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Biomedical subjects

A N Mooss

Publications and source records attributed to A N Mooss.

At least 19 recordsLinked to original sources
PubMed1994

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.

Adrenergic beta-Antagonists↗
PubMed1992

Comparative pharmacodynamics of intravenous lidocaine in patients with acute and chronic ventricular arrhythmias.

OBJECTIVE: To evaluate the pharmacodynamics of intravenous lidocaine in patients with acute-onset and chronic ventricular arrhythmias. DESIGN: Open-label, pharmacodynamic evaluation. SETTING: Private, university-affiliated, hospital coronary-care unit. PATIENTS: Twenty cardiac patients with acute-onset ventricular ectopy and 20 with chronic ventricular ectopy. INTERVENTIONS: Intravenous lidocaine was administered to all patients as a 1-mg/kg bolus, a 0.5-mg/kg bolus, and a 2.8-mg/min constant infusion for 48 hours. MAIN OUTCOME MEASURES: Changes in ventricular premature beat (VPB) frequency against total treatment period frequency and by an hour-to-hour assessment of changes in VPB frequency compared with total baseline frequencies. Response was defined as greater than or equal to 80 percent total VPB reduction, greater than or equal to 90 percent paired VPB reduction, and total abolition of nonsustained ventricular tachycardia events. RESULTS: A statistically significant difference in the pharmacodynamic effects of lidocaine were observed during the first eight hours of treatment in patients with acute-onset and chronic VPBs. The number of patients with acute-onset VPBs who responded to lidocaine in the first hour of treatment did not change significantly over the remaining hours of treatment. Response to lidocaine was less in patients with chronic VPBs than in patients with acute-onset VPBs. The response rate to lidocaine was significantly less during the first eight hours in patients with chronic VPBs than in patients with acute-onset VPBs. Following eight hours of treatment, the response rates between acute-onset and chronic VPB patients were not significantly different. Mean lidocaine plasma concentrations were not different between the groups. In addition, there were no significant differences in the incidence of adverse effects between the two groups. CONCLUSIONS: The onset of antiarrhythmic effect as measured by suppression of ventricular ectopy is delayed in patients with chronic VPBs compared with patients with acute-onset VPBs. Decisions about lidocaine response in patients with chronic VPBs cannot be made accurately in the first eight hours of therapy.

Acute Disease↗
PubMed1992

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.

Animals↗
PubMed1991

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.

Adult↗
PubMed1990

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.

Administration, Oral↗
PubMed1989

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.

Angiography↗
PubMed1989

Nifedipine in the treatment of hypertensive episodes in the coronary care unit.

The effectiveness of nifedipine for the treatment of acute hypertensive episodes in patients already taking chronic calcium-channel blocker therapy is unknown. We report our experience with 43 consecutive patients who received nifedipine for acute hypertensive episodes in the coronary care unit. Of the 43 patients (24 men, 19 women), 23 (53 percent) were taking chronic (greater than 2 mo) calcium-channel blocker therapy. Nifedipine 10 mg capsules were chewed and swallowed with repeat doses given at hourly intervals if necessary. Target BP was 140/90 mm Hg, which was achieved in 31 of 43 patients (72 percent). In patients already taking calcium-channel blockers, target BP was achieved in 18 of 23 patients (78 percent). Response in patients not taking chronic calcium-channel blockers was observed in 13 of 20 patients (65 percent). Overall, adverse effects occurred in 16 of 43 patients (37 percent): 11 of 23 patients (48 percent) taking calcium-channel blockers, and 5 of 20 patients (25 percent) not taking calcium-channel blockers. Nifedipine is equally effective in lowering BP in patients taking calcium-channel blockers as it is in patients not taking them. Although associated with a higher incidence of adverse effects in patients already taking calcium-channel blockers, these effects were not considered serious. Nifedipine is an effective agent in acute hypertensive episodes, even in patients receiving chronic calcium-channel blocker therapy.

Adult↗
PubMed1989

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.

Adult↗
PubMed1987

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)

Death, Sudden↗
PubMed1987

Double-blind randomized comparison of intravenous tocainide versus lidocaine in the treatment of chronic ventricular arrhythmias.

The efficacy and safety of intravenous tocainide were compared with intravenous lidocaine in patients with chronic ventricular arrhythmias in a double-blind, parallel study. Twenty-nine patients were randomized to a tocainide (n = 15) or lidocaine (n = 14) group. Antiarrhythmic efficacy was defined as a greater than or equal to 50% reduction in single ventricular premature complex (VPC) frequency, greater than or equal to 90% reduction in paired VPC frequency, and total abolition of ventricular tachycardia. Efficacy was observed in 40% (6 of 15) of patients in the tocainide group and in 36% (5 of 14) patients in the lidocaine group. A 75% or greater reduction in total VPCs occurred in 40% (6 of 15) of patients in the tocainide group and in 57% (8 of 14) of patients in the lidocaine group. Greater than 90% suppression of paired VPCs occurred in 9 of 13 (69%) patients taking tocainide and in 6 of 11 (54%) patients taking lidocaine. Total abolition of ventricular tachycardia was documented in 5 of 11 (45%) patients given tocainide and in two of six (33%) patients given lidocaine. A total of 17 adverse reactions affecting 86% (12 of 14) of patients taking lidocaine and 11 adverse reactions affecting 53% (8 of 15) of patients taking tocainide occurred. Four patients in each treatment group suffered dose-limiting adverse effects. This study suggests that the efficacy and safety of intravenous tocainide are similar to that of intravenous lidocaine in patients with chronic ventricular arrhythmias.

Anti-Arrhythmia Agents↗
PubMed1983

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.

Aged↗
PubMed1983

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.

Adult↗
PubMed1983

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.

Adult↗
PubMed1982

Ventricular fibrillation complicating pacemaker insertion in acute myocardial infarction.

Temporary transvenous pacing catheters were placed in 101 patients with acute myocardial infarction (MI) for the management of bradyarrhythmias or conduction disturbances. Fourteen (14%) patients (group A) developed ventricular fibrillation (VF) at the time of pacing catheter manipulation in the right ventricle. Compared to the remaining 87 (86%) patients (group B), the patients in group A were younger (56.1 vs 65.8 yrs, P = 0.007). Thirteen (92.8%) of 14 patients in group A had inferior MI compared to 58 (66.6%) of 87 patients in group B (P = 0.04). All but one patient in group A had pacemaker insertion within 24 h of the onset of symptoms of MI compared to 55 (63%) of 87 in group B (P = 0.02). In 12 of the 14 patients in group A, following defibrillation and intravenous bolus administration of lidocaine, the pacing catheter was positioned in the right ventricle without further episodes of VF. It is concluded that 1) in patients with acute MI temporary transvenous pacemaker insertion may be complicated by VF; 2) VF is most likely to occur in younger patients with inferior MI infarction when the pacing catheter is inserted within 24 h of the onset of symptoms of infarction; and 3) administration of an intravenous bolus of lidocaine may be effective in preventing the induction of VF by catheter manipulation.

Adult↗
PubMed1981

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.

Adult↗