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Left bundle branch block with left axis deviation
LETTERS
TO
THE
EDITOR
TREATMENT OF POLYMORPHOUS VENTRICULAR TACHYCARDIA
LEFT BUNDLE BRANCH BLOCK WITH LEFT AXIS DEVIATION
Nicholson et al.’ report on three cases of ventricular fibrillation provoked by usual dosages of disopyramide. The association of ventricular tachyarrhythmias and prolongation of Q-T interval is a feature of the arrhythmia known as “torsade de pointes.” 2 The illustration of the arrhythmias in their cases, most noticeably in Case 2, indeed suggests the presence of torsade de pointes. The refractoriness of the arrhythmia to orthodox treatment, as found in their Case 1, was mentioned by Krikler and Curry,2 who commented that drugs with actions similar to those of quinidine may disastrously aggravate the arrhythmia. Among the drugs used by Nicholson et al. in their Case 1 were lidocaine and procainamide, both of which have been reported to cause torsade de pointes. 2 Krikler and Curry* recommended treatment with isoprenaline in such cases, but did not refer to results obtained with such therapy. In a similar patient treated by one of us (M.M.Z.) the arrhythmia did not recur after electrical defibrillation, and drug therapy was not administered. We wonder whether Nicholson and his associates considered using isoprenaline in their patients? Indeed, we would be interested to know the experience of other cardiologists in treating cases of torsade de pointes with isoprenaline.
Lichstein et a1.l reported on 49 patients with chronic left bundle branch block and left axis deviation and concluded that the majority of their patients with these combined findings have associated left anterior hemiblock. In support of their conclusion we2 recently described a patient who manifested acute left anterior hemiblock at the onset of myocardial ischemia induced by exercise followed a minute later by complete left bundle branch block that disappeared after 3 minutes of recovery. We believe that the cause of the conduction abnormality in our patient was myocardial ischemia because we could not reproduce this exercise-related electrocardiographic abnormality after successful myocardial revascularization had been performed.
Monty M. Zion, MD, FRCP, FACC lvor Geft MB, MRCP Institute of Cardiology Shaare Zedek Medical Centre Jerusalem, Israel
References 1. Nkhotron WJ, Martin CB, &acsy JG, Knot% HR. Dlsopyramide-induced ventricular fibrillatbn. Am J Cardbl 1979343~1053-5. 2. Krlkhv DM, Curvy PVL. Tomada de pohtes, an atypical venklcular tachycardia. Br HearI J 1978;38:117-20.
Rene A. Oliveros, Lt Col, USA MC Department of Cardiology Division of Medicine Department of the Air Force Wilford Hall USAF Medical Center (AFSC Lackland Air Force Base, Texas References 1. Lkhtek~ E, Mwatra R. Gupta PK, Chodda KD. S@itlcanCa ot complete left bundle branch block with left axis deviation. Am J Cardlol 1979;44:239-42. 2. OlIvema RA. Boaworth J. Welland FL, BOwher CA. Intermittent left anterior hemiblock during treadhill exe& test. Chest 1977;72:492-4
REPLY
In Oliveros’ patient left anterior hemiblock developed and then left bundle branch block with left axis deviation 1 minute later. Although this time interval is much shorter than in our patients with chronic disease, the fact that the conduction defects occurred separately is similar. Unfortunately, neither of our observations answers the question whether these findings are related to an anatomic defect or can be explained by a functional abnormality of conduction. Edgar Lichstein, MD, FACC Maimonides Medical Center Division of Cardiology Brooklyn, New York
REPLY
We agree that Case 2 in our recent report represents “torsade de point& as described by Krikler and Curry. All three cases in our report are best characterized by the recently suggested phrase “polymorphous ventricular tachycardia.” In our management of Case 1 no significant lessening of the arrhythmia occurred with any drug management attempted. Overdrive pacing proved to be the definitive treatment in this case. Such management has been suggested in the past. Only recently’ has successful control of this arrhythmia with isoproterenol in 10 patients been documented. Seventeen other patients were successfully managed with overdrive pacing, as in our Case 1. Consequently, we believe that the management of recurrihg polymorphous ventricular tachycardia should be (1) discontinuance of the offending drug, and (2) administration of overdrive pacing or isoproterenol, or both. The use of type I antiarrhythmic agents such as quinidine and pronestyl should be avoided. W. Jay Nicholson, MD, FACP, FACC Department of Medicine Division of Cardiology York Hospital York, Pennsylvania Reference 1. &bowky S, sbcukrg B. Lowh Clinical features and treatment.
RF, Agmon J. Fulymorphow Am J Cardlol 1979;44:339-44.
ventricular tachycardia:
OCCULT THYROTOXICOSIS AND THYROTROPINRELEASING HORMONE TEST-l
This commentary is presented in the hope that the study of Forfar et al.’ will not be uncritically accepted by the medical community2 and result in an unwarranted increase in the use of the thyrotropin-releasing hormone (TRH) test. That thyrotoxicosis can exist in the elderly, in the absence of classical clinical signs, has been known for many years, as has the ability of hyperthyroidism to produce atria1 fibrillation. Although most observers agree that the thyrotropinreleasing hormone test is the most sensitive study for the diagnosis of primary hyperthyroidism, I question whether it was necessary to use it in any of the patients in their report. Of the 10 patients, only 2 (Cases 1 and 10) had normal values of both triiodothyronine (Ts) and total thyroxine (Td). Both patients were women, but at or p&t the usual age of menopause. In the absence of estrogens they would be expected to have relatively low levels of thyroxine-binding globulin and thus high-normal values would be unusual. Studies of free thyroxine, or a Free
September 1980
The American Journal of CARDIOLOGY
Volume 48
821
TO
THE
EDITOR
TREATMENT OF POLYMORPHOUS VENTRICULAR TACHYCARDIA
LEFT BUNDLE BRANCH BLOCK WITH LEFT AXIS DEVIATION
Nicholson et al.’ report on three cases of ventricular fibrillation provoked by usual dosages of disopyramide. The association of ventricular tachyarrhythmias and prolongation of Q-T interval is a feature of the arrhythmia known as “torsade de pointes.” 2 The illustration of the arrhythmias in their cases, most noticeably in Case 2, indeed suggests the presence of torsade de pointes. The refractoriness of the arrhythmia to orthodox treatment, as found in their Case 1, was mentioned by Krikler and Curry,2 who commented that drugs with actions similar to those of quinidine may disastrously aggravate the arrhythmia. Among the drugs used by Nicholson et al. in their Case 1 were lidocaine and procainamide, both of which have been reported to cause torsade de pointes. 2 Krikler and Curry* recommended treatment with isoprenaline in such cases, but did not refer to results obtained with such therapy. In a similar patient treated by one of us (M.M.Z.) the arrhythmia did not recur after electrical defibrillation, and drug therapy was not administered. We wonder whether Nicholson and his associates considered using isoprenaline in their patients? Indeed, we would be interested to know the experience of other cardiologists in treating cases of torsade de pointes with isoprenaline.
Lichstein et a1.l reported on 49 patients with chronic left bundle branch block and left axis deviation and concluded that the majority of their patients with these combined findings have associated left anterior hemiblock. In support of their conclusion we2 recently described a patient who manifested acute left anterior hemiblock at the onset of myocardial ischemia induced by exercise followed a minute later by complete left bundle branch block that disappeared after 3 minutes of recovery. We believe that the cause of the conduction abnormality in our patient was myocardial ischemia because we could not reproduce this exercise-related electrocardiographic abnormality after successful myocardial revascularization had been performed.
Monty M. Zion, MD, FRCP, FACC lvor Geft MB, MRCP Institute of Cardiology Shaare Zedek Medical Centre Jerusalem, Israel
References 1. Nkhotron WJ, Martin CB, &acsy JG, Knot% HR. Dlsopyramide-induced ventricular fibrillatbn. Am J Cardbl 1979343~1053-5. 2. Krlkhv DM, Curvy PVL. Tomada de pohtes, an atypical venklcular tachycardia. Br HearI J 1978;38:117-20.
Rene A. Oliveros, Lt Col, USA MC Department of Cardiology Division of Medicine Department of the Air Force Wilford Hall USAF Medical Center (AFSC Lackland Air Force Base, Texas References 1. Lkhtek~ E, Mwatra R. Gupta PK, Chodda KD. S@itlcanCa ot complete left bundle branch block with left axis deviation. Am J Cardlol 1979;44:239-42. 2. OlIvema RA. Boaworth J. Welland FL, BOwher CA. Intermittent left anterior hemiblock during treadhill exe& test. Chest 1977;72:492-4
REPLY
In Oliveros’ patient left anterior hemiblock developed and then left bundle branch block with left axis deviation 1 minute later. Although this time interval is much shorter than in our patients with chronic disease, the fact that the conduction defects occurred separately is similar. Unfortunately, neither of our observations answers the question whether these findings are related to an anatomic defect or can be explained by a functional abnormality of conduction. Edgar Lichstein, MD, FACC Maimonides Medical Center Division of Cardiology Brooklyn, New York
REPLY
We agree that Case 2 in our recent report represents “torsade de point& as described by Krikler and Curry. All three cases in our report are best characterized by the recently suggested phrase “polymorphous ventricular tachycardia.” In our management of Case 1 no significant lessening of the arrhythmia occurred with any drug management attempted. Overdrive pacing proved to be the definitive treatment in this case. Such management has been suggested in the past. Only recently’ has successful control of this arrhythmia with isoproterenol in 10 patients been documented. Seventeen other patients were successfully managed with overdrive pacing, as in our Case 1. Consequently, we believe that the management of recurrihg polymorphous ventricular tachycardia should be (1) discontinuance of the offending drug, and (2) administration of overdrive pacing or isoproterenol, or both. The use of type I antiarrhythmic agents such as quinidine and pronestyl should be avoided. W. Jay Nicholson, MD, FACP, FACC Department of Medicine Division of Cardiology York Hospital York, Pennsylvania Reference 1. &bowky S, sbcukrg B. Lowh Clinical features and treatment.
RF, Agmon J. Fulymorphow Am J Cardlol 1979;44:339-44.
ventricular tachycardia:
OCCULT THYROTOXICOSIS AND THYROTROPINRELEASING HORMONE TEST-l
This commentary is presented in the hope that the study of Forfar et al.’ will not be uncritically accepted by the medical community2 and result in an unwarranted increase in the use of the thyrotropin-releasing hormone (TRH) test. That thyrotoxicosis can exist in the elderly, in the absence of classical clinical signs, has been known for many years, as has the ability of hyperthyroidism to produce atria1 fibrillation. Although most observers agree that the thyrotropinreleasing hormone test is the most sensitive study for the diagnosis of primary hyperthyroidism, I question whether it was necessary to use it in any of the patients in their report. Of the 10 patients, only 2 (Cases 1 and 10) had normal values of both triiodothyronine (Ts) and total thyroxine (Td). Both patients were women, but at or p&t the usual age of menopause. In the absence of estrogens they would be expected to have relatively low levels of thyroxine-binding globulin and thus high-normal values would be unusual. Studies of free thyroxine, or a Free
September 1980
The American Journal of CARDIOLOGY
Volume 48
821