ABSTRACT WITHDRAWN

Abstract

Introduction

Reappraisal of electrocardiographic changes in pediatric patients with acute myocarditis

To evaluate the prognostic significance of electrocardiographic (ECG) changes in pediatric patients with acute myocarditis.

Methods

This study recruited 21 children with acute myocarditis at Kaohsiung Veterans General Hospital, Taiwan. Medical records were reviewed for age, sex, presenting symptoms, ECG findings, treatment, and clinical course. ECG was analyzed for rhythm, conduction times, signs of hypertrophy, and repolarization abnormalities.

Results

ECG analysis was undertaken in 21 pediatric patients (M/F 15/6, 11.0 +/- 5.7 years). In 12 patients with the predominant symptoms of chest pain, sinus rhythm, normal QRS, and repolarization abnormalities were the prevailing ECG features on admisson. Repolarization abnormalitis improved under symptomatic treatment. In 3 patients with the predominant symptoms of tachycardia, sinus rhythm, normal QRS, and repolarization abnormalities were also the prevailing ECG features on admission, which improved on discharge. In the remaining 6 patients with acute fulminant myocarditis, sinus tachycardia, wide QRS, VPC, VT, LBBB, AV block, and repolarization abnormalities were the prevailing ECG features on admission. Severe hypotension required immediate intravenous inotropic support. ECMO was performed in 2 patients. Of the 21 patients, 17 were discharged with normal ECG, 2 were discharged with RBBB, and 2 children died.

Conclusions

ECG changes varied greatly in pediatrc patients with acute myocarditis. Repolarization abnormalities in stable patients generally improved after symptomatic treatment. In patients with acute fulminant myocarditis, ECG changes may be early signs of severe LV dysfunction and an indication for aggressive inotropic support, even ECMO. Most patients with resolved myocarditis had normal ECG, but RBBB may persist in some patients.

Electrocardiographic characterisation of ventricular ectopy originating from the Para-Hisian Region

Abstract

Background

Ventricular premature beats (VPBs) originating from the right ventricular outflow tract (RVOT) are highly amenable to radiofrequency (RF) ablation. RVOT VPBs result in a typical ECG with a left bundle branch block, inferior axis morphology. VPBs originating near the His bundle require careful consideration due to the risk of heart block. We therefore sought to investigate the ECG characteristics of VPBs arising from the para-Hisian (PH) region.

Methods

A retrospective analysis of 91 consecutive patients undergoing ablation for symptomatic VPBs between 2006-2011 was undertaken. Activation and pacemapping were performed in all patients and the successful ablation site recorded. Digitized ECGs were analysed. We defined the PH area as < 1cm from a well-positioned His catheter displaying a His bundle electrogram.

Results

Of 91 patients studied, 48 had VPBs arising from the RVOT and 6 (6.6%) from the PH region. See figure. Mean age of PH group was 53 ± 19 vs 45 ± 16 years in the RVOT group (p = 0.4). 4/6 in the PH group and 35/48 in the RVOT group were female. There was no difference in QRS duration in PH vs RVOT origin (164 ± 17.6ms vs. 167 ± 19.5ms p = 0.8). Precordial transition was earlier, as expressed by a significantly lower transitional zone index, in the PH group compared to the RVOT group (-1.2 ± 0.98 vs 0.12 ± 0.31, p = 0.001). Notching in the S wave of lead V1 (p = 0.022, sensitivity 67%, specificity 92%), a dominant R wave in aVL (p = 0.09, sensitivity 100%, specificity 75%) and an S wave in either leads III or aVF (p = 0.02, sensitivity 67%, specificity 92%) were significantly associated with PH vs. RVOT VPBs. R wave amplitude in the inferior leads was significantly lower in the PH group (0.63 ± 0.37 mV vs 1.29 ± 0.34 mV, p < 0.001). The combination of a dominant R wave in lead aVL and an S wave in leads III or aVF had a sensitivity of 66% and specificity of 100% for predicting a PH origin. 5/6 in the PH group were ablated 2 with cryo. There were no instances of AV block.

Conclusion

In VPBs with left bundle-inferior axis morphology, the combination of an R wave in lead aVL and an S wave in lead III or aVF had a 66% sensitivity and a 100% specificity for predicting a PH origin. The performance of these criteria merit prospective validation.

graphic

Case series of pregnancy associated incessant ectopic atrial tachycardia

Abstract

Background

Sustained arrhythmia during pregnancy is uncommon in the absence of structural heart disease. There are isolated reports of incessant ectopic atrial tachycardia (AT) during pregnancy but this group of patients is not well characterised. We report a case series of 5 patients who developed incessant AT during pregnancy.

Methods

Over a 2 year period five pregnant patients presented with incessant AT necessitating hospitalisation and medical notes were reviewed.

Results

The baseline clinical characteristics are summarised in the Table 1. Mean age at first presentation was 31.8 ± 5.5 years. 4/5 patients were multigravida and two of them had had palpitations (no documented arrhythmia) during previous pregnancies. All patients were asymptomatic prior to their pregnancies. 4/5 presented in the 3rd trimester of their pregnancy. Dyspnoea and palpitations were the most common presenting symptoms, one patient presented with heart failure symptoms. Electrocardiogram (ECG) showed narrow complex tachycardia suggestive of a long RP tachycardia with variable cycle lengths and P-wave morphology suggested right atrial origin in 4/5 patients. 4/5 patients had Adenosine acutely with transient termination of the AT. Echocardiogram demonstrated impaired left ventricular systolic function (LVSF) in all patients. Beta-blockers and/or Flecainide were the most common anti-arrhythmic drugs (AADs) used with variable response. 2/5 patients went on to have urgent deliveries on the same admission as patients remained symptomatic without satisfactory rhythm or rate control on AADs (one caesarean section (CS), one induction). 2/5 had semi-elective CS six weeks after discharge (for recurrent AT with LV dysfunction and for pre-eclampsia). All patents delivered healthy infants and AT resolved after delivery. There was no recurrence of documented AT off AADs and repeat echocardiogram confirmed recovery of LVSF in all patients.

Table 1

Pt #1Pt #2Pt#3Pt #4Pt #5
Age3634233630
Pregnancy5th2nd2nd2nd1st
Gestation 1st admission / delivery33/3323/3737/3830/3630/37
Delivery modeurgent / CSelective / inducedurgent / inducedelective / CSelective / CS
Total / post-partum hospital stay (days)18/112/114/106/69/6
Structural changesnonenonemod-sev MR (rheum. fever)small ASDnone
LVSF impairment pre / post deliverymild / normalmild / normalmild / normalmod-sev / normalmod / normal
Termination (Adenosine)yesyesDNAyesyes
Rhythm control (AAD)partialpartialrate controlfullpartial
AT originright superiorright inferiorleft inferiorright superiorright superior
Pt #1Pt #2Pt#3Pt #4Pt #5
Age3634233630
Pregnancy5th2nd2nd2nd1st
Gestation 1st admission / delivery33/3323/3737/3830/3630/37
Delivery modeurgent / CSelective / inducedurgent / inducedelective / CSelective / CS
Total / post-partum hospital stay (days)18/112/114/106/69/6
Structural changesnonenonemod-sev MR (rheum. fever)small ASDnone
LVSF impairment pre / post deliverymild / normalmild / normalmild / normalmod-sev / normalmod / normal
Termination (Adenosine)yesyesDNAyesyes
Rhythm control (AAD)partialpartialrate controlfullpartial
AT originright superiorright inferiorleft inferiorright superiorright superior
Pt #1Pt #2Pt#3Pt #4Pt #5
Age3634233630
Pregnancy5th2nd2nd2nd1st
Gestation 1st admission / delivery33/3323/3737/3830/3630/37
Delivery modeurgent / CSelective / inducedurgent / inducedelective / CSelective / CS
Total / post-partum hospital stay (days)18/112/114/106/69/6
Structural changesnonenonemod-sev MR (rheum. fever)small ASDnone
LVSF impairment pre / post deliverymild / normalmild / normalmild / normalmod-sev / normalmod / normal
Termination (Adenosine)yesyesDNAyesyes
Rhythm control (AAD)partialpartialrate controlfullpartial
AT originright superiorright inferiorleft inferiorright superiorright superior
Pt #1Pt #2Pt#3Pt #4Pt #5
Age3634233630
Pregnancy5th2nd2nd2nd1st
Gestation 1st admission / delivery33/3323/3737/3830/3630/37
Delivery modeurgent / CSelective / inducedurgent / inducedelective / CSelective / CS
Total / post-partum hospital stay (days)18/112/114/106/69/6
Structural changesnonenonemod-sev MR (rheum. fever)small ASDnone
LVSF impairment pre / post deliverymild / normalmild / normalmild / normalmod-sev / normalmod / normal
Termination (Adenosine)yesyesDNAyesyes
Rhythm control (AAD)partialpartialrate controlfullpartial
AT originright superiorright inferiorleft inferiorright superiorright superior

Conclusion

Incessant AT may be uniquely associated with pregnancy even in the absence of structural heart disease. Delivery of the infants abolished the ATs in all patients. LVSF was impaired during AT, at follow up all patients were asymptomatic off AADs and LVSF had normalised.

Patients with “Idiopathic” Ventricular Fibrillation and an ICD

Abstract

Introduction

Idiopathic VF (IVF) maybe over diagnosed depending on which definition is used. The aim of this study was to investigate the incidence of IVF and the frequency with which patients are inappropriately labelled with IVF in a tertiary centre with a specialist inherited arrhythmia clinic.

Methods

Medical notes were retrospectively reviewed on all patients who had an ICD inserted between June 1994 and May 2012. All patients who had undergone a secondary prevention ICD for either “unknown” or “idiopathic” reasons were selected. The electronic records and medical notes were reviewed to reveal whether in light of further testing a different diagnosis would be given. IVF was defined as VF with no identifiable cause after full clinical investigation.

Results

Of 2189 patients, 135 had a working diagnosis of IVF. Of these 7 had limited clinical data and were excluded. Of the remaining 128 patients (98M), only 28 (22%) had a confirmed diagnosis of IVF. 15 patients (12%) required further testing before all causes could be excluded resulting in a diagnosis of IVF (9 need an exercise test and 12 need an ajmaline test). The remaining 85 patients were found to have dilated cardiomyopathy or ischaemic heart disease 72 (56%), hypertrophic cardiomyopathy 3 (2%), ARVC 4 (3%), Long QT syndrome 2 (1.5%), Brugada syndrome 2 (1.5%), 1 with cardiac sarcoidosis and 1 with Wolff Parkinson White syndrome. Of the 28 patients with confirmed IVF (mean age 43 +/- 13) and follow up ranging from 2 - 216 months, 16 (57%) had evidence of early repolarization on their ECG (J point notching/slurring in ≥ 2 leads). 8/28 (28%) IVF patients had at least one appropriate therapy during follow up and 1 patient required catheter ablation for recurrent VF.

Conclusion

IVF may be diagnosed prematurely which can result in a failure to screen the family for inherited causes of VF. Appropriate therapy is common in these patients and there is a high prevalence of early repolarization and IVF but because of its frequency in the general population this is not a useful screening marker.

Electrophysiological differentiation of early ARVC from benign outflow tract ectopy utilising high density mapping

Abstract

Background

The differentiation of arrhythmogenic right ventricular cardiomyopathy (ARVC) from benign RV outflow tract ectopy (RVOTE) remains a significant clinical challenge. Although endocardial voltage mapping and assessment of conduction delay can resolve differences between these groups, this has principally been examined in advanced disease. The ability of electrophysiological parameters to distinguish early ARVC from benign RVOTE is untested. We compared dynamic conduction-repolarization kinetics in patients with early ARVC with data from benign RVOTE and controls with supraventricular tachycardia (SVT).

Methods

23 ARVC patients (definite or probable by modified task force criteria with no RV structural features) underwent high density mapping of the right ventricle (RV). These were compared to data from 14 RVOTE and 12 SVT patients. Local conduction and repolarization parameters were assessed in sinus rhythm steady state pacing and during a standard S1-S2 protocol. Signal analysis was performed using custom semi-automated software. Results were compared using mixed-effects regression modeling and statistical significance inferred from the models.

Results

Progressively greater local repolarisation times developed in ARVC patients as coupling intervals decreased towards ventricular effective refractory period (VERP), this effect was greatest in the RVOT (ARVC: 18 ± 20ms;RVOTE ±14, Control: 1 ± 18, p <0.05). The increase in conduction delay at VERP from steady-state was the most effective single predictor of ARVC versus RVOTE - AUC 0.73 (p < 0.001), see figure (red line and inset boxplot), with a sensitivity and specificity of 65% and 67% in distinguishing ARVC from RVOTE. A combination of conduction delay, repolarisation time prolongation and fractionation had a peak sensitivity and specificity of 72% and 70% respectively in separating ARVC from benign RVOTE (figure, thick grey line).

graphic

Conclusions

The earliest manifestations of ARVC are electrophysiological, resulting in significant changes of conduction and repolarisation kinetics. These could be of value in guiding the management and follow-up of patients with RVOT ectopy.

Short telomeres and telomerase activity in ischaemic cardiomyopathy patients – predictors of ventricular arrhythmia

Abstract

Introduction

Implantable cardioverter defibrillators (ICDs) reduce mortality in patients with ischaemic cardiomyopathy at high risk of ventricular arrhythmias(VA),which are the commonest cause of sudden death. However, ICDs are associated with morbidity and mortality. Importantly 67% of patients never receive an appropriate shock after ICD implantation under the current indication, suggesting a need for better risk stratification tools.Telomere and telomerase in leukocytes have recently been shown to correlate with biological aging and pathogenesis of various cardiovascular diseases. We hypothesise that leukocyte telomere length, load-of-short telomeres and/or telomerase activity correlate with the incidence of VA in ischaemic cardiomyopathy patients and could be used to guide ICD therapy more precisely.

Methods

90 ischaemic cardiomyopathy patients with primary prevention ICDs were recruited over one year at St Bartholomew's Hospital.Those with chronic inflammatory conditions, cancer, unwilling to consent were excluded.Concentrated leukocyte fraction was obtained from venous blood samples and stored at -80°C in an anonymous manner. Genomic DNA was extracted from these and mean leukocyte telomere length analysed by qPCR, load-of-short telomeres by U-STELA and telomerase activity by TRAP assay.All samples were analysed in duplicate and investigators were semi-blinded to arrhythmia history.Continuous data were compared using unpaired T-test and categorical data by Chi-square test. Logistic regression analysis was performed to determine if telomere dynamics(adjusted for age,sex&time since ICD implant) independently predict the likelihood of a shock (fatal VA).

Results

There were no significant differences in demographics between the fatal VA(shock) and no fatal VA(non shock) group. Age related telomere attrition (p = 0.03) was observed as expected. There was no significant difference in the age and sex adjusted mean telomere length between the two groups (p = 0.44). The load-of-short telomeres was significantly different between the two groups both at 1500bp (p = 0.014) and 1000bp (0.001) as shown in IMG1.The telomerase activity was significantly higher in the shock group (0.50) than in the non shock group (0.18).

graphic

Both the load-of-short telomeres and telomerase independently predicted the likelihood of shock (p = 0.003,0.02). Also, the sensitivity and specificity of load-of-short telomeres and telomerase in predicting fatal VA was higher than the current gold-standard i.e. LVEF (AUC 0.82,0.74 vs 0.50).

Conclusion

This is the first study to characterise the telomere dynamics of patients at high risk of sudden cardiac death and co-relate this with the incidence of VA. The load-of-short telomeres and telomerase activity independently predict the likelihood of shock in ischaemic cardiomyopathy patients with primary prevention ICDs. These have a place as potential biomarkers for prediction of fatal VA and guide ICD prescription.

What are the risk factors for arrhythmogenesis in grown up congenital heart disease (guch) patients following cardiac surgery?

Abstract

Background

Arrhythmias in Grown Up Congenital Heart Disease (GUCH) patients are the main reason for hospital admission, and a major cause of morbidity and mortality. Although patients have been extensively studied in the longer term, there is little information regarding perioperative arrhythmias. The aim of the study was to identify independent risk factors for arrhythmias in GUCH patients following cardiac surgery.

VariableArrhythmia
Univariate ModelpMultivariable modelp
NoYesOdds ratio (95%CI)Odds ratio (95%CI)
Age : mean (SD)30.3 (+/-12.5)37.2 (+/-13.5)1.04 (1.02, 1.06)0.0001.06 (1.03, 1.09)0.000
CPB (mins) (%)65 (20.8)26 (8.3)1.20 (0.43, 3.36)0.7292.07 (0.56, 7.66)0.273
1-6038 (12.2)43 (13.8)3.39 (1.22, 9.43)0.0193.92 (1.09, 14.17)0.037
61-12032 (10.3)53 (17.0)4.97 (1.79, 13.81)0.0025.49 (1.52, 19.83)0.009
121-18011 (3.5)20 (6.4)0.0055.34 (1.19, 24.02)0.029
>1815.45 (1.67, 17.77)
Temp admit: mean oC (SD)35.4 (+/-0.9)35.8 (+/-1.1)1.37 (1.08, 1.73)0.0091.56 (1.14, 2.12)0.005
MAP max: mean (sd)91.9 (+/-11.4)88.3 (+/-9.5)0.97 (0.94, 0.99)0.0040.95 (0.92, 0.99)0.007
Transfusion given (%)104 (33.3)128 (41.0)3.23 (1.80, 5.83)0.0002.21 (1.01, 4.85)0.047
Days AICU (%)
2-632 (10.3)61 (19.6)3.64 (2.16,6.13)0.0002.77 (1.39, 5.52)0.004
>68 (2.6)22 (7.1)5.25 (2.21,12.44)0.0003.92 (0.94, 16.38)0.061
VariableArrhythmia
Univariate ModelpMultivariable modelp
NoYesOdds ratio (95%CI)Odds ratio (95%CI)
Age : mean (SD)30.3 (+/-12.5)37.2 (+/-13.5)1.04 (1.02, 1.06)0.0001.06 (1.03, 1.09)0.000
CPB (mins) (%)65 (20.8)26 (8.3)1.20 (0.43, 3.36)0.7292.07 (0.56, 7.66)0.273
1-6038 (12.2)43 (13.8)3.39 (1.22, 9.43)0.0193.92 (1.09, 14.17)0.037
61-12032 (10.3)53 (17.0)4.97 (1.79, 13.81)0.0025.49 (1.52, 19.83)0.009
121-18011 (3.5)20 (6.4)0.0055.34 (1.19, 24.02)0.029
>1815.45 (1.67, 17.77)
Temp admit: mean oC (SD)35.4 (+/-0.9)35.8 (+/-1.1)1.37 (1.08, 1.73)0.0091.56 (1.14, 2.12)0.005
MAP max: mean (sd)91.9 (+/-11.4)88.3 (+/-9.5)0.97 (0.94, 0.99)0.0040.95 (0.92, 0.99)0.007
Transfusion given (%)104 (33.3)128 (41.0)3.23 (1.80, 5.83)0.0002.21 (1.01, 4.85)0.047
Days AICU (%)
2-632 (10.3)61 (19.6)3.64 (2.16,6.13)0.0002.77 (1.39, 5.52)0.004
>68 (2.6)22 (7.1)5.25 (2.21,12.44)0.0003.92 (0.94, 16.38)0.061
VariableArrhythmia
Univariate ModelpMultivariable modelp
NoYesOdds ratio (95%CI)Odds ratio (95%CI)
Age : mean (SD)30.3 (+/-12.5)37.2 (+/-13.5)1.04 (1.02, 1.06)0.0001.06 (1.03, 1.09)0.000
CPB (mins) (%)65 (20.8)26 (8.3)1.20 (0.43, 3.36)0.7292.07 (0.56, 7.66)0.273
1-6038 (12.2)43 (13.8)3.39 (1.22, 9.43)0.0193.92 (1.09, 14.17)0.037
61-12032 (10.3)53 (17.0)4.97 (1.79, 13.81)0.0025.49 (1.52, 19.83)0.009
121-18011 (3.5)20 (6.4)0.0055.34 (1.19, 24.02)0.029
>1815.45 (1.67, 17.77)
Temp admit: mean oC (SD)35.4 (+/-0.9)35.8 (+/-1.1)1.37 (1.08, 1.73)0.0091.56 (1.14, 2.12)0.005
MAP max: mean (sd)91.9 (+/-11.4)88.3 (+/-9.5)0.97 (0.94, 0.99)0.0040.95 (0.92, 0.99)0.007
Transfusion given (%)104 (33.3)128 (41.0)3.23 (1.80, 5.83)0.0002.21 (1.01, 4.85)0.047
Days AICU (%)
2-632 (10.3)61 (19.6)3.64 (2.16,6.13)0.0002.77 (1.39, 5.52)0.004
>68 (2.6)22 (7.1)5.25 (2.21,12.44)0.0003.92 (0.94, 16.38)0.061
VariableArrhythmia
Univariate ModelpMultivariable modelp
NoYesOdds ratio (95%CI)Odds ratio (95%CI)
Age : mean (SD)30.3 (+/-12.5)37.2 (+/-13.5)1.04 (1.02, 1.06)0.0001.06 (1.03, 1.09)0.000
CPB (mins) (%)65 (20.8)26 (8.3)1.20 (0.43, 3.36)0.7292.07 (0.56, 7.66)0.273
1-6038 (12.2)43 (13.8)3.39 (1.22, 9.43)0.0193.92 (1.09, 14.17)0.037
61-12032 (10.3)53 (17.0)4.97 (1.79, 13.81)0.0025.49 (1.52, 19.83)0.009
121-18011 (3.5)20 (6.4)0.0055.34 (1.19, 24.02)0.029
>1815.45 (1.67, 17.77)
Temp admit: mean oC (SD)35.4 (+/-0.9)35.8 (+/-1.1)1.37 (1.08, 1.73)0.0091.56 (1.14, 2.12)0.005
MAP max: mean (sd)91.9 (+/-11.4)88.3 (+/-9.5)0.97 (0.94, 0.99)0.0040.95 (0.92, 0.99)0.007
Transfusion given (%)104 (33.3)128 (41.0)3.23 (1.80, 5.83)0.0002.21 (1.01, 4.85)0.047
Days AICU (%)
2-632 (10.3)61 (19.6)3.64 (2.16,6.13)0.0002.77 (1.39, 5.52)0.004
>68 (2.6)22 (7.1)5.25 (2.21,12.44)0.0003.92 (0.94, 16.38)0.061

Methods

Data was gathered on 312 consecutive GUCH patients undergoing cardiac surgery at our institution 1997-2002. Development of an arrhythmia was defined as requiring post-operative pacing, cardioversion or amiodarone; and independent risk factors determined using a multivariable model (STATA v12).

Results

Independent risk factors identified for arrhythmia development in the post-operative GUCH patient included increasing age (p < 0.001), higher core body temperature (p = 0.009), longer cardiopulmonary bypass (p = 0.002), transfusion (p < 0.001), lower blood pressure post-operatively (p = 0.004) and ICU length of stay (LOS). Arrhythmia was not associated with increased mortality, but was associated with increased duration of ICU admission (p < 0.001).

Conclusion

Development of arrhythmia post-cardiac surgery in GUCH patients is associated with increased ICU morbidity and LOS. The mechanisms of arrhythmia development have been well studied in the outpatient setting, however critical care arrhythmias remain relatively unexplored. These data suggest further investigation of acute GUCH arrhythmogenesis may be of value, as some of the identified factors are modifiable. Further, development of a scoring system to identify high risk patients who may require surgical arrhythmia intervention, and/or pharmacological arrhythmia prophylaxis may be of value to prevent these acute arrhythmias and potentially reduce morbidity.

Heart rate variability as a prognostic marker of mortality in patients with myocardial infarction. Systematic review and meta-analysis

Abstract

Objective

To evaluate the role of HRV as a prognostic marker of mortality in post-myocardial infarction patients.

Methods

Medline, Embase, Cochrane, Scielo databases, gray literature, Manual search and cross references were searched. Authors were contacted looking for primary data. Two authors independently selected articles using Quorum statements. Disagreements were solved by consensus. Quality was assessed using the Hayden's scale for prognostic studies. Clinical, statistical heterogeneity, publication bias, sensitivity and subgroups analysis were performed. HRV measurements included were: SDNN, SDANN, HRV-index, HF, LF/HF, VLF, ULF, Total-Power. The softwares used were Revman 4.2, EPIDAT 3.1 and Reference Manager 11.0.

Results

32 articles were included from 351 potential publications. Low values of SDNN (RR 3.97 CI 95% 3.21-4.91, I2: 29.7%), VLF(RR 3.36 CI 95% 2,40-4,70 I2: 0%) and HRV index (RR 6,24 CI 95% 4,94-7,88 I2: 22,2%) were significantly associated with cardiac mortality. VLF (RR 2.83 CI 95% 2.40-3.35 I2: 15.3%) was the only index associated with total mortality. Both associations had high consistency during subgroups analysis that included, quality, year of publicaction and differents cut-off points.

Conclusions

Reduced HRV is a true prognostic marker for cardiac mortality in MI. In contrast VLF was significantly associated with total mortality. These indexes were consistently and significantly associated with each outcome.

graphic

The relationship between left ventricular scar and ventricular repolarisation in patients with coronary artery disease – insights from late gadolinium enhancement mri

Abstract

Introduction

The markers of ventricular repolarisation QTc, QT dispersion (QTD) and the Tpeak to Tend interval (Tpeak-end) are associated with ventricular arrhythmogenesis in long QT syndrome where the mechanistic link is well established. Such markers are also associated with the occurrence of sudden cardiac death (SCD) in the general population, though in this context the mechanistic link is less clear. The extent of LV scar quantified by late gadolinium enhancement cardiac magnetic resonance imaging (LGE-CMR) predicts the occurrence of ventricular arrhythmias in patients with coronary artery disease (CAD) and the role of scar in arrhythmogeneis is well established. Understanding the relationship between the extent of LV scar and ECG markers of repolarisation may help explain the mechanism underlying the association between the ECG markers and SCD in the non-channelopathy population.

The study aim was to evaluate the relationship between the markers of ventricular repolarisation - QTc, QTD and Tpeak-end - and the extent and distribution of LV scar in patients with CAD at high SCD risk.

Methods

We included 64 consecutive ICD recipients (66 ± 11 years, 80% male, median LVEF 30%) who had undergone LGE-CMR prior to device implantation over 4 years.

Scar was quantified using the CMR images and characterised in terms of percent LV scar and number of LV segments in a 17-segment model with quartiles (1-25%, 26-50%, 51-75% and 76-100%) of transmural scar. Repolarisation parameters were measured on an ECG performed prior to ICD implantation.

Results

In the study population mean QTc was 472 ± 56 ms, mean QTD 69 ± 45ms and mean Tpeak-end 85 ± 18ms. Fifty-eight patients (91%) had evidence of LV scar on the late enhancement images and the median amount of scar was 12.6% (5.9-21.2%). There was a significant association between the number of LV segments with subendocardial scar (1-25% transmurality) and markers of repolarization. The greater the number of segments of subendocardial scar the higher the value of QTc (p = 0.009), QTD (p = 0.026) and Tpeak-end (0.029). These associations remained significant when corrected for potential confounders (diabetes, amiodarone use, QRS width and LVEF) - QTc (P = 0.003), QTD (p = 0.002) and Tpeak-end (p = 0.008). However there was no association between any of the repolarisation variables and percent LV scar or the number of LV segments with scar greater than 25% transmurality.

Conclusion

In this study there was a strong association between the presence of subendocardial LV scar and prolonged QTc, QTD, and Tpeak-end. It may be that in some patients these ECG parameters are predictors of SCD due to their association with previous subendocardial myocardial infarction.

A systematic comparison of late gadolinium enhancement magnetic resonance imaging and left atrial endocardial voltage

Abstract

Introduction

Following catheter ablation of atrial fibrillation (AF), late gadolinium enhancement magnetic resonance imaging (LGE MRI) may be able to visualise areas of fibrosis and therefore reduced endocardial voltage. Unlike previous qualitative visual comparisons, we describe a new quantitative technique for comparison of left atrial (LA) endocardial voltage with 3D LGE MRI signal intensity and have applied it in patients undergoing repeat atrial ablation.

Methods

Ten patients who had previous catheter ablation for AF, and represented with either paroxysmal AF (n = 4) or atrial tachycardia (AT) (n = 6) underwent pre-ablation LGE MRI. A 3D LA reconstruction was created by projecting the LGE data on to a segmented LA shell (signal intensities were displayed as the number of standard deviations (SD) from the mean intensity of the atrial blood pool).

During the ablation procedure, high density (mean number of points: 368 ± 127) LA endocardial voltage maps were acquired in either sinus rhythm or AT using CARTO 3 (Biosense Webster).

The 3D LGE MRI reconstructions and endocardial voltage maps were manually segmented into LA regions (left and right WACA, roof, mitral line, anterior, posterior, inferior, septum and lateral) using custom-written software to derive the mean signal intensity and endocardial voltage for each segment.

Results

Mean LGE MRI signal intensity and endocardial voltage were derived for a total of 131 atrial segments in ten patients.

In the atrial segments in which the mean LGE MRI signal intensity was low (0 to 3 SD from the mean intensity of the atrial blood pool - ‘healthy’), the mean ± SD endocardial voltage was 0.86 ± 0.7 mV, whereas when the mean LGE MRI signal intensity was high (>3 SD - ‘scar’), the mean endocardial voltage was significantly lower at 0.51 ± 0.4 mV (p < 0.004) (Figure 1).

Top and middle rows: Corresponding posteroanterior (top) and superior (middle) views of a 3D LGE MRI (left; SD= number of standard deviations from mean intensity of atrial blood pool) and a CARTO endocardial voltage map (right) from two different patients. Bottom row: Graph showing endocardial voltage (mean +/− standard deviation) for low and high MRI signal intensities.
Figure 1

Top and middle rows: Corresponding posteroanterior (top) and superior (middle) views of a 3D LGE MRI (left; SD= number of standard deviations from mean intensity of atrial blood pool) and a CARTO endocardial voltage map (right) from two different patients. Bottom row: Graph showing endocardial voltage (mean +/− standard deviation) for low and high MRI signal intensities.

Conclusions

High LGE MRI signal intensity correlates with low endocardial voltage, however, low voltage can still occur in areas of low signal intensity on LGE MRI. Refinement of this technique is needed to permit non-invasive assessment of atrial substrate prior to repeat catheter ablation.

How studying at Master's level influences the professional practice of specialist nurses within an acute hospital trust

Abstract

Introduction

The theme for the study was to evaluate in reality how Master's level study impacts on the clinical practice of specialist nurses and on their perceptions as working professionals. Under consideration was whether the master's programmes available were relevant to specialist nurse roles. With this in mind the purpose of the study was to gain an in depth perspective of the impact and relevance of master's level study for the professional practice of specialist nurses within an acute hospital trust.

Method

An interpretive phenomenological design was chosen to reflect this, with a purposive sample of six participants. Participants were recruited following an invitation email to the entire specialist nurse group and the first six respondents that met the inclusion criteria chosen. Data was collected using semi-structured interviews and analysed using Burnard's (1991) thematic content analysis.

Results

Five categories emerged: reason's for undertaking Master's level study, relevance to clinical practice, enhancing career opportunities, experience of studying at Master's level and earlier nursing career perspective of Master's. Transpiring strongly was the drive within the author's organisation for specialist nurses to achieve Master's status and the strong leadership in place impelling developments in nursing academia. The practical utility of Master's degrees was particularly relevant and of most value. There was specific reference to the more nebulous modules and their associated relevance to clinical practice. The monumental task of completing a Master's degree was clear particularly in relation to the personal impact of studying at this level. All participants indicated that support both within their organisation and educational institute was deficient. Participant's clearly identified the changes that had taken place in nursing education influencing career development and progression. Participants who did not envisage studying at this level in their earlier careers had since recognised the national drive for advances in nursing academia as a vehicle to improve patient care.

Conclusion

The limitations of the study hinged upon two factors, explicitly time and funding. Both of which little could be done since the study was conducted as part of an educational programme, self-funded by the researcher. The sample size should not be considered a weakness as it was appropriate to the study design.

The development of extensive clinical knowledge was seen as fundamental adding depth to professional knowledge required in undertaking specialist nurse roles. Studying at this level placed great pressure on the students particularly in relation to personal development; support both from an organisational and academic level was an influential factor. The findings endorse the need to improve the support offered to specialist nurses undertaking Master's level study as a requirement of their advanced clinical roles.