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Left Bundle Branch Block with Intermittent QRS Axis Switching Observation of a Hypertensive Patient for 18 Years

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Left Bundle Branch Block with Intermittent QRS Axis Switching Observation of a Hypertensive Patient for 18 Years Case Reports Left Bundle Branch Block With Intermittent QRS Axis Switching Observation of a Hypertensive Patient for 18 Years Tetsuya Takato,1 MD, Namie Yamada,1 MD, Jun Fujii,1 MD, Saburo Mashima,2 MD, and Terunao Ashida,1 MD Summary A 64-year-old man who had been prescribed antihypertensive drugs since 1971 at- tended our clinic in 1988 with hypertension and electrocardiographic abnormalities. An electrocardiogram revealed left axis deviation (LAD) in 1988 and slightly prolonged PQ intervals in 1993. Complete left bundle branch block (CLBBB) with LAD developed in May 1995. The wide QRS of the CLBBB had never returned to the normal narrow QRS and had intermittently alternated between LAD and normal axis. The PQ intervals were longer when the QRS axis showed LAD compared to that with normal QRS axis. The QRS complexes in leads V1-V3 revealed an R wave at LAD and a QS pattern at normal axis. During a deep breathing test, the QRS axis switched from normal axis to LAD at the end of forced expiration and also switched from normal axis to LAD within a few minutes after the exercise test. These results suggest that the shift of the QRS axis might be related to the tone of the autonomic nervous system. (Int Heart J 2009; 50: 677-684) Key words: Left bundle branch block, QRS axis alternation, Electrocardiogram LEFT bundle branch block (LBBB) usually occurs in patients with cardiac disease. However, Rosenbaum and others1-3) have reported that as many as 12% of patients with LBBB have no demonstrable heart disease. The QRS axis of CLBBB is usually normal axis or LAD. Only a few reports have described CLBBB with a changing QRS axis,4-8) whereas all reported cases describe acute symptoms and follow-up periods ranging from 1 day to 10 months. The present patient developed a narrow QRS complex over 6 years followed by LBBB with a changing QRS axis over the next 12 years. From the 1 Division of Cardiovascular Disease, The Institute for Adult Diseases Asahi Life Foundation and 2 School of Medicine, Showa University, Tokyo, Japan. Address for correspondence: Terunao Ashida, MD, Division of Cardiovascular Disease, The Institute for Adult Diseases Asahi Life Foundation, 1-6-1 Marunouchi, Chiyoda-ku, Tokyo 100-0005, Japan. Received for publication March 17, 2009. Revised and accepted May 15, 2009. 677 Int Heart J 678 TAKATO, ET AL September 2009 Case Report A 64-year-old man who had been treated with antihypertensive drugs since 1971 was referred to our clinic with hypertension and abnormal electrocardio- grams in 1988. At his first visit to our clinic, his blood pressure was 180/86 mmHg and his electrocardiogram (ECG) showed LAD and poor R wave pro- gression in leads V1-V4. The PQ interval was slightly increased to 0.22 seconds Figure 1. Electrocardiogram obtained during first visit on December 21, 1988 indicat- ing LAD (-35 degrees), QRS duration of 0.10 seconds, and poor progression of R wave in leads V1-V4. Figure 2. An electrocardiogram on May 2, 1995 indicating LAD (-58 degrees) and first appearance of CLBBB (QRS 0.15 seconds). Vol 50 No 5 LBBB AND INTERMITTENT LAD AND NORMAL AXIS 679 in about 1993. He developed chest pain for 2-3 minutes on one occasion when he got up from bed in 1994. The result of the Master double exercise test was negative. An ECG revealed CLBBB with LAD on May 2, 1995, and the wide QRS of CLBBB never returned to normal narrow QRS. Unexpectedly, the QRS axis changed from LAD to normal axis on October 28, 1996. Thereafter, ECGs showed CLBBB with intermittent alternation of QRS axis between LAD and normal axis. Figure 3. An electrocardiogram on October 28, 1996 indicating changing QRS axis to normal axis (+56 degrees) and CLBBB (QRS 0.15 seconds). Figure 4. An electrocardiogram of 3 minutes after exercise testing on October 29, 2007. Black arrows show normal axis and white arrows show left axis deviation. PQ in- tervals were longer at LAD than at normal axis. Int Heart J 680 TAKATO, ET AL September 2009 Blood and urine examination data at the first visit were almost all within normal limits, with the exception of a slight increase in uric acid, though he had been administered allopurinol. Laboratory findings on October 5, 2007 revealed mild anemia, mild creatinine elevation (1.14 mg/dL), proteinuria, and glycosuria with a normal HbA1c. A chest X-ray on July 2, 2007 showed a cardiothoracic ratio of 42% and a mildly calcified aorta. Echocardiography on September 6, 2006 revealed an interventricular septum (IVS) of 12 mm, a left ventricular posterior wall (LVPW) of 11 mm, left ventricular diastolic dimension (LVDd) of 55 mm, left atrial dimension (LAD) of 50 mm, left ventricular ejection frac- tion (LVEF) of 0.84, left ventricular fractional shortening (LVFS) of 22%, left ventricular mass index (LVMI) of 175 g/cm2, and an E/A of 0.7, all of which indicated mild left atrial enlargement and left ventricular hypertrophy. Carotid echography on November 28, 2006 indicated a right maximum intima-media thickness (IMT) of 2.7 mm (bulbus) and left maximum IMT of 2.5 mm (internal carotid artery). Myocardial thallium scintigraphy at The University of Tokyo Hospital on March 8, 2007 revealed mildly reduced deposition in the upper to lower septum after stress. Redistribution was complete and the findings were compatible with CLBBB. The washout rate was normal. Electrocardiography: The initial ECG findings on December 21, 1988 indicated LAD, QRS duration of 0.10 seconds, and poor progression of R wave in leads V1-V4 (Figure 1). An ECG on May 2, 1995 revealed CLBBB of a wide QRS complex (0.15 seconds) with LAD and a prolonged PQ interval of 0.22 seconds and small R waves in leads V1-V4 (Figure 2). An ECG on October 28, 1996 showed CLBBB with a normal axis and no small R waves in the QRS complex of leads V1 and V2 (Figure 3). Another ECG 3 minutes after an exercise test on Figure 5. An electrocardiogram during deep breathing testing on July 7, 1997. At the end of forced expiration, the axis of ECG changed from normal axis to LAD transiently ( ■ ). Minimal differences in QRS complex were found between those with normal axis and LAD (See text). Vol 50 No 5 LBBB AND INTERMITTENT LAD AND NORMAL AXIS 681 Figure 6. Diagram of PQ interval, QRS duration, HR, and QRS axis. October 29, 2007 showed CLBBB with a QRS that intermittently switched be- tween the normal axis and LAD (Figure 4). The PQ interval was longer (0.24 - 0.26 seconds) when the LAD was present compared with that (0.22 - 0.23 sec- onds) accompanying the normal QRS axis. An ECG during a deep breathing test on July 7, 1997 showed that the QRS axis suddenly changed from normal axis to LAD at the end of forced expiration (Figure 5). The QRS in leads V1 and V3 showed a QS pattern when the axis was normal and an rS pattern when the axis deviated to the left. Figure 6 shows the serial changes in electrocardiographic findings over 18 years. The QRS duration that was initially normal with LAD, gradually increased and then CLBBB developed in 1995. Thereafter, the QRS axis switched back and forth between LAD and normal axis. Discussion The study by Lichstein, et al in 19799) reviewed ECG data from 84 patients with LBBB (LAD, n = 49; normal axis, n = 35) whose earlier ECGs were avail- able. They concluded that most patients with LBBB and LAD have a separate left anterior hemiblock (either before or after LBBB appearance). In 1978, Dhingra, et al10) compared 49 and 53 patients with chronic LBBB accompanied by a normal axis and by LAD, respectively. They concluded that among patients with LBBB, those with LAD had a greater incidence of myocardial dysfunc- tion, more advanced conduction disease, and greater cardiovascular mortality Int Heart J 682 TAKATO, ET AL September 2009 than those with a normal axis. In 1982, Havelda, et al11) examined 70 hearts with LBBB in a series of 1410 sequential dissections. Thirty-two hearts had LAD and 34 had normal axes. As a result, of the 70 hearts with LBBB, 42 had infarction. Inferoposterolateral and basal infarctions were larger in patients with LBBB and LAD than in those with LBBB and a normal axis. A prospective study by Das, et al12) in 2001 examined the relationship between LAD (axis between -30° and -90°) and left ventricular ejection fraction (LVEF) and found that the presence of LAD in LBBB did not signify a further decrease in EF. Rosenbaum13) proposed the theoretical possibility of an intermittent QRS axis change in CLBBB in 1969 and Vera, et al4) described the first actual case 3 years later in 1972. The Table summarizes the findings of previous reports and of the present case. All 6 patients were over 60 years of age. Vera, et al described a patient who had diabetes mellitus for over 20 years, chronic renal insufficien- cy, and CLBBB with several episodes of intermittent obvious RAD. They con- cluded that a coexistent left posterior hemiblock and predivisional LBBB caused the CLBBB with intermittent RAD in their patient. Ranginani, et al5) described a 73-year-old patient with CLBBB and intermittent LAD who had hypertension, diabetes, myocardial infarction, coronary aorta bypass graft (CABG), and aortic valve replacement (AVR) in 2000. In 2006, Cheng, et al6) described a 69-year- old woman with congestive heart failure, CLBBB, and intermittent RAD. Coex- istent left posterior hemiblock and predivisional LBBB were suggested.
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