ObjectivePresentations of non-cardiac chest pain (NCCP) to the emergency department (ED) are increasing. More knowledge of prognosis and healthcare utilisation of patients with NCCP is necessary to optimise their management.MethodsThis study is a prospective, observational, prevalence-based cohort study conducted from September 2015 to February 2016 with 1-year follow-up including all patients 18 years and older referred to the ED with chest pain. Discharge diagnoses, mortality, major adverse cardiac events (MACE), re-presentations to the ED, hospitalisations, cardiac interventions and outpatient monitoring were assessed.ResultsMore than 60% of the 1239 patients presenting with chest pain were discharged with NCCP. The all-cause 1-year mortality rate of patients with NCCP was 2.3% compared with 7.2% in patients with cardiac chest pain (CCP) (p<0.001) and the occurrence of MACE was 5.1% vs 8.3%, respectively (p=0.026). Previous history of coronary artery disease (CAD) in patients with NCCP was identified as a predictive factor for MACE (OR 4.30 (95% CI 1.24 to 14.89), p=0.021). Patients with NCCP had more non-invasive interventions than patients with CCP (proportion of 0.225 vs 0.165 per patient, p<0.001) and 13.7% of patients with NCCP re-presented at the ED within 1 year.ConclusionThe majority of patients referred to the ED with chest pain are discharged with NCCP. The prognosis of patients with NCCP is better than patients with CCP; however, they are at risk for MACE due to a history of CAD. Patients with NCCP moreover use a substantial amount of medical resources, stressing the importance of good triage to minimise unnecessary healthcare utilisation while still preventing MACE.
Ventricular arrhythmias, consisting of single ectopic beats (sEB), multiple EB (mEB), and Torsades de Pointes (TdP, defined as >5 beats with QRS vector twisting around isoelectric line) can be induced in the anesthetized chronic AV-block (CAVB) dog by dofetilide (IKr-blocker). The interplay between temporal dispersion of repolarization, quantified as short-term variability (STV), and spatial dispersion of repolarization (SDR) in the initiation and perpetuation of these arrhythmias remains unclear. Five inducible (>3 TdPs/10') CAVB dogs were observed for 10' from the start of dofetilide infusion (0.025mg/kg, 5'). An intracardiac decapolar electrogram (EGM) catheter and 30 intramural cardiac needles in the left ventricle (LV) were introduced. STVARI was derived from 31 consecutive activation recovery intervals (ARI) on the intracardiac EGM, using the formula: . The mean SDR3D in the LV was determined as the three-dimensional repolarization time differences between the intramural cardiac needles. Moments of measurement included baseline (BL) and after dofetilide infusion prior to first 1) sEB (occurrence at 100±35"), 2) mEB (224±96"), and 3) non self-terminating TdP (454±298"). STVARI increased from 2.15±0.32ms at BL to 3.73±0.99ms* prior to the first sEB and remained increased without further significant progression to mEB (4.41±0.45ms*) and TdP (5.07±0.84ms*) (*p<0.05 compared to BL). SDR3D did not change from 31±11ms at BL to 43±13ms prior to sEB, but increased significantly prior to mEB (68±7ms*) and to TdP (86±9ms*+) (+p<0.05 compared to sEB). An increase in STV contributes to the initiation of sEB whereas an increase in SDR is important for the perpetuation of non self-terminating TdPs.
Ventricular remodelling can make the heart more susceptible to ventricular arrhythmias like torsades de pointes. Understanding the underlying mechanisms of initiation of ventricular arrhythmias and the determining factors for its severity has the potential to uncover new interventions. Beat-to-beat variation of repolarisation, quantified as short-term variability of repolarisation (STV), has been identified as an important factor contributing to arrhythmogenesis. This article provides an overview of experimental data about STV in relation to the initiation of torsades de pointes in a canine model of complete chronic atrioventricular block susceptible to torsades de pointes arrhythmias. Furthermore, it explores STV in relation to the severity of the arrhythmic outcome.
BACKGROUND The anesthetized, complete chronic atrioventricular block (CAVB) dog model allows reproducible inducibility of torsades de pointes (TdP) arrhythmias due to ventricular remodeling and after a challenge with an I Kr blocker. High-rate pacing (HRP) prevents ventricular arrhythmias but has long-term detrimental effects on cardiac function when applied continuously. Temporal dispersion of repolarization, quantified as short-term variability (STV), increases before ventricular arrhythmias and has been proposed as a marker to guide HRP.OBJECTIVE The purpose of this proof-of-principle study was to show that automatically determined STV can guide HRP to prevent imminent ventricular arrhythmias.METHODS Eight CAVB dogs were implanted with an implantable cardioverter-defibrillator (ICD) with software to automatically determine STV (STV ICD ) in real time. During HRP, STV was measured offline from right ventricular (RV) electrograms (EGMs) and left ventricular (LV) monophasic action potential durations (MAPDs) (STV RV,EGM/LV,MAPD ). The CAVB dogs were challenged twice with dofetilide (0.025 mg/kg intravenously over 5 minutes or until the first TdP). In experiment 1, the individual STV ICD threshold before the first arrhythmic event was determined and programmed into the ICD. In experiment 2, HRP with 100 bpm was initiated automatically once the STV ICD threshold was reached. RESULTSIn experiment 1, 8 of 8 dogs had repetitive TdP, and STV ICD increased from 0.96 6 0.42 ms to 2.10 6 1.26 ms (P ,.05). In experiment 2, all dogs reached the STV threshold. HRP decreased STV RV,EGM/LV,MAPD from 2.02 6 1.12 ms to 0.78 6 0.28 ms, which was accompanied by prevention of TdP in 7 of 8 dogs.CONCLUSION STV can guide HRP automatically by an ICD to prevent ventricular arrhythmias.
Background Short‐term variability of the QT interval (STV QT ) has been proposed as a novel electrophysiological marker for the prediction of imminent ventricular arrhythmias in animal models. Our aim is to study whether STV QT can predict imminent ventricular arrhythmias in patients. Methods and Results In 2331 patients with primary prophylactic implantable cardioverter defibrillators, 24‐hour ECG Holter recordings were obtained as part of the EU‐CERT‐ICD (European Comparative Effectiveness Research to Assess the Use of Primary Prophylactic Implantable Cardioverter Defibrillators) study. ECG Holter recordings showing ventricular arrhythmias of >4 consecutive complexes were selected for the arrhythmic groups (n=170), whereas a control group was randomly selected from the remaining Holter recordings (n=37). STV QT was determined from 31 beats with fiducial segment averaging and calculated as , where D n represents the QT interval. STV QT was determined before the ventricular arrhythmia or 8:00 am in the control group and between 1:30 and 4:30 am as baseline. STV QT at baseline was 0.84±0.47 ms and increased to 1.18±0.74 ms ( P <0.05) before the ventricular arrhythmia, whereas the STV QT in the control group remained unchanged. The arrhythmic patients were divided into three groups based on the severity of the arrhythmia: (1) nonsustained ventricular arrhythmia (n=32), (2) nonsustained ventricular tachycardia (n=134), (3) sustained ventricular tachycardia (n=4). STV QT increased before nonsustained ventricular arrhythmia, nonsustained ventricular tachycardia, and sustained ventricular tachycardia from 0.80±0.43 ms to 1.18±0.78 ms ( P <0.05), from 0.90±0.49 ms to 1.14±0.70 ms ( P <0.05), and from 1.05±0.22 ms to 2.33±1.25 ms ( P <0.05). This rise in STV QT was significantly higher in sustained ventricular tachycardia compared with nonsustained ventricular arrhythmia (+1.28±1.05 ms versus +0.24±0.57 ms [ P <0.05]) and compared with nonsustained ventricular arrhythmia (+0.34±0.87 ms [ P <0.05]). Conclusions STV QT increases before imminent ventricular arrhythmias in patients, and the extent of the increase is associated with the severity of the ventricular arrhythmia.
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