Asian Cardiovasc Thorac Ann 1998;6:203-207
© 1998 Asia Publishing EXchange Pte Ltd
Intravenous Diltiazem for Treatment of Supraventricular Tachycardia After Coronary Artery Bypass Surgery
C Levent Birincio
lu, MD,
A Tulga Ulus, MD,
Birol Yamak, MD,
S Fehmi Katirciolu, MD,
Binali Mavita
, MD,
Ouz Tademir, MD
Department of Cardiovascular Surgery Türkiye Yüksek  htisas Hospital Ankara, Turkey
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For reprint information contact: C Levent Birinciolu, MD Department of Cardiovascular Surgery Türkiye Yüksek htisas Hospital Sihhiye, Ankara 06100, Turkey Tel: 90 312 310 3080 Ext. 1247 Fax: 90 312 312 4122 Email: ulus{at}escortnet.com
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ABSTRACT
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Between 1995 and 1997, 180 patients who had undergone coronary artery bypass grafting were given intravenous diltiazem for conversion of supraventricular tachycardia to sinus rhythm or control of ventricular rhythm in atrial fibrillation. The patients were divided into three groups of 60 each: group 1 required no inotropic support; group 2 had mild inotropic support with dopamine; group 3 had high-dose inotropic support with adrenalin and dopamine. Thirty-eight patients in group 1 (63%), 40 in group 2 (67%), and 32 in group 3 (53%) responded to one or two doses of diltiazem. There was no difference between the groups in terms of the success rate of the treatment (p > 0.05). Additional procedures were needed in 70 patients including cardioversion in 20 (12 in group 1, 8 in group 2). Mean cardiac index was significantly increased and mean pulmonary artery pressure was significantly decreased in all three groups after diltiazem treatment. After the first dose of diltiazem (0.25 mg·kg–1), the mean heart rate decreased from 141.5mg·kg–1 ± 3.8, 136.9 ± 8.5, and 140.2 ± 4.7 to 118.2 ± 5.1, 101.2 ± 6.7, and 105.6 ± 16.8 in groups 1, 2, and 3, respectively. The maximum decrease was seen after 5 minutes. After the second dose of diltiazem (0.35 mg·kg–1), although mean heart rates were not significantly decreased, 45% of group 1, 44% of group 2, and 46% of group 3 patients who did not respond to the first dose of diltiazem, converted to sinus rhythm. In the early postoperative period after coronary artery bypass graft surgery, diltiazem was of benefit in the treatment of supraventricular tachycardia and atrial fibrillation or flutter. This treatment may be especially useful in patients who are in poor hemodynamic condition.
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INTRODUCTION
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Diltiazem hydrochloride is a slow-channel blocker or calcium channel antagonist. Oral forms are used in the treatment of angina pectoris and systemic hypertension.1–7 Currently, oral diltiazem is recommended for the treatment of atrial arrhythmias.8,9 Intravenous diltiazem was found in several studies to be useful for the conversion of supraventricular tachycardia to sinus rhythm and control of ventricular rhythm in atrial fibrillation.10–14 After open-heart surgery, rhythm problems are frequently encountered in the early postoperative period. A number of patients with arrhythmias may have low cardiac output requiring inotropic agents that tend to exacerbate rhythm disturbances. In this study, we evaluated the use of intravenous diltiazem to stabilize heart rhythm after cardiac surgery.
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MATERIALS AND METHODS
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Between 1995 and 1997, 180 patients were given intravenous diltiazem for conversion of supraventricular tachycardia to sinus rhythm or control of ventricular rhythm in atrial fibrillation. All of the patients had undergone coronary artery bypass grafting at Türkiye Yüksek htisas Hospital. The indications for treatment were atrial fibrillation or flutter in patients with a ventricular response above 120 beats per minute, supraventricular tachycardia, or sick sinus syndrome (second or third degree atrioventricular block was not included). The contraindications were hypotension below 80 mm Hg, hypersensitivity to diltiazem, or pregnancy.
The patients were divided into three groups of 60 patients each. Group 1 consisted of patients who did not need inotropic support, patients in group 2 required mild inotropic support with dopamine, and those in group 3 needed high-dose inotropic support with adrenalin and dopamine. The patient characteristics are shown in Table 1
. Systolic and diastolic blood pressures, heart rate, cardiac index, pulmonary artery pressure, and electrocardiography were recorded before and after treatment. Effective treatment was defined as conversion to sinus rhythm or persistent atrial fibrillation with at least a 20% decrease in ventricular rate and below 100 beats per minute.
Heart rates were recorded over a 1-minute period by 12-lead electrocardiogram monitoring. Patients who sustained a ventricular rhythm above 120 beats per minute for 15 minutes were given 0.25 mg·kg–1 diltiazem intravenously over a period of 2 minutes. Blood pressure and heart rate were recorded every 5 minutes during the following 15 minutes. If the effective treatment criteria were not achieved after 15 minutes, a further infusion of 0.35 mg·kg–1 diltiazem was given over a 2-minute period. Heart rate and blood pressure were monitored as before.
STATISTICAL METHODS
Repeated measurements of analysis of variance, Kruskal-Wallis one-way analysis of variance, Wilcoxon matched-pairs signed-ranks test, t test for paired samples, and the Student-Newman-Keuls test as a post-hoc test were used for statistical analysis. A p value less than 0.05 was considered statistically significant. All values were reported as mean ± standard deviation.
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RESULTS
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The mean serum potassium levels were 4.02 ± 0.4 mEq·L–1 in group 1, 4.1 ± 0.6 mEq·L–1 in group 2, and 4.29 ± 0.7 mEq·L–1 in group 3 (p > 0.05).
Twenty patients (33%) in group 1, 24 patients (40%) in group 2, and 8 patients (13%) in group 3 responded satisfactorily to the first dose of diltiazem. Effective response to the second dose of diltiazem was achieved in 18, 16, and 24 patients in groups 1, 2, and 3 respectively. Thus, the responses to one or two doses of diltiazem were 63% in group 1, 67% in group 2, and 53% in group 3. There was no difference between the groups in terms of the success rate after treatment at the end of the studyc (p > 0.05). Additional procedures were required in 70 patients including cardioversion in 20 (12 in group 1, 8 in group 2).
Neither heart rate nor blood pressure changes were statistically significant between the three groups following the first or second doses of diltiazem. Systolic and diastolic blood pressures decreased significantly (p < 0.05) at 5, 10, and 15 minutes after the first treatment in all groups (Figures 1 and 2). Mean heart rates also decreased significantly within each group at 5, 10, and 15 minutes after the first treatment (Figure 3). The maximum decrease was seen 5 minutes after the first dose of diltiazem. After the second treatment, although the mean heart rates did not statistically decrease further, 45% of the patients in group 1, 44% of the patients in group 2, and 46% of the patients in group 3 who had not responded to the first dose of diltiazem, converted to sinus rhythm.
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Figure 1. Mean systolic blood pressure changes after treatment with intravenous diltiazem. *Values at 5, 10, and 15 minutes were significantly decreased in all groups (p < 0.01).
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Figure 2. Mean diastolic blood pressure changes after treatment with intravenous diltiazem. *Values at 5, 10, and 15 minutes were significantly decreased in all groups (p < 0.05).
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Figure 3. Heart rate changes after treatment with intravenous diltiazem. *Values at 5, 10, and 15 minutes were significantly decreased in all groups (p < 0.05).
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Mean cardiac index increased significantly (p < 0.05) over time in all three groups (Figure 4). Although there was no difference between the three groups after the first dose, there were differences after the second dose at 10 and 15 minutes; at 10 minutes after the second dose, group 1 had a significantly higher mean cardiac index than groups 2 and 3; at 15 minutes after the second treatment the mean cardiac index in group 3 was lower than the other two groups (Figure 4). Mean pulmonary artery pressures decreased significantly over time in all three groups (p < 0.05). However, the mean pulmonary artery pressure at all times was significantly higher in group 3 compared to the other 2 groups (Figure 5).
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Figure 4. Cardiac index differences after treatment with intravenous diltiazem. *Values at 5, 10, and 15 minutes were significantly increased in all groups (p < 0.05).  Values at 10 and 15 minutes were significantly different between groups (p < 0.05).
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Figure 5. Pulmonary artery pressure changes after treatment with intravenous diltiazem. *Values at 5, 10, and 15 minutes were significantly decreased in all groups (p < 0.05). Values at 5, 10, and 15 minutes were significantly different between groups (p < 0.05).
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DISCUSSION
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Atrial arrhythmias occur frequently after coronary artery bypass grafting.1,2 Tyras and colleagues15 reported an incidence of only 11.4%, whereas White and colleagues16 using continuous 24-hour electrocardiographic monitoring and including nonsustained supraventricular tachycardia found an incidence of 100%. Other studies examining only sustained supraventricular arrhythmia reported an incidence in the range of 11.4% to 40.1%.3–9
The occurrence of atrial fibrillation has been correlated with abnormal phase IV depolarization, conduction velocity, and transmembrane action potential in patients aged 40 years and older.3–6 Atrial infarction, left atrial hypertension, local surgical trauma (cannulation of atria), pericarditis, and age-dependent atrial atrophic changes may be contributing factors to postoperative atrial fibrillation.7–14 The toleration of atrial fibrillation depends on the ventricular rate, the degree of underlying left ventricular systolic and diastolic dysfunction, and the duration of the arrhythmia. The loss of atrial systole when combined with tachycardia and a reduced filling time as well as increased myocardial oxygen consumption, may have deleterious effects. This is especially true in patients with ischemic heart disease or acute myocardial infarction, hypertensive or hypertrophic hearts, or a dilated or hypertrophic cardiomyopathy. Coronary artery bypass grafting reduces the ischemic jeopardy imposed by arrhythmias. Only in patients with poor left ventricular function and a markedly hypertrophied myocardium does atrial fibrillation become a major concern. In such patients, atrial fibrillation can precipitate serious hemodynamic compromise so that urgent termination of the arrhythmia and its further prevention are of paramount importance.16–22
Atrial fibrillation may cause low cardiac output and conversely, low cardiac output may cause atrial fibrillation. Atrial fibrillation may be a sign of decreased vertricular performance during low cardiac output, so it must be controlled by antiarrhythmic agents that do not depress left ventricular function.1–6 Because atrial fibrillation following coronary artery bypass grafting requires treatment, there is a potential for adverse consequences secondary to antiarrhythmic drugs including digoxin, beta blockers, verapamil, and type V antiarrhythmic agents. Hypotension, atrioventricular block, and increased predisposition to ventricular arrhythmias have been reported.10–14 In addition, organ toxicity related to type I antiarrhythmic agents frequently occurs.9
Optimum bolus doses of diltiazem are reported to be 0.25 mg·kg–1 and 0.35 mg·kg–1 infused intravenously over 2 minutes.1,2,6,7 In our study, a positive response was seen in 29% of patients with the 0.25 mg·kg–1 dose. An additional 32% of the patients had a positive response to the second dose of 0.35 mg·kg–1 giving an overall response rate of 61%. The remaining 31% of patients required additional procedures. The maximum response was achieved 5 minutes after the treatment in agreement with other reports.3 This rapid response is important and in order to sustain the effect, we prescribed oral diltiazem 30 mg 3 times daily, when possible.
Intravenous diltiazem causes prolongation of atrioventricular (AV) node conduction during supraventricular tachycardia. After diltiazem infusion, no change was reported in the electrophysiologic properties of accessory AV conduction in patients with Wolff-Parkinson-White syndrome.2 In addition, there was no change in retrograde AV nodal parameters or accessory path conduction-refractory periods. It decreased AV nodal conduction and increased the AV node refractory period in a dose-dependant manner. In view of this, it is considered that the therapeutic effect of diltiazem occurs through an influence on the AV node (especially in supraventricular tachycardia with an antegrade path).1–6
In this study, intravenous diltiazem effectively reduced the mean heart rate in all three groups. None of the patients had AV block. Diltiazem has no clinically important negative inotropic effect so it may be used safely for hidden or manifest cardiac insufficiency.3–5 We found that systolic and diastolic blood pressures decreased in all three groups but the mean pressures did not fall below 88 mm Hg systolic and 40 mm Hg diastolic in any group. The increases in cardiac index and pulmonary artery pressure were attributed to the improved rhythm and deceased heart rate.
Beta-blocking agents are effective in 50% to 60% of such patients but they have a negative inotropic effect.5 Because of this, especially for high-risk patients, beta blockers are not the first choice. Electrical cardioversion was necessary in 33.3% of patients in the literature. The drawbacks of this therapy are that the patient may need intubation via sedation and in patients with edematous ventricles, cardioversion may lead to ventricular fibrillation.7–14 In our study, 12 patients from the first group (20%) and 8 patients from the second group (13.3%) had cardioversion and successfully returned to sinus rhythm.
Our finding of an overall 61% success rate with diltiazem for treating cardiac rhythm disturbances in the early postoperative period following coronary artery bypass grafting, confirms the usefulness of this drug. It may be especially beneficial in patients who are in poor hemodynamic condition.
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ABSTRACT
INTRODUCTION
