Wolff-Parkinson-White syndrome associated with Brugada syndrome.
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Adult↗
Biomedical subjects
M Borggrefe
Publications and source records attributed to M Borggrefe.
Brugada syndrome and supraventricular tachyarrhythmias: a novel association?
INTRODUCTION: The Brugada syndrome is a distinct form of idiopathic ventricular fibrillation characterized by a unique ECG pattern consisting of a right bundle branch block-like aspect and ST segment elevation in leads V1 to V3. As a high induction rate of ventricular tachyarrhythmias has been reported in Brugada syndrome, we hypothesized that this also may be true for supraventricular tachycardias in these patients. METHODS AND RESULTS: Between January 1995 and December 2000, we identified 35 consecutive patients with Brugada syndrome; 26 had a history of cardiac arrest or syncope and 9 were asymptomatic. All patients underwent electrophysiologic study, including an atrial and ventricular stimulation protocol. Ten patients (29%) were found to have supraventricular tachyarrhythmias (SVT) in addition to the Brugada syndrome. These 10 patients presented with aborted sudden cardiac death (n = 3) and/or a family history of sudden cardiac death (n = 4), syncope (n = 4), or primarily with a Brugada typical ECG, a positive family history, and palpitations (n = 2). Eight of them underwent genetic testing, but only 1 had a mutation in the SCN5A gene. In 6 patients, an AV nodal reentrant tachycardia was easily and reproducibly inducible. Two patients had clinical documented and inducible episodes of an atrial tachycardia (1 in addition to an AV nodal reentrant tachycardia). One patient had paroxysmal atrial fibrillation alternating with sinus rhythm, and 2 patients with accessory pathways were identified. CONCLUSION: This is the first description of an association of the Brugada syndrome with SVT. Thus, the arrhythmogenic substrate in Brugada syndrome may not be restricted to the ventricular level. Palpitations in this syndrome should raise the possibility of SVT. Conversely, in patients with SVT and aborted sudden cardiac death or syncope not related to SVT, the Brugada syndrome should be considered a possible additional electrophysiologic abnormality.
Adult↗
Targeting the slow pathway for atrioventricular nodal reentrant tachycardia: initial results and long-term follow-up in 379 consecutive patients.
OBJECTIVES: This study is designed to examine the immediate and short-term outcomes of patients who have undergone slow pathway ablation/modification for atrioventricular nodal reentrant tachycardia. BACKGROUND: Targeting the slow pathway has emerged as the superior form of treatment for atrioventricular nodal reentrant tachycardia. This technique has been found effective and is associated with a low complication rate. However, little is known of the long-term outcome of patients undergoing this procedure. METHODS: Over a 40-month period the slow pathway was targeted in 379 consecutive patients with proven atrioventricular nodal reentrant tachycardia. The case records of all patients were examined. Accurate follow-up data is available in 96% of patients a mean of 20.6 months after the procedure. RESULTS: The initial success rate was 97%. The incidence of complete heart block was 0.8% and the mean fluoroscopy duration was 27.3 min. The recurrence rate was 6.9%. Age, number of pulses and fluoroscopy time were positively associated with either initial failure or recurrence. A total of 11.3% of patients were still taking antiarrhythmic medication at follow-up. CONCLUSIONS: Targeting the slow pathway is an effective form of treatment for atrioventricular nodal reentrant tachycardia. The technique has a high initial success rate, a low complication rate and a low recurrence rate at long-term follow-up. Slow pathway modification is associated with similar success rates and recurrence rates as slow pathway ablation and may confer theoretical long-term benefits.
Catheter Ablation↗
Impact of radiofrequency catheter ablation of accessory pathways on the frequency of atrial fibrillation during long-term follow-up; high recurrence rate of atrial fibrillation in patients older than 50 years of age.
AIMS: Atrial fibrillation represents a frequent and potentially life-threatening arrhythmia in patients with accessory atrioventricular pathways. Radiofrequency ablation has become the curative treatment of first choice for these patients. Investigations after successful surgical pathway dissection reported an almost complete elimination of paroxysmal atrial fibrillation. However, there are only a few reports which include a small number of patients undergoing radiofrequency ablation. The purpose of this study was to examine whether successful radiofrequency ablation of accessory pathways prevents the occurrence of paroxysmal atrial fibrillation, and to identify possible predictors of atrial fibrillation recurrence. METHODS AND RESULTS: A total of 116 consecutive patients (mean age 42+/-15 years) with manifest or concealed accessory pathways and documented paroxysmal atrial fibrillation underwent radiofrequency catheter ablation. The patients were reexamined at 6 and 12 months. Long-term follow-up information was obtained by questionnaire and/or by consulting the referring physician. Pathway conduction was abolished in 101 cases (87%). Late follow-up information was obtained from 91 of these 101 patients (90%) with successful ablation with a mean follow-up duration of 23.9+/-12.3 months. During follow-up, 25 of 91 patients (27%) experienced arrhythmias. Recurrent episodes of atrial fibrillation were observed in 18 of these 25 cases (i.e. 20% of the 91 patients). Differences between patients with and without recurrences of atrial fibrillation were examined for age, sex, associated cardiac disease, presence of multiple pathways, pathway location, atrial fibrillation inducibility during the procedure and cycle length of the atrioventricular reentrant tachycardia. Only older age was a significant independent predictor of atrial fibrillation recurrence (P=0.02). Eleven of 31 patients (35%) older than 50 years of age had atrial fibrillation recurrences during follow-up compared to seven of 60 patients (12%) under age 50. The recurrence rate of atrial fibrillation was even higher in patients older than 60 years (6 of 11 patients, i.e. 55%). In comparison, the occurrence rate of atrial fibrillation during follow-up in a control group of 100 consecutive patients with successful accessory pathway ablation, who did not have evidence of paroxysmal atrial fibrillation prior to ablation, was 4% and, thus, significantly lower than in the study group of the 91 patients (P=0.001). CONCLUSIONS: The recurrence rate of paroxysmal atrial fibrillation after successful radiofrequency ablation of accessory pathways shows an age-related increase, being low in patients younger than 50 years of age (12%) and high in the older patients: 35% in patients older than 50 years and 55% in patients older than 60. These results have significant therapeutic implications concerning the decisions on pharmacological therapy after successful ablation in patients older than 50 years. Furthermore, these data will help physicians advise older patients properly about their risk of recurrence of atrial fibrillation after ablation.
Adult↗
A multicentre, double-blind randomized crossover comparative study on the efficacy and safety of dofetilide vs sotalol in patients with inducible sustained ventricular tachycardia and ischaemic heart disease.
BACKGROUND: Antiarrhythmic drugs are still used for the treatment of ventricular tachyarrhythmias, in combination with implantable cardioverter-defibrillators or without them. AIM OF THE STUDY: In a double-blind randomized crossover design, the short- and long-term efficacy and safety of oral dofetilide or oral sotalol were compared in 135 patients with ischaemic heart disease and inducible sustained ventricular tachycardia. METHODS: The inducibility of ventricular tachycardia was determined by programmed electrophysiological stimulation at baseline. Patients were then blindly randomized to receive either oral dofetilide 500 microg twice daily or oral sotalol 160 mg twice daily, for 3 to 5 days. Suppression of inducible ventricular tachycardia on the drug was then assessed by programmed electrophysiological stimulation. After a wash-out period of at least 2.5 days, the patients received the alternative treatment for 3 to 5 days. Suppression of inducible ventricular tachycardia on the alternate drug was again determined by programmed electrophysiological stimulation. Selection of long-term treatment was allocated blindly according to programmed electrophysiological stimulation results. RESULTS: During the acute phase, 128 patients received both dofetilide and sotalol. Sixty-seven patients were responders to either drug. Forty-six patients (35.9%) were responders to dofetilide compared with 43 (33.6%) to sotalol (P=ns). Only 23 patients responded to both dofetilide and sotalol. Adverse events, deemed to be treatment related, were seen in 2.3% of patients receiving dofetilide and 8.6% of patients receiving sotalol (P=0.016). Three patients on dofetilide had torsade de pointes. Two patients receiving sotalol died during the acute phase (one was arrhythmic death, and the other was due to heart failure). During the long-term phase, two of 42 patients (4.8%) receiving dofetilide and three of 27 patients (11.1%) receiving sotalol withdrew from treatment due to lack of efficacy. Overall, during the long-term phase, 23.8% of the patients receiving dofetilide and 37.0% of the patients receiving sotalol, withdrew from treatment with a similar pattern of withdrawals for the two drugs. CONCLUSION: Dofetilide was as efficacious as sotalol in preventing the induction of sustained ventricular tachycardia. There was no concordance in the response rate in two-thirds of the patients. Dofetilide was significantly better tolerated during the acute phase than sotalol. Both dofetilide and sotalol were well tolerated during the long term with no statistically significant difference in the adverse events.
Adult↗
Haemodynamic quantification of different provocation manoeuvres by simultaneous measurement of right and left atrial pressure: implications for the echocardiographic detection of persistent foramen ovale.
AIMS: Persistent foramen ovale (PFO) is found in 9.2--32% of echocardiographic examinations. The gold standard for the detection of a PFO is transoesophageal echocardiography (TEE) and the mostly used provocation test is the Valsalva manoeuvre. The aim of our study was to evaluate the effectiveness of the Valsalva manoeuvre compared to other provocation tests by simultaneous haemodynamic measurements of the right and left atrial pressure. METHODS: Fifty patients underwent Swan-Ganz catheterization. Right atrial pressure and pulmonary capillary wedge pressure, which corresponds to the left atrial pressure, were measured simultaneously. The following manoeuvres were compared: the Valsalva manoeuvre, coughing, deep inspiration and expiration pressures of 20 mmHg, 40 mmHg and 60 mmHg. The main objective of our study was to compare the occurrence of pressure gradients (right atrial pressure> left atrial pressure). For further quantification mean gradients, time duration of pressure overlap, as well as products of mean gradients and overlap time were analysed. RESULTS: During the Valsalva manoeuvre a significant pressure gradient could be observed in 84% of the patients, followed by an expiration pressure of 60 mmHg (82%), inspiration (78%), expiration pressure of 40 mmHg (76%), coughing (75%) and an expiration pressure of 20 mmHg (62%). Comparing the mean gradients and the products of mean gradients and overlap time duration during the different manoeuvres, we could detect the significantly best results with the Valsalva manoeuvre. CONCLUSIONS: The Valsalva manoeuvre might be the most effective test to provoke a right-to-left atrial shunt for the detection of a PFO during echocardiographic examinations.
Adult↗
Abnormalities of cardiac sympathetic innervation in arrhythmogenic right ventricular cardiomyopathy : quantitative assessment of presynaptic norepinephrine reuptake and postsynaptic beta-adrenergic receptor density with positron emission tomography.
BACKGROUND: The frequent provocation of ventricular tachycardia by stress or catecholamines and the efficacy of antiarrhythmic drugs with antiadrenergic properties suggest an involvement of the cardiac adrenergic system in arrhythmogenesis in patients with arrhythmogenic right ventricular cardiomyopathy (ARVC). Previous studies demonstrated abnormalities of the presynaptic uptake-1 assessed by (123)I-MIBG-single-photon emission computed tomography. METHODS AND RESULTS: This study investigated neuronal reuptake of norepinephrine (uptake-1) and beta-adrenergic receptor density in 8 patients with ARVC and 29 age-matched control subjects. All subjects underwent positron emission tomography with the volume of distribution (V(d)) of [(11)C]hydroxyephedrine ((11)C-HED) used to assess presynaptic norepinephrine reuptake, the maximum binding capacity (B(max)) of [(11)C]CGP-12177 ((11)C-CGP-12177) to assess postsynaptic beta-adrenergic receptor density, and [(15)O]H(2)O for quantification of myocardial blood flow. Patients with ARVC demonstrated a highly significant global reduction in postsynaptic beta-adrenergic receptor density compared with that in control subjects (B(max) of (11)C-CGP-12177: 5.9+/-1.3 vs 10.2+/-2.9 pmol/g tissue, P<0.0007), whereas the presynaptic uptake-1 tended toward reduction only (V(d) of (11)C-HED: 59.1+/-25.2 vs 71.0+/-18.8 mL/g tissue, NS). There were no differences in myocardial blood flow between the groups, and plasma norepinephrine was within normal limits in patients and control subjects. CONCLUSIONS: The findings demonstrate a significant reduction of myocardial beta-adrenergic receptor density in patients with ARVC. This may result from a secondary downregulation after increased local synaptic norepinephrine levels caused by increased firing rates of the efferent neurons or as the result of impaired presynaptic catecholamine reuptake. These findings give new insights into the pathophysiology of arrhythmogenesis in ARVC, with potential impact on diagnostic evaluation and therapeutic management.
Adult↗
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↗
Effects of antiarrhythmic drugs on cloned cardiac voltage-gated potassium channels expressed in Xenopus oocytes.
The effects of 17 commonly used antiarrhythmic drugs on the rapidly activating cardiac voltage-gated potassium channels (Kv1.1, Kv1.2, Kv1.4, Kv1.5, Kv2.1 and Kv4.2) were studied in the expression system of the Xenopus oocyte. A systematic overview on basic properties was obtained using a simple and restricted experimental protocol (command potentials 10 mV and 50 mV positive to the threshold potential; concentration of 100 micromol/l each). The study revealed that 8 of 17 drugs yielded significant effects (changes >10% of control) on at least one type of potassium channel in the oocyte expression system. These drugs were ajmaline, diltiazem, flecainide, phenytoin, propafenone, propranolol, quinidine and verapamil, whereas the effects of adenosine, amiodarone, bretylium, disopyramide, lidocaine, mexiletine, procainamide, sotalol and tocainide were negligible. The drug effects were characterized by reductions of the potassium currents (except for quinidine and ajmaline). A voltage-dependence of drug effect was found for quinidine, verapamil and diltiazem. The different effect of the drugs was not related to the fast or slow current inactivation of the potassium channels (except for verapamil). Profiles of the individual drug effects at the different potassium channel types were identical for propafenone and flecainide and differed for all other substances. The study demonstrates marked differences in sensitivity to antiarrhythmic drugs within the group of voltage-operated cardiac potassium channel types. Taking the restrictions of the oocyte system into consideration, the findings suggest that several antiarrhythmic drugs exert significant effects at rapidly activating cardiac potassium channels.
Animals↗
[New knowledge in arrhythmogenesis--role of ion channels and genetic aspects].
Recent advances in molecular biology have had a major impact on our understanding of the mechanisms of human diseases. Electrophysiology is one of the areas which, besides others, has substantially benefited from this development. Our understanding of the structure, function and mechanisms of the regulation of ion channels as well as their contribution to the pathogenesis of cardiac arrhythmias has substantially increased. The results of these studies are not only of special interest from the scientific point of view. It is likely to assume that, in the future, they will increasingly influence the diagnosis and treatment of arrhythmias.
Arrhythmias, Cardiac↗
Molecular genetics of arrhythmias--a new paradigm.
The molecular genetic background of inherited cardiac arrhythmias has only recently been uncovered. This late development in comparison to other inherited cardiac disorders has partly been due to the high mortality and early disease onset of these arrhythmias resulting in mostly small nucleus families. Thus, traditional genetic linkage studies, which are based on the genetic information obtained from large multi-generation families, were made difficult. Inherited arrhythmogenic disorders can be divided into 'primary electrical disorders' (e.g., long-QT [LQT] syndrome) in which a detectable, organic heart disease is not evident, and into inherited diseases of the myocardial structure (e.g., hypertrophic cardiomyopathies) in which the arrhythmias occur combined with the structural alterations. To date, all inherited arrhythmogenic disorders in which the causative genes have been identified turned out to be channelopathies, since the genes encode channel subunits that regulate important ion currents that tune the cardiac action potential. The discovery of the genetic bases of the LQT syndrome became a new methodologic paradigm; because with the use of 'classical' genetic linkage strategies (named [positional] candidate strategies) not only the causative genes have been found, but moreover, functional components with a previously unknown but fundamental role for a normal repolarization process were discovered. Disease mutations turned out to be not only a family-specific event with a distinct phenotype and the potential of an additional diagnostic tool, but also, when expressed in heterologous expression systems, characterize the defective ion channel in a topological way and lead to a more specific understanding of ion channel function. Most, if not all, primary electrical cardiac disorders show a high genetic diversity. For the LQT syndromes, sixth disease loci and the responsible gene have been recently discovered (so-called locus or genetic heterogeneity). Within all disease genes, the mutations are spread over the entire gene (allelic heterogeneity); in addition, more than one disease mutation may be present. This complexity requires, at least, complete mutation analysis of all LQT genes before medical advice should be given. Meanwhile, genotype-phenotype correlations in large families are being used to evaluate intergene, interfamilial and intrafamilial differences in the clinical phenotype, reflecting gene specific, gene-site specific and individual consequences of a given mutation. A widespread phenotypic heterogeneity even within mutation carriers in the same family raises the importance of modifying factors and genes that are mostly unknown to date. The reduced penetrance and variable expressivity associated with the LQT mutations remain still to be explained. First insights into the complex actions of mutations are being extracted, from expression data; these preliminary results may lead to potential implications for a specific (gene-site directed) therapy. This paper discusses the current data on molecular genetics and genotype-phenotype correlations in LQT syndrome and related disorders and the potential implications for diagnosis and treatment.
Arrhythmias, Cardiac↗
Is there a need for routine testing of ICD defibrillation capacity? Results from more than 1000 studies.
AIMS: Benefits and complications of postoperative implantable cardioverter-defibrillator tests are controversial matters. This study sought to assess the necessity of defibrillation function tests after implantation. METHODS AND RESULTS: We retrospectively analysed 1007 implantable cardioverter-defibrillator tests in 587 systems and 556 patients. Nine hundred and thirty implantable cardioverter-defibrillator tests (89.4%) were routinely performed. Seventy-one tests (7%) were performed after a change in the antiarrhythmic drug regimen and six tests (0.60%) because of a suspected dysfunction of the implantable cardioverter-defibrillator. During routine tests, four systems (0.4%) failed to defibrillate the patient. However, in all but one test, abnormalities of the system had been observed before the test. After the addition of antiarrhythmic drugs, two of 71 implantable cardioverter-defibrillator systems (2.8%) failed to defibrillate the patient. One of six systems tested due to a suspected dysfunction failed to defibrillate the patient. During 16 tests (1.6%), complications occurred. CONCLUSIONS: Our experience demonstrates that postoperative tests of the defibrillation function of implantable cardioverter-defibrillators rarely reveal dysfunctions. As testing is unpleasant for the patient and not free of complications, tests might be restricted to those patients in whom a dysfunction is suspected and to those patients in whom class I or class III antiarrhythmic drugs have been added to the antiarrhythmic drug regimen.
Adolescent↗
Prevalence of coronary artery disease in a general population without suspicion of coronary artery disease: angiographic analysis of subjects aged 40 to 70 years referred for catheter ablation therapy.
BACKGROUND: The prevalence of coronary vessel wall alterations in the general population is not known. Therefore, the aim of our study was to determine the prevalence of coronary artery disease in persons in whom the underlying disease was not related to coronary artery disease and could therefore be regarded as a near normal population. METHODS: We included 331 consecutive patients (173 men, 158 women, aged between 40 and 70 years) who were referred for catheter ablation of an accessory pathway (67.4% ) or atrioventricular-node modification (32.6%) and who underwent coronary angiography as part of their routine baseline evaluation before radiofrequency current application. Most of the patients (79%) of this cohort were free of symptoms of coronary artery disease. Based on visual inspection of coronary angiograms in multiple projections, patients were classified to have one-, two- or three-vessel disease if stenoses greater than 50% of lumen diameter were present. In addition, diffuse vessel wall alterations were assessed using two different score systems. RESULTS: The prevalence of coronary artery disease in this near normal population was 7.3%, with a significant difference in coronary asymptomatic (3.8%) vs symptomatic patients (17.1%). Mean levels of total cholesterol and other risk factors were not significantly different in patients with coronary artery disease compared to those without. But levels of low-density lipoprotein (LDL) cholesterol and lipoprotein(a) were significantly higher and high-density (HDL) cholesterol lower in patients with a stenosis or extent score higher than zero compared to a score of zero. The values of all vessel scores evaluating the extent of critical and diffuse coronary vessel alterations were very low in patients affected with coronary artery disease, indicating a low degree of diffuse alteration of the vessel wall. CONCLUSIONS: The prevalence of coronary artery disease with at least one critical stenosis in subjects aged 40-70 years with an average cholesterol level of 238+/-42 mg. dl(-1)is 7.3%.
Arrhythmias, Cardiac↗
The bad ventricle--revascularization versus transplantation.
BACKGROUND: The proportion of patients with left-ventricular dysfunction (LVD) undergoing high risk revascularization is increasing. In this patient group, the perioperative risk is elevated because of the pre-existing pathophysiology. Detailed evaluation and interdisciplinary differential therapeutic considerations on the basis of the comparative benefit rationale, with cardiac transplantation alternative, is mandatory. METHODS: Among 7275 patients who underwent coronary artery bypass grafting between 1990 and 1998 in our institution, we found 51 patients who had had an ejection fraction <20%, and thus were candidates for transplantation (group CABG); these were compared with 163 patients who were listed for cardiac transplantation because of ischemic cardiomyopathy (group HTX). The survival analysis was performed on the basis of the intention-to-treat principle independent of subsequent transplantation. RESULTS: Both groups were comparable with regard to left-ventricular ejection fraction; pulmonary capillary wedge pressure and serum creatinine, but patients in the CAGB group were older (63+/-11 vs 56+/-8; p = 0.001) and included a higher percentage of women (m/f: 42/9 vs 152/11; p = 0.03). Nevertheless, there was a similar 1-year survival in both groups (group BP 71.9% vs group HTX 66.3%; p = ns). Looking at the CABG group, the internal thoracic artery was used in 36/51 patients, an intra-aortic balloon pump was used preoperatively in 26 patients, and intraoperatively in 6. Left-ventricular assist devices had to be inserted in three patients, extracorporeal membrane oxygenation once. Perioperative (30 day) survival was 88.2 %. An elevated preoperative serum creatinine and the nonusage of the internal thoracic artery predicted an adverse outcome. In the long-term course, the NYHA functional class improved in most cases from III preoperatively to I after 26 (2-66) months. CONCLUSION: We conclude that patients with ischemic cardiomyopathy, viable myocardium, and graftable vessels can be revascularized with acceptable risk. Since for these patients a standby of mechanical circulatory support must be anticipated perioperatively, this infrastructure should be established within the center.
Aged↗
Modification of stretch-induced shortening of repolarization by streptomycin in the isolated rabbit heart.
The exact mechanism of mechano-electrical feedback and stretch-induced arrhythmias is unknown, but the role of stretch-activated ion channels and specific calcium channels has been proposed. The aim of the present study was to test the hypothesis that stretch-activated ion channels and not calcium channels contribute to stretch-related alterations of repolarization and that these effects can be neutralized by stretch-activated channel block. We studied the interaction of acute ventricular dilatation and the stretch-activated channel blocker streptomycin and the specific calcium channel blocker verapamil in an isolated retrogradely perfused rabbit heart model in which the left ventricular size is modified by abruptly changing the volume of a fluid-filled balloon placed in the left ventricle. Acute ventricular dilatation led to a rate-dependent decrease in repolarization. The mean effective refractory period (ERP) and monophasic action potential duration (MAP90) for cycle lengths between 300 and 1,000 ms decreased from 174.2+/-9 ms and 178.9+/-7 ms to 161.6+/-11 ms and 169.7+/-5 ms, respectively. Streptomycin (80 microM) inhibited this stretch-related shortening of repolarization (ERP: 175.4+/-8 ms; MAP90: 179.7+/-8 ms, p < 0.05) but had almost no effect on already dilated ventricles. Counteraction of the observed electrophysiologic changes could only be achieved by increasing the streptomycin concentration to 200 microM. Streptomycin nearly completely suppressed stretch-related ectopic ventricular complexes. In contrast, verapamil (1 microM) had no effect on stretch-related changes in repolarization and stretch-induced arrhythmias. The present study indirectly implicates stretch-activated ion channels in the genesis of stretch-related changes in repolarization and arrhythmias. The electrophysiologic changes after ventricular dilatation to a degree that increases left ventricular pressure in a clinically relevant range can be influenced by the stretch-activated channel blocker streptomycin but not by specific calcium channel block. This may have clinically important implications for the development of new antiarrhythmic drugs.
Animals↗
Infarct related artery patency: relation to serial electropharmacological studies and outcome in patients with previous myocardial infarction and ventricular tachyarrhythmias.
Evidence suggests that infarct related artery (IRA) patency may improve survival after acute myocardial infarction, which is thought to be partially due to a lower incidence of malignant ventricular tachyarrhythmias. However, little is known about the effect of IRA patency on antiarrhythmic drug response and long-term outcome in patients with previous infarction who already experienced sustained ventricular tachyarrhythmias. A total of 152 patients with remote myocardial infarction and documented ventricular tachycardia (VT) or ventricular fibrillation (VF) underwent coronary angiography and programmed ventricular stimulation before and after oral administration of d,l-sotalol (240-640 mg/day). D,l-sotalol suppressed inducibility of VT/VF in 37 (25.2%) patients. The IRA was patent in 38.1% of all patients. There was no significant difference in the frequency of drug response between patients with patent or occluded IRAs (26.8% vs 24.2%, P = 0.87). In patients with a patent IRA, d,l-sotalol tended to be more effective in the absence of a left ventricular aneurysm, although this difference did not reach statistical significance (P = 0.38). Ejection fraction and collateral blood flow had no effect on drug response in the presence or absence of IRA patency. During follow-up (13.0 +/- 19.9 months) of 29 patients discharged on oral d,l-sotalol, 3 patients experienced symptomatic VT and 4 sudden death. Arrhythmia recurrence and death of all cause (n = 6) and cardiac death (n = 4) were independent of IRA patency status. IRA patency had no effect on short-term drug response to d,l-sotalol in patients with remote myocardial infarction and documented VT/VF. Long-term outcome of patients with sustained ventricular tachyarrhythmias is independent of IRA patency status. In contrast to a previous report, outcome of electropharmacological testing was not predicted by the patency of the IRA.
Aged↗
A patient with "atrial torsades de pointes".
A patient with long QT syndrome and a history of palpitations underwent electrophysiologic study. Runs of polymorphic self-terminating atrial tachyarrhythmias were easily induced and occurred spontaneously several times. Atrial monophasic action potential (MAP) durations were prolonged at short pacing cycle lengths. Premature high right atrial extrastimuli prolonged MAP durations in the low right atrium, resulting in an inverse electrical restitution curve, and increased dispersion of repolarization. MAP morphology showed gradually increasing early afterdepolarizations. When the arrhythmia was initiated, a new action potential reproducibly emerged from these afterdepolarizations. To the knowledge of the authors, this is the first reported case of "atrial torsades de pointes" in a patient.
Action Potentials↗
Reproducible conversion from wide to narrow complex tachycardia: what is the mechanism?
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Adult↗