Joseph Galvin
Mater Misericordiae University Hospital
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Europace | 2010
Ronan Margey; McCann Ha; Gavin Blake; Edward Keelan; Joseph Galvin; Maureen Lynch; Niall Mahon; D. Sugrue; James O'Neill
AIMS To describe the incidence and management of cardiac device infection. Infection is a serious, potentially fatal complication of device implantation. The numbers of device implants and infections are rising. Optimal care of device infection is not well defined. METHODS AND RESULTS We retrospectively identified cases of device infection at our institution between 2000 and 2007 by multiple source record review, and active surveillance. Device infection was related to demographics, clinical, and procedural characteristics. Descriptive analysis was performed. From 2000 to 2007, a total of 2029 permanent pacemakers and 1076 biventricular/implantable cardioverter-defibrillators (ICDs) or ICDs were implanted. Thirty-nine cases of confirmed device infections were identified--27 pacemaker and 12 bivent/ICD or ICD infections, giving an infection rate of 1.25%. Median time from implant or revision to presentation was 150 days (range 2915 days, IQR25% 35-IQR75% 731). Ninety percent of patients presented with generator-site infections. The most common organism was methicillin-sensitive Staphylococcus aureus (30.8%), followed by coagulase negative Staphylococcus (20.5%). Complete device extraction occurred in 82%. Of these, none had relapse, and mortality was 7.4% (n = 2/27). With partial removal or conservative therapy (n = 13), relapse occurred in 67% (n = 8/12), with mortality of 8.4% (n = 1/12). Median duration of antibiotics was 42 days (range 47 days, IQR25% 28-IQR75% 42 days). Re-implantation of a new device occurred in 54%, at a median of 28 days (range 73 days, IQR25% 8.5-IQR75% 35 days). Methicillin-Resistant Staphylococcus Aureus infection predicted mortality (P < 0.004, RR 37, 95% CI 5.3-250). Median follow-up was 36 months. CONCLUSION Cardiac device infection is a rare complication, with significant morbidity and mortality. Complete hardware removal with appropriate duration of antimicrobial therapy results in the best outcomes for patients.
Europace | 2011
Ronan Margey; Andrew Roy; Sandra Tobin; Conor O'Keane; Catherine McGorrian; Valerie Morris; Siobhan Jennings; Joseph Galvin
INTRODUCTION Sudden cardiac death (SCD) in young people is a rare but devastating event for families and communities. Ireland has previously had no measure of the incidence of SCD in young people. We report the incidence and causes of SCD in persons <35 years of age. METHODS AND RESULTS We undertook a retrospective study of SCD between 2005 and 2007 in persons aged 15-35 years in the Republic of Ireland. We identified potential cases of out of hospital SCD through the Central Statistics Office (CSO) death certificate records. Autopsy, toxicology, and inquest reports were then obtained and analysed by an expert panel who adjudicated on the cause of death. A total of 342 potential SCD cases were identified through the CSO. Fifty were younger than 15 years of age, and 86 had either incomplete or unavailable post-mortem reports. Of 206 full reports obtained, 116 were adjudicated as cases of SCD. Cases were predominantly male (75%), with a mean age of 25.8 years (standard deviation 6.3). The incidence of SCD in this age range was 2.85 per 100,000 person-years (4.36 for males and 1.30 for females) and the incidence of sudden arrhythmic death syndrome (SADS) was 0.76 per 100,000 person-years. The commonest causes were SADS, 26.7% (31 of 116), followed by coronary artery disease, 20.7% (24 of 116), hypertrophic cardiomyopathy (HCM), 14.7% (17 of 116), and idiopathic left ventricular hypertrophy not fulfilling criteria for HCM, 10.3% (12 of 116). CONCLUSIONS The incidence of SCD in the young in Ireland was 4.96 (95% CI 3.06, 6.4) for males and 1.3 (95% CI 0.62, 2.56) for females per 100 000 person-years. Sudden arrhythmic death syndrome was the commonest cause of SCD in the young, and the incidence of SADS was more than five times that in official reports of the Irish CSO.
BMC Medical Genetics | 2013
Catherine McGorrian; Charlene McShane; Colin McQuade; Ted Keelan; Jim O’Neill; Joseph Galvin; Kevin M. Malone; Niall Mahon; Mary B. Codd
BackgroundFamily-based cardiac screening programmes for persons at risk for genetic cardiac diseases are now recommended. However, the psychological wellbeing and health related quality of life (QoL) of such screened patients is poorly understood, especially in younger patients. We sought to examine wellbeing and QoL in a representative group of adults aged 16 and over in a dedicated family cardiac screening clinic.MethodsProspective survey of consecutive consenting patients attending a cardiac screening clinic, over a 12 month period. Data were collected using two health measurement tools: the Short Form 12 (version 2) and the Hospital Anxiety and Depression Scale (HADS), along with baseline demographic and screening visit-related data. The HADS and SF-12v.2 outcomes were compared by age group. Associations with a higher HADS score were examined using logistic regression, with multi-level modelling used to account for the family-based structure of the data.ResultsThere was a study response rate of 86.6%, with n=334 patients providing valid HADS data (valid response rate 79.5%), and data on n=316 retained for analysis. One-fifth of patients were aged under 25 (n=61). Younger patients were less likely than older to describe significant depression on their HADS scale (p<0.0001), although there were overall no difference between the prevalence of a significant HADS score between the younger and older age groups (18.0% vs 20.0%, p=0.73). Significant positive associates of a higher HADS score were having lower educational attainment, being single or separated, and being closely related to the family proband. Between-family variance in anxiety and depression scores was greater than within-family variance.ConclusionsHigh levels of anxiety were seen amongst patients attending a family-based cardiac screening clinic.Younger patients also had high rates of clinically significant anxiety. Higher levels of anxiety and depression tends to run in families, and this has implications for family screening and intervention programmes.
Europace | 2013
Catherine McGorrian; Orla Constant; Nicola Harper; Catherine O'Donnell; Mary B. Codd; Edward Keelan; Andrew Green; James O'Neill; Joseph Galvin; Niall Mahon
AIMS Sudden arrhythmic death syndrome (SADS) occurs when a person suffers a sudden, unexpected death, with no cause found at postmortem examination. We aimed to describe the cardiac screening outcomes in a population of relatives of SADS victims METHODS AND RESULTS Prospective and retrospective cohort study of consecutive families attending the Family Heart Screening clinic at the Mater Misericordiae Hospital in Dublin, Ireland, from January 2007 to September 2011. Family members of SADS victims underwent a standard screening protocol. Adjunct clinical and postmortem information was sought on the proband. Families who had an existing diagnosis, or where the proband had epilepsy, were excluded. Of 115 families identified, 73 were found to fit inclusion criteria and were retained for analysis, with data available on 262 relatives. Over half of the screened family members were female, and the mean age was 38.6 years (standard deviation 15.6). In 22 of 73 families (30%), and 36 of 262 family members (13.7%), a potentially inheritable cause of SADS was detected. Of the population screened, 32 patients (12.2%) were treated with medication, and 5 (1.9%) have received implantable cardiac defibrillators. Of the five families with long QT syndrome (LQTS) who had a pathogenic gene mutation identified, three carried two such mutations. CONCLUSION In keeping with international estimates, 30% of families of SADS victims were found to have a potentially inherited cardiac disease. The most common positive finding was LQTS. Advances in postmortem standards and genetic studies may assist in achieving more diagnoses in these families.
Scientific Reports | 2015
Jillian P. Casey; Svein Isungset Støve; Catherine McGorrian; Joseph Galvin; Marina Blenski; Aimee M. Dunne; Sean Ennis; Francesca Brett; Mary D. King; Thomas Arnesen; Sally Ann Lynch
We report two brothers from a non-consanguineous Irish family presenting with a novel syndrome characterised by intellectual disability, facial dysmorphism, scoliosis and long QT. Their mother has a milder phenotype including long QT. X-linked inheritance was suspected. Whole exome sequencing identified a novel missense variant (c.128 A > C; p.Tyr43Ser) in NAA10 (X chromosome) as the cause of the family’s disorder. Sanger sequencing confirmed that the mutation arose de novo in the carrier mother. NAA10 encodes the catalytic subunit of the major human N-terminal acetylation complex NatA. In vitro assays for the p.Tyr43Ser mutant enzyme showed a significant decrease in catalytic activity and reduced stability compared to wild-type Naa10 protein. NAA10 has previously been associated with Ogden syndrome, Lenz microphthalmia syndrome and non-syndromic developmental delay. Our findings expand the clinical spectrum of NAA10 and suggest that the proposed correlation between mutant Naa10 enzyme activity and phenotype severity is more complex than anticipated; the p.Tyr43Ser mutant enzyme has less catalytic activity than the p.Ser37Pro mutant associated with lethal Ogden syndrome but results in a milder phenotype. Importantly, we highlight the need for cardiac assessment in males and females with NAA10 variants as both patients and carriers can have long QT.
Europace | 2011
Ronan Margey; Lisa Browne; Eamonn Murphy; Martin O'Reilly; Niall Mahon; Gavin Blake; McCann Ha; D. Sugrue; Joseph Galvin
AIMS Out-of-hospital cardiac arrest (OOHCA) survival remains poor, estimated at 3-7%. We aim to describe the incidence of OOHCA, survival from OOHCA, and the impact of improved pre-hospital care on survival from OOHCA. METHODS AND RESULTS A retrospective registry was established using multi-source information to assess survival from cardiac arrest following the introduction of several improvements in pre-hospital emergency medical care from 2003. Survival from OOHCA, from asystole/pulseless electrical activity, and from ventricular tachycardia/ventricular fibrillation was estimated. Adjusted per 100 000 population annual incidence rates from national population census data were calculated. Mean and median emergency medical services (EMS) response times to OOHCA calls were assessed. A total of 962 OOHCAs occurred from 1 January 2003 until 31 December 2008. Sixty-nine per cent (69%, n = 664) were male. Seventy-two per cent (72%, n = 693) occurred at home with 28% occurring in a public venue. Of these public venues, 33.9% (91 of 268) had an automated external defibrillator available. Bystander cardiopulmonary resuscitation (CPR) was in progress when emergency services arrived in 11% (n = 106) of the cases. Nineteen per cent (19.4%, n = 187) had a known prior cardiac history or chest pain prior to circulatory collapse. Overall survival to hospital discharge improved significantly from 2.6 to 11.3%, P = 0.001. Survival from ventricular fibrillation (VF) to hospital admission, rose from 28.6 to 86.3%, P = 0.001. Survival to hospital discharge from VF improved from 21.4 to 33%, P = 0.007. Mean EMS response times to the scene of arrest decreased from 9.18 to 8.34 min. Emergency medical services scene time, reflecting acute pre-hospital medical care, rose from 14.46 to 18.12 min. The adjusted incidence of OOHCA for our catchment population declined from 109.4 to 88.2 per 100,000 population between 2003 and 2008. CONCLUSIONS The incidence of OOHCA has declined but importantly, survival to hospital discharge has improved dramatically. Reduction in ambulance response time, resulting in earlier initiation of basic and advanced life support and earlier defibrillation, was associated with an increase in the proportion of victims found in VF rather than asystole and likely accounted for most of the improvement. Further improvements in response times and public education to improve bystander CPR rates should remain a priority.
American Journal of Roentgenology | 2010
Darra T. Murphy; Suzanne C. Shine; Andrea Cradock; Joseph Galvin; Edward Keelan; John G. Murray
OBJECTIVE Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a cause of sudden cardiac death in otherwise healthy young adults. This article outlines the spectrum of MRI findings in ARVC using a combination of static and cine images. CONCLUSION The detection of right ventricular enlargement, fatty infiltration, fibrosis, and wall motion abnormalities at MRI is useful in the diagnosis of ARVC.
BMC Cardiovascular Disorders | 2013
Catherine McGorrian; Sarah Lyster; Andrew Roy; Heloise Tarrant; Mary B. Codd; Peter Doran; Maria Fitzgibbon; Joseph Galvin; Niall Mahon
BackgroundHypertrophic cardiomyopathy (HCM) is a genetic condition, and relatives of affected persons may be at risk. Cardiac troponin biomarkers have previously been shown to be elevated in HCM. This study examines the new highly-sensitive cardiac troponin I (hsTnI) assay in a HCM screening population.MethodsNested case–control study of consecutive HCM sufferers and their relatives recruited from May 2010 to September 2011. After informed consent, participants provided venous blood samples and clinical and echocardiographic features were recorded. Associations between the natural log (ln) of the contemporary troponin I (cTnI) and hsTnI assays and markers of cardiac hypertrophy were examined. Multiple regression models were fitted to examine the predictive ability of hsTnI for borderline or definite HCM.ResultsOf 107 patients, 24 had borderline and 19 had definite changes of HCM. Both TnI assays showed significant, positive correlations with measures of cardiac muscle mass. After age and sex adjustment, the area under the receiver operator characteristic (AUROC) curve for the outcome of HCM was 0.78, 95% CI [0.65, 0.90], for ln(hsTnI), and 0.66, 95% CI [0.51, 0.82], for ln(cTnI) (p=0.11). Including the hsTnI assay in a multiple-adjusted “screening” model for HCM resulted in a non-significant improvement in both the AUROC and integrated discrimination index.ConclusionsBoth cTnI and hsTnI show a graded, positive association with measures of cardiac muscle mass in persons at risk of HCM. Further studies will be required to evaluate the utility of these assays in ECG- and symptom-based identification of HCM in at-risk families.
Clinical Research in Cardiology | 2018
Katie A. Walsh; Joseph Galvin; John F. Keaney; Edward Keelan; Gábor Széplaki
AimsZero- and near-zero-fluoroscopic ablation techniques reduce the harmful effects of ionizing radiation during invasive electrophysiology procedures. We aimed to test the feasibility and safety of a zero-fluoroscopic strategy using a novel integrated magnetic and impedance-based electroanatomical mapping system for radiofrequency ablation (RFA) of supraventricular tachycardias (SVTs).MethodsWe retrospectively studied 92 consecutive patients undergoing electrophysiology studies with/without RFA for supraventricular tachycardia (SVT) performed by a single operator at a single center. The first 42 (Group 1) underwent a conventional fluoroscopic-guided approach and the second 50 (Group 2) underwent a zero-fluoroscopic approach using the Ensite Precision™ 3-D magnetic and impedance-based mapping system (Abbott Inc).ResultsGroup 1 comprised 14 AV-nodal re-entrant tachycardia (AVNRT), 12 typical atrial flutter, 4 accessory pathway (AP), 2 atrial tachycardia (AT), and 9 diagnostic EP studies (EPS). Group 2 comprised 16 AVNRT, 17 atrial flutter, 6 AP, 3 AT, 2 AV-nodal ablations, and 7 EPS. A complete zero-fluoroscopic approach was achieved in 94% of Group 2 patients. All procedures were acutely successful, and no complications occurred. There was a significant reduction in fluoroscopy dose, dose area product, and time (p < 0.0001, for all), with no difference in procedure times. Ablation time for typical atrial flutter was shorter in Group 2 (p = 0.006).ConclusionsA zero-fluoroscopic strategy for diagnosis and treatment of SVTs using this novel 3D-electroanatomical mapping system is feasible in majority of patients, is safe, reduces ionizing radiation exposure, and does not compromise procedural times, success rates, or complication rates.
Clinical Research in Cardiology | 2018
Katie A. Walsh; Joseph Galvin; John F. Keaney; Edward Keelan; Gábor Széplaki
Catheter ablation of symptomatic premature atrial complexes (PACs) can be challenging, but the use of a 3D-electroanatomical mapping systems might improve accuracy [1]. Ultra-high-density (HD) mapping during routine atrial ablations leads to rapid and accurate generation of the electroanatomical maps [2]. We report on a case of a 72-year-old mildly overweight male patient (body mass index of 27.1 kg/ m2), with a history of coronary artery disease, percutaneous intervention to the left anterior descending artery and hypertension, who presented with high burden of symptomatic PACs (27% on Holter ECG monitor). Surface ECG P-wave morphology was almost identical to sinus p-waves, suggesting high right atrial or superior vena cava or right superior pulmonary vein origin (Fig. 1a). Continuous, automatic ultra-HD activation mapping of the left and right atrium (RA) during PACs was performed (Orion mapping catheter, Rhythmia, Boston Scientific). Typically, with this system, a second timing reference is sufficient to discriminate between atrial rhythms; however, this metric was insufficient due to the proximity of the PAC to the sinus node and the distance of the reference catheter. The PACs were automatically detected and discriminated from sinus rhythm using a strict ‘ECG Morphology Reference’ criterion (typically used for ventricular mapping), where a template of the PAC was compared with subsequent beats (Fig. 1b, PAC template—yellow, rejected sinus beat— white). Using this tool, the user can determine a tolerance level for the match of the template to the actual beat. The points are included in the map if they fulfil the match criteria and the electrograms are within 2 mm of the surface of the geometry. Moreover, in this case, ventricular beat overlap (to detect different PR intervals), respiratory, and motion filters were also used. In summary, the following settings were applied: 5 mm for propagation reference, 0.18 for ECG reference, 1 mm for motion, final 50% end expiration for respiration, 3 for tracking, and 23 ms for ventricular overlap beat metric. The system accurately identified the focus at the high lateral RA (panel C, signals from the mapping catheter in panel D and signals from ablation catheter in panel E), in close vicinity of the sinus node, where a single radiofrequency application (red dots) resulted in automaticity and immediate termination of PACs (43 °C and 30W limit, 30 s, white dots represent consolidation ablation points). The use of activation sequence mapping only would likely be inaccurate in this case. The patient was completely asymptomatic at the 6-month follow-up visit, with 0.8% PAC burden on the Holter. To our knowledge, this is the first known report using an ECG matching criterion with 3D mapping to automatically discriminate between sinus rhythm and a PAC focus, in such close proximity to the sinus node. Ultra-HD mapping allows accurate identification of the substrate for atrial arrhythmias [3–6]. The use of multiple discrimination algorithms, including ECG morphology analysis might be able to improve the accuracy of PAC mapping.