lntracoronary electrocardiogram coronary angioplasty
during
This prospective study examines the data derived from the intracoronary electrocardiogram (ECG) (derived from the coronary guide wire) compared with that from four standard surface leads (I, II, Ill, and V,) in documenting myocardial ischemia during coronary angioplasty. lntracoronary and surface ECGs were simultaneously recorded in 300 consecutive patients (mean age 59 k IO; range 33 to 80 years; 246 males [82%] during coronary angioplasty in 368 lesions (167 left anterior descending [46%], 85 left circumflex [23%], 107 right coronary arteries [29%], and nine bypass grafts [2%]), before balloon inflation, at 1 minute of inflation, and at the end of the procedure. ST segment changes (>O.l mV) were observed in the intracoronary ECG in 306 lesions (83%) (151 left anterior descending [88%], 75 left circumflex [89%], and 80 right coronary arteries [73%]) versus in 245 lesions (67%) in the surface ECG (126 left anterior descending [73%], 43 left circumflex [47%], and 76 right coronary arteries [70%]; [p < O.OOOl]). The mean ST segment shift was 0.5 + 0.4 mV in intracoronaq and 0.1 k 0.2 mV in standard leads (p < 0.0001). ST elevation was seen in 97% of cases with intracoronary ECG changes versus in 83% with surface ECG changes. The remainder had ST depression. A total of 48 lesions (13%) did not produce ECG changes and 62 (16%) had silent ischemia. In 75 lesions (21%), ECG changes were seen only in the intracoronary ECG, compared with 14 lesions (4%) with changes only in the surface ECG (p < 0.001). The intracoronary ECG more readily detects acute ischemia and is a valuable adjunct to surface leads during coronary angioplasty, particularly in the left circumflex coronary artery. (AM HEART J 1992;124:337.)
Abhay K. Pande, Bernhard Meier, Philip and Josiane Favre Geneva, Switzerland
Urban, Victor Moles, Pierre-Andre
Myocardial ischemia is frequently provoked during coronary angioplasty. In most cases ischemia is transient, appearing after the advancement of the angioplasty catheter across a critical lesion or during balloon inflations, and disappearing promptly after balloon deflation. The detection of myocardial ischemia is important for the decisions regarding seating of the guiding catheter, adjustment of balloon position, timing of balloon inflation and deflation, and also to assess the clinical relevance of the angioplasty procedure. Conventional means to detect myocardial ischemia include the presence or absence of angina and surface electrocardiographic (ECG) changes. However, such monitoring is not infallible. A patient may not experience angina although myocardial ischemia is present. Usually one to four surface ECG leads are monitored during angioplasty and these leads may poorly represent the myocardial area at risk. Moni-
From Received Reprint Hospital, 4/l/38101
the Cardiology for publication
Center,
University
Oct. 24, 1991;
Hospital, accepted
requests: Bernhard M&r, MD, 1211. Geneva 14, Switzerland.
Geneva. Feb.
Cardiology
14, 1992. Center,
University
Dorsaz,
toring 12 leads may demonstrate myocardial ischemia in the majority of patients; however, this is cumbersome and the chest electrodes may interfere with visualization during angioplasty. Use of only limb leads decreases the sensitivity of detecting myocardial ischemia, particularly in the anterior and lateral areas. To overcome these pitfalls in monitoring myocardial ischemia during coronary angioplasty, we introduced the clinical use of the intracoronary ECG derived from a coronary guide wire in 1985.l. 2 This represents a summation ECG of the myocardial territory around the coronary artery containing the bare coronary guide wire. Its feasibility was subsequently confirmed by others.3a 4 A similar technique had been used in an experimental animal model to detect myocardial ischemia during acute coronary occlusion.5 This prospective study examines the data derived from the intracoronary ECG in detecting myocardial ischemia during coronary angioplasty compared with that derived from surface ECG leads I, II, III, and Vz. The chest lead Vs was selected because it has been shown to be most sensitive in detecting myocardial ischemia of the left anterior descending coronary artery territory.6 337
338
Pande et al.
Table
1. Baseline
August 1992 Heart Journal
American
Table
characteristics
Patients Males Age (yr) Mean Range
300 243 (82C< )
Lesions Mean diameter stenosis (“a ) Left anterior descending coronary artery Left circumflex coronary artery Right coronary artery Bypass grafts To left anterior descending coronary artery To left circumflex coronary artery To right coronary artery
368 (100’; 89 -t 11 167 (46 5 85 (23”; 107 (29Y 9 (2r ) 5 (1’0) 2 (0.5’, 2 (0.5“;
II. Material Schneider Schneider ACS 0.014 Schneider
59 t 10 33-88 ) ) ) )
) )
METHODS Patients and lesions. The study group consisted of 300 consecutive unselected patients undergoing coronary balloon angioplasty for 368 lesions. The baseline characteristics are depicted in Table I. Technique. The intracoronary ECG was recorded using conventional coronary guide wires or fixed-wire balloons for coronary angioplasty (Table II). The guide wire or fixed-wire balloon serves as a unipolar electrode placed distal to the lesion. The external end is connected to the chest lead terminal of a multichannel ECG using a torquing clamp modified as a female plug (Fig. l), or an alligator clamp for fixed-wire balloons. The guiding and balloon catheters provide insulation of the guide wire in the aorta and in the proximal part of the coronary artery. In this study, Monorail (Schneider Europe, Biilach, Switzerland) or fixed-wire systems were used exclusively. While using the Monorail system, the guide wire is usually placed in the most distal position possible. With fixed-wire balloons, recording is only possible from a site immediately distal to the balloon. Protocol. The intracoronary and four surface ECG leads were recorded before the first balloon inflation, at 1 minute of inflation, and at the end of the angioplasty procedure, in addition to being monitored continuously during the angioplasty procedure (Fig. 2). In all the patients balloon was inflated for at least 1 minute. The changes were recorded at 1 minute for standardization. Presence of myocardial ischemia was defined as an ST segment shift of 20.01 mV at 80 msec after the J point using the TP segment as the isoelectric reference. The ECG measurements were done in the surface ECG lead showing maximum changes. One millivolt calibration was used for calculating the amplitude changes. The presence or absence of angina in association with ECG changes was noted. Bypass grafts were grouped with their target coronary arteries. Statistical analysis was done using Student’s t test. The values are expressed as the mean t standard deviation.
used as an intracoronary
0.014 in Magnum in 0.012 in
lead 247 :,fj 12 4
0.021 in
Fixed wire balloons SciMed ACE USC1 Probe Datascope Integra
(67’, 115’, (3°C (I ’ ,
) ) ) 1
49 (13’1 1 41 (I l’,’ ) 5 (I’,) .? ( 1 ( If )
RESULTS
ECG signs of myocardial ischemia were found during angioplasty in 306 arteries (83?:,) in the intracoronary ECG and in 245 arteries (67 !‘, ) in the surface ECG (p < 0.001). The difference was statistically significant regarding the left circumflex and left anterior descending coronary artery (Fig. 3). The mean ST shift was 0.5 * 0.4 mV in the intracoronary ECG and 0.1 i 0.2 mV in the surface ECG (p < 0.0001). ST elevation was the ECG change seen in 97 % of positive intracoronary ECG tracings and in 83Y of surface tracings. The remainder had ST depression. The mean magnitude of ST change was similar in the left anterior descending, left, circumflex, and right coronary arteries. A total of 48 arteries (13”; ) had no ECG changes. In 62 lesions (16:; ), angioplasty provoked silent myocardial ischemia. In 75 lesions (21 “C), ECG changes were seen only in the intracoronary ECG as opposed to 14 lesions (4’;) ) with changes only in the surface ECG (p < 0.001). These 14 patients with no ECG changes in the intracoronary ECG and with changes in the surface ECG included six patients with fixed wire balloons (Ace, SciMed Life Systems, Inc., Maple Grove, Minn.), and eight patients who had occlusion of a side branch. Chest pain was reported by patients during occlusion of 283 arteries (77 “C), with ischemic changes in the intracoronary ECG in 208 arteries (74r; ) and in the surface ECG in 167 arteries (59”(. ) (p < 0.001). The incidence of intracoronary and surface ECG changes and pain is shown in Fig. 4. DISCUSSION
This study’s aim was to prospectively assessthe ability of the intracoronary ECG to detect myocardial ischemia during coronary angioplasty and compare it with the ability of surface ECG leads I, II, III, and V.J. ST segment changes were significantly more readily detected by the intracoronary ECG in the left anterior descending and the left circumflex coronary arteries.
In right
coronary
arteries,
the differences
Volume Number
124 2
Intracoronary
ECG during PTCA
339
indicates centimeters).
did not reach statistical significance. This could be because the limb leads that were monitored (I, II, and III) have a high sensitivity for myocardial ischemia in the territory of the right coronary artery. To obtain the same sensitivity for the anterior region subtended by the left anterior descending artery, a single lead does not suffice, as previously shown with respect to lead V.5.7 Monitoring six chest leads improves the sensitivity,’ but it is cumbersome and frequently interferes with the fluoroscopic visualization of the coronary artery. The intracoronary ECG displays its potential best when dealing with the left circumflex coronary artery. In this study, only 45% of patients had surface ECG changes reflecting myocardial ischemia during angioplasty of the left circumflex coronary artery as against 89% with changes in the intracoronary ECG. Similar results were obtained by Berry et al9 The myocardium dependent upon the left circumflex coronary artery is poorly represented even by a 12-lead ECGPIOsl1 whereas the coronary guide wire always records in the exact region of the int,erest. Leads positioned on the back of the chest could increase the detection of ischemia of the circumflex territory by t,he surface ECG. However, this is less practical than obtaining the intracoronary ECG. The magnitude of ST changes was more marked in the intracoronary ECG compared with the surface ECG leads. This is the result of the proximity of the intracoronary electrode to the site of ischemia, which makes the changes more obvious. This difference can of course be artificially corrected by increasing the amplitude in the surface ECG, but this also increases background noise. There was no difference in the magnitude of ST elevation with the intracoronary lead between the left anterior descending, circumflex, or right coronary arteries. The intracoronary ECG can be monitored during angioplasty without loss of time, additional material,
before
1 min of balloon inflation
after
Fig. 2. Intracoronary (IC) and surface ECG (I, II, III, V,) during angioplasty of a left circumflex coronary artery showing marked ST elevation in the intracoronary ECG not detectable in the surface ECG. Calibration marks indicate 1 mV.
or risk. It helps to assessthe clinical relevance of the procedure by reporting the viability of myocardium at risk and the potential of collaterals to prevent ischemia. The intracoronary ECG is therefore of some prognostic value. It also is a reliable indicator of flow return after balloon deflation and provides a model to study myocardial ischemia during acute coronary occlusion. There were 14 patients with no ECG changes in the intracoronary ECG and ischemic changes in the surface ECG. Of these, six patients had angioplasty with fixed wire balloons. With these devices the intracoronary ECG is captured immediately distal to the balloon and may fail to reflect ischemia, which usually develops more remote from the balloon catheter. This holds particularly true for the right coronary artery, where ischemia may be limited to the left ventricle, which is not reached by the wire of a fixed
340
Pande et al.
American
August 1992 Heact Journal
Fig. 3. ST changesand chest pain at 1 minute of balloon inflation. ZCECG,Intracoronary ECG; Surface,
surface ECG; LAD, left anterior descendingcoronary artery; LCX, left circumflex coronary artery; RCA, right coronary artery.
Pain + IC ECG + S ECG Pain + IC ECG No pain + No ECG Ic ECG + S ECG + No pain IC ECG + No pain Pain Pain + S ECG S ECG + No pain
n= 368
4. Incidence of intracoronary and surface ECG changesand chest pain or any combination of these manifestations at 1 minute of balloon inflation. ZCECG, Intracoronary ECG; S ECG, surface ECG.
Fig.
wire balIoon dilating a proximal stenosis. The remaining patients probably had occlusion of a side branch, producing ischemia that was not reflected by the intracoronary ECG. There are a number of limitations of the intracoronary ECG. (1) It can be obtained only while a guide wire resides in the coronary artery. (2) Some fixedwire balloons (e.g., Cordis Orion, Medtronic Omniflex, Sorin one-to-one) are fully insulated, which prevents their use as an electrode. (3) The configuration of the ECG changes with the displacement of the guide wire. (4) ManipuIations of the guide wire produce artifacts. (5) The intracoronary ECG ignores is-
chemia of other myocardial areas or side branches occluded by the balloon. A problem in an artery dilated previously can be missed if the operator relies solely on the intracoronary ECG while attempting a second vessel. Hence the intracoronary ECG should be seen as a complement rather than a replacement of surface leads for monitoring during coronary angioplasty. REFERENCES
1. Meier B, Killisch JP, Adatte JJ, Casalini P, Rutishauser W. Intrakoronares Elektrokardiogramm wshrend transluminaler Koronarangioplastie. Schweiz Med Wochenschr 1985;115: 1590-3.
Volume
124
Number
2
Intracoronury
2. Meier B, Rutishauser W. Coronary pacing during percutaneous transluminal coronary angioplasty. Circulation 1985; 71:557-61. 3. Friedman PL, Shook TL, Kirshenbaum JM, Selwyn AP, Ganz P. Value of the intracoronary electrocardiogram to monitor myocardial ischemia during percutaneous transluminal coronary angioplasty. Circulation 1986;74:330-9. 4. Feldman T, Chua KG, Childers RW. R wave of the surface and intracxonary electrocardiogram during acute coronary occlusion. Am J Cardiol 1986;58:885-90. 5. Hashimoto K, Corday E, Lang T, Rubin G, Meerbaum S, Osher J, Farcot J, Davidson RM. Significance of ST segment elevations in acute myocardial ischemia: evaluation with intracoronary electrode technique. Am J Cardiol 1976;37:493500. 6. Feldman T, Childers RW, Chua KG. Optimal ECG monitoring during percutaneous transluminal coronary angioplasty of left anterior descending artery. Cathet Cardiovasc Diagn 1987;13:271-4. 7. Hauser AM, Gangadhartan V, Ramos RG, Gordon S, Timmis GC, Dudlets P. Sequence of mechanical, electrocardiographic
8.
9.
10.
11.
ECG during PTCA
and clinical effects of repeated coronary artery occlusion in human beings: echocardiographic observations during coronary angioplasty. J Am Co11 Cardiol 1985;5:193-7. Wohlgelernter D, Cleman M, Highman HA, Fetterman RC, Duncan JS, Zaret BL, Jaffe CC. Regional myocardial dysfunction during coronary angioplasty: evaluation by two-dimensional echocardiography and 12-lead electrocardiography. J Am Co11 Cardiol 1986;7:1245-54. Berry C, Zalewski A, Kovach R, Savage M, Goldberg S. Surface electrocardiogram in the detection of transmural myocardial ischemia during coronary artery occlusion. Am J Cardiol 1989;63:21-6. Boden WE, Kleiger RE, Gibson RS, Schwartz DJ, Schectman KB, Capone RJ, Roberts R, and the Diltiazem Reinfarction Study Group. Electrocardiographic evolution of posterior myocardial infarction: importance of early precordial ST segment depression. Am J Cardiol 1987;59:782-7. Sclarovsky S, Topaz 0, Rechavia E, Strasberg B, Agman J. Ischemic ST segment depression in leads Vz-Va as the presenting electrocardiographic feature of posterolateral wall infarction. AM HEART J 1987;113:1085-96.
Efficacy of directional coronary atherectomy in cases unsuitable for percutaneous transluminal coronary angioplasty (PTCA) and after unsuccessful PTCA Directional coronary atherectomy (DCA) was used in 10 female and 50 male patients with an average age of 58 years. They were categorized into three different groups depending on the indications for atherectomy. Group 1 included all patients who had atherectomy as their primary intervention (n = 20) because they were assumed to be unsuitable for percutaneous transluminal coronary angioplasty (PTCA). Group 2 consisted of patients in whom DCA was used after failed balloon dilatation with unsuccessful but uneventful treatment (n = 17). Group 3 (n = 23) included patients in whom DCA was performed as a “rescue” or “bailout” procedure after unsuccessful PTCA resulting in critical ischemia (ECG changes, chest pain, hypotension, and shock). The target lesions were located in the left main artery in two, left anterior descending artery in 43, right coronary artery in 15, and aortocoronary venous bypass in five. The mean length of the lesions was 8 mm (2 to 25 mm). The overall success rate for 65 lesions was 92%. The mean stenosis was reduced from 87 & 12% to 19 & 17% in patients with primary success. Presently available follow-up angiograms (30) showed six restenoses. Major complications occurred in seven patients (myocardial infarction in two and coronary artery bypass graft surgery within 24 hours in five); there were no deaths. Our results show that DCA is a safe and effective technique that can extend the use of percutaneous procedures and provide a promising nonsurgical option in cases of unsuccessful PTCA. (AM HEART J 1992;124:341.)
B. Hiifling, P. Gonschior, Lindi Simpson, G. Bauriedel, and A. Nerlich Munich,
German31
From the Medizinische Department I, Klinikum Grosshadern, and the Institute of Pathology, UCersity of Munich. Supported by Sanderstiftung grant 90.026.1 and a grant from Deutsche Herzetiftung (Dr. Gonschior).
Received for publication Sept. 26, 1991; accepted Feb. 3, 1992. Reprint requests: Peter Gonschior, Medizinische Department I, Klinikum Grosshadern, Marchioninistr. 15,BOOO Munich 70, Germany. 4/1/38Q99
341
during
This prospective study examines the data derived from the intracoronary electrocardiogram (ECG) (derived from the coronary guide wire) compared with that from four standard surface leads (I, II, Ill, and V,) in documenting myocardial ischemia during coronary angioplasty. lntracoronary and surface ECGs were simultaneously recorded in 300 consecutive patients (mean age 59 k IO; range 33 to 80 years; 246 males [82%] during coronary angioplasty in 368 lesions (167 left anterior descending [46%], 85 left circumflex [23%], 107 right coronary arteries [29%], and nine bypass grafts [2%]), before balloon inflation, at 1 minute of inflation, and at the end of the procedure. ST segment changes (>O.l mV) were observed in the intracoronary ECG in 306 lesions (83%) (151 left anterior descending [88%], 75 left circumflex [89%], and 80 right coronary arteries [73%]) versus in 245 lesions (67%) in the surface ECG (126 left anterior descending [73%], 43 left circumflex [47%], and 76 right coronary arteries [70%]; [p < O.OOOl]). The mean ST segment shift was 0.5 + 0.4 mV in intracoronaq and 0.1 k 0.2 mV in standard leads (p < 0.0001). ST elevation was seen in 97% of cases with intracoronary ECG changes versus in 83% with surface ECG changes. The remainder had ST depression. A total of 48 lesions (13%) did not produce ECG changes and 62 (16%) had silent ischemia. In 75 lesions (21%), ECG changes were seen only in the intracoronary ECG, compared with 14 lesions (4%) with changes only in the surface ECG (p < 0.001). The intracoronary ECG more readily detects acute ischemia and is a valuable adjunct to surface leads during coronary angioplasty, particularly in the left circumflex coronary artery. (AM HEART J 1992;124:337.)
Abhay K. Pande, Bernhard Meier, Philip and Josiane Favre Geneva, Switzerland
Urban, Victor Moles, Pierre-Andre
Myocardial ischemia is frequently provoked during coronary angioplasty. In most cases ischemia is transient, appearing after the advancement of the angioplasty catheter across a critical lesion or during balloon inflations, and disappearing promptly after balloon deflation. The detection of myocardial ischemia is important for the decisions regarding seating of the guiding catheter, adjustment of balloon position, timing of balloon inflation and deflation, and also to assess the clinical relevance of the angioplasty procedure. Conventional means to detect myocardial ischemia include the presence or absence of angina and surface electrocardiographic (ECG) changes. However, such monitoring is not infallible. A patient may not experience angina although myocardial ischemia is present. Usually one to four surface ECG leads are monitored during angioplasty and these leads may poorly represent the myocardial area at risk. Moni-
From Received Reprint Hospital, 4/l/38101
the Cardiology for publication
Center,
University
Oct. 24, 1991;
Hospital, accepted
requests: Bernhard M&r, MD, 1211. Geneva 14, Switzerland.
Geneva. Feb.
Cardiology
14, 1992. Center,
University
Dorsaz,
toring 12 leads may demonstrate myocardial ischemia in the majority of patients; however, this is cumbersome and the chest electrodes may interfere with visualization during angioplasty. Use of only limb leads decreases the sensitivity of detecting myocardial ischemia, particularly in the anterior and lateral areas. To overcome these pitfalls in monitoring myocardial ischemia during coronary angioplasty, we introduced the clinical use of the intracoronary ECG derived from a coronary guide wire in 1985.l. 2 This represents a summation ECG of the myocardial territory around the coronary artery containing the bare coronary guide wire. Its feasibility was subsequently confirmed by others.3a 4 A similar technique had been used in an experimental animal model to detect myocardial ischemia during acute coronary occlusion.5 This prospective study examines the data derived from the intracoronary ECG in detecting myocardial ischemia during coronary angioplasty compared with that derived from surface ECG leads I, II, III, and Vz. The chest lead Vs was selected because it has been shown to be most sensitive in detecting myocardial ischemia of the left anterior descending coronary artery territory.6 337
338
Pande et al.
Table
1. Baseline
August 1992 Heart Journal
American
Table
characteristics
Patients Males Age (yr) Mean Range
300 243 (82C< )
Lesions Mean diameter stenosis (“a ) Left anterior descending coronary artery Left circumflex coronary artery Right coronary artery Bypass grafts To left anterior descending coronary artery To left circumflex coronary artery To right coronary artery
368 (100’; 89 -t 11 167 (46 5 85 (23”; 107 (29Y 9 (2r ) 5 (1’0) 2 (0.5’, 2 (0.5“;
II. Material Schneider Schneider ACS 0.014 Schneider
59 t 10 33-88 ) ) ) )
) )
METHODS Patients and lesions. The study group consisted of 300 consecutive unselected patients undergoing coronary balloon angioplasty for 368 lesions. The baseline characteristics are depicted in Table I. Technique. The intracoronary ECG was recorded using conventional coronary guide wires or fixed-wire balloons for coronary angioplasty (Table II). The guide wire or fixed-wire balloon serves as a unipolar electrode placed distal to the lesion. The external end is connected to the chest lead terminal of a multichannel ECG using a torquing clamp modified as a female plug (Fig. l), or an alligator clamp for fixed-wire balloons. The guiding and balloon catheters provide insulation of the guide wire in the aorta and in the proximal part of the coronary artery. In this study, Monorail (Schneider Europe, Biilach, Switzerland) or fixed-wire systems were used exclusively. While using the Monorail system, the guide wire is usually placed in the most distal position possible. With fixed-wire balloons, recording is only possible from a site immediately distal to the balloon. Protocol. The intracoronary and four surface ECG leads were recorded before the first balloon inflation, at 1 minute of inflation, and at the end of the angioplasty procedure, in addition to being monitored continuously during the angioplasty procedure (Fig. 2). In all the patients balloon was inflated for at least 1 minute. The changes were recorded at 1 minute for standardization. Presence of myocardial ischemia was defined as an ST segment shift of 20.01 mV at 80 msec after the J point using the TP segment as the isoelectric reference. The ECG measurements were done in the surface ECG lead showing maximum changes. One millivolt calibration was used for calculating the amplitude changes. The presence or absence of angina in association with ECG changes was noted. Bypass grafts were grouped with their target coronary arteries. Statistical analysis was done using Student’s t test. The values are expressed as the mean t standard deviation.
used as an intracoronary
0.014 in Magnum in 0.012 in
lead 247 :,fj 12 4
0.021 in
Fixed wire balloons SciMed ACE USC1 Probe Datascope Integra
(67’, 115’, (3°C (I ’ ,
) ) ) 1
49 (13’1 1 41 (I l’,’ ) 5 (I’,) .? ( 1 ( If )
RESULTS
ECG signs of myocardial ischemia were found during angioplasty in 306 arteries (83?:,) in the intracoronary ECG and in 245 arteries (67 !‘, ) in the surface ECG (p < 0.001). The difference was statistically significant regarding the left circumflex and left anterior descending coronary artery (Fig. 3). The mean ST shift was 0.5 * 0.4 mV in the intracoronary ECG and 0.1 i 0.2 mV in the surface ECG (p < 0.0001). ST elevation was the ECG change seen in 97 % of positive intracoronary ECG tracings and in 83Y of surface tracings. The remainder had ST depression. The mean magnitude of ST change was similar in the left anterior descending, left, circumflex, and right coronary arteries. A total of 48 arteries (13”; ) had no ECG changes. In 62 lesions (16:; ), angioplasty provoked silent myocardial ischemia. In 75 lesions (21 “C), ECG changes were seen only in the intracoronary ECG as opposed to 14 lesions (4’;) ) with changes only in the surface ECG (p < 0.001). These 14 patients with no ECG changes in the intracoronary ECG and with changes in the surface ECG included six patients with fixed wire balloons (Ace, SciMed Life Systems, Inc., Maple Grove, Minn.), and eight patients who had occlusion of a side branch. Chest pain was reported by patients during occlusion of 283 arteries (77 “C), with ischemic changes in the intracoronary ECG in 208 arteries (74r; ) and in the surface ECG in 167 arteries (59”(. ) (p < 0.001). The incidence of intracoronary and surface ECG changes and pain is shown in Fig. 4. DISCUSSION
This study’s aim was to prospectively assessthe ability of the intracoronary ECG to detect myocardial ischemia during coronary angioplasty and compare it with the ability of surface ECG leads I, II, III, and V.J. ST segment changes were significantly more readily detected by the intracoronary ECG in the left anterior descending and the left circumflex coronary arteries.
In right
coronary
arteries,
the differences
Volume Number
124 2
Intracoronary
ECG during PTCA
339
indicates centimeters).
did not reach statistical significance. This could be because the limb leads that were monitored (I, II, and III) have a high sensitivity for myocardial ischemia in the territory of the right coronary artery. To obtain the same sensitivity for the anterior region subtended by the left anterior descending artery, a single lead does not suffice, as previously shown with respect to lead V.5.7 Monitoring six chest leads improves the sensitivity,’ but it is cumbersome and frequently interferes with the fluoroscopic visualization of the coronary artery. The intracoronary ECG displays its potential best when dealing with the left circumflex coronary artery. In this study, only 45% of patients had surface ECG changes reflecting myocardial ischemia during angioplasty of the left circumflex coronary artery as against 89% with changes in the intracoronary ECG. Similar results were obtained by Berry et al9 The myocardium dependent upon the left circumflex coronary artery is poorly represented even by a 12-lead ECGPIOsl1 whereas the coronary guide wire always records in the exact region of the int,erest. Leads positioned on the back of the chest could increase the detection of ischemia of the circumflex territory by t,he surface ECG. However, this is less practical than obtaining the intracoronary ECG. The magnitude of ST changes was more marked in the intracoronary ECG compared with the surface ECG leads. This is the result of the proximity of the intracoronary electrode to the site of ischemia, which makes the changes more obvious. This difference can of course be artificially corrected by increasing the amplitude in the surface ECG, but this also increases background noise. There was no difference in the magnitude of ST elevation with the intracoronary lead between the left anterior descending, circumflex, or right coronary arteries. The intracoronary ECG can be monitored during angioplasty without loss of time, additional material,
before
1 min of balloon inflation
after
Fig. 2. Intracoronary (IC) and surface ECG (I, II, III, V,) during angioplasty of a left circumflex coronary artery showing marked ST elevation in the intracoronary ECG not detectable in the surface ECG. Calibration marks indicate 1 mV.
or risk. It helps to assessthe clinical relevance of the procedure by reporting the viability of myocardium at risk and the potential of collaterals to prevent ischemia. The intracoronary ECG is therefore of some prognostic value. It also is a reliable indicator of flow return after balloon deflation and provides a model to study myocardial ischemia during acute coronary occlusion. There were 14 patients with no ECG changes in the intracoronary ECG and ischemic changes in the surface ECG. Of these, six patients had angioplasty with fixed wire balloons. With these devices the intracoronary ECG is captured immediately distal to the balloon and may fail to reflect ischemia, which usually develops more remote from the balloon catheter. This holds particularly true for the right coronary artery, where ischemia may be limited to the left ventricle, which is not reached by the wire of a fixed
340
Pande et al.
American
August 1992 Heact Journal
Fig. 3. ST changesand chest pain at 1 minute of balloon inflation. ZCECG,Intracoronary ECG; Surface,
surface ECG; LAD, left anterior descendingcoronary artery; LCX, left circumflex coronary artery; RCA, right coronary artery.
Pain + IC ECG + S ECG Pain + IC ECG No pain + No ECG Ic ECG + S ECG + No pain IC ECG + No pain Pain Pain + S ECG S ECG + No pain
n= 368
4. Incidence of intracoronary and surface ECG changesand chest pain or any combination of these manifestations at 1 minute of balloon inflation. ZCECG, Intracoronary ECG; S ECG, surface ECG.
Fig.
wire balIoon dilating a proximal stenosis. The remaining patients probably had occlusion of a side branch, producing ischemia that was not reflected by the intracoronary ECG. There are a number of limitations of the intracoronary ECG. (1) It can be obtained only while a guide wire resides in the coronary artery. (2) Some fixedwire balloons (e.g., Cordis Orion, Medtronic Omniflex, Sorin one-to-one) are fully insulated, which prevents their use as an electrode. (3) The configuration of the ECG changes with the displacement of the guide wire. (4) ManipuIations of the guide wire produce artifacts. (5) The intracoronary ECG ignores is-
chemia of other myocardial areas or side branches occluded by the balloon. A problem in an artery dilated previously can be missed if the operator relies solely on the intracoronary ECG while attempting a second vessel. Hence the intracoronary ECG should be seen as a complement rather than a replacement of surface leads for monitoring during coronary angioplasty. REFERENCES
1. Meier B, Killisch JP, Adatte JJ, Casalini P, Rutishauser W. Intrakoronares Elektrokardiogramm wshrend transluminaler Koronarangioplastie. Schweiz Med Wochenschr 1985;115: 1590-3.
Volume
124
Number
2
Intracoronury
2. Meier B, Rutishauser W. Coronary pacing during percutaneous transluminal coronary angioplasty. Circulation 1985; 71:557-61. 3. Friedman PL, Shook TL, Kirshenbaum JM, Selwyn AP, Ganz P. Value of the intracoronary electrocardiogram to monitor myocardial ischemia during percutaneous transluminal coronary angioplasty. Circulation 1986;74:330-9. 4. Feldman T, Chua KG, Childers RW. R wave of the surface and intracxonary electrocardiogram during acute coronary occlusion. Am J Cardiol 1986;58:885-90. 5. Hashimoto K, Corday E, Lang T, Rubin G, Meerbaum S, Osher J, Farcot J, Davidson RM. Significance of ST segment elevations in acute myocardial ischemia: evaluation with intracoronary electrode technique. Am J Cardiol 1976;37:493500. 6. Feldman T, Childers RW, Chua KG. Optimal ECG monitoring during percutaneous transluminal coronary angioplasty of left anterior descending artery. Cathet Cardiovasc Diagn 1987;13:271-4. 7. Hauser AM, Gangadhartan V, Ramos RG, Gordon S, Timmis GC, Dudlets P. Sequence of mechanical, electrocardiographic
8.
9.
10.
11.
ECG during PTCA
and clinical effects of repeated coronary artery occlusion in human beings: echocardiographic observations during coronary angioplasty. J Am Co11 Cardiol 1985;5:193-7. Wohlgelernter D, Cleman M, Highman HA, Fetterman RC, Duncan JS, Zaret BL, Jaffe CC. Regional myocardial dysfunction during coronary angioplasty: evaluation by two-dimensional echocardiography and 12-lead electrocardiography. J Am Co11 Cardiol 1986;7:1245-54. Berry C, Zalewski A, Kovach R, Savage M, Goldberg S. Surface electrocardiogram in the detection of transmural myocardial ischemia during coronary artery occlusion. Am J Cardiol 1989;63:21-6. Boden WE, Kleiger RE, Gibson RS, Schwartz DJ, Schectman KB, Capone RJ, Roberts R, and the Diltiazem Reinfarction Study Group. Electrocardiographic evolution of posterior myocardial infarction: importance of early precordial ST segment depression. Am J Cardiol 1987;59:782-7. Sclarovsky S, Topaz 0, Rechavia E, Strasberg B, Agman J. Ischemic ST segment depression in leads Vz-Va as the presenting electrocardiographic feature of posterolateral wall infarction. AM HEART J 1987;113:1085-96.
Efficacy of directional coronary atherectomy in cases unsuitable for percutaneous transluminal coronary angioplasty (PTCA) and after unsuccessful PTCA Directional coronary atherectomy (DCA) was used in 10 female and 50 male patients with an average age of 58 years. They were categorized into three different groups depending on the indications for atherectomy. Group 1 included all patients who had atherectomy as their primary intervention (n = 20) because they were assumed to be unsuitable for percutaneous transluminal coronary angioplasty (PTCA). Group 2 consisted of patients in whom DCA was used after failed balloon dilatation with unsuccessful but uneventful treatment (n = 17). Group 3 (n = 23) included patients in whom DCA was performed as a “rescue” or “bailout” procedure after unsuccessful PTCA resulting in critical ischemia (ECG changes, chest pain, hypotension, and shock). The target lesions were located in the left main artery in two, left anterior descending artery in 43, right coronary artery in 15, and aortocoronary venous bypass in five. The mean length of the lesions was 8 mm (2 to 25 mm). The overall success rate for 65 lesions was 92%. The mean stenosis was reduced from 87 & 12% to 19 & 17% in patients with primary success. Presently available follow-up angiograms (30) showed six restenoses. Major complications occurred in seven patients (myocardial infarction in two and coronary artery bypass graft surgery within 24 hours in five); there were no deaths. Our results show that DCA is a safe and effective technique that can extend the use of percutaneous procedures and provide a promising nonsurgical option in cases of unsuccessful PTCA. (AM HEART J 1992;124:341.)
B. Hiifling, P. Gonschior, Lindi Simpson, G. Bauriedel, and A. Nerlich Munich,
German31
From the Medizinische Department I, Klinikum Grosshadern, and the Institute of Pathology, UCersity of Munich. Supported by Sanderstiftung grant 90.026.1 and a grant from Deutsche Herzetiftung (Dr. Gonschior).
Received for publication Sept. 26, 1991; accepted Feb. 3, 1992. Reprint requests: Peter Gonschior, Medizinische Department I, Klinikum Grosshadern, Marchioninistr. 15,BOOO Munich 70, Germany. 4/1/38Q99
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