Novel application of intravascular lithotripsy in stent under-expansion: A single-center experience.

INTRODUCTION: Stent under-expansion due to calcification is associated with a less durable result. The development of intravascular lithotripsy (IVL) has provided clinicians with a readily available, simple-to-use treatment option for coronary calcification, but the use of IVL within a previously stented segment is currently off-license. There are, however, developing data suggesting that the use of IVL can be an effective treatment option for patients with calcific stent under-expansion. METHOD: This was a single-center study of all patients treated with IVL for calcific stent under-expansion between January 2019 and June 2021. The impact of IVL on quantitative coronary angiography (QCA) stenosis and on the minimal stent area (MSA) derived from intracoronary imaging were recorded. The presence of periprocedural complications and adverse cardiovascular events was obtained from the clinical record during the study timeframe. RESULTS: Thirty-nine patients underwent IVL for calcific stent under-expansion during the study time frame with one patient treated with more than one lesion in the same session. In all lesions, there was an improvement in the QCA stenosis with 37 (92.5%) having a residual stenosis of ≤30%. The mean QCA stenosis pre-IVL was 68 ± 21% and following IVL the mean QCA was 18 ± 9% (p < 0.001). In all lesions, there was an improvement in the MSA, with 26 (92.9%) achieving an MSA of more than 4.5 mm2 . The mean MSA pre-IVL was 3.88 ± 1.51 mm2 and following IVL the mean MSA was 7.41 ± 2.34 mm2 (p < 0.001). There were no major procedural complications. Over a mean follow-up of 506 ± 277 days, one patient died from ventricular arrhythmia but there were no other major adverse cardiovascular events. CONCLUSION: This single-center study demonstrates that IVL is a safe and effective treatment for calcific stent under-expansion with good medium-term results.

Distribution of High-Sensitivity Troponin Taken Without Conventional Clinical Indications in Critical Care Patients and Its Association With Mortality.

OBJECTIVES: To describe the distribution of high-sensitivity troponin in a consecutive cohort of patients in critical care units, regardless of clinical indication, and its association with clinical outcomes. DESIGN: Prospective observational study. SETTING: Single-center teaching hospital. PATIENTS: Consecutive patients admitted to two adult critical care units (general critical care unit and neuroscience critical care unit) over a 6-month period. INTERVENTIONS: All patients had high-sensitivity troponin tests performed at admission and tracked throughout their critical care stay, regardless of whether the supervising team felt there was a clinical indication. The results were not revealed to patients or clinicians unless clinically requested. MEASUREMENTS AND MAIN RESULTS: There were 1,033 patients in the study cohort (general critical care unit 750 and neuroscience critical care unit 283). The median high-sensitivity troponin was 21 ng/L (interquartile range, 7-86 ng/L), with 560 patients (54.2%) above the upper limit of normal as defined by the manufacturer. Admission high-sensitivity troponin concentrations above the upper limit of normal in general critical care unit and neuroscience critical care unit were associated with increasing age, comorbidity, markers of illness severity, and the need for organ support. On adjusted analysis, the high-sensitivity troponin concentration remained an independent predictor of critical care mortality in general critical care unit and neuroscience critical care unit. CONCLUSIONS: High-sensitivity troponin elevation, taken outside the context of conventional clinical indications, was common in the critically ill. Such elevations were associated with increasing age, comorbidity, illness severity, and the need for organ support. Admission high-sensitivity troponin concentration is an independent predictor of critical care mortality and as such may represent a novel prognostic biomarker at admission.

Changes in platelet function with inflammation in patients undergoing vascular surgery.

The role of platelets in ischaemic events is well established. Aspirin represents the default antiplatelet and blocks the metabolism of arachidonic acid (AA) at the cyclo-oxygenase enzyme (COX). AA is commonly used as a test of response to aspirin, but recent data raise uncertainty about the validity of this approach. Specifically, in some patients AA-induced clotting is not suppressed, but the level of COX-dependent AA metabolite, thromboxane B2 (TXB2) is negligible. Furthermore, AA-induced whole blood clotting varies dynamically in individuals, who are aspirin responsive according to TXB2 levels. The aim of this study was to assess the level of AA-, ADP- and thrombin-mediated platelet reactivity in patients on aspirin before, during, and after major vascular surgery, which represents a model of on/off vascular inflammation. Firstly, we hypothesized, that in association with this inflammatory episode AA-, ADP- and thrombin-induced clotting would change in a dynamic manner. Secondly, that AA-induced clotting will be modified despite complete suppression of platelet TXB2 production by aspirin throughout the periprocedural period, possibly via a lipoxygenase-mediated mechanism. Fourty patients underwent major vascular surgery (open abdominal aortic aneurysm operation, infrainguinal bypass for subcritical limb ischaemia or peripheral aneurysm repair with bypass). They were all on 75 mg of aspirin prior to and throughout the perioperative period and received 5000 units of unfractionated heparin intraoperatively. AA-, ADP-, and thrombin-induced clotting, AA metabolites (TXB2 and 12-Hyroxyeicosatetraenoic acid (12-HETE)) and inflammatory markers (CRP, IL-6, TNF-α and CD40) were measured pre-procedure and at 2, 24, 48 hours, 3 to 5 days and 3 months after surgery. AA-, ADP- and thrombin-induced platelet reactivity was assessed using thrombelastography. TXB2, 12-HETE, IL-6, TNF-α, CD40 were determined using the sequential competitive binding Enzyme-Linked ImmunoAssay technique and CRP was determined using an immune-turbidimetric test on human serum. There was a transient rise in inflammatory markers in the early perioperative period (CRP at 24, 48 hours and 3 to 5 days p < 0.001 and IL-6 at 2, 24, 48 hours and 3 to 5 days p < 0.001 as compared to baseline). Patients had negligible levels of TXB2 throughout, confirming a consistent therapeutic response to aspirin. There was a transient rise in thrombin-mediated clotting (MAThrombin at 48 hours p = 0.001 and 3 to 5 days p < 0.001) and a fall in AA- and ADP-induced clotting in the early post op period (both MAAA and MAADP p = 0.001 at 2 hours). At 3 months, the level of AA- and ADP-induced clotting was significantly higher than at baseline (p = 0.008 for MAAA and p = 0.002 for MAADP), hence demonstrating a rebound effect. These data demonstrate a novel dynamic variation in platelet aggregation with acute vascular inflammation, including AA-induced whole blood clotting which is apparently COX-1 independent.

Is high sensitivity troponin, taken regardless of a clinical indication, associated with 1 year mortality in critical care patients?

The aim of this study was to assess whether high sensitivity troponin (hs-cTnI) is associated with 1 year mortality in critical care (CC). One year mortality data were obtained from NHS Digital for a consecutive cohort of patients admitted to general CC unit (GCCU) and neuroscience CC unit (NCCU) who had hs-cTnI tests performed throughout their CC admission, regardless of whether the test was clinically indicated. Cox proportional hazards were used to estimate the risk of 1-year mortality. A landmark analysis was undertaken to assess whether any relationship at 1 year was driven by mortality within the first 30 days. A total of 1033 consecutive patients were included. At 1 year 254 (24.6%) patients had died. The admission log(10)hs-cTnI concentration in the entire cohort (HR 1.35 (95% CI 1.05-1.75) p = 0.009 with a bootstrap of 1000 samples) was independently associated with 1 year mortality. On landmark analysis the association with 1 year mortality was driven by 30 day mortality. These results indicate that admission hs-cTnI concentration is independently associated with 1 year mortality in CC and this relationship may be driven by differences in mortality at 30 days.

Association between troponin level and medium-term mortality in 20 000 hospital patients.

INTRODUCTION: Cardiac troponin (cTn) concentrations above the manufacturer recommended upper limit of normal (ULN) are frequently seen in hospital patients without a clinical presentation consistent with type 1 myocardial infarction, and the significance of this is uncertain. The aim of this study was to assess the relationship between medium-term mortality and cTn concentration in a large consecutive hospital population, regardless of whether there was a clinical indication for performing the test. METHOD: This prospective observational study included 20 000 consecutive in-hospital and outpatient patients who had a blood test for any reason at a large teaching hospital, and in whom a hs-cTnI assay was measured, regardless of the original clinical indication. Mortality was obtained via NHS Digital. RESULTS: A total of 20 000 patients were included in the analysis and 18 282 of these (91.4%) did not have a clinical indication for cardiac troponin I (cTnI) testing. Overall, 2825 (14.1%) patients died at a median of 809 days. The mortality was significantly higher if the cTnI concentration was above the ULN (45.3% vs 12.3% p<0.001 log rank). Multivariable Cox analysis demonstrated that the log10 cTnI concentration was independently associated with mortality (HR 1.76 (95% CI 1.65 to 1.88)). Landmark analysis, excluding deaths within 30 days, showed the relationship between cTnI concentration and mortality persisted. CONCLUSION: In a large, unselected hospital population, in 91.4% of whom there was no clinical indication for testing, cTnI concentration was independently associated with medium-term cardiovascular and non-cardiovascular mortality in the statistical model tested.

Validation of the MIRACLE2 Score for Prognostication After Out-of-hospital Cardiac Arrest.

Background: Out-of-hospital cardiac arrest (OHCA) is associated with very poor clinical outcomes. An optimal pathway of care is yet to be defined, but prognostication is likely to assist in the challenging decision-making required for treatment of this high-risk patient cohort. The MIRACLE2 score provides a simple method of neuro-prognostication but as yet it has not been externally validated. The aim of this study was therefore to retrospectively apply the score to a cohort of OHCA patients to assess the predictive ability and accuracy in the identification of neurological outcome. Methods: Retrospective data of patients identified by hospital coding, over a period of 18 months, were collected from a large tertiary-level cardiac centre with a mature, multidisciplinary OHCA service. MIRACLE2 score performance was assessed against three existing OHCA prognostication scores. Results: Patients with all-comer OHCA, of presumed cardiac origin, with and without evidence of ST-elevation MI (43.4% versus 56.6%, respectively) were included. Regardless of presentation, the MIRACLE2 score performed well in neuro-prognostication, with a low MIRACLE2 score (≤2) providing a negative predictive value of 94% for poor neurological outcome at discharge, while a high score (≥5) had a positive predictive value of 95%. A high MIRACLE2 score performed well regardless of presenting ECG, with 91% of patients receiving early coronary angiography having a poor outcome. Conclusion: The MIRACLE2 score has good prognostic performance and is easily applicable to cardiac-origin OHCA presentation at the hospital front door. Prognostic scoring may assist decision-making regarding early angiographic assessment.

Incidence and 1-year outcome of periprocedural myocardial infarction following cardiac surgery: are the Universal Definition and Society for Cardiovascular Angiography and Intervention criteria fit for purpose?

OBJECTIVES: The diagnosis and clinical implications of periprocedural myocardial infarction (PPMI) following coronary artery bypass grafting (CABG) are contentious, especially the importance of PPMI in the interpretation of trial data. METHODS: Consecutive patients admitted to a cardiothoracic critical care unit over a 6-month period following open cardiac surgery had high-sensitivity cardiac troponin I assay performed on admission and every day for 48 h, regardless of whether there was a request by the supervising clinical team. Patients were categorized as PPMI using both the Universal Definition of Myocardial Infarction (UDMI) and Society of Cardiovascular Angiography and Interventions (SCAI) criteria. Multivariable Cox regression analysis was performed to assess whether any relationships between PPMI diagnoses and 1-year mortality were independent. RESULTS: There were 2 groups of consecutive patients: (i) after CABG (n = 245) and (ii) after non-CABG surgery (n = 243). Of the CABG patients, 20.4% met criteria for UDMI PPMI and 87.6% for SCAI PPMI. The diagnosis of UDMI PPMI was independently associated with 1-year mortality on multivariable Cox regression analysis [hazard ratio 4.16 (95% confidence interval 1.28-13.49)]. Of 243 patients who had non-CABG cardiac surgery, 11.4% met criteria for UDMI PPMI and 85.2% for SCAI PPMI but neither were associated with 1-year mortality. CONCLUSIONS: The incidence of SCAI PPMI in a real-world cohort of cardiac surgery patients is so high as to be of limited clinical value. In contrast, a diagnosis of UDMI PPMI post-CABG is independently associated with 1-year mortality, so may have clinical (and research) utility.

Relation of High-Sensitivity Troponin to 1 Year Mortality in 20,000 Consecutive Hospital Patients Undergoing a Blood Test for Any Reason.

This was an observational study of the 1-year outcomes of the 20,000 patients included in the original CHARIOT study. The aim of the study was to assess the association between high sensitivity troponin I (hs-cTnI) concentration and 1 year mortality in this cohort. The original CHARIOT study included a consecutive cohort of in- and out-patients undergoing blood tests for any reason. Hs-cTnI concentrations were measured regardless of whether the clinician requested them. These results were nested and not revealed to the team unless requested for clinical reasons. One year mortality data was obtained from NHS Digital as originally planned. Overall, 1782 (8.9%) patients had died at 1 year. Multivariable Cox regression analysis showed that a hs-cTnI concentration above the upper limit of normal was independently associated with the hazard of mortality (HR 2.23; 95% confidence intervals 1.97 to 2.52). Furthermore, the log (10) hs-cTnI concentration was independently associated with the hazard of 1 year mortality (HR 1.77; 95% confidence intervals 1.64 to 1.91). In conclusion, in a large, unselected hospital population of both in- and out-patients, in 18,282 (91.4%) of whom there was no clinical indication for testing, hs-cTnI concentration was associated with 1 year mortality.

High sensitivity troponin measurement in critical care: Flattering to deceive or 'never means nothing'?

INTRODUCTION: Troponin elevation is central to the diagnosis of acute type 1 myocardial infarction. It is, however, elevated in a range of other conditions, including type 2 myocardial infarction, and this setting is increasingly associated with adverse clinical outcomes. Patients within intensive care frequently have at least one organ failure together with a range of co-morbidities. Interpretation of troponin assay results in this population is challenging. This clinical uncertainty is compounded by the introduction of ever more sensitive troponin assays. AREAS COVERED: The aims of this review are to (a) describe the currently available literature about the use of troponin assays in intensive care, (b) analyse the challenges presented by the introduction of increasingly sensitive troponin assays and (c) assess whether the role of troponin assays in intensive care may change in the future, dependent upon recent and ongoing research suggesting that they are predictive of outcome regardless of the underlying cause: the 'never means nothing' hypothesis.

Distribution of contemporary sensitivity troponin in the emergency department and relationship to 30-day mortality: The CHARIOT-ED substudy.

BACKGROUND: Contemporary sensitivity troponin (cs-cTn) concentrations above the upper limit of normal (ULN) are seen in a wide range of clinical conditions and evidence is growing that suggests cs-cTn may be a biomarker of future morbidity and mortality. OBJECTIVES: Our aim was to test the hypothesis that cs-cTn, measured in the emergency department, may be a biomarker for 30-day mortality, irrespective of the patient's presentation. METHOD: In all 5,708 consecutive cases, contemporary sensitivity troponin I (cs-cTnI) was measured either as requested by the clinical team or as part of the study, in which case both the clinical team and the patient were unaware of the result. Basic demographics were available from the original study and 30-day mortality was derived from NHS Digital data. RESULTS: In patients whose cs-cTnI test was requested solely as part of the study, 30-day mortality increased with increasing cs-cTnI concentrations (0% with undetectable concentrations to 14.7% with concentrations above the ULN). Multivariable Cox regression analysis showed that log(10)cs-cTnI concentration was independently associated with 30-day mortality. CONCLUSION: Increasing cs-cTnI concentrations are associated with higher short-term mortality as well as length of stay. As such, cs-cTnI measurements may provide useful prognostic information.

True 99th centile of high sensitivity cardiac troponin for hospital patients: prospective, observational cohort study.

OBJECTIVE: To determine the distribution, and specifically the true 99th centile, of high sensitivity cardiac troponin I (hs-cTnI) for a whole hospital population by applying the hs-cTnI assay currently used routinely at a large teaching hospital. DESIGN: Prospective, observational cohort study. SETTING: University Hospital Southampton NHS Foundation Trust, Southampton, United Kingdom, between 29 June 2017 and 24 August 2017. PARTICIPANTS: 20 000 consecutive inpatients and outpatients undergoing blood tests for any clinical reason. Hs-cTnI concentrations were measured in all study participants and nested for analysis except when the supervising doctor had requested hs-cTnI for clinical reasons. MAIN OUTCOME MEASURES: Distribution of hs-cTnI concentrations of all study participants and specifically the 99th centile. RESULTS: The 99th centile of hs-cTnI for the whole population was 296 ng/L compared with the manufacturer's quoted level of 40 ng/L (currently used clinically as the upper limit of normal; ULN). Hs-cTnI concentrations were greater than 40 ng/L in one in 20 (5.4%, n=1080) of the total population. After excluding participants diagnosed as having acute myocardial infarction (n=122) and those in whom hs-cTnI was requested for clinical reasons (n=1707), the 99th centile was 189 ng/L for the remainder (n=18 171). The 99th centile was 563 ng/L for inpatients (n=4759) and 65 ng/L for outpatients (n=9280). Patients from the emergency department (n=3706) had a 99th centile of 215 ng/L, with 6.07% (n=225) greater than the recommended ULN. 39.02% (n=48) of all patients from the critical care units (n=123) and 14.16% (n=67) of all medical inpatients had an hs-cTnI concentration greater than the recommended ULN. CONCLUSIONS: Of 20 000 consecutive patients undergoing a blood test for any clinical reason at our hospital, one in 20 had an hs-cTnI greater than the recommended ULN. These data highlight the need for clinical staff to interpret hs-cTnI concentrations carefully, particularly when applying the recommended ULN to diagnose acute myocardial infarction, in order to avoid misdiagnosis in the absence of an appropriate clinical presentation. TRIAL REGISTRATION: Clinicaltrials.gov NCT03047785.

DNA Damage and Repair in Patients With Coronary Artery Disease: Correlation With Plaque Morphology Using Optical Coherence Tomography (DECODE Study).

OBJECTIVE: The aim of this study was to examine DNA ligase activity and expression of DNA damage response pathway (DDR) genes in patients with stable angina (SA) and non-ST elevation myocardial infarction (NSTEMI) and determine whether they correlate with plaque morphology. BACKGROUND: Patients with coronary artery disease (CAD) have evidence of deoxyribonucleic acid (DNA) damage in peripheral blood mononuclear cells (PBMCs). It is unclear whether this represents excess damage or defective DNA repair activity. METHODS: DNA ligase activity and the expression of 22 DDR genes were measured in PBMCs of patients (both SA (n = 47) and NSTEMI (n = 42)) and in age and gender-matched controls (n = 35). Target lesion anatomical assessment was undertaken with frequency domain optical coherent tomography. RESULTS: DNA ligase activity was different across the three groups of patients (control = 119 ±â€¯53, NSTEMI = 115.6 ±â€¯85.1, SA = 81 ±â€¯55.7 units/g of nuclear protein; ANOVA p = 0.023). Pair wise comparison demonstrated that this significance is due to differences between the control and SA patients (p = 0.046). Genes involved in double strand break repair and nucleotide excision repair pathways were differentially expressed in patients with SA and NSTEMI. In SA patients, fibrocalcific plaques were strongly associated with GTSE1, DDB1, MLH3 and ERCC1 expression. By contrast, in NSTEMI patients the strongest association was observed between fibrous plaques and ATM and XPA expression. CONCLUSION: PBMCs from patients with CAD exhibit differences in DNA ligase activity and expression of DDR genes. Expression levels of certain DDR genes are strongly associated with plaque morphology and may play a role in plaque development and progression. Trial Registration Number URL: www.Clinicaltrials.gov; NCT02335086.

High sensitivity troponins in contemporary cardiology practice: are we turning a corner?

INTRODUCTION: Troponin is considered to be the gold standard biomarker for ruling out MI. There has been a drive to improve the diagnostic speed, and as such the high sensitivity cardiac troponin (hs-cTn) assays have been introduced into clinical practice and are now part of international guidelines. Their novel value in clinical practice more generally is becoming apparent. Areas covered: In this review we will evaluate the evidence for the use of hs-cTn assays in clinical practice, the issues with the assay and how the hs-cTn can be utilized in the future as a biomarker of cardiovascular risk. Expert commentary: The use of the hs-cTn assays as a 'rule out' test for MI is compelling, as a 'rule in' there are significant issues relating the specificity of the assay for MI. The future of the assay may lie in population screening and risk modeling.

High sensitivity troponin in the management of tachyarrhythmias.

BACKGROUND: The introduction of the highly sensitive troponin (hs-trop) assays into clinical practice has allowed for the more rapid diagnosis or exclusion of type 1 myocardial infarctions (T1MI) by clinicians, in addition type 2 myocardial infarctions (T2MI) are now more frequently detected. Tachyarrhythmias are one of the common causes of T2MI, the medium and long term outcome for this cohort of T2MI is yet to be clarified. METHODS: Retrospective review of consecutive patients admitted with a diagnosis of either (a) non ST-elevation myocardial infarction (NSTEMI) or (b) tachyarrhythmia was performed. Data were collected on patient demographics and investigations. Patient mortality status was recorded through the Personal Demographics Service (PDS) via NHS Digital. RESULTS: A total of 704 patients were eligible for inclusion to the study. 264 patients were included in the study with a final discharge diagnosis of NSTEMI and 440 patients with a final discharge diagnosis of tachyarrhythmia. There was a significantly higher peak troponin in NSTEMI patients compared to the tachyarrhythmia troponin positive group (4552ng/L vs 571ng/L, p<0.001). Mortality was significantly higher in the troponin positive tachyarrhythmia patients than the troponin negative patients (54 vs 34, 26.2% vs 14.5%, log rank p=0.003), furthermore, the mortality of NSTEMI and troponin positive tachyarrhythmia patients was similar (55 vs 54, 20.8% vs 26.2%, log rank p=0.416). Only one patient (0.14%) was given a formal diagnosis of T2MI. CONCLUSIONS: These data suggest that troponin positive tachyarrhythmia is not a benign diagnosis, and has a mortality rate similar to NSTEMI. Formal labeling as T2MI is rare in real life practice. More investigation into the detection and management of T2MI and troponin positive arrhythmia patients is now warranted.

Detection of individual responses to clopidogrel: Validation of a novel, rapid analysis using thrombelastography 6s.

INTRODUCTION: There is potential value in testing individual response to P2Y12 inhibitors to predict ischemic and bleeding risk in patients undergoing percutaneous coronary intervention. The aims of this study were: (1) to validate the ability of a novel point of care (POC) assay, thrombelastography (TEG) 6s, to detect changes in adenosine diphosphate (ADP)-induced whole blood clotting in volunteers and patients given clopidogrel using TEG 5000 as a reference and (2) to compare a novel, rapid parameter, area under the curve at 15 minutes (AUC15), with the traditional maximum clot amplitude (MA) in TEG 6s. METHODS: A total of 25 participants were included in whom ADP-induced clotting was measured at 4 time points: (1) 12 healthy volunteers given 600 mg of clopidogrel; (2) 12 patients with ACS given 600 mg of clopidogrel; (3) 1 healthy volunteer given 600 mg of clopidogrel on 5 separate occasions. All samples were tested using conventional TEG 5000 and the new POC TEG 6S, and a new parameter called AUC15 was compared with MA in TEG 6s. RESULTS: (1) TEG 5000 and TEG 6s both detected changes in ADP-induced platelet activation. Bland-Altman analysis demonstrated a good level of agreement between them. (2) For TEG 6S, correlation between MA and the novel AUC15 was strong for both thrombin and ADP channels (R2  = 0.867, R = .936, P < .001), and the AUC15 result was available on average 13.3 minutes earlier. CONCLUSIONS: Thrombelastography 6s is a rapid, easy to use and accurate test of ADP-induced clotting using TEG 5000 as a reference. A novel parameter, AUC15, is a viable, time-saving option for this test and has potential value in personalized P2Y12 inhibitor therapy.

Transcatheter aortic valve implantation: where are we now?

Transcatheter aortic valve implantation (TAVI) was first used in clinical practice in 2002. Since 2002, there has been a rapid increase in TAVI activity in patients with symptomatic severe aortic stenosis. This has been supported by systematic randomized data comparing TAVI against the gold standard treatment for the last 50 years' surgical aortic valve replacement. TAVI is now currently a recommended therapeutic intervention in the treatment of severe aortic stenosis patients who are deemed either high risk or inoperable. The indications for TAVI continue to expand. Within this review we will focus on the current guidelines for TAVI, the evidence for it, the complications of TAVI, postprocedure care, the technology available to clinicians now and finally the future perspectives for TAVI.

Does the evidence really suggest that we should completely revascularise bystander disease in patients with ST elevation myocardial infarction undergoing primary angioplasty? Why we still need more definitive trial data to change routine practice.

INTRODUCTION: There remains considerable heterogeneity in the management of significant lesions in non culprit coronary arteries in STEMI patients undergoing primary percutaneous coronary intervention (PPCI). Three recent randomised trials have shown clinical outcome benefit in a complete revascularisation approach when compared to PPCI of the culprit artery alone. By contrast, observational data suggest that an aggressive complete revascularisation may not confer clinical benefit and may, in some cases, be harmful. Areas covered: In this review we discuss the three recent randomised trials that have advocated a complete revasculariation approach in addition to data available from registries. Expert commentary: An adequately powered, randomised controlled trial is required to answer the question of whether complete revascularisation in STEMI patients is beneficial and, if so, whether it should be ischaemia directed and whether it should be at the index procedure or staged.

Is arachidonic acid stimulation really a test for the response to aspirin? Time to think again?

INTRODUCTION: Platelets play a key role in pathogenesis of atherothrombosis. Activated platelets initiate thrombus formation. Antiplatelet therapy (APT) modifies these properties. APT involves aspirin. The existence of 'aspirin resistance' is reported in many populations with cardiovascular disease. The prevalence of this phenomenon is highly variable, affecting more than 50% of patient subgroups in some papers. Areas covered: This review describes the prevalence of 'aspirin resistance', analyses why there is so much apparent variation and addresses whether the commonly used tests of aspirin response are in fact accurately assessing its functional performance. The clinical consequences if arachidonic acid(AA)-mediated assays do not accurately assess the functional performance of aspirin could be important. Expert commentary: Two important issues arise, firstly, that it can no longer be considered robust to use AA-induced platelet activation as a true diagnostic test of functional response to aspirin. It is clear that the output from PFT using AA as an agonist are not even a surrogate for the pharmacological activity of aspirin. Secondly, current data raise important and clinically relevant questions about, how AA stimulation induces clotting in individuals in whom aspirin is effective at its COX-1 target. The evidence indicates at least one recruitable, COX-1-independent pathway that is associated with vascular inflammation.