[Anniversary of catheterization in cardiology (Andreas Ronald Grüentzing)].
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Biomedical subjects
Publications and source records attributed to L Szatmáry.
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The study was aimed to investigate the electrophysiological properties of long QT syndrome associated with permanent bradycardia. The investigations were performed in 26 patients suffering from long QT duration (QTC-frequency adapted QT-:484 +/- 34 ms) with permanent, marked bradycardia (heart rate: 42 +/- 7 min-1). Adams Stokes syncopal attack appeared in 12 patients, while in 14 cases ventricular tachycardia attack with syncope could be observed (study group). As control served the data of 30 patients suffering from long lasting marked bradycardia (heart rate: 44 +/- 7 min-1) with normal QT (QTC:420 +/- 28 ms). Each patient was candidate for pacemaker implantation. The following questions were studied: 1. The effect of heart rate on QT duration. The experiments were performed by electrical ventricular stimulation. 2. The effect of sympathetic and parasympathetic-pharmacologic-blockade on QT time. The study was performed under electrical ventricular stimulation by administration of propranolol and atropine. 3. The dispersion of QT time was studied by using electrical heart stimulation and 12 lead ECG recording. Electrophysiological investigations were performed in 14 patients with long QT and permanent bradycardia. On augmentation of the cycle length (bradycardia) the increase in the QT duration was more-out of all proportion-expressed in long QT. On pharmacologic sympathetic blockade in long QT syndrome the QT duration significantly diminished. The QT dispersion was more expressed in patients with prolonged QT interval and on bradycardia the QT dispersion further increased significantly. The irritability of the ventricle was markedly augmented in patients with long QT and bradycardia. Appearance of polymorphous ventricular tachycardia could frequently be observed and could be regularly induced by early ventricular extrastimuli and bradycardia.(ABSTRACT TRUNCATED AT 250 WORDS)
BACKGROUND: This study followed up the natural history of T-wave inversion and assessed the short-term prognosis associated with the condition. METHODS: Forty patients with acute ischemic syndrome, without infarction, and with postischemic T-wave inversion (group 1) were followed during the persistence (inverted T-wave period) and after the resolution of T-wave inversion (positive T-wave period). Another 40 patients with acute ischemic syndrome, without infarction and with normal T waves (group 2), were also followed. RESULTS: Postischemic inverted T waves showed resolution within 3-21 days of presentation in 31 patients from group 1 on medical treatment alone. Further ischemic events (acute myocardial infarction, acute ischemic syndrome, angina pectoris, silent ischemia), inducible ischemia (during treadmill test), wall-motion abnormalities (demonstrated by echocardiography), all developing in the primarily ischemic myocardial area, were more frequent (P < 0.02) in group 1 patients during the inverted T-wave period compared with those experienced in the positive T-wave period of group 1 patients, and compared with group 2 patients. CONCLUSION: In most patients on medical treatment, postischemic inverted T-waves tended to resolve within 3 weeks. The presence of postischemic inverted T waves appears to be an independent marker of further ischemic events.
This study has followed up the natural history of postischemic inverted T waves and assessed the prognosis. 40 consecutive patients with unstable angina with postischemic precordial inverted T waves in the noninfarcted, previously ischemic area were followed during the persistence (negative T wave period) and after resolution of inverted T waves (positive T wave period). The outcome with frequencies of acute myocardial infarction, acute ischemic syndrome, angina pectoris, positive exercise test, silent myocardial ischemia, anterior wall motion abnormalities on echocardiogram, positive coronary arteriography were determined and compared in the negative versus positive T wave periods. Postischemic inverted T waves showed resolution within the postischemic 3-21 days (at a mean of 10.6 days) in 31 patients on medical treatment alone during the whole study period. Frequencies of parameters/patients determined in negative versus positive T wave periods are as follows: acute myocardial infarction: 5/40 versus 0/31 (non significant), acute ischemic syndrome: 25/40 versus 2/31 (p < 0.001), angina pectoris: 32/40 versus 11/31 (p < 0.001), positive treadmill exercise test: 14/16 versus 14/30 (p < 0.02), silent myocardial ischemia: 14/14 versus 16/31 (p < 0.01), hypokinesis 26/34 versus 4/24 (p < 0.001), positive coronary arteriography: 4/4 versus 11/11 (non significant). In most patients on medical treatment, the postischemic inverted T waves tend to resolve within 3 weeks. Attention has to be paid to the patients with postischemic inverted T waves during the negative T wave period: the high ischemic risk gradually decreases with resolution of negative T waves.
The coexistence of congenital complete heart block and QT prolongation represents a special type of arrhythmia. The electrophysiological and clinical characteristics of this syndrome were studied in eight patients suffering from congenital AV block and QT prolongation. Data from 22 patients suffering from congenital complete heart block only, served as a control. In the study group, the appearance of a torsade de pointes type of ventricular tachycardia could regularly be observed and the tachycardial attack could usually be provoked by ventricular extrastimuli. The corrected QT time was markedly prolonged; on ventricular stimulation, at higher pacing rates the QT interval shortened, but remained significantly higher than in the control group. Syncopal attacks--with the character of polymorphic tachycardia--appeared in each patient of the study group while occurring in only three patients from the control group. Patients were given pacemaker implants (using a higher pacing rate) and long-term administration of beta-receptor blockers. The outcome was favourable; no ventricular tachycardia or syncopal attack was observed in the follow-up period.
The authors have investigated the haemodynamic effects of verapamil on the pulmonary circulation by 24 patients suffering from secondary pulmonary hypertension, caused by mitral and/or aortic valve diseases. For this purpose the numeric and graphometric analysis of intracavitary right ventricle pressure curve and pulmonary artery pressure tracing was applied. It was observed a selective antihypertensive effect on the lesser circulation. The pulmonary and systemic systolic tension decreased comparing in percentage 3:1, in case of diastolic tension this comparison was 2:1. The decrease in pulmonary circulation was strongly significant. The diminishing of heart rate and the improving of right heart function was not significant. The elevation of end-diastolic pressure of the right ventricle, just as the shape-analysis of pressure curves suggested right ventricle overload.
The effect of parasympathetic and sympathetic pharmacologic blockade (atropine and propranolol) on QT duration was studied in 26 patients. Of this number 17 had a normal QT time, while in 9 patients the QT interval was prolonged (greater than 460 ms). QT time was determined before and after the pharmacologic blockade with sinus rhythm (under a non fixed cycle length) and with atrial pacing (with a fixed cycle length). Atropine administration did not change QT duration significantly. On the effect of beta receptor blockade in normal patients only the corrected QT time shortened, while in long QT syndrome a very pronounced shortening in QT time, independent of the changes in the cycle length, could be observed. In QT prolongation an overactivity in the sympathetic tone can be supposed.
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Percutaneous transluminal coronary angioplasty (PTCA) in acute myocardial infarction (AMI) was performed in 42 patients (37 males, 5 females, average age 53 years). Recanalization of the stenosed or occluded infarction-related coronary artery was achieved within the first 14 to 50 min from the start of catheterization in 95% of cases. Three patients were transferred for emergency coronary bypass graft surgery (CABG) because of major multiple coronary lesions, immediately after angiographically successful PTCA. One of the patients died in cardiogenic shock. Four patients died between days 5 to 15 of hospitalization. Repeat coronary angiography was done in 27 of the 37 survivors at a mean interval of 2.5 months after AMI. Total reocclusion was found in 6 patients. The recanalized coronary artery had prevented its patency in 78% of the cases; restenosis was found in 5 patients, and was successfully dealt with renewed angioplasty in 3 patients. While the ejection fraction (EF) had remained largely unchanged, there was some improving tendency of left ventricular segmental kinetics, particularly in case of anterior wall infarction. PTCA without thrombolytic therapy seems to provide an effective and relatively prompt recanalizing procedure in the complex management of AMI.
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The electrophysiological characteristics of the long QT syndrome (LQTS) associated with permanent bradycardia and ventricular tachycardiac attacks were electrophysiologically studied in 12 patients. Tachycardia could be induced by ventricular electrical stimulation in 11 cases. The following electrophysiological properties could be revealed: 1) a very short ventricular refractory period (VERP) compared with QT length; 2) inhomogeneity in VERP and QT interval in different areas of the ventricles; 3) repetitive ventricular responses on early ventricular electrical stimuli. Patients were successfully treated by pacemaker implantation and beta-blockers. In two patients a comparatively high pacing rate was required to reduce the QT interval.
The acute effect of ajmaline was investigated in the treatment of postoperative ventricular arrhythmias. Ajmaline (Glurytmal--Giulini Pharma GMBH) was applied intravenously in 15 patients suffering from ventricular premature beats (Lown II--IV/b), tachycardia and/or ventricular fibrillation after open heart surgery. Ajmaline infusion produced in 40% of the cases a total suppression and in 100% a significant improvement of malignant ventricular arrhythmia. In patients with recurrent and resistant ventricular tachycardia, ajmaline proved effective even when other antiarrhythmic drugs had failed. It was shown to be effective in reducing ventricular premature contractions and recurrent ventricular tachycardia after heart surgery, without haemodynamic side effects. Because of recurrent ventricular premature beats in 11 patients after acute ajmaline administration further oral application of prajmalium bitartarate (Neo-Gilurytmal) was necessary. The maintenance of these patients on oral ajmaline treatment seemed important.
The electrophysiological characteristics and the antiarrhythmic indication areas of lorcainide were studied by using electrophysiological investigations and clinical studies in patients suffering from sustained arrhythmias. According to the data of the arrhythmia analyses (30 patients) the most important electrophysiological effects of lorcainide are: increase of the effective refractory period of the atria and ventricles; prolongation of the conduction time in the His bundle; prolongation of the refractory period and conduction of the accessory pathways. In the course of clinical studies (55 patients) lorcainide proved to be very effective in treating ventricular arrhythmias and preventing or disrupting ventricular tachyarrhythmic attacks. Lorcainide has a very promising antiarrhythmic effect in the suppression of tachyarrhythmias with accessory pathway conduction, too.
The electric sign of sinus node activity, the sinus node electrogram, was recorded in animal experiments and in 22 patients. In humans the electric sign of the sinus node precedes the atrial activation by 60 msec on the average. Atrial impulse conduction time is somewhat longer than the sinoauricular one. Canine sinus node electrogram is very similar to that recorded in humans but sinoauricular impulse conduction is somewhat quicker in dogs. The pathological importance of the sinus node electrogram is discussed.
The clinical, electrocardiographic, pharmacologic, electrophysiologic and Holter monitoring findings are described in four patients with autonomic sinus node dysfunction and one patient with autonomic binodal disease. All showed cerebral symptoms, and had attacks of dizziness, weakness, near-syncope or syncope. After a pharmacologic autonomic blockade with propranolol and atropine, all patients had normal intrinsic heart rates. Electrophysiological studies revealed normal corrected intrinsic node recovery time (less than or equal to 240 msec) a gradual return to the basic cycle length in the secondary postpacing cycles after autonomic blockade, and no intrinsic paroxysmal atrioventricular block. Continuous ECG monitoring (1-3 X 24 hours) revealed severe sinus bradycardia, SA-block, severe sinus arrest, cardiac standstill, atrial fibrillation and in two patients associated AV-block. Autonomic blockade with electrophysiological studies exclude the intrinsic involvement of the sinoatrial and atrioventricular node. Holter monitoring is the best method for assessing the autonomic neurovegetative component of dysrhythmias. Therapy regarding isolated autonomic sinus node dysfunction depended on the pathomechanisms of rhythm disorders: two patients received permanent pacemakers, antiarrhythmic drugs were applied in the case of two patients, and etiological treatment in the case of one. During the follow-up, all patients became symptom-free.
Electrophysiological analysis of 20 patients in child or adolescent age affected by paroxysmal tachycardia has been performed. In 16 cases the tachycardia was supraventricular and in 4 cases it was ventricular. Evaluation of the electrophysiological parameters revealed certain characteristics of childhood tachyarrhythmias, viz. (1) adequate sinus node function, absence of sinus dysfunction, (2) absence of brachycardia, (3) acceleration of anterograde and retrograde atrioventricular impulse conduction systems.
To study the diagnostic possibilities and mechanisms involved in sinus node dysfunction (SND), 26 patients with sick sinus syndrome were evaluated by basic electrophysiological tests before and after autonomic blockade, and by Holter monitoring. Based on intrinsic heart rate (IHR), two groups, a normal and a pathologic one, were separated. With Holter recordings, significant differences were manifested in minimal heart rate during sleeping and also in sinus cycles averaged for 24 h between the two groups. In patients with pathological IHR (n = 9) abnormal intrinsic rhythmicity were verified by electrophysiological means, while we found positive ECGs referring to sinoatrial dysfunction during the first 24 h of rhythm recording. The group of normal IHR (n = 17) covers patients with intrinsic SND (intrinsic SA block, 3/17 patients) and patients (14/17) where the electrophysiologic properties of the pacemaker cells were normal: normal intrinsic recovery time, gradual return to the stable intrinsic sinus cycle length in the postpacing secondary cycles, biphasic postextrasystolic patterns with a well-estimated intrinsic sinoatrial conduction time. Repeated Holter recording (total 26 X 24 h) revealed severe bradycardia (2 cases), SA block (4 cases), SA arrest (2 cases), tachybradyarrhythmia (1 case). Electrophysiological studies have a low diagnostic value in autonomic SND; repeated rhythm monitoring is obviously the best complementary method for appreciating the role and significance of autonomic tone in sick sinus syndrome.