International Journal of Cardiology, 36 (1992) 234-235
234 0 1992 Elsevier
Science Publishers B.V. All rights reserved 0167-5273/92/$05.00
CARD10 14994
Are late potentials operative in arrhythmias following methylprednisolone pulse therapy S. Ozen ‘, L. Tokgozoglu b and U. Saatci a Departments of ’ Pediatric Nephrology and ’ Cardiology, Hacettepe University, School of Medicine, Sihhiye, Ankara, Turkey
(Received 4 November 1991; revision accepted 20 February 1992)
We have evaluated 11 patients for the presence of late potentials in an attempt to investigate whether pulse methylprednisolone exerted its arrhythmogenic effect via this mechanism. All patients received pulse steroid therapy for their glomerulopathies. One of the patients developed bradycardia, no electrocardiographic abnormalities were present in the rest of these patients. Late potentials were not detected in any of the patients. Thus, in this preliminary study we have not been able to demonstrate that pulse steroid therapy plays a role in the genesis of late potentials. Key words: Late potential;
Ventricular
arrhythmia;
Methylprednisolone
Introduction
Pulse methylprednisolone therapy is becoming increasingly popular as a treatment modality in various childhood diseases, especially in the field of pediatric nephrology. It has been shown to improve survival in resistant nephrotic syndromes [l]. On the other hand, high-dose methylprednisolone therapy has been occasionally associated with arrhythmias and even sudden death [2,3]. Despite sporadic case reports on the subject the exact mechanism of these arrhythmias and sudden death have not been elucidated yet. Detection of late potentials by signal averaged electrocardiography has proved to be useful in defining patients at high risk for developing ventricular fibrillation [4j. We have carried out a preliminary study to investigate whether pulse steroid therapy could exert its arrhythmogenic effect via late potentials. Patients and Methods
All the 11 patients studied had primary glomerulopathies. The age range was 5 to 17 yr with a mean of 12 yr. There were 5 girls and 6 boys. None of the
Correspondence to: Dr. S. Ozen, Kuleli Osman Pasa, 06700, Ankara, Turkey.
sok.
9/2,
Gazi
patients had symptoms or signs of cardiac disease except for hypertension in 4 patients. The histopathological diagnosis of these renal patients were: focal glomerulosclerosis (FGS) in 5 cases, recurrence of the primary glomerulopathy (FGS) in 2 transplant patients, rapidly progressive glomerulonephritis in 2 cases, membranoproliferative glomerulonephritis in one patient and mesangial proliferative glomerulonephritis in one patient. All were decided to put on pulse therapy due to their resistant disease. Bolus methylprednisolone was administered intravenously, at a dose of 30 mg/kg over l-2 h. Baseline and follow-up ECGs were performed in all and were found to be normal. In all patients baseline signal averaged ECG was performed followed by recordings 24 and 72 h after the pulse treatment. Late potentials were investigated by the following representative criteria: (1) the filtered QRS complex was to be !onger than 114-120 ms; (2) there was to be < 20 WV of signal in the last 40 ms of the filtered QRS complex; and (3) a terminal filtered QRS complex was to remain below 40 PV for longer than 38 ms 141. Results
None of the patients developed clinically detectable arrhythmias following the infusion of methylprednisolone except for one patient who developed sinus
735 TABLE
1
Average
QRS and root mean
QRS RMS
square
(RMS) values.
Before treatment
24 h after treatment
72 h after treatment
16.6 220.1
76.2 249.8
77.6 223.6
(pulse rate 54-58/min) during the infusion which lasted for 20 h and remitted spontaneously. In the remaining patients pre- and post-treatment ECGs were found to be normal with no changes in PR, QRS and QT intervals. Serum electrolytes remained within normal limits. When the signal averaged ECGs were evaluated the QRS duration and the root mean square voltage 40 did not change significantly (Table I). bradycardia
Discussion In spite of the current enthusiasm for the use of pulse methylprednisolone therapy in resistant glomerulopathies as well as other clinical settings, questions about its safety are still unclear [2]. There have been several reports concerning arrhythmias and sudden death following pulse methylprednisolone treatment [2,3]. However, some of these patients had multisystem disease. A variety of arrhythmias have been reported and no consistent agreement on the mechanism has been reached. Studies in animals have suggested that intravenous steroids can be arrhythmogenic and speed of administration has been suggested as an important factor [3]. Late potentials appear to originate from small areas of delayed and disorganised ventricular activation [S]. Their role in causing ventricular tachycardia or fibrillation has been well defined in patients with myocardial
infarction or cardiomyopathy. Late potentials have also been shown to be an indicator of increased ventricular vulnerability in a small group of patients without a previous history of organic heart disease [5]. It is thought that the interaction of factors such as autonomic tone, ischemia, electrolyte imbalance and other unknown factors in a patient with electrophysiologic or anatomic derangement is important in the generation of late potentials. In this preliminary study we investigated whether high dose methylprednisolone therapy could be a potential factor in generating late potentials and thus increasing ventricular vulnerability in arrhythmia. We have not been able to demonstrate that this therapy plays a role in the genesis of late potentials. Acknowledgement We would like to thank contribution to our study.
Prof.
Dr. Ali Oto for his
References Mendoza SA, Reznik VM, Griswold WR, Krensky AM, Yorgin PD, Tune BM. Treatment of steroid-resistant FGS with pulse methylprednisolone and alkylating agents, Pediatr Nephrol 1990;4:303. Bocanegra TS. Castaneda MO, Espinoza LR. Vasy FB, Germain BF. Sudden death after methylprednisolone pulse therapy. Ann Intern Med 1981;95:122. Gardiner PVG, Griffiths ID. Sudden death after treatment with pulsed methylprednisolone. Br Med J 1990;300:125. McGuire M, Kuchar D, Ganis J, Sammel N, Thorburn C. Natural history of late potentials in the first ten days after acute myocardial infarction and relation to early ventricular arrhythmias. Am J Cardiol 1988;61:1187. Breithardt G, Borggrefe M, Quantius B et al. Ventricular vulnerability assessed by programmed ventricular stimulation in patients with and without late potentials. Circulation 1983;68:275.
234 0 1992 Elsevier
Science Publishers B.V. All rights reserved 0167-5273/92/$05.00
CARD10 14994
Are late potentials operative in arrhythmias following methylprednisolone pulse therapy S. Ozen ‘, L. Tokgozoglu b and U. Saatci a Departments of ’ Pediatric Nephrology and ’ Cardiology, Hacettepe University, School of Medicine, Sihhiye, Ankara, Turkey
(Received 4 November 1991; revision accepted 20 February 1992)
We have evaluated 11 patients for the presence of late potentials in an attempt to investigate whether pulse methylprednisolone exerted its arrhythmogenic effect via this mechanism. All patients received pulse steroid therapy for their glomerulopathies. One of the patients developed bradycardia, no electrocardiographic abnormalities were present in the rest of these patients. Late potentials were not detected in any of the patients. Thus, in this preliminary study we have not been able to demonstrate that pulse steroid therapy plays a role in the genesis of late potentials. Key words: Late potential;
Ventricular
arrhythmia;
Methylprednisolone
Introduction
Pulse methylprednisolone therapy is becoming increasingly popular as a treatment modality in various childhood diseases, especially in the field of pediatric nephrology. It has been shown to improve survival in resistant nephrotic syndromes [l]. On the other hand, high-dose methylprednisolone therapy has been occasionally associated with arrhythmias and even sudden death [2,3]. Despite sporadic case reports on the subject the exact mechanism of these arrhythmias and sudden death have not been elucidated yet. Detection of late potentials by signal averaged electrocardiography has proved to be useful in defining patients at high risk for developing ventricular fibrillation [4j. We have carried out a preliminary study to investigate whether pulse steroid therapy could exert its arrhythmogenic effect via late potentials. Patients and Methods
All the 11 patients studied had primary glomerulopathies. The age range was 5 to 17 yr with a mean of 12 yr. There were 5 girls and 6 boys. None of the
Correspondence to: Dr. S. Ozen, Kuleli Osman Pasa, 06700, Ankara, Turkey.
sok.
9/2,
Gazi
patients had symptoms or signs of cardiac disease except for hypertension in 4 patients. The histopathological diagnosis of these renal patients were: focal glomerulosclerosis (FGS) in 5 cases, recurrence of the primary glomerulopathy (FGS) in 2 transplant patients, rapidly progressive glomerulonephritis in 2 cases, membranoproliferative glomerulonephritis in one patient and mesangial proliferative glomerulonephritis in one patient. All were decided to put on pulse therapy due to their resistant disease. Bolus methylprednisolone was administered intravenously, at a dose of 30 mg/kg over l-2 h. Baseline and follow-up ECGs were performed in all and were found to be normal. In all patients baseline signal averaged ECG was performed followed by recordings 24 and 72 h after the pulse treatment. Late potentials were investigated by the following representative criteria: (1) the filtered QRS complex was to be !onger than 114-120 ms; (2) there was to be < 20 WV of signal in the last 40 ms of the filtered QRS complex; and (3) a terminal filtered QRS complex was to remain below 40 PV for longer than 38 ms 141. Results
None of the patients developed clinically detectable arrhythmias following the infusion of methylprednisolone except for one patient who developed sinus
735 TABLE
1
Average
QRS and root mean
QRS RMS
square
(RMS) values.
Before treatment
24 h after treatment
72 h after treatment
16.6 220.1
76.2 249.8
77.6 223.6
(pulse rate 54-58/min) during the infusion which lasted for 20 h and remitted spontaneously. In the remaining patients pre- and post-treatment ECGs were found to be normal with no changes in PR, QRS and QT intervals. Serum electrolytes remained within normal limits. When the signal averaged ECGs were evaluated the QRS duration and the root mean square voltage 40 did not change significantly (Table I). bradycardia
Discussion In spite of the current enthusiasm for the use of pulse methylprednisolone therapy in resistant glomerulopathies as well as other clinical settings, questions about its safety are still unclear [2]. There have been several reports concerning arrhythmias and sudden death following pulse methylprednisolone treatment [2,3]. However, some of these patients had multisystem disease. A variety of arrhythmias have been reported and no consistent agreement on the mechanism has been reached. Studies in animals have suggested that intravenous steroids can be arrhythmogenic and speed of administration has been suggested as an important factor [3]. Late potentials appear to originate from small areas of delayed and disorganised ventricular activation [S]. Their role in causing ventricular tachycardia or fibrillation has been well defined in patients with myocardial
infarction or cardiomyopathy. Late potentials have also been shown to be an indicator of increased ventricular vulnerability in a small group of patients without a previous history of organic heart disease [5]. It is thought that the interaction of factors such as autonomic tone, ischemia, electrolyte imbalance and other unknown factors in a patient with electrophysiologic or anatomic derangement is important in the generation of late potentials. In this preliminary study we investigated whether high dose methylprednisolone therapy could be a potential factor in generating late potentials and thus increasing ventricular vulnerability in arrhythmia. We have not been able to demonstrate that this therapy plays a role in the genesis of late potentials. Acknowledgement We would like to thank contribution to our study.
Prof.
Dr. Ali Oto for his
References Mendoza SA, Reznik VM, Griswold WR, Krensky AM, Yorgin PD, Tune BM. Treatment of steroid-resistant FGS with pulse methylprednisolone and alkylating agents, Pediatr Nephrol 1990;4:303. Bocanegra TS. Castaneda MO, Espinoza LR. Vasy FB, Germain BF. Sudden death after methylprednisolone pulse therapy. Ann Intern Med 1981;95:122. Gardiner PVG, Griffiths ID. Sudden death after treatment with pulsed methylprednisolone. Br Med J 1990;300:125. McGuire M, Kuchar D, Ganis J, Sammel N, Thorburn C. Natural history of late potentials in the first ten days after acute myocardial infarction and relation to early ventricular arrhythmias. Am J Cardiol 1988;61:1187. Breithardt G, Borggrefe M, Quantius B et al. Ventricular vulnerability assessed by programmed ventricular stimulation in patients with and without late potentials. Circulation 1983;68:275.
