Author + information
- Received November 25, 1998
- Revision received March 29, 1999
- Accepted June 11, 1999
- Published online October 1, 1999.
- Kuo-Chun Hung, MDa,
- Fun-Chung Lin, MDa,
- Ming-Shyan Chern, MDa,
- Hern-Jia Chang, MDa,
- I-Chang Hsieh, MDa and
- Delon Wu, MD, FACCa,* ()
- ↵*Reprint requests and correspondence: Dr. Delon Wu, Chang Gung Memorial Hospital, 199 Tung Hwa North Road, Taipei, Taiwan
The purpose of this study was to investigate the possible mechanism and the clinical significance of transient atrioventricular block (AVB) during dobutamine stress echocardiography (DSE).
Transient AVB occurs rarely during DSE; however, the mechanisms responsible for blocks are unclear.
A retrospective analysis of clinical, echocardiographic, catheterization, revascularization and head-up tilting test data was conducted in patients who developed transient AVB during DSE.
A total of 302 patients with known or suspected coronary artery disease (CAD) underwent DSE before coronary angiography between November 1997 and August 1998. Transient AVB developed in 12 patients during the test. Mobitz I block was noted in six patients and Mobitz II block in the other six patients. Nine of these 12 patients were subsequently shown to have CAD and three had no significant coronary artery stenosis. Mobitz II block was observed only in patients with CAD, while Mobitz I block occurred in three patients with and three patients without CAD (p < 0.05). Eight of the nine patients with CAD underwent a successful coronary angioplasty with or without stenting and a repeat DSE revealed no recurrence of heart block except in one patient. Head-up tilting test in the 12 patients revealed a positive response in three of the nine patients with and all three patients without CAD. A negative head-up tilting test was likely to be observed in patients with, as compared with those without, CAD in this study population (p < 0.05).
Transient AVB is not an infrequent manifestation during DSE. Both myocardial ischemia and neurally mediated vagal reflex may be responsible for this phenomenon. The development of Mobitz II block during DSE is indicative of the presence of CAD. A successful revascularization in patients with CAD who develop transient AVB may abolish this phenomenon.
Dobutamine stress echocardiography (DSE) is an effective and safe tool for diagnosis of coronary artery disease (CAD) (1–4). The most common adverse experiences during DSE are angina pectoris and arrhythmias, which are usually mild and well-tolerated by the patients without specific treatment (5–7). Transient atrioventricular block (AVB) during DSE has been described only occasionally (5,6), but the mechanism and significance of transient AVB during DSE have not been elucidated. This study was conducted to investigate the possible mechanism and the clinical significance of transient AVB during DSE.
From November 1997 through August 1998, 302 patients underwent DSE for evaluation of CAD at Chang Gung Memorial Hospital in Taipei, Taiwan. Twelve (4%) of the 302 patients who developed transient second degree AVB during DSE were the population of this study. All study patients received cardiac catheterization and coronary angiography within two days after DSE. Percutaneous transluminal coronary angioplasty (PTCA) with or without stenting was performed to lesions with ≥50% stenosis. Follow-up DSE was performed in patients who had a successful coronary revascularization three to seven days later. A head-up tilting test was performed in all patients. The study was retrospective in nature and the protocol of DSE was reviewed and approved by the institutional review board and was in accordance with the local ethical standards.
Dobutamine stress echocardiography was performed using a Vingmed CFM 800 system (Vingmed Sound, Horten, Norway) with a 2.5-MHz transducer. Images were acquired from parasternal long- and short-axis views as well as apical two- and four-chamber views, with the patient in the left lateral recumbent position. After recording the baseline echocardiography, dobutamine was administered intravenously by an infusion pump at 5 μg/kg body weight per min for 3 min, which was subsequently increased at a step of 10 μg/kg per min every 3 min to a maximum of 40 μg/kg per min. Atropine (0.25 mg per min to a maximum of 1 mg) was then injected if 85% of the predicted maximal heart rate (220 minus age for men and 200 minus age for women) was not reached. A 3-lead electrocardiogram (ECG) was continuously monitored and the blood pressure was measured by an automatic device every 3 min. The echocardiogram was continuously monitored throughout the test, recorded on videotape and digitized on floppy disk which could be displayed side by side in a quad screen format to facilitate the comparison of the images at various stages. The test was discontinued if severe angina pain, achievement of 85% of the predicted maximal heart rate, extensive new wall motion abnormalities, ST segment elevation >0.1 mV, severe hypertension (blood pressure ≥240/120 mm Hg), hypotension (decrease in systolic blood pressure ≥40 mm Hg), significant tachyarrhythmias or other intolerable side effects developed during the test. In the event of severe angina and manifestation of ischemia, sublingual nitroglycerin or intravenous esmolol or both were administered.
Analysis of echocardiography
The wall motion was analyzed by dividing the left ventricle into 16 segments, as recommended by the American Society of Echocardiography (8). Regional wall motion was semiquantified using a 4-point scoring system: 1 = normal contraction, 2 = hypokinesia, 3 = akinesia, 4 = dyskinesia. Global wall motion score index (WMSI) at each stage was calculated according to the standard formula: sum of the segment scores/number of segments scored. A positive test was defined as the development of a new or worsening of wall motion dyssynergy. In addition, a biphasic response with an initial improvement of dyssynergy followed by worsening of dyssynergy was considered as a positive test.
Coronary angiography and revascularization
Coronary angiography using the Judkins technique was performed within one to two days after DSE. The severity of coronary stenosis was determined by calipers and expressed as a percent of luminal diameter reduction to the nearby normal segment. Significant CAD was defined as ≥50% stenosis of at least one epicardial artery.
Coronary angioplasty with or without stent implantation was performed on all lesions with significant stenosis using standard techniques through the femoral artery. Successful revascularization was defined as ≥20% reduction in luminal diameter stenosis with <50% final residual diameter stenosis. Complete revascularization was defined when all diseased vessels displayed no residual stenosis ≥50% in all coronary arteries.
Follow-up DSE was performed in those patients with successful coronary revascularization within three to seven days. The hemodynamic variables and WMSI were compared before and after revascularization in these patients.
Head-up tilting test
The head-up tilting test was performed several days after coronary angiography or coronary revascularization in all patients after fasting for at least 8 h. All cardiovascular drugs were discontinued 48 h before the test. The ECG was continuously displayed and the blood pressure measured at 2-min intervals. After a 10-min resting period in supine position, the patients were elevated to an 80° head-tilt position for 5 min. If syncope, bradycardia or hypotension was not observed, the same procedure was repeated with isoproterenol infusion at a stepwise dose increment of 1, 2 and 4 μg/min sequentially. A positive head-up tilting test was defined as the development of near-syncope or syncope in association with bradycardia, hypotension or both. Bradycardia was defined as the heart rate below 60 beats/min and a decline in the heart rate by at least 20 beats/min from the baseline value. Hypotension was considered when the absolute systolic blood pressure was less than 90 mm Hg or the decrease in systolic blood pressure was more than 50% of the maximal value observed in the upright position (9,10).
Mobitz I block is a type of second degree AVB with progressive lengthening of PR (interval between p wave and QRS complex) interval before a blocked P wave, while Mobitz II block is a sudden unexpected blocked P wave without changes in PR interval. For the purpose of analysis, 2:1 or high grade AVB associated with Mobitz I block was analyzed as Mobitz I block, while 2:1 or high grade AVB without changes in PR interval or Mobitz I block was analyzed as Mobitz II block.
Data are expressed as mean ± SD. Paired Student ttest was used for comparison of paired data. Differences between the groups with and without CAD were assessed by chi-square analysis. Student ttests were used to assess the association of each variable separately for the patients with and without transient AVB. A value of p < 0.05 was considered statistically significant.
Clinical characteristics (table 1)
All 12 patients were men with an average age of 51 ± 12 years (range 32–72). Five patients had angina pectoris, 4 had recent myocardial infarction, 1 had congestive cardiomyopathy with an ECG suggestive of old myocardial infarction and 2 had atypical chest pain. The baseline ECG was normal in five patients and displayed anterior myocardial infarction in four patients and inferior myocardial infarction in three patients. All 12 patients were in sinus rhythm with 1:1 atrioventricular (AV) conduction and normal PR interval. Mobitz type I Wenckebach block developed in six patients and Mobitz type II block developed in the other six patients during DSE (Fig. 1); one of the type I (case 9) and two of the type II block (cases 2 and 7) were associated with 2:1 AVB. Atrioventricular block appeared during dobutamine infusion at a dose of 20 μg/kg per min in 1 patient, 30 μg/kg per min in two patients and at 40 μg/kg per min in 9 patients. The sinus rate at the time of AVB was 74 ± 16 beats/min as compared with a rate of 61 ± 9 beats/min during control. The duration of transient AVB ranged from 0.75 to 3.93 min. One to one AV conduction resumed after intravenous injection of atropine in the six patients with type I AVB, but not in the six patients with type II AVB. In the latter six patients, 1:1 AV conduction resumed after discontinuance of dobutamine.
Coronary angiography and revascularization (table 2)
Coronary angiography demonstrated two-vessel disease in seven patients, one-vessel disease in two patients and patent coronary arteries in the remaining three patients (cases 9, 10 and 12). The lesion was noted in the left anterior descending artery in 5, the circumflex artery in 4 and the right coronary artery in 7. The AV nodal artery was visible in all patients except the 5 patients (cases 2, 4–6 and 11) who had a total occlusion of the right coronary artery. The left ventricular ejection fraction (LVEF) ranged from 0.31 to 0.77 and was normal in nine patients and abnormal in three patients. Wall motion abnormality with local hypokinesia or akinesia was observed in seven patients. Coronary revascularization with balloon angioplasty and stent implantation was performed in the nine patients with significant CAD and was successful in 8 patients. Complete revascularization was achieved in 7 of the latter 8 patients except 1 patient (case 1) who had a residual 55% stenosis in the left circumflex artery. After angioplasty or stenting, the AV nodal artery was visible in all patients except the one (case 2) who had an unsuccessful revascularization.
DSE before and after revascularization (table 1)
Dobutamine stress echocardiography was performed in all 12 patients with or without CAD before coronary angiography and it was repeated in the eight patients who had CAD but with successful revascularization. Dobutamine stress echocardiography demonstrated abnormal wall motion with and without new wall motion abnormalities in 10 of the 12 patients before coronary angiography. Nine of these 10 patients exhibited a CAD by angiogram. Mobitz II AVB developed only in the 6 patients with CAD while Mobitz I AVB occurred in 3 patients with and 3 patients without (χ2= 4, p < 0.05). In the 10 patients with CAD, new wall motion abnormalities were noted during DSE in 8 patients. In 6 of these 8 patients (cases 1, 3, 4, 6, 7 and 12), AVB occurred concomitantly with the onset of new wall motion abnormalities, while in the other 2 patients (cases 8 and 11) it occurred before the onset of new wall motion abnormalities. The repeat DSE in the eight patients with successful revascularization displayed an improvement in the WMSI at rest (1.22 ± 0.23 before and 1.13 ± 0.20 after revascularization, p = 0.02) and during peak dose of dobutamine (1.41 ± 0.23 before and 1.13 ± 0.20 after revascularization, p = 0.001). Only one patient developed AVB during the follow-up DSE (case 11); this patient had Mobitz I block before and after revascularization. In this patient, AVB occurred before the onset of new wall motion abnormalities before revascularization. After revascularization, there were no new wall motion abnormalities during DSE.
Head-up tilting test (table 1)
The head-up tilting test was conducted in all 12 patients. Six displayed a positive response. Three of these 6 patients had CAD and 3 had patent coronary arteries. Four of these six patients manifested with Mobitz I AVB and 2 with Mobitz II AVB during DSE. All 6 patients developed hypotension and severe sinus bradycardia during head-up tilting; 2 experienced syncope and 4 experienced near-syncope. None of these six patients developed AVB during the head-up tilting test. A negative head-up tilting test was observed to be more common in patients with CAD than it was in those without in this group of patients who developed transient AVB during DSE (chi-square = 4, p < 0.05).
Clinical and stress echocardiographic parameters in patients with and without AVB (table 3)
There were no significant differences between patients with and without AVB in gender, cardiac risk factors, previous myocardial infarction, incidence of CAD and medications; however, patients with AVB were younger. There were also no significant differences in the stress echocardiographic parameters between these two groups, including symptoms, heart rate, blood pressure, LVEF, WMSI and new wall motion abnormalities.
Transient AVB is a relatively rare complication during DSE with a reported incidence ranging from 0.6% to 1.1% (5,6). The nature of this complication had not been investigated previously. Transient AVB has been known to occur spontaneously in patients without obvious structural heart disease (11). The type of block is Mobitz type I, usually occurring at midnight, and is associated with sinus bradycardia. Paroxysmal AVB may also occur during exercise in patients with latent disease in the His-Purkinje system (12). In the present series, transient AVB occurred in 4% of patients who underwent a DSE test before coronary angiography and both Mobitz I and Mobitz II block were observed.
Myocardial ischemia and AVB
Mobitz type I second degree AVB is a common manifestation of acute inferior wall infarction because the AV nodal artery arises from the dominant coronary artery at the origin of the posterior descending artery (13). However, the distal AV node may also receive collateral blood supplies from the septal perforating arteries of the proximal left anterior descending artery (14). Bassan et al. (15)analyzed 51 consecutive patients with acute inferior wall infarction and noted some degree of AVB in 11 patients. They found that patients with inferior infarction and proximal left anterior descending artery lesion had a six-fold greater chance of developing block during acute phase of infarction as compared with those without left anterior artery lesion. In contrast, Mobitz type II second degree AVB is a less common complication of acute myocardial infarction and is usually associated with extensive anteroseptal infarction because the His bundle and the proximal bundle branches receive blood supplies from the septal perforating arteries of the left anterior descending artery as well as the posterior descending artery and the AV nodal artery (16). Atrioventricular block, regardless of the type or site of the block complicating acute infarction, is usually transient; the AV conduction resumes during recovery phase of infarction. Histologic studies in patients who had succumbed to acute infarction complicated by AVB usually revealed interstitial edema and cell swelling with only scattered necrosis of the conducting tissue (17). These findings suggest that conducting tissue survives better than the working myocardial cells and ischemia, edema, increased vagal tone or the effects of endogenous adenosine may contribute to the occurrence of AVB during acute infarction. Wilber et al. (18)reported two patients with complete heart block complicating extensive anterior myocardial infarction in whom a late angioplasty was performed. One to one AV conduction resumed within minutes of reperfusion despite a lack of measurable ventricular muscle salvage as demonstrated by ventriculography one week later. Moreyra et al. (19)reported a patient with congestive heart failure and complete AVB with no evidence of acute infarction. Coronary angiography revealed a 95% stenosis of the middle third of the right coronary artery, 50% stenosis of the left main coronary artery and 50% stenosis of the proximal left anterior descending artery. Coronary angioplasty to the right coronary artery was conducted one week after the onset of AVB. Within 24 h after reperfusion, 1:1 AV conduction with first degree block was observed. Four days after reperfusion, the PR interval returned to normal. Kovac et al. (20)described a patient with recurrent syncope and episodes of paroxysmal AVB preceded by asymptomatic ST elevation on ambulatory monitoring. Coronary angiography revealed a severe stenosis in the midsegment of the right coronary artery. Successful angioplasty with stent implantation abolished the episodes of syncope and AVB.
Vagally-mediated paroxysmal AVB has been observed during vomiting (21), swallowing (22), carotid massage (23)and coronary angiography (24). It has also been observed during the head-up tilting test (25). The head-up tilting test is a very useful diagnostic tool in patients with neurocardiogenic or vasovagal syncope (9,10,26,27). Although the methodology of this test varies, it requires patients to be tilted to a semiupright position using a motorized table with a footboard. If hypotension or bradycardia are not observed during the observation period, the test is repeated during isoproterenol infusion. Although the exact mechanism of head-up tilting test is not entirely clear, the test is probably operating through the Bezold-Jarisch axis (26,27). The Bezold-Jarisch reflex results from stimulation of the inhibitory cardiac sensory receptors that lead to vagal activation and sympathetic inhibition, producing vasodilation, hypotension and bradycardia (28). Prolonged asystole due to sinus arrest or sinoatrial block is common, but AVB is rare, probably due to the accompanying sinus bradycardia (24,25). The Bezold-Jarisch reflex may play a role in the genesis of AVB during myocardial ischemia or the acute phase of infarction (28).
AVB during DSE
This study showed that AVB occurred during DSE in both patients with and without CAD and that both Mobitz type I and Mobitz type II block were observed during AVB. Mobitz type II block was observed only in patients with CAD, usually in those with left anterior descending artery disease or those with two-vessel disease. In contrast, Mobitz type I block was noted in patients with and without CAD. Several mechanisms could be operating. First, myocardial ischemia induced by dobutamine infusion was the most likely mechanism responsible for AVB in patients with CAD. The observation that AVB developed concomitantly with the onset of new wall motion abnormalities is consistent with this hypothesis. The abolition of AVB during repeat DSE following successful revascularization further supports this assumption. Second, vagally mediated effects could be a contributing factor in some patients. Although dobutamine instead of isoproterenol was used in stress echocardiography, dobutamine could initiate vagal reflex through the Bezold-Jarisch reflex. The finding that all three patients without CAD had a positive head-up tilting test and that all three manifested with Mobitz I block during DSE is consistent with this assumption. However, the fact that AVB is a rare manifestation of the head-up tilting test appears to be contradictory to this hypothesis. This may be explained by the accompanying sinus bradycardia during head-up tilting which prevented the occurrence of AVB (24,25). Last, there may be latent disease in the conducting system. If this is the case, dobutamine infusion could unravel the abnormality in the His-Purkinje system producing Mobitz type II block, while enhancing the AV nodal conduction preventing the occurrence of Mobitz type I block. This possibility is less likely because the block in patients with CAD disappeared after revascularization, while the block in those without CAD was a Mobitz type I AV nodal block.
This study demonstrates that transient second degree AVB is not an infrequent complication during DSE. Both Mobitz type I and Mobitz type II blocks may be observed. The occurrence of Mobitz type II block during DSE is indicative of the presence of CAD, usually involving the left anterior descending artery or two coronary arteries. Mobitz type I block may occur in both patients with and without CAD. In patients with CAD and development of AVB during DSE, successful revascularization may abolish the occurrence of AVB.
☆ This study was supported in part by grants from the National Science Council (NSC88-2314-B182-085, NSC88-2314-B182-089 and NSC88-2314-B182-079) of the Republic of China, Taipei.
- atrioventricular block
- coronary artery disease
- dobutamine stress echocardiography
- left ventricular ejection fraction
- percutaneous transluminal coronary angioplasty
- interval between p wave and QRS complex
- wall motion score index
- Received November 25, 1998.
- Revision received March 29, 1999.
- Accepted June 11, 1999.
- American College of Cardiology
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