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PubMed1987

[Incidence and kind of reperfusion arrhythmias in thrombolytic therapy of acute myocardial infarct].

UNLABELLED: In 200 consecutive patients with acute myocardial infarction combined medical-mechanical recanalization was attempted. Coronary angiography revealed an occluded vessel in 150 patients. This vessel could be opened in 127 patients. There were 112 men and 15 women, aged 32 to 72 years (mean age 61.2 years); 60 patients had an anterior and 67 patients presented with an inferior myocardial infarction. 103 from 127 patients presented with arrhythmias during the ischemic phase and 112 from 127 patients during the reperfusion phase. The following arrhythmias had a significantly higher incidence in the reperfusion phase compared to the ischemic phase: sinus bradycardia (29 pts. - 22.8% - vs. 15 pts. - 11.8%; p less than 0.05), ventricular bigeminy (28 pts. - 29.9% - vs. 5 pts. - 3.9%; p less than 0.01), ventricular couplets (34 pts. - 26.8% - vs. 20 pts. - 15.7%; p less than 0.05) and accelerated idioventricular rhythm (32 pts. - 25.2% - vs. 5 pts. - 3.9%; p less than 0.01). Ventricular fibrillation occurred during the ischemic phase in 9 patients and during the reperfusion phase in 7 patients (n.s.). None of the patients presented with sustained ventricular tachycardia, neither in the ischemic, nor in the reperfusion phase. CONCLUSIONS: The following rhythm disturbances can be called reperfusion arrhythmias: sinus bradycardia, ventricular bigeminy, ventricular couplets and accelerated idioventricular rhythm. The observed reperfusion arrhythmias were short-living and did not need special therapeutic measures.

Adult↗
PubMed1988

Arrhythmias in the assessment of coronary artery reperfusion following thrombolytic therapy.

Arrhythmias are used as markers of coronary reperfusion after administration of thrombolytic agents. We studied the effects of coronary recanalization on the development of arrhythmias in patients receiving thrombolytic agents during the early hours of acute myocardial infarction. Acute cardiac catheterization, assessing perfusion of the infarction-related artery and identifying the arrhythmias, was performed within eight hours of onset of symptoms. Fifty-six of 67 patients (84 percent) studied had total occlusion of the infarction-related artery, 25 of whom had restoration of coronary flow during the 90 minutes after initiation of therapy; 31 had no evidence of reperfusion. Eleven patients had subtotal vessel occlusion that did not change appreciably during therapy, and 20 patients (30 percent) had transient arrhythmias. There were no significant differences in the frequency of arrhythmias: 36 percent of reperfused patients, 19 percent of nonreperfused, and 45 percent of subtotal occlusion patients. Only bradyarrhythmia was significantly related to the restoration of flow of the right coronary artery. Other rhythm disturbances, including accelerated idioventricular rhythm, did not correlate with a change in the perfusion status of the vessel. Bradycardia may be a useful marker for right coronary artery reperfusion. Arrhythmias in general are not specific for coronary reperfusion and should not be used as event markers.

Adult↗
PubMed1987

[The Flack test: a test exploring the sinus function in athletes. Apropos of 351 tests].

A standardized Flack's test with continuous electrocardiographic recording was performed in 351 moderately trained athletes (317 men and 34 women; mean age 23.7 years). The test gave normal results in 310 subjects (88.3%). Tachycardia in excess of 100 beats/min was observed in 12 subjects (3.4%), and 56 abnormalities which were not present on previous ECG recordings at rest were noted in 29 subjects (8.3%); 27 of these abnormalities appeared immediately after a previous one. Out of these 56 abnormalities, 26 (44.6%) were associated with sinus dysfunction: sinus bradycardia in 8 cases, second degree sinoatrial block in 2 cases, third degree sinoatrial block in 3 cases and sinus arrest in 13 cases. In 16 cases of third degree sinoatrial block or sinus arrest escape rhythms were observed, including coronary sinus rhythm (3), junctional rhythm (12) and accelerated idioventricular rhythm (1). Five of the 56 abnormalities (8.9%) were disorders of conduction, i.e. first or second degree atrioventricular block, atrioventricular dissociation and blocked P waves. These disorders are known to be frequently associated with sinus dysfunction. In 9 out of 56 abnormalities (16.1%) disorders of excitability were present as atrial, junctional and ventricular extrasystoles. In 8 subjects the Flack's test resulted in the disappearance of disorders of conduction or excitability of the "athlete" type present at rest, as the Ruffier-Dickinson test, or the cycloergometric exercise test.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

Arrhythmias during the acute phase of reperfusion therapy for acute myocardial infarction: effects of beta-adrenergic blockade.

In 107 patients with acute myocardial infarction, the incidence of ventricular arrhythmias during the acute phase of thrombolysis was examined by means of Holter monitoring. In patients with a patient infarct-related artery as assessed angiographically at 90 minutes, the occurrence of accelerated idioventricular rhythms was noted significantly more frequently than in patients with a permanent occluded vessel. This arrhythmia peaked in the first 180 minutes after the start of thrombolysis. In addition, single ventricular premature beats and runs of ventricular tachycardia were also more common in patients with successful reperfusion. The effects of acute intravenous administration of beta-blockers were examined in 66 patients without contraindications to this therapeutic approach. There were no differences in the occurrence of any type of rhythm disorders in patients with (n = 43) or without beta-blockade (n = 23). Thus ventricular arrhythmias particularly accelerated idioventricular rhythms, and single ventricular premature beats occur more frequently in patients with a patent infarct artery within the first 24 hours after thrombolysis. Acute intravenous beta-blockade does not appear to exert significant antiarrhythmic effects during this period.

Adrenergic beta-Antagonists↗
PubMed1991

The oral dopamine agonist, ibopamine, in normal man: effects on rhythm, heart rate, blood pressure and catecholamines.

To evaluate the effects of the oral aselective dopamine congener ibopamine, heart rate, blood pressure, cardiac rhythm, electrocardiographic (ECG) parameters and plasma catecholamines were studied in ten healthy subjects on three occasions: without medication, after 100 mg oral ibopamine and after combined treatment of ibopamine and the dopamine antagonist metoclopramide. Ibopamine was well tolerated by all subjects. No significant changes in heart rate or blood pressure were seen during either ibopamine alone or during concomitant metoclopramide administration. In addition, there were no differences in PR-, QRS- and QTc- intervals on the ECG and plasma norepinephrine, epinephrine and dopamine levels were unchanged. None of the ten volunteers showed proarrhythmia from ibopamine. However, in one subject, episodes of accelerated idioventricular rhythm were observed after ibopamine, which were asymptomatic and did not exceed a rate of 51 beats/minute. During concomitant metoclopramide infusion, ibopamine did not induce accelerated idioventricular rhythm. In conclusion, in healthy subjects ibopamine appears to be a safe drug and causes neither proarrhythmia, nor changes in heart rate, blood pressure, ECG-parameters, or plasma catecholamines.

Administration, Oral↗
PubMed1990

Monomorphic repetitive rhythms originating from the outflow tract in patients with minor forms of right ventricular cardiomyopathy.

We studied in detail 17 patients presenting with monomorphic repetitive ventricular rhythms having left bundle branch block morphology and right axis deviation. All had an apparently normal heart at physical examination. At chest radiography, three patients had mild cardiomegaly, and at electrocardiography, five patients had inverted T waves beyond V2. Five patients had syncope or near syncope. In seven patients the tachycardia occurred on effort. One patient died suddenly. The patients were extensively investigated, using cross-sectional echocardiography, complete haemodynamic and angiographic studies, electrophysiology and histology, to search for any structural basis of the arrhythmias. Tachycardia was sustained in 8 patients, nonsustained in 3, and consistent with accelerated idioventricular rhythm and repetitive paroxysmal ventricular tachycardia in 5 and 1 patients, respectively. Despite the differences in clinical and arrhythmologic features, similar abnormalities of right ventricular structure and/or wall motion were detected in all patients, consistent with localized forms of right ventricular cardiomyopathy. Different antiarrhythmic drugs were successfully used in twelve patients (the four patients with accelerated idioventricular rhythm were not treated). The patient who died suddenly had previously had a sustained ventricular tachycardia and was being treated by beta-blockade. Postmortem study revealed massive fibro-adipose substitution of the right ventricular free wall and pulmonary infundibulum.

Adolescent↗
PubMed1986

Reperfusion ventricular arrhythmias during intracoronary thrombolysis.

While coronary reperfusion arrhythmias are well defined in animal models, their prevalence and predisposing factors are still uncertain during pharmacologic coronary reperfusion in patients with acute myocardial infarction. In 80 patients, who underwent this procedure and had a continuous electrocardiographic monitoring (associated with a Holter recording in 34), 6 patients developed ventricular fibrillation. Ventricular fibrillation was the terminal event in 2/19 non-reperfused patients. The other episodes of ventricular fibrillation (controlled with DC countershock) occurred within 5 minutes and 3 minutes after angiographic documentation of coronary reperfusion. Ventricular fibrillation was observed in 4/10 patients with a residual stenosis less than or equal to 80% but in no case among the 39 patients with a residual stenosis greater than 80% (P = 0.01). Holter recordings in 19 reperfused patients showed ventricular tachycardia or accelerated idioventricular rhythm at reperfusion in 8/10 patients with a coronary stenosis less than or equal to 80% and only in 3/9 with a higher degree stenosis (P less than 0.05). Reperfusion ventricular fibrillation was found to occur in 8.1% of patients. A residual stenosis of 80% or less was found to be a predisposing factor in the occurrence of ventricular fibrillation, ventricular tachycardia or accelerated idioventricular rhythm at reperfusion.

Adult↗
PubMed1993

[Reperfusion arrhythmia].

Reperfusion arrhythmias were described from the first trials of intracoronary thrombolysis for myocardial infarction. The prevalence of ventricular fibrillation during intravenous thrombolysis is low (< 7%) and comparable to that observed with classical treatment. Holter recording shows that ventricular tachycardia and accelerated idioventricular rhythms occur in over 80% of cases. These arrhythmias are generally well tolerated and do not require specific therapy. A bradycardia-hypotension syndrome is observed in about a quarter of reperfused patients, nearly always in inferior wall infarction. It normally resolves spontaneously or after atropine or vascular filling. Reperfusion is associated with a clearcut increase in the number of episodes of arrhythmia. Some arrhythmias such as sustained ventricular tachycardia, early accelerated idioventricular rhythms (occurring in the first 6 hours) or the bradycardia-hypotension syndrome may be considered as non-invasive criteria of reperfusion. More severe ischemia and sudden reperfusion favour the arrhythmogenicity of reperfusion in the animal. Recent data suggest that this may be the case in the clinical context. In some uncontrolled studies, lidocaine, betablockers and aspirin did not affect the prevalence of the arrhythmias. Preliminary trials indicate that flunarizine and captopril may reduce the incidence of reperfusion arrhythmias in man. Ventricular arrhythmias and myocardial stunning could be the result of sa single phenomenon (the extent of the ischemic lesions or reperfusion lesions). Studies currently under way should clarify the relationship between the incidence of arrhythmias, the severity of stunning and myocardial recovery. Protocols evaluating therapeutic interventions on the reperfusate should include Holter monitoring.

Animals↗
PubMed1987

Time course and characteristics of ventricular arrhythmias after reperfusion in acute myocardial infarction.

The time course and characteristics of ventricular arrhythmias were studied in 45 consecutive patients with acute myocardial infarction who received intravenous streptokinase and underwent 24-hour Holter monitoring both after admission and before discharge 8 +/- 3 days later. In 41 of the 45 patients, thrombolytic treatment resulted in reperfusion as determined by characteristic clinical signs, i.e., rapid relief of pain associated with rapid resolution of ST-segment elevation and simultaneous abrupt increase in serum creatine kinase-MB activity. During the first 24 hours after reperfusion, the prevalence of ventricular premature complexes (VPCs) and couplets was nearly 100%, with an average frequency of 67 VPCs (range 1 to 1,336, median 44) and 6 couplets per hour per patient (range 1 to 97, median 4). Ninety percent of patients had an average of 8 runs of accelerated idioventricular rhythm per hour per patient (range 1 to 226, median 5) and 23% of the patients had an average of 2 runs of ventricular tachycardia per hour per patient (range 1 to 22, median 2) during the first 24 hours after reperfusion. The frequency of arrhythmias began to decrease 8 to 12 hours after reperfusion. Except for VPCs, ventricular arrhythmias were rare during the predischarge Holter study. Arrhythmias after reperfusion did not produce clinical symptoms and did not degenerate into ventricular fibrillation even though the patients were not receiving antiarrhythmic therapy. In the 4 patients without signs of reperfusion, the prevalence and frequency of all ventricular arrhythmias during the 24 hours after treatment was lower than in patients with reperfusion, and none had an accelerated idioventricular rhythm.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Complexes, Premature↗
PubMed1993

Angiographic validation of bedside markers of reperfusion.

OBJECTIVES: We sought to validate with coronary angiography several primary and ancillary markers of reperfusion. BACKGROUND: The availability of bedside markers of reperfusion is of major importance in the thrombolytic therapy of acute myocardial infarction. However, the reliability of current markers is still controversial. METHODS: Changes in chest pain, ST segment elevation and heart rate and rhythm were assessed every 5 to 10 min for up to 3 h after initiation of recombinant tissue-type plasminogen activator therapy in 82 patients with acute myocardial infarction. Coronary angiography was performed within 24 h. RESULTS: At angiography, 69 of the 82 patients had a patent infarct-related artery with Thrombolysis in Myocardial Infarction trial (TIMI) grade 3 flow and a rapid and progressive decrease in chest pain and ST elevation. The pain resolved in 24 +/- 23 min (range 3 to 50). The ST elevation decreased by > or = 50% within 16 +/- 14 min (range 5 to 41). Accelerated idioventricular rhythm developed in 49% of patients and sinus bradycardia in 23%; conduction abnormalities and atrial fibrillation resolved. All markers appeared in close temporal proximity to the onset of an abrupt increase in plasma creatine kinase (CK) and CK-MB isoenzyme activity, a previously validated marker of the time of reperfusion. Before its final resolution, ST elevation transiently decreased and increased in 58% of patients. Comparison of one pretreatment and one posttreatment electrocardiogram significantly reduced the reliability of ST segment change as a marker of reperfusion. In 13 of 82 patients, the infarct-related artery demonstrated TIMI grade < or = 2 flow; in 9, pain and ST elevation did not lessen and CK and CK-MB activity showed no abrupt increase. The remaining four patients initially demonstrated a decrease in pain and ST elevation; however, within 3 h and before angiography, the recurrence of pain and ST elevation suggested reocclusion. CONCLUSIONS: A rapid and progressive decrease in pain and ST elevation is a reliable marker of reperfusion with TIMI grade 3 flow. Because ST elevation and pain often fluctuate before undergoing final resolution with reperfusion, frequent or continuous monitoring of ST elevation is essential for reliable recognition of the fact and time of reperfusion. Accelerated idioventricular rhythm and episodes of sudden sinus bradycardia, although specific to reperfusion, do not occur in all patients with reperfusion.

Aged↗
PubMed1992

[Experience with the use of streptokinase in acute myocardial infarct at the prehospital stage].

The authors analyze the experience gained with the systemic thrombolytic therapy (STLT) at the prehospital stage of the treatment of acute myocardial infarction by specialized emergency cardiological teams. The screening of patients to be given STLT was performed via the remote diagnostic center. STLT was provided to 43 patients who were given intravenous injections of 500,000 PU streptokinase (Avalizin, GDR) for 15-30 minutes. The control group included 16 patients given standard therapy. After STLT 62.8% of the patients demonstrated moderate arterial hypotension, which could readily be corrected. Myocardial reperfusion after STLT manifested by rapid removal of the painful syndrome, characteristic dynamics of ECT, and by the appearance of specific reperfusion disorders of rhythm and conduction. The accelerated idioventricular rhythm, ventricular premature heart beat and A-V rhythm of the junction were recorded most frequently. The indicated rhythm disorders were removed readily enough. It is recommended that STLT may be carried out at the prehospital stage of AMI treatment by the cardiological emergency teams, which is likely to appreciably enhance the efficacy of the given therapy form.

Electrocardiography↗
PubMed2006

Study of pathogenesis of ventricular arrhythmia in experimental rats by separation of sinus and ventricular substitutional rhythms.

Pathogenesis of cardiac arrhythmia was determined by EEC changes after ATP-induced complete atrioventricular block. The re-entry mechanism underlays extrasystoles with equal coupling intervals with complexes of ventricular substitution rhythms, which transformed into paroxysmal tachycardia with equal R-R intervals, ventricular flutter, and ventricular fibrillation. Ectopic automaticity was characterized by extrasystole unrelated to the complexes of substitutional rhythms, which was transformed into accelerated idioventricular rhythm and asystole. During trigger activity, the extrasystoles were associated with complexes of basic rhythm and transformed themselves into torsades de pointes and ventricular fibrillation.

Adenosine Triphosphate↗
PubMed1980

[Ventricular tachycardia. A possible complication of intravenous atropine in the coronary patient].

Ventricular tachycardia occurred with chest pain in a 64 year old man with coronary artery disease after an intravenous injection of atropine. The particular feature of this case as compared to the other 8 reported cases is the restoration of sinus rhythm after a passage of accelerated idioventricular rhythm by the administration of oxygen and nitroglycerin. The increased oxygen consumption and myocardial ischaemia due to the tachycardia seem to be the factors responsible for these ventricular arrhythmias. Such cases, though rare, incite caution in the administration of atropine to patients with coronary artery disease.

Atropine↗
PubMed1993

[Early clinical, electrocardiographic and biological criteria of reperfusion after intravenous fibrinolysis during the acute phase of myocardial infarction].

Between May 1991 and February 1992, 31 consecutive patients were included in a prospective study, the aims of which were to determine the criteria of early coronary revascularisation after intravenous thrombolysis in the acute phase of myocardial infarction. The rise in serum myoglobin, the ST segment elevation, accelerated idioventricular rhythm and the evolution of chest pain were analysed. All patients underwent coronary angiography. Twenty-six were revascularized and 5 remained with coronary occlusion. Two types of serum myoglobin curves were demonstrated. Those with a sudden , decrease and a well defined peak in the first 4 hours were specific for revascularisation and easily identified (Group A: 16 patients). The graphs with a progressively rising slope to a peak after the 4th hour were observed in patients with coronary occlusion, but also in 10 patients with recanalized arteries (Group B). No significant difference was demonstrated with regards to the clinical and coronary angiographic parameters between patients in Group A and Group B. On the other hand, the time between the onset of chest pain and peak myoglobin was shorter in Group A (298 +/- 81 min) than in recanalised patients in Group B (380 +/- 54 min) (p < 0.05). The difference in the profile of the serum myoglobin could therefore reflect restoration of arterial flow in myocardial cells which had not suffered the same period of ischemia. ST segment elevation may increase, decrease of remain stable at 120 minutes in patients revascularised and those remaining occluded. In 9 patients, the ST elevation increased compared with the initial electrocardiogram .(ABSTRACT TRUNCATED AT 250 WORDS)

Accelerated Idioventricular Rhythm↗
PubMed1985

Arrhythmias with brief, high-dose intravenous streptokinase infusion in acute myocardial infarction.

Cardiac arrhythmias are described during the first 2 h after brief, high-dose, intravenous streptokinase infusion in 23 patients with evolving myocardial infarction was given. A control group consisted of 22 similar patients with acute myocardial infarction not treated with streptokinase infusion. On the basis of an early peak of creatine kinase activity successful reperfusion was achieved in 60.9% of patients. Significantly more ventricular premature complexes (P less than 0.01) and paroxysms of idioventricular rhythm (P less than 0.05) were noticed in the treated group. Premature ventricular complexes did not predict any severe ventricular arrhythmia. Accelerated idioventricular rhythm appears to be the most specific arrhythmia encountered with thrombolytic therapy of acute myocardial infarction. We propose that in routine clinical work it can be used as a bedside sign of successful reperfusion.

Adult↗
PubMed1983

[Ventricular pre-excitation revealed by idioventricular rhythm and large QRS tachycardias. Apropos of an operated case].

A 15 year old boy presented with palpitations of sudden onset and termination over a two month period. The heart was clinically and radiologically normal. The electrocardiogramme showed sinus rhythm with a short PR interval (0,11 sec) and narrow QRS complexes (0,08 sec) associated with an intermittent escape accelerated idioventricular rhythm (AIVR). During an attack of palpitations a regular tachycardia (250/min) with wide QRS complexes of the same configuration as those of the AIVR (left side delay). The diagnosis of ventricular tachycardia was retained. Endocavitary electrophysiological recording demonstrated preexcitation of the right ventricle associated with accelerated nodal conduction explaining the narrow QRS complexes in sinus rhythm. The wide complex tachycardias initiated and terminated by paired ventricular stimulation were identical to the spontaneous attacks and were attributed to an antidromic reciprocating rhythm. The hypothesis of a rhythm arising from the accessory pathway is suggested. This would explain the identical configuration of the QRS complexes of the AIVR and of the antidromic reciprocating-rhythm and the disappearance of the AIVR after surgical section of the accessory pathway.

Adolescent↗
PubMed1995

Upright tilt table testing in the evaluation of syncope.

OBJECTIVES: To review our experience with the upright tilt table test for the diagnosis of vasovagal syncope in a group of unselected patients with a history of syncope or presyncope. METHODS: 179 patients with a history of syncope or presyncope were subjected to upright tilt test. After carotid sinus massage to exclude carotid sinus hypersensitivity, the patients were tilted on a motorised tilt table with footplate support to an angle of sixty to seventy degrees for thirty minutes. If syncope was not induced, isoprenaline was then infused for a further fifteen minutes. A positive response was defined as fulfilling at least two out of three criteria: (i) syncope or presyncope similar to the spontaneous episodes of syncope, (ii) relative slowing of the heart rate at the onset of symptoms, (iii) drop of systolic pressure to less than 90 mmHg or by more than 50 mmHg. STATISTICAL METHODS: Continuous variables are expressed as mean values +/- one standard deviation and analysed for statistical significance by the unpaired Student's t-test. Chi-squared test with continuity correction was used for dichotomous variables. RESULTS: Ninety-four patients (53%) were positive for vasovagal syncope. Fourteen patients (8%) were positive at baseline tilt. An additional 80 patients (45%) were positive with the use of isoprenaline. Ten percent of the positive responses were purely cardioinhibitory, 10% purely vasodepressor and 80% mixed. The commonest cardiac rhythm during a positive response was junctional rhythm (46%) followed by sinus rhythm (44%). Sinus arrest with ventricular standstill occurred in only 5%. Accelerated idioventricular rhythm, 2:1 atrioventricular block and ventricular bigeminy accounted for the remaining 5%. CONCLUSION: The upright tilt table test is useful for the diagnosis of vasovagal syncope.

Adolescent↗