Coronary Angiographic Characteristics of Patients With Permanent Artificial Pacemakers
Background The cause of severe cardiac conduction disturbances is often uncertain. The aim of this study was to examine a group of patients with permanent pacemakers who underwent coronary arteriography to determine the extent of coronary atherosclerotic disease that might be responsible for the conduction disturbances.
Methods and Results Forty-three consecutive patients with a permanent pacemaker and 36 matched control patients were investigated. The coronary angiographic study included measurement of diameter and stenosis severity, qualitative assessment of flow, and classification of pathological anatomy, particularly the blood supply to territories supplying the different segments of the conduction system. Among 43 patients with a permanent pacemaker, 27 had ischemic heart disease (17 after coronary artery bypass graft surgery). The conduction disturbance was infranodal in 28 patients, sinus nodal in 6, AV nodal in 4, and complete AV block of unspecified origin in 5. Patients with permanent pacemakers had a coronary artery pathology compromising blood flow to the septal branches and the right coronary artery (type IV anatomy). This pattern was significantly different from the matched control patients, in whom the most prevalent coronary anatomy was the combination of right coronary artery with distal left anterior descending artery (not involving the septal branches) lesions (P=.007).
Conclusions Patients with coronary artery disease and severe conduction disturbances that require implantation of permanent pacemakers are more likely to have a specific pathological coronary anatomy that combines a compromised blood flow to the septal branches of the left anterior descending artery with right coronary artery lesions. The location of lesions in the coronary tree rather than severe diffuse atherosclerosis appears to be responsible for the conduction disturbances.
Conduction disturbances of the heart may affect the sinoatrial and AV nodes and the intraventricular conduction system. Symptomatology ranges from weakness to loss of consciousness and death. Patients with persistent or recurrent symptomatic conduction disturbances need permanent pacemaker implantation. Acute conditions that may cause conduction disturbances include myocardial infarction, electrolyte disturbances, drugs (eg, digitalis), myocarditis (eg, rheumatic or viral), cardiac trauma, cardiac surgery, and others. The chronic conduction disturbances are due to degenerative conditions, often without other identifiable myocardial disease. They may also be due to cardiomyopathy or hypertensive or congenital heart disease. Some patients with permanent pacemakers have overt or latent atherosclerotic heart disease, which causes conduction disturbances, probably by inducing conduction-system ischemia. The results of several small studies have been inconclusive.1 2 3 4 In many patients, the cause is not known.
The present study examined retrospectively the coronary anatomy and pathology of 43 consecutive patients who had permanent pacemaker implantation and coronary angiography to find a common pathological-anatomic basis for conduction disturbances and compared them with a group of matched patients with angiographically proven coronary artery disease.
We studied 458 consecutive patients who underwent permanent pacemaker implantation between 1984 and 1992. Forty-three of these patients had also undergone coronary angiography within 2 years before or after pacemaker implantation. They composed the study group. None of these patients received β-blockers, calcium blockers, or other medications responsible for sinus node dysfunction or conduction disturbances.
Matched Control Group
To each patient from the study group, we matched a patient without a pacemaker using the following criteria: sex, age within 5 years of the study group patient, presence or absence of diabetes mellitus and hypertension, with or without CABG, and presence or absence of significant (>50%) narrowing in the coronary arteries responsible for supplying blood to the conduction system (LAD [source of the septal branches] and the artery that gives rise to the branches to the SA and AV nodes [either RCA or LCx]). For matching, we used the presence or absence of lesions in each coronary artery but without regard to their locations in a specific segment.
Hypertension, diabetes mellitus, and left ventricular dysfunction were used as matching criteria because they are known causes of conduction disturbances and left ventricular dysfunction, which may result in conduction disturbances.5 6 7 Smoking and hypercholesterolemia, risk factors for atherosclerosis but not for conduction disturbances, were not used as matching criteria.
Age, sex, height, weight, performance of PTCA or CABG, previous conduction disturbances, and the conduction abnormality for which the pacemaker was implanted were recorded. Details of underlying cardiac disease, blood pressure, and fasting blood glucose and serum cholesterol levels were also recorded or measured.
Coronary angiography was performed with the use of diagnostic catheters of known and recorded diameter (6F to 8F). Two investigators blinded to the clinical data of the patients (except for 10 cineangiography films in which the electrodes of previously implanted permanent pacemakers were visible) read the ECGs and analyzed the cine films. Coronary artery diameter was measured with manual calipers. This method has been validated in our laboratory against computerized quantitative coronary angiography measurements (r=.91), and the interobserver and intraobserver repeatability of this method in our laboratory is 0.94 and 0.93, respectively.
The dominance of the coronary tree was determined and documented according to the criteria of Dodge et al.8
Assessment of Pathological Coronary Anatomy Findings
Narrowings in the coronary tree were identified in the following arteries and branches: left main, LAD, first three perforators, first diagonal, LCx, first marginal, RCA, right ventricular branch, PL, PDA, SAN, and AVN. Each lesion diameter was compared with an adjacent distal normal-looking segment, and lesion severity was graded in the following manner: 0% to 50%, insignificant; 50% to 70%, significant; 70% to 90%, moderate; and >90%, severe. Left main coronary artery, LAD, and LCx were measured in the anteroposterior view; perforators, ramus medianus, and first marginal in the RAO view; first diagonal in the RAO or caudocranial LAO view; and RCA, right ventricular branch, PL, PDA, SAN, and AVN in the LAO view. The diameter of the diagnostic catheter was used as a reference for calculating absolute arterial diameters. All measurements were made in the field center to reduce pincushion distortion.
Classification of Pathological Coronary Anatomy Supplying the Conduction System
The location of narrowings in the LAD and RCA (or LCx for dominant left coronary system) as the arteries supplying the conduction system was documented accurately and classified as follows (Figure⇓)9 :
Type I: Anatomy not compromising blood supply to the conduction system, namely, either the absence of significant narrowing in the LAD, RCA, LCx, PL, or PDA or the presence of mid-distal LAD lesions past the septal branches.
Type II: Pathological coronary anatomy involving septal branches emerging from the LAD (and without significant lesions in the RCA)—II-0, narrowing of the LAD before the septal branches; II-A, narrowing of the LAD at the origin of the septal arteries; II-B, narrowings of the LAD both before and after the origin of the septal branches; and II-C, narrowing of the septal branches.
Type III: Pathological coronary anatomy compromising blood supply to the SA or AV node but not compromising blood flow to the septal branches. This subset included patients with distal LAD lesions after the septal branches.
Type IV: Combination of types II and III—pathological coronary anatomy that compromises blood supply both to the septal branches and to the SA or AV branch. IV-0 indicates narrowing of the LAD before emergence of the septal branches and narrowing of the RCA; IV-A, narrowing of the LAD at the origin of the septal arteries and narrowing of the RCA; IV-B, narrowings of the LAD both before and after the origin of the septal branches and narrowing of the RCA; and IV-C, narrowing of the septal branches and of the RCA.
In our original classification of post-CABG patients, narrowing of the LAD before the septal branches was classified as type I-B (without compromised flow to the conduction system) because a bypass graft implanted distally could supply the septal branches retrogradely.9 Because many patients in the present study did not have a bypass graft to protect the septal branches, this lesion was classified as type II-0.
Coronary Artery Diameter of Apparently Normal Segments
To determine whether patients with permanent pacemakers have diffuse atherosclerosis of all the coronary arteries, we measured the diameter of each artery in apparently normal segments and in defined locations: the largest segment of the distal 1.5 cm of the RCA before the bifurcation to the PDA and PL and the largest segment of the proximal 1.5 cm of the studied artery in all other vessels.5 Comparison of grouped arterial diameters was then performed with the use of absolute diameters and diameters adjusted for body surface area.
Measurements of Branches Supplying the Conduction System
Coronary artery measurements included the length as well as the diameter of the following conduction-system supply branches: SA node and AV node arteries emerging from the RCA or LCx were measured close to their origins; the first, second, and third perforating septal branches (P1, P2, and P3) supplying the interventricular septum, which contains the bundle of His and the left and right bundle branches, were measured close to their origins. Although the PDA supplies the inferior part of the interventricular septum, which does not contain specialized conduction tissue, it was studied because it provides retrograde blood flow to the septum in case of compromised flow of LAD septal branches. The lengths of the AV node and perforating branches were also measured. The length of the SA node was not always measured because the angiographer did not focus on this artery. The SAN and AVN branches were measured in the LAO view. The septal branches were measured in the anteroposterior or RAO view.
Qualitative Assessment of Antegrade and Retrograde Flows
Antegrade flow and retrograde flow to branches supplying the conduction system were graded qualitatively in each patient as good, moderate, or poor.
Measurement of Left Ventricular Ejection Fraction
The left ventricular endocardial silhouette was traced from the projected left ventriculogram in end systole and diastole, and volumes were calculated after accurate planimetry.10 The diameter of the diagnostic catheter measured from the same projections was used as a reference for calculating left ventricular volumes.
Comparison of clinical data and of coronary diameters and lengths (absolute and adjusted for body surface area) between the study group and matched control group (patients matched according to coronary anatomy) was performed by use of a paired t test. Distribution of study patients and their matched control patients according to stenosis severity or pathological anatomy types was analyzed with the χ2 test. Distribution of study patients and their matched control patients according to direction (antegrade or retrograde) and quality of blood supply to the conduction system was studied with the χ2 test.
Patients and Clinical Data
The study group comprised 43 patients who had permanent pacemakers and had had coronary angiography. We matched 36 patients without pacemakers from our computerized angiography database (matched control group) to each of 36 patients from the study group. The clinical data of the two groups were comparable (Table 1⇓). Similarly, there were no significant differences in any of the parameters between the 36 study patients and their 36 matched control patients. Twenty-seven patients from the study group had infranodal and no other conduction disturbance. Some patients had underlying cardiac disease known to cause conduction disturbances (valvular heart disease, dilated cardiomyopathy, and heart transplantation). Sixteen patients had infranodal conduction disturbances and no cardiac disease other than coronary disease. We therefore also compared the coronary anatomy of these 16 study patients with their matched control patients.
Characteristics of the Study Group
The clinical diagnosis, location of conduction disturbance in the conduction system, and pathological coronary arterial type of each patient in the study group are given in Table 2⇓. Table 2⇓ also gives the anatomic type of each matched control patient. The pathological anatomic types were not identical in pairs of matched patients because matching took into account the presence of a significant lesion in the coronary arteries without regard to its location in specific segments. In 12 study patients, there was no apparent reason for the conduction disturbance. Of these 12 patients, 6 had coronary artery disease (3 with type I and 3 with type III coronary anatomy) that was unrelated to blood flow to the conduction system. Twenty-seven control patients had ischemic heart disease. In 17 of these patients, conduction disturbances appeared within 1 week of CABG; in 2, it appeared immediately after catheterization and PTCA; and in 8, it was not related to a revascularization procedure. Of 27 control patients with ischemic heart disease, 16 had had a previous myocardial infarction (8 inferior, 5 anterior, 2 anterior and inferior, and 1 anterolateral and posterior). Table 3⇓ describes the conduction disturbances in the study group. Lesions were usually infranodal. Five study patients had complete AV block of unspecified origin.
Comparison of the Study and Matched Control Groups
All matched patients had a dominant RCA (possibly because dominant LCx anatomy is less prevalent in the general population and therefore is more difficult to match). There was no difference in the distribution of patients according to lesion severity between patients in the study group and their matched control patients (Table 4⇓).
Thirty-six patients from the study group and 36 patients from the control group were matched. The distribution of pathological anatomic types in regard to blood supply to the conduction system of these groups is described in Table 5⇓. A statistically significant difference was found between the two groups (P=.007 by χ2): more patients had type IV anatomy (16 patients) in the study group and type III anatomy (10 patients) in the control group. If one combines the anatomic types that compromise blood flow to septal branches (types II and IV) and the anatomic types that do not (types I and III), a significant difference is found between the study group (19 and 17 patients for these combinations, respectively) and control group (8 and 28 patients, respectively) (P=.015 by χ2). Sixteen patients with permanent pacemakers had an infranodal conduction disturbance and no cardiac disease other than coronary disease. Comparison of these patients with their matched control patients yielded similar highly significant differences between the two groups (Table 6⇓). By stratifying on the basis of our matching criteria, including age, sex, diabetes mellitus, and hypertension, we ruled out a possible confounding influence of these criteria on the pathological coronary anatomy. Thus, the difference between the study and the matched control groups is caused by the location of the narrowings in the LAD and the combination with RCA lesions.
RCA lesions were present in an equal number of patients (17 in each group) in both groups (type III or IV anatomy) because the presence or absence of significant lesions in any RCA segment was a matching criterion. None of the patients had a lesion compromising blood flow to the SA node (eg, origin or very proximal RCA lesions). Seventeen patients had pacemaker implantation shortly after CABG; 13 of them had type IV, 2 had type II, and 2 had type III coronary anatomy, whereas none had type I anatomy. Another 10 patients had ischemic heart disease without CABG; 7 of them had type IV, 1 had type II, and 2 had type I coronary anatomy.
There was a tendency for reduced blood flow in the conduction-system supply branches in the study group, but this was not statistically significant (Table 7⇓). A similar analysis of the subset of patients with type IV anatomy did not show a significant difference between the study and control groups.
There was no difference in coronary diameter (absolute or adjusted for body surface area) of apparently normal segments or in the length of the septal arteries and the AVN when the 36 matched control patients were compared with the study group patients (either the 43 patients in the entire study group or the 36 matched patients in the study group). There was also no difference in these parameters when patients with or without ischemic heart disease in the study group were compared.
Chronic degenerative heart diseases may involve the conduction system only (Lenègre’s disease) or calcification and sclerosis of the fibrous cardiac skeleton (Lev’s disease). Other chronic cardiac diseases, such as valvular heart disease (rheumatic or others), cardiomyopathies, hypertensive heart disease, and congenital heart defects, may injure the conduction system. The relationship between conduction disturbances and the underlying pathology has been studied at autopsy, but these patients do not represent the general population, and many of the studies were conducted more than 20 years ago. Since then, the natural history of conduction disturbances has changed, longevity has improved, the spectrum of cardiac diseases has altered, and the treatment of conduction disturbances has been revolutionized by the use of pacemakers. The association between conduction disturbances and atherosclerotic coronary disease has been investigated in only a few small studies in the early 1970s.1 2 3 Coronary angiography performed in some series did not reveal specific coronary arterial lesions, and the anatomy of the branches supplying the conduction system was not studied. Hamby et al4 examined 42 patients with ECG conduction disturbances and symptomatic coronary artery disease. Although most patients had a significant lesion in the LAD coronary artery, there was no correlation with specific lesions. None of the patients in that study needed a permanent pacemaker.
We hypothesized that an atherosclerotic process in arteries that supply regions of conduction may cause disturbances that require pacemaker implantation. We have correlated post-CABG conduction disturbances and preoperative pathological coronary anatomy of the septal branches and have identified specific coronary pathology in the LAD and RCA that compromises blood flow to the conduction system.9 We found that retrograde blood flow to septal branches from the PDA protects the patient against postoperative conduction disturbance. Our present study includes all patients who had pacemaker implantation and coronary angiography at our institution between the years of 1984 and 1992. This series, like the autopsy series, does not represent the general population of patients who require pacemaker implantation. It includes more patients with coronary artery disease. It is unethical to undertake coronary angiography in all patients who have pacemaker implantation, and for this reason, we matched patients in the study group with other patients who had identical coronary artery anatomy and in whom a pacemaker was not inserted. The two groups were then compared.
Pathological Coronary Anatomy in Patients With Permanent Pacemakers
The study and matched control groups had lesions in the same coronary arteries because this was a matching criterion. The severity of the lesions was identical in the two groups (Table 4⇑). The location of the lesions in the proximal LAD in relation to the proximal septal branches and in combination with RCA lesions distinguished the two groups; patients in the study group usually had type IV coronary anatomy: lesions in the proximal LAD that involved the septal branches, together with lesions in the RCA. Patients from the matched control group had more type III lesions: lesions in the RCA with lesions in the distal LAD not involving the septal branches (Tables 5⇑ and 6⇑). This was also true for a subset of patients with infranodal conduction disturbances and coronary artery disease. Thus, the combination of lesions compromising the septal branches and interfering with retrograde flow from the PDA (and possibly disturbing flow to the AV node) is important in the pathogenesis of severe conduction disturbances.
Type II anatomy (involving septal branches) occurred more often in patients in the study group, whereas type I anatomy (not involving septal branches) occurred more often in patients in the matched control group, again emphasizing the importance of lesions in the LAD related to the septal branches.
More patients in the study group had poor blood flow (antegrade and retrograde) to branches supplying the conduction system, but the difference was not significant statistically. Assessment of flow (as well as other coronary anatomy characteristics) was made from the angiographic films, which were not always performed at the time of pacemaker implantation. Thus, in some patients, the flow to these branches may have been altered after angiography, particularly in patients undergoing CABG in whom operative factors may have impaired septal blood flow and caused ischemia of the conduction system.
Degenerative cardiac disease is the most prevalent cause of severe conduction disturbances. Clinically, patients with permanent pacemakers are not known to have more frequent ischemic events than the general population. Our findings may thus seem provocative. On the other hand, the study group comprised only 10% of our overall permanent-pacemaker population. The average age in the study group was 61 years, 10 years younger than that of patients with permanent pacemakers who did not undergo coronary angiography. This implies a different origin for conduction disturbances in the study group patients who underwent coronary angiography: ischemic heart disease. Thus, in patients younger than 65 years old with severe conduction disturbances, further investigation for coronary artery disease should be considered.
Clinical and Conduction Disturbance Characteristics in Patients With Permanent Pacemakers
The most prevalent conduction disturbance in the study group was infranodal (28 of 43 patients), and of these 28 patients, 20 had complete AV block. This may represent the susceptibility of the infranodal region to ischemic or other injuries.
Thirty-one of 43 patients had cardiac disease that could account for their conduction disturbances, the most prevalent being ischemic heart disease. An underlying cardiac disease responsible for conduction disturbance was absent in only 12 patients. Previous studies1 2 included a higher rate of unexplained conduction disturbances.
Fourteen patients with pathological coronary artery anatomy involving the septal branches developed a conduction disturbance shortly after CABG; in 11, the conduction disturbance was infranodal, whereas it was an unspecified complete AV block in the others. This confirms our hypothesis that coronary anatomy that compromises blood flow to septal branches is a risk factor for developing severe conduction disturbance after CABG.9
Diameter and Length of Coronary Arteries and Their Branches in Patients With Permanent Pacemakers
Longer coronary arteries have more branches and supply a larger myocardial mass.8 We found no difference in the length of the septal branches or the AVN between the groups in the present study. This suggests that the volume of tissue containing the AV node and the His bundle and bundle branches is constant and that this factor is irrelevant to the development of conduction disturbances. There was also no difference in coronary artery diameter or the severity of lesions between the two groups. Thus, diffuse atherosclerosis and lesion severity are not responsible for severe conduction disturbances. Rather, it is the location of lesions along the coronary tree that compromises blood flow to the conduction system.
Our cohort of patients with permanent pacemakers who also underwent coronary angiography is biased, has more patients with than without ischemic heart disease, and does not represent the general population of patients with a permanent pacemaker. Nevertheless, the comparison of the study group with a matched control group is valid and yields meaningful results. Coronary angiography is not indicated routinely in patients with permanent pacemakers, and there is no other way to study the pathological anatomy of these patients.
In this study, we found it more convenient to use manual rather than computerized measurements. Because grades of stenosis (severe, moderate, etc) were compared in the first place and exact diameters were compared only for normal segments, manual measurements do not pose a methodological problem. As mentioned in “Methods,” the accuracy of this method at our laboratory is high.
Optimal angiographic views for diameter measurements of each segment were chosen. In some of these views, the distance of the diagnostic catheter (used as a reference) to the x-ray tube was not identical to the distance from the measured segment to the tube. This may cause deviation of measured absolute diameters from the actual ones. Also, pincushion distortion and image magnification may add some inaccuracy. These are inherent drawbacks of any angiographic study. The differences between groups, however, remain undistorted because identical views were used in all groups.
In conclusion, patients with coronary artery disease and severe conduction disturbances that require implantation of permanent pacemakers have a specific pathological coronary anatomy (type IV) with a compromised blood flow to septal branches of the LAD and RCA lesions. The specific location of the lesions in the coronary tree rather than the severity or diffuseness of the atherosclerosis seems to be responsible for these conduction disturbances.
Selected Abbreviations and Acronyms
|AVN||=||artery to AV node|
|CABG||=||coronary artery bypass graft surgery|
|LAD||=||left anterior descending coronary artery|
|LAO||=||left anterior oblique|
|LCx||=||left circumflex coronary artery|
|PDA||=||posterior descending artery|
|PTCA||=||percutaneous transluminal coronary angioplasty|
|RAO||=||right anterior oblique|
|RCA||=||right coronary artery|
|SAN||=||artery to sinoatrial node|
- Received September 5, 1996.
- Revision received February 10, 1997.
- Accepted February 20, 1997.
- Copyright © 1997 by American Heart Association
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