- Email: [email protected]
Coronary pathology predicts conduction disturbances after coronary artery bypass grafting
Coronary Pathology Predicts Conduction Disturbances After Coronarv Arterv Bypass Grafting Morris Mosseri, MD, Gilath Meir, MD, Chaim Lotan, MD, Yonathan Hasin, MD, Azai Applebaum, MD, Shimon Rosenheck, MD, Dov Shimon, MD, and Mervyn S. Gotsman, MD, FRCC Departments of Cardiology and Cardiovascular Surgery, Hadassah University Hospital, Jerusalem, Israel
Conduction disturbances after coronary artery bypass grafting may result from compromised septal blood flow. To examine this hypothesis we reviewed the preoperative coronary angiography of 55 consecutive patients undergoing coronary artery bypass grafting. Thirty-five patients had either no lesion or a discrete lesion in the left anterior descending coronary artery that did not include the septal perforator (type I anatomy). Twenty patients had a lesion of the left anterior descending coronary artery at the origin of the first septal branch, a lesion of the first septal artery, or a pair of lesions in the left anterior descending coronary artery that straddled the origin of the first septal artery; all lesions were praximal to the graft site (type I1 anatomy). None of the patients with type I anatomy had a major conduction disturbance after coronary artery bypass grafting. Eleven of the patients with type I1 anatomy had major conduc-
tion disturbances after coronary artery bypass grafting; right bundle-branch block in 1, right bundle-branch block and left anterior hemiblock in 2, left bundlebranch block in 5, and complete atrioventricular block that required pacemaker implantation in 3 ( p < 0.001). In the 20 patients with type 11 anatomy, the appearance of conduction disturbances correlated well with the absence of retrograde flow to the septal branches from the right coronary artery ( p < 0.01). Pathological lesions in the left anterior descending coronary artery that compromise flow in the first perforator and that do not provide an adequate circulation produce localized damage and conduction disturbances after coronary artery bypass grafting. This can be predicted from the preoperative angiographic anatomy.
C
Patients and Methods
onduction disturbances (CD) after coronary artery bypass grafting (CABG) are well known and occur with an incidence of 4% to 34% [1-4]. Improved myocardial preservation and the use of cardioplegia has decreased the incidence of intraoperative myocardial injury [5,6]. Nonetheless, the incidence of postoperative CD has remained high [4, 7-10]. Cold potassium cardioplegia used today is associated with a 34% incidence of right bundle-branch block (RBBB) (often temporary) compared with 6% in a control group using ischemic arrest and intermittent perfusion [ll]. The suggestion that CD are induced by global ischemia during CABG is probably too simplistic. The present study was undertaken to determine whether there is a specific anatomical group of patients who are at risk for postoperative CD after CABG. We studied 55 consecutive patients who underwent open heart operations.
Accepted for publication Oct 17, 1990. Address reprint requests to Dr Gotsman, Department of Cardiology, Kiryat Hadassah, PO Box 12000, Jerusalem, Israel 91-120.
0 1991 by The
Society of Thoracic Surgeons
(Ann Thoruc Surg 1992;52:248-52)
Three hundred twenty-nine patients underwent their first coronary artery bypass graft operation in the Surgical Department at Hadassah Hospital during a 3-year period. Of them, 55 consecutive patients were referred from the Cardiological Department in Hadassah Hospital. These patients are the subjects of the present study. Patients who also had aneurysmectomy, ventricular septal defect repair, or valvar operation were not included. All patients underwent coronary artery bypass grafting under general anesthesia. Cardiopulmonary bypass was instituted with a bubble oxygenator. Myocardial preservation was achieved by core cooling to 24" to 26°C. St. Thomas' cardioplegic solution (1,400 to 2,500 mL per patient) was delivered through the ascending aorta. Cardiac and septal temperatures were monitored and were in the range of 8" to 15°C. Supplemental cardioplegia was delivered through vein grafts and the ascending aorta every 30 minutes. The heart was further cooled with topical iced saline solution. The following preoperative and perioperative details were noted: age, sex, previous myocardial infarction, cardiopulmonary bypass and aortic clamp time, perioperative myocardial infarction, old and perioperative conduction disturbances, and number and site of coronary bypass grafts. 0003-4975/91/$3.50
MOSSERI ET AL POST-CABG CONDUCTION & CORONARY ANATOMY
Ann Thorac Surg 1991;51:24%52
\
11 a
la
Fig 1 . Classification of lesions in the left corona y system: type 1, lesions not related to septal branches; type 11, lesions related to septal branches (a, left anterior descending [LAD] lesion at the origin of a septa/ branch; b, pair of LAD lesions straddling the septal artey ; c, discrete lesion of the septal artey). (G = graft to LAD; 1P = first perforator.)
I b
I1 b
Twelve-lead electrocardiograms were routinely recorded within 6 hours after operation and daily thereafter until discharge. Earlier electrocardiograms were recorded when the monitor was suggestive of ST-T changes or conduction disturbances. Blood creatine kinase examinations were performed in all patients with suspected myocardial infarction and in some patients with conduction disturbances without electrocardiographic evidence for myocardial infarction. Perioperative transmural myocardial infarction was diagnosed whenever a new Q wave unrelated to CD appeared in two leads in the electrocardiogram. A subendocardial wall infarction was diagnosed when ST-T changes (unrelated to CD and with no Q wave) appeared in any two leads and were accompanied with an increase in blood creatine kinase-MB level (>160 IUL). Perioperative “major” CD were defined as complete right or left bundle-branch block (LBBB)or complete atrioventricular block. Conduction disturbances were persistent if they were still existing in the electrocardiogram at discharge. A postoperative thallium effort test (1 to 6 months after operation) to confirm or exclude septal hypoperfusion was available only in a minority of patients. To increase the number of patients with postoperative CD, we analyzed the 11 of our consecutive 55 patients in whom CD developed and added another 12 patients with postoperative CD who had undergone angiography and operation in previous years. This created an extended group of patients with perioperative CD who were examined separately. Coronary angiography was performed on a 4.5-inch General Electric image intensifier with an overframing lens to obtain maximum magnification. Angiograms were
249
I1 c
made in at least five different oblique projections including the craniocaudal projection. The coronary angiographic examinations performed before CABG were reviewed by a cardiologist who was blinded to the presence of CD. Lesions of more than 70% in one view were graded as serious. A detailed description of the lesions in the coronary arteries and their branches was drawn. Type I anatomy was defined as either no lesion (type Ia) or a discrete lesion in the left anterior descending coronary artery unrelated to the septal branches (type Ib) (Fig 1). Type I1 anatomy was defined as a lesion of the left anterior descending coronary artery (LAD)at the origin of a septal branch (IIa), a pair of lesions in the LAD straddling the septal artery (IIb), or a discrete lesion of the septal artery (IIc) all proximal to the graft anastomosis (Fig 1). Retrograde filling of the septum and the perforating arteries from the right coronary system was assessed qualitatively as good, moderate, poor, or none. All continuous data were presented as mean standard deviation. The correlation between the anatomical types and the CD and between CD and retrograde filling of the septal arteries were tested by the Fisher’s exact test. A comparison of the number of grafts in the two anatomical groups was performed using Student’s t test.
*
Results We studied 55 patients, 48 men and 7 women. Their mean age was 59 ? 7 years (range, 46 to 70 years). Thirty-five patients (age, 60 ? 4.7 years) had type I anatomy; 14 had type Ia and 21 had type Ib. Twenty patients (age, 58.2 6.6 years) were found to have type I1 anatomy. Of these, 3 patients had type IIa lesions, 8 patients had a type IIb
*
250
MOSSERI ET AL POST-CABG CONDUCTION & CORONARY ANATOMY
lesion, and 5 patients had type IIc lesions. Four patients had both type IIb and IIc lesions. Twenty-nine of the 35 patients with type I anatomy and 19 of the 20 with type I1 anatomy were male.
Correlation Between Conduction Disturbances and Pathological Anatomy None of the 35 patients with type I anatomy had postoperative CD. Of the 20 patients with type I1 anatomy, 11 (55%)had major postoperative CD ( p < 0.001). Only 1 patient with type I1 anatomy had preoperative CD (RBBB + left anterior hemiblock [LAHB]). After CABG he had temporary complete atrioventricular (AV) block that did not require permanent pacemaker implantation. No patient with type I anatomy had preoperative CD. Four patients with type I and 1 patient with type I1 anatomy had left main coronary disease (>40% narrowing), and none had CD.
Correlation Between Retrograde Filling of Septa1 Branches and Conduction Disturbances Of patients with type I1 anatomy, 6 of the 9 patients without CD and only 1of the 11with CD had moderate or good retrograde filling of the septum from the posterior interventricular branch of the right coronary artery ( p < 0.01). In patients with type I anatomy, 16 of 35 patients (all of them with type Ib) had moderate or good retrograde filling.
Types of Conduction Disturbances in Type II Anatomy Eleven of the 20 patients with type I1 anatomy had one or more CD. Four of them had permanent LBBB, one had permanent RBBB, two had permanent RBBB and LAHB and 2 had permanent complete AV block that required implantation of a permanent pacemaker. Another patient had temporary LBBB that was followed by permanent LAHB, whereas another had temporary complete AV block requiring a permanent pacemaker implantation.
Correlation Between Previous Myocardial Infarction and Conduction Disturbances One patient of 18 with a previous inferior myocardial infarction, 1 of 12 with previous anterior wall infarction, and 1 of 4 with both previous inferior and anterior myocardial infarctions had a major conduction disturbance. Three of the 21 patients with no previous myocardial infarction had major CD ( p = not significant [NS]).
Distribution of Conduction Disturbances in the Extended Group In the extended group with CD, 20 of 23 patients had type I1 anatomy. Their CD included complete AV block in 10 patients (temporary in 2), LBBB in 9 patients (temporary in 3), and RBBB in 4 patients. Four of them had LAHB and 1 had left posterior hemiblock. Three of the 23 patients had complete AV block (temporary in one) and type Ib anatomy and in all 3 there was no retrograde flow to septal branches. In 1 of them there was a 90% left main coronary artery lesion and in another total LAD coronary artery occlusion proximal to the first perforator. Other CD did not appear in patients with type I anatomy.
Ann Thorac Surg 1991;51:24&52
Correlation Between Operative Technique and Conduction Disturbances
*
The cardiopulmonary bypass time was 107 22 minutes in type I anatomy and 111 24 minutes in type I1 anatomy ( p = NS). The aortic cross-clamp time was 53 ? 12 minutes in the group with type I anatomy and 57 2 9 minutes in the group with type I1 anatomy ( p = NS).
*
Correlation Between Anatomy Type and Number of Grafts The average number of grafts in the group with a type I lesion was was 2.8 ? 0.6 and in the group with type 11, 3.2 2 0.6 ( p = NS).
Correlation Between Conduction Disturbances and Number of Grafts
*
The 11 patients with CD had 3 0.4 grafts per patient and the 44 patients without CD had 2.8 0.6 grafts per patient ( p = NS).
*
Correlation Between Perioperative Acute Myocardial Infarction and Anatomical Type Five patients with type I anatomy had myocardial infarction (2 subendocardial and 3 transmural) without CD. Two patients with type I1 had myocardial infarction (one subendocardial anterior and one transmural lateral) without CD ( p = NS). Blood creatine kinase-MB level was examined in 4 patients with CD (all had complete AV block); it was increased in 2 and normal in the remaining 2. Results of a postoperative thallium effort test were available in 6 patients. In 5 of them (4 with type I anatomy) it did not show septal hypoperfusion, and these patients did not have CD. The sixth patient had a reversible septal hypoperfusion and a large fixed defect in the inferoposterolateral wall. This patient had type IIa anatomy with no retrograde filling of septal branches, and after operation he had new permanent LBBB.
Comment Preoperative and perioperative factors that have been investigated to determine the cause of CD include previous CD, left ventricular function, previous digitalis therapy, previous myocardial infarction, number of grafts, and the duration of cardiopulmonary bypass and aortic clamp time. Some workers found a positive correlation, but this was not confirmed by others. The relevant literature is summarized in Table 1. Several anatomical data of the coronary arteries have been investigated and related to post-CABG conduction disturbances: the number of diseased coronary arteries was not found to be predictive (4, 81 but a correlation between RBBB and triple-vessel disease has been described [9]. Total occlusion of the LAD or right coronary artery [4, 81 or occlusion of both arteries [4] were unrelated to CD. Recently, RBBB and LAHB were found to be common in patients with left main coronary artery disease (41. The present study was undertaken to determine the anatomical basis for predicting post-CABG CD. The prox-
MOSSERI ET AL POST-CABG CONDUCTION & CORONARY ANATOMY
Ann Thorac Surg 1991;51:2&52
Table 1 . Perioperative Factors in the Genesis of Postoperative Conduction Disturbances as Described in the Literature Rela tionship
Factor Preoperative Previous conduction disturbances Left ventricular function Digitalis Old anterior wall infarction Old inferior wall infarction Angiographic characteristics Left main coronary artery disease Triple-vessel disease Combined LAD and RCA disease Operative Cold potassium cardioplegia Number of grafts Cardiopulmonary bypass time
Aortic clamp time
Positive
None 181 [41 (91
[4, 7",9'1
[41 [9a1
[4r 81 141
PlbI
PI [I, 81
(71 [4,71
[I, 8, 9"l
[4,71
Related to temporary conRelated to right bundle-branch block. duction disturbances. RCA = right coronary LAD = left anterior descending coronary artery; artery.
a
imal bundle branches are located in the upper interventricular septum and are supplied by the first perforating branch of the LAD artery. It is obvious that a normal LAD is unrelated to postoperative CD. In contrast, we found that discrete lesions of the LAD (even when severe) that do not include the origin of the perforating branch did not put the patient at risk. In this anatomical subset (type Ib) coronary blood flow to the septal branches is maintained from the native coronary artery or the graft. On the other hand, in type I1 lesions, flow to the septal branches is compromised. The lesions are more important when retrograde flow from the right coronary artery to the septal branches is poor or absent. The damage to the conduction system in these cases may appear in this locus minoris resistentia during the period before or after aortopulmonary bypass if flow decreases and is inadequate or if cardioplegia is imperfect or prolonged. The combination of the coronary anatomy type with the operative technique may thus be important. Even if cardiopulmonary bypass is optimal, the improved flow from the graft may increase the perfusion pressure in the distal LAD and thereby decrease competitive flow proximal to the LAD graft including the perforator branch. Indeed, progression of proximal artery disease is accelerated in grafted arteries [12] and may be due to decreased laminar flow proximally
251
to the graft. Good septal collateral flow, however, may prevent CD. The differentiation between type I and I1 anatomy is straightforward. Because anatomical patterns ranging from a single large proximal septal perforator to a multitude of smaller septal vessels do exist, the subclassification in group I1 is sometimes more difficult; in a diffusely diseased LAD system with very little or no flow in the septal branches, it is difficult to decide what was the original size of the perforator arteries. Also, some of the patients were classified as having combined IIb and IIc lesions. Such anatomical differences between patients may contribute to the type, severity, and permanence of CD manifested in an individual patient. However, because the difference in rate of CD was found between anatomy types I and 11, the results should not be altered. The most frequent conduction disturbance was LBBB followed by complete AV block and RBBB. Similar findings were noted when the extended group of patients with CD after CABG was examined. The relatively low frequency of RBBB may be related to the good blood supply to this bundle both from the left and right coronary systems. For RBBB to occur, one needs compromised flow to both systems. However, we did not find a significant difference in the frequency of previous inferior or anterior myocardial infarctions in patients with CD. Three patients in the extended group had CD despite type I anatomy. One of them had left main coronary artery disease and another had total LAD occlusion proximal to the first perforator. Occlusion of the graft to the LAD may be the reason for the CD, but none of the patients was recatheterized to support this suggestion. It is also possible that intraoperative factors played a greater role in these patients. Notably, we did not find a correlation between left main coronary lesions and CD as suggested by others [4]. No correlation was found between CD and sex or age. However, the male predominance and the narrow range of age in both anatomy types preclude definite conclusions. No correlation was found between CD and the number of grafts, aortic clamp time, and cardiopulmonary bypass time. In 4 of the patients with CD (complete AV block), the level of creatine kinase-MB was examined. It was increased in 2 and normal in 2. Two patients with type I1 anatomy had electrocardiographic and enzymatic evidence of perioperative acute myocardial infarction but neither had CD. In addition, 5 patients with type I anatomy (and no CD) had perioperative myocardial infarction. Thus, the CD are not related to acute myocardial infarction in general, but rather to localized ischemia in the region of the first perforating branch, which supplies the conduction system. The information obtained by thallium efforttest, in the few patients tested, agreed with the concept presented here to correlate between CD and septal vascularization. Because this study is retrospective and anatomy may have been changed since operation, we did not perform a thallium test on every patient. Two practical implications may be derived from this study. First, intraoperative angioplasty, endarterectomy, or septal artery grafting should be considered in patients
252
MOSSERI ET AL POST-CABG CONDUCTION & CORONARY ANATOMY
with type I1 lesions. Second, patients with type I1 anatomy undergoing CABG require more prolonged monitoring because CD may develop in them and require further interventions such as pacemaker implantation. In conclusion, CD after CABG were found to be related to specific anatomical lesions involving the first perforating artery, which supplies the interventricular septum. Good retrograde filling of the septa1 branches from the right coronary artery before operation protects the heart against postoperative CD. Patients who have anatomical lesions involving the first perforating artery need a direct graft to the first perforating artery, endarterectomy, or intraoperative dilation of the offending lesion.
Ann Thorac Surg 1991;51:24652
6. 7. 8. 9. 10.
References 1. Satinsky JD, Collins JJ Jr, Dalen JE. Conduction defects after cardiac surgery. Circulation 1974;5O(Suppl2):170-4. 2. Selzer A, Cohn K. Asymptomatic coronary artery disease and coronary bypass surgery. Am J Cardiol 1977;39:614-6. 3. Brewer DL, Bilbro RH, Barthel AG. Myocardial infarction as a complication of coronary bypass surgery. Circulation 1973; 4758-64. 4. Caspi Y, Safadi T, Ammar R, Elamy A, Fishman NH, Merin G. The significance of bundle branch block in the immediate postoperative electrocardiograms of patients undergoing coronary artery bypass. J Thorac Cardiovasc Surg 1987;93442-6. 5. Davids HA, Hermans WTH, Hollaar L, Van der Laarse A,
11.
12.
Hysmans HA. Extent of myocardial damage after open heart surgery assessed from serial plasma enzyme level in either of two periods (1975 and 1980). Br Heart J 1982;47167-72. Espinoza J, Lipski J, Litwak R, Donoso E, Dack S . New Q waves after coronary artery bypass surgery for angina pectons. Am J Cardiol 1974;332214. Zeldis SM, Morganroth J, Horowitz LN, et al. Fascicular conduction disturbances after coronary bypass surgery. Am J Cardiol 1978;41:860-4. Baerman JM, Kirsh Mh4, De Buitleir M, et al. Natural history and determinants of conduction defects following coronary artery bypass surgery. Ann Thorac Surg 1987;44:150-3. Bantea C. Bundle branch block after coronary bypass surgery. Am Heart J 1982;104:1114. Rippe JM, Browning C, Vander Salm T, Goldberg R, Alpert JS, Dalen JE. Fascicular conduction disturbances following aortocoronary bypass surgery: the role of hypothermia versus potassium-arrest cardioplegia. J Cardiovasc Surg 1984;25: 456-61. OConnell JB, Wallis D, Johnson SA, Pifarre R, Gunnar RM. Transient bundle branch block following use of hypothermic cardioplegia in coronary artery bypass surgery: high inadence without perioperative myocardial infarction. Am Heart J 1982;103:85-92. 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 1):144-50.
Conduction disturbances after coronary artery bypass grafting may result from compromised septal blood flow. To examine this hypothesis we reviewed the preoperative coronary angiography of 55 consecutive patients undergoing coronary artery bypass grafting. Thirty-five patients had either no lesion or a discrete lesion in the left anterior descending coronary artery that did not include the septal perforator (type I anatomy). Twenty patients had a lesion of the left anterior descending coronary artery at the origin of the first septal branch, a lesion of the first septal artery, or a pair of lesions in the left anterior descending coronary artery that straddled the origin of the first septal artery; all lesions were praximal to the graft site (type I1 anatomy). None of the patients with type I anatomy had a major conduction disturbance after coronary artery bypass grafting. Eleven of the patients with type I1 anatomy had major conduc-
tion disturbances after coronary artery bypass grafting; right bundle-branch block in 1, right bundle-branch block and left anterior hemiblock in 2, left bundlebranch block in 5, and complete atrioventricular block that required pacemaker implantation in 3 ( p < 0.001). In the 20 patients with type 11 anatomy, the appearance of conduction disturbances correlated well with the absence of retrograde flow to the septal branches from the right coronary artery ( p < 0.01). Pathological lesions in the left anterior descending coronary artery that compromise flow in the first perforator and that do not provide an adequate circulation produce localized damage and conduction disturbances after coronary artery bypass grafting. This can be predicted from the preoperative angiographic anatomy.
C
Patients and Methods
onduction disturbances (CD) after coronary artery bypass grafting (CABG) are well known and occur with an incidence of 4% to 34% [1-4]. Improved myocardial preservation and the use of cardioplegia has decreased the incidence of intraoperative myocardial injury [5,6]. Nonetheless, the incidence of postoperative CD has remained high [4, 7-10]. Cold potassium cardioplegia used today is associated with a 34% incidence of right bundle-branch block (RBBB) (often temporary) compared with 6% in a control group using ischemic arrest and intermittent perfusion [ll]. The suggestion that CD are induced by global ischemia during CABG is probably too simplistic. The present study was undertaken to determine whether there is a specific anatomical group of patients who are at risk for postoperative CD after CABG. We studied 55 consecutive patients who underwent open heart operations.
Accepted for publication Oct 17, 1990. Address reprint requests to Dr Gotsman, Department of Cardiology, Kiryat Hadassah, PO Box 12000, Jerusalem, Israel 91-120.
0 1991 by The
Society of Thoracic Surgeons
(Ann Thoruc Surg 1992;52:248-52)
Three hundred twenty-nine patients underwent their first coronary artery bypass graft operation in the Surgical Department at Hadassah Hospital during a 3-year period. Of them, 55 consecutive patients were referred from the Cardiological Department in Hadassah Hospital. These patients are the subjects of the present study. Patients who also had aneurysmectomy, ventricular septal defect repair, or valvar operation were not included. All patients underwent coronary artery bypass grafting under general anesthesia. Cardiopulmonary bypass was instituted with a bubble oxygenator. Myocardial preservation was achieved by core cooling to 24" to 26°C. St. Thomas' cardioplegic solution (1,400 to 2,500 mL per patient) was delivered through the ascending aorta. Cardiac and septal temperatures were monitored and were in the range of 8" to 15°C. Supplemental cardioplegia was delivered through vein grafts and the ascending aorta every 30 minutes. The heart was further cooled with topical iced saline solution. The following preoperative and perioperative details were noted: age, sex, previous myocardial infarction, cardiopulmonary bypass and aortic clamp time, perioperative myocardial infarction, old and perioperative conduction disturbances, and number and site of coronary bypass grafts. 0003-4975/91/$3.50
MOSSERI ET AL POST-CABG CONDUCTION & CORONARY ANATOMY
Ann Thorac Surg 1991;51:24%52
\
11 a
la
Fig 1 . Classification of lesions in the left corona y system: type 1, lesions not related to septal branches; type 11, lesions related to septal branches (a, left anterior descending [LAD] lesion at the origin of a septa/ branch; b, pair of LAD lesions straddling the septal artey ; c, discrete lesion of the septal artey). (G = graft to LAD; 1P = first perforator.)
I b
I1 b
Twelve-lead electrocardiograms were routinely recorded within 6 hours after operation and daily thereafter until discharge. Earlier electrocardiograms were recorded when the monitor was suggestive of ST-T changes or conduction disturbances. Blood creatine kinase examinations were performed in all patients with suspected myocardial infarction and in some patients with conduction disturbances without electrocardiographic evidence for myocardial infarction. Perioperative transmural myocardial infarction was diagnosed whenever a new Q wave unrelated to CD appeared in two leads in the electrocardiogram. A subendocardial wall infarction was diagnosed when ST-T changes (unrelated to CD and with no Q wave) appeared in any two leads and were accompanied with an increase in blood creatine kinase-MB level (>160 IUL). Perioperative “major” CD were defined as complete right or left bundle-branch block (LBBB)or complete atrioventricular block. Conduction disturbances were persistent if they were still existing in the electrocardiogram at discharge. A postoperative thallium effort test (1 to 6 months after operation) to confirm or exclude septal hypoperfusion was available only in a minority of patients. To increase the number of patients with postoperative CD, we analyzed the 11 of our consecutive 55 patients in whom CD developed and added another 12 patients with postoperative CD who had undergone angiography and operation in previous years. This created an extended group of patients with perioperative CD who were examined separately. Coronary angiography was performed on a 4.5-inch General Electric image intensifier with an overframing lens to obtain maximum magnification. Angiograms were
249
I1 c
made in at least five different oblique projections including the craniocaudal projection. The coronary angiographic examinations performed before CABG were reviewed by a cardiologist who was blinded to the presence of CD. Lesions of more than 70% in one view were graded as serious. A detailed description of the lesions in the coronary arteries and their branches was drawn. Type I anatomy was defined as either no lesion (type Ia) or a discrete lesion in the left anterior descending coronary artery unrelated to the septal branches (type Ib) (Fig 1). Type I1 anatomy was defined as a lesion of the left anterior descending coronary artery (LAD)at the origin of a septal branch (IIa), a pair of lesions in the LAD straddling the septal artery (IIb), or a discrete lesion of the septal artery (IIc) all proximal to the graft anastomosis (Fig 1). Retrograde filling of the septum and the perforating arteries from the right coronary system was assessed qualitatively as good, moderate, poor, or none. All continuous data were presented as mean standard deviation. The correlation between the anatomical types and the CD and between CD and retrograde filling of the septal arteries were tested by the Fisher’s exact test. A comparison of the number of grafts in the two anatomical groups was performed using Student’s t test.
*
Results We studied 55 patients, 48 men and 7 women. Their mean age was 59 ? 7 years (range, 46 to 70 years). Thirty-five patients (age, 60 ? 4.7 years) had type I anatomy; 14 had type Ia and 21 had type Ib. Twenty patients (age, 58.2 6.6 years) were found to have type I1 anatomy. Of these, 3 patients had type IIa lesions, 8 patients had a type IIb
*
250
MOSSERI ET AL POST-CABG CONDUCTION & CORONARY ANATOMY
lesion, and 5 patients had type IIc lesions. Four patients had both type IIb and IIc lesions. Twenty-nine of the 35 patients with type I anatomy and 19 of the 20 with type I1 anatomy were male.
Correlation Between Conduction Disturbances and Pathological Anatomy None of the 35 patients with type I anatomy had postoperative CD. Of the 20 patients with type I1 anatomy, 11 (55%)had major postoperative CD ( p < 0.001). Only 1 patient with type I1 anatomy had preoperative CD (RBBB + left anterior hemiblock [LAHB]). After CABG he had temporary complete atrioventricular (AV) block that did not require permanent pacemaker implantation. No patient with type I anatomy had preoperative CD. Four patients with type I and 1 patient with type I1 anatomy had left main coronary disease (>40% narrowing), and none had CD.
Correlation Between Retrograde Filling of Septa1 Branches and Conduction Disturbances Of patients with type I1 anatomy, 6 of the 9 patients without CD and only 1of the 11with CD had moderate or good retrograde filling of the septum from the posterior interventricular branch of the right coronary artery ( p < 0.01). In patients with type I anatomy, 16 of 35 patients (all of them with type Ib) had moderate or good retrograde filling.
Types of Conduction Disturbances in Type II Anatomy Eleven of the 20 patients with type I1 anatomy had one or more CD. Four of them had permanent LBBB, one had permanent RBBB, two had permanent RBBB and LAHB and 2 had permanent complete AV block that required implantation of a permanent pacemaker. Another patient had temporary LBBB that was followed by permanent LAHB, whereas another had temporary complete AV block requiring a permanent pacemaker implantation.
Correlation Between Previous Myocardial Infarction and Conduction Disturbances One patient of 18 with a previous inferior myocardial infarction, 1 of 12 with previous anterior wall infarction, and 1 of 4 with both previous inferior and anterior myocardial infarctions had a major conduction disturbance. Three of the 21 patients with no previous myocardial infarction had major CD ( p = not significant [NS]).
Distribution of Conduction Disturbances in the Extended Group In the extended group with CD, 20 of 23 patients had type I1 anatomy. Their CD included complete AV block in 10 patients (temporary in 2), LBBB in 9 patients (temporary in 3), and RBBB in 4 patients. Four of them had LAHB and 1 had left posterior hemiblock. Three of the 23 patients had complete AV block (temporary in one) and type Ib anatomy and in all 3 there was no retrograde flow to septal branches. In 1 of them there was a 90% left main coronary artery lesion and in another total LAD coronary artery occlusion proximal to the first perforator. Other CD did not appear in patients with type I anatomy.
Ann Thorac Surg 1991;51:24&52
Correlation Between Operative Technique and Conduction Disturbances
*
The cardiopulmonary bypass time was 107 22 minutes in type I anatomy and 111 24 minutes in type I1 anatomy ( p = NS). The aortic cross-clamp time was 53 ? 12 minutes in the group with type I anatomy and 57 2 9 minutes in the group with type I1 anatomy ( p = NS).
*
Correlation Between Anatomy Type and Number of Grafts The average number of grafts in the group with a type I lesion was was 2.8 ? 0.6 and in the group with type 11, 3.2 2 0.6 ( p = NS).
Correlation Between Conduction Disturbances and Number of Grafts
*
The 11 patients with CD had 3 0.4 grafts per patient and the 44 patients without CD had 2.8 0.6 grafts per patient ( p = NS).
*
Correlation Between Perioperative Acute Myocardial Infarction and Anatomical Type Five patients with type I anatomy had myocardial infarction (2 subendocardial and 3 transmural) without CD. Two patients with type I1 had myocardial infarction (one subendocardial anterior and one transmural lateral) without CD ( p = NS). Blood creatine kinase-MB level was examined in 4 patients with CD (all had complete AV block); it was increased in 2 and normal in the remaining 2. Results of a postoperative thallium effort test were available in 6 patients. In 5 of them (4 with type I anatomy) it did not show septal hypoperfusion, and these patients did not have CD. The sixth patient had a reversible septal hypoperfusion and a large fixed defect in the inferoposterolateral wall. This patient had type IIa anatomy with no retrograde filling of septal branches, and after operation he had new permanent LBBB.
Comment Preoperative and perioperative factors that have been investigated to determine the cause of CD include previous CD, left ventricular function, previous digitalis therapy, previous myocardial infarction, number of grafts, and the duration of cardiopulmonary bypass and aortic clamp time. Some workers found a positive correlation, but this was not confirmed by others. The relevant literature is summarized in Table 1. Several anatomical data of the coronary arteries have been investigated and related to post-CABG conduction disturbances: the number of diseased coronary arteries was not found to be predictive (4, 81 but a correlation between RBBB and triple-vessel disease has been described [9]. Total occlusion of the LAD or right coronary artery [4, 81 or occlusion of both arteries [4] were unrelated to CD. Recently, RBBB and LAHB were found to be common in patients with left main coronary artery disease (41. The present study was undertaken to determine the anatomical basis for predicting post-CABG CD. The prox-
MOSSERI ET AL POST-CABG CONDUCTION & CORONARY ANATOMY
Ann Thorac Surg 1991;51:2&52
Table 1 . Perioperative Factors in the Genesis of Postoperative Conduction Disturbances as Described in the Literature Rela tionship
Factor Preoperative Previous conduction disturbances Left ventricular function Digitalis Old anterior wall infarction Old inferior wall infarction Angiographic characteristics Left main coronary artery disease Triple-vessel disease Combined LAD and RCA disease Operative Cold potassium cardioplegia Number of grafts Cardiopulmonary bypass time
Aortic clamp time
Positive
None 181 [41 (91
[4, 7",9'1
[41 [9a1
[4r 81 141
PlbI
PI [I, 81
(71 [4,71
[I, 8, 9"l
[4,71
Related to temporary conRelated to right bundle-branch block. duction disturbances. RCA = right coronary LAD = left anterior descending coronary artery; artery.
a
imal bundle branches are located in the upper interventricular septum and are supplied by the first perforating branch of the LAD artery. It is obvious that a normal LAD is unrelated to postoperative CD. In contrast, we found that discrete lesions of the LAD (even when severe) that do not include the origin of the perforating branch did not put the patient at risk. In this anatomical subset (type Ib) coronary blood flow to the septal branches is maintained from the native coronary artery or the graft. On the other hand, in type I1 lesions, flow to the septal branches is compromised. The lesions are more important when retrograde flow from the right coronary artery to the septal branches is poor or absent. The damage to the conduction system in these cases may appear in this locus minoris resistentia during the period before or after aortopulmonary bypass if flow decreases and is inadequate or if cardioplegia is imperfect or prolonged. The combination of the coronary anatomy type with the operative technique may thus be important. Even if cardiopulmonary bypass is optimal, the improved flow from the graft may increase the perfusion pressure in the distal LAD and thereby decrease competitive flow proximal to the LAD graft including the perforator branch. Indeed, progression of proximal artery disease is accelerated in grafted arteries [12] and may be due to decreased laminar flow proximally
251
to the graft. Good septal collateral flow, however, may prevent CD. The differentiation between type I and I1 anatomy is straightforward. Because anatomical patterns ranging from a single large proximal septal perforator to a multitude of smaller septal vessels do exist, the subclassification in group I1 is sometimes more difficult; in a diffusely diseased LAD system with very little or no flow in the septal branches, it is difficult to decide what was the original size of the perforator arteries. Also, some of the patients were classified as having combined IIb and IIc lesions. Such anatomical differences between patients may contribute to the type, severity, and permanence of CD manifested in an individual patient. However, because the difference in rate of CD was found between anatomy types I and 11, the results should not be altered. The most frequent conduction disturbance was LBBB followed by complete AV block and RBBB. Similar findings were noted when the extended group of patients with CD after CABG was examined. The relatively low frequency of RBBB may be related to the good blood supply to this bundle both from the left and right coronary systems. For RBBB to occur, one needs compromised flow to both systems. However, we did not find a significant difference in the frequency of previous inferior or anterior myocardial infarctions in patients with CD. Three patients in the extended group had CD despite type I anatomy. One of them had left main coronary artery disease and another had total LAD occlusion proximal to the first perforator. Occlusion of the graft to the LAD may be the reason for the CD, but none of the patients was recatheterized to support this suggestion. It is also possible that intraoperative factors played a greater role in these patients. Notably, we did not find a correlation between left main coronary lesions and CD as suggested by others [4]. No correlation was found between CD and sex or age. However, the male predominance and the narrow range of age in both anatomy types preclude definite conclusions. No correlation was found between CD and the number of grafts, aortic clamp time, and cardiopulmonary bypass time. In 4 of the patients with CD (complete AV block), the level of creatine kinase-MB was examined. It was increased in 2 and normal in 2. Two patients with type I1 anatomy had electrocardiographic and enzymatic evidence of perioperative acute myocardial infarction but neither had CD. In addition, 5 patients with type I anatomy (and no CD) had perioperative myocardial infarction. Thus, the CD are not related to acute myocardial infarction in general, but rather to localized ischemia in the region of the first perforating branch, which supplies the conduction system. The information obtained by thallium efforttest, in the few patients tested, agreed with the concept presented here to correlate between CD and septal vascularization. Because this study is retrospective and anatomy may have been changed since operation, we did not perform a thallium test on every patient. Two practical implications may be derived from this study. First, intraoperative angioplasty, endarterectomy, or septal artery grafting should be considered in patients
252
MOSSERI ET AL POST-CABG CONDUCTION & CORONARY ANATOMY
with type I1 lesions. Second, patients with type I1 anatomy undergoing CABG require more prolonged monitoring because CD may develop in them and require further interventions such as pacemaker implantation. In conclusion, CD after CABG were found to be related to specific anatomical lesions involving the first perforating artery, which supplies the interventricular septum. Good retrograde filling of the septa1 branches from the right coronary artery before operation protects the heart against postoperative CD. Patients who have anatomical lesions involving the first perforating artery need a direct graft to the first perforating artery, endarterectomy, or intraoperative dilation of the offending lesion.
Ann Thorac Surg 1991;51:24652
6. 7. 8. 9. 10.
References 1. Satinsky JD, Collins JJ Jr, Dalen JE. Conduction defects after cardiac surgery. Circulation 1974;5O(Suppl2):170-4. 2. Selzer A, Cohn K. Asymptomatic coronary artery disease and coronary bypass surgery. Am J Cardiol 1977;39:614-6. 3. Brewer DL, Bilbro RH, Barthel AG. Myocardial infarction as a complication of coronary bypass surgery. Circulation 1973; 4758-64. 4. Caspi Y, Safadi T, Ammar R, Elamy A, Fishman NH, Merin G. The significance of bundle branch block in the immediate postoperative electrocardiograms of patients undergoing coronary artery bypass. J Thorac Cardiovasc Surg 1987;93442-6. 5. Davids HA, Hermans WTH, Hollaar L, Van der Laarse A,
11.
12.
Hysmans HA. Extent of myocardial damage after open heart surgery assessed from serial plasma enzyme level in either of two periods (1975 and 1980). Br Heart J 1982;47167-72. Espinoza J, Lipski J, Litwak R, Donoso E, Dack S . New Q waves after coronary artery bypass surgery for angina pectons. Am J Cardiol 1974;332214. Zeldis SM, Morganroth J, Horowitz LN, et al. Fascicular conduction disturbances after coronary bypass surgery. Am J Cardiol 1978;41:860-4. Baerman JM, Kirsh Mh4, De Buitleir M, et al. Natural history and determinants of conduction defects following coronary artery bypass surgery. Ann Thorac Surg 1987;44:150-3. Bantea C. Bundle branch block after coronary bypass surgery. Am Heart J 1982;104:1114. Rippe JM, Browning C, Vander Salm T, Goldberg R, Alpert JS, Dalen JE. Fascicular conduction disturbances following aortocoronary bypass surgery: the role of hypothermia versus potassium-arrest cardioplegia. J Cardiovasc Surg 1984;25: 456-61. OConnell JB, Wallis D, Johnson SA, Pifarre R, Gunnar RM. Transient bundle branch block following use of hypothermic cardioplegia in coronary artery bypass surgery: high inadence without perioperative myocardial infarction. Am Heart J 1982;103:85-92. 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 1):144-50.