Diagnostic and prognostic significance of exercise-induced premature ventricular complexes in men and women: a four year follow-up.

Two hundred eighty patients (197 men and 83 women) with normal rest electrocardiograms and no history of prior myocardial infarction were referred for evaluation of chest pain. It was found that exercise-induced premature ventricular complexes had a lower sensitivity, specificity, positive predictive value and negative predictive value in predicting significant coronary artery disease than exercise-induced ST segment depression greater than or equal to 1 mm. The incidence of exercise-induced premature ventricular complexes was not significantly different in patients with no significant coronary artery disease, single vessel disease or multivessel disease. The site of origin of exercise-induced premature ventricular complexes was not helpful in predicting the presence or severity of coronary artery disease. At a mean follow-up period of 47.1 months, exercise-induced premature ventricular complexes did not predict coronary events (cardiac death or nonfatal myocardial infarction) in men or women.

Tocainide kinetics in congestive heart failure.

Our subjects were 20 patients with life-threatening or symptomatic ventricular arrhythmias refractory to standard oral antiarrhythmic drugs but responsive to intravenous lidocaine. After evaluation of arrhythmias and treatment with intravenous lidocaine, oral tocainide dosage regimens were based on age, weight, and clinical status. During initial tocainide treatment, six plasma tocainide concentrations were recorded within a single dosing interval in 17 of 20 patients, by which standard kinetic parameters were calculated. Eventual trough steady-state tocainide plasma concentrations were predicted from the derived patient-specific kinetic parameters. Mean daily tocainide dose was 1800 mg (1200 to 2400). Mean daily tocainide doses (milligram per kilogram) did not differ significantly among responders and nonresponders or among patients with or without congestive heart failure. Mean peak and trough plasma concentrations 48 hr after initiation of therapy were 9.8 and 7.5 mcg/ml. Tocainide plasma concentrations did not correlate with responders and nonresponders or identify patients who were developing adverse reactions to tocainide. There were no significant differences in any of the calculated kinetic parameters as a function of response to tocainide or the presence of congestive heart failure, but there was a trend toward smaller volumes of distribution and higher average plasma concentrations at steady state in patients with congestive heart failure. There were no significant kinetic differences among patients with and without congestive heart failure, but a trend toward higher plasma concentrations in patients with congestive heart failure and the small number of patients suggests that further data collection is necessary before dosage recommendations can be made.

Effect of digoxin on ST-segment changes detected by ambulatory electrocardiographic monitoring in healthy subjects.

Digoxin causes false-positive ST depression during exercise stress testing, but it is unknown if digoxin produces ST depression during ambulatory electrocardiographic monitoring. Fifty healthy volunteers underwent both exercise stress testing and ambulatory electrocardiographic monitoring before and after 14 days of digoxin (0.25 mg/day) administration. Significant ST depression was defined as greater than or equal to 1 mm of horizontal or downsloping ST depression 80 ms after the J point lasting for greater than or equal to 60 seconds. During therapy, 13 subjects (26%) had at least 1 episode of ST depression and 5 subjects (10%) had multiple episodes of ST depression detected by ambulatory monitoring. Ten subjects (20%) had ST depression that occurred during exercise that was detected by both stress test and ambulatory monitoring. Three subjects (6%) had ST depression that was detected on the ambulatory recording only at times other than during the stress test. Stratification of demographic and clinical variables did not predict digoxin-induced ST depression. Thus, digoxin causes false-positive ST depression detected by ambulatory monitoring. The incidence is similar to that observed during stress testing, but also occurs at heart rates lower than that achieved during stress tests. Ambulatory electrocardiographic monitoring will be less useful in the noninvasive assessment of coronary artery disease in patients receiving digoxin.

Digoxin-induced positive exercise tests: their clinical and prognostic significance.

To evaluate the influence of digoxin on the results of exercise testing and the prognostic significance of digoxin-induced positive exercise tests, 98 healthy men, aged 22 to 70 years, were studied. All had normal initial exercise test results. All took digoxin, 0.25 mg daily, for 14 days, and then performed daily exercise tests until each had a negative test response. Five years after these initial tests, a medical history was obtained from 92 of the 98 subjects, and 76 subjects performed repeat exercise tests. Six subjects were lost to follow-up study. Twenty-five percent of subjects (22 of 98) had a digoxin-induced positive exercise test. There was a direct relation between age and the incidence of digoxin-positive tests. The incidence of digoxin-positive tests in men over age 60 years was 100 percent. By 30 seconds after exercise no subject had greater than 1.9 mm S-T depression. No test remained positive for more than 6 minutes after exercise was discontinued. No test was positive 12 days after digoxin was withdrawn. With logistic regression analysis, it was possible to estimate the probability that a subject would have a digoxin-induced positive test. No subject had had a cardiovascular event at follow-up study, but five subjects had a positive repeat exercise test. Four of these subjects had had a digoxin-positive test initially. It is concluded that (1) useful information can be obtained from exercise studies of patients who receive digoxin, (2) the probability that a positive exercise test is due to digoxin can be estimated, (3) to remove the exercise-induced electrocardiographic effect, the drug should be withdrawn for 12 days, and (4) digoxin may unmask subclinical coronary arterial stenosis.

Efficacy and tolerance of high-dose intravenous amiodarone for recurrent, refractory ventricular tachycardia.

High-dose intravenous amiodarone was given to 35 patients with recurrent life-threatening ventricular tachycardia (VT) refractory to conventional antiarrhythmic agents. Intravenous amiodarone was given as a 5 mg/kg dose over 30 minutes followed by 20 to 30 mg/kg/day as a constant infusion for 5 days. Twenty-two (63%) patients responded to intravenous amiodarone. All 22 responders received oral amiodarone. Thirteen (59%) continue to receive oral amiodarone after an average follow-up of 19 months, 4 (18%) had sudden cardiac death on oral amiodarone, 2 (9%) died while receiving amiodarone, secondary to left ventricular failure, and 3 (14%) discontinued amiodarone because of side effects. Of the 13 (37%) nonresponders, 10 died in the hospital while receiving intravenous amiodarone, secondary to lethal arrhythmia. Three nonresponders were discharged from the hospital; 2 with automatic cardioverter/defibrillators and 1 receiving a combination of antiarrhythmic agents. Serious adverse events occurred in 13 (37%) patients during intravenous amiodarone therapy. These included hypotension in 8 patients, symptomatic bradycardia in 4 patients and sinus arrest with bradycardia and hypotension in 1 patient. Minor side effects occurred in 23 (66%) patients. In conclusion, high dose intravenous amiodarone is effective in most patients with recurrent, sustained VT but is associated with an unacceptably high incidence of serious adverse events. The optimal dose and duration of intravenous amiodarone for patients with recurrent, refractory sustained VT remain unknown.

Effects of verapamil on postextrasystolic potentiation.

To assess the effects of verapamil on postextrasystolic potentiation (PESP), contrast left ventriculography was performed in ten healthy anesthetized dogs before and after the intravenous administration of verapamil, 0.1 mg/kg. During the contrast ventriculography, a single atrial premature stimulus was introduced. Ejection fractions of a control beat and postpremature beat were measured before and after verapamil. Before verapamil, the mean ejection fractions of the control beat and the postpremature beat were 60 +/- 10 percent and 67 +/- 10 percent, respectively (p less than 0.05). Following the administration of verapamil, the mean ejection fraction of the control beat decreased from 60 +/- 10 percent to 55 +/- 11 percent (p less than 0.05). However, the mean ejection fraction of the postpremature beats increased when compared with the control beats following intravenous verapamil (65 +/- 8 percent and 55 +/- 11 percent, respectively; p less than 0.05). These results suggest that PESP is not inhibited by the administration of intravenous verapamil.

Long-term antiarrhythmic therapy with cibenzoline.

This single-blind, placebo-controlled study evaluated long-term therapy with cibenzoline in 19 patients with chronic ventricular arrhythmias. Antiarrhythmic efficacy, defined as greater than or equal to 75% reduction in single premature ventricular complexes (PVCs), greater than or equal to 90% reduction in paired PVCs, and total abolition of ventricular tachycardia (VT), was established after dose titration in 14 of 19 (74%) patients. Mean frequency of single PVCs was reduced by 65%, mean paired PVC frequency was reduced by 68%, and mean VT event frequency was reduced by 82%. Antiarrhythmic efficacy was maintained during long-term therapy in five of the 14 (36%) short-term responders. Of the nine patients who discontinued cibenzoline during long-term follow-up, five had a loss of arrhythmia control, three failed to redevelop arrhythmias during placebo reintroduction, and one developed an adverse reaction. Three patients (16%) experienced a proarrhythmic effect. Echocardiographic evaluation did not reveal any deleterious effect of cibenzoline on left ventricular function in the group as a whole. In six patients with preexisting left ventricular dysfunction, left ventricular ejection fraction and fractional shortening improved significantly (P less than .05) during cibenzoline therapy. Adverse effects occurred in seven patients (37%) but necessitated drug discontinuation in only one patient (5%). Cibenzoline provides effective short-term therapy for patients with chronic ventricular arrhythmias. Long-term therapy must be assessed periodically to ensure continued efficacy. Drug-related adverse effects occur infrequently. Cibenzoline can be used safely in patients with compensated left ventricular dysfunction.

Economic impact of inappropriate histamine2-receptor antagonist use.

Histamine2 (H2)-receptor antagonists are widely prescribed for a variety of acid-mediated gastrointestinal disorders. The objective of the present study was to quantify the frequency of inappropriate H2-receptor antagonist use and its economic impact in patients who were admitted to a critical care bed at our hospital and followed as outpatients for 1 year. Eighty-eight (72%) of 123 patients admitted to the coronary care unit (CCU) or the intensive care unit over a 14-day period received H2-receptor antagonists. Forty-five (51%) of the 88 patients did not have a documented indication for H2-receptor antagonist therapy. Most of the patients without indications were admitted to the CCU for cardiac diagnoses. Thirty-eight patients (43%) were discharged on oral H2-receptor antagonist therapy. Twenty (53%) of the 38 patients had no documented indication for therapy; 17 of these patients continued H2-receptor antagonist therapy for 1 year, whereas the remaining 3 patients received therapy for 1, 2, and 3 months, respectively. The cost of therapy for the 45 patients receiving inappropriate therapy during hospitalization was $5,084.31. Outpatients costs for the 20 patients remaining on inappropriate therapy was $8,619.75. The total cost of inappropriate therapy was $13,704.06. If data collected during this 2-week period were extrapolated to 1 year, the projected annual cost of inappropriate therapy would be $356,305.56. The economic impact of inappropriate H2-receptor antagonist therapy at our institution is great. Programs designed to reduce such inappropriate use must be implemented and evaluated for their ability to decrease the associated costs.

Restenosis, the Achilles' heel of coronary angioplasty.

Coronary angioplasty is widely performed for the management of symptomatic coronary artery disease. With improvements in technique, operator experience, and tools, more complex lesions are being treated. Unfortunately, luminal renarrowing continues to limit the long-term success of the procedure, resulting in the need for repeat revascularization in approximately 30% of patients within 6 months. As the pathophysiologic process of restenosis is better defined, various pharmacologic and mechanical interventions have been tried to attenuate the process. Some agents are antithrombotics, antiplatelets, angiotensin-converting enzyme inhibitors, lipid-lowering drugs, and calcium channel blockers. Improvement has been noted with the newer glycoprotein IIb- and IIIa-blocking agents, mechanical stents, and radioactive materials. Whether these new compounds will withstand the test of time is unknown.

Potential influence of timing of low-density lipoprotein cholesterol evaluation in patients with acute coronary syndrome.

OBJECTIVE: To determine the significance of timing of low-density lipoprotein (LDL) cholesterol evaluation in patients with chest pain as it relates to subsequent National Cholesterol Education Program (NCEP) treatment decisions. DESIGN: Prospective, observational study. SETTING: A university-affiliated tertiary care hospital. PATIENTS: Sixty-two patients with coronary heart disease who were not receiving lipid-lowering therapy and whose LDL levels were obtained 25-48 hours after onset of chest pain. INTERVENTION: We evaluated laboratory test results of patients with chest pain admitted to the cardiac care unit to determine risk to patients when LDL levels obtained inappropriately are used to make decisions regarding antihyperlipidemic therapy. MEASUREMENTS AND MAIN RESULTS: Inpatient and outpatient LDL levels were compared, and changes in NCEP treatment decisions analyzed. Differences between inpatient and outpatient LDL levels were significant (p<0.05), which frequently resulted in changes in therapy using the NCEP guidelines. The LDL levels of most inpatients were consistent with NCEP goals for patients with coronary heart disease, whereas the outpatient levels showed a need for drug therapy. CONCLUSION: Lipid values obtained 25-48 hours after hospital admission in patients with acute coronary syndromes do not represent baseline values and may significantly alter the treatment approach; thus, they should not be used to direct drug therapy.

Double-blind, randomized, placebo-controlled evaluation of atropine to prevent vasovagal reaction during removal of femoral arterial sheaths.

STUDY OBJECTIVE: To evaluate the efficacy and safety of atropine in preventing vasovagal reactions (VVRs) during removal of femoral arterial sheaths after diagnostic left heart catheterization. DESIGN: Prospective, double-blind, randomized, placebo-controlled study. SETTING: University-affiliated, 450-bed teaching hospital. PATIENTS: One hundred sixty-five patients undergoing left heart catheterization. INTERVENTIONS: Eighty-eight patients were assigned to receive atropine 0.5 mg intravenously and 77 received placebo 5 minutes before sheath removal. MEASUREMENTS AND MAIN RESULTS: The frequency of VVRs was significantly reduced in the atropine group compared with the placebo group, 2.3% and 10.4%, respectively (overall relative risk in the atropine group 0.22, 95% CI 0.12-0.41, p=0.03). Significant decreases in systolic (35.2 +/- 5.8 mm Hg, p<0.001) and diastolic blood pressures (12.6 +/- 12.6 mm Hg, p=0.002) occurred in the 10 patients with VVRs compared with those without VVR. No cardiac arrhythmias occurred after atropine administration. Dry mouth was the only side effect reported with atropine (8/88, 9%). CONCLUSION: Atropine significantly reduced the frequency of VVRs associated with removal of femoral arterial sheaths after diagnostic left heart catheterization. The drug should be studied in a larger series of patients to assess its ability to decrease the morbidity and costs associated with VVR.

Comparison of 24-hour ambulatory blood pressure data in hypertensive patients switched from nifedipine-GITS to nifedipine-CC.

STUDY OBJECTIVE: To evaluate 24-hour blood pressure control and frequency of adverse effects in patients with mild to moderate hypertension switched from nifedipine gastrointestinal therapeutic system (Nif-GITS) to nifedipine coat core (Nif-CC). DESIGN: Open-label, prospective, switch study SETTING: University-affiliated outpatient cardiology clinic. SUBJECTS: Twenty patients with mild to moderate essential hypertension, who were taking Nif-GITS 30, 60, or 90 mg/day for 8 weeks or longer. INTERVENTIONS: Patients stabilized with Nif-GITS 30, 60, or 90 mg were monitored over 24 hours with an ambulatory blood pressure monitor and were then switched to an equivalent dosage of Nif-CC. After 8 weeks+/-1 week taking Nif-CC, they were again monitored with a 24-hour blood pressure monitor. The 24-hour blood pressure load (percentage of values > 135/85 mm Hg for 24 hrs), daytime blood pressure load (percentage of values > 140/90 mm Hg from 7:00 A.M.-10:00 P.M.), nighttime blood pressure load (percentage of values > 120/80 mm Hg from 10:00 P.M.-7:00 A.M.), diurnal blood pressure variation, average 24-hour blood pressure, daytime blood pressure, nighttime blood pressure, mean blood pressure for the first 4 hours, and last 8 hours of the dosing interval were measured. Adverse effects such as headache, dizziness, and edema were also reported. MEASUREMENTS AND MAIN RESULTS: No differences in average 24 hour-blood pressure readings were observed but significant differences in blood pressure control during the first 4 and last 8 hours of the dosing interval were seen. Systolic and diastolic blood pressures were higher after approximately 16 hours in patients switched from Nif-GITS to Nif-CC. Although Nif-CC caused a greater initial response, it was less effective than Nif-GITS after 16 hours. This could explain the lack of differences in average 24-hour blood pressure values between formulations. Of the 20 patients, 20% experienced increased headaches, 20% showed signs of increased peripheral edema, and 10% reported occasional dizziness after switching agents. Three patients discontinued Nif-CC, two as ordered by their primary care physician and one on his own due to headache. CONCLUSION: This study suggests that patients switched from Nif-GITS to Nif-CC could experience increased blood pressure during the night or toward the end of the dosing interval. They could also experience adverse effects such as headache, edema, and dizziness, which could result in more physician visits and put patients with other disease states such as coronary heart disease at increased risk.

Serial ambulatory monitoring in patients with unstable angina pectoris.

We performed a prospective study by dual-channel ambulatory monitoring performed for 24 to 72 hours immediately after hospitalization for unstable angina. The incidence of ST-segment depression or elevation or ventricular tachycardia or complex premature ventricular complexes (PVCs) in 42 consecutive patients with unstable angina due to coronary artery disease (39 by coronary arteriography) was investigated. During ambulatory monitoring, 28 of 42 patients (67%) exhibited ST-segment depression or elevation, 13 of 42 patients (31%) had ventricular tachycardia or complex PVCs, and 31 of 42 patients (74%) had either ST-segment depression or elevation, ventricular tachycardia, or complex PVCs. Ventricular tachycardia or complex PVCs occurred in 10 of 20 patients (50%) with abnormal left ventricular function and in 3 of 22 patients (14%) with normal left ventricular function (p less than 0.025). We found that 72 hours of ambulatory monitoring was not more useful than 48 hours in detecting the incidence of ST-segment depression or elevation, ventricular tachycardia, or complex PVCs. Ambulatory monitoring did not help in clinically differentiating patients with left main or 3-vessel disease from 1-vessel or 2-vessel disease. In addition, ambulatory monitoring did not help in predicting which patients with unstable angina would require coronary artery surgery.

Efficacy and tolerance of tocainide during long-term treatment of malignant ventricular arrhythmias.

A group of 51 patients with malignant ventricular arrhythmias refractory to standard oral antiarrhythmic agents were treated with oral tocainide. Antiarrhythmic efficacy was defined as total abolition of occurrences of ventricular tachycardia (VT) or ventricular fibrillation (VF) as assessed by hospital admissions for arrhythmias and the occurrence of sudden cardiac death (SCD). Of the 51 patients, 32 (63%) initially tolerated tocainide and were discharged from the hospital. Of the 19 patients not initially responding to tocainide, 6 (12%) had arrhythmia recurrence and 13 (25%) developed intolerable central nervous system or gastrointestinal side effects. Of these 19 short-term nonresponders, 8 (42%) patients suffered SCD over an average follow-up of 24 months (annual SCD rate of 21%). Two patients suffered SCD during the first week of tocainide therapy. Discounting the 2 patients with SCD on tocainide therapy, 6 of 17 (35%) patients initially withdrawn from tocainide suffered SCD (annual SCD rate of 18%). Twenty-four of the 32 short-term responders did not have arrhythmia recurrence over a mean follow-up of 38 months resulting in an overall long-term efficacy of 47% (24/51). Over an average follow-up of 38 months for these 24 short-term responders, 12 patients expired from nonarrhythmic causes, 3 patients were withdrawn for non-drug-related causes, and 9 patients remain on tocainide therapy. Of the 8 long-term nonresponders, 3 patients had arrhythmia recurrence and died suddenly while 5 patients developed intolerable side effects. The annual SCD rate in short-term responders was 3%. Eighteen of the 51 patients (35%) were withdrawn from the study because of adverse effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Percutaneous transluminal angioplasty of anomalous right coronary artery.

Angioplasty of anomalous coronary arteries can be technically challenging because of difficulty in selectively cannulating the aberrant vessel. We present our experience with angioplasty of an anomalous right coronary artery. A Judkins-type left coronary catheter with an eccentric tip, the FL4-G type catheter was used to obtain stable position in the right coronary artery and angioplasty was performed.

Treatment of asymptomatic myocardial ischemia.

BACKGROUND: Asymptomatic myocardial ischemia is commonly observed in patients with coronary artery disease. Numerous studies have shown that patients with asymptomatic ischemia are at higher risk for adverse outcome than those without ischemia. Several recent studies have investigated the therapeutic options available in the management of patients with asymptomatic myocardial ischemia. METHODS: Recently published randomized controlled trials investigating the treatment of asymptomatic myocardial ischemia were reviewed. RESULTS: The controlled trials suggest that (1) asymptomatic ischemia can be suppressed to various degrees using pharmacologic therapy or revascularization, (2) beta-blockers are in general superior to calcium channel blockers or nitrates in relieving asymptomatic ischemia, and (3) revascularization is superior to pharmacologic therapy. CONCLUSIONS: A growing body of evidence suggests that in patients with coronary artery disease, treatment of asymptomatic ischemia may result in improved outcome. However, because of significant limitations in the published studies, additional studies with large sample sizes and broader inclusion criteria are needed.

Safety of esmolol in patients with acute myocardial infarction treated with thrombolytic therapy who had relative contraindications to beta-blocker therapy.

OBJECTIVE: This study was conducted to evaluate the safety of esmolol in 114 patients treated with thrombolytic therapy for acute myocardial infarction who also had relative contraindications to beta-blockade, and the predictive value of patient tolerance to esmolol and subsequent patient tolerance of oral beta-blocker therapy. PATIENTS: One hundred and fourteen patients with myocardial infarction documented by enzyme concentrations and electrocardiographic changes who also had relative contraindications to beta-blockade. METHODS: Esmolol was initiated during acute myocardial infarction for myocardial ischemia (n = 88), hypertension (n = 13), or supraventricular tachycardia (n = 13). Relative contraindications to beta-blocker therapy included either active signs/symptoms of left ventricular dysfunction or a history of congestive heart failure (n = 40), a history of chronic obstructive pulmonary disease or asthma (n = 31), bradycardia (HR < 60 beats/min; n = 18), peripheral vascular disease (n = 15), or hypotension (systolic BP < 100 mm Hg; n = 14). RESULTS: During initial esmolol dose titration, 69 patients tolerated 300 micrograms/kg/min, 12 patients tolerated 200 micrograms/kg/min, 17 patients tolerated 100 micrograms/kg/min, and 16 patients tolerated 50 micrograms/kg/min. Twenty-eight patients (25 percent) developed dose-limiting adverse effects during esmolol maintenance infusions. Sixteen patients required esmolol dose reduction and 12 required esmolol discontinuation. Adverse effects reversed within 30-45 minutes following dose reduction or discontinuation. The 86 patients who tolerated esmolol infusions without dose reduction or drug discontinuation were subsequently treated with oral beta-blockers. Eleven of these patients (13 percent) developed adverse effects requiring oral beta-blocker discontinuation. Nine of these patients had tolerated only 50 micrograms/kg/min of esmolol, and the other 2 patients had tolerated only 100 micrograms/kg/min. CONCLUSIONS: Esmolol can be used safely in most patients treated with thrombolytic therapy for acute myocardial infarction who have relative contraindications to beta-blockers. Tolerance to higher maintenance doses of esmolol is a good predictor of subsequent outcome with oral beta-blocker therapy.

A comparison of sublingual nifedipine versus nitroglycerin in the treatment of acute angina pectoris.

The administration of nifedipine by the sublingual rather than the oral route has been suggested to provide a more rapid onset of effect. We compared the safety and efficacy of sl nifedipine to sl nitroglycerin in patients who developed anginal chest pain during diagnostic exercise stress testing. Consecutive patients undergoing diagnostic Bruce treadmill exercise who had not had a recent myocardial infarction or undergone coronary bypass graft surgery and who were not taking nitrates, beta-blockers, digoxin, or calcium antagonists were eligible. Seventy-eight patients meeting the inclusion/exclusion criteria consented to participate. Of these 78, 13 developed chest pain necessitating exercise cessation and were randomized to either nitroglycerin or nifedipine. Nitroglycerin was initially given to seven patients and nifedipine to six patients. Complete pain relief was observed in five of seven (71 percent) nitroglycerin patients at two minutes postdose. At four minutes postdose, the remaining two nitroglycerin patients were essentially pain-free. At two minutes postdose, no patient receiving nifedipine had complete pain resolution, and only one patient (17 percent) had partial (greater than 50 percent) pain relief. At four minutes postdose, four of the nifedipine patients were crossed over to nitroglycerin. At two minutes after the nitroglycerin dose, all four patients had total pain relief. The remaining two nifedipine patients had partial pain relief and were not crossed over to nitroglycerin. Subjective side effects and changes in heart rate and blood pressure were not significantly different between nitroglycerin and nifedipine.(ABSTRACT TRUNCATED AT 250 WORDS)

Automated and nomographic analysis of exercise tests.

A study was conducted to evaluate the validity and usefulness of a commercially available microprocessor for automated exercise ECG analysis and to develop a nomogram for estimating the severity of coronary artery disease. Results of visual analysis, automated analysis, and coronary arteriography were correlated for the 107 patients studied. Automated analysis was shown to be valid and useful. The ST integrals (area of ST depression) recorded after exercise were superior to those recorded during exercise because they manifested higher specificity and predictive value, even though their sensitivity was slightly lower. Using postexercise integrals, it was possible to differentiate mild and severe disease. From multiple-regression analysis of ST integrals, duration of exercise, and the severity of coronary artery disease, a nomogram was derived to estimate severity of coronary artery disease.

Crossover comparison of cibenzoline and quinidine in ambulatory patients with chronic ventricular arrhythmias.

This study was designed to compare the efficacy and safety of cibenzoline and quinidine in ambulatory patients with ventricular arrhythmias. Following washout of previous antiarrhythmic treatment, a 48-h ambulatory electrocardiographic (ECG) recording was obtained. Twenty-seven patients were screened, of whom 20 met the entry criteria of greater than or equal to 30 ventricular premature beats (VPBs)/h. Cibenzoline was started at 130 mg every 12 h and was increased to 160 mg every 12 h if necessary. Quinidine was started at 300 mg every 6 h and was increased to 400 mg every 6 h if necessary. Treatment was assessed by 24-h ambulatory ECG recording. Efficacy was defined as greater than 75% reduction in single VPBs, greater than 90% reduction in paired VPBs, and total abolition of ventricular tachycardia events. A 7-day washout with repeat 24-h ambulatory ECG recording to document return of ventricular arrhythmias was required prior to crossover. Efficacy was documented in 9 of 20 (45%) patients receiving cibenzoline and in 9 of 20 (45%) patients receiving quinidine. Response to cibenzoline 130 mg every 12 h was documented in 8 of 20 (40%) patients and in 1 of 11 (9%) patients receiving cibenzoline 160 mg every 12 h. Response to quinidine 300 mg every 6 h was documented in 8 of 20 (40%) patients and in 2 of 6 (33%) patients receiving 400 mg every 6 h. Dose-limiting side effects occurred in 1 of 20 (5%) patients receiving cibenzoline and in 7 of 20 (35%) patients receiving quinidine. Cibenzoline and quinidine are equal in efficacy, but cibenzoline is significantly better tolerated.