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PubMed1982

Effects of lignocaine on bidirectional tachycardia and on digitalis-induced atrial tachycardia with block.

Most recent studies discussing tachycardias with alternating QRS polarity have referred to those known as torsade de pointes. This report, in contrast, deals with bidirectional tachycardia and the effects of lignocaine on 10 patients with this arrhythmia. Three of the patients also had digitalis-induced atrial tachycardia with block. In one patient, a single bolus of lignocaine was followed (five minutes later) by ventricular fibrillation, but the other nine patients received two boluses of 75 mg followed by a drip infusion of 3 mg/min. The drug terminated the episodes of atrial tachycardia with block and bidirectional tachycardia in all patients thus treated. Whereas the abolition of the bidirectional tachycardia was permanent in the seven patients with digitalis intoxication, it recurred after stopping the drip infusion in the two patients without digitalis toxicity. It is concluded that lignocaine can be useful in the treatment of digitalis-induced bidirectional tachycardia and atrial tachycardia with block. From this study no conclusions can be drawn, however, as to whether lignocaine is superior to other class I or class IV agents.

Adult↗
PubMed1988

Entrainment of ventricular tachycardia: explanation for surface electrocardiographic phenomena by analysis of electrograms recorded within the tachycardia circuit.

Transient entrainment was demonstrated during 59 pacing events in 18 episodes of sustained uniform ventricular tachycardia (VT) while recording electrograms from the site of origin of tachycardia (LE-SOO). During entrainment, the morphology of the initial component of the LE-SOO was identical to the morphology observed during the tachycardia in 13 VTs (group I), but in five VTs (group II), the initial component changed at a "critical" paced cycle length. The presence of the proposed surface electrocardiographic criteria for entrainment--fixed fusion and a first postpacing complex without fusion but occurring at the paced cycle length--were integrally dependent on the morphologic changes in the local presystolic electrogram. Fixed fusion of the surface electrocardiogram at one or more paced cycle lengths was detected during entrainment at 35 of 59 paced cycle lengths in 12 of 18 tachycardias, 10 of which were group I and two of which were group II VTs. Fixed fusion demonstrated by analysis of the LE-SOO was observed at one or more pacing cycle lengths in 17 of 18 VTs. In five tachycardias in which surface electrocardiographic fusion was not observed, fixed fusion was evident on analysis of the left ventricular LE-SOO during right ventricular pacing. The first postpacing interval, as measured at the surface electrocardiogram, was consistently equal to the paced cycle length in only one of 18 tachycardias and was greater than the VT cycle length in eight of 17 tachycardias. A pathway with a long conduction time was demonstrated during entrainment. However, in those 12 VTs in patients in whom pacing was performed at more than one cycle length and there was preservation of the LE-SOO morphology, the conduction time between the stimulus and presystolic electrogram remained constant. Thus, no evidence for "atrioventricular nodal-like" decremental conduction was observed over a wide range of pacing cycle lengths. We conclude that: (1) two of the previously proposed criteria for diagnosis of entrainment (fixed fusion on the surface electrocardiogram and a first postpacing interval equal to the paced cycle length) are overly restrictive criteria for definition of "entrainment" of VT, (2) analysis of endocardial recordings from the site of origin of tachycardia during attempted entrainment of VT is useful for documenting the presence of entrainment, and (3) such analysis provides a basis for the understanding of surface electrocardiographic phenomenon associated with entrainment.

Cardiac Pacing, Artificial↗
PubMed1988

Tachycardia cycle length and maximum capacity of anterograde and retrograde atrioventricular conduction in paroxysmal supraventricular tachycardia.

Anterograde and retrograde pathways are the two major components of the reentry circuit in patients with paroxysmal supraventricular reentrant tachycardias. Therefore, the capacity of each pathway to maintain 1:1 conduction would be expected to determine the cycle length (CL) of the tachycardia. In this study, the possible relationship between the CL of reentrant tachycardia and the maximum capacities of anterograde and retrograde conduction in the maintenance of a 1:1 response during atrial and ventricular pacing were examined. This relationship was analyzed in 26 patients with orthodromic reentrant tachycardia due to Wolff-Parkinson-White syndrome (group 1) and compared with that in 26 patients with atrioventricular nodal reentrant tachycardia (group 2). There were no statistically significant differences between the two groups in the shortest tachycardia CLs (mean +/- SD, 325 +/- 44 versus 329 +/- 52 ms); in the shortest ventricular pacing CLs with 1:1 response (314 +/- 63 versus 319 +/- 38 ms); nor in the CLs that produced retrograde atrioventricular block (306 +/- 62 versus 301 +/- 37 ms). In contrast, the longest atrial pacing CL that produced Wenckebach's phenomenon and the shortest atrial pacing CL with 1:1 response were significantly shorter for group 1 than for group 2 patients (290 +/- 38 versus 390 +/- 88 ms, P less than 0.001) and (305 +/- 38 versus 406 +/- 90 ms, P less than 0.001), respectively. It was concluded that the CL of orthodromic tachycardia can best be predicted from the shortest atrial pacing CL that maintains 1:1 anterograde conduction via the normal pathway.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2000

Antidromic atrioventricular reentrant tachycardia mimicking ventricular tachycardia in the setting of previous myocardial infarction.

The differentiation between ventricular tachycardia and broad-complex supraventricular tachycardia can be extremely difficult, particularly in emergency situations. We report a case of hemodynamically compromising broad-complex tachycardia in a 63-year-old man. The patient had previously sustained an anteroseptal myocardial infarction and had subsequently undergone coronary artery bypass surgery because of triple-vessel coronary artery disease. Intravenous treatment with ajmalin terminated the tachycardia and revealed preexcited QRS complexes compatible with the presence of a left-sided atrioventricular accessory pathway. An antidromic atrioventricular reentrant tachycardia (identical to the clinical tachycardia) was induced during an electrophysiologic study. In conclusion, there are several causes of broad-complex tachycardia, even in patients with previous myocardial infarction, and, where doubt exists, electrophysiologic studies should be performed.

Coronary Artery Bypass↗
PubMed1987

Differentiation of ventricular tachycardia from supraventricular tachycardia with aberration: value of the clinical history.

The purpose of this study was to assess whether the clinical history is of any value in the differentiation in the emergency department of ventricular tachycardia (VT) from supraventricular tachycardia (SVT) with aberration. The records of 84 patients who presented with a wide-complex tachycardia and who were able to provide a history were reviewed. The wide-complex tachycardia was proven by a later electrophysiologic study to be VT in 62 patients and SVT with aberration in 22 patients. History of prior myocardial infarction, history of congestive heart failure, and history of recent angina pectoris all had positive predictive values for VT of greater than 95%, but had sensitivities of 66%, 24%, and 24%, respectively. Age greater than 35 years had a sensitivity of 92% and a positive predictive value of 85% for VT. None of the clinical characteristics was strongly predictive for SVT; the best was age less than or equal to 35 years, which had a positive predictive value of 70%. We conclude that clinical variables may be helpful in the emergency department diagnosis of wide-complex tachycardias. If a patient with a wide-complex tachycardia has a history of myocardial infarction, congestive heart failure, or recent angina pectoris, the tachycardia has a high likelihood of being ventricular in origin. However, there are no clinical variables that are highly predictive of SVT with aberration.

Adult↗
PubMed1997

Atypical atrioventricular node reciprocating tachycardia masquerading as tachycardia using a left-sided accessory pathway.

OBJECTIVES: The study was performed to document that atrioventricular node reciprocating tachycardia (AVNRT) can be associated with eccentric retrograde left-sided activation, masquerading as tachycardia using a left accessory pathway. BACKGROUND: The eccentric retrograde left-sided activation during tachycardia is thought to be diagnostic of the presence of a left free wall accessory pathway. However, it is not known whether AVNRT can occur with eccentric retrograde left-sided activation. METHODS: We studied 356 patients with AVNRT who underwent catheter ablation. Retrograde atrial activation during tachycardia and ventricular pacing were determined by intracardiac recordings, including the use of a decapolar coronary sinus catheter. RESULTS: The retrograde atrial activation was eccentric in 20 patients (6%). Eight of these patients had the earliest retrograde atrial activation recorded in the lateral coronary sinus leads, and 12 had the earliest retrograde atrial activation recorded in the posterior coronary sinus leads, with the most proximal coronary sinus electrode pair straddling the coronary sinus orifice. These tachycardias were either the fast-slow or the slow-slow form of AVNRT. The slow-fast form of AVNRT was also inducible in 17 of the 20 patients. Successful ablation of the slow pathway in the right atrial septum near the coronary sinus ostium prevented the induction and clinical recurrence of reciprocating tachycardia in all patients. CONCLUSIONS: Atypical AVNRT with eccentric retrograde left-sided activation was demonstrated in 6% of all patients with AVNRT masquerading as tachycardia using a left-sided accessory pathway. Ablation of the slow pathway at the posterior aspects of the right atrial septum resulted in a cure in these patients.

Adult↗
PubMed2006

A modified electrocardiographic algorithm for differentiating typical atrioventricular node re-entrant tachycardia from atrioventricular reciprocating tachycardia mediated by concealed accessory pathway.

Non-invasive prediction of tachycardia mechanism is becoming clinically important in the era of catheter ablation for curing supraventricular tachycardia. Twelve-lead electrocardiograms (ECGs) during sinus rhythm and atrioventricular node re-entrant tachycardia (AVNRT) or atrioventricular reciprocating tachycardia (AVRT) with a narrow QRS complex were obtained from 154 consecutive adult patients who had received successful radiofrequency catheter ablation. The ECGs of initial 104 patients were analysed by three observers without knowledge of the electrophysiological diagnosis. The two arrhythmias were accurately diagnosed in 68% of cases. Three criteria were found to be discriminators of tachycardia mechanism by univariable analysis. Pseudo r/Q/S waves predicated AVNRT in 92% of cases (sensitivity 71%; specificity 95%). Retrograde P wave predicated AVRT in 86% of cases (sensitivity 75%; specificity 85%), RP interval > or =100 ms in 93% (sensitivity 71%; specificity 94%) and ST-segment elevation in lead aVR in 83% (sensitivity 71%; specficity 83%). According to the initial results, we proposed a modified stepwise ECG algorithm which used pseudo r/S/Q waves, RP interval and ST-segment elevation in lead aVR during tachycardia. Two observers assessed the modified algorithm in the remaining 50 patients. The algorithm was able to correctly diagnose the tachycardia mechanism in 84% and 87%, respectively. Using the modified algorithm can improve the accuracy and simplify the differential diagnosis between typical AVNRT and AVRT via concealed accessory pathway in adult patients.

Adult↗
PubMed1999

Junctional tachycardia during radiofrequency ablation of the slow pathway in patients with AV nodal reentrant tachycardia: effects of autonomic blockade.

INTRODUCTION: The autonomic nervous system richly innervates the peri-AV nodal region and may be activated during radiofrequency (RF) ablation for AV nodal reentrant tachycardia, resulting in the generation of junctional tachycardia. The purpose of this prospective study was to determine the role of the autonomic nervous system in the genesis of junctional tachycardia. METHODS AND RESULTS: We compared the characteristics of junctional tachycardia in patients with (n = 10) and without (n = 10) autonomic blockade undergoing RF ablation for AV nodal reentrant tachycardia. Intravenous administration of atropine (0.04 mg/kg) and propranolol (0.2 mg/kg) were used to block the autonomic nervous system. There were no differences in clinical variables and baseline electrophysiologic characteristics between the two groups except for slightly longer effective refractory periods of the fast pathway and of the atrium in the autonomic blockade group. The autonomic blockade shortened the baseline sinus cycle length and effective refractory period of the ventricle only but not other electrophysiologic characteristics of the AV node. The junctional tachycardia was observed during ablation in each patient, but its occurrence and cycle length, as well as numbers of consecutive junctional beats, were not altered by the autonomic blockade. CONCLUSION: Our results indicate that the muscarinic and beta-adrenergic components of the autonomic nervous system play no role in the genesis of junctional tachycardia.

Atrioventricular Node↗
PubMed2005

Two unusual cases of coincident atrioventricular nodal reentrant tachycardia and ventricular tachycardia.

The simultaneous occurrence of narrow and wide QRS complex tachycardias was observed in 2 patients evaluated at our electrophysiological centers. Electrophysiological testing revealed the coexistence of two types of arrhythmia (atrioventricular nodal reentrant tachycardia and verapamil-sensitive left ventricular tachycardia) in one patient and of three types of arrhythmia (atrioventricular nodal reentrant tachycardia, ventricular tachycardia originating from the right ventricular outflow tract, and left ventricular tachycardia) in the other. Both patients underwent successful radiofrequency ablation of all the types of tachycardia.

Aged↗
PubMed1989

Predictors of sustained ventricular tachycardia inducibility in patients with nonsustained ventricular tachycardia and chronic coronary artery disease.

To assess the likelihood of inducing sustained ventricular tachycardia, we analyzed a cohort of 58 retrospective and 18 prospective patients with chronic coronary artery disease who underwent electrophysiologic study because of spontaneous nonsustained ventricular tachycardia (three or more beats, lasting less than 30 seconds, at a rate greater than 100/min). In 24 of the 58 retrospective patients (41%) sustained ventricular tachycardia was inducible. Stepwise logistic regression identified two "major" variables--left ventricular aneurysm/dyskinesis/akinesis (p = 0.0001; relative risk = 11.88) and ejection fraction less than 40% (p = 0.0002; relative risk = 9.69)--and one "minor" variable--nonsustained ventricular tachycardia longer than 10 beats (p = 0.0151; relative risk = 4.21)--as significant predictors of inducibility. Nineteen patients with both major variables had a high probability of inducibility (greater than 90%). Nineteen patients with neither major variable had a low probability of inducibility (less than 5%). The remaining 20 patients with only one of the major variables had an intermediate probability of inducibility (14% to 75%). The significance of the third minor factor, nonsustained ventricular tachycardia longer than 10 beats, was confined to this intermediate group, in which it could be used to segregate relatively high (65% to 75%) and relatively low (14% to 20%) probability of inducibility. Prospective application of the predictor function stratified 18 additional patients into three groups with high (six patients), intermediate (seven patients), and low (five patients) probability of inducibility. The observed rate of inducibility in each group was 5 of 6 (83%), 2 of 7 (29%), and 0 of 5 (0%), respectively. These data suggest that patients with nonsustained ventricular tachycardia and chronic coronary artery disease can be stratified into subgroups with high, intermediate, and low probability of inducibility of sustained ventricular tachycardia on the basis of ejection fraction and regional ventricular wall motion defects alone.

Aged↗
PubMed2001

Is sinus node modification appropriate for inappropriate sinus tachycardia with features of postural orthostatic tachycardia syndrome?

Inappropriate sinus tachycardia and postural orthostatic tachycardia are ill-defined syndromes with overlapping features. Although sinus node modification has been reported to effectively slow the sinus rate, long-term clinical response has not been adequately assessed. Furthermore, whether patients with postural orthostatic tachycardia would benefit from sinus node modification is unknown. The study prospectively assessed the short- and long-term clinical outcomes of seven consecutive female patients with postural orthostatic tachycardia syndrome and inappropriate sinus tachycardia who were treated with sinus node modification. The study was conducted in a tertiary care center. The electrophysiological and clinical responses were prospectively assessed as defined by autonomic function testing, including Valsalva maneuver, deep breathing, tilt table testing, and quantitative sudomotor axonal reflex testing. Among the study population (mean age was 41+/-6 years), 5 (71%) patients had successful sinus node modification. At baseline, heart rates were 101+/-12 beats/min before modification and 77+/-9 beats/min after modification (P = 0.001). With isoproterenol, heart rates were 136+/-9 and 105+/-12 beats/min (P = 0.002) before and after modification, respectively. The mean heart rate during 24-hour Holter monitoring was also significantly reduced: 96+/-9 and 72+/-6 beats/min (P = 0.005) before and after modification, respectively. Despite the significant reduction in heart rate, autonomic symptom score index (based on ten categories of clinical symptoms) was unchanged before (15.6+/-4.1) and after (14.6+/-3.6) sinus node modification (P = 0.38). Sinus rate can be effectively slowed by sinus node modification. Clinical symptoms are not significantly improved after sinus node modification in patients with inappropriate sinus tachycardia and postural orthostatic tachycardia. A primary subtle autonomic disregulation is frequently present in this population. Sinus node modification is not recommended in this patient population.

Adult↗
PubMed1995

Effect of almokalant, a selective potassium channel blocker, on the termination and inducibility of paroxysmal supraventricular tachycardias: a study in patients with Wolff-Parkinson-White syndrome and atrioventricular nodal reentrant tachycardia. Almokalant PSVT Study Group.

Almokalant is a newly developed selective blocker of the delayed outward K+ current and exhibits the electrophysiological properties of a class III antiarrhythmic agent. In a Scandinavian multicenter, placebo-controlled trial, the antiarrhythmic efficacy of almokalant was investigated in patients with paroxysmal supraventricular tachycardia: 87 patients with mean age of 50 +/- 14 years (range 21-71 years), with reciprocating tachycardia due to either Wolff-Parkinson-White (WPW) syndrome (n = 58) or atrioventricular nodal reentry tachycardia (AVNRT) (n = 29) were studied with transesophageal atrial stimulation. After a baseline procedure, during which sustained tachycardia was induced and overdrive terminated, tachycardia was reinduced and an intravenous (i.v.) infusion of either placebo or almokalant (aiming at a pseudoequilibrium plasma level of 20, 50, 100, or 150 nM) (Cpl 20-Cpl 150), was administered. Each patient was studied at two Cpl. Thirty-nine patients were randomly assigned in a double-blind fashion to either placebo+almokalant at Cpl 20 or Cpl 20 + Cpl 50; 26 patients were studied openly at Cpl 50 + Cpl 100, and 22 were studied openly at Cpl 100 + Cpl 150 almokalant. The antiarrhythmic efficacy was assessed as the ability to terminate induced tachycardia and to suppress inducibility: The proportion of patients in which the tachycardia was terminated was placebo 3 of 20 (15%); Cpl 20, 7 of 36 (19%): Cpl 50, 10 of 36 (28%); Cpl 100, 14 of 35 (40%); and Cpl 150, 5 of 9 (56%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1983

Atrial tachycardia facilitating initiation of ventricular tachycardia.

A 17-year-old male was studied because of clinically documented tachycardias showing narrow and wide QRS complexes. He was found to suffer from an atrial and a ventricular tachycardia. It was demonstrated that initiation of ventricular tachycardia occurred on reaching a critical ventricular rate during atrial tachycardia. Our study illustrates the value of electrophysiological studies in patients suspected of suffering from double or multiple tachycardias. It also shows that the occurrence of one type of tachycardia may be critically related to another type of tachycardia.

Adolescent↗
PubMed1985

Autonomic control of ventricular tachycardia: sympathetic neural influence on spontaneous tachycardia 24 hours after coronary occlusion.

This study was performed to determine whether sympathetic nerves influence the rate of ventricular tachycardia occurring spontaneously in dogs 24 hr after occlusion of the anterior descending coronary artery. Seventeen chloralose-anesthetized dogs underwent activation mapping during spontaneous ventricular tachycardia with QRS morphologies similar to those recorded in the conscious state. Bilateral stellate ganglionectomy (n = 8) decreased mean arterial pressure from 71 +/- 4 (mean +/- SE) to 52 +/- 5 mm Hg (p less than .001) and heart rate from 121 +/- 9 to 79 +/- 15 beats/min (p less than .025) by decreasing the number of complexes of ventricular tachycardia from 120 +/- 9 to 49 +/- 15 per minute (p less than .001). Subsequent unilateral sympathetic nerve stimulation (n = 4) was shown to accelerate ventricular tachycardia foci originating from the ipsilateral aspect of the infarction. Regional sympathetic denervation (n = 7) was performed by application of phenol to the epicardium surrounding an electrode at the site of origin of at least one morphology of ventricular tachycardia. Mean arterial pressure did not change, but total heart rate decreased from 122 +/- 9 to 106 +/- 9 beats/min (p less than .01) and the number of complexes of ventricular tachycardia with a morphology arising from the phenol-treated area fell from 68 +/- 12 to 28 +/- 9 (p less than .001). Evidence for regional denervation was documented by prolongation of duration of electrograms and local repolarization times limited to the phenol-treated area. We conclude that sympathetic nerves directly control rate of spontaneous ventricular tachycardia 24 hr after myocardial infarction in the dog.

Animals↗
PubMed2001

Demonstration of the exact anatomic tachycardia circuit in the fast-slow form of atrioventricular nodal reentrant tachycardia.

BACKGROUND: The tachycardia circuit in the fast-slow form of atrioventricular nodal reentrant tachycardia (FS-AVNRT) has not been convincingly defined. METHODS AND RESULTS: To define the tachycardia circuit, single extrastimuli were delivered during FS-AVNRT to 9 intra-atrial sites in 12 patients: the His bundle (HB) site; the superior portion of the HB site (S-HB); 3 arbitrarily divided sites on the AV junction extending from the HB site to the coronary sinus ostium (CSOS) (sites S, M, and I); the superior, posterior, and posteroinferior portions of the CSOS (S-CSOS, P-CSOS, and PI-CSOS, respectively); and the CSOS. The inferior portion of coronary sinus ostium (I-CSOS), at which the earliest retrograde activation was observed, was excluded. At each site, the longest coupling interval of the single extrastimulus that reset the tachycardia and the subsequent return cycle was measured. The mean tachycardia cycle length was 370+/-55 ms. The longest coupling intervals at sites S-HB, HB, S, M, I, CSOS, S-CSOS, P-CSOS, and PI-CSOS were 328+/-53, 360+/-55, 358+/-55, 358+/-54, 360+/-55, 338+/-56, 323+/-54, 331+/-56, and 321+/-58 ms, respectively, and the subsequent return cycles were 408+/-58, 371+/-55, 370+/-55, 372+/-56, 370+/-55, 396+/-56, 411+/-60, 405+/-58, and 412+/-59 ms, respectively. The longest coupling intervals at sites HB, S, M, and I were longer than those at S-HB, CSOS, S-CSOS, P-CSOS, and PI-CSOS (P<0.0001). The return cycles at sites HB, S, M, and I did not differ from the tachycardia cycle length, whereas those at CSOS, S-CSOS, P-CSOS, and PI-CSOS were longer than the tachycardia cycle length (P<0.0001). CONCLUSIONS: The perinodal atrium extending from the HB site to the I-CSOS is an integral limb of the reentry circuit in FS-AVNRT.

Adolescent↗
PubMed1999

[Tachycardia-induced tachycardia: definitive treatment with radiofrequency ablation. Presentation of three cases].

Tachycardia-induced tachycardia is the phenomenon in which one tachycardia degenerates into another. Few data are available in patients suffering from AV nodal reentrant tachycardia an atrial fibrillation. For related to AV nodal reentrant triggered by tachycardia; there is a possible effective treatment by eliminating the slow nodal pathway, with radiofrequency ablation, as shown by other authors. In this study we present data on three patients with repeated episodes of documented atrial fibrillation and at least one episode of AV nodal reentrant tachycardia or regular palpitations. Radiofrequency ablation of the slow AV nodal pathway was successfully performed in both, and at a follow up of 6, 9 and 10 months, respectively, no new episode of AV nodal reentrant tachycardia or atrial fibrillation was documented.

Adult↗
PubMed2000

[Bundle of His tachycardia and chronic reciprocating rhythm: rare forms of prenatal tachycardia].

In cases of permanent tachycardia, ante-natal diagnosis of chronic reciprocating rhythms with long RP' intervals or His bundle tachycardias is difficult. The authors report two cases of permanent foetal tachycardia with 1/1 atrioventricular conduction. In one case, the tachycardia rate was 170/min with anasarca treated by amiodarone in view of a family history of His bundle tachycardia. In the other case, the tachycardia rate was 200/min but with no signs of cardiac failure and was, therefore, not treated. The ECG at birth confirmed the diagnosis of His bundle tachycardia in the first case and identified a chronic reciprocating rhythm in the other.

Adult↗
PubMed1996

Tachycardia induced cardiomyopathy in dogs; relation between chronic supraventricular and chronic ventricular tachycardia.

Long-standing ventricular tachycardia (VT) and supraventricular tachycardia (SVT) can produce a reversible left ventricular dysfunction. The onset of cardiomyopathy and the severity of posttachycardic changes depend at least on three parameters of tachycardia, including its type (VT or SVT), rate and duration. Ten dogs (beagles) were paced at 180 beats/min for 3 weeks. Two pacing modalities, supraventricular and ventricular, were used in each dog. In half of them, the study was started by ventricular, and in the other half by supraventricular high-rate pacing. The alternate pacing modality was applied after complete recovery of left ventricular function. Ventricular function and morphology were evaluated by radionuclide ventriculography, echocardiography and Swan-Ganz catheterisation. Posttachycardic changes were studied in sinus rhythm after cessation of pacing. Left ventricular ejection fraction (LVEF) fell significantly after either type of tachycardia (SVT: 53 +/- 5%, VT: 48 +/- 7%, P < 0.05) compared with baseline values (69.5 +/- 2.3%). Significant increases (P < 0.05) in end-systolic (SVT: 2.1 +/- 0.3 cm, VT: 2.4 +/- 0.2 cm vs. 1.6 +/- 0.3 cm) and end-diastolic dimensions (SVT: 3.0 +/- 0.3 cm, VT: 3.3 +/- 0.4 cm vs. 2.7 +/- 0.3 cm) indicated ventricular dilation in paced animals. Left ventricular pulmonary capillary wedge pressure increased significantly after either type of tachycardia as compared with baseline values (SVT: 7.5 +/- 1.2 mmHg, VT: 8.4 +/- 1.1 mmHg vs. 1.9 +/- 1.5 mmHg, P < 0.05); the difference between tachycardias was not significant. The present study demonstrates that chronic SVT and VT result in left ventricular dysfunction in a relatively short time, even if the heart rate is not very high. Deterioration of left ventricular ejection fraction and dilation of the left ventricle are more marked in chronic VT than in chronic SVT.

Animals↗