Search

Cardiac chamber weight was determined at necropsy in 323 men to develop correlative studies of electrocardiographic criteria for ventricular hypertrophy. Thirty recommended criteria for left ventricular (LV) hypertrophy, 10 for right ventricular (RV) hypertrophy, and combinations of both criteria for combined hypertrophy were evaluated. Four methods for electrocardiographic diagnosis of LV hypertrophy were derived: (1) a modification of the Romhilt-Estes point system; (2) the presence of any 1 of 3 criteria: (a) S V1 + R V5 or V6 greater than 35 mm, (b) left atrial abnormality, or (c) intrinsicoid deflection in lead V5 or V6 greater than or equal to 0.05 second; (3) a combination of any 2 criteria or of 1 criterion (above) plus at least 1 of the following 3 additional criteria: (a) left-axis deviation greater than -30 degrees, (b) QRS duration greater than 0.09 second, or (c) T-wave inversion in lead V6 of 1 mm or more; and (4) the use of a single criterion--left atrial abnormality. Sensitivity varied from 57 to 66% and specificity from 85 to 93% among these 4 methods. Myocardial infarction increased sensitivity of the foregoing methods, but the specificity was reduced. Method 2 is preferred for the electrocardiographic diagnosis of LV hypertrophy. Two methods were useful for right ventricular (RV) hypertrophy: (1) the use of any 1 of 4 criteria: (a) R/S ratio in lead V5 or V6 less than or equal to 1; (b) S V5 or V6 greater than or equal to 7 mm; (c) right-axis deviation of more than +90 degrees, or (d) P pulmonale; and (2) use of any 2 combinations of the foregoing criteria. Sensitivity ranged from 18 to 43% and specificity from 83 to 95%. Combined hypertrophy was best diagnosed using left atrial abnormality as the sole criteria of LV hypertrophy, plus any 1 of 3 criteria of RV hypertrophy: (a) R/S ratio in lead V5 or V6 less than or equal to 1, (b) S V5 or V6 greater than or equal to 7 mm, or (c) right axis deviation greater than +90 degrees.(ABSTRACT TRUNCATED AT 250 WORDS)

Summary Analysis of clinical ventricular ectopy hasprovided deductive evidence for the existence of concealed ventricular rhythms. Studies in the experimental animal have demonstrated that when ventricular extrastimuli are applied near the ventricular effective refractory period of consecutive sinus beats, extrastimuli may not be conducted after sinus beats immediately following the postextrasystolic pause. This sequence may be due to a prolongation of the effective refractory period of ventricular muscle produced by the increased cycle length resulting from the post-extrasystolic pause. The purpose of this study was to extend these observations to the human ventricle in an attempt to produce concealed ventricular rhythms by programmed ventricular extrastimuli. Twelve patients with normal PR intervals and QRS complexes with a mean age of 49 years were studied with ventricular extrastimuli at programmed intervals following normally conducted sinus impulses. Premature ventricular impulses were introduced after every sinus beat at intervals 10 to 120 msec outside the effective refractory period. In eleven patients without ventricular interpolation,stimuli applied within 40 msec of the effective refractory period produced from one to three concealed (non-conducted) ventricular stimuli following the postextrasystolic pause; stimuli applied greater than 40 msec outside the effective refractory period at identical current levels produced manifested bigeminy in all cases. In one patient with interpolated premature ventricular beats without a compensatory pause, programmed ventricular extrastimuli produced manifest bigeminy at all coupling intervals. This study demonstrates the experimental production of concealed and manifest ventricular rhythms in man and confirms the importance of the relationship between the ventricular effective refractory period, the timing of the premature ventricular impulse, and the occurence of a compensatory pause.

The short-term efficacy of oral acebutolol was evaluated in 20 patients with coronary artery disease and frequent premature ventricular contractions (PVCs) by serial 24-hour Holter monitoring before and while the patients were receiving an average daily dose of 1,100 mg. of acebutolol for four weeks. Fifty-five percent of the 20 patients showed a greater than 70% PVC reduction from baseline values. The only serious side effect during short-term therapy was mild, reversible cardiac decompensation in one patient. The long-term safety and continued efficacy of acebutolol was then evaluated over the next 11 months in nine of the 11 patients showing greater than 70% PVC reduction at four weeks. Two-thirds of these nine patients continued to show greater than 80% PVC reduction from baseline values at 12 months. One patient developed alopecia during long-term therapy. The majority of patients not responding well to acebutolol at four weeks had an actual increase in PVCs on acebutolol therapy. We conclude that acebutolol produces long-term, effective reduction in PVCs without serious toxicity in the majority of patients with ventricular ectopy. However, this drug appears to either produce an excellent response or no response with regard to PVC control in most instances.

This study shows significant changes occurring in systolic time intervals in an experimental animal model of aortic outflow obstruction with cardiac hypertrophy. The left ventricular ejection time is markedly prolonged and the preejection period/left ventricular ejection time ratio shortened. These changes are in the opposite direction of those usually observed with left ventricular dysfunction in man but similar to those described in man with aortic stenosis. Furthermore, the changes observed in systolic time intervals after digoxin in this experimental model are not comparable to those reported in man with normal or abnormal left ventricular function. Hence, the use of systolic time intervals, including digitalis effect, to evaluate the functional state of the left ventricle in aortic outflow obstruction are probably unreliable.

The influence of aorto-coronary bypass surgery (ACBS) on ventricular arrhythmia was examined in 57 patients. Six-hour Holter monitoring was done on the day prior to and 3 mth after ACBS. None of the patients were on any antiarrhythmic drugs during these recordings. Ventricular arrhythmia was classified into three groups: Group I (45 patients) had an average of less than 10 premature ventricular contractions (PVCs) per hour, Group II (7 patients), 11-30 PVCs per hour and Group III (5 patients), greater than 30 PVCs per hour. There was no significant change in the number of patients in each group after ACBS. Complex PVCs were present in 8 patients preoperatively and in 9 patients after ACBS. The number of diseased vessels and the extent of left ventricular wall motion abnormality noted preoperatively, had no effect on ventricular arrhythmia following surgery. These data show that ACBS, when performed to relieve angina, does not have a significant effect on the prevalence of PVCs and does not prevent or reduce the occurrence of complex PVCs.

To evaluate the refractory periods of the atrioventricular (A-V) conducting system in patients with a short P-R interval and normal QRS complex, 57 patients with a P-R interval of 110 to 280 msec were studied with His bundle recording and premature atrial stimulation at similar cycle lengths of 660 to 720 msec. In 13 patients with a short P-R interval (120 msec or less) the mean value for the functional refractory period of the A-V node was 368 plus or minus 36 msec (standard deviation), which was significantly lower (P smaller than 0.01) than the mean value of 415 plus or minus 50 msec in 36 patients with a normal P-R interval (between 120 and 200 msec) and the mean value of 492 plus or minus 57 msec in 8 patients with an increased P-R interval (200 msec or greater). Patients with a short P-R interval had a mean value for the effective refractory period of the A-V conducting system of 247 plus or minus 26 msec, which was significantly lower (P smaller than 0.01) than the mean values of 297 plus or minus 51 msec in patients with a normal P-R interval and 369 plus or minus 87 msec in patients with an increased P-R interval. The results identify a characteristic conduction abnormality that is compatible with a partial A-V nodal bypass or dual A-V nodal conduction pathways. The relation between the duration of the P-R interval and the regractory period may aid understanding of the clinical significance of the scalar electrocardiogram.

The clinical presentation and echocardiographic findings in a patient with rupture of a noncoronary sinus of Valsalva aneurysm into the right atrium with associated aortic regurgitation are described. Preoperatively, only the right coronary cusp could be visualized by echocardiography. Following surgical repair of the defect, both right and noncoronary cusps were easily seen. It is felt that the inability to demonstrate the noncoronary cusp was caused by the aneurysm pulling the cusp out of alignment with the uninvolved cusps. The echocardiogram appears to be useful in the diagnosis of a rupture of the noncoronary sinus of Valsalva.

Propafenone is a new anti arrhythmic agent with primarily membrane-stabilizing action. Three U.S. controlled double-blind cross-over studies demonstrated the efficacy of propafenone in suppressing ventricular premature complexes (VPCs), including repetitive forms: 67–83% of patients had greater than 80% reduction of VPCs, 62% achieved greater than 90% reduction of couplets and 80%–100% achieved 200% abolition of ventricular tachycardia runs. Other studies showed that propafenone is effective in controlling ventricular arrhythmias refractory to conventional anti arrhythmic agents. Propafenone is at least as effective as these agents. Long-term sustained efficacy of propafenone was shown in some preliminary studies. Because of the variation in individual response to the drug, therapy should be individualized for each patient. Propafenone is well tolerated: side effects of propafenone are few and involve mostly the cardiac conduction system. Propafenone would be a significant addition to the anti arrhythmic armamentarium.

In order to determine the role of the coupling interval of a premature ventricular contraction (PVC) in the development of paroxysmal ventricular tachycardia (PVT) during the early phase of acute myocardial infarction in man, 52 male patients with documented acute myocardial infarction had 24-hour Holter monitoring commenced within 24 hours of the onset of prolonged chest pain. Review of the tape recordings revealed that 27 patients had PVT documented, while 25 patients did not. Analysis of the data on the two groups showed that the frequency of PVCs, coupled PVCs, and accelerated idioventricular rhythm (AIVR) were found to be associated with a significantly increased incidence of ventricular tachycardia. The mean coupling interval of the PVCs initiating episodes of ventricular tachycardia was not significantly different from either the mean coupling interval of the isolated PVCs in the patients with PVT or the mean coupling interval of the PVCs in the patients without PVT. This suggests that the coupling interval of a ventricular ectopic is a poor predictor of ventricular tachycardia in the early phases of acute myocardial infarction.

The long-term prognosis of paroxysmal ventricular tachycardia (PVT) complicating acute myocardial infarction remains unevaluated. Significant ventricular arrhythmia in the patient after infarction is said to carry a poor prognosis with regard to survival. To evaluate these two important aspects of myocardial infarction in man, 56 patients with documented myocardial infarction had Holter monitoring performed during the initial 24 hours and prior to hospital discharge. In 38 of the 45 survivors, Holter monitoring was repeated an average of 19 months after infarction. There were eight cardiac deaths during follow-up. Data analysis revealed that of 18 patients with PVT during the acute phase, one died during follow-up and 17 survived long-term. Even though the incidence of complex PVCs prior to hospital discharge and at long-term follow-up was higher in patients with PVT during the acute phase than in those without PVT, survival appeared unaffected. Thus, PVT during the acute phase of myocardial infarction and complex PVCs at the time of hospital discharge are not incompatible with long-term survival.

Most measurements establishing standard values for the normal electrocardiogram have been derived from a healthy population, whereas many electrocardiographic interpretations are necessary in hospitalized or seriously ill patients. Therefore, the characteristics of the electrocardiogram were described from 48 autopsied men known to be free of cardiopulmonary disease by clinical assessment and by a special cardiac examination using postmortem coronary angiography and a chamber partition technique. Highest values, mean and standard deviation, and the upper 97.5 percentile or lower 2.5 percentile when appropriate were noted for QRS voltage, QRS axis and duration, and intrinsicoid deflection in V5 or V6. Any ST-segment and T-wave changes were noted as well as left and right atrial abnormalities. Twenty-eight electrocardiographic criteria recommended to detect left ventricular hypertrophy and 10 recommended to detect right ventricular hypertrophy were evaluated for percentage of false-positive results and the 97.5 percentile value for each criterion was developed from the present data base. The data in this study can be used as a standard for comparing electrocardiographic variation in middle-aged men with specific relevance for electrocardiographic criteria of ventricular hypertrophy.

The sensitivity of 30 electrocardiographic criteria for left ventricular (LV) hypertrophy, isolated or combined, was examined to determine the relation to the underlying disease. Patients with coronary artery disease (CAD), systemic hypertension, valvular heart disease and cardiomyopathy were evaluated. A cardiac partition technique was used to define ventricular hypertrophy. Single electrocardiographic criteria often showed high sensitivity for 1 disease state, but not for others. Precordial voltage criteria were most sensitive for those with hypertensive and valvular disease. A QRS axis of more than −30 ° occurred most often in patients with CAD. Both left atrial abnormality and abnormal T-wave inversion of more than 1 mm in V6 occurred with a high sensitivity in general; however, T-wave inversion of more than 1 mm in V6 had a low sensitivity in cardiomyopathy. Methods using combinations of various electrocardiographic criteria improved sensitivity. Using these methods, sensitivity of the electrocardiogram for LV hypertrophy was excellent for patients with systemic hypertension and valvular heart disease and acceptable by usual standards for patients with CAD and cardiomyopathy. Because the use of a single criterion is often ineffective, methods using multiple electrocardiographic criteria to detect LV hypertrophy are recommended when the patients under study have diverse cardiac diseases.

Although sinus node function has been evaluated during premature atrial stimulation, no study of retrograde ventriculoatrial sinus node activation following premature ventricular stimuli has been reported. The purpose of this study was to investigate the production of compensatory and noncompensatory pauses by premature ventricular contractions through a comparison of the effects of atrial and ventricular stimulation on sinus node function. Eleven patients in sinus rhythm were studied with programmed introduction of premature atrial and ventricular stimuli outside the ventricular vulnerable period. The onset of sinus node reset, duration of return sinus cycle (A2-A3) during reset, and estimated sinoatrial conduction times were recorded. Sinus node function during premature ventricular stimulation was approximated by utilizing the interval between the last sinus beat and onset of retrograde atrial depolarization (A1-A2 interval). The return cycle length (A2-A3) during sinus reset compared at equal A1-A2 intervals was significantly less with ventriculoatrial conduction (1,145 +/- 52 msec. atrial vs. 1,076 +/- 52 msec ventriculoatrial; P less than 0.01 by paired t test) and the estimated sinoatrial conduction time was significantly less with ventriculoatrial conduction (71 +/- 7 msec. atrial vs. 25 +/- 7 msec. ventriculoatrial; P less than 0.01 by paired t test). Ventriculoatrial sinus reset occurred later in the sinus cycle than atrial reset in three of seven patients with sinus reset produced by both atrial and ventricular prematures. This study shows that the effects of ventriculoatrial conduction on sinus node function are significantly different from those of atrial stimulation alone. The return sinus cycle length during reset and estimated sinoatrial conduction time are significantly reduced with ventriculoatrial conduction. Although the zones of sinus reset with atrial and ventricular stimulation are approximately equal, ventriculoatrial depolarization may produce sinus reset later in the sinus cycle in some cases.

A 20-year-old man presented with cardiomegaly, frequent PVC's, and abdominal pain. On the nineteenth hospital day the patient developed ventricular fibrillation and died. Analysis of a Holter recording initiated 16 hours previously demonstrated an increase in the corrected QT interval (QTc) to 0.48 second and a prematurity index less than 1.0 only during the minute terminated by ventricular fibrillation. This report documents changes in sinus rate, coupling interval, QTc, and prematurity index for 16 hours preceding ventricular fibrillation in a patient with cardiomyopathy. The timing of the terminal arrhythmia coincided with significant changes in the QTc and prematurity index characterized by bradycardia-dependent QTc prolongation and a post-extrasystolic reduction in prematurity index.

Thirty patients with clinically significant ventricular ectopy were treated with propafenone, a new potent antiarrhythmic agent with membrane stabilizing action. Patients had a minimum mean of greater than 30 ventricular premature beats per hour documented by continuous 48-hour ambulatory ECG recording. Twenty-five patients qualified as responders, defined as greater than 85% reduction of ventricular ectopy compared to baseline, and completed a double-blind placebo-crossover phase. Significant reduction in single ventricular ectopy per hour, paired ventricular ectopy per hour, and ventricular tachycardia beats per hour were observed. Almost total abolition of ventricular tachycardia and paired ventricular ectopy was achieved. Side effects were minimal and well tolerated. A significant prolongation of the PR interval occurred. QRS prolongation and prolongation of the corrected QT interval was observed in some patients, with new left bundle branch block developing in two patients. Long-term efficacy and safety studies will be necessary to determine the ultimate role of this new agent in the selection of antiarrhythmic therapy, but these inital results are encouraging.

Since both propranolol therapy and saphenous-vein bypass surgery have become accepted treatments for patients with symptomatic coronary-artery disease, it is important to determine if either influences the prevalence of ventricular arrhythmias in these patients. Six-hour dynamic electrocardiography was done on 130 patients with chronic stable angina pectoris at least 1 year after being randomized to surgical or medical therapy. All surgical patients had saphenous-vein grafting; 90% of the medical patients received propranolol. Data analysis showed that even though the overall prevalence of premature ventricular contractions was no different in medical and surgical patients, the prevalence of complex premature ventricular contractions was significantly higher in surgically treated patients not receiving propranolol than in propranolol-treated medical patients (p less than 0.05). However, the survival rate was no different in either group, and the quality of life in the surgical patients remained superior.

To determine the effect of diphenylhydantoin on intraventricular conduction in man, we utilized His bundle recordings and coupled atrial pacing to record the relative refractory period of the His-Purkinje system and the functional refractory period of the atrioventricular (A-V) node in 14 patients before and after administration of diphenylhydantoin at a rate of 50 mg/min. Before infusion of diphenylhydantoin (5 mg/kg at a rate of 50 mg/min) His-Purkinje conduction delay occurred with right bundle branch block in nine patients and with left bundle branch block in five patients. After infusion of diphenylhydantoin the onset or degree of His-Purkinje delay was altered in all patients. In nine patients diphenylhydantoin reduced the relative refractory period of the His-Purkinje system to a value less than that of the functional refractory period of the A-V node so that His-Purkinje conduction delay could not be demonstrated after diphenylhydantoin. In five patients, diphenylhydantoin reduced the relative refractory period of the His-Purkinje system or altered the degree of aberrant conduction, or both. Diphenylhydantoin reduced the minimal H 1 –H 2 interval achieved before the onset of His-Purkinje block from 421 ± 27 (standard deviation) to 384 ± 34 msec ( P P > 0.1). These results establish that diphenylhydantoin has a significant effect on intraventricular conduction in man.

Left atrial (LA) abnormality determined from precordial lead V1 was assessed by 2 observers as a criterion of left ventricular (LV) hypertrophy in the presence of right bundle branch block (BBS) in 23 patients. The presence of LV hypertrophy was confirmed from a postmortem cardiac partition technique and defined at 2 levels of confidence: probable and definite hypertrophy. Observers reliably differentiated between the hypertrophied and normal-sized ventricle in the presence of right BBB by using LA abnormality as an electrocardiographic criterion. When defined as definite hypertrophy, observer 1 correctly identified LV hypertrophy in 78% of the cases and observer 2 in 67% of the cases. False-positive results were present in 21% of cases by observer 1 and 14% by observer 2. Comparable results were achieved when a definition of probable hypertrophy was used. Observer performance of recognition of LA abnormality in this study was satisfactory with 91% agreement between observers. Our results are comparable and in some instances superior to conventional criteria commonly recommended to diagnose LV hypertrophy on the electrocardiogram without right BBB.

Although rapid atrial pacing is frequently used as a test of atrioventricular conduction, no studies have compared this method with other conduction parameters. The purpose of this study was to compare the results of rapid atrial pacing with refractory period measurements utilizing the extrastimulus technique. Determination of the refractory periods of the atrium, A-V node, and His-Purkinje system were accomplished in 41 patients undergoing diagnostic cardiac catheterization, and the results compared with rapid atrial pacing to the point at which A-V Wenckebach occurred (WP). The results showed significant correlation (P less than 0.01) between the WP and functional refractory period (FRP) of the A-V node (r=0.89, FRP=865-2.6 WP), and significant correlation between the WP and the effective refractory period (ERP) of the total A-V conducting system(r=0.81, ERP=729-2.6 WP). The relationship between WP and the refractory periods also allowed prediction of the occurrence of physiological His-Purkinje block during introduction of premature atrial contractions and the site of the effective refractory period of the total A-V conducting system. This study establishes a close relationship between these methods and confirms the usefulness of rapid atrial pacing as a reliable test of A-V conduction in man.

Thirty-two men with chronic ventricular arrhythmias responded to propafenone, a new potent antiarrhythmic agent, in short-term trials with 85% or greater reduction of total ventricular premature complexes (VPCs) per hour, 95% or greater reduction of ventricular couplets (VCs) per hour, and 100% abolition of ventricular tachycardia (VT) beats per 24 hours. These patients were continued on long-term propafenone therapy to assess sustained therapeutic efficacy and safety. Thirty patients completed 1 year and 26 patients completed 2 years of testing with this agent; one patient died of sudden death and another died of a noncardiac cause. Although there were significantly fewer patient responders at 1 and 2 years, the majority of patients (greater than 79%) continued to respond optimally to propafenone. Side effects were minor and included bitter taste, dizziness, congestive heart failure, fatigue, and significant prolongation of the PR and QRS intervals. Propafenone has sustained antiarrhythmic efficacy after 2 years without serious toxicity.

Atrioventricular conduction patterns suggestive of dual A-V nodal pathways have been reported in patients with and without a history of paroxysmal A-V nodal re-entrant tachycardia (PSVT). The purpose of this study was to determine whether significant association exists between this conduction pattern and the occurrence of PSVT in man. The pattern of A-V conduction was evaluated at similar pacing rates in 13 patients with documented PSVT and 135 patients with PSVT. Patients without PSVT were divided into groups with normal PR intervals (106 patients), PR intervals of 120 msec. or less (12 patients), and PR intervals of 200 msec. or greater (17 patients). Evidence of dual A-V nodal pathways was found in seven of 13 patients with PSVT and nine of 135 patients without PSVT, including eight of 106 patients with normal PR intervals, none of 12 patients with short PR intervals, and one of 17 patients with PR intervals of 200 msec. or greater. The incidence of dual A-V nodal pathways was significantly greater (P less than 0.01) in patients with PSVT when compared with all other groups. In two of four patients with PSVT, propranolol was found to unmask evidence of dual pathways; no evidence of dual pathways was produced by propranolol in 23 patients without PSVT. The data show that the pattern of dual A-V nodal pathways is common only in patients with PSVT and is significantly less frequent in patients without PSVT regardless of the presence of short or long PR intervals. The results of this study establish a strong association between this conduction pattern and the occurrence of PSVT in man.

The effects of orally administered propafenone on ejection fraction (EF) determined by radionuclide angiography were studied in 2 groups of patients receiving different dosing regimens. Fourteen group A patients had no clinical evidence of left ventricular (LV) dysfunction and were not receiving digoxin therapy. In this group a mean daily dosage of 879 mg resulted in a decrease in resting LVEF from 52 +/- 9% to 48 +/- 11% (p less than 0.05). Eight group B patients had clinical radionuclide evidence of LV dysfunction and were receiving digoxin therapy. In this group, a daily dosage of propafenone of 600 mg/day resulted in no significant change in LVEF. No clinically significant effects on cardiac compensation were evident in either group. These data suggest a negative inotropic effect that is either related to propafenone dosage or at least partially attenuated by digoxin therapy. Further studies are necessary to define precisely the effects of propafenone on LV function.

This study examined the hearts of 55 patients dying of chronic obstructive pulmonary disease, with and without cor pulmonale, quantitated histologically the degree of myocardial fibrosis in the left and right ventricle, and determined the relationship to associated disease states. Comparison has been made to a control group of 17 patients free of cardiopulmonary disease. Patients with associated and advanced ischemic heart disease, as proved by marked atherosclerosis and myocardial infarction, have significantly increased myocardial fibrosis throughout all layers of the left ventricular wall in comparison to control patients or patients with chronic obstructive pulmonary disease free of associated cardiac disease. Right ventricular fibrosis was not significantly increased; however, one case showed a marked degree of fibrosis related to myocardial infarction. Subdivision of patients with chronic obstructive pulmonary disease into groups with definite anatomic right ventricular hypertrophy, a clinical diagnosis of cor pulmonale, or with chronic hypoxemia failed to show any difference in the percentage of myocardial fibrosis of the ventricles among these groups. Increased fibrosis of the right or left ventricle in patients with chronic obstructive pulmonary disease, therefore, is not related to the degree of myocardial hypertrophy pathologically, the hypoxemic state, or clinical heart failure, but to ischemic heart disease with myocardial infarction.

Although previous studies have suggested that accelerated idioventricular rhythm rarely coexists with paroxysmal ventricular tachycardia, this relation has not been systematically evaluated in acute myocardial infarction. To examine this relation, the frequency and characteristics of the two arrhythmias were analyzed by performing 24 hour Holter monitoring during the initial 24 hours of acute myocardial infarction in 52 successive patients. Twenty-four of these patients had documented accelerated idioventricular rhythm; 28 patients did not. Paroxysmal ventricular tachycardia occurred in 83 percent of patients with accelerated idioventricular rhythm but in only 18 percent of patients without this arrhythmia (P < 0.001). The results remained at the same level of significance whether paroxysmal ventricular tachycardia was defined by rates greater than 100, 120 or 140 beats/min. These findings suggest that accelerated idioventricular rhythm complicating acute myocardial infarction is not always benign and is frequently associated with more serious forms of ventricular arrhythmia.

We studied 71 patients with 12-hour Holter monitoring to determine if the incidence and complexity of ventricular arrhythmias in symptomatic coronary artery disease patients were related to the extent of left ventricular dysfunction. Their average age was 51 years, and each had cardiac catheterization within 3 months of study. Thirty-six patients had left ventricular aneurysms, 10 had normal left ventricular angiograms and 25 had left ventricular hypokinesis or akinesis without dyskinesis. The patients with aneurysms had significantly more heart failure, prior infarction, cardiomegaly and impaired ejection fractions. The mean premature ventricular contractions per hour for the aneurysm patients was 34 +/- 52, 3 +/- 5 for those with normal left ventricles, and 11 +/- 24 in the remainder. Complex premature ventricular contraction were noted in 50% of the aneurysm patients, in 10% of the patients with normal left ventricles and in 23% of the patients with hypokinesis or akinesis. Ventricular arrhythmias increase with greater left ventricular wall motion abnormality in patients with symptomatic coronary artery disease.

The effectiveness of Holter monitoring is compared to modified treadmill exercise for detecting ventricular arrhythmia in 54 patients during the third week after a documented myocardial infarction. Treatment with digoxin and antiarrhythmic agents had been discontinued for 48 hours. Whereas 76% of the patients had no PVCs during treadmill exercise, only 7% were free of PVCs during Holter monitoring. Complex PVCs occurred in 37% of the subjects during Holter monitoring and in 4% of the subjects during treadmill stress. Although Holter monitoring was significantly more reliable in detecting ventricular arrhythmia, assessment of exercise tolerance and angina status during modified treadmill stress makes both technics desirable in carefully selected patients awaiting discharge from the hospital after myocardial infarction.