MedWire News: Left atrial (LA) linear lesions are nearly always necessary for successful catheter ablation of atrial fibrillation (AF), French researchers have demonstrated.
Their study found that although persistent AF could be terminated without LA linear lesions, most patients require such lesions to prevent the later development of macro re-entrant atrial tachycardia.
A team led by Sébastien Knecht (Université Victor Segalen Bordeaux II) retrospectively studied 180 patients with persistent AF who had undergone catheter ablation.
AF was successfully terminated in 154 patients, report Knecht et al in the European Heart Journal. Of these, 69 had required both LA linear lesions (ie, the roofline and the mitral isthmus line) to terminate AF whereas 85 had not.
Patients who required linear lesions had a longer duration of AF (9 vs 12 months), but otherwise the two groups were similar with regard to clinical and echocardiographic characteristics.
After 28 months of follow-up, however, the incidence of LA macro re-entrant atrial tachycardia was significantly higher among patients who had not required LA lesions than those who had, at 78% versus 33% (p=0.002).
And the vast majority of patients ultimately required a roof line and/or a mitral line in order to remain in sinus rhythm.
“This study highlights that although pulmonary vein isolation and electrogram-based ablation without linear lesions are effective for terminating persistent AF in a significant number of patients, macro re-entrant AT requiring LA linear ablation is very likely to occur during the overall follow-up period,” Knecht and co-authors conclude.
In a related editorial, Thomas Rostock and Stephan Willems from University Hospital Eppendorf in Germany said it remains unclear whether the atrial tachycardias are a cause or a consequence of AF; nevertheless they added: “It has become clearer that LA linear ablation remains an imperative step on the road to sinus rhythm in patients with chronic AF.”
Eur Heart J 2008; 29: 2359–2366
segunda-feira, 20 de outubro de 2008
Post-CABG AF affects early and late mortality
MedWire News: Postoperative atrial fibrillation (AF) affects both early and late mortality in patients who undergo isolated coronary artery bypass graft (CABG) surgery, say researchers who call for careful postoperative surveillance.
There is an ongoing debate surrounding the prognostic implications of postoperative AF, which is recognized as a difficult complication associated with significant adverse events and increased length of stay in intensive care and in hospital.
Giovanni Mariscalco, from Varese University Hospital in Italy, and colleagues studied 1832 patients who underwent isolated CABG between 2000 and 2005 at two cardiac centers, identifying patients who experienced postoperative AF and following them up until death or 2007.
The team reports in the journal Circulation that AF developed in 31% of the patients. Patients who developed AF were significantly older than those who did not, at 68.4 years versus 63.7 years.
The length of hospital stay was significantly longer for patients with AF than for those without, at 9.4 days versus 8.1 days. Patients with AF also experienced significantly higher in-hospital mortality than those without, at 3.3% versus 0.5%.
In all, 1806 patients were alive at discharge, of whom 143 were lost to follow-up. The remaining patients were followed up for a median of 51 months. After a median of 14 months, 126 patients died.
Long-term mortality was significantly higher for patients with AF than for those without, at 2.99 compared with 1.34 per 100 person-years, giving an adjusted hazard ratio (HR) of 2.13, which rose to 2.56 when also taking into account warfarin prescription at discharge.
Cox regression analysis revealed that AF patients had a significantly increased risk for cardiac causes of death, at a HR of 2.83, compared with non-AF patients. Of the cardiac causes, AF patients were significantly more likely than non-AF patients to die of embolism, at a HR of 4.33. AF patients did not face an elevated risk for non-cardiac causes of death.
The team writes: “Our results imply that appropriate antiarrhythmic and antithrombotic prophylaxis should be considered in patients after CABG.”
Circulation 2008; 118: 1612–1618
There is an ongoing debate surrounding the prognostic implications of postoperative AF, which is recognized as a difficult complication associated with significant adverse events and increased length of stay in intensive care and in hospital.
Giovanni Mariscalco, from Varese University Hospital in Italy, and colleagues studied 1832 patients who underwent isolated CABG between 2000 and 2005 at two cardiac centers, identifying patients who experienced postoperative AF and following them up until death or 2007.
The team reports in the journal Circulation that AF developed in 31% of the patients. Patients who developed AF were significantly older than those who did not, at 68.4 years versus 63.7 years.
The length of hospital stay was significantly longer for patients with AF than for those without, at 9.4 days versus 8.1 days. Patients with AF also experienced significantly higher in-hospital mortality than those without, at 3.3% versus 0.5%.
In all, 1806 patients were alive at discharge, of whom 143 were lost to follow-up. The remaining patients were followed up for a median of 51 months. After a median of 14 months, 126 patients died.
Long-term mortality was significantly higher for patients with AF than for those without, at 2.99 compared with 1.34 per 100 person-years, giving an adjusted hazard ratio (HR) of 2.13, which rose to 2.56 when also taking into account warfarin prescription at discharge.
Cox regression analysis revealed that AF patients had a significantly increased risk for cardiac causes of death, at a HR of 2.83, compared with non-AF patients. Of the cardiac causes, AF patients were significantly more likely than non-AF patients to die of embolism, at a HR of 4.33. AF patients did not face an elevated risk for non-cardiac causes of death.
The team writes: “Our results imply that appropriate antiarrhythmic and antithrombotic prophylaxis should be considered in patients after CABG.”
Circulation 2008; 118: 1612–1618
Episodic amiodarone not advantageous in AF
MedWire News: Episodic amiodarone therapy cannot be recommended for persistent atrial fibrillation (AF), say Dutch researchers, who found that most patients required continuous therapy to adequately suppress arrhythmias.
Amiodarone is the most effective drug used to prevent AF but can cause a range of noncardiac adverse events, particularly when used in high dosages and over long periods of time.
In the present study, Sheba Ahmed (University of Groningen) and colleagues hypothesized that episodic amiodarone therapy would be as effective as continuous treatment, but with an improved safety and tolerability profile.
They tested this in a multicenter trial known as CONVERT, in which 209 patients with recurrent symptomatic persistent AF were randomized to receive either episodic or continuous amiodarone therapy following successful electrical cardioversion and a loading dose of amiodarone.
After a median follow-up of 2.1 years, continuous therapy exhibited a range of advantages over episodic therapy. These included a higher proportion of patients in sinus rhythm (62% vs 48%, p=0.05), a lower incidence of AF recurrence (54% vs 80%, p<0.001), a lower rate of all-cause mortality and cardiovascular hospitalizations (34% vs 53%, p=0.02), and a trend to fewer underlying heart disease-related major events (9% vs 16%).
Conversely, episodic therapy was associated with a nonsignificant trend toward fewer amiodarone-related major events (19% vs 24%), while there was no difference between the groups in the incidence of the primary endpoint – a composite of amiodarone and underlying heart disease-related major events (35% episodic vs 33% continuous).
“Considering the above, episodic amiodarone treatment cannot be advocated for most patients with persistent atrial fibrillation,” Ahmed and co-authors conclude.
“This study shows that episodic amiodarone treatment – in contrast to our expectations – has no clinical advantage over continuous treatment because it did not lower morbidity in patients with persistent atrial fibrillation over 2 years of follow-up.”
The study is published in the Journal of the American Medical Association.
JAMA 2008; 300: 1784–1792
Amiodarone is the most effective drug used to prevent AF but can cause a range of noncardiac adverse events, particularly when used in high dosages and over long periods of time.
In the present study, Sheba Ahmed (University of Groningen) and colleagues hypothesized that episodic amiodarone therapy would be as effective as continuous treatment, but with an improved safety and tolerability profile.
They tested this in a multicenter trial known as CONVERT, in which 209 patients with recurrent symptomatic persistent AF were randomized to receive either episodic or continuous amiodarone therapy following successful electrical cardioversion and a loading dose of amiodarone.
After a median follow-up of 2.1 years, continuous therapy exhibited a range of advantages over episodic therapy. These included a higher proportion of patients in sinus rhythm (62% vs 48%, p=0.05), a lower incidence of AF recurrence (54% vs 80%, p<0.001), a lower rate of all-cause mortality and cardiovascular hospitalizations (34% vs 53%, p=0.02), and a trend to fewer underlying heart disease-related major events (9% vs 16%).
Conversely, episodic therapy was associated with a nonsignificant trend toward fewer amiodarone-related major events (19% vs 24%), while there was no difference between the groups in the incidence of the primary endpoint – a composite of amiodarone and underlying heart disease-related major events (35% episodic vs 33% continuous).
“Considering the above, episodic amiodarone treatment cannot be advocated for most patients with persistent atrial fibrillation,” Ahmed and co-authors conclude.
“This study shows that episodic amiodarone treatment – in contrast to our expectations – has no clinical advantage over continuous treatment because it did not lower morbidity in patients with persistent atrial fibrillation over 2 years of follow-up.”
The study is published in the Journal of the American Medical Association.
JAMA 2008; 300: 1784–1792
quinta-feira, 16 de outubro de 2008
Novel mutation implicated in familial AF
10 October 2008
MedWire News: Japanese researchers have identified a novel genetic mutation in the cardiac sodium channel that can give rise to familial atrial fibrillation (AF).
The gain-of-function mutation in the SCN5A gene was found to cause increased atrial excitability in patients without underlying structural heart disease, thereby representing a novel pathogenic mechanism underlying AF.
The research, by Takeru Makiyama (Kyoto University) and colleagues, centered on a Japanese family with autosomal dominant hereditary AF that spanned three generations.
Seven family members presented with AF or frequent premature atrial contraction (PAC) in the absence of structural heart disease. The affected members had a remarkably similar clinical course, the authors comment, exhibiting recurrent atrial arrhythmias that were resistant to ablation or drug therapy.
Mutational analysis of the proband identified a novel missense mutation, M1875T, in the Na+ channel gene SCN5A, which was subsequently identified in all affected family members.
Functional studies revealed a distinct gain-of-function type modulation characterized by a +16.4 mV shift in the steady-state inactivation. “This is, to the best of our knowledge, the greatest depolarization shift in all of the previously reported SCN5A mutants,” remark Makiyama et al.
The researchers propose various mechanisms by which the novel mutation might lead to PAC or AF. However they are unable to explain why the SCN5A mutant is associated with atrial but not ventricular arrhythmias, given that Na+ channels encoded by SCN5A are expressed in both chambers of the heart.
Writing in the Journal of the American College of Cardiology, they conclude: “We identified a novel SCN5A gain-of-function mutation that causes a familial form of AF without any underlying structural heart diseases, which provides us with new insight into the pathogenesis of the commonly occurring form of AF.”
J Am Coll Cardiol 2008; 52: 1326–1334
MedWire News: Japanese researchers have identified a novel genetic mutation in the cardiac sodium channel that can give rise to familial atrial fibrillation (AF).
The gain-of-function mutation in the SCN5A gene was found to cause increased atrial excitability in patients without underlying structural heart disease, thereby representing a novel pathogenic mechanism underlying AF.
The research, by Takeru Makiyama (Kyoto University) and colleagues, centered on a Japanese family with autosomal dominant hereditary AF that spanned three generations.
Seven family members presented with AF or frequent premature atrial contraction (PAC) in the absence of structural heart disease. The affected members had a remarkably similar clinical course, the authors comment, exhibiting recurrent atrial arrhythmias that were resistant to ablation or drug therapy.
Mutational analysis of the proband identified a novel missense mutation, M1875T, in the Na+ channel gene SCN5A, which was subsequently identified in all affected family members.
Functional studies revealed a distinct gain-of-function type modulation characterized by a +16.4 mV shift in the steady-state inactivation. “This is, to the best of our knowledge, the greatest depolarization shift in all of the previously reported SCN5A mutants,” remark Makiyama et al.
The researchers propose various mechanisms by which the novel mutation might lead to PAC or AF. However they are unable to explain why the SCN5A mutant is associated with atrial but not ventricular arrhythmias, given that Na+ channels encoded by SCN5A are expressed in both chambers of the heart.
Writing in the Journal of the American College of Cardiology, they conclude: “We identified a novel SCN5A gain-of-function mutation that causes a familial form of AF without any underlying structural heart diseases, which provides us with new insight into the pathogenesis of the commonly occurring form of AF.”
J Am Coll Cardiol 2008; 52: 1326–1334
Differential diagnosis of wide QRS tachycardia under scrutiny
6 October 2008
MedWire News: The standard approach to the differential diagnosis of wide QRS tachycardia in patients with fixed bundle branch block (BBB) is flawed and may cause some patients to be wrongly diagnosed with ventricular tachycardia, say researchers.
The claim is made by Spanish cardiologists based on a prospective study of patients with fixed BBB and reported in the European Heart Journal.
It is widely held that the differentiation of wide QRS tachycardia in patients with preexisting wide QRS complex is simple: If the QRS complexes during tachycardia are identical to those in sinus rhythm, the tachycardia is supraventricular tachycardia (SVT); if they are different, the arrhythmia is ventricular in origin.
“This concept may be too simplistic and has not been tested in a systematic way,” write Tomás Datino (Hospital General Universitario, Madrid) and co-authors.
For this study, Datino et al analyzed QRS morphology during incremental rapid atrial pacing in 59 patients in sinus rhythm and QRS =120 ms but no pre-excitation.
On pacing, minor QRS changes were seen in 37% of subjects and major changes in 39%, the researchers report. One patient showed major axis shifts and none showed a change to the contralateral BBB pattern.
QRS changes were significantly and independently related to pacing rate and BBB type, being more frequent in those with right BBB. Furthermore, of 14 subjects with SVT, 13 displayed the same QRS changes during pacing.
Based on their observations Datino et al conclude: “If the 12-lead ECG morphology of a wide QRS tachycardia is different to that during sinus rhythm, but with the same BBB pattern, it does not necessarily imply that the tachycardia is ventricular.”
In an accompanying editorial, Hein Wellens (Cardiovascular Research Institute Maastricht, The Netherlands) remarked: “To make the correct diagnosis in a wide QRS tachycardia remains a challenge.
“In patients with the same type of BBB during sinus rhythm and tachycardia, there may be differences in QRS configuration without implying that the tachycardia is ventricular.”
Eur Heart J 2008; 29: 2351–2358
MedWire News: The standard approach to the differential diagnosis of wide QRS tachycardia in patients with fixed bundle branch block (BBB) is flawed and may cause some patients to be wrongly diagnosed with ventricular tachycardia, say researchers.
The claim is made by Spanish cardiologists based on a prospective study of patients with fixed BBB and reported in the European Heart Journal.
It is widely held that the differentiation of wide QRS tachycardia in patients with preexisting wide QRS complex is simple: If the QRS complexes during tachycardia are identical to those in sinus rhythm, the tachycardia is supraventricular tachycardia (SVT); if they are different, the arrhythmia is ventricular in origin.
“This concept may be too simplistic and has not been tested in a systematic way,” write Tomás Datino (Hospital General Universitario, Madrid) and co-authors.
For this study, Datino et al analyzed QRS morphology during incremental rapid atrial pacing in 59 patients in sinus rhythm and QRS =120 ms but no pre-excitation.
On pacing, minor QRS changes were seen in 37% of subjects and major changes in 39%, the researchers report. One patient showed major axis shifts and none showed a change to the contralateral BBB pattern.
QRS changes were significantly and independently related to pacing rate and BBB type, being more frequent in those with right BBB. Furthermore, of 14 subjects with SVT, 13 displayed the same QRS changes during pacing.
Based on their observations Datino et al conclude: “If the 12-lead ECG morphology of a wide QRS tachycardia is different to that during sinus rhythm, but with the same BBB pattern, it does not necessarily imply that the tachycardia is ventricular.”
In an accompanying editorial, Hein Wellens (Cardiovascular Research Institute Maastricht, The Netherlands) remarked: “To make the correct diagnosis in a wide QRS tachycardia remains a challenge.
“In patients with the same type of BBB during sinus rhythm and tachycardia, there may be differences in QRS configuration without implying that the tachycardia is ventricular.”
Eur Heart J 2008; 29: 2351–2358
Gene variant identified in sinus node dysfunction
9 October 2008
MedWire News: A gene variant that causes sick sinus syndrome has been identified, offering new insights into the cellular mechanisms involved in arrhythmias and other diseases of cell excitability.
The research was a collaboration between scientists in the USA and France involving two large families with highly penetrant and severe sinus node dysfunction (SND).
SND causes “sick sinus syndrome,” a potentially lethal disease associated with heart-rate variability and bradycardia, and the reason for over half of permanent pacemaker implantations. Until now, the genetic and molecular mechanisms underlying SND were unknown.
The researchers began by mapping the two families – 108 individuals in total, 39 of whom had SND – to the human ANK2 locus, which encodes ankyrin-B (AnkB).
“Mutant ANK2 alleles associated with AnkB expression or AnkB loss-of function are strongly associated with severe human SND,” write Peter Mohler (University of Iowa Carver College of Medicine, Iowa City, USA) and fellow researchers in the Proceedings of the National Academy of Sciences.
The team then studied knockout mice, finding that AnkB is highly expressed in the sinoatrial node (SAN) and that AnkB activity is essential for the posttranslational organization of SAN channels and transporters.
Most importantly, Mohler et al showed that AnkB is required for physiological cardiac pacing and that dysfunction in AnkB-based pathways leads to abnormal SAN activity and SND.
“Together, our findings associate abnormal channel targeting with human SND and highlight the critical role of local membrane organization for sinoatrial node excitability,” the researchers write.
“We predict that there are likely additional unidentified ankyrin variants in the larger general population that predispose humans to a combination of heart disease symptoms, including sinus node dysfunction, atrial fibrillation and ventricular arrhythmias.”
The discovery has implications beyond SND, they add, since genes that encode ankyrin and related proteins are likely involved in other diseases characterized by cell excitability, such as epilepsy, bipolar disorder, and diabetes.
PNAS 2008; 105: 15617–15622
MedWire News: A gene variant that causes sick sinus syndrome has been identified, offering new insights into the cellular mechanisms involved in arrhythmias and other diseases of cell excitability.
The research was a collaboration between scientists in the USA and France involving two large families with highly penetrant and severe sinus node dysfunction (SND).
SND causes “sick sinus syndrome,” a potentially lethal disease associated with heart-rate variability and bradycardia, and the reason for over half of permanent pacemaker implantations. Until now, the genetic and molecular mechanisms underlying SND were unknown.
The researchers began by mapping the two families – 108 individuals in total, 39 of whom had SND – to the human ANK2 locus, which encodes ankyrin-B (AnkB).
“Mutant ANK2 alleles associated with AnkB expression or AnkB loss-of function are strongly associated with severe human SND,” write Peter Mohler (University of Iowa Carver College of Medicine, Iowa City, USA) and fellow researchers in the Proceedings of the National Academy of Sciences.
The team then studied knockout mice, finding that AnkB is highly expressed in the sinoatrial node (SAN) and that AnkB activity is essential for the posttranslational organization of SAN channels and transporters.
Most importantly, Mohler et al showed that AnkB is required for physiological cardiac pacing and that dysfunction in AnkB-based pathways leads to abnormal SAN activity and SND.
“Together, our findings associate abnormal channel targeting with human SND and highlight the critical role of local membrane organization for sinoatrial node excitability,” the researchers write.
“We predict that there are likely additional unidentified ankyrin variants in the larger general population that predispose humans to a combination of heart disease symptoms, including sinus node dysfunction, atrial fibrillation and ventricular arrhythmias.”
The discovery has implications beyond SND, they add, since genes that encode ankyrin and related proteins are likely involved in other diseases characterized by cell excitability, such as epilepsy, bipolar disorder, and diabetes.
PNAS 2008; 105: 15617–15622
sábado, 11 de outubro de 2008
Rate-related changes in QRS morphology in patients with fixed bundle branch block: implications for differential diagnosis of wide QRS complex tachyca
Tomás Datino, Jesús Almendral*, Esteban González-Torrecilla, Felipe Atienza, Francisco J. García-Fernández, Ángel Arenal, Leonardo Atea and Francisco Fernández-Avilés
Cardiology Department, Hospital General Universitario, Gregorio Marañón, Doctor Esquerdo 46, Madrid 28007, Spain
Received 3 December 2007; revised 15 June 2008; accepted 8 July 2008; online publish-ahead-of-print 29 July 2008.
* Corresponding author. Tel/Fax: +34 915 868 276, Email: almendral@secardiologia.es
See page 2319 for the editorial comment on this article (doi:10.1093/eurheartj/ehn391)
Aims: To analyse QRS morphology in response to rapid atrial pacing (RAP) and supraventricular tachycardia (SVT) in patients with pre-existing bundle branch block (BBB).
Methods and results: We prospectively studied 59 patients in sinus rhythm (SR), with QRS 120 ms, and no pre-excitation. Trains of RAP were introduced at increasing rates until atrioventricular block. QRS during SR and last QRS complex of each RAP train were compared on the 12-leads. Previously described criteria for minor and major configuration differences were used to identify QRS changes. During RAP minor QRS changes were seen in 22 (37%) and major changes in 23 (39%) subjects. One patient showed major axis shifts and no one showed a change to the contralateral BBB pattern. QRS changes were significantly and independently related to RAP rate and type of BBB (more frequent if right-BBB). Of 14 subjects (24%) with SVT, 13 displayed the same QRS changes during RAP.
Conclusion: In patients with organic BBB, important changes in QRS morphology, except for a change in the contralateral BBB, can appear during RAP and SVT. Thus, in these patients, a change in QRS morphology during tachycardia does not necessarily imply that it is ventricular tachycardia.
Key Words: Tachycardia • Bundle branch block • Diagnosis • Wide QRS complex tachycardia • Electrocardiography
Comentario de incirculation.net:
Differential diagnosis of wide QRS tachycardia under scrutiny
6 October 2008
MedWire News: The standard approach to the differential diagnosis of wide QRS tachycardia in patients with fixed bundle branch block (BBB) is flawed and may cause some patients to be wrongly diagnosed with ventricular tachycardia, say researchers.
The claim is made by Spanish cardiologists based on a prospective study of patients with fixed BBB and reported in the European Heart Journal.
It is widely held that the differentiation of wide QRS tachycardia in patients with preexisting wide QRS complex is simple: If the QRS complexes during tachycardia are identical to those in sinus rhythm, the tachycardia is supraventricular tachycardia (SVT); if they are different, the arrhythmia is ventricular in origin.
“This concept may be too simplistic and has not been tested in a systematic way,” write Tomás Datino (Hospital General Universitario, Madrid) and co-authors.
For this study, Datino et al analyzed QRS morphology during incremental rapid atrial pacing in 59 patients in sinus rhythm and QRS =120 ms but no pre-excitation.
On pacing, minor QRS changes were seen in 37% of subjects and major changes in 39%, the researchers report. One patient showed major axis shifts and none showed a change to the contralateral BBB pattern.
QRS changes were significantly and independently related to pacing rate and BBB type, being more frequent in those with right BBB. Furthermore, of 14 subjects with SVT, 13 displayed the same QRS changes during pacing.
Based on their observations Datino et al conclude: “If the 12-lead ECG morphology of a wide QRS tachycardia is different to that during sinus rhythm, but with the same BBB pattern, it does not necessarily imply that the tachycardia is ventricular.”
In an accompanying editorial, Hein Wellens (Cardiovascular Research Institute Maastricht, The Netherlands) remarked: “To make the correct diagnosis in a wide QRS tachycardia remains a challenge.
“In patients with the same type of BBB during sinus rhythm and tachycardia, there may be differences in QRS configuration without implying that the tachycardia is ventricular.”
Eur Heart J 2008; 29: 2351–2358
Cardiology Department, Hospital General Universitario, Gregorio Marañón, Doctor Esquerdo 46, Madrid 28007, Spain
Received 3 December 2007; revised 15 June 2008; accepted 8 July 2008; online publish-ahead-of-print 29 July 2008.
* Corresponding author. Tel/Fax: +34 915 868 276, Email: almendral@secardiologia.es
See page 2319 for the editorial comment on this article (doi:10.1093/eurheartj/ehn391)
Aims: To analyse QRS morphology in response to rapid atrial pacing (RAP) and supraventricular tachycardia (SVT) in patients with pre-existing bundle branch block (BBB).
Methods and results: We prospectively studied 59 patients in sinus rhythm (SR), with QRS 120 ms, and no pre-excitation. Trains of RAP were introduced at increasing rates until atrioventricular block. QRS during SR and last QRS complex of each RAP train were compared on the 12-leads. Previously described criteria for minor and major configuration differences were used to identify QRS changes. During RAP minor QRS changes were seen in 22 (37%) and major changes in 23 (39%) subjects. One patient showed major axis shifts and no one showed a change to the contralateral BBB pattern. QRS changes were significantly and independently related to RAP rate and type of BBB (more frequent if right-BBB). Of 14 subjects (24%) with SVT, 13 displayed the same QRS changes during RAP.
Conclusion: In patients with organic BBB, important changes in QRS morphology, except for a change in the contralateral BBB, can appear during RAP and SVT. Thus, in these patients, a change in QRS morphology during tachycardia does not necessarily imply that it is ventricular tachycardia.
Key Words: Tachycardia • Bundle branch block • Diagnosis • Wide QRS complex tachycardia • Electrocardiography
Comentario de incirculation.net:
Differential diagnosis of wide QRS tachycardia under scrutiny
6 October 2008
MedWire News: The standard approach to the differential diagnosis of wide QRS tachycardia in patients with fixed bundle branch block (BBB) is flawed and may cause some patients to be wrongly diagnosed with ventricular tachycardia, say researchers.
The claim is made by Spanish cardiologists based on a prospective study of patients with fixed BBB and reported in the European Heart Journal.
It is widely held that the differentiation of wide QRS tachycardia in patients with preexisting wide QRS complex is simple: If the QRS complexes during tachycardia are identical to those in sinus rhythm, the tachycardia is supraventricular tachycardia (SVT); if they are different, the arrhythmia is ventricular in origin.
“This concept may be too simplistic and has not been tested in a systematic way,” write Tomás Datino (Hospital General Universitario, Madrid) and co-authors.
For this study, Datino et al analyzed QRS morphology during incremental rapid atrial pacing in 59 patients in sinus rhythm and QRS =120 ms but no pre-excitation.
On pacing, minor QRS changes were seen in 37% of subjects and major changes in 39%, the researchers report. One patient showed major axis shifts and none showed a change to the contralateral BBB pattern.
QRS changes were significantly and independently related to pacing rate and BBB type, being more frequent in those with right BBB. Furthermore, of 14 subjects with SVT, 13 displayed the same QRS changes during pacing.
Based on their observations Datino et al conclude: “If the 12-lead ECG morphology of a wide QRS tachycardia is different to that during sinus rhythm, but with the same BBB pattern, it does not necessarily imply that the tachycardia is ventricular.”
In an accompanying editorial, Hein Wellens (Cardiovascular Research Institute Maastricht, The Netherlands) remarked: “To make the correct diagnosis in a wide QRS tachycardia remains a challenge.
“In patients with the same type of BBB during sinus rhythm and tachycardia, there may be differences in QRS configuration without implying that the tachycardia is ventricular.”
Eur Heart J 2008; 29: 2351–2358
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