International Journal of cardiology ELSEVIER International Journal of Cardiology 56 (1996)75-81 Tachycardia induced cardiomyopathy in dogs; relation between chronic supraventricular and chronic ventricular tachycardia I. Zupan”‘“, P. Rakovec”, N. Budihnab, A. Brecelj”, M. Koielj” “Department of Cardiology, University Medical Centre Ljubljana, ZaloSka 7, 1000 Ljubljana, Slovenia bDepartment of Nuclear Medicine, University Medical Centre Ljubljana, ZuloSka 7, 1000 Ljubljana, Slovenia ‘Department of Cardiovascular Surgery, University Medical Centre Ljubljana, ZaloSka 7, 1000 Ljubljana, Slovenia Received 22 April 1996; accepted 23 May 1996 Abstract Long-standing ventricular tachycardia (VT) and supraventricular tachycardia (SVT) can produce a reversible left ventricular dysfunction. The onset of cardiomyopathy and the severity of posttachycardicchangesdepend at least on three parametersof tachycardia, including its type (VT or SVT), rate and duration. Ten dogs (beagles) were paced at 180 beats/min for 3 weeks. Two pacing modalities, supraventricular and ventricular, were used in each dog. In half of them, the study was started by ventricular, and in the other half by supraventricular high-rate pacing. The alternate pacing modality was applied after complete recovery of left ventricular function. Ventricular function and morphology were evaluated by radionuclide ventriculography, echocardiography and Swan-Ganz catheterisation. Posttachycardicchangeswere studied in sinus rhythm after cessation of pacing. Left ventricular ejection fraction (LVEF) fell significantly after either type of tachycardia (SVT: 53?.5%, VT: 48?7%, PcO.05) compared with baseline values (69522.3%). Significant increases (P<O.O5) in end-systolic (SVT: 2.lkO.3 cm,VT: 2.4kO.2 cm vs. 1.6kO.3 cm) and end-diastolic dimensions (SVT: 3.0+0.3 cm, VT: 3.31-0.4 cm vs. 2.720.3 cm) indicated ventricular dilation in paced animals. Left ventricular pulmonary capillary wedge pressure increased significantly after either type of tachycardia as compared with baseline values (SVT: 7.52 1.2 mmHg, VT: 8.421.1 mmHg vs. 1.9? 1.5 mmHg, JYO.05); the difference between tachycardias was not significant. The present study demonstrates that chronic SVT and VT result in left ventricular dysfunction in a relatively short time, even if the heart rate is not very high. Deterioration of left ventricular ejection fraction and dilation of the left ventricle are more marked in chronic VT than in chronic SVT. Keywords: Chronic tachycardia; Ventricular; Supraventricular; Cardiomyopathy 1. Introduction Chronic ventricular tachycardia (VT) and sup- raventricular tachycardia (SVT) have been shown to *Corresponding author. Tel: +386-61.317057; Fax: +386-61- 302455. produce dilated, congestive cardiomyopathy in both humans [l-14] and experimental animals [5-211. In clinical practice, chronic high-rate tachycardias have to be treated promptly and the therapy is clear and well defined. Tachycardias with slower or ‘bor- derline’ rates have an unpredictable outcome and are still being investigated. 0167-5273/96/$15.00 0 1996 Elsevier Science Ireland Ltd. All rights reserved PII SO167-5273(96)02728-3
Transcript
International Journal of
cardiology ELSEVIER International Journal of Cardiology 56 (1996) 75-81
Tachycardia induced cardiomyopathy in dogs; relation between chronic supraventricular and chronic ventricular tachycardia
I. Zupan”‘“, P. Rakovec”, N. Budihnab, A. Brecelj”, M. Koielj” “Department of Cardiology, University Medical Centre Ljubljana, ZaloSka 7, 1000 Ljubljana, Slovenia
bDepartment of Nuclear Medicine, University Medical Centre Ljubljana, ZuloSka 7, 1000 Ljubljana, Slovenia ‘Department of Cardiovascular Surgery, University Medical Centre Ljubljana, ZaloSka 7, 1000 Ljubljana, Slovenia
Received 22 April 1996; accepted 23 May 1996
Abstract
Long-standing ventricular tachycardia (VT) and supraventricular tachycardia (SVT) can produce a reversible left ventricular dysfunction. The onset of cardiomyopathy and the severity of posttachycardic changes depend at least on three parameters of tachycardia, including its type (VT or SVT), rate and duration. Ten dogs (beagles) were paced at 180 beats/min for 3 weeks. Two pacing modalities, supraventricular and ventricular, were used in each dog. In half of them, the study was started by ventricular, and in the other half by supraventricular high-rate pacing. The alternate pacing modality was applied after complete recovery of left ventricular function. Ventricular function and morphology were evaluated by radionuclide ventriculography, echocardiography and Swan-Ganz catheterisation. Posttachycardic changes were studied in sinus rhythm after cessation of pacing. Left ventricular ejection fraction (LVEF) fell significantly after either type of tachycardia (SVT: 53?.5%, VT: 48?7%, PcO.05) compared with baseline values (69522.3%). Significant increases (P<O.O5) in end-systolic (SVT: 2.lkO.3 cm,VT: 2.4kO.2 cm vs. 1.6kO.3 cm) and end-diastolic dimensions (SVT: 3.0+0.3 cm, VT: 3.31-0.4 cm vs. 2.720.3 cm) indicated ventricular dilation in paced animals. Left ventricular pulmonary capillary wedge pressure increased significantly after either type of tachycardia as compared with baseline values (SVT: 7.52 1.2 mmHg, VT: 8.421.1 mmHg vs. 1.9? 1.5 mmHg, JYO.05); the difference between tachycardias was not significant. The present study demonstrates that chronic SVT and VT result in left ventricular dysfunction in a relatively short time, even if the heart rate is not very high. Deterioration of left ventricular ejection fraction and dilation of the left ventricle are more marked in chronic VT than in chronic SVT.
produce dilated, congestive cardiomyopathy in both humans [l-14] and experimental animals [5-211.
In clinical practice, chronic high-rate tachycardias have to be treated promptly and the therapy is clear and well defined. Tachycardias with slower or ‘bor- derline’ rates have an unpredictable outcome and are still being investigated.
0167-5273/96/$15.00 0 1996 Elsevier Science Ireland Ltd. All rights reserved PII SO167-5273(96)02728-3
76 I. Zupan et al. I International Journal of Cardiology 56 (1996) 7.5-81
Reports by several other authors and our ex- perience suggest that chronic supraventricular tachy- cardia in humans causes a picture of dilated car- diomyopathy if the heart rate exceeds 150 beats/mm, whereas the rate of 130-150 beats/min has a less clear relation to cardiomyopathy. Chronic ventricular tachycardia usually leads to congestive heart failure even at lower rates [5,22-251. It is, however, unclear if the severity of myocardial dysfunction depends upon the type of tachycardia, i.e. on whether tachy- cardia is supraventricular or ventricular.
In the present study we hypothesized that there is a difference between chronic SVT and chronic VT in terms of the severity of the resulting car- diomyopathy, even with comparable heart rates. We tested this hypothesis by studying left ventricular function following atrial and ventricular pacing of the same heart.
2. Methods
Ten adult dogs were studied (beagles, weight: 13 + 1.4 kg, age 3 t 1 years old). Each dog underwent a 3-week protocol of rapid ventricular (or atrial) pacing, followed by atrial (or ventricular) pacing at 180 beats/min.
The experiment was approved by the Republic Veterinary Department (No. 323-01/38-90/V-LE).
2.1. Pacemaker implant
Dogs were anesthetized with 2% halothane (1.5 l/mm) and nitrous oxide (0.5 l/mm), intubated and ventilated. Sterile left thoracotomy of the fourth intercostal space was performed. The heart was exposed through pericardiotomy. Two stimulating sutureless electrodes (Mod. 6917AT, Medtronic, Inc., Minneapolis, MN) were screwed-m each heart, one on the auricula of the right atrium, and the other on the apex of the left ventricle. The electrodes were connected to a subcutaneous pacemaker, modified to permit programmed pacing of up to 300 beats/mm (Activitrax II 8414, Medtronic Inc.). The pacemaker was buried in a subcutaneous pocket adjacent to the thoracotomy skin incision. The implanted electrodes were tested with the pacing analyzer (Pacing System analyzer, Mod. 53 11, Medtronic) prior to the closure
of thoracotomy. The pericardium was left partly opened, the thoracotomy was closed and air was evacuated from the pleural space. After recovering from anesthesia the dogs were closely monitored in an observation room for l-2 days. Then they were returned to a chronic care facility, where they received a 5-day course of penicillin, a standard diet, and free access to water.
2.2. Pacing protocol
Ten dogs were randomly assigned to two protocols of pacing. Two pacing modalities, supraventricular and ventricular, were used in each dog. In half of them the study was started by ventricular and in the other half by supraventricular pacing. The alternate pacing modality was applied after complete recovery of left ventricular function. To perform an alternate pacing modality, a small sterile skin incision above the subcutaneous pocket was made in order to switch the electrodes on the pacemaker.
Dogs were paced in an asynchronous mode at a rate of 180 beats/min for 3 weeks, after which time the pacemaker was programmed in to a demand mode at a rate of 60 beats/mm.
Posttachycardic changes were evaluated in sinus rhythm, after cessation of pacing.
2.3. Measurements
There were no differences in the measurements protocol between animals with tachycardia induced by atrial pacing and those with tachycardia induced by ventricular pacing. The observers making the measurements were blinded as to whether SVT or VT had been conducted. All measurements were performed five times in each animal as follows: at basal condition, at 2 h and at 4 weeks after termina- tion of SVT, and at 2 h and at 4 weeks after termination of VT. The studies were conducted in conscious animals sedated with phenothiazine.
2.3.1. Radionuclide ventriculography Ventricular performance, i.e. ejection fraction, was
studied by the resting equilibrium-gated blood pool imaging performed after in vivo labeling of red blood cells [26]: starmous pyrophosphate (6.3 mg) was injected to prime red cells, followed at 20-30
I. Zupan et al. I International Journal of Cardiology 56 (1996) 75-81 II
min by the administration 35 mCi of 99mTc-pertech- netate.
A Siemens Basicam gamma camera with low energy all-purpose collimator with the energy peak centered at 140 keV with a 20% window, connected to a computer (Macintosh IIf equipped with Nuclear MAC 1.a9.7 software for scintigraphy) was used for scintigraphic studies.
Heart images were obtained from a modified left anterior oblique (septal) projection. Data were col- lected using physiological triggering with R deflec- tion from the dog’s ECG signal. During the acquisi- tion, nuclear medicine digital computer system used a real time list mode processing allowing for the integration of several hundred heart beats (R-R intervals) and construction of multiple, identically phased composite images. A forward-backward framing was performed. Each cardiac cycle was divided into 32 parts, and 32 frames with an average of 10 000 counts per frame were formed. Edges of the left ventricle were designed manually on the end-diastolic and end-systolic frames, and the com- puter program was used to calculate the ejection fraction (EF), peak systolic ejection rate (peak ejection rate) and peak diastolic filling rate (peak filling rate).
The ejection fraction was calculated from the background corrected end-diastolic and end-systolic frames.
2.3.2. Echocardiographic evaluation Two dimension directed, M-mode echocardiog-
raphic studies (35 MHz transducers, Diasonics VS 60) were performed from the right parasternal area. Standard left ventricular cross-sectional views were taken at the chordal level [27]. M-mode echocardiog- rams were taken using a 2-D echocardiogram as a guide. Left ventricular end-diastolic and left ven- tricular end-systolic dimensions were measured from the printed picture. End diastole was measured at the peak of the electrocardiographic R wave, and the smallest systolic frame was assumed to represent end systole.
2.3.3. Hemodynamic evaluation Under direct vision a 20-gauge plastic cannula was
inserted into the right or left jugular vein of each dog, and a No. 5F Swan-Ganz catheter was passed
from the jugular vein to the pulmonary artery. Pulmonary arterial diastolic pressure was used and the data were tabulated as pulmonary capillary wedge pressure (PCWP).
2.4. Statistical analysis
The differences in the parameters of left ventricu- lar function were analyzed by ANOVA using the Scheffe method for multiple comparison. PcO.05 was regarded as statistically significant. All data are presented as the mean 2 standard deviation.
3. Results
All ten animals completed the protocol. Weekly physical examination demonstrated that the dogs tolerated the elevated heart rate well, and continued with their normal eating and drinking behavior until the completion of the protocol. They showed no signs of respiratory distress, fatigue or ascites.
The results are presented in Table 1. The left ventricular ejection fraction was significantly lower after SVT and VT compared with baseline values. There was also a significant difference between the deterioration of left ventricular function in VT com- pared with SVT (Fig. 1). Ejection fraction fell by nearly 30% from control level to the level of peak heart failure. Four weeks after cessation of pacing, the ejection fraction was comparable with baseline values.
Left ventricular systolic and left ventricular dias- tolic diameters increased in chronic ventricular and supraventricular high rate pacing. The difference was highly significant as compared to basal values and also with respect to both tachycardlas. Left ventricu- lar diastolic cavity size and left ventricular systolic cavity size decreased to baseline values within 4 weeks after cessation of pacing.
Peak ejection rate (PER) and peak filling rate (PFR) fell significantly after SVT and VT compared with baseline values. Systolic dysfunction was more pronounced than diastolic in both types of chronic tachycardia. Systolic and diastolic dysfunction index- es were restored 4 weeks after cessation of pacing.
There was a significant difference in left ventricu- lar pulmonary capillary wedge pressure between
78 1. Zupcm et al. I hternational Journal of Curdiology 56 (1996) 75-X1
Table I Effects of rapid ventricular and supraventricular pacing at 180 beats/min for 3 weeks in dogs
Basal 2 h after cessation of pacing 4 weeks after cessation of pacing
All data represent means%S.D. n = 10. HR, heart rate; LVEF, left ventricular ejection fraction; LVEDD, left ventricular end-diastolic dimension; LVESD, left ventricular end-systolic dimension; PCWP, pulmonary capillary wedge pressure; PER, peak ejection rate; PFR, peak filling rate; EDV/s, end-diastolic volume per second. *P<O.O5 (compared with basal); tP<0.05 (compared with ‘after SVT’ status).
baseline values and after each type of tachycardia. The difference between tachycardias was not statisti- tally significant.
4. Discussion
The present study compares the hemodynamic effects of chronic SVT and VT.
We demonstrated that in a relatively short time chronic SVT and VT resulted in left ventricular dysfunction, even with lower heart rates. Previous studies reported considerable variability in the time needed to produce severe heart failure, ranging from 14 days at 240-280 beats/min [28] to 2 months at 220 beats/min [21] in dogs and 14 days at 225 beats/min in sheep [29]. Pigs respond to chronic tachycardia in similar manner as dogs [20]. In many
Fig. 1. Gated radionuclide ventriculography in basal condition, after SVT, and after VT is presented. End-diastolic and end-systolic computed images are demonstrated. We see gradual increasing of left ventricular end-diastolic and end-systolic volumes. Iv, left ventricle; rv, right ventricle.
I. &pan et al. / International Journal of Cardiology 56 (1996) 75-81 79
studies the 3-week protocol was used [15,17,21,30] and we considered that time period as a good reference.
We chose pacing at 180 beats/min for the follow- ing reasons: first, this particular rate in dogs resem- bles heart rates of 140-150 beats/min in humans. It is known from human physiology that a 75% dias- tolic shortening occurs at a rate of 150 beats/mm compared to basal heart rate of 70 beats/min [3 11. In dogs, following mitral valve movement, the same percentage of diastole shortening was found ech- ocardiographically at a pacing rate of 180 beats/min. Second, the canine heart is prone to develop AV node block when rapidly paced from the atria [32,33], which was not the case in our experiment.
In our study we found that left ventricular EF and dilation of the left ventricle were more pronounced in chronic VT than in chronic SVT. False depolariza- tion in VT probably alters the time course of contraction which has mechanical consequences. Mechanisms of LV impairment may be the same in both types of chronic tachycardia. Studies employing atria1 and ventricular high-rate pacing (230-250 beats/min) separately, showed similar results [16,30].
In our study complete recovery of tachycardia- induced cardiomyopathy occurred regardless of the pacing modality used (either supraventricular or ventricular). Some authors reported permanent dias- tolic dysfunction [17], but the pacing rate they employed was much higher than in our study. The underlying pathophysiologic mechanisms of tach- ycardia-induced impairment of left ventricular func- tion have not been fully identified, although several have been proposed: decreased coronary perfusion [34,35], energy substrate depletion [36,37], altera- tions in myocyte function and structure [38-421. Irrespective of the mechanism, the important finding of the study is the complete reversibility of the abnormalities.
Each dog was used as its own control, allowing us to measure changes occurring in each animal. We did not study sham control animals to document the variability of measurements over time and to com- pare them with heart failure animals as the variability of measurements proved to be low, and the com- parison was considered relatively unimportant in view of the large changes observed [43].
Some of the findings in our model are similar to
those reported previously in animal models of chronic tachycardia [44,45]. Our dog model differs technically from those used by other authors. We assessed ventricular ejection fraction using radionu- elide ventriculography, which is a non-invasive and exact technique, reproducible at a single application of isotope and showing a high degree of correlation with the ‘golden standard’ of contrast ventriculog- raphy. Studies can be made in conscious animals with intact reflexes, which is of great clinical signih- came [46].
Another significant difference between our model and previous animal models is that we investigated changes occurring in same heart due to two different types of tachycardia (source in the atrium versus source in the ventricle). Other factors determining the severity of cardiomyopathy - the tachycardia rate and the duration of tachycardia - remained constant.
Our findings and those from other investigators suggest that there may be two tachycardia rate limits (one for chronic VT and the other one for chronic SVT) under which induction of cardiomyopathy may no longer be possible. However, the tachycardia rate limit for SVT tends to be surprisingly low, which is in accordance with a report about 10 patients with atria1 fibrillation (lowest heart rate 120 beats/min) and initially believed idiopathic cardiomyopathy ~251.
5. Conclusions
In conclusion, the present study demonstrates that within a relatively short time, chronic ventricular and chronic supraventricular tachycardia result in left ventricular dysfunction, even with lower heart rates. Deterioration of left ventricular ejection fraction and dilation of the left ventricle are more pronounced in chronic VT than in chronic SVT. Recovery from tachycardia-induced cardiomyopathy is complete, regardless of whether atria1 or ventricular pacing is used.
Acknowledgments
We thank Medtronic company, for their generous cooperation and technical support. The study was
80 I. Zupan et al. / International Journal of Cardiology S6 (1996) 75-81
supported by the Slovenian Ministry of Science and Technology.
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