Bivalirudin is superior to heparins alone with bailout GP IIb/IIIa inhibitors in patients with ST-segment elevation myocardial infarction transported emergently for primary percutaneous coronary intervention: a pre-specified analysis from the EUROMAX trial.

AIMS: In the HORIZONS trial, in-hospital treatment with bivalirudin reduced bleeding and mortality in primary percutaneous coronary intervention (PCI) compared with heparin and routine glycoprotein IIb/IIIa inhibitors (GPI). It is unknown whether this advantage of bivalirudin is observed in comparison with heparins only with GPI used as bailout. METHODS AND RESULTS: In the EUROMAX study, 2198 patients with ST-segment elevation myocardial infarction (STEMI) were randomized during transport for primary PCI to bivalirudin or to heparins with optional GPI. Primary and principal outcome was the composites of death or non-CABG-related major bleeding at 30 days. This pre-specified analysis compared patients receiving bivalirudin (n = 1089) with those receiving heparins with routine upstream GPI (n = 649) and those receiving heparins only with GPI use restricted to bailout (n = 460). The primary outcome death and major bleeding occurred in 5.1% with bivalirudin, 7.6% with heparin plus routine GPI (HR 0.67 and 95% CI 0.46-0.97, P = 0.034), and 9.8% with heparins plus bailout GPI (HR 0.52 and 95% CI 0.35-0.75, P = 0.006). Following adjustment by logistic regression, bivalirudin was still associated with significantly lower rates of the primary outcome (odds ratio 0.53, 95% CI 0.33-0.87) and major bleeding (odds ratio 0.44, 95% CI 0.24-0.82) compared with heparins alone with bailout GPI. Rates of stent thrombosis were higher with bivalirudin (1.6 vs. 0.6 vs. 0.4%, P = 0.09 and 0.09). CONCLUSION: Bivalirudin, started during transport for primary PCI, reduces major bleeding compared with both patients treated with heparin only plus bailout GPI and patients treated with heparin and routine GPI, but increased stent thrombosis.

Low-tilt monophasic and biphasic waveforms compared with standard biphasic waveforms in the transvenous defibrillation of ventricular fibrillation.

BACKGROUND: Commercially available implantable defibrillators utilize a high-tilt waveform. Studies in atrial fibrillation and transthoracic defibrillation of ventricular fibrillation (VF) have shown improved defibrillation efficacy using low-tilt (LT) waveforms. We investigated the feasibility, efficacy, and safety of a LT waveform in the transvenous defibrillation of VF and hypothesized that it would be more efficacious than standard tilted biphasic (STB) waveforms. METHODS AND RESULTS: The investigation was performed in four phases in a porcine model: an efficacy study of LT monophasic waveforms (n = 9), an efficacy study of LT biphasic waveforms (n = 9), a comparison study between the most successful LT waveforms and clinically available STB waveforms (n = 15), and a safety study (n = 9). A total of 1,056 shocks were delivered (phase 1: 288, phase 2: 288, phase 3: 480). The LT biphasic 8/4-ms waveform was significantly more likely to successfully defibrillate than the LT monophasic and STB waveforms with an odds ratio of 122.3 (95% confidence interval: 32.5, 460.2, P < 0.001). The calculated defibrillation threshold (E50) for the LT 8/4-ms waveform was 12.7 J compared to 43.5 J and 45.5 J for STB waveforms 6/6 ms and 8/4 ms, respectively, and 47.7 J for LT 12-ms waveform. The LT 8/4-ms waveform had no lasting detrimental effect on cardiac function, and any transient hemodynamical or biochemical changes observed were comparable to those observed with STB waveforms. CONCLUSION: LT waveforms are effective and appear safe in transvenous defibrillation in a porcine model of VF. The LT biphasic 8/4-ms waveform is more efficacious than conventional waveforms.

Temporal analysis of continuous chest compression rate and depth performed by firefighters during out of hospital cardiac arrest.

BACKGROUND: Quality of chest compressions (CC) during cardiopulmonary resuscitation (CPR) often do not meet guideline recommendations for rate and depth. This may be due to the fatiguing nature of physically compressing a patient's chest, meaning that CPR quality reduces over time. OBJECTIVE: This analysis investigates the effect of CPR duration on the performance of continuous CCs delivered by firefighters equipped with CPR feedback devices. METHODS: Data were collected from a first responder group which used CPR feedback and automatic external defibrillator devices when attending out-of-hospital cardiac arrest events. Depth and rate of CC were analysed for 134 patients. Mean CC depth and rate were calculated every 5 s during two-minute episodes of CPR. Regression models were created to evaluate the relationship between applied CC depth and rate as a function of time. RESULTS: Mean (SD) CC depth during the investigation was 48 (9) mm. An inverse relationship was observed between CC depth and CPR duration, where CC depth decreased by 3.39 mm, over two-minutes of CPR (p < 0.001). Mean (SD) CC rate was 112.06 (5.87) compressions per minute. No significant relationship was observed between CC rate and CPR duration (p = 0.077). Mean depth was within guideline range for 33.58% of patient events, while guideline rate was observed in 92.54% of cases. CONCLUSIONS: A reduction in CC depth was observed during two-minutes of continuous CCs while CC rate was not affected. One third of patients received a mean CC depth within guideline range (50 to 60 mm).

Thrombolysis during resuscitation for out-of-hospital cardiac arrest.

BACKGROUND: Approximately 70% of persons who have an out-of-hospital cardiac arrest have underlying acute myocardial infarction or pulmonary embolism. Therefore, thrombolysis during cardiopulmonary resuscitation may improve survival. METHODS: In a double-blind, multicenter trial, we randomly assigned adult patients with witnessed out-of-hospital cardiac arrest to receive tenecteplase or placebo during cardiopulmonary resuscitation. Adjunctive heparin or aspirin was not used. The primary end point was 30-day survival; the secondary end points were hospital admission, return of spontaneous circulation, 24-hour survival, survival to hospital discharge, and neurologic outcome. RESULTS: After blinded review of data from the first 443 patients, the data and safety monitoring board recommended discontinuation of enrollment of asystolic patients because of low survival, and the protocol was amended. Subsequently, the trial was terminated prematurely for futility after enrolling a total of 1050 patients. Tenecteplase was administered to 525 patients and placebo to 525 patients; the two treatment groups had similar clinical profiles. We did not detect any significant differences between tenecteplase and placebo in the primary end point of 30-day survival (14.7% vs. 17.0%; P=0.36; relative risk, 0.87; 95% confidence interval, 0.65 to 1.15) or in the secondary end points of hospital admission (53.5% vs. 55.0%, P=0.67), return of spontaneous circulation (55.0% vs. 54.6%, P=0.96), 24-hour survival (30.6% vs. 33.3%, P=0.39), survival to hospital discharge (15.1% vs. 17.5%, P=0.33), or neurologic outcome (P=0.69). There were more intracranial hemorrhages in the tenecteplase group. CONCLUSIONS: When tenecteplase was used without adjunctive antithrombotic therapy during advanced life support for out-of-hospital cardiac arrest, we did not detect an improvement in outcome, in comparison with placebo. (ClinicalTrials.gov number, NCT00157261.)

Heart fatty acid-binding protein in combination with the 80-lead body surface potential map improves early detection of acute myocardial infarction in patients who are cardiac troponin T-negative at presentation.

UNLABELLED: Of patients who present with ischemic-type chest pain and a negative cardiac troponin T (cTnT) at first medical contact, there are patients at a very early stage of infarction. The aim of this research was to assess heart fatty acid-binding protein (H-FABP), a novel marker of myocyte necrosis, in combination with the 80-lead body surface potential map (BSPM) in the early diagnosis of acute myocardial infarction (AMI). METHODS: In this prospective study, consecutive patients presenting with acute ischemic-type chest pain between 2003 and 2006 were enrolled. At first medical contact, blood was sampled for cTnT and H-FABP; in addition, a 12-lead electrocardiogram (ECG) and BSPM were recorded. A second cTnT was sampled 12 hours or more after presentation. Peak cTnT 0.03 µg/L or higher diagnosed AMI. Elevated H-FABP was 5 ng/mL or higher. A cardiologist blinded to both the clinical details and 12-lead ECG interpreted the BSPM. RESULTS: Enrolled were 407 patients (age 62 ± 13 years; 70% men). Of these 407, 180 had cTnT less than 0.03 µg/L at presentation. Acute myocardial infarction occurred in 52 (29%) of 180 patients. Of these 180 patients, 27 had ST-segment elevation (STE) on ECG, 104 had STE on BSPM (sensitivity, 88%; specificity, 55%), and 95 (53%) had H-FABP elevation. The proportion with elevated H-FABP was higher in the AMI group compared with non-AMI group (P < .001). Body surface potential map STE was significantly associated with H-FABP elevation (P < .001). Of those with initial cTnT less than 0.03 µg/L, the c-statistic for the receiver operating characteristic curve distinguishing AMI from non-AMI using H-FABP alone was 0.644 (95% confidence interval [CI], 0.521-0.771), using BSPM alone was 0.716 (95% CI, 0.638-0.793), and using the combination of BSPM and H-FABP was 0.812 (95% CI, 0.747-0.876; P < .001). CONCLUSION: In patients with acute ischemic-type chest pain who have a normal cTnT at presentation, the combination of H-FABP and BSPM at first assessment identifies those with early AMI (c-statistic, 0.812; P < .001), thus allowing earlier triage to reperfusion therapy and secondary prevention.

Real-world insight into public access defibrillator use over five years.

BACKGROUND: Public access defibrillators (PADs) represent unique life-saving medical devices as they may be used by untrained lay rescuers. Collecting representative clinical data on these devices can be challenging. Here, we present results from a retrospective observational cohort study, describing real-world PAD utilisation over a 5-year period. METHODS: Data were collected between October 2012 and October 2017. Responders voluntarily submitted electronic data downloaded from HeartSine PADs, and patient demographics and other details using a case report form in exchange for a replacement battery and electrode pack. RESULTS: Data were collected for 977 patients (692 males, 70.8%; 255 females, 26.1%; 30 unknown, 3.1%). The mean age (SD) was 59 (18) years (range <1 year to 101 years). PAD usage occurred most commonly in homes (n=328, 33.6%), followed by public places (n=307, 31.4%) and medical facilities (n=128, 13.1%). Location was unknown in 40 (4.09%) events. Shocks were delivered to 354 patients. First shock success was 312 of 350 patients where it could be determined (89.1%, 95% CI 85.4% to 92.2%). Patients with reported response times ≤5 min were more likely to survive to hospital admission (89/296 (30.1%) vs 40/250 (16.0%), p<0.001). Response time was unknown for 431 events. CONCLUSION: This is the first study to report global PAD usage in voluntarily submitted, unselected real-world cases and demonstrates the real-world effectiveness of PADs, as confirmed by first shock success.

Body surface mapping vs 12-lead electrocardiography to detect ST-elevation myocardial infarction.

A prospective, multicenter trial was conducted in patients with nontraumatic chest pain in 4 hospitals to determine whether an 80-lead body surface map electrocardiogram system (80-lead BSM ECG) improves detection of ST-segment elevation in acute myocardial infarction (STEMI) compared with a standard 12-lead electrocardiogram (ECG) in an emergency department (ED) setting. A trained ED or cardiology staff member (technician or nurse) recorded a 12-lead ECG and 80-lead BSM ECG from each subject at initial presentation. Serial biomarkers (total creatine kinase [CK], CK-MB, and/or troponin) were obtained according to individual hospital practice. Of the 647 patients evaluated, 589 had available biomarkers results. Eighty-lead BSM ECG improved detection of biomarker-confirmed STEMI compared with the 12-lead ECG for CK-MB-defined STEMI (100% vs 72.7%, P = .031; n = 364) or troponin-defined STEMI (92.9% vs 60.7%, P = .022; n = 225). Specificity for STEMI was high (range, 94.9%-97.1%) with no significant difference between 80-lead BSM ECG and 12-lead ECG. Right ventricular involvement complicating inferior STEMI was detected by 80-lead BSM ECG in 2 (22%) of 9 patients with CK-MB-defined MI and in 2 (22%) of 9 patients with troponin-defined MI. The infarct location missed most commonly on 12-lead ECG but detected by 80-lead BSM ECG was inferoposterior MI. We conclude that BSM using 80-lead BSM ECG is more sensitive for detection of STEMI than 12-lead ECG, while retaining similar specificity.

Novel biomarkers in early diagnosis of acute myocardial infarction compared with cardiac troponin T.

AIMS: To evaluate the role of novel biomarkers in early detection of acute myocardial infarction (MI) in patients admitted with acute chest pain. METHODS AND RESULTS: A prospective study of 664 patients presenting to two coronary care units with chest pain was conducted over 3 years from 2003. Patients were assessed on admission: clinical characteristics, ECG (electrocardiogram), renal function, cardiac troponin T (cTnT), heart fatty acid binding protein (H-FABP), glycogen phosphorylase-BB, NT-pro-brain natriuretic peptide, D-dimer, hsCRP (high sensitivity C-reactive protein), myeloperoxidase, matrix metalloproteinase-9, pregnancy associated plasma protein-A, soluble CD40 ligand. A > or = 12 h cTnT sample was also obtained. MI was defined as cTnT > or = 0.03 microg/L. In patients presenting <4 h of symptom onset, sensitivity of H-FABP for MI was significantly higher than admission cTnT (73 vs. 55%; P = 0.043). Specificity of H-FABP was 71%. None of the other biomarkers challenged cTnT. Combined use of H-FABP and cTnT (either one elevated initially) significantly improved the sensitivities of H-FABP or cTnT (85%; P < or = 0.004). This combined approach also improved the negative predictive value, negative likelihood ratio, and the risk ratio. CONCLUSION: Assessment of H-FABP within the first 4 h of symptoms is superior to cTnT for detection of MI, and is a useful additional biomarker for patients with acute chest pain.

Improving the Diagnosis of Culprit Left Circumflex Occlusion With Acute Myocardial Infarction in Patients With a Nondiagnostic 12-Lead ECG at Presentation: A Retrospective Cohort Study.

Background Left circumflex culprit is often missed by the standard 12-lead ECG . Extended lead systems (body surface potential map [ BSPM ]) should improve the diagnosis of culprit left circumflex stenosis with myocardial infarction. Methods and Results Retrospective analysis of a hospital research registry (August 2000-August 2010) comprising consecutive patients with (1) ischemic-type chest pain at rest; (2) 12-lead ECG and 80-lead BSPM at first medical contact; and (3) cardiac troponin-T 12 hours after symptom onset and/or creatine kinase MB fraction, were undertaken. Enrolled in the cohort were patients with culprit left circumflex stenosis (thrombolysis in myocardial infarction flow grade 0/1) at angiography. Acute myocardial infarction AMI was defined as cardiac troponin-T ≥0.1 µg/L and/or creatine kinase MB fraction >2 upper limits of normal. Enrolled were 482 patients: 168 had exclusion criteria. Of the remaining 314 (age 64±11 years; 62% male), 254 (81%) had AMI : of these, 231 had BSPM STE -sensitivity 0.91, specificity 0.72, positive predictive value 0.93, negative predictive value 0.65, and c-statistic 0.803 for AMI ( P<0.001). Of those with BSPM STE and AMI (n=231), STE was most frequently detected in the posterior (n=111, 48%), lateral (n=53, 23%), inferior (n=39, 17%), and right ventricular (n=21, 9%) territories. Conclusions Among patients with 12-lead ECG non-ST-segment-elevation myocardial infarction and culprit left circumflex stenosis, initial BSPM identifies ST-segment elevation beyond the territory of the 12-lead ECG . Greater use of the BSPM may result in earlier identification of AMI , which may lead to more rapid reperfusion.

Comparison of value of leads from body surface maps to 12-lead electrocardiogram for diagnosis of acute myocardial infarction.

We aimed to develop 12-lead electrocardiographic (ECG) models testing ST-elevation criteria with QRST variables and compare their performance with the 80-lead body surface map (BSM) in detection of acute myocardial infarction (AMI). Because the prevalence of non-ST-elevation AMI is increasing worldwide, advances in early ECG detection of AMI are urgently needed. The study population was 755 consecutive patients presenting with ischemic chest pain from January 2002 to June 2004. All patients had electrocardiography and body surface mapping performed at initial presentation. AMI occurred in 519 patients (69%, cardiac troponin T or I level > or =0.1 ng/ml). Of these 519 patients, 303 (58%) had no ST-elevation on the initial 12-lead electrocardiogram. Ten patients were classified as having an "aborted AMI" and were included in the AMI analysis. The American College of Cardiology/European Society of Cardiology criteria for ST-elevation on 12-lead electrocardiogram identified 236 patients with AMI (sensitivity 45%, specificity 92%). Additional QRST features improved sensitivity (51% to 68%) but with decreased specificity (71% to 89%), with the optimal multivariate ECG model having a c-statistic of 0.75. The optimal BSM model identified 402 patients as having AMI (sensitivity 76%, specificity 92%, c-statistic 0.84). This improvement in sensitivity over the 12-lead electrocardiogram was due mainly to detection of ST-elevation in the high right anterior, posterior, and right ventricular territories and AMI in the presence of left bundle branch block. In conclusion, QRST variables added to criteria for ST-elevation result in improvement in sensitivity of the 12-lead electrocardiogram, although with decreased specificity. The BSM is superior in detecting AMI and demonstrates the importance of electroanatomic evaluation of patients with acute coronary syndromes.

A pilot study of a low-tilt biphasic waveform for transvenous cardioversion of atrial fibrillation: improved efficacy compared with conventional capacitor-based waveforms in patients.

BACKGROUND: The optimal waveform tilt for defibrillation is not known. Most modern defibrillators used for the cardioversion of atrial fibrillation (AF) employ high-tilt, capacitor-based biphasic waveforms. METHODS: We have developed a low-tilt biphasic waveform for defibrillation. This low-tilt waveform was compared with a conventional waveform of equivalent duration and voltage in patients with AF. Patients with persistent AF or AF induced during a routine electrophysiology study (EPS) were randomized to receive either the low-tilt waveform or a conventional waveform. Defibrillation electrodes were positioned in the right atrial appendage and distal coronary sinus. Phase 1 peak voltage was increased in a stepwise progression from 50 V to 300V. Shock success was defined as return of sinus rhythm for >/=30 seconds. RESULTS: The low-tilt waveform produced successful termination of persistent AF at a mean voltage of 223 V (8.2 J) versus 270 V (6.7 J) with the conventional waveform (P = 0.002 for voltage, P = ns for energy). In patients with induced AF the mean voltage for the low-tilt waveform was 91V (1.6 J) and for the conventional waveform was 158 V (2.0 J) (P = 0.005 for voltage, P = ns for energy). The waveform was much more successful at very low voltages (less than or equal to 100 V) compared with the conventional waveform (Novel: 82% vs Conventional 22%, P = 0.008). CONCLUSION: The low-tilt biphasic waveform was more successful for the internal cardioversion of both persistent and induced AF in patients (in terms of leading edge voltage).

An early phase of slow myocardial activation may be necessary in order to benefit from cardiac resynchronization therapy.

BACKGROUND: Not all patients with a QRS duration longer than 140 milliseconds respond to cardiac resynchronization therapy (CRT). The same QRS duration may correspond to different spatiotemporal patterns of myocardial activation that influence response to CRT. METHODS: Electrocardiographic imaging based on 80 chest wall electrodes was used to construct the spatiotemporal myocardial activation map in 46 consecutive patients before CRT. The cumulative percentage of myocardium activated was plotted against time expressed in terms of quintiles of the overall QRS duration. Changes in the left ventricular ejection fraction and end-diastolic diameter, maximum oxygen consumption per minute, brain natriuretic peptide level, and 6-minute walk distance after 6 months of CRT were compared across different patterns with 1-way analysis of variance. RESULTS: Data from 34 patients were available for analysis. Four spatiotemporal patterns of myocardial activation could be identified: triphasic (fast-slow-fast) (13), uniform (8), fast-slow (7), and slow-fast (6). The overall QRS duration was similar in the 4 groups (166 +/- 19 vs 138 +/- 21 vs 157 +/- 26 vs 152 +/- 37 milliseconds, P = not significant [NS]). The ejection fraction showed a trend of greater increases for the triphasic (6.5% +/- 7.0%) and slow-fast (15.5% +/- 6.4%) patterns than for the uniform (4.0% +/- 13.3%) and fast-slow (8.0% +/- 6.1%) patterns (P = NS). The end-diastolic diameter showed a trend of greater decreases for the triphasic (-3.7% +/- 5.3%) and slow-fast (-7.0% +/- 6.7%) patterns than for the uniform (0.8% +/- 6.7%) and fast-slow (0.0% +/- 4.6%) patterns (P = NS). The maximum oxygen consumption per minute showed a trend of greater increases for the triphasic (1.2 +/- 4.2 mL/kg/min) and slow-fast (4.1 +/- 2.7 mL/kg/min) patterns than for the uniform (0.1 +/- 4.1 mL/kg/min) and fast-slow (1.0 +/- 2.1 mL/kg/min) patterns (P = NS). The brain natriuretic peptide level decreased significantly more for the triphasic (-450 +/- 1269) and slow-fast (-3121 +/- 1512) patterns than for the uniform (762 +/- 1036) and fast-slow (718 +/- 2530) patterns (P = .0003). The 6-minute walk distance increased significantly more for the triphasic (29 +/- 89) and slow-fast (40 +/- 23) patterns than for the uniform (6 +/- 87) and fast-slow (37 +/- 45) patterns (P = .0003). CONCLUSIONS: Different spatiotemporal patterns of myocardial activation exist among patients with broad QRS complex and may affect response to CRT. An early phase of slow myocardial activation (the triphasic fast-slow-fast and the slow-fast patterns) may be necessary for a patient to benefit from CRT.

Risk stratification of chest pain patients in the emergency department by a nurse utilizing a point of care protocol.

OBJECTIVE: Risk stratification of patients with ischaemic type chest pain assessed in the emergency department utilizing a point of care (POC) protocol. METHODS: Patient demographics, cardiac biomarkers, management and follow-up at 6 months were reviewed for patients seen over 20 months. RESULTS: Out of 546 patients, 351 (64%) were admitted. The diagnoses after admission were confirmed as acute myocardial infarction in 59 patients and unstable angina, (cTroponin T<0.09 ng/ml) in 92 patients. The c-statistic of the receiver operating curves for myocardial infarction (myocardial infarction, cTroponinT at 12 h >0.09 ng/ml) as determined by the POC assay was cTroponin I=0.884, CK-MB=0.883, myoglobin=0.845 and beta-type natriuretic peptide (BNP)=0.755. The c-statistic for the same sample assessed by the hospital laboratory was cTroponin T=0.893: for CK-MB within 12 h of admission it was 0.918; the 12 h cTroponin T was 0.982 and within 24 h of admission NT pro-BNP was 0.789. POC BNP in patients admitted was 68 ng/l (median) vs. 24 ng/l (median) for those not admitted, (P<0.001). POC BNP for patients admitted with unstable angina (12 h cTroponin T <0.09 ng/ml) was 47 ng/l (median, P<0.001). At 6 months, 14 patients had died; five during admission, two within 30 days and seven up to 6 months. During admission two died from heart failure, two with respiratory tract infection and one from carcinoma. Of those not admitted one had died from asbestosis. CONCLUSION: Risk stratification by a specialist nurse utilizing a POC protocol is an appropriate means of assessing patients with chest pain.

Predictors of excess mortality after myocardial infarction in women.

BACKGROUND: Research suggests that women have higher mortality after acute myocardial infarction (AMI) than men. Potential factors to explain this disparity include delay to presentation, less aggressive interventional strategies, and more severe disease at coronary angiography in women. METHODS: Consecutive patients (n=663) presenting to coronary care between Jan 2002 and Jan 2005 with ischemic type chest pain and AMI (troponin T >0.09ng/ml) were recruited. Details of the presentation and management were obtained from the medical notes. The primary endpoint was three month all cause mortality. RESULTS: Of these patients 31% (205/663) were female. Mean age of women was 70 (SD 11) and 63 (SD 13) for men (p<0.001). There was no difference between the sexes for delay in presentation or treatment or for ST elevation infarction site. Women had prior hypertension more than men (49% 100/205 vs. 38% 174/458, p=0.008). Women were less likely to have diagnostic catheterisation (67% 137/205 vs. 80% 365/458 p<0.001). Both genders had similar coronary artery disease extent and frequencies of LV impairment (EF<45%) and were equally likely to undergo revascularisation (79% 108/137 vs. 81% 295/365 p=NS). There was an excess 3 month mortality among women (11% 23/205 vs. 5% 24/458 in men p=0.006). INDEPENDENT: predictors of 3 month mortality by logistic regression analysis were age (OR 1.06, 95% CI 1.03 -1.09, p<0.001) and LV impairment (OR 0.28, 95% CI 0.13-0.56, p<0.001). CONCLUSION: As LV impairment was comparable in men and women, the excess mortality identified is due to older age at presentation of women.

Epicardial potentials computed from the body surface potential map using inverse electrocardiography and an individualised torso model improve sensitivity for acute myocardial infarction diagnosis.

INTRODUCTION: Epicardial potentials (EPs) derived from the body surface potential map (BSPM) improve acute myocardial infarction (AMI) diagnosis. In this study, we compared EPs derived from the 80-lead BSPM using a standard thoracic volume conductor model (TVCM) with those derived using a patient-specific torso model (PSTM) based on body mass index (BMI). METHODS: Consecutive patients presenting to both the emergency department and pre-hospital coronary care unit between August 2009 and August 2011 with acute ischaemic-type chest pain at rest were enrolled. At first medical contact, 12-lead electrocardiograms and BSPMs were recorded. The BMI for each patient was calculated. Cardiac troponin T (cTnT) was sampled 12 hours after symptom onset. Patients were excluded from analysis if they had any ECG confounders to interpretation of the ST-segment. A cardiologist assessed the 12-lead ECG for ST-segment elevation myocardial infarction by Minnesota criteria and the BSPM. BSPM ST-elevation (STE) was ⩾0.2 mV in anterior, ⩾0.1 mV in lateral, inferior, right ventricular or high right anterior and ⩾0.05 mV in posterior territories. To derive EPs, the BSPM data were interpolated to yield values at 352 nodes of a Dalhousie torso. Using an inverse solution based on the boundary element method, EPs at 98 cardiac nodes positioned within a standard TVCM were derived. The TVCM was then scaled to produce a PSTM using a model developed from computed tomography in 48 patients of varying BMIs, and EPs were recalculated. EPs >0.3 mV defined STE. A cardiologist blinded to both the 12-lead ECG and BSPM interpreted the EP map. AMI was defined as cTnT ⩾0.1 µg/L. RESULTS: Enrolled were 400 patients (age 62 ± 13 years; 57% male); 80 patients had exclusion criteria. Of the remaining 320 patients, the BMI was an average of 27.8 ± 5.6 kg/m2. Of these, 180 (56%) had AMI. Overall, 132 had Minnesota STE on ECG (sensitivity 65%, specificity 89%) and 160 had BSPM STE (sensitivity 81%, specificity 90%). EP STE occurred in 165 patients using TVCM (sensitivity 88%, specificity 95%; p < 0.001) and in 206 patients using PSTM (sensitivity 98%, specificity 79%; p < 0.001). Of those with AMI by cTnT and EPs ⩽0.3 mV using TVCM ( n = 22), 18 (82%) patients had EPs >0.3 mV when an individualised PSTM was used. CONCLUSION: Among patients presenting with ischaemic-type chest pain at rest, EPs derived from BSPM using a novel PSTM significantly improve sensitivity for AMI diagnosis.

Early clinical outcomes as a function of use of newer oral P2Y12 inhibitors versus clopidogrel in the EUROMAX trial.

Objective: To ascertain whether different oral P2Y12 inhibitors might affect rates of acute stent thrombosis and 30-day outcomes after primary percutaneous coronary intervention (pPCI). Methods: The European Ambulance Acute Coronary Syndrome Angiography (EUROMAX) randomised trial compared prehospital bivalirudin with heparin with optional glycoprotein IIb/IIIa inhibitor treatment in patients with ST-segment elevation myocardial infarction triaged to pPCI. Choice of P2Y12 inhibitor was at the investigator's discretion. In a prespecified analysis, we compared event rates with clopidogrel and newer oral P2Y12 inhibitors (prasugrel, ticagrelor). Rates of the primary outcome (acute stent thrombosis) were examined as a function of the P2Y12 inhibitor used for loading and 30-day outcomes (including major adverse cardiac events) as a function of the P2Y12 inhibitor used for maintenance therapy. Logistic regression was used to adjust for differences in baseline characteristics. Results: Prasugrel or ticagrelor was given as the loading P2Y12 inhibitor in 49% of 2198 patients and as a maintenance therapy in 59%. No differences were observed in rates of acute stent thrombosis for clopidogrel versus newer P2Y12 inhibitors (adjusted OR 0.50, 95% CI 0.13 to 1.85). After adjustment, no difference was observed in 30-day outcomes according to maintenance therapy except for protocol major (p=0.029) or minor (p=0.025) bleeding and Thrombolysis In Myocardial Infarction minor bleeding (p=0.002), which were less frequent in patients on clopidogrel. Consistent results were observed in the bivalirudin and heparin arms. Conclusions: The choice of prasugrel or ticagrelor over clopidogrel was not associated with differences in acute stent thrombosis or 30-day ischaemic outcomes after pPCI. Trial registration number: NCT01087723.

Age, outcomes, and treatment effects of fibrinolytic and antithrombotic combinations: findings from Assessment of the Safety and Efficacy of a New Thrombolytic (ASSENT)-3 and ASSENT-3 PLUS.

BACKGROUND: Elderly patients with acute myocardial infarction are at particularly high risk for death and bleeding complications. The efficacy and safety of antithrombotic strategies in these patients remain unclear. METHODS: To provide more insight into the risk and benefit of antithrombotic strategies in the elderly, we examined patients from the ASSENT-3 and ASSENT-3 PLUS trials with STEMI who were treated with tenecteplase (TNK) and unfractionated heparin (UFH) or enoxaparin, or half-dose TNK with abciximab and reduced-dose UFH. RESULTS: Older patients had a higher risk profile, and lower use of concomitant therapies and revascularization procedures. We found an interaction between age and treatment effect for the efficacy end point (P = .0007) and the efficacy plus safety end point (P < .0001). Younger patients (<65 years) had a lower risk of the composite efficacy plus safety end point with enoxaparin (relative risk [RR] 0.84, 95% CI 0.74-0.94) or abciximab (RR 0.79, 95% CI 0.69-0.90) compared with UFH. In patients >65 years of age, the benefit of enoxaparin appeared to be offset by an increased risk of bleeding complications. The risk of the efficacy plus safety end point tended to be higher in elderly patients receiving abciximab and half-dose TNK (RR 1.18, 95% CI 0.91-1.51 for 76-85 years of age and RR 1.48, 95% CI 0.88-2.49 for >85 years of age). CONCLUSIONS: Although TNK with either enoxaparin or abciximab appeared to be more effective than with standard UHF in younger patients, these combinations tended to be less effective and even may be unsafe in the elderly. Development of new combination strategies and dosing schemes of fibrinolytics and antithrombotics with improved efficacy and safety in the elderly remains a high priority.

Improved detection of acute myocardial infarction using a diagnostic algorithm based on calculated epicardial potentials.

BACKGROUND: New methods for detecting myocardial infarction in patients with suspected acute coronary syndromes are needed particularly in an era where the majority of patients with myocardial infarction present with non-diagnostic 12-lead electrocardiograms (ECG). We compared a novel epicardial diagnostic algorithm using epicardial potentials from the 80-lead body surface map with other electrocardiographic techniques in detection of myocardial infarction. METHODS: Between February 1999 and February 2001, consecutive patients (n=427) with ischemic type chest pain had an initial 12-lead ECG and body surface map recorded. Detecting myocardial infarction using an epicardial algorithm was first performed in a training set (n=213) and tested in a validation set of patients (n=214). The results from this epicardial algorithm in myocardial infarction detection were compared with the physician's interpretation of the 12-lead ECG, the body surface map algorithm (PRIME) and physician's interpretation of the body surface map. RESULTS: Myocardial infarction occurred in 205 patients (creatine kinase >or=2x upper limit of normal with creatine kinase-MB >or=7% CK). The physician's interpretation of the 12-lead ECG identified 122 with myocardial infarction (sensitivity 60%, specificity 99%), the body surface map algorithm 137 (sensitivity 67%, specificity 89%), the physician's interpretation of the body surface map 153 (sensitivity 75%, specificity 91%) and the epicardial algorithm 158 (sensitivity 77% specificity 99%). Combining the physician's interpretation of the 12-lead ECG with the epicardial algorithm increased significantly the detection of myocardial infarction (sensitivity 85%, specificity 98%, p<0.001) compared with the 12-lead ECG. CONCLUSIONS: An epicardial algorithm based on epicardial potentials increases significantly the detection of myocardial infarction particularly among those with non-diagnostic 12-lead ECG's.

Comparing the efficacy and safety of a novel monophasic waveform delivered by the passive implantable atrial defibrillator with biphasic waveforms in cardioversion of atrial fibrillation.

BACKGROUND: The passive implantable atrial defibrillator (PIAD) (with no battery or discharging capacitor and powered transcutaneously by radio-frequency energy) delivering a novel monophasic low-tilt waveform is more efficacious than the standard monophasic waveform at atrial defibrillation. Standard biphasic (STB) waveforms, however, are more efficacious and safer than monophasic waveforms. This study compared the efficacy and safety of the PIAD waveform with biphasic waveforms. METHODS AND RESULTS: Sustained atrial fibrillation (AF) was induced by rapid atrial pacing. Cardioversion was attempted via 2 atrial defibrillation leads. The efficacy of the PIAD was compared with 3 biphasic waveforms (standard, single rounded, and double rounded) at varying voltage settings in 10 pigs. After a synchronized shock, hemodynamic changes between the PIAD, standard biphasic, and monophasic waveforms were compared at 1.5 and 3.0 J in 12 pigs. Myocardial injury (biochemical and histological) after ten 5-J PIAD shocks was compared with a no-shock group in 14 pigs. The PIAD 100-V setting was significantly more efficacious than the STB (100/-50 V: 100% [1.88+/-0.02 J] versus 90% [0.89+/-0.0 J]; P=0.025). No arrhythmic, hemodynamic, or myocardial injury was observed with the PIAD waveform. CONCLUSIONS: Defibrillation with the PIAD is more efficacious than with the STB waveform and appears safe. This device could provide a more effective option for cardioversion.