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).

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.

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.

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.

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.

An investigation of thrust, depth and the impedance cardiogram as measures of cardiopulmonary resuscitation efficacy in a porcine model of cardiac arrest.

OBJECTIVE: Optimising the depth and rate of applied chest compressions following out of hospital cardiac arrest is crucial in maintaining end organ perfusion and improving survival. The impedance cardiogram (ICG) measured via defibrillator pads produces a characteristic waveform during chest compressions with the potential to provide feedback on cardiopulmonary resuscitation (CPR) and enhance performance. The objective of this pre-clinical study was to investigate the relationship between mechanical and physiological markers of CPR efficacy in a porcine model and examine the strength of correlation between the ICG amplitude, compression depth and end-tidal CO2 (ETCO2). METHODS: Two experiments were performed using 24 swine (12 per experiment). For experiment 1, ventricular fibrillation (VF) was induced and mechanical CPR commenced at varying thrusts (0-60 kg) for 2 min intervals. Chest compression depth was recorded using a Philips QCPR device with additional recording of invasive physiological parameters: systolic blood pressure, ETCO2, cardiac output and carotid flow. For experiment 2, VF was induced and mechanical CPR commenced at varying depths (0-5 cm) for 2 min intervals. The ICG was recorded via defibrillator pads attached to the animal's sternum and connected to a Heartsine 500 P defibrillator. ICG amplitude, chest compression depth, systolic blood pressure and ETCO2 were recorded during each cycle. In both experiments the within-animal correlation between the measured parameters was assessed using a mixed effect model. RESULTS: In experiment 1 moderate within-animal correlations were observed between physiological parameters and compression depth (r=0.69-0.77) and thrust (r=0.66-0.82). A moderate correlation was observed between compression depth and thrust (r=0.75). In experiment 2 a strong within-animal correlation and moderate overall correlations were observed between ICG amplitude and compression depth (r=0.89, r=0.79) and ETCO2 (r=0.85, r=0.64). CONCLUSION: In this porcine model of induced cardiac arrest moderate within animal correlations were observed between mechanical and physiological markers of chest compression efficacy demonstrating the challenge in utilising a single mechanical metric to quantify chest compression efficacy. ICG amplitude demonstrated strong within animal correlations with compression depth and ETCO2 suggesting its potential utility to provide CPR feedback in the out of hospital setting to improve performance.

Aborted myocardial infarction in ST-elevation myocardial infarction: insights from the STrategic Reperfusion Early After Myocardial infarction trial.

BACKGROUND: We evaluated the prespecified endpoint, aborted myocardial infarction (AbMI), according to the use of a pharmacoinvasive (PI) strategy versus primary percutaneous coronary intervention (PCI) in 1754 patients randomised within 3 h of symptom onset in the STrategic Reperfusion Early After Myocardial infarction (STREAM) trial. METHODS: Based on sequential ECG's and biomarkers, AbMI was defined as ST-elevation resolution ≥50% (90 min posttenecteplase (TNK) in the PI arm or 30 min postprimary PCI) with minimal biomarker rise. RESULTS: In the PI arm 11.1% (n=99) had AbMI versus 6.9% (n=59) in primary PCI arm (p<0.01). In a multivariable model, AbMI patients overall had less baseline ΣST-deviation, fewer baseline Q-waves and shorter total ischaemic times. PI AbMI patients had faster time to TNK (90 vs 100 min, p=0.015): total ischaemic time was 100 min longer in primary PCI AbMI patients and no difference in ischaemic time existed between AbMI and non-AbMI patients within this group. Although no significant interaction between treatment and AbMI on the composite endpoint of death/shock/congestive heart failure/recurrent MI occurred (p=0.292), PI AbMI patients had a lower incidence in this endpoint than non-AbMI patients (5.1 vs 12%, p=0.038); this was not evident in primary PCI patients. Forty-five patients (ie, 2.5%) had masquerading MI with minimal biomarker elevation and no evolution in baseline ST-elevation. CONCLUSIONS: A PI strategy of early fibrinolysis more frequently aborts MI than primary PCI. Such PI patients had more favourable outcomes as compared with non-AbMIs. Diligent review of ECG evolution in STEMI distinguishes AbMI from infarct masquerade. ClinicalTrials.gov ID: NCT00623623.

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.

A support vector machine for predicting defibrillation outcomes from waveform metrics.

BACKGROUND: Algorithms to predict shock success based on VF waveform metrics could significantly enhance resuscitation by optimising the timing of defibrillation. OBJECTIVE: To investigate robust methods of predicting defibrillation success in VF cardiac arrest patients, by using a support vector machine (SVM) optimisation approach. METHODS: Frequency-domain (AMSA, dominant frequency and median frequency) and time-domain (slope and RMS amplitude) VF waveform metrics were calculated in a 4.1Y window prior to defibrillation. Conventional prediction test validity of each waveform parameter was conducted and used AUC>0.6 as the criterion for inclusion as a corroborative attribute processed by the SVM classification model. The latter used a Gaussian radial-basis-function (RBF) kernel and the error penalty factor C was fixed to 1. A two-fold cross-validation resampling technique was employed. RESULTS: A total of 41 patients had 115 defibrillation instances. AMSA, slope and RMS waveform metrics performed test validation with AUC>0.6 for predicting termination of VF and return-to-organised rhythm. Predictive accuracy of the optimised SVM design for termination of VF was 81.9% (± 1.24 SD); positive and negative predictivity were respectively 84.3% (± 1.98 SD) and 77.4% (± 1.24 SD); sensitivity and specificity were 87.6% (± 2.69 SD) and 71.6% (± 9.38 SD) respectively. CONCLUSIONS: AMSA, slope and RMS were the best VF waveform frequency-time parameters predictors of termination of VF according to test validity assessment. This a priori can be used for a simplified SVM optimised design that combines the predictive attributes of these VF waveform metrics for improved prediction accuracy and generalisation performance without requiring the definition of any threshold value on waveform metrics.

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.

The inverse problem utilizing the boundary element method for a nonstandard female torso.

This paper proposes a new method of rapidly deriving the transfer matrix for the boundary element method (BEM) forward problem from a tailored female torso geometry in the clinical setting. The method allows rapid calculation of epicardial potentials (EP) from body surface potentials (BSP). The use of EPs in previous studies has been shown to improve the successful detection of the life-threatening cardiac condition--acute myocardial infarction. The MRI scanning of a cardiac patient in the clinical setting is not practical and other methods are required to accurately deduce torso geometries for calculation of the transfer matrix. The new method allows the noninvasive calculation of tailored torso geometries from a standard female torso and five measurements taken from the body surface of a patient. This scaling of the torso has been successfully validated by carrying out EP calculations on 40 scaled torsos and ten female subjects. It utilizes the BEM in the calculation of the transfer matrix as the BEM depends only upon the topology of the surfaces of the torso and the heart, the former can now be accurately deduced, leaving only the latter geometry as an unknown.

Early detection of acute posterior myocardial infarction using body surface mapping and SPECT scanning.

BACKGROUND: Many patients with non-ST elevation myocardial infarction (NSTEMI) may have posterior STEMI, which should be emergently treated with reperfusion strategies but is difficult to identify by 12-lead ECG. OBJECTIVES: To compare the initial ECG and body surface map (BSM) for the diagnosis of posterior MI as verified by single-photon emission computed tomography (SPECT) and cTroponin T. METHODS: Patients with chest pain greater than 20 min at rest with either ST depression of at least 0.1 mV in at least one of leads I, aVL or V1-V6 on ECG or STE at least 0.05 mV in at least one posterior lead on the BSM which underwent early SPECT scan. RESULTS: Sixty patients (87%, 60 out of 69 with interpretable SPECT) had a posterior wall perfusion defect, all had cTroponinT (>0.09 ng/ml) and thus had posterior MI. Initial ECG showed STE in 24 (40%, 24 out of 60): 36 were non-diagnostic (60%, 36 out of 60). STE on BSM identified inferior MI in seven patients (12%, 7 out of 60), posterior in 32 patients (53%, 32 out of 60), and nine patients had right ventricular (15%, 9 out of 60). Twelve had no STE (20%, 12 out of 60). Of the patients with posterior MI and non-diagnostic ECGs, 53% (19 out of 36) were posterior MI by the BSM and six (17%, 6 out of 36) right ventricular MI only. The BSM correctly identified 53% (32 out of 60) (95% confidence interval 40-66%) of posterior MI. Of the 60 patients with posterior MI, 60% (36) had non-diagnostic ECGs: the BSM identified 42% (25) either as posterior MI or right ventricular MI only. CONCLUSION: We have shown that the BSM diagnoses significantly more posterior MI than the 12-lead ECG, allowing early identification of these patients so that maximum benefit from early reperfusion strategies can be gained.

Myocardial wall motion and thickening assessment in early gated SPECT images of acute coronary syndrome patients likely to have inferolateral perfusion defects.

The purpose of this study was to compare semi-quantitative visual scores of perfusion, motion and thickening with an automated hypoperfusion index (HI) in patients with suspected acute inferolateral perfusion defects. In the absence of perfusion defects motion and thickening abnormalities were assessed. Sixty-eight patients with chest pain at rest and either ST depression ≥0.1 mV in ≥1 of leads I, aVL, V1-V6 on 12-lead ECG or ST elevation ≥0.05 mV in ≥1 posterior lead on the body surface map comprised the study population. A rest gated perfusion scan was performed within 24 h of symptoms. Scans were scored for perfusion, motion and thickening semi-quantitatively. The scores were compared to the automated HI. A 12 h Troponin T >0.09 ng/ml indicated myocardial infarction (MI). Sixty-five patients (96%, 65/68) had MI. The summed perfusion score correlated well with the HI (ρ = 0.90, P < 0.01) and agreement between scorers was good (κ = 0.77, 95% CI = 0.57-0.94). The summed motion score correlated with the HI (ρ = -0.61, P < 0.01) and agreement between scorers was moderate (κ = 0.65, 95% CI = 0.52-0.79). Summed thickening score correlated with HI (ρ = -0.67, P < 0.01) and agreement between scorers was good (κ = 0.74, 95% CI = 0.64-0.88). Of the 1156 segments assessed (68 × 17), 542 had normal perfusion. Of these normally perfused segments, 113 (21%, 113/542) had a motion abnormality and 102 (19%, 102/542) had a thickening abnormality. Three patients with proven myocardial infarction had normal myocardial perfusion (HI ≤ 5) but exhibited wall motion and thickening abnormalities. In conclusion, assessment of wall motion and thickening in addition to perfusion in acute myocardial perfusion imaging may improve the diagnostic sensitivity for acute MI. Of the scores addressing motion and thickening, interobserver agreement was better for the summed thickening score.

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.

In-hospital percutaneous coronary intervention improves in-hospital survival in patients with acute inferior myocardial infarction particularly with right ventricular involvement.

OBJECTIVE: Assess the interaction between fibrinolysis and in-hospital percutaneous coronary intervention (PCI) in patients with inferior myocardial infarction (MI), particularly those with electrocardiographic evidence of right ventricular infarction (RVI). DESIGN: Retrospective observational study. PATIENTS: Consecutive patients with inferior MI identified from an MI registry between January 1998 and January 2004. INTERVENTIONS: Propensity analyses and multiple regression analysis were used to determine the mortality benefit of PCI. MAIN OUTCOME MEASURES: In-hospital morbidity and mortality. RESULTS: In total, 465 patients with inferior MI received fibrinolytic therapy (median pain-to-needle time of 167 minutes; IQR 100-311 minutes). The main predictors of PCI were recurrent chest pain, peak creatine kinase, age, reinfarction, presence of heart failure and male gender. Significant independent predictors of in-hospital mortality were age > or = 75 years, RVI, initial systolic blood pressure < or = 80 mmHg, female gender and no in-hospital PCI. In-hospital PCI was performed in 184/465 (40%) patients; 55 (30%) had rescue PCI performed < or = 6 hours post fibrinolysis, 45 (24%) within 6-24 hours and 84 (46%) > or = 24 hours. In-hospital PCI was associated with reduced in-hospital mortality (PCI: 9 [5%] vs. no PCI: 40 [14%]; p < 0.001) mainly in those with RVI (PCI: 8 [8%] vs. no PCI 33 [23%]; p = 0.002) compared with no RVI (PCI: 1 [1%] vs. no PCI 7 [5%]; p = 0.1). CONCLUSION: A strategy of timely fibrinolysis combined with in-hospital PCI including rescue PCI may result in a significant reduction in in-hospital mortality and morbidity in patients with inferior MI, particularly those with RVI.

Prognostic value of a multimarker approach for patients presenting to hospital with acute chest pain.

To evaluate the prognostic role of novel biomarkers for the risk stratification of patients admitted with ischemic-type chest pain, a prospective study of 664 patients presenting to 2 coronary care units with ischemic-type chest pain was conducted over 3 years beginning in 2003. Patients were assessed on admission for clinical characteristics, electrocardiographic findings, renal function, cardiac troponin T (cTnT), markers of myocyte injury (heart fatty acid-binding protein [H-FABP] and glycogen phosphorylase BB), neurohormonal activation (N-terminal-pro-brain natriuretic peptide [NT-pro-BNP]), hemostatic activity (fibrinogen and D-dimer), and vascular inflammation (high-sensitivity C-reactive protein, myeloperoxidase, matrix metalloproteinase-9, pregnancy-associated plasma protein-A, and soluble CD40 ligand). A >or=12-hour cTnT sample was also obtained. Myocardial infarction (MI) was defined as peak cTnT >or=0.03 microg/L. Patients were followed for 1 year from the time of admission. The primary end point was death or MI. Elevated fibrinogen, D-dimer, H-FABP, NT-pro-BNP, and peak cTnT were predictive of death or MI within 1 year (unadjusted odds ratios 2.5, 3.1, 5.4, 5.4, and 6.9, respectively). On multivariate analysis, H-FABP and NT-pro-BNP were selected, in addition to age, peak cTnT, and left ventricular hypertrophy on initial electrocardiography, as significant independent predictors of death or MI within 1 year. Patients without elevations of H-FABP, NT-pro-BNP, or peak cTnT formed a very low risk group in terms of death or MI within 1 year. A very high risk group had elevations of all 3 biomarkers. In conclusion, the measurement of H-FABP and NT-pro-BNP at the time of hospital admission for patients with ischemic-type chest pain adds useful prognostic information to that provided by the measurement of baseline and 12-hour cTnT.

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.)

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.