aust 1991;154:808-814. 6. Jelinek M. Routine coronary angiography after each major coronary event. In: Broustet J, cd. Proceedings of the Vth World Congress on Cardiac Rehabilitation. Andover, Hampshire, UK: Intercept Ltd., 1993:39-44.
In Vivo Assessment by Intravascular Ultrasound of Enlargement in Saphenous Vein Bypass Grafts Farrell 0. Mendelsohn, MD, Gary P. Foster, MD, lgor F. Palacios, MD, Arthur E. Weyman, MD, and Neil J. Weissman, MD
ocal compensatory enlargement has been described as a mechanismto maintain a luminal cross-sectional F area at a stenotic site in human femoral, carotid, and coronary arteries.lA Compensatoryenlargementmay be due to an increased shear stress caused by the atherosclerotic plaque in conjunction with endothelial-dependent factors7-lo or, alternatively, to medial attenuation with loss of underlying structural s~pport.‘~~~Although vascular remodeling in muscular arteries has been well described in both pathologic series1*4and in vivo intravascular ultrasound studies,2*3,5 the responseto progressive atherosclerosis in venous grafts is unknown. Atherosclerotic plaque may cause similar alterations of vascular flow and shear stressesin vein grafts and arteries. However, veins may lack the endothelial-mediated function required for remodeling. Likewise, the media of veins are structurally different from arteries and may not respond to plaque in an analogous fashion. Intravascular ultrasound is ideally suited to assesscompensatory vessel enlargement because of its ability to provide tomographic images of the vessel wall and its components. The purpose of this study was therefore to determine if compensatoryenlargement occurs in veins used as arterial conduits in vivo using intravascular ultrasound. ... Patients with reverse saphenousvein bypass grafts were selected from among those undergoing angiography for the evaluation of angina or a recent myocardial From the Cardiac Ultrasound and Catheterization laboratories, Cardiac Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts. Dr. Weissman’s current address is: Division of Cardiology, M42 18, Georgetown University Medical Center, 3800 Reservoir Road NW, Washington, D.C. 20007. Manuscript received May 30, 1995; revised manuscript received and accepted August 1.5, 1995.
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infarction. Patients were excluded if there was evidence of active ischemia, arrhythmia, or hemodynamic instability. Intravascular ultrasound was performed in each patient at the discretion of the interventional cardiologist for clinical evaluation of plaque extent, distribution, and morphology. Intravascular ultrasound was performed before vascular intervention using a variety of imaging catheters. A 4.3Fr (n = 4) or 2.9Fr (n = 5) ultrasound catheter with a 30 MHz transducer (Cardiovascular Imaging Systems, Sunnyvale, California) or a 4.8Fr 20 MHz (n = 6) or 3SFr 30 MHz (n = 4) ultrasound catheter (Boston Scientific, Watertown, Massachusetts)was used. Under fluoroscopic guidance, the ultrasound catheter was advanced over a O.Olbinch guidewire to a distal site in the saphenous vein graft. Continuous ultrasound imaging commencedas the catheter was slowly withdrawn until the transducer reached the guiding catheter at the aortoostial junction. Ultrasound images were recorded on 0.5-inch s-VHS videotape for further review. Intravascular ultrasound images were reviewed by 2 observers (FOM, NJW), and only images in which the intima, media,,and adventitia of arterialized vein grafts could be clearly identified were used for subsequent analysis. Luminal area was defined as the area enclosed by the leading edge of the luminal-intimal border, and vessel area as the area enclosed by the media-adventitial border. Vessel area minus luminal area constituted the effective plaque area.l2 All areaswere measuredby direct planimetry using a computer analysis system (Sony SUM 1010,Sony Medical Electronic, Park Ridge, New Jersey).Percentvessel area stenosiswas defined as plaque areadivided by vesselarea.3The site of increased plaque area with the smallest luminal area constituted the lesion segment. Because saphenous veins are reversed when implanted as arterial conduits, a site immeNOVEMBER
15,
1995
FIGURE 1. Intravascular ultrasound images of a saphenous vein raft at the site of a focal stenosis /A) and at an immediately adjacent reference site (Bj. Note that the vessel size is larger at tf e lesion sit6 than at the referen’ce site.
diately distal to the lesion segment (within 1 cm) with regardlessof whether a proximal or distal reference was ~50% vessel area stenosis was chosen as the reference. used for comparison. Lesion vessel area was larger than If the intravascular ultrasound catheter was unable to the reference vessel area in 23 of 24 lesions (95.8%) cross the lesion (n = S), a proximal reference was used (Figures 1 and 2). For the lesion segments,there was a for comparison. For each lesion and reference.segment, significant correlation between plaque and vessel areas the cross-sectional area of the vessel, lumen, and plaque (r = 0.83, p
-1
I
BRIEF REPORTS 1067
Saphenous vein grafts used as coronary arterial conduits undergo compensatory enlargementin a manner similar to . muscular arteries. There is a highly significant correlation between vessel area and plaque area (r = 0.83, p cO.OOl),with 95.8% of the stenotic sitesenlarging comparedwith their immediately adjacentreference segment. Compensatory enlargement maintains the luminal size when up to 30% of the vessel is occupied by plaque. These findings are consistent with the original observation of Glagov et al’ in a postmortem series of left main coronary arteries. Whether veins used as arterial conduits undergo compensatoryenlargement in responseto atherosclerotic plaque was previously unknown. Native saphenous 5 10 15 20 25 30 35 40 0 veins, while possessinga 3-layered strucPique area (mm2) ture (intima, media, and adventitia), have a histologic organization different from FWRE 3. lhe saphous vein vessd area is significady and posihdy rdakC arteries with only a rudimentary internal tathepkquearea. elastic lamina and no external elastic lamina.t3After insertion into the coronary circulation, saphenousvein grafts undergo 86 morphologic changes (“arterialization”) I rt0.32 , rr0.70 including intimal fibrous thickening, me=p=m : p30% of the vessel area occupied by plaque, there the cube of the luminal radius, small decreasesin the luwas an inverse relation with the lumen area.In this group men from increased plaque burden will produce a large (with >30% effective plaque area stenosis), the lumen increase in shear stresson the vessel walLi Arteries reareadecreasedas the percentageof vesselarea occupied spond to the altered shear stressby expanding to restore by plaque increased (r = 0.75, p cO.OOl).Similar to the normal luminal dimensions, thus normalizing the shear initial report of Glagov et al,’ this relation remained sig- stress.“* Since this responseis endothelium-dependent,9 nificant (p
l.-l::I
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may help our understanding of vascular remodeling and arterialization. Becausea growing proportion of patients presenting with acute ischemic syndromes have saphenous vein bypass grafts, the clinical implications of these findings cannot be overstated. As with coronary arteries, the degree of atherosclerotic plaque cannot be adequately assessedwith angiography. For example, compensatory enlargement may make a culprit lesion angiographically silent“ after successfulthrombolysis. In addition, segments adjacent to a stenotic lesion may not be adequate references because they underestimate vessel dimensions. Thus, sizing an interventional device to perform optimized transcatheter revascularization may be difficult without intravascular ultrasound. Furthermore, angiography may prove insensitive for a study on atherosclerotic plaque progression or regression in venous bypass grafts becauseof its inability to detect compensatory enlargement. These data demonstrate that saphenous vein grafts enlarge at sites of focal atherosclerosis and preserve luminal area for narrowing of ~30% of the cross-sectional vessel area. 1. Glagov S, Weisenerg E, Zarins CK, Stankunavicius R, Kolettis GJ. Compensatory enlargement of human atherosclerotic coronary arteries. N Engl J Med 1987:316:1371-1375.
Cardiac Rehabilitation Electrocardiographic Donald
2. Hermiller JB, Tenaglia AN, Kisslo KB, Phillips HR. Bashore TM, Stack RS, Davidson CJ. In viva validation of compensatory enlargement of atherosclerotic coronary arteries. Am J Cardiol 1993;71:665-668. 3. Losordo DW, Rosenfield K, Kaufman J, Piecmk A, lsner JM. Focal cotnpensatoty enlargement of human arteries in response to progressive atherosclerosis: in viva documentation using intravascular ultrasound. Circukzti~n 1994;89: 2570-2577. 4. Stiel GM, Stiel LSG, Schafer J, Donath K, Mathey DC. Impact of compensatory enlargement of atherosclerotic coronary arteries on angiographic assessment of coronary artery disease. Circulation 1989;80: 1603-1609. 5. McPherson DD, Sima SJ, Hiratzka LF, Thorpe L, Armstrong ML, Marcus ML, Kerber RE. Coronary arterial remodeling studied by high-frequency epicardial echocardiography: an early compensatory mechanism in patients with obstructive coronaly atherosclerosis. J Am Cull Cardiol 1991;17:7%86. 6. Beere PA, Glagov S, Zatins CK. Experimental atherosclerosis at the carotid bifurcation of the cynomologus monkey. Localization, compensatory enlargement, and the sparing effect of lowered heart rate. Arkkoscler Thrmnb 1992;12: 1245-1253. 7. Kamiya A, Togawa T. Adaptive regulation of wall shear stress to flow change in the canine carotid artery. Am J Physiol 1980;239:H14-H21. 8. Zarins CK, Zatina MA, Giddens DP, Ku DN, Glagov S. Shear stress regulation of artery lumen diameter in experimental atherogenesl5. J Vfw Surg 1987; 5:413420. 9. Langille BL, O’Donnell F. Reductions in atterial diameter produced by chronic decreases in blood flow are endothelium-dependent. Science 1986;23 1:405407. 10. Glagov S, Zarins C, Giddens DP, Ku DN. Hemodynamics and atherosclerosis: insights and perspectives gained from studies of human arteries. Arch P&al Lab Med 1988;112:1018-1031. 11. Crawford T, Levene Cl. Medial thinning in atheroma. J Pufhol 1953;66: 19-23. 12. Keren G, Douek P, Oblon C, Banner RF, Pichard AD, Leon MB. Atherosclerotic saphenous vein grafts treated with different interventional procedures assessed by intravascular ultrasound. Am Hem J 1992; 124: 198-206. 13. Spray TL, Roberts WC. Changes in saphrnous veins used as aonocoronary bypass grafts. Am Heart J 1977;94:50&5 16. 14. Isner JM, Donaldson RF, Fortin AH, Tischler A, Clarke RH. Attenuation of the media of coronary arteries in advanced atherosclerosis. Am J Cardiol 1986:58: 937-939. 15. MacIsaac AI, Thomas JD, Topel EJ. Toward the quiescent coronary plaque. J Am Coil Cardiol 1993;22:1228-1241.
Using Simultaneous Voice and l’runstelephonic Monitoring
K. Shaw, PhD, Kenneth E. Sparks, PhD, Henry S. Jennings III, MD, and Janice C. Vantrease, RN
n 1984,Fletcher,’ Miller,* and their co-workers found Itientstranstelephonic electrocardiographicmonitoring of pawith coronary artery disease who exercised at home to be both efficacious and safe. Subsequentstudies support these initial findings,3,4with the scope of investigations expanding to include compliance5 and reimbursement6issues. Research data reveal those particularly benefiting from transtelephonic exercise monitoring (TEM) are patients located in rural areas where community hospitals frequently lack resourcesto establish and maintain viable outpatient programs.7For these persons,TEM provides a workable compromisebetween exercising alone and lengthy travel to metropolitan hospital-based programs. More recently, the concept of tandem sites has developed.7Patients exercisein rural medical facilities rather than at home with TEM provided by metropolitan hospital personnel located miles away.The From the Saint Thomas Heart Institute, Saint Thomas Hospital, Nashville, Tennessee, and the Department of Ph sical Education, Cleveland State Universrty, Cleveland, Ohio. Dr. S t: aw’s address is: Cardiac Health and Rehabilitation, Saint Thomas Heart Institute, Saint Thomas Hospital, 4220 Harding Road, Nashville, Tennessee 37205. Manuscript received May 30, 1995, revrsed manuscript received and accepted August 8, 1995.
simultaneoustransmissionof voice and rhythm strip over the sametelephone line was not commercially available until 198S6Before this time, basestation operatorswere required to “toggle” between analog voice and digital electrocardiographic signals. This potentially presented an increased risk for patients and proved cumbersome to operators who received voice communication at the expense of heart rhythm and vice versa. Although the simultaneous transmission feature corrected this fault and improved product acceptance,the proliferation of this new technology has not been studied. This investigation examinesthe current statusof simultaneous voice and electrocardiographic TEM in hospital, home, and clinic settings. ... We polled all facilities (n = 32) with simultaneous voice and electrocardiographic TEM capability. Because simultaneous transmission technology is marketed by only 1 company (Scott&e Inc., Cleveland, Ohio), ScottCare’s assistancewas obtainedin providing a list of product owners, leasees,and program supervisors. Each site was then sent a packet containing a sample22-item questionnaire with accompanying letter of explanation. One month later, program supervisorswere contactedby teleBRIEF REPORTS
1069
to define risk and management options when there has been a change in symptoms suggestive of unstable or progressive angina or the occurrence of an acute myocardial infarction.‘j 1. Jelinek VM, Krafchek J, McDonald IG. Prognosis of cardiac disease in ambulant patients. Med JAW 1984;141:33+337. 2. Jelinek MV, Chow MO, Santamaria I. The low risk cardiac patient: an opportunity for cost containment. J Clin Epidemiol 1994,47:1013-1020. 3. Breslow N. A generalised Kmskal-Wallis test for comparing K samples subject to unequal patterns of censorship. Biometrika 1970;57:579-594. 4. Mantel N. Evaluation of survival data and two new rank order statistics arising in its consideration. Cancer Chemofher Repotis 1966;50: 163-170. 5. Jelinek MV, Becker NG, Ryan WF, Clemens A. Routine coronary angiography for effort angina. Med J Aust 1991;154:808-814. 6. Jelinek M. Routine coronary angiography after each major coronary event. In: Broustet J, cd. Proceedings of the Vth World Congress on Cardiac Rehabilitation. Andover, Hampshire, UK: Intercept Ltd., 1993:39-44.
In Vivo Assessment by Intravascular Ultrasound of Enlargement in Saphenous Vein Bypass Grafts Farrell 0. Mendelsohn, MD, Gary P. Foster, MD, lgor F. Palacios, MD, Arthur E. Weyman, MD, and Neil J. Weissman, MD
ocal compensatory enlargement has been described as a mechanismto maintain a luminal cross-sectional F area at a stenotic site in human femoral, carotid, and coronary arteries.lA Compensatoryenlargementmay be due to an increased shear stress caused by the atherosclerotic plaque in conjunction with endothelial-dependent factors7-lo or, alternatively, to medial attenuation with loss of underlying structural s~pport.‘~~~Although vascular remodeling in muscular arteries has been well described in both pathologic series1*4and in vivo intravascular ultrasound studies,2*3,5 the responseto progressive atherosclerosis in venous grafts is unknown. Atherosclerotic plaque may cause similar alterations of vascular flow and shear stressesin vein grafts and arteries. However, veins may lack the endothelial-mediated function required for remodeling. Likewise, the media of veins are structurally different from arteries and may not respond to plaque in an analogous fashion. Intravascular ultrasound is ideally suited to assesscompensatory vessel enlargement because of its ability to provide tomographic images of the vessel wall and its components. The purpose of this study was therefore to determine if compensatoryenlargement occurs in veins used as arterial conduits in vivo using intravascular ultrasound. ... Patients with reverse saphenousvein bypass grafts were selected from among those undergoing angiography for the evaluation of angina or a recent myocardial From the Cardiac Ultrasound and Catheterization laboratories, Cardiac Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts. Dr. Weissman’s current address is: Division of Cardiology, M42 18, Georgetown University Medical Center, 3800 Reservoir Road NW, Washington, D.C. 20007. Manuscript received May 30, 1995; revised manuscript received and accepted August 1.5, 1995.
1066
THE AMERICAN
JOURNAL
OF CARDIOLOGY@
VOL. 76
infarction. Patients were excluded if there was evidence of active ischemia, arrhythmia, or hemodynamic instability. Intravascular ultrasound was performed in each patient at the discretion of the interventional cardiologist for clinical evaluation of plaque extent, distribution, and morphology. Intravascular ultrasound was performed before vascular intervention using a variety of imaging catheters. A 4.3Fr (n = 4) or 2.9Fr (n = 5) ultrasound catheter with a 30 MHz transducer (Cardiovascular Imaging Systems, Sunnyvale, California) or a 4.8Fr 20 MHz (n = 6) or 3SFr 30 MHz (n = 4) ultrasound catheter (Boston Scientific, Watertown, Massachusetts)was used. Under fluoroscopic guidance, the ultrasound catheter was advanced over a O.Olbinch guidewire to a distal site in the saphenous vein graft. Continuous ultrasound imaging commencedas the catheter was slowly withdrawn until the transducer reached the guiding catheter at the aortoostial junction. Ultrasound images were recorded on 0.5-inch s-VHS videotape for further review. Intravascular ultrasound images were reviewed by 2 observers (FOM, NJW), and only images in which the intima, media,,and adventitia of arterialized vein grafts could be clearly identified were used for subsequent analysis. Luminal area was defined as the area enclosed by the leading edge of the luminal-intimal border, and vessel area as the area enclosed by the media-adventitial border. Vessel area minus luminal area constituted the effective plaque area.l2 All areaswere measuredby direct planimetry using a computer analysis system (Sony SUM 1010,Sony Medical Electronic, Park Ridge, New Jersey).Percentvessel area stenosiswas defined as plaque areadivided by vesselarea.3The site of increased plaque area with the smallest luminal area constituted the lesion segment. Because saphenous veins are reversed when implanted as arterial conduits, a site immeNOVEMBER
15,
1995
FIGURE 1. Intravascular ultrasound images of a saphenous vein raft at the site of a focal stenosis /A) and at an immediately adjacent reference site (Bj. Note that the vessel size is larger at tf e lesion sit6 than at the referen’ce site.
diately distal to the lesion segment (within 1 cm) with regardlessof whether a proximal or distal reference was ~50% vessel area stenosis was chosen as the reference. used for comparison. Lesion vessel area was larger than If the intravascular ultrasound catheter was unable to the reference vessel area in 23 of 24 lesions (95.8%) cross the lesion (n = S), a proximal reference was used (Figures 1 and 2). For the lesion segments,there was a for comparison. For each lesion and reference.segment, significant correlation between plaque and vessel areas the cross-sectional area of the vessel, lumen, and plaque (r = 0.83, p
-1
I
BRIEF REPORTS 1067
Saphenous vein grafts used as coronary arterial conduits undergo compensatory enlargementin a manner similar to . muscular arteries. There is a highly significant correlation between vessel area and plaque area (r = 0.83, p cO.OOl),with 95.8% of the stenotic sitesenlarging comparedwith their immediately adjacentreference segment. Compensatory enlargement maintains the luminal size when up to 30% of the vessel is occupied by plaque. These findings are consistent with the original observation of Glagov et al’ in a postmortem series of left main coronary arteries. Whether veins used as arterial conduits undergo compensatoryenlargement in responseto atherosclerotic plaque was previously unknown. Native saphenous 5 10 15 20 25 30 35 40 0 veins, while possessinga 3-layered strucPique area (mm2) ture (intima, media, and adventitia), have a histologic organization different from FWRE 3. lhe saphous vein vessd area is significady and posihdy rdakC arteries with only a rudimentary internal tathepkquearea. elastic lamina and no external elastic lamina.t3After insertion into the coronary circulation, saphenousvein grafts undergo 86 morphologic changes (“arterialization”) I rt0.32 , rr0.70 including intimal fibrous thickening, me=p=m : p
l.-l::I
1068
THE AMERICAN JOURNAL OF CARDIOLOGY”
VOl
76
NOVEMBER 15, 1995
may help our understanding of vascular remodeling and arterialization. Becausea growing proportion of patients presenting with acute ischemic syndromes have saphenous vein bypass grafts, the clinical implications of these findings cannot be overstated. As with coronary arteries, the degree of atherosclerotic plaque cannot be adequately assessedwith angiography. For example, compensatory enlargement may make a culprit lesion angiographically silent“ after successfulthrombolysis. In addition, segments adjacent to a stenotic lesion may not be adequate references because they underestimate vessel dimensions. Thus, sizing an interventional device to perform optimized transcatheter revascularization may be difficult without intravascular ultrasound. Furthermore, angiography may prove insensitive for a study on atherosclerotic plaque progression or regression in venous bypass grafts becauseof its inability to detect compensatory enlargement. These data demonstrate that saphenous vein grafts enlarge at sites of focal atherosclerosis and preserve luminal area for narrowing of ~30% of the cross-sectional vessel area. 1. Glagov S, Weisenerg E, Zarins CK, Stankunavicius R, Kolettis GJ. Compensatory enlargement of human atherosclerotic coronary arteries. N Engl J Med 1987:316:1371-1375.
Cardiac Rehabilitation Electrocardiographic Donald
2. Hermiller JB, Tenaglia AN, Kisslo KB, Phillips HR. Bashore TM, Stack RS, Davidson CJ. In viva validation of compensatory enlargement of atherosclerotic coronary arteries. Am J Cardiol 1993;71:665-668. 3. Losordo DW, Rosenfield K, Kaufman J, Piecmk A, lsner JM. Focal cotnpensatoty enlargement of human arteries in response to progressive atherosclerosis: in viva documentation using intravascular ultrasound. Circukzti~n 1994;89: 2570-2577. 4. Stiel GM, Stiel LSG, Schafer J, Donath K, Mathey DC. Impact of compensatory enlargement of atherosclerotic coronary arteries on angiographic assessment of coronary artery disease. Circulation 1989;80: 1603-1609. 5. McPherson DD, Sima SJ, Hiratzka LF, Thorpe L, Armstrong ML, Marcus ML, Kerber RE. Coronary arterial remodeling studied by high-frequency epicardial echocardiography: an early compensatory mechanism in patients with obstructive coronaly atherosclerosis. J Am Cull Cardiol 1991;17:7%86. 6. Beere PA, Glagov S, Zatins CK. Experimental atherosclerosis at the carotid bifurcation of the cynomologus monkey. Localization, compensatory enlargement, and the sparing effect of lowered heart rate. Arkkoscler Thrmnb 1992;12: 1245-1253. 7. Kamiya A, Togawa T. Adaptive regulation of wall shear stress to flow change in the canine carotid artery. Am J Physiol 1980;239:H14-H21. 8. Zarins CK, Zatina MA, Giddens DP, Ku DN, Glagov S. Shear stress regulation of artery lumen diameter in experimental atherogenesl5. J Vfw Surg 1987; 5:413420. 9. Langille BL, O’Donnell F. Reductions in atterial diameter produced by chronic decreases in blood flow are endothelium-dependent. Science 1986;23 1:405407. 10. Glagov S, Zarins C, Giddens DP, Ku DN. Hemodynamics and atherosclerosis: insights and perspectives gained from studies of human arteries. Arch P&al Lab Med 1988;112:1018-1031. 11. Crawford T, Levene Cl. Medial thinning in atheroma. J Pufhol 1953;66: 19-23. 12. Keren G, Douek P, Oblon C, Banner RF, Pichard AD, Leon MB. Atherosclerotic saphenous vein grafts treated with different interventional procedures assessed by intravascular ultrasound. Am Hem J 1992; 124: 198-206. 13. Spray TL, Roberts WC. Changes in saphrnous veins used as aonocoronary bypass grafts. Am Heart J 1977;94:50&5 16. 14. Isner JM, Donaldson RF, Fortin AH, Tischler A, Clarke RH. Attenuation of the media of coronary arteries in advanced atherosclerosis. Am J Cardiol 1986:58: 937-939. 15. MacIsaac AI, Thomas JD, Topel EJ. Toward the quiescent coronary plaque. J Am Coil Cardiol 1993;22:1228-1241.
Using Simultaneous Voice and l’runstelephonic Monitoring
K. Shaw, PhD, Kenneth E. Sparks, PhD, Henry S. Jennings III, MD, and Janice C. Vantrease, RN
n 1984,Fletcher,’ Miller,* and their co-workers found Itientstranstelephonic electrocardiographicmonitoring of pawith coronary artery disease who exercised at home to be both efficacious and safe. Subsequentstudies support these initial findings,3,4with the scope of investigations expanding to include compliance5 and reimbursement6issues. Research data reveal those particularly benefiting from transtelephonic exercise monitoring (TEM) are patients located in rural areas where community hospitals frequently lack resourcesto establish and maintain viable outpatient programs.7For these persons,TEM provides a workable compromisebetween exercising alone and lengthy travel to metropolitan hospital-based programs. More recently, the concept of tandem sites has developed.7Patients exercisein rural medical facilities rather than at home with TEM provided by metropolitan hospital personnel located miles away.The From the Saint Thomas Heart Institute, Saint Thomas Hospital, Nashville, Tennessee, and the Department of Ph sical Education, Cleveland State Universrty, Cleveland, Ohio. Dr. S t: aw’s address is: Cardiac Health and Rehabilitation, Saint Thomas Heart Institute, Saint Thomas Hospital, 4220 Harding Road, Nashville, Tennessee 37205. Manuscript received May 30, 1995, revrsed manuscript received and accepted August 8, 1995.
simultaneoustransmissionof voice and rhythm strip over the sametelephone line was not commercially available until 198S6Before this time, basestation operatorswere required to “toggle” between analog voice and digital electrocardiographic signals. This potentially presented an increased risk for patients and proved cumbersome to operators who received voice communication at the expense of heart rhythm and vice versa. Although the simultaneous transmission feature corrected this fault and improved product acceptance,the proliferation of this new technology has not been studied. This investigation examinesthe current statusof simultaneous voice and electrocardiographic TEM in hospital, home, and clinic settings. ... We polled all facilities (n = 32) with simultaneous voice and electrocardiographic TEM capability. Because simultaneous transmission technology is marketed by only 1 company (Scott&e Inc., Cleveland, Ohio), ScottCare’s assistancewas obtainedin providing a list of product owners, leasees,and program supervisors. Each site was then sent a packet containing a sample22-item questionnaire with accompanying letter of explanation. One month later, program supervisorswere contactedby teleBRIEF REPORTS
1069