Target temperature in post-arrest comatous patients. Is something changed in the postpandemic era?

INTRODUCTION: The recommended target temperature in the treatment of comatous patients after cardiac arrest has recently changed. We analyzed the impact on the neurological outcome of a change in the target temperature from July 2021. MATERIAL AND METHODS: This was a retrospective analysis comparing the discharge status of 78 patients with a target temperature of 33 °C (group 1) with that of 24 patients with a target temperature of 36.5 °C (group 2). Pearson chi-square and Mann-Whitney U tests were used. RESULTS: The initial rhythm was defibrillable in 65% of group 1 and 71% of group 2, and cardiac arrest was witnessed in 93% of group 1 and 96% of group 2. There was an adverse outcome (death or vegetative state) in 37 patients in group 1 (47%) compared to 18 in group 2 (74%) (Pearson chi-square 5.612, p = 0.018). CONCLUSIONS: In our series of patients, the temperature control target temperature change from 33 °C to 36.5 °C was associated with worse neurological outcome. Further studies are needed to evaluate the outcome of a generalized modification of temperature control targets in comatose patients after cardiac arrest in our postpandemic era.

False ST-segment elevation by artifact due to an infusion pump.

A patient admitted for non-ST-elevation acute coronary syndrome showed an episode of ST-segment elevation on the monitor. These alterations were due to an artifact produced by the administration of a saline bolus through an infusion pump that disappeared at the end of the bolus. Our findings highlight that the interpretation of the electrocardiogram requires careful analysis and correlation with the clinical situation and with other physiological parameters.

Elevation of ST-segment in aVR is predictive of cardiogenic shock but not of multivessel disease in inferior myocardial infarction.

INTRODUCTION: Some studies suggest that ST elevation in aVR (aVR-STE) can predict the presence of left main or multivessel disease (MVD) and relates to prognosis. Our purpose was to analyze the relationship of aVR-STE to MVD disease or cardiogenic shock (CS) in patients with inferior myocardial infarction (inferior STEMI). METHODS: We analyzed two cohorts of consecutive patients admitted for inferior STEMI in the Coronary Unit of two university hospitals. ST elevation and ST depression in each derivation were compared between patients with and without MVD and with and without CS. RESULTS: We included 342 patients-19.6% women and 80.4% men-with a median age of 60 (52, 70); 18 patients (5.2%) had MVD, and 25 (7.3%) patients presented CS. There was no relationship between ST elevation or ST depression in either derivation and MVD. In contrast, CS was associated with aVR-STE, ST-segment depression in lead aVL, and the sum of ST-segment depression. aVR-STE of 0.25 mm had a sensitivity of 24.0% and a specificity of 95.9% for CS. After multivariate analysis including clinical variables, aVR-STE was independently associated with CS. CONCLUSIONS: In patients with inferior STEMI, ST-segment analysis was not useful in predicting multivessel disease. aVR-STE was an independent predictor of CS, with high specificity but low sensitivity.

Localization of the culprit artery in inferior myocardial infarction: Influence of the point of measurement of ST segment.

BACKGROUND: There are several approaches widely used in the localization of the responsible artery in inferior myocardial infarction. However, the existing papers show differences in the point where the ST segment is measured. The purpose of our investigation is to analyse the influence of the point at which elevation of the ST segment is measured on the results of these algorithms. METHODS: We analysed the 12­lead electrocardiograms of 90 consecutive patients with inferior myocardial infarction. The ST segment elevation or depression was measured at the J-point and at 80 ms, and three algorithms were applied to predict the culprit artery with both measurements. Sensitivity, specificity, the area under the curve, and the kappa index of agreement were analysed to compare each algorithm at the J-point and at 80 ms. RESULTS: The area under the curve was better at the J-point than at 80 ms in two algorithms (0.696 vs. 0.635, p < 0.043, and 0.754 vs. 0.661, p < 0.045) and did not change in one. Agreement between the J-point and 80 ms was suboptimal in all three algorithms (0.71, 0.65, and 0.58). CONCLUSIONS: The result of different algorithms to detect the culprit artery in inferior STEMI patients can change significantly depending on the point where ST elevation or depression is measured.

Safety and efficacy of in-hospital clopidogrel-to-prasugrel switching in patients with acute coronary syndrome. An analysis from the 'real world'.

Antiplatelet switching in the management of acute coronary syndrome (ACS) seems to be safe, but prospective data are limited. This retrospective study assessed the safety and efficacy of in-hospital clopidogrel-to-prasugrel switching in patients with ACS. We analysed 525 consecutive patients with ACS admitted to our coronary care unit. We assessed the prevalence and the short-term outcomes of in-hospital clopidogrel-to-prasugrel switching. Bleeding and thrombotic events were assessed using propensity score matching analysis. A total of 468 patients received acetylsalicylic acid and a P2Y12 ADP receptor inhibitor. Medication switching occurred in 117 patients (25 %). Compared with the clopidogrel group, the switching group consisted preferentially of younger males with STEMI, exhibited fewer comorbidities, and had lower ischaemic risk. We found no differences between the switching group and the clopidogrel group in the bleeding rate [3.6 vs. 2.3 %, odds ratio (OR):1.59 95 % confidence interval (CI): 0.26-9.7, p NS], and in adverse cardiac or cerebrovascular events (MACCE) (5 vs. 8.4 %, OR: 0.57 95 % CI 0.16-2, p NS). In-hospital switching from clopidogrel to prasugrel in a selected high-risk ACS population resulted in a similar incidence of in-hospital haemorrhagic and thrombotic events. This strategy should be clarified in further randomised studies.

Effect of early metoprolol on infarct size in ST-segment-elevation myocardial infarction patients undergoing primary percutaneous coronary intervention: the Effect of Metoprolol in Cardioprotection During an Acute Myocardial Infarction (METOCARD-CNIC) trial.

BACKGROUND: The effect of ß-blockers on infarct size when used in conjunction with primary percutaneous coronary intervention is unknown. We hypothesize that metoprolol reduces infarct size when administered early (intravenously before reperfusion). METHODS AND RESULTS: Patients with Killip class II or less anterior ST-segment-elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention within 6 hours of symptoms onset were randomized to receive intravenous metoprolol (n=131) or not (control, n=139) before reperfusion. All patients without contraindications received oral metoprolol within 24 hours. The predefined primary end point was infarct size on magnetic resonance imaging performed 5 to 7 days after STEMI. Magnetic resonance imaging was performed in 220 patients (81%). Mean ± SD infarct size by magnetic resonance imaging was smaller after intravenous metoprolol compared with control (25.6 ± 15.3 versus 32.0 ± 22.2 g; adjusted difference, -6.52; 95% confidence interval, -11.39 to -1.78; P=0.012). In patients with pre-percutaneous coronary intervention Thrombolysis in Myocardial Infarction grade 0 to 1 flow, the adjusted treatment difference in infarct size was -8.13 (95% confidence interval, -13.10 to -3.16; P=0.0024). Infarct size estimated by peak and area under the curve creatine kinase release was measured in all study populations and was significantly reduced by intravenous metoprolol. Left ventricular ejection fraction was higher in the intravenous metoprolol group (adjusted difference, 2.67%; 95% confidence interval, 0.09-5.21; P=0.045). The composite of death, malignant ventricular arrhythmia, cardiogenic shock, atrioventricular block, and reinfarction at 24 hours in the intravenous metoprolol and control groups was 7.1% and 12.3%, respectively (P=0.21). CONCLUSIONS: In patients with anterior Killip class II or less ST-segment-elevation myocardial infarction undergoing primary percutaneous coronary intervention, early intravenous metoprolol before reperfusion reduced infarct size and increased left ventricular ejection fraction with no excess of adverse events during the first 24 hours after STEMI. CLINICAL TRIAL REGISTRATION URL: http://www.clinicaltrials.gov. Unique identifier: NCT01311700. EUDRACT number: 2010-019939-35.

Nonadherence to ticagrelor versus clopidogrel and clinical outcomes in patients with ACS. Results from the CREA-ARIAM registry.

INTRODUCTION AND OBJECTIVES: Prior studies have not determined whether the effect of dual antiplatelet therapy (DAPT) cessation on the subsequent risk of major adverse cardiac events (MACE) varies by the choice of P2Y12-inhibitor after acute coronary syndrome (ACS). METHODS: We performed a prespecified subanalysis of a multicenter, prospective registry of ACS patients discharged on ticagrelor or clopidogrel between 2015 and2019. Nonadherence to DAPT was categorized as physician-guided discontinuation and disruption due to adverse effects, nonadherence, or bleeding. The association between DAPT cessation and 1-year MACE was analyzed using multivariate time-updated Cox models with inverse probability of censoring weighted estimators. RESULTS: Out of 2180 patients, 174 (8.3%) prematurely discontinued DAPT (physician-guided, n=126; disruption, n=48). Nonadherent patients were older and had more comorbidities than those on DAPT. Compared with physician-guided discontinuation, disruption occurred earlier after discharge and was more frequent with ticagrelor than with clopidogrel. In time-varying analysis, DAPT cessation was associated with an increased risk of MACE (adjusted HR, 1.32, 95%CI, 1.10-1.76), largely driven by disruption (adjusted HR, 1.47, 95%CI, 1.22-1.73). There was an exponential increase in MACE risk after DAPT cessation within 90 days after ACS, especially after disruption of ticagrelor compared with clopidogrel (Pinteraction<.001). After adjustment for DAPT duration, this interaction was not statistically significant on the additive scale (relative excess risk due to interaction 0.12, 95%CI,-0.99-1.24). CONCLUSIONS: In this all-comers registry, 1 in 12 patients prematurely discontinued DAPT within 1 year after ACS. Compared with physician-recommended discontinuation, disruption resulted in a significantly higher risk of MACE. After adjustment for DAPT duration, this association was not moderated by the choice of P2Y12-inhibitor. Clinical trial registered at ClinicalTrials.gov (Identifier: NCT02500290).

Timing of P2Y12 Inhibitor Administration in Patients With STEMI Undergoing Primary PCI.

BACKGROUND: The optimal timing of P2Y12 inhibitor administration in patients with ST-segment elevation myocardial infarction (STEMI) has not been completely elucidating. OBJECTIVES: This analysis from a prospective multicenter registry sought to assess the safety and effectiveness of P2Y12 inhibitor pretreatment in patients transferred for primary percutaneous coronary intervention (PCI) within a regional STEMI network. METHODS: Pretreatment was defined as P2Y12 inhibitor administration before coronary angiography. Endpoints were major adverse cardiac events (MACE), major bleeding, and net adverse clinical events, a composite of MACE or major bleeding, within 30 days of index admission. Association of P2Y12 inhibitor pretreatment with outcomes was modeled using doubly robust weighted estimators based on propensity score analysis. RESULTS: Of 1,624 patients included, 1,033 received P2Y12 inhibitors before angiography and 591 in the catheterization laboratory (cath lab). The non-pretreated cohort more often had history of coronary artery disease and were more likely to receive antiplatelet therapy before the index admission. After adjustment for confounding and dependent censoring, pretreatment with P2Y12 inhibitors predicted lower risk of MACE (adjusted HR: 0.53; 95% CI: 0.37-0.76), without increasing bleeding risk (adjusted HR: 0.62; 95% CI: 0.36-1.05), resulting in superior net clinical benefit (adjusted HR: 0.47; 95% CI: 0.26-0.86) compared with in-cath lab administration of P2Y12 inhibitors. There was a significant treatment-by-time interaction for MACE risk, whereby the observed benefits of pretreatment only became apparent when time between P2Y12 inhibitor administration and PCI was longer than 80 minutes. CONCLUSIONS: In contemporary patients with STEMI transferred for primary PCI, pretreatment with P2Y12 inhibitors was associated with a significant time-dependent reduction of 30-day MACE without increasing bleeding risk.

N-terminal pro-B-type natriuretic peptide and pulmonary echography are predictors of acute heart failure needing early mechanical ventilation in acute coronary syndrome.

AIM: The aim of this study was to determine the best clinical predictors of acute heart failure needing mechanical ventilation (MV) in the first 48 h of evolution of patients admitted because of acute coronary syndrome (ACS). METHODS: We analyzed a cohort of patients admitted for ACS between February 2017 and February 2018. A pulmonary ultrasound was performed on admission and was considered positive (PE+) when there were three or more B-lines in two quadrants or more of each hemithorax. It was compared with N-terminal pro-B-type natriuretic peptide (NT-proBNP), peak troponin T-us value GRACE (Global Registry of Acute Coronary Events), CRUSADE (Can Rapid risk stratification of Unstable angina patients Suppress ADverse outcomes with Early implementation of the American College of Cardiology and American Heart Association guidelines - Bleeding Score), CACS (Canada Acute Coronary Syndrome risk score), and HAMIOT (Heart Failure after Acute Myocardial Infarction with Optimal Treatment score) scores, shock index, ejection fraction, chest X-ray, and Killip class at admission as predictors of MV in the first 48 h of admission. RESULTS: A total of 119 patients were included: 54.6% with ST elevation and 45.4% without ST elevation. Twelve patients (10.1%) required MV in the first 48 h of evolution. The sensitivity of PE+ was 100% (73.5-100%), specificity 91.6% (84.6-96.1%), and area under the curve was 0.96 (0.93-0.96). The sensitivity of an NT-proBNP value more than 3647 was 88.9% (51.9-99.7%), specificity 92.1% (84.5-96.8%), and area under the curve was 0.905 (0.793-1). The κ statistic between both predictors was 0.579. All the other scores were significantly worse than PE + . CONCLUSION: Lung ultrasound and a high NT-proBNP (3647 ng/L in our series) on admission are the best predictors of acute heart failure needing MV in the first 48 h of ACS. The agreement between both tests was only moderate.

Recovery of Left Ventricular Function and Long-Term Outcomes in Patients With Takotsubo Syndrome.

BACKGROUND: Takotsubo syndrome (TTS) is a form of transient left ventricular (LV) dysfunction that usually resolves within days to weeks. OBJECTIVES: We aimed to assess the predictors and prognostic impact of time-to-LV recovery after TTS. METHODS: Prospective serial imaging data from the nationwide, multicenter RETAKO (REgistry on TAKOtsubo Syndrome) were comprehensively reviewed to assess the timing of LV recovery. Multivariable logistic regression was used to assess factors associated with late (≥10 days) vs early (<10 days) recovery. The long-term risk of all-cause mortality was compared between the late and early recovery groups using fully adjusted Cox models, and using flexible parametric survival models with recovery time included as a continuous variable. RESULTS: Of 1,463 patients included (median age 73 years, 13% men), 373 (25%) had late and 1,090 (75%) had early LV recovery. Older age, history of neurological disorders, bystander coronary artery disease, active cancer, physical triggers, elevated inflammatory biomarkers, cardiogenic shock, and lower LV ejection fraction at admission were independent predictors of late recovery. At 4-year follow-up, the adjusted risk of death was significantly higher in patients with late recovery compared with those with early recovery (16.0% vs 8.6%, adjusted HR: 1.31; 95% CI: 1.12-1.60), with the risk of death increasing by 8% for every additional 10-day delay in time-to-LV recovery (adjusted HR: 1.08; 95% CI: 1.04-1.13). CONCLUSIONS: Late recovery of LV function after TTS is associated with reduced short- and long-term survival. In TTS patients without early LV recovery, closer clinical follow-up might be considered.

Influence of HbA1c levels on platelet function profiles associated with tight glycemic control in patients presenting with hyperglycemia and an acute coronary syndrome. A subanalysis of the CHIPS Study ("Control de HIperglucemia y Actividad Plaquetaria en Pacientes con Síndrome Coronario Agudo").

Patients with hyperglycemia, an acute coronary syndrome and poor glycemic control have increased platelet reactivity and poor prognosis. However, it is unclear the influence of a tight glycemic control on platelet reactivity in these patients. This is a subanalysis of the CHIPS study. This trial randomized patients with hyperglycemia to undergo an intensive glucose control (target blood glucose 80-120 mg/dL), or conventional glucose control (target blood glucose <180 mg/dL). We analyzed platelet function at discharge on the subgroup of patients with poor glycemic control, defined with admission levels of HbA1c higher than 6.5%. The primary endpoint was maximal platelet aggregation following stimuli with 20 µM ADP. We also measured aggregation following collagen, epinephrine, and thrombin receptor-activated peptide, as well as P2Y12 reactivity index and surface expression of glycoprotein IIb/IIIa and P-selectin. A total of 67 patients presented HbA1c ≥ 6.5% (37 intensive, 30 conventional), while 42 had HbA1c < 6.5% (20 intensive, 22 conventional). There were no differences in baseline characteristics between groups. At discharge, patients with HbA1c ≥6.5% had significantly reduced MPA with intensive glucose control compared with conventional control (46.1 ± 22.3 vs. 60.4 ± 20.0%; p = 0.004). Similar findings were shown with other measures of platelet function. However, glucose control strategy did not affect platelet function parameters in patients with HbA1c < 6.5%. Intensive glucose control in patients presenting with an acute coronary syndrome and hyperglycemia results in a reduction of platelet reactivity only in the presence of elevated HbA1c levels.

Comparative Safety and Effectiveness of Ticagrelor versus Clopidogrel in Patients With Acute Coronary Syndrome: An On-Treatment Analysis From a Multicenter Registry.

Background: The net clinical benefit of ticagrelor over clopidogrel in acute coronary syndrome (ACS) has recently been questioned by observational studies which did not account for time-dependent confounders. We aimed to assess the comparative safety and effectiveness of ticagrelor vs. clopidogrel accounting for non-adherence in a real-life setting. Methods: This is a prospective, multicenter cohort study of patients with ACS discharged on ticagrelor or clopidogrel between 2015 and 2019. Major exclusions were previous intracranial bleeding, and the use of prasugrel or oral anticoagulation. Association of P2Y12 inhibitor therapy with 1-year risk of Bleeding Academic Research Consortium Type 3 or 5 bleeding; major adverse cardiac events (MACEs), a composite endpoint of all-cause death, nonfatal myocardial infarction (MI), nonfatal stroke, or urgent target lesion revascularization; definite/probable stent thrombosis; vascular death; and net adverse clinical event (a composite endpoint of major bleeding and MACE) were analyzed according to the "on-treatment" principle, using fully adjusted Cox and Fine-Gray regression models with doubly robust inverse probability of censoring weighted estimators. Results: Among 2,070 patients (mean age 63 years, 27% women, 62.5% ST-elevation MI), 1,035 were discharged on ticagrelor and clopidogrel, respectively. Ticagrelor-treated patients were younger and had few comorbidities, but high rates of medication non-compliance, compared with clopidogrel users. After comprehensive multivariate adjustments, ticagrelor did not increase the risk of major bleeding compared with clopidogrel [subhazard ratio, 1.40; 95% confidence interval (CI), 0.96-2.05], while proved superior in reducing MACE (hazard ratio 0.62; 95% CI, 0.43-0.90), vascular death (subhazard ratio, 0.71; 95% CI, 0.52-0.97) and definite/probable stent thrombosis (subhazard ratio, 0.54; 95% CI, 0.30-0.79); thereby resulting in a favorable net clinical benefit (hazard ratio 0.78; 95% CI, 0.60-0.98) compared with clopidogrel. Results from sensitivity analyses were consistent with those from the primary analysis, whereas those from the intention-to-treat (ITT) analysis went in the opposite direction. Conclusion: Among all-comers with ACS, ticagrelor did not significantly increase the risk of major bleeding, while resulting in a net clinical benefit compared with clopidogrel. Further research is warranted to confirm these findings in high bleeding risk populations. CREA-ARIAM Andalucía: (ClinicalTrials.gov Identifier: NCT02500290); Current pre-specified analysis (ClinicalTrials.gov Identifier: NCT04630288).

[Smoking paradox in acute coronary syndrome without ST-segment elevation]. / La paradoja del tabaco en el síndrome coronario agudo sin elevación del ST.

BACKGROUND AND OBJECTIVE: Although smoking habit is a well-known cardiovascular risk factor, it has been described that smokers admitted because of myocardial infarction have better prognosis than non smoker patients, which is known as "the smoking paradox". The purpose of our work is to investigate whether this phenomenon occurs among patients admitted because of acute coronary syndrome without ST-segment elevation (NSTACS), and which factors help to explain it. PATIENTS AND METHODS: We analysed 563 consecutive patients admitted because of NSTACS on the Coronary Unit of our hospital from January 2005 to December 2006. We analysed clinic and angiographic characteristics and their relationship with in-hospital complications and prognosis. RESULTS: 155 Patients were smokers (27.53%). Smoker patients were younger, more often male, had less risk factors, and more often had a Killip I class at admission (91.6% vs. 79.3%). They had less commonly the combined endpoint of death, reinfarction or Killip Class IV (6.5 vs 13.6%, odds ratio 0.439, confidence interval 0.218 a 0.885, P=.018). This relationship was lost after adjusting to other significant clinical and angiographic data by logistic regression. CONCLUSIONS: Our study confirms the "smoking paradox" amongst NSTACS patients, which is explained by the lower prevalence of previous myocardial infarction, diabetes or multivessel disease. It is essential to recommend quitting the smoking habit.

Prevalence and clinical significance of totally occluded infarct-related arteries in patients with non-ST-segment elevation acute coronary syndromes.

Background Seemingly conflicting findings exist regarding the prognostic impact of totally occluded infarct-related arteries (oIRA) in non-ST elevation acute coronary syndromes (NSTE-ACS). Methods Retrospective analysis of prospective multicenter registry data comprising a single-center NSTE-ACS cohort, aimed at assessing the impact of occluded (TIMI flow 0/1) versus patent culprit vessels (pIRA, TIMI flow 2/3) on the composite endpoint of all-cause death and cardiogenic shock events at 30 days. Results Of 568 patients, 183 (32.5%) had oIRA. Male sex, refractory angina, ECG suggestive of multivessel or left main disease, and larger infarct sizes with inferior/posterolateral wall involvement, were identified as highly specific markers of oIRA. Successful culprit-lesion revascularization occurred more frequently in patent than in oIRA (90% vs. 96%; P = 0.013). Conversely, patients with oIRA more frequently achieved successful revascularization of concurrent non-IRAs including chronic total occlusions than did those with pIRA (28% vs. 3%; P = 0.0005). Multivariate analysis revealed neutral effects of oIRA on outcomes and identified incomplete revascularization as a powerful predictor of mortality. Moderation analysis revealed a significant interaction between completeness of revascularization and IRA patency, whereby among the incompletely revascularized patients, those with oIRA enjoyed a significant survival advantage over their counterparts with pIRA (11.8% vs. 28%, adjusted OR 0.34; 95% CI 0.10-0.73; Pinteraction = 0.012). Conclusions Approximately one third of NSTE-ACS patients in this cohort had oIRA. However, compared with pIRA, the occurrence of oIRA did not portend poor outcomes, likely resulting from the higher rate of incomplete revascularization and increased risk of subsequent mortality in patients with pIRA. These exploratory findings warrant further investigation.

Fondaparinux versus enoxaparin in the contemporary management of non-ST-elevation acute coronary syndromes. Insights from a multicenter registry.

BACKGROUND: Fondaparinux is thought to have the most favorable risk-benefit profile among all anticoagulants in non-ST-elevation acute coronary syndrome (NSTE-ACS). However, conflicting findings exist whether this holds true in current clinical practice. We aimed to assess the net clinical benefit of fondaparinux versus enoxaparin in the contemporary management of NSTE-ACS. METHODS: Analysis of prospective multicenter registry data of NSTE-ACS patients who received fondaparinux or enoxaparin from February 2015, through December 2017. Survival models within a competing risks framework including site-specific random effects, were used to assess the composite of clinically relevant bleedings and major adverse cardiovascular events at 30 days. RESULTS: Of 2094 patients, 1724 (82%) received enoxaparin and 370 (18%) fondaparinux. Both groups were comparable except for a lower prevalence of diabetes and renal impairment, and greater use of transradial approach in the fondaparinux group. Multivariate analysis revealed a net clinical benefit in favour of fondaparinux versus enoxaparin (Subhazard Ratio [SHR] 0.59; 95%CI 0.37-0.92), mainly driven by a reduction in bleeding (SHR 0.57; 95%CI 0.37-0.89). Exploratory analysis suggested greater reductions in bleeding with fondaparinux among patients undergoing transradial approach, revealing a significant interaction between treatment and vascular access on the multiplicative scale (Pinteraction = 0.0056), but not on an additive scale (P = 0.457). Propensity-score-matching analysis yielded similar results. CONCLUSIONS: In contemporary management of NSTE-ACS, fondaparinux seems to provide a favorable net clinical benefit compared with enoxaparin, primarily driven by a bleeding reduction. Effect modification on the safety profile of fondaparinux by the vascular access approach warrants further investigation.

Identification of the culprit artery in inferior myocardial infarction through the 12-lead ECG.

BACKGROUND: Identification of the culprit artery can be helpful in the management of inferior infarction with ST-segment elevation myocardial infarction. Some studies suggest that previously published algorithms intended to help identify the infarct-related artery are suboptimal. Our aim is to develop a better method to localise the culprit artery on the basis of the 12-lead ECG. PATIENTS AND METHODS: We analysed the ECG and coronary angiograms of two different cohorts of patients with inferior ST-segment elevation myocardial infarction. Patients from the first cohort were labelled the derivative cohort (group A), whereas patients in the second cohort were labelled the validation cohort (group B). ST-segment elevation was measured in each lead, and a multiple logistic regression analysis was carried out to determine the best equation to predict the culprit artery. A derived algorithm was then applied to the validation cohort. Next, our algorithm was applied to the total cohort of both groups and compared with four different previously published algorithms. We analysed differences in sensitivity, specificity and area under the curve (AUC). RESULTS: We included 252 patients in the derivative group and 90 in the validation group. The multiple models analysis concluded that the best model should include five leads. This model was validated by internal bootstrapping with 1000 repetitions in group A and externally in group B. The resultant algorithm was as follows: (ST-elevation in III + aVF + V3) - (ST-elevation in II + V6) less than 0.75 mm means that the culprit artery is the left circumflex artery (Cx). If the result is at least 0.75, the culprit artery is the right coronary artery. The total group of both cohorts comprised 342 patients, aged 61.2 ± 12.4 years, of whom 19.6% were female and 80.4% were male. The Cx was the culprit artery in 67 (19.6%) patients. Our algorithm had a sensitivity of 72.3, a specificity of 80.9 and an AUC of 0.766. The AUC value was better compared with the other algorithms. CONCLUSION: The best algorithm to localise the culprit artery includes ST-elevation in leads II and V6 related to Cx, and ST-elevation in leads III, aVF and V3 related to right coronary artery. Our algorithm has been validated internally and externally, and works better than other previously published algorithms.

Role of coronary angiography in patients with a non-diagnostic electrocardiogram following out of hospital cardiac arrest: Rationale and design of the multicentre randomized controlled COUPE trial.

BACKGROUND: Coronary artery disease (CAD) is a major cause of out-of-hospital cardiac arrest (OHCA). The role of emergency coronary angiography (CAG) and percutaneous coronary intervention (PCI) following cardiac arrest in patients without ST-segment elevation myocardial infarction (STEMI) remains unclear. AIMS: We aim to assess whether emergency CAG and PCI, when indicated, will improve survival with good neurological outcome in post-OHCA patients without STEMI who remain comatose. METHODS: COUPE is a prospective, multicentre and randomized controlled clinical trial. A total of 166 survivors of OHCA without STEMI will be included. Potentially non-cardiac aetiology of the cardiac arrest will be ruled out prior to randomization. Randomization will be 1:1 for emergency (within 2 h) or deferred (performed before discharge) CAG. Both groups will receive routine care in the intensive cardiac care unit, including therapeutic hypothermia. The primary efficacy endpoint is a composite of in-hospital survival free of severe dependence, which will be evaluated using the Cerebral Performance Category Scale. The safety endpoint will be a composite of major adverse cardiac events including death, reinfarction, bleeding and ventricular arrhythmias. CONCLUSIONS: This study will assess the efficacy of an emergency CAG versus a deferred one in OHCA patients without STEMI in terms of survival and neurological impairment.

Distortion of the terminal portion of the QRS is associated with poor collateral flow before and poor myocardial perfusion after percutaneous revascularization for myocardial infarction.

AIMS: The distortion of the terminal portion of the QRS has been related to adverse outcome in patients with ST-segment elevation myocardial infarction. METHODS: We studied the relationship of this electrocardiographic pattern with the angiographic findings in patients treated with percutaneous revascularization for ST-segment elevation myocardial infarction. We included 349 patients, 318 treated with primary angioplasty and 31 with rescue angioplasty after failed thrombolysis. RESULTS: Eighty-five patients were found with distortion of the terminal portion of the QRS complex (group 1) and 264 without it (group 2). Collateral flow was absent in 30 patients (35%) from group 1, versus 52 patients (20%) from group 2 [odds ratio (OR) 1.806, 1.097-2.974, P 0.019]. No-reflow occurred in 12 (14%) patients in group 1 versus 17 (6.4%) in group 2 (OR 2.388, 1.091-5.230, P 0.016). Myocardial perfusion was graded 2-3 in 28 patients (58%) of group 1 versus 98 (76%) in group 2 (OR 0.443, 0.220-0.893, P 0.021). CONCLUSION: Patients with ST-segment elevation myocardial infraction showing distortion of the terminal portion of the QRS have worse collateral flow, and present more often no-reflow or poor myocardial perfusion after percutaneous revascularization. These data contribute to explain the worse clinical outcome of these patients.