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Prognostic significance of exercise-induced complex ventricular arrhythmias in coronary artery disease with normal and abnormal left ventricular ejection fraction
1136
BRIEF REPORTS
FIGURE 2. Left coronary angiogram in anterior view 3 hours after onset of chest pain. Left anterior descending coronary artery is normal.
prior intracoronary thrombolytic therapy have been demonstrated in about 3% of patients with proved AMI on angiography at 4 weeks to 12 months after AMI. 2 There has been 1 other published report of 3 episodes of AMI in 2 patients with normal or near normal coronary arteries supplying the site of AMI. 3 Angiography was performed at 12 hours in the patient with normal coronary arteries and at 4 and 12 hours in the patient with near normal coronary arteries. The cause of AMI in our patient is uncertain. Three possibilities have been considered: a coronary artery lesion missed at angiography, an episode of prolonged coronary artery spasm, or an obstructing thrombus or embolus with early spontaneous lysis. At coronary angiography, several projections, including angulated
Prognostic Significance of ExerciseInduced Complex Ventricular Arrhythmias in Coronary Artery Disease with Normal and Abnormal Left Ventricular Ejection Fraction CHANDRA K. NAIR, MD WADE THOMSON, MS WlLBERT S. ARONOW, MD TOM PAGANO, MD KAY RYSCHON, MS MICHAEL H. SKETCH, MD
Ventricular arrhythmias on the electrocardiogram at rest and during prolonged ambulatory monitoring are From the Division of Cardiology, Creighton University School of Medicine, 601 North 30th Street, Omaha, Nebraska 68131. Manuscript received April 16, 1984; revised manuscript received June 19, 1984, accepted June 26, 1984.
views, were taken and a major stenotic lesion was not seen. Coronary artery spasm was unlikely as he had no previous angina, no visible spasm on angiography, and no angina in the 6 months after the AMI. Heupler et al 4 was unable to provoke coronary spasm with ergonovine in any of 6 patients with normal coronary arteries and a history of AMI as an isolated clinical event. The most likely cause of the infarct would appear to be obstruction of the left anterior descending artery by thrombus superimposed on a nonobstructive atherosclerotic plaque not seen on angiography, or obstruction by an embolus. In each case rapid lysis must be postulated. Indirect evidence of spontaneous lysis of coronary thrombi has been provided by de Wood et al, 6 who performed angiography up to 24 hours after the onset of symptoms of AMI. He found that the incidence of total coronary occlusion decreased with time. Anderson et al 6 described 2 patients with normal coronary arteries after streptokinase lysis of a completely occluding coronary thrombus 8 and 3 hours after the onset of anterior AMI. References 1. Maddahl J, Ganz W, Nlmomlya K, Hashlda J, Flshbeln MC, Mondkar A, Buchblnder N, Marcus H, Geft I, Shah PK, Rozanskl A, Swan HJC, Berman DS. Myocardial salvage by intracoronary thrombolysis in evolving acute myocardial infarction: evaluation using in1~acorouaryinjection of thallium-201. Am Heart J 1981; 102:664-674. 2. Belrlu A, Pare JC, Sanz GA, Casals F, Magrlna J, Castaner A, NavarroLopoz F. Myocardial Infarction with normal coronary arteries: a prospective cllnical--anglographic study. Am J Cardlol 1981;48:28-32. 3. Olive PB, Brecklnddge JC. Acute myocardial infarction with normal and near normal coronary arteries. Documentation with coronary arteriography within 12 112 hours of the onset of symptoms in two cases (three episodes). Am J Cardlol 1977;40:1000-1007. 4. Heupler FA, Prouclflt WL, Razavl M, Shlrey EK, Grsonslreet R, Sheldon WC. Ergonovlne maleete provocative test for coronary arterial spasm. Am J Cardiol 1978;41:631-640. 5. De Wood MA, Spores J, Nolske R, Mouser LT, Burroughs R, Golden MS, Lang HT. Prevalence of total coronary occlusion during the early hours of transmural myocardial infarction. N Engl J Mad 1980;303:897-902. 6. Anderson JL, Marshall HW, While RS, Datz F. Streptoklnase thrombolysis for acute myocardial Infarction in young adults with normal coronary arteries. Am Heart J 1983;106:1437-1438.
associated with increased risk of both sudden and nonsudden cardiac death. However, the prognostic significance of exercise-induced ventricular arrhythmias is controversialj -4 Recently, we reported that exercise-induced simple premature ventricular complexes in patients without prior myocardial infarction (MI) did not predict coronary events during a mean follow-up of 4 years. 4 Therefore, we studied the prognostic value of exercise-induced complex ventricular arrhythmias in patients with both a normal and an abnormal left ventricular (LV) ejection fraction (EF) to delineate whether exercise-induced ventricular arrhythmias predict mortality independent of LV function. One hundred eighty-six patients with coronary artery disease (CAD) documented by coronary arteriography were studied. There were 157men (mean age 59 4- 9years) and 29 women (mean age 59 4- 9 years). Ninety-seven patients (52%) had documented previous MI. Patients with cardiomyopathy, valvular heart disease, anemia, thyroid disease, electrolyte imbalance, complete left bundle branch block, intraventricular conduction defect, or premature ventricular complexes on the electrocardiogram at rest were excluded.
November 1, 1984 THE AMERICANJOURNAL OF CARDIOLOGY Volume54
TABLE I
Correlation of Exercise-Induced Complex Ventricular Arrhythmlas and Simple or No Premature Ventricular Complexes with Sudden Death and Total Cardiac Death in Patients with Coronary Artery Disease During 4-Year Follow-Up
TABLE III
Sudden Death Total Cardiac Death n n Exercise-induced complex ventricular arrhythmias Exercise-induced simple or no premature ventricular complexes
2•30 (7% ")
4•30 (13% •)
12/156 (8%)
17/156 (11%)
• Difference not significant.
1137
CorrelaUon of Exercise-Induced Complex Ventricular Arrhythmlas and Simple or No Premature Ventrlcular Complexes with Sudden Death and Total Cardiac Death In PaUents with Coronary Artery Disease and Abormal Left Ventrlcular Ejection Fraction During 4-Year Follow-Up Sudden Death Total Cardiac Death n n
Exercise-induced complex ventricular arrhythmias Exercise-induced simple or no premature ventricular complexes
219 (22% •)
3/9 (33% ")
8•56 (14%)
10/56 (18%)
• Difference not significant. TABLE II
Correlation of Exercise-Induced Complex Ventrlcular Arrhythmlas and Simple or No Premature Ventricular Complexes with Sudden Death and Total Cardiac Death in Patients with Coronary Artery Disease and Normal Left Ventricular Ejection Fraction During 4-Year Follow-Up Sudden Death Total Cardiac Death n n
Exercise-induced complex ventricular arrhythmias Exercise-induced simple or no premature ventricular complexes
0/21 (0% °)
1/21 (5% •)
4/100 (4%)
7/100 (7%)
TABLE IV
Correlation of Abnormal Left Ventricular Ejection Fraction and of Normal Left Ventricular Ejection Fraction with Sudden Death and Total Cardiac Death in Patients with Coronary Artery Disease During 4-Year Follow-Up
Abnormal left ventricular ejection fraction Normal left ventricular ejection fraction
Sudden Death n
Total Cardiac Death n
10/65 (15% *)
13/65 (20%t)
4/121 (3%)
8/121 (7%)
• p <0.005; 1"p <0.01.
• Difference not significant.
Seventy-one patients were taking antiarrhythmic agents including quinidine, procainamide, disopyramide, mexiletine, tocainide, a miodarone or ~-blocking drugs (46 patients) at the time of exercise testing, and 73 patients (51 patients receiving f3-blocking drugs) were taking antiarrhythmic agents during the follow-up period. During follow-up, 87 patients underwent coronary artery bypass surgery, and none had coronary angioplasty. All 186 patients performed a continuous multistage treadmill exercise test using the Bruce protocol. Standard 12-1ead electrocardiograms were recorded at the end of each 3-minute stage and at the end of exercise. After exercise, electrocardiograms were recorded with the patients in the supine position immediately after exercise and at 1,2, 3, 4, 5 and 6 minutes after exercise. The patients were monitored continuously during and for 6 or more minutes after exercise. Of the 186 patients, 132 (71% ) exercised until chest pain, marked dyspnea or fatigue developed, 30 (16%) exercised until they had marked STsegment changes, 20 (11%) exercised until 100% of the maximal predicted heart rate was achieved, 3 (2%) exercised until complex ventricular arrhythmias developed, and 1 patient (1% ) exercised until symptoms of lightheadedness occurred. Exercise-induced premature ventricular complexes were considered complex if they occurred in pairs or runs, if they were multiform, or if they occurred at a frequency of more than 10 beats/rain. Ventricular arrhythmias detected on hard copy were included. Selective coronary arteriograms were performed in all 186 patients, using either the Sones or Judkins technique, within 14 days of exercise testing. EF was calculated from the left ventriculogram in the right anterior oblique view using a simplified modification of the area-length method. L VEF
was considered normal if it was 50% or greater and abnormal if it was less than 50%. Significant CAD was defined as a decrease in luminal diameter greater than 50% as judged by 2 or more of the investigators without knowledge of the results of exercise testing. Follow-up of all 186 patients was obtained from each patient's physician as well as from the patient, if alive, or from the patient's family if the patient had died. The mean follow-up was 4.1 4- 1.3years {range 2.1 to 8.1). In this study, sudden death was defined as death from cardiac cause occurring within i hour of onset of symptoms. The incidence of total cardiac death included both sudden and nonsudden cardiac deaths. All data were analyzed using an I B M System 4341 computer and programs from the statistical package for social sciences (SPSS). Chi-square tests and a life-table analysis were used. Table I lists the incidence of sudden death and total cardiac death in patients with and without exercise-induced complex ventricular arrhythmias. No significant differences were found. Table H lists the incidence of sudden death and total cardiac death in patients with CAD and a normal L VEF both with and without exercise-induced complex ventricular arrhythmias. No significant differences were found. Table I I I illustrates the incidences of sudden death and total cardiac death in patients with CAD and an abnormal L VEF both with and without exercise-induced complex ventricular arrhythmias. No significant differences were found. Table I V shows the incidences of sudden death and of total cardiac death in patients with CAD and abnormal L VEF and in patients with CAD and a normal L VEF. Patients with an abnormal L VEF had a higher incidence of sudden death (chi-square = 8.86, p <0.005) and of total cardiac death (chi-square = 7.57, p <0.01). Life-table analysis showed that the incidence of total cardiac death did not differ between
1136
BRIEFREPORTS
v 100
Q
(3
P
P < 0.005
e-
o
FIGURE 1. Life-table analysis of patients with coronary artery disease and an abnormal and a normal left ventricular ejection fraction (LVEF).
n
2 O.
40
E U
I
0
0
I
1
i
I
2
I
i
i
3
i
4
i
17
Normal
•
Abnormal LVEF I
5
LVEF
I
i
8
Years
patients with and without exercise-induced complex ventricular arrhythmias, between patients with a normal L VEF with and without exercise-induced complex ventricular arrhythmias, or between patients with an abnormal L VEF with and without exercise-induced complex ventricular arrhythmias. Figure 1 depicts a life-table analysis for patients with CAD and an abnormal L VEF and a normal L VEF. Using the Lee-Desu statistic, survival curves showed a significant difference between patients with CAD with an abnormal L VEF and those with a normal L VEF, p <0.005.
Ambulatory monitoring studies have documented that complex ventricular arrhythmias are prognosticaUy significant independent of LV function.5,6 However, the prognostic significance of exercise-induced complex ventricular arrhythmias is controversial.1-~ Our data revealed no significant difference in the incidences of sudden or total cardiac death in patients with exercise-induced complex ventricular arrhythmias when compared with those in patients without exercise-induced complex ventricular arrhythmias. However, patients with an abnormal LVEF had a higher incidence of sudden and total cardiac death than did patients with a normal LVEF. These differences were independent of exercise-induced complex ventricular arrhythmias.
Long-Term Therapy of Paroxysmal Supraventricular Tachycardia: A Randomized, Double-Blind Comparison of Digoxin, Propranolol and Verapamil MICHAEL D. WINNIFORD, MD KAY L. FULTON, MD L. DAVID HILLIS, MD
Although most patients with paroxysmal supraventricular tachycardia (SVT) have episodes with such From the Department of Internal Medicine (Cardiovascular Division), Room L5.134, the University of Texas Health Science Center, 5323 Harry Hines Boulevard, Dallas, Texas 75235. Manuscript received July 19, 1984, accepted July 23, 1984.
Our study is a retrospective analysis of a select group of patients with CAD who were referred for cardiac catheterization and exercise testing. In these patients, our data suggest that exercise-induced complex ventricular arrhythmias do not predict sudden death or total cardiac mortality independent of LV function and are in agreement with the recent data reported by Califf et al. 3 References 1. Udall JA, Ellestad MH. Predictive implications of ventrlcular premature contractions associated with treadmill stress testing. Circulation 1977;56: 985-989. 2. Cohn K, Kamm B, Fetech N, Brand R, Goldschlager N. Use of a treadmill score to predict presence and severity of coronary artery disease. Circulation 1979;59:286-296. 3. Callff RM, McKInnla RA, McNeer JF, Harrell FE, Lee KL, Pryor DB, Waugh RA, Harris PJ, Rosatl RA, Wagner GS. Prognostic value of ventricular arrhythmlas associated with treadmill exercise testing in patients studied with cardiac catheterization for suspected ischemic heart disease. JACC 1983;2:1060-1067. 4. Nalr CK, Aronow WS, Sketch MH, Pagano T, Lynch JD, Mooss AN, Esterbrooks D, Runco V, Ryschon K. Diagnostic and prognostic significance of exercise-induced premature ventricular complexes in men and women: a four year follow-up. JACC 1983; 1:1201- 1206. 5. Ruberman W, Welnblatt E, Goldberg JD, Frank CW, Shapiro S. Ventricular premature beats in the prognosis of angina. Am J Cardiol 1973;297:750757. 6. Calm RM, McKinnis RA, Barks J, Lee KL, Harrell FE, Bahar VS, Pryor DB, Wagner GS, Rosatl RA. Prognostic implications of ventrlcular arrhythmias during 24 hour ambulatory monitoring in patients undergoing catheterization for coronary artery disease. Am J Cardiol 1982;50:23-31.
infrequency and lack of symptoms that prophylactic therapy is not warranted, some have frequent or especially symptomatic episodes and may benefit from the chronic administration of an antiarrhythmic agent. Several drugs have been used as prophylactic therapy for SVT, including digitalis, z propranolol2,3 and verapamil. 4-6 The present study was performed to compare the long-term efficacy and safety of these 3 agents in patients with frequent SVT. Eleven patients (2 men and 9 women, mean age 48 years [range 30 to 72]) were identified as having more than 2 episodes per month of symptomatic S V T (documented electrocardiographicaUy) when no antiarrhythmic drugs were given. Patients were ineligible for study if they had electrocardiographic evidence of ventricular preexcitation. After informed consent was obtained, each patient was randomly and blindly assigned to receive I month each of digoxin (0.375 rag]day), propranolol (240 mg]day in 3 equal doses) and
BRIEF REPORTS
FIGURE 2. Left coronary angiogram in anterior view 3 hours after onset of chest pain. Left anterior descending coronary artery is normal.
prior intracoronary thrombolytic therapy have been demonstrated in about 3% of patients with proved AMI on angiography at 4 weeks to 12 months after AMI. 2 There has been 1 other published report of 3 episodes of AMI in 2 patients with normal or near normal coronary arteries supplying the site of AMI. 3 Angiography was performed at 12 hours in the patient with normal coronary arteries and at 4 and 12 hours in the patient with near normal coronary arteries. The cause of AMI in our patient is uncertain. Three possibilities have been considered: a coronary artery lesion missed at angiography, an episode of prolonged coronary artery spasm, or an obstructing thrombus or embolus with early spontaneous lysis. At coronary angiography, several projections, including angulated
Prognostic Significance of ExerciseInduced Complex Ventricular Arrhythmias in Coronary Artery Disease with Normal and Abnormal Left Ventricular Ejection Fraction CHANDRA K. NAIR, MD WADE THOMSON, MS WlLBERT S. ARONOW, MD TOM PAGANO, MD KAY RYSCHON, MS MICHAEL H. SKETCH, MD
Ventricular arrhythmias on the electrocardiogram at rest and during prolonged ambulatory monitoring are From the Division of Cardiology, Creighton University School of Medicine, 601 North 30th Street, Omaha, Nebraska 68131. Manuscript received April 16, 1984; revised manuscript received June 19, 1984, accepted June 26, 1984.
views, were taken and a major stenotic lesion was not seen. Coronary artery spasm was unlikely as he had no previous angina, no visible spasm on angiography, and no angina in the 6 months after the AMI. Heupler et al 4 was unable to provoke coronary spasm with ergonovine in any of 6 patients with normal coronary arteries and a history of AMI as an isolated clinical event. The most likely cause of the infarct would appear to be obstruction of the left anterior descending artery by thrombus superimposed on a nonobstructive atherosclerotic plaque not seen on angiography, or obstruction by an embolus. In each case rapid lysis must be postulated. Indirect evidence of spontaneous lysis of coronary thrombi has been provided by de Wood et al, 6 who performed angiography up to 24 hours after the onset of symptoms of AMI. He found that the incidence of total coronary occlusion decreased with time. Anderson et al 6 described 2 patients with normal coronary arteries after streptokinase lysis of a completely occluding coronary thrombus 8 and 3 hours after the onset of anterior AMI. References 1. Maddahl J, Ganz W, Nlmomlya K, Hashlda J, Flshbeln MC, Mondkar A, Buchblnder N, Marcus H, Geft I, Shah PK, Rozanskl A, Swan HJC, Berman DS. Myocardial salvage by intracoronary thrombolysis in evolving acute myocardial infarction: evaluation using in1~acorouaryinjection of thallium-201. Am Heart J 1981; 102:664-674. 2. Belrlu A, Pare JC, Sanz GA, Casals F, Magrlna J, Castaner A, NavarroLopoz F. Myocardial Infarction with normal coronary arteries: a prospective cllnical--anglographic study. Am J Cardlol 1981;48:28-32. 3. Olive PB, Brecklnddge JC. Acute myocardial infarction with normal and near normal coronary arteries. Documentation with coronary arteriography within 12 112 hours of the onset of symptoms in two cases (three episodes). Am J Cardlol 1977;40:1000-1007. 4. Heupler FA, Prouclflt WL, Razavl M, Shlrey EK, Grsonslreet R, Sheldon WC. Ergonovlne maleete provocative test for coronary arterial spasm. Am J Cardiol 1978;41:631-640. 5. De Wood MA, Spores J, Nolske R, Mouser LT, Burroughs R, Golden MS, Lang HT. Prevalence of total coronary occlusion during the early hours of transmural myocardial infarction. N Engl J Mad 1980;303:897-902. 6. Anderson JL, Marshall HW, While RS, Datz F. Streptoklnase thrombolysis for acute myocardial Infarction in young adults with normal coronary arteries. Am Heart J 1983;106:1437-1438.
associated with increased risk of both sudden and nonsudden cardiac death. However, the prognostic significance of exercise-induced ventricular arrhythmias is controversialj -4 Recently, we reported that exercise-induced simple premature ventricular complexes in patients without prior myocardial infarction (MI) did not predict coronary events during a mean follow-up of 4 years. 4 Therefore, we studied the prognostic value of exercise-induced complex ventricular arrhythmias in patients with both a normal and an abnormal left ventricular (LV) ejection fraction (EF) to delineate whether exercise-induced ventricular arrhythmias predict mortality independent of LV function. One hundred eighty-six patients with coronary artery disease (CAD) documented by coronary arteriography were studied. There were 157men (mean age 59 4- 9years) and 29 women (mean age 59 4- 9 years). Ninety-seven patients (52%) had documented previous MI. Patients with cardiomyopathy, valvular heart disease, anemia, thyroid disease, electrolyte imbalance, complete left bundle branch block, intraventricular conduction defect, or premature ventricular complexes on the electrocardiogram at rest were excluded.
November 1, 1984 THE AMERICANJOURNAL OF CARDIOLOGY Volume54
TABLE I
Correlation of Exercise-Induced Complex Ventricular Arrhythmlas and Simple or No Premature Ventricular Complexes with Sudden Death and Total Cardiac Death in Patients with Coronary Artery Disease During 4-Year Follow-Up
TABLE III
Sudden Death Total Cardiac Death n n Exercise-induced complex ventricular arrhythmias Exercise-induced simple or no premature ventricular complexes
2•30 (7% ")
4•30 (13% •)
12/156 (8%)
17/156 (11%)
• Difference not significant.
1137
CorrelaUon of Exercise-Induced Complex Ventricular Arrhythmlas and Simple or No Premature Ventrlcular Complexes with Sudden Death and Total Cardiac Death In PaUents with Coronary Artery Disease and Abormal Left Ventrlcular Ejection Fraction During 4-Year Follow-Up Sudden Death Total Cardiac Death n n
Exercise-induced complex ventricular arrhythmias Exercise-induced simple or no premature ventricular complexes
219 (22% •)
3/9 (33% ")
8•56 (14%)
10/56 (18%)
• Difference not significant. TABLE II
Correlation of Exercise-Induced Complex Ventrlcular Arrhythmlas and Simple or No Premature Ventricular Complexes with Sudden Death and Total Cardiac Death in Patients with Coronary Artery Disease and Normal Left Ventricular Ejection Fraction During 4-Year Follow-Up Sudden Death Total Cardiac Death n n
Exercise-induced complex ventricular arrhythmias Exercise-induced simple or no premature ventricular complexes
0/21 (0% °)
1/21 (5% •)
4/100 (4%)
7/100 (7%)
TABLE IV
Correlation of Abnormal Left Ventricular Ejection Fraction and of Normal Left Ventricular Ejection Fraction with Sudden Death and Total Cardiac Death in Patients with Coronary Artery Disease During 4-Year Follow-Up
Abnormal left ventricular ejection fraction Normal left ventricular ejection fraction
Sudden Death n
Total Cardiac Death n
10/65 (15% *)
13/65 (20%t)
4/121 (3%)
8/121 (7%)
• p <0.005; 1"p <0.01.
• Difference not significant.
Seventy-one patients were taking antiarrhythmic agents including quinidine, procainamide, disopyramide, mexiletine, tocainide, a miodarone or ~-blocking drugs (46 patients) at the time of exercise testing, and 73 patients (51 patients receiving f3-blocking drugs) were taking antiarrhythmic agents during the follow-up period. During follow-up, 87 patients underwent coronary artery bypass surgery, and none had coronary angioplasty. All 186 patients performed a continuous multistage treadmill exercise test using the Bruce protocol. Standard 12-1ead electrocardiograms were recorded at the end of each 3-minute stage and at the end of exercise. After exercise, electrocardiograms were recorded with the patients in the supine position immediately after exercise and at 1,2, 3, 4, 5 and 6 minutes after exercise. The patients were monitored continuously during and for 6 or more minutes after exercise. Of the 186 patients, 132 (71% ) exercised until chest pain, marked dyspnea or fatigue developed, 30 (16%) exercised until they had marked STsegment changes, 20 (11%) exercised until 100% of the maximal predicted heart rate was achieved, 3 (2%) exercised until complex ventricular arrhythmias developed, and 1 patient (1% ) exercised until symptoms of lightheadedness occurred. Exercise-induced premature ventricular complexes were considered complex if they occurred in pairs or runs, if they were multiform, or if they occurred at a frequency of more than 10 beats/rain. Ventricular arrhythmias detected on hard copy were included. Selective coronary arteriograms were performed in all 186 patients, using either the Sones or Judkins technique, within 14 days of exercise testing. EF was calculated from the left ventriculogram in the right anterior oblique view using a simplified modification of the area-length method. L VEF
was considered normal if it was 50% or greater and abnormal if it was less than 50%. Significant CAD was defined as a decrease in luminal diameter greater than 50% as judged by 2 or more of the investigators without knowledge of the results of exercise testing. Follow-up of all 186 patients was obtained from each patient's physician as well as from the patient, if alive, or from the patient's family if the patient had died. The mean follow-up was 4.1 4- 1.3years {range 2.1 to 8.1). In this study, sudden death was defined as death from cardiac cause occurring within i hour of onset of symptoms. The incidence of total cardiac death included both sudden and nonsudden cardiac deaths. All data were analyzed using an I B M System 4341 computer and programs from the statistical package for social sciences (SPSS). Chi-square tests and a life-table analysis were used. Table I lists the incidence of sudden death and total cardiac death in patients with and without exercise-induced complex ventricular arrhythmias. No significant differences were found. Table H lists the incidence of sudden death and total cardiac death in patients with CAD and a normal L VEF both with and without exercise-induced complex ventricular arrhythmias. No significant differences were found. Table I I I illustrates the incidences of sudden death and total cardiac death in patients with CAD and an abnormal L VEF both with and without exercise-induced complex ventricular arrhythmias. No significant differences were found. Table I V shows the incidences of sudden death and of total cardiac death in patients with CAD and abnormal L VEF and in patients with CAD and a normal L VEF. Patients with an abnormal L VEF had a higher incidence of sudden death (chi-square = 8.86, p <0.005) and of total cardiac death (chi-square = 7.57, p <0.01). Life-table analysis showed that the incidence of total cardiac death did not differ between
1136
BRIEFREPORTS
v 100
Q
(3
P
P < 0.005
e-
o
FIGURE 1. Life-table analysis of patients with coronary artery disease and an abnormal and a normal left ventricular ejection fraction (LVEF).
n
2 O.
40
E U
I
0
0
I
1
i
I
2
I
i
i
3
i
4
i
17
Normal
•
Abnormal LVEF I
5
LVEF
I
i
8
Years
patients with and without exercise-induced complex ventricular arrhythmias, between patients with a normal L VEF with and without exercise-induced complex ventricular arrhythmias, or between patients with an abnormal L VEF with and without exercise-induced complex ventricular arrhythmias. Figure 1 depicts a life-table analysis for patients with CAD and an abnormal L VEF and a normal L VEF. Using the Lee-Desu statistic, survival curves showed a significant difference between patients with CAD with an abnormal L VEF and those with a normal L VEF, p <0.005.
Ambulatory monitoring studies have documented that complex ventricular arrhythmias are prognosticaUy significant independent of LV function.5,6 However, the prognostic significance of exercise-induced complex ventricular arrhythmias is controversial.1-~ Our data revealed no significant difference in the incidences of sudden or total cardiac death in patients with exercise-induced complex ventricular arrhythmias when compared with those in patients without exercise-induced complex ventricular arrhythmias. However, patients with an abnormal LVEF had a higher incidence of sudden and total cardiac death than did patients with a normal LVEF. These differences were independent of exercise-induced complex ventricular arrhythmias.
Long-Term Therapy of Paroxysmal Supraventricular Tachycardia: A Randomized, Double-Blind Comparison of Digoxin, Propranolol and Verapamil MICHAEL D. WINNIFORD, MD KAY L. FULTON, MD L. DAVID HILLIS, MD
Although most patients with paroxysmal supraventricular tachycardia (SVT) have episodes with such From the Department of Internal Medicine (Cardiovascular Division), Room L5.134, the University of Texas Health Science Center, 5323 Harry Hines Boulevard, Dallas, Texas 75235. Manuscript received July 19, 1984, accepted July 23, 1984.
Our study is a retrospective analysis of a select group of patients with CAD who were referred for cardiac catheterization and exercise testing. In these patients, our data suggest that exercise-induced complex ventricular arrhythmias do not predict sudden death or total cardiac mortality independent of LV function and are in agreement with the recent data reported by Califf et al. 3 References 1. Udall JA, Ellestad MH. Predictive implications of ventrlcular premature contractions associated with treadmill stress testing. Circulation 1977;56: 985-989. 2. Cohn K, Kamm B, Fetech N, Brand R, Goldschlager N. Use of a treadmill score to predict presence and severity of coronary artery disease. Circulation 1979;59:286-296. 3. Callff RM, McKInnla RA, McNeer JF, Harrell FE, Lee KL, Pryor DB, Waugh RA, Harris PJ, Rosatl RA, Wagner GS. Prognostic value of ventricular arrhythmlas associated with treadmill exercise testing in patients studied with cardiac catheterization for suspected ischemic heart disease. JACC 1983;2:1060-1067. 4. Nalr CK, Aronow WS, Sketch MH, Pagano T, Lynch JD, Mooss AN, Esterbrooks D, Runco V, Ryschon K. Diagnostic and prognostic significance of exercise-induced premature ventricular complexes in men and women: a four year follow-up. JACC 1983; 1:1201- 1206. 5. Ruberman W, Welnblatt E, Goldberg JD, Frank CW, Shapiro S. Ventricular premature beats in the prognosis of angina. Am J Cardiol 1973;297:750757. 6. Calm RM, McKinnis RA, Barks J, Lee KL, Harrell FE, Bahar VS, Pryor DB, Wagner GS, Rosatl RA. Prognostic implications of ventrlcular arrhythmias during 24 hour ambulatory monitoring in patients undergoing catheterization for coronary artery disease. Am J Cardiol 1982;50:23-31.
infrequency and lack of symptoms that prophylactic therapy is not warranted, some have frequent or especially symptomatic episodes and may benefit from the chronic administration of an antiarrhythmic agent. Several drugs have been used as prophylactic therapy for SVT, including digitalis, z propranolol2,3 and verapamil. 4-6 The present study was performed to compare the long-term efficacy and safety of these 3 agents in patients with frequent SVT. Eleven patients (2 men and 9 women, mean age 48 years [range 30 to 72]) were identified as having more than 2 episodes per month of symptomatic S V T (documented electrocardiographicaUy) when no antiarrhythmic drugs were given. Patients were ineligible for study if they had electrocardiographic evidence of ventricular preexcitation. After informed consent was obtained, each patient was randomly and blindly assigned to receive I month each of digoxin (0.375 rag]day), propranolol (240 mg]day in 3 equal doses) and