Low prevalence of cardiac troponin T mutations in a Greek hypertrophic cardiomyopathy cohort.
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Adolescent↗
Biomedical subjects
I Rizos
Publications and source records attributed to I Rizos.
Coronary artery ectasia, aneurysm of the basilar artery and varicose veins: common presentation or generalized defect of the vessel wall? A case report.
A young man who suffered from an acute myocardial infarction is presented. He presented coronary artery ectasia along with coronary artery disease. Further evaluation revealed the presence of both a saccular aneurysm of the basilar artery as well as varicose veins of the lower limbs. A common pathogenic mechanism is discussed since all these findings are characterized by similar histologic substrate with the most profound defect being destruction of the myoelastic elements of the media.
Adult↗
Three-year survival of patients with heart failure caused by dilated cardiomyopathy and L-carnitine administration.
We examined the efficacy of long-term L-carnitine administration for the treatment of heart failure caused by dilated cardiomyopathy in adult patients. To accomplish this, we studied 80 patients with moderate to severe heart failure (New York Heart Association classification III to IV) caused by dilated cardiomyopathy. This article reports on the nearly 3 years of follow-up data on patient mortality. Primary results will be published in the future. After a period of stable cardiac function up to 3 months, patients were randomly assigned to receive either L-carnitine (2 g/d orally) or placebo. There were no statistical differences between the 2 groups at baseline examination in clinical and hemodynamic parameters, such as ejection fraction, Weber classification, maximal time of cardiopulmonary exercise test, peak VO(2) consumption, arterial and pulmonary blood pressure, and cardiac output. After a mean of 33.7 +/- 11.8 months of follow-up (range 10 to 54 months), 70 patients were in the study: 33 in the placebo group and 37 in the L-carnitine group. At the time of analysis, 63 patients were alive. There were 6 deaths in the placebo group and 1 death in the L-carnitine group. Survival analysis with the Kaplan-Meier method showed that patients' survival was statistically significant (P <.04) in favor of the L-carnitine group. L-carnitine appears to possess considerable potential for the long-term treatment of patients with heart failure attributable to dilated cardiomyopathy.
Administration, Oral↗
Serum lipoprotein(a) levels in a Greek population sample without a history of premature myocardial infarction.
OBJECTIVE: To investigate lipoprotein(a) levels in a Greek population sample. METHOD: Serum apolipoprotein [Apo(a)] concentrations were measured in 220 men and 190 women aged 55-65 years without a history of effort angina or myocardial infarction. RESULTS: The distributions of Apo(a) and lipoprotein(a) [LP(a)] levels were highly skewed both in men and in women. The level of 30 mg/dl Lp(a) corresponded to the 77th percentile of the Lp(a) distribution in men but to the 66th percentile in women. Women had significantly higher values of Apo(a) or Lp(a) concentration than men. High-density lipoprotein cholesterol levels tended to be higher in women, but not in men, belonging to the fourth and fifth quintiles of the Lp(a) distribution than in those belonging to the three lower quintiles.
Aged↗
Electropharmacology of the bradycardic agents alinidine and zatebradine (UL-FS 49) in a conscious canine ventricular arrhythmia model of permanent coronary artery occlusion.
Myocardial infarction was produced in 27 anesthetized dogs by ligating the left anterior descending (LAD) coronary artery proximal to the septal branch. Nineteen of these animals survived the operation and were studied by programmed stimulation in a random sequence between the third and seventh days after the infarct. Complete electrophysiologic testing was implemented in each animal prior to and after single doses of either alinidine (1 mg/kg IV) or zatebradine (0.5 mg/kg IV). Alinidine prevented reinduction of sustained ventricular tachycardia (SVT) in only 2 of 9 dogs and zatebradine in 1 of 8 dogs. The SVT cycle length was not significantly changed in all cases in which it was still inducible despite drug administration (p > 0.05). Alinidine lengthened the effective refractory period (ERP) in the AV node (p < 0.01), whereas zatebradine did not induce a statistically significant prolongation. Conversely, zatebradine increased the left ventricular ERP, while alinidine left it almost unchanged. The rate-corrected QT interval (QTc) did not significantly differ from control values after the administration of either agents. Also, the duration and the ERP of infarctzone potentials, defined as late potentials, remained unaltered. The results indicate that the bradycardic agents alinidine and zatebradine do not exert antiarrhythmic efficacy against SVT induced during subacute myocardial infarction in conscious dogs. None of these drugs substantially changed ventricular electrophysiology or showed a drug-specific proarrhythmic effect.
Animals↗
Time domain analysis of the signal averaged electrocardiogram in patients with a conduction defect or a bundle branch block.
Doubts have been expressed about the clinical usefulness of time domain analysis of the signal averaged electrocardiogram in patients with prolonged QRS complex duration. We studied 147 patients using a signal averaged ECG (40-250 Hz) whose QRS complex was longer than 100 ms. A baseline electrophysiology study was also performed in 128 of these patients. Seventy-seven patients had a minor (QRS < 120 and > 100 ms) conduction defect. Thirty-seven of these 77 had either induced or spontaneous sustained ventricular tachycardia (group I) and 40 had no sustained ventricular tachycardia (group II). Seventy patients had a major (QRS > or = 120 ms) conduction defect, 44 of whom had sustained ventricular tachycardia (group A). The remaining 26 without this condition formed Group B. Group I compared to group II patients had a longer filtered QRS duration (120.8 +/- 14 vs 104.5 +/- 9.5 ms, P < 0.001), a longer low amplitude signal duration (41 +/- 12.1 vs 31 +/- 12.6 ms, P < 0.0001) and a lower root mean square of the last 40 ms of the filtered QRS complex (27 +/- 29.8 vs 35 +/- 25.3 microV, P = ns). Group A compared to group B had a longer filtered QRS duration (157.7 +/- 20.2 vs 140.7 +/- 15.7 ms, P < 0.001), a longer low amplitude signal duration (57.3 +/- 24.9 vs 37.8 +/- 20.3 ms P < 0.001) and a lower root mean square of the last 40 ms of the filtered QRS complex (14.3 +/- 11.2 vs 22.0 +/- 10.5 microV, P < 0.01). Using conventional late potential criteria, the sensitivity and specificity of the signal averaged ECG for the detection of sustained ventricular tachycardia patients with a minor conduction defect were 89% and 75%, respectively. The same criteria applied to patients with a major conduction defect were sensitive (sensitivity: 87%) but non-specific (specificity: 50%). However, by using modified late potential criteria, such as the presence of two of any of the following three signal averaged parameters: filtered QRS duration > or = 145 ms, low amplitude signal duration > or = 50 ms, root mean square of the last 40 ms of the filtered QRS complex < or = 17.5 microV, we derived a non-optimal but still acceptable combination of sensitivity (68%) and specificity (73%). We conclude that traditional late potential criteria can be applied in patients with a minor conduction defect, but modification of these criteria is necessary to derive useful clinical information for risk stratification of patients with a QRS complex duration > or = 120 ms.
Adult↗
Electrophysiological mechanisms of action of the levorotatory isomer of sotalol in a canine infarct model of inducible ventricular tachycardia: comparison with the beta-1 receptor antagonist bisoprolol.
To evaluate the antiarrhythmic efficacy of l-sotalol and bisoprolol on inducible ventricular arrhythmias, conscious dogs with 4- to 8-day-old myocardial infarction were studied by programmed electrical stimulation. Direct recordings from infarcted and adjacent normal subepicardium were made using a specially designed composite electrode. From 18 dogs developing sustained ventricular tachycardia (sVT) during control stimulation, l-sotalol (1.5 mg/kg i.v.) prevented reinducibility of sVT in 10 animals, while in seven other animals it significantly reduced the rate of tachycardia. Bisoprolol (0.2 mg/kg i.v.), tested in a separate group of 10 dogs susceptible to sVT, was mostly ineffective in preventing or slowing the tachycardia. Both agents significantly prolonged conduction time and refractoriness within the atrioventricular conduction system, and decreased heart rate. However, while l-sotalol lengthened ventricular refractoriness and QT interval, bisoprolol exerted only a minor effect on these parameters. Neither of the drugs affected conduction in normal and infarcted myocardium, as indicated by almost unchanged QRS complex width and duration of ventricular late potentials, respectively. The results indicate that acute beta-blockade is ineffective against sVT induced during the subacute stage of myocardial infarction. The antiarrhythmic efficacy of l-sotalol may predominantly be related to its prolonging effect on ventricular refractoriness, supporting the concept of pure class III action.
Animals↗
Electrophysiological mechanisms of action of ethmozine that explain its antiarrhythmic efficacy in the late stage of experimental myocardial infarction in dogs.
The effects of intravenous ethmozine (3 mg.kg-1) on electrophysiological parameters of ischaemically damaged myocardium and induced ventricular tachyarrhythmias were studied by programmed stimulation in 17 conscious dogs with 4 to 8 day-old ligation of the left anterior descending coronary artery. Ethmozine showed a beneficial effect on sustained ventricular tachycardia by suppressing its inducibility in five of 14 animals or by slowing its rate in six of 14 animals. Ethmozine prolonged the ventricular effective refractory period in normal and infarcted myocardium, and impaired depressed conduction in ischaemically damaged tissue. The latter was indicated by significant lengthening of late potentials recorded from the infarction zone. The QT interval was only slightly increased with ethmozine. Our findings indicate an antiarrhythmic action of ethmozine in the late stage of myocardial infarction. Major mechanisms accounting for its efficacy may predominantly be associated with marked depression of slow conduction in the infarction zone, as well as with prolongation of ventricular refractoriness without significant changes of ventricular repolarization.
Animals↗
Lidocaine converts inducible ventricular fibrillation into sustained ventricular tachycardia in conscious dogs with recent myocardial infarction.
The aim of the present study was to investigate the effect of lidocaine (L) on ventricular tachyarrhythmias with special reference to ventricular fibrillation (VF). Myocardial infarction (MI) was created in 39 dogs by doubly ligating the left anterior descending (LAD) coronary artery. All animals surviving the infarction (n = 33) were subjected to programmed ventricular stimulation 7.6 +/- 3.2 days later. Local electrical activity was recorded from the subepicardium of the left ventricular wall by means of a specially designed composite electrode. L (2 and 4 mg/kg i.v.) facilitated the induction of sustained monomorphic ventricular tachycardia (sVT) in 8 dogs with nonsustained polymorphic ventricular tachycardia (nsVT) in the control. In 13 dogs developing sVT during control stimulation, L slowed the rate of tachycardia in 8 animals (first-dose effect), while it abolished arrhythmia induction in 5 animals (second-dose effect). It was interesting that L (2 mg/kg) abolished reproduction of control VF in 12 animals by converting it into sVT. L significantly depressed conduction and prolonged ventricular refractoriness in the infarction zone. The results suggest that L facilitates induction of sVT in conscious dogs with recent MI, thereby decreasing susceptibility of infarcted myocardium to aggressive polymorphic nsVT or VF. The capability of L to exacerbate slow conduction in the infarction zone seems not to favor the development of VF during this stage of MI.
Animals↗
Intraindividual comparison of diltiazem and verapamil on induction of paroxysmal supraventricular tachycardia.
The effects of i.v. diltiazem (0.25 mg/kg) and i.v. verapamil (0.15 mg/kg) were studied in 18 patients with recurrent paroxysmal supraventricular tachycardia (SVT) who underwent serial electrophysiological studies. In 10 of 18 patients with extranodal accessory pathways the effects of diltiazem and verapamil were similar in comparable plasma concentrations. SVT was prevented in 10/10 cases after diltiazem and 9/10 cases after verapamil, furthermore there as an increase in antegrade refractoriness of the normal AV nodal pathway of 22 and 27%, respectively; accessory pathway refractoriness and conduction remained unchanged in both drugs. In 8 of 18 patients with dual AV nodal pathways diltiazem was significantly less effective as compared to verapamil (p < 0.02) regarding prevention ov SVT (3/8 vs. 8/8 cases) and increase in the antegrade refractoriness of the slow AV nodal pathway (+21 vs. +34%). However, both drugs produced equivalent slowing of antegrade AV nodal conduction and a similar increase in antegrade refractoriness of the fast AV nodal pathway. In all 18 patients, the site of action of both drugs was the antegrade limb, regardless of SVT mechanism. The data suggest that the two calcium antagonists are equipotent in AV reentrance but verapamil may offer greater benefit in AV nodal reentrance than diltiazem.
Adult↗
Amiodarone in patients with recurrent sustained ventricular tachyarrhythmias: results of programmed electrical stimulation and long-term clinical outcome in chronic treatment.
Thirty-three patients with clinically recurrent ventricular tachyarrhythmias were treated with amiodarone (200 to 600 mg/day) during a mean follow-up period of 23.7 months. Prior to amiodarone therapy, sustained ventricular tachycardia or ventricular fibrillation was initiated in all patients at control electrophysiologic study; patients failed a mean of 5.7 drugs, as assessed by programmed electrical stimulation. At electrophysiologic study after a loading phase (1000 mg/day for 10 days), 10 patients had no inducible ventricular tachycardia, nine patients had nonsustained ventricular tachycardia, 13 patients had persistent sustained ventricular tachycardia, and one patient had ventricular fibrillation. Patients were continued on amiodarone alone regardless of the findings at the electrophysiologic study, and during follow-up patients with no inducible sustained ventricular tachycardia or fibrillation on amiodarone had no recurrent arrhythmias or sudden death. Six of 14 patients (43%) with sustained ventricular tachyarrhythmias still inducible had recurrent ventricular tachycardia/fibrillation, and four of them died suddenly (29%). Programmed electrical stimulation predicts a good clinical long-term outcome during amiodarone therapy. Patients with persisting fast tachyarrhythmias (cycle length less than or equal to 300 msec) on amiodarone and a low ejection fraction (less than 35%) seem to have a higher incidence of sudden death. In these patients, therapeutic approaches such as antiarrhythmic surgery or implantation of antitachycardia devices should be considered.
Amiodarone↗
Effects of intravenous disopyramide and quinidine on normal myocardium and on the characteristics of arrhythmias: intraindividual comparison in patients with sustained ventricular tachycardia.
Intraindividual comparison of the acute response to intravenous quinidine and to intravenous disopyramide was performed in 27 patients with sustained ventricular tachycardia (VT) who underwent serial electrophysiological studies. In each patient, sustained VT could be reproducibly initiated by programmed ventricular stimulation during control studies. Quinidine and disopyramide prevented inducibility of sustained VT in 7 and 8 of the 27 patients, respectively. Six patients were concordant responders to both drugs and 18 patients were concordant non-responders resulting in a total of 24 patients (89%) who had a concordant result (P less than 0.01). In the 18 non-responders with inducible sustained VT after both drugs, quinidine and disopyramide caused qualitatively and quantitatively similar changes in the characteristics of the VT: prolongation of the interval between the initiating extrastimulus and the first beat of VT by 36 and 39%, and an increase in VT cycle length by 21 and 29%, respectively. The QRS morphology of VT was concordantly altered in 13 of these 18 patients (72%). In all 27 patients, quinidine and disopyramide caused a quantitatively similar prolongation of ventricular refractoriness by 12 and 14%, of the QRS duration by 14 and 13% and of the QTc interval by 13 and 13%, respectively. The clinical data obtained at comparable plasma concentrations confirm the experimental presumption that quinidine and disopyramide have qualitatively and quantitatively similar electrophysiological effects not only on normal myocardium but also on the characteristics of VT, resulting in a significant concordance of antiarrhythmic responses.
Adult↗
Contribution of delayed ventricular repolarization to the anti-arrhythmic efficacy of sotalol.
Eighteen patients with sustained ventricular tachycardia underwent serial electrophysiological studies to establish the therapeutic efficacy of sotalol as compared to other available anti-arrhythmic agents. One or more acutely effective drug was found in 14 of the 18 patients (78%). Sotalol was tested in all 18 patients and was effective in 12 of them (67%). For assessment of the prophylactic efficacy of other anti-arrhythmic agents, an average of 3.5 additional studies per patient were performed resulting in successful prevention of ventricular tachycardia in a total of 10 of 63 (16%) additional trials. Nine patients were placed on chronic oral therapy with sotalol. In these nine patients long-term prophylaxis against ventricular tachycardia was documented over a mean follow-up period of 9.6 months (range 2-18 months). The study suggests that sotalol can provide effective prophylaxis against ventricular tachycardia in a significant proportion of patients refractory to other available drugs and that this prophylactic efficacy is predominantly due to its Class III anti-arrhythmic properties. Experimental studies were performed in eight conscious dogs 3-7 days following proximal LAD ligation. Epicardial recordings were obtained using implanted composite electrodes. Sotalol prevented sustained VT by a predominant increase in refractoriness of the infarcted zone. In vitro, sotalol caused a significant prolongation of the action potential of epicardial and endocardial fibres within both the infarcted and noninfarcted myocardium. Refractoriness of epicardial ventricular fibres was significantly more prolonged in ischemically damaged cells as compared to normal fibres.
Animals↗
Intraindividual comparison of intravenous ajmaline and quinidine in patients with sustained ventricular tachycardia: effects on normal myocardium and on arrhythmia characteristics.
Intraindividual comparison of the acute response to intravenous quinidine and to intravenous ajmaline was performed in 23 patients with sustained ventricular tachycardia (VT) who underwent serial electrophysiological studies. In each patient, sustained VT could be reproducibly initiated by programmed ventricular stimulation during control studies. Inducibility of sustained VT was prevented after quinidine in 6 of the 23 patients (26%) and after ajmaline in 8 of the same 23 cases (35%). Agreement between the effects of both drugs was not significant: 2 patients had a similar response to both quinidine and ajmaline and 11 patients did not have a response to either of the two drugs, resulting in a total of only 13 patients (57%) who had a similar response to both drugs. In the 11 non-responders with inducible sustained VT before and after both drugs, quinidine and ajmaline caused qualitatively and quantitatively similar alterations of VT characteristics including a significant prolongation of the interval between the initiation extrastimulus and the first beat of VT by 38 and 42% (P less than 0.01), an increase in VT cycle length by 15 and 22% (P less than 0.01) and a prolongation of the QRS duration during VT by 15 and 18% (P less than 0.01), respectively. In all 23 patients, quinidine and ajmaline caused a quantitatively similar prolongation of ventricular refractoriness by 11 and 9% (P less than 0.05), of the QRS duration at sinus rhythm by 10 and 15% (P less than 0.01) and of the QTc interval by 13 and 10% (P less than 0.05), respectively. Thus, ajmaline and quinidine appear to have similar electrophysiological effects on both normal myocardium and on indirect parameters of reentry; in individual patients with sustained VT, however, such electrophysiological similarities do not result in significant agreement of preventive responses.
Adult↗
[Electrophysiological effects of sotalol on the sinus node, atrium, AV node and his-bundle cells in the rabbit heart].
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Action Potentials↗
Differential effects of sotalol and metoprolol on induction of paroxysmal supraventricular tachycardia.
Seventeen patients with recurrent paroxysmal supraventricular tachycardia (SVT) underwent serial electrophysiologic studies to compare the effects of i.v. sotalol (1.5 mg/kg) and i.v. metoprolol (0.15 mg/kg). The plasma concentrations of sotalol (2.1 +/- 1.1 microgram/ml) and metoprolol (67 +/- 15 ng/ml) were within the therapeutic range. Before drug administration, sustained SVT could be reproducibly induced in all patients. Sotalol prevented induction of sustained SVT in 10 of 17 patients (59%) and metoprolol in 4 (28%) (p less than 0.05). In 6 of 8 patients with atrioventricular (AV) nodal reentrance, the site of action of sotalol was the anterograde or the retrograde limb, reflecting an increase in refractoriness in both pathways of the circus movement. In 4 of 9 patients with AV reentrance, the site of action of sotalol was exclusively the AV nodal pathway; conduction through the extranodal accessory tract appeared to be unchanged, but its anterograde effective refractory period was prolonged (from 285 +/- 25 to 322 +/- 28 ms, p less than 0.001; mean +/- standard deviation). In the 7 patients in whom sotalol did not prevent sustained SVT, the tachycardia cycle length increased from 347 +/- 42 to 392 +/- 45 ms (p less than 0.01). Compared with sotalol, metoprolol had qualitatively similar but quantitatively less potent effects on the AV nodal pathways; however, different from sotalol, metoprolol had no effect on extranodal accessory tracts. The study suggests that at therapeutic plasma concentrations, sotalol would be effective in preventing clinical SVT in a significant proportion of patients refractory to metoprolol; because sotalol not only has beta-blocking properties but also results in acute prolongation of the action potential duration, this combination of class II and III activity may contribute to its superior prophylactic efficacy compared with pure beta blockade.
Adult↗
Electrophysiologic testing in assessment of therapy with sotalol for sustained ventricular tachycardia.
Eighteen patients with sustained ventricular tachycardia underwent electrophysiologic studies to establish the therapeutic efficacy of sotalol. In each patient ventricular tachycardia could be reproducibly initiated by programmed stimulation during control studies. Sotalol prevented induction of sustained ventricular tachycardia in 12 of the 18 patients (67%). Prolongation of the QTC interval and of ventricular refractoriness was regularly observed after sotalol but did not reliably predict prophylactic efficacy. Severe adverse effects, including congestive heart failure and sinus node dysfunction, were noted early during sotalol therapy in three patients. Nine patients were placed on long-term oral treatment with sotalol and four patients on another effective agent. In these 13 patients, complete (12 patients) or partial (one patient) long-term prophylaxis against ventricular tachycardia was documented over a mean follow-up period of 16 months (range 8 to 24). The study suggests that sotalol can provide effective prophylaxis against sustained ventricular tachycardia; this prophylactic efficacy is not typical for pure beta-adrenergic antagonism but may at least partly result from experimentally observed prolongation of the ventricular action potential duration.
Administration, Oral↗
[Programmed stimulation in patients with malignant ventricular arrhythmias. I: Diagnostic value].
Sudden cardiac death is a leading cause of death in industrially developed countries and accounts for approximately 90 000 deaths yearly in the FRG. While the majority of victims have severe coronary heart disease, sudden cardiac death is infrequently caused by acute myocardial infarction (20%) but is predominantly related to malignant ventricular arrhythmias (i.e., ventricular fibrillation or sustained ventricular tachycardia). Patients with a history of such malignant ventricular arrhythmias are at high risk for sudden death. Spontaneous occurrence of sustained ventricular tachycardia and of ventricular fibrillation is critically related to two factors: 1. trigger-arrhythmias consisting usually of complex ventricular extrasystoles (Lown classification IV to V); 2. increased vulnerability of the myocardium representing the target organ for trigger-arrhythmias. While trigger-arrhythmias can be easily recorded by noninvasive techniques including Holter monitoring or exercise and stress ECG, ventricular vulnerability is more difficult to determine and often requires ventricular stimulation with intracardiac electrocatheters. In patients with documented spontaneous malignant ventricular arrhythmias, two aspects of programmed stimulation must be considered: 1. diagnostic, and more importantly, 2. therapeutic purposes of this method. Diagnostic purposes include determination of the mode of initiation and unequivocal ventricular localization of the tachycardia excluding other arrhythmias with broad QRS complex. In patients with spontaneous sustained ventricular tachycardia, programmed stimulation can reproducibly initiate the clinical arrhythmia in 85% (sensitivity and specificity of the method approximately 90%). In patients with cardiac arrest due to ventricular fibrillation, programmed stimulation is less reliable (50%). However, the main purpose of programmed stimulation in patients with documented clinical malignant arrhythmias is not diagnostic or prognostic evaluation but is serial electrophysiological studies for individual optimization of antiarrhythmic therapy.
Arrhythmias, Cardiac↗