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Biomedical subjects

M Talajic

Publications and source records attributed to M Talajic.

At least 91 records · Page 5Linked to original sources
PubMed1989

Value of induction of pleomorphic ventricular tachycardia during programmed stimulation.

The morphology of the first documented, the recurrent and the induced ventricular tachycardia were studied in 41 patients with an old myocardial infarction and documented sustained ventricular tachycardia. During a mean follow-up of 29 +/- 11 months recurrent ventricular tachycardia was present in 24 of 41 patients with the same morphology as the first ventricular tachycardia in nine (37.5%) and a different morphology in 15 patients (62.5%). Ventricular tachycardia with the same morphology as the spontaneous ventricular tachycardia were induced without significant differences between patients with recurrent events and those without. However, multiple morphologies of ventricular tachycardia (pleomorphism) were induced more frequently in patients with subsequent recurrence of ventricular tachycardia (off drugs: 9 of 13, 69%, on drugs: 14 of 23, 61%) than in patients without (off drugs: 4 of 10, 40%, on drugs: 2 of 11, 18%) (P less than 0.05). Pleomorphism of ventricular tachycardia induced during programmed stimulation identifies patients at a higher risk of subsequent recurrent events. Recurrent ventricular tachycardia has a different morphology than the first one in two thirds of patients.

Aged↗
PubMed1989

The value of the clinical history to assess prognosis of patients with ventricular tachycardia or ventricular fibrillation after myocardial infarction.

Multivariate analysis using 70 variables in 200 patients who suffered from ventricular tachycardia or ventricular fibrillation after myocardial infarction detected eleven variables that were associated with an increased risk of sudden arrhythmic death and cardiac death during a mean follow-up period of 2 years. Four of the 11 variables came from the patient's clinical history: (1) cardiac arrest at the time of the first spontaneous episode of arrhythmia, (2) New York Heart Association functional class for dyspnoea = III, (3) ventricular tachycardia or ventricular fibrillation occurring early (after 3 days and within 2 months) after myocardial infarction, (4) multiple myocardial infarctions before the first episode of ventricular tachyarrhythmia. Total mortality, incidence of sudden arrhythmic death and of non-sudden cardiac death increased with an increasing number (zero, one, two, three, four) of variables seen in individual patients. Patients with zero or one variable had an incidence of sudden death of 2.8% and a 4.2% incidence of non-sudden cardiac death at 26 months, while patients with more than two variables had a 13.5% and a 20.3% incidence respectively of sudden and non-sudden cardiac death. The strongest predictor of sudden death was the occurrence of cardiac arrest during the first spontaneous episode of ventricular arrhythmia. The strongest predictor of non-sudden cardiac death was the New York Heart Association functional class. The use of the four variables to stratify risk revealed seven subgroups of patients with incidences of sudden death ranging from 0 to 28%.(ABSTRACT TRUNCATED AT 250 WORDS)

Death, Sudden↗
PubMed1989

Predictors of long-term success during closed-chest catheter ablation of the atrioventricular junction.

The predictors of long-term success during closed-chest catheter ablation of the atrioventricular junction remain unclear. Catheter ablation was performed in 32 consecutive patients, 18 male and 14 female, mean age 57 years, with intractable supraventricular tachycardia, in spite of a mean of 4.9 antiarrhythmic drugs. Duration of symptoms averaged 9.2 years, and the mean heart rate during tachycardia was 180 beats min-1. Paroxysmal atrial fibrillation or flutter was the presenting arrhythmia in 23 patients, intranodal tachycardia in four patients, and reciprocating tachycardia using an accessory pathway in five patients. There were no immediate complications, and 29 patients received a permanent transvenous pacemaker. A total of 94 shocks of 300 J (in 94% of cases) were given, (mean 2.96 shocks per patient). Chronic complete heart block was produced after one shock in nine patients (28%), and after two or more shocks (mean 3.3 +/- 1.1) in 13 patients. Modification of conduction was seen in four patients (12%). Failure to achieve any improvement of symptoms occurred in six patients (19%). There was no significant difference between the amplitude of atrial and His electrograms between patients who had complete heart block after one shock and those in whom conduction persisted. Catheter ablation was successful in 92% of patients who were given five shocks or less, but in only one of five patients (20%) who received six or more shocks. During a mean follow-up of 12 months, no patient with successful ablation during the first 24 h after catheter ablation resumed conduction or had recurrent symptomatic supraventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Attenuation of class 3 and sinus node effects of amiodarone by experimental hypothyroidism.

Amiodarone's class III effects may be due to inhibition of the cardiac effects of thyroid hormone. If so, amiodarone would not be expected to cause QT prolongation in hypothyroid subjects. The electrocardiographic (ECG) changes induced after treatment with amiodarone were compared in euthyroid and hypothyroid guinea pigs. Hypothyroidism was induced with intraperitoneal (i.p.) administration of 1 mCi I131 (eight animals). Three of these animals also received oral methimazole to block any residual thyroid hormone production. Significant increases in body weight (28 +/- 9%), RR (14 +/- 8%), QT (14 +/- 5%), and QTc (7 +/- 2%) intervals occurred after induced hypothyroidism. Pilot studies with amiodarone treatment for 4 weeks in euthyroid guinea pigs demonstrated that maximal effects on ECG intervals were achieved after 1 week of drug therapy. Therefore, both euthyroid and hypothyroid groups were treated with daily i.p. amiodarone (80 mg/kg) for 7 days. Euthyroid guinea pigs treated with amiodarone had significant increases in RR (33 +/- 10%), QT (31 +/- 15%), and corrected QT (13 +/- 11%) intervals. In contrast, when hypothyroid animals were treated with amiodarone, no statistically significant changes occurred in ECG intervals. Plasma concentrations of amiodarone did not differ between the two groups (0.7 +/- 0.6 vs. 0.7 +/- 0.4 mg/L in hypothyroid and euthyroid groups, respectively). We conclude that intact thyroid function is a prerequisite for class III and sinus node effects of amiodarone in the guinea pig. This implies that at least some of amiodarone's effects are mediated through antagonism of thyroid action.

Amiodarone↗
PubMed1989

Sinus node dysfunction and sudden cardiac death following treatment with encainide.

Encainide, a class Ic drug, is generally thought of as having little effect on sinus node function. In this article, we present the clinical course and electrophysiological findings of a patient who had cardiac arrest after 1 week of encainide therapy for ventricular extrasystoles. No ventricular tachyarrhythmias were induced during programmed ventricular stimulation (baseline study and while receiving encainide therapy). Prior to encainide therapy, sinus node function was normal, but clinical observations after admission for cardiac arrest and subsequent electrophysiological study revealed that encainide had caused striking impairments in sinus node function. During a 6-month follow-up without antiarrhythmic drug treatment, this patient has had an uneventful course. We concluded that encainide can cause severe and life-threatening sinus node dysfunction.

Anilides↗
PubMed1989

Amplification of flecainide-induced ventricular conduction slowing by exercise. A potentially significant clinical consequence of use-dependent sodium channel blockade.

Proarrhythmic effects of flecainide acetate have been reported during exercise, but the mechanism for the arrhythmogenic interaction between flecainide and exercise is unknown. We hypothesized that the sinus tachycardia of exercise may enhance flecainide-induced conduction slowing by increasing use-dependent sodium channel blockade, thereby facilitating the occurrence of ventricular reentry. To evaluate the modulation of flecainide's effects by exercise, we studied 19 patients who were receiving therapeutic doses of flecainide for the treatment of cardiac arrhythmias. Sixteen patients underwent treadmill exercise testing by a modified Bruce protocol. During exercise, QRS duration increased progressively from 94 +/- 22 msec (mean +/- SD) at rest to 116 +/- 25 msec (p less than 0.001) at a mean heart rate increase of 84 +/- 32 beats/min. The patient with the greatest QRS increase developed a monomorphic ventricular tachycardia at peak exercise. At rest, the QRS duration after treatment with flecainide increased 12.1 +/- 10.0% compared with the pretreatment value, and with exercise, the QRS duration increased by a further 28.1 +/- 17.0% compared with the predrug value. We found that the best predictor of further exercise-induced QRS slowing was the change in QRS duration produced by flecainide at rest (r = 0.76, p = 0.001). In an age- and disease-matched control group, the QRS duration did not change during exercise that caused a similar heart rate increase.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1989

Frequency-dependent effects of diltiazem on the atrioventricular node during experimental atrial fibrillation.

Calcium channel blockers depress atrioventricular (AV) nodal properties in vivo in a frequency-dependent manner, suggesting that selective drug action during supraventricular arrhythmias may result from use-dependent properties. The present study was designed to examine whether or not the rate-dependent actions of diltiazem account for its therapeutic effects during atrial fibrillation. The determinants of the ventricular response to atrial fibrillation (concealed AV nodal conduction and AV node functional refractory period, AVFRP) were evaluated at multiple cycle lengths (with extrastimulus techniques) and during electrically induced atrial fibrillation (with indirect indexes from RR interval histograms) in anesthetized dogs. In the presence of diltiazem, AVFRP increased progressively relative to control as rate accelerated. At cycle lengths comparable to sinus rhythm in humans, AVFRP increased 10%, 17%, and 32% after doses 1, 2, and 3 of diltiazem, respectively. Drug-induced increases in AVFRP were greater at basic cycle lengths just above the Wenckebach point (17%, 48%, and 81%) and were maximal during atrial fibrillation (39%, 86%, and 154% increases for doses 1, 2, and 3, respectively). Diltiazem also increased the AV conduction system effective refractory period, thereby increasing the potential zone of concealment into the AV node. Frequency-dependent increases in the zone of concealment were produced by diltiazem and were associated with marked increases in the standard deviation of RR interval histograms during atrial fibrillation (257%, 526%, and 923% increases after doses 1, 2, and 3, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

[Prognosis and follow-up of patients with ventricular tachycardias or ventricular fibrillation without coronary heart disease].

We studied the follow-up of 49 patients (pts), mean age 34 +/- 9 years, without coronary artery disease who had sustained (duration greater than 30 s) monomorphic ventricular tachycardia (smvt) (n = 42) or ventricular fibrillation (vf) (n = 7). There were 9/49 pts (18%) with smvt who had right ventricular dysplasia (RVD) and 32/49 pts (65%) without structural heart disease ("idiopathic" ventricular arrhythmia) (26/32 pts with smvt and 6/32 pts with vf). There were 6/49 pts (12%) with congestive (COCM) and 2/49 pts (4%) with hypertrophic (HOCM) cardiomyopathy. Mean follow-up was 49 +/- 13 months. During the follow-up 1/9 pts (11%) with RVD died postoperatively from heart failure, 1/26 pts (4%) with idiopathic smvt from cancer and 2/6 pts (33%) with COCM from heart failure. There were no deaths in pts with idiopathic vf. Recurrent smvt occurred in 5/9 pts (56%) with RVD, in 10/26 pts (39%) with idiopathic smvt, in 2/6 pts (33%) with idiopathic vf, in 3/6 pts (50%) with COCM and in 1/2 pts (50%) with HOCM. Our data show that pts with smvt or vf without coronary artery disease have a good prognosis. However, there is a high incidence of recurrent ventricular arrhythmia in these patients.

Adolescent↗
PubMed1988

Prognosis of patients with ventricular tachycardia and ventricular fibrillation: role of the underlying etiology.

The prognosis of 149 patients with ventricular tachycardia (n = 108) or ventricular fibrillation (n = 41) was analyzed to assess the importance of the underlying etiology of the arrhythmia. Seventy-three patients (Group I) had a previous myocardial infarction and documented late sustained monomorphic ventricular tachycardia. Thirty-five (Group II) also had a previous myocardial infarction but had late ventricular fibrillation. There were 41 patients (Group III) without coronary artery disease: 9 patients with right ventricular dysplasia, 26 with idiopathic sustained ventricular tachycardia and 6 with idiopathic ventricular fibrillation. The mean follow-up period for all patients was 22 to 57 months. The total mortality rate in Group I (16%) and Group II (34%) and the arrhythmic mortality rate in Group I (5%) and Group II (11%) were significantly higher than the rates in Group III. In the latter group the total mortality rate was 4% for those with idiopathic ventricular tachycardia and 11% for those with right ventricular dysplasia, and there were no deaths due to arrhythmia (p less than 0.05). Left ventricular ejection fraction was significantly lower and left ventricular end-diastolic pressure was significantly higher in Group I and Group II than in Group III. There were nonfatal recurrences of ventricular tachycardia in 33 to 56% of patients, and the number of these episodes did not differ significantly in those with and without coronary artery disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

[Ventricular tachycardia and ventricular fibrillation following myocardial infarct: determinants of prognosis and disease course].

To assess the risk of sudden death 79 patients (pts) with sustained monomorphic ventricular tachycardia (SMVT) and 37 patients with ventricular fibrillation (VF) after myocardial infarction (MI) were studied by coronary angiography, ambulatory monitoring, and programmed electrical stimulation. Mean follow-up was 28 +/- 12 months. Total mortality was significantly higher in pts with VF (13/37, 35%) than in pts with SMVT (15/79, 19%) (p less than 0.05), whereas there were no significant differences in the incidence of sudden death between pts with VF (6/37, 16%) and those with SMVT (5/79, 6%) (p = 0.09). Patients with VF had more frequent anterior and multiple MI's (33/37, 89%) than pts with SMVT (42/79, 53%) (p less than 0.05) and more often presented their arrhythmia earlier (within 2 months) after MI (23/37, 62%) than SMVT pts (28/79, 36%) (p less than 0.05). In addition, there were significant differences in mean left-ventricular ejection fraction between pts with VF (30 +/- 8%) and those with SMVT (35 +/- 12%) (p less than 0.05). Our data show that pts with VF after myocardial infarction have more severe left ventricular dysfunction and more extensive coronary disease and a somewhat higher risk of sudden death than pts with SMVT.

Adult↗
PubMed1987

A transcardiac lead system for identification and termination of supraventricular and ventricular tachycardia.

The value of a transcardiac lead system (coronary sinus to right ventricular apex) to record atrial and ventricular electrical activity and its pacing capabilities was assessed in 20 patients with a variety of tachycardias (atrial tachycardia in 3 patients, atrial flutter in 4, intranodal tachycardia in 6, circus movement tachycardia using an accessory pathway in 1 patient, and ventricular tachycardia in 9). The transcardiac lead invariably showed both atrial and ventricular electrical activity during sinus rhythm and tachycardias, allowing application of the same criteria as used when analyzing cardiac rhythm on the surface electrocardiogram. Atrial complexes had a mean amplitude of 4.2 mV during sinus rhythm and varied from 3.0 to 4.1 mV during the different types of tachycardia. Ventricular complexes had a mean amplitude of 9.8 mV during sinus rhythm, 13.8 mV during supraventricular tachycardia and 16.1 mV during ventricular tachycardia. The duration of the QRS complex on the transcardiac lead was equal to the duration of the QRS complex on the surface electrocardiogram during tachycardias with a small or wide QRS complex. By varying the intensity of current delivered through the transcardiac lead, only right ventricular pacing (mean current intensity 1.2 +/- 0.4 mA) or simultaneous atrioventricular pacing (mean current intensity 4.7 +/- 3.3 mA) could be achieved. Termination of all episodes of tachycardia was achieved with either ventricular pacing or simultaneous atrioventricular pacing. This transcardiac lead system allows clear identification of atrial and ventricular events, is suitable for tachycardia analysis using simple surface electrocardiographic algorithms and allows pacing termination of a variety of tachycardias.

Atrioventricular Node↗
PubMed1987

Comparative electrophysiologic effects of intravenous amiodarone and desethylamiodarone in dogs: evidence for clinically relevant activity of the metabolite.

It has been suggested that some of the effects of long-term amiodarone therapy may be due to accumulation of a metabolite, desethylamiodarone. To evaluate the pharmacologic actions of the metabolite, we gave single intravenous doses (10 or 25 mg/kg) of amiodarone or desethylamiodarone to anesthetized dogs. The resulting plasma and myocardial concentrations of both agents were similar to levels achieved with long-term oral amiodarone therapy in man. Amiodarone and desethylamiodarone produced frequency-dependent slowing in ventricular and atrioventricular nodal conduction and increased atrial and ventricular refractory periods. The relative effects of these agents on fast- and slow-channel tissues differed, with amiodarone producing significantly greater prolongation of Wenckebach cycle length and desethylamiodarone producing larger increases in QRS duration, atrial refractory period, and ventricular refractory period. We conclude that desethylamiodarone has substantial electrophysiologic effects at clinically relevant concentrations and has relatively greater effect on fast-channel tissue in vivo than does amiodarone. The accumulation of desethylamiodarone probably accounts for some of the delayed electrophysiologic effects in patients receiving long-term treatment with amiodarone.

Amiodarone↗
PubMed1987

Frequency-dependent effects of amiodarone on atrioventricular nodal function and slow-channel action potentials: evidence for calcium channel-blocking activity.

The purpose of these experiments was to determine the frequency dependence of the effects of amiodarone and its active desethyl metabolite on slow-channel tissues. Intravenous amiodarone and desethylamiodarone (10 or 25 mg/kg) increased atrioventricular conduction time (AVCT) and refractory period (AVERP) in open-chest, chloralose-anesthetized dogs. Drug effects on AVCT and AVERP were greatly augmented by increasing atrial stimulation frequency. The frequency dependence of drug effects was quantified by studying the response of atrioventricular (AV) conduction to changes in coupling interval. Under control conditions, premature atrial stimulation increased AVCT with a time constant of 70 msec. In the presence of amiodarone and desethylamiodarone, a biexponential relationship between AVCT and coupling interval was observed. One component had a time constant similar to control, and a slower component with a time constant of about 1 sec appeared. Slow-channel action potentials produced in canine cardiac false tendons by elevated potassium (25 mM) and isoproterenol in vitro showed interval-dependent changes in Vmax with a time constant averaging 74 msec in the absence of amiodarone. In the presence of amiodarone, a slower recovery phase of Vmax with a time constant averaging 0.94 sec was observed. These results indicate that amiodarone and its metabolite produce heart rate-dependent changes in AV nodal function in vivo and suggest use-dependent calcium-channel blockade as a mechanism of this action. Amiodarone's rate-related effects on slow-channel properties should produce selective depression of supraventricular tachyarrhythmias involving rapid activation of the AV node.

Action Potentials↗
PubMed1986

Frequency-dependent effects of calcium antagonists on atrioventricular conduction and refractoriness: demonstration and characterization in anesthetized dogs.

Calcium-channel blockers are known to affect slow inward current in a frequency-dependent fashion. The purpose of these experiments was to study use-dependent effects of verapamil, diltiazem, and nifedipine on atrioventricular conduction in vivo. Loading and maintenance infusion techniques were developed to study each drug at a series of stable plasma concentrations in autonomically blocked dogs anesthetized with morphine and alpha-chloralose. All three agents produced changes in atrioventricular conduction and refractoriness that increased with increasing stimulation frequency. The time dependence of drug-induced changes in atrioventricular conduction was characterized both by varying the coupling of single test stimuli and by abruptly changing activation frequency. The time constants for onset of (tau on) and recovery from (tau off) block were typical for each drug, with nifedipine having a faster time constant (tau off = 0.36 +/- 0.12 sec) than verapamil (tau off = 3.2 +/- 1.0 sec, tau on = 28 +/- 8 sec) or diltiazem (tau off = 2.7 +/- 1.2 sec, tau on = 13 +/- 4 sec). The time constants for each drug were independent of concentration but the magnitude of time-dependent change increased with increasing drug concentration. We conclude that calcium-channel blockers have important frequency-dependent effects on atrioventricular conduction in vivo. This frequency dependence may result in selective depression of atrioventricular conduction in the presence of supraventricular tachyarrhythmias, with important potential implications for the clinical use of these agents.

Animals↗
PubMed1985

Age-dependent lidocaine disposition in patients with acute myocardial infarction.

To evaluate age-dependent changes in lidocaine disposition in patients with acute myocardial infarction, we measured plasma concentrations of lidocaine and its metabolites monoethylglycinexylidide and glycinexylidide after discontinuation of a maintenance lidocaine infusion. Plasma lidocaine clearance was calculated by dividing the lidocaine concentration at the end of the infusion into the maintenance infusion rate. Lidocaine clearance in 35 patients was related to body weight and was reduced by heart failure. Heart failure was more common in the elderly, occurring in 15 of 27 (56%) patients over 65 years old and seven of 29 (24%) patients under 65 years old. There was a reduction in lidocaine clearance with age due, in part, to lower body weight and a higher prevalence of heart failure in the elderly. Multilinear regression analysis showed that age and weight contributed to the prediction of lidocaine plasma clearance in patients with and without heart failure. Age was a particularly important predictor of lidocaine clearance in patients with heart failure. Adjustment of lidocaine maintenance doses based on age, weight, and heart failure may help control the frequency of lidocaine adverse reactions in the elderly.

Adult↗
PubMedDate not supplied

Depression and health-care costs during the first year following myocardial infarction.

OBJECTIVE: Depression in the hospital after myocardial infarction (MI) has been associated with a substantial increase in the long-term risk of cardiac mortality, but little is known about other outcomes. This study uses Quebec Medicare data to examine the relationship between post-MI depression and physician costs, including both out-patient care and hospital readmissions. METHODS: The sample consists of 848 1-year survivors of an acute MI who had completed the Beck Depression Inventory (BDI) in hospital. Two hundred sixty subjects had BDI scores of >/=10 (30.7%), indicative of mild to moderate symptoms of depression. Quebec Medicare data during the index admission for an acute MI and during the year following discharge were compared for the patients with elevated BDI scores and those with normal scores. RESULTS: Total costs, in Canadian dollars (out-patient physician charges plus physician costs during admissions plus estimates of associated direct costs), were about 41% higher (p = 0.004) for patients with elevated BDI scores. The difference was primarily related to out-patient and emergency room visits and readmission costs associated with longer stays in hospital wards, and was not accounted for by use of psychiatric services or readmissions for revascularization. CONCLUSION: Results suggest that, in addition to the survival risks associated with post-MI depression, there are increased health care costs linked to both readmissions and out-patient contacts among depressed patients who survive the first post-MI year. The extent to which the increased use of health care may have reduced depression and enhanced survival remains unclear.

Adult↗
PubMedDate not supplied

Major depression before and after myocardial infarction: its nature and consequences.

The prevalence and prognostic impact of previous depression, depression in the hospital, and depression after discharge were studied in 222 patients admitted for acute myocardial infarction (MI). Patients were interviewed 1 week, 6 months, and 12 months after the index MI using a modified version of the Diagnostic Interview Schedule (DIS); patients also completed the Beck Depression Inventory (BDI). Patients or family members were recontacted at 18 months to determine survival. Some 27.5% of patients had at least one episode of major depression before their MI, but only 7.7% were depressed at some point during the year preceding the infarct. Overall, 31.5% of patients experienced depression in the hospital or during the year postdischarge. Some 35 patients were depressed in the hospital, 30 became depressed between discharge and 6 months, and five more between 6 and 12 months after the MI. History of depression increased the risk of depression in the hospital and after discharge. Depression in the hospital was associated with an increased risk of mortality over 18 months. Patients who experienced a recurrent depression in the hospital were at particularly high risk. Although patients who became depressed after discharge differed from those who remained depression-free in terms of age, history of depression, BDI scores, and the number of depression symptoms on the DIS in the hospital, a model including these variables identified only 14.7% of the patients who became depressed after returning home. Post-MI depression is common and largely unrelated to medical and psychosocial factors.

Adult↗