Simone Savastano

Failure of implantable cardioverter-defibrillator leads: A matter of lead size?

BACKGROUND Small-diameter implantable cardioverter-defibrillator (ICD) Sprint Fidelis and Riata leads have been recalled owing to an increased risk of lead failure, thus arousing the suspicion that lead size might be a critical issue. OBJECTIVE To compare the incidence of failure of small-diameter (≤8 F) and standard-diameter (>8 F) ICD leads implanted in a single center. METHODS From January 2003 to December 2010, 190 Sprint Fidelis, 182 Riata/Riata ST, 99 Optim (Riata Optim/Durata), and 419 standard-diameter leads were implanted in our center. RESULTS During a median follow-up of 33 months, the overall failure rate was 6.3%. Follow-up duration was similar for Sprint Fidelis, Riata, and standard-diameter leads but shorter for the Optim group. The failure rate was significantly higher in Sprint Fidelis leads than in both standard-diameter (4.8%/year vs 0.8%/year; P<.001) and Riata/Riata ST (4.8%/year vs 2.6%/year; P = .03) leads. The incidence of lead failure in Riata/Riata ST leads proved significantly higher than in standard-diameter leads (2.6%/year vs 0.8%/year; P = .001). No cases of lead failure were recorded in the Optim group. On multivariable analyses, small-diameter (hazard ratio [HR] 5.03, 2.53-10.01, P<.001), Sprint Fidelis (HR 6.3, 3.1-13.3, P<.001), or Riata/Riata ST (HR 4.5, 1.9-10.5, P = .001) leads and age<60 years (HR 2.3, 1.3-4.3, P = .005) were found to independently increase the risk of lead failure. CONCLUSIONS Compared with standard-diameter leads, both Sprint Fidelis and Riata/Riata ST small-diameter ICD leads are at an increased risk of failure, although the incidence of events is significantly lower in the Riata than in the Sprint Fidelis group.

Positive trend in survival to hospital discharge after out-of-hospital cardiac arrest: a quantitative review of the literature

Background Seven editions of cardiopulmonary resuscitation (CPR) and emergency cardiovascular care guidelines have been published with many changes, in particular, about CPR. Objectives The aim of our study was to evaluate the temporal trend of survival to hospital discharge after out-of-hospital cardiac arrest (OHCA) as a possible effect of guidelines changes. Methods We searched PubMed for observational studies on ‘survival to hospital discharge after OHCA’. Survival to discharge was the primary outcome; prehospital return of spontaneous circulation and survival to hospital admission were our secondary endpoints. All data were analyzed according to the year of inclusion: group 1 before 2000; group 2 between 2000 and 2005; and group 3 after 2005. Mortality rates were compared between groups by means of a group frequency-weighted log-linear model. Results We considered 38 of 201 studies for a total of 156 301 patients. Survival to hospital discharge rate was 5.0% [95% confidence interval (CI) 4.9–5.2) in group 1; 6.1% (95% CI 5.9–6.4) in group 2; and 9.1% (95% CI 8.9–9.4) in group 3 (P < 0.001). A statistically significant decrease in risk of mortality in group 2 vs. group 1 (risk ratio 0.988, 95% CI 0. 985–0.0.992, P < 0.001) and in group 3 vs. group 2 (risk ratio 0.967, 95% CI 0.964–0.971, P < 0.001) was observed. Similar trends were observed for return of spontaneous circulation and survival to hospital admission. Conclusion Survival to hospital discharge after OHCA has significantly improved. Many aspects may influence survival, but surely, the reduction of time and an early and good quality CPR have positively influenced the outcome.

A comprehensive electrocardiographic, molecular, and echocardiographic study of Brugada syndrome: Validation of the 2013 diagnostic criteria

BACKGROUND The debate on the diagnostic value of high intercostal spaces (ICSs) and of the number of diagnostic leads in Brugada syndrome (BrS) has been settled by a recent expert consensus statement. OBJECTIVE To test the validity, and the underlying anatomy, of the new electrocardiographic (ECG) diagnostic criteria using echocardiographic, molecular, and clinical evidence in 1 clinical study population with BrS. METHODS We analyzed 114 patients with BrS and with a spontaneous or drug-induced type 1 ECG pattern recorded in 1 or more right precordial leads in fourth, third, and second ICSs. The right ventricular outflow tract (RVOT) was localized by using echocardiography. All probands were screened on the SCN5A gene. RESULTS The percentage of mutation carriers (MCs) and the event rate were similar regardless of the diagnostic ICS (fourth vs high ICSs: MCs 23% vs 19%; event rate 22% vs 28%) and the number of diagnostic leads (1 vs ≥2: MCs 20% vs 22%; event rate 22% vs 27%). The concordance between RVOT anatomical location and the diagnostic ICSs was 86%. The percentage of the diagnostic ECG pattern recorded was significantly increased by the exploration of the ICSs showing RVOT by echocardiography (echocardiography-guided approach vs conventional approach 100% vs 43%; P < .001). CONCLUSION The high ICSs are not inferior to the standard fourth ICS for the ECG diagnosis of BrS, and the interindividual variability depends on the anatomical location of the RVOT as assessed by using echocardiography. This approach significantly increases diagnostic sensitivity without decreasing specificity and fully supports the recently published new diagnostic criteria.

Pharmacological therapy following catheter ablation of atrial fibrillation.

Catheter ablation has been proven to be an effective treatment for patients with drug-resistant atrial fibrillation. Nevertheless its efficacy is limited to 60–80% of patients in different studies. Whether the use of pharmacological therapy after catheter ablation of atrial fibrillation might increase the procedural success rate is still a matter of debate. There is general agreement that antiarrhythmic drugs (AADs) are useful in the management of arrhythmias occurring in the very early period after catheter ablation (blanking period). On the contrary, limited data are available on the efficacy of AADs over a longer period. Some patients remain free of arrhythmia recurrences by the use of AADs that were ineffective before catheter ablation: whether this latter situation is to be considered a partial success of catheter ablation or a treatment failure, thus demanding a redo procedure, is still an open question. Some studies have also investigated the role of non-AADs [angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers, statins and corticosteroids] in preventing atrial fibrillation recurrences after catheter ablation, reporting conflicting results. Whereas there is a general consensus on the use of anticoagulation therapy in the first phase after catheter ablation, no definite data are available on the proper long-term management of anticoagulation therapy after catheter ablation. This review focuses on the still open issue of what is the optimal pharmacological treatment of patients after catheter ablation of atrial fibrillation.

End-tidal carbon dioxide and defibrillation success in out-of-hospital cardiac arrest

PURPOSE Basing on the relationship between the quality of cardiopulmonary resuscitation (CPR) and the responsiveness of VF to the defibrillation we aimed to assess whether the values of ETCO2 in the minute before defibrillation could predict the effectiveness of the shock. MATERIALS AND METHODS We retrospectively evaluated the reports generated by the manual monitor/defibrillator (Corpuls by GS Elektromedizinische Geräte G. Stemple GmbH, Germany) used for cases of VF cardiac arrest from January 2015 to December 2016. The mean ETCO2 value of the minute preceding the shock (METCO260) was computed. A blind evaluation of the effectiveness of each shock was provided by three cardiologists. RESULTS A total amount of 207 shocks were delivered for 62 patients. When considering the three tertiles of METCO260 (T1:METCO260 ≤ 20mmHg; T2: 20mmHg < METCO260 ≤ 31mmHg and T3: METCO260 > 31mmHg) a statistically significant difference between the percentages of shock success was found (T1: 50%; T2: 63%; T3: 78%; Chi square p=0.003; p for trend <0.001). When the METCO260 was lower than 7mmHg no shock was effective and when the METCO260 was higher than 45mmHg no shock was ineffective. Shocks followed by ROSC were preceded by higher values of METCO260 as compared either to ineffective shocks or effective ones without ROSC. CONCLUSIONS This is the first demonstration of the relation between ETCO2 and defibrillation effectiveness. Our findings stress the pivotal role of High Quality CPR, monitored via ETCO2, and suggest ETCO2 monitoring as an additional weapon to guide defibrillation.

Global T waves inversion and QT prolongation. An uncommon presentation of acute pulmonary embolism

This is the case of a man presenting to the emergency department for dyspnea. Despite a very common symptom he presented an uncommon twelve leads electrocardiogram (ECG). At a first glance it could have suggested an acute coronary syndrome, a Takotsubo cardiomyopathy or a hypertrophic cardiomyopathy. However the further investigations showed an acute pulmonary embolism (APE) whose pre-test probability was low with a Wells score of 0 and a Geneva simplified score of 1. Negative T waves have been described in APE, however, such a morphology associated with QT prolongation is a very rare presentation. This case confirms how the diagnosis of APE could be often insidious representing a challenge for the emergency physician.

Post ROSC pulse-oximetry derived perfusion index and thirty days survival after out-of-hospital cardiac arrest. New insights from the Pavia CARe (Pavia Cardiac Arrest Registry)

The perfusion index (PI) is the ratio of the pulsatile blood flow o the nonpulsatile or static blood in peripheral tissue thus it repesents a noninvasive measure of peripheral perfusion that can be ontinuously and noninvasively obtained from a pulse oximeter. eripheral PI has been proposed for different clinical uses with ome applications in critical patients [1–3]. No data are available bout cardiac arrest survivors, however It is likely that a good eripheral perfusion after the return of spontaneous circulation ROSC) could increase the chance of survival at least in the short erm. Our aim was to assess whether peripheral PI measured after OSC could predict thirty days survival after an out-of-hospital ardiac arrest (OHCA). To address our aim the reports from those atients who achieved ROSC generated by the manual monior/defibrillator (Corpuls by GS Elektromedizinische Geräte G. temple GmbH, Germany) after every case of OHCA were retropectively evaluated. The mean values of PI were automatically rovided in the report every minute from the ROSC onwards and he mean value of 30 min of monitoring (MPI30) was calculated. From January 2015 to December 2016 1501 patients have een enrolled in our OHCA registry (Pavia CARe); in 931 patients ardiopulmonary resuscitation was attempted and 156 patients howed a prehospital ROSC. Among these patients with prehospi-

La sindrome del QT lungo nella morte improvvisa infantile: una malattia diagnosticabile e curabile

Nei paesi occidentali la sindrome della morte improvvisa infantile (SIDS) rappresenta la causa principale di morte nel primo anno di vita. Le ipotesi finora formulate sulla patogenesi della SIDS rimandano ad un quadro di tipo multifattoriale, in cui fattori di rischio diversi cooperano sinergicamente. Tra le possibili cause non cardiache, sono stati indagati diversi aspetti genetici tra i quali quelli legati a fattori immunitari, neuromodulatori ed enzimatici, che risultano tuttavia di difficile definizione sul piano clinico, soprattutto alla luce di possibili interventi terapeutici. Al contrario e possibile svolgere un’azione preventiva in quei potenziali casi SIDS, riconducibili ad aritmie cardiache su base genetica. Tra le canalopatie, la sindrome del QT lungo riveste un ruolo molto importante, essendo responsabile di circa il 10% dei casi SIDS. Un semplice elettrocardiogramma, eseguito nelle prime settimane dopo la nascita, consente di fare diagnosi di sindrome del QT lungo, individuando quindi i neonati a piu alto rischio aritmico per i quali e possibile iniziare una terapia beta-bloccate, efficace nella prevenzione delle aritmie maligne.

La denervazione simpatica cardiaca sinistra nel trattamento della sindrome del QT lungo: un’opzione efficace e ben tollerata

La sindrome del QT lungo (LQTS) e una patologia genetica che espone ad un aumentato rischio di aritmie ventricolari maligne; ad oggi diversi presidi terapeutici sono applicabili nella prevenzione degli aventi aritmici. La terapia farmacologica, pur riducendo di molto il rischio aritmico, non e totalmente efficace soprattutto nelle forme piu severe di patologia. Il defibrillatore cardiaco impiantabile (ICD) e efficace nel cardiovertire prontamente le aritmie, ma non ne previene l’insorgenza: inoltre, l’accettazione dell’impianto di un ICD, soprattutto per i bambini, puo essere un processo difficile sia per l’impatto psicologico delle potenziali numerose scariche sia per le conseguenze a lungo termine della gestione medica. La denervazione simpatica cardiaca sinistra (LCSD) e un’opzione terapeutica efficace sia nella prevenzione degli eventi aritmici, soprattutto in pazienti sintomatici nonostante la terapia farmacologica massimale, che nel ridurre il numero di scariche dell’ICD. Inoltre, la LCSD presenta il vantaggio della sicurezza e della buona tollerabilita da parte del paziente; percio va considerata in alternativa o in associazione all’impianto di ICD in pazienti LQTS con alto rischio aritmico.

Modificatori genetici del rischio aritmico nella morte cardiaca improvvisa: dalla sindrome del QT lungo alle patologie cardiache più comuni

Gli studi sulla patogenesi della morte cardiaca improvvisa si sono concentrati sul rapporto tra background genetico individuale e suscettibilita aritmica. Questa relazione, inizialmente descritta nelle patologie cardiache ereditarie come la sindrome del QT lungo (LQTS), e stata poi estesa alla ricerca di fattori genetici modulanti il rischio aritmico (genetic modifiers) nella popolazione generale. La sindrome del QT lungo e una patologia aritmogena, che predispone a tachicardie ventricolari maligne e morte cardiaca improvvisa, il cui substrato patogenetico e costituito da mutazioni nei geni codificanti i canali ionici implicati nel potenziale d’azione cardiaco. Tuttavia, il quadro clinico dei pazienti LQTS spesso mostra una spiccata variabilita fenotipica, anche in portatori della stessa mutazione, suggerendo la presenza di altri fattori genetici modificanti il rischio aritmico. In questo senso, gli studi sulla sindrome del QT lungo possono rappresentare una risorsa fondamentale per l’identificazione di genetic modifiers in patologie cardiache piu comuni: infatti, e stato dimostrato come un polimorfismo nella popolazione caucasica (K897T), localizzato in gene codificante un canale ionico cardiaco, possa modulare il rischio aritmico sia nella sindrome del QT lungo che nella fase subacuta dell’infarto. Allo stesso modo l’individuazione di un particolare substrato genetico in grado di modificare la lunghezza dell’intervallo QT nella popolazione generale puo fornire utili indicazioni per la ricerca di nuovi target genetici nella sindrome del QT Lungo: l’esempio paradigmatico e rappresentato da alcune varianti genetiche comuni di NOS1AP. Tutti questi risultati suggeriscono la strada per future applicazioni cliniche dei genetic modifiers nella stratificazione del rischio aritmico individuale.