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Chest pain is a common general practice presentation that requires careful diagnostic assessment because of its diverse and potentially serious causes. However, the evaluation of acute chest pain remains challenging, despite many new insights over the past two decades. The percentage of patients presenting to the emergency departments because of acute chest pain appears to be increasing. Nowadays, there are two essential chest pain-related issues: (i) the missed diagnoses of acute coronary syndromes with a poor short-term prognosis; and (ii) the increasing percentage of hospitalizations of low-risk cases. It is well known that hospitalization of a low-risk chest pain patient can lead to unnecessary tests and procedures, with an increasing trend of complications and burden of costs. Therefore, the significantly reduced financial resources of healthcare systems induce physicians and administrators to improve the efficiency of care protocols for patients with acute chest pain. Despite the efforts of the Scientific Societies in producing statements on this topic, in Italy there is still a significant difference between emergency physicians and cardiologists in managing patients with chest pain. For this reason, the aim of the present consensus document is double: first, to review the evidence-based efficacy and utility of various diagnostic tools, and, second, to delineate the critical pathways (describing key steps) that need to be implemented in order to standardize the management of chest pain patients, making a correct diagnosis and treatment as uniform as possible across the entire country.
Revised by: Luisa Cacciavillani, Aldo Clerico, Emilio Di Lorenzo, Luigi Raffaele Elia, Alberto Menozzi, Adriano Murrone, Marco Sicuro, Massimo Uguccioni
Consensus Document Approval Faculty in Appendix
‘Chest pain’ is the symptom causing 5–9% of admissions to hospital emergency departments (ED) in the western countries.1 The most frequent cause of chest pain is acute coronary syndrome (ACS), at rates of up to 45%.2 In about 2% of cases, ACS is not correctly detected and patients are mistakenly discharged,3 at a cost estimated to be higher than 6 billion dollars,4,5 with missed diagnoses of ACS triggering increases in legal and medical expenses.6
Issues associated with the management of these patients are two-fold, prompting the need: (i) on one hand, to avoid missed diagnoses of ACS, which has a high-mortality rate; and (ii) on the other, to avoid extensive hospitalization of cases at low risk.
The preparation of this consensus paper was prompted by the evolution and innovative implementation of diagnostic tools available in this setting of patients, following publication of the previous ANMCO-SIMEU Italian consensus document in 2009.7
The mentioned evolution is reflected in: (i) the introduction of high-sensitivity troponins and new biomarkers; (ii) the adoption of the newer ESC guidelines on ACS; (iii) the development of non-invasive imaging tests (at rest and with stress); and (iv) the need to introduce the concept of the ‘Chest Pain Team’.
Technically, a chest pain is any pain occurring, anteriorly, between the base of the nose and the umbilicus and, posteriorly, between the occiput and the 12th vertebra, which has no traumatic or other clearly identifiable underlying cause.7
Among patients entering ED with chest pain, ACS is diagnosed and confirmed in 10–20% of cases.8
When a patient is admitted to ED because of acute chest pain, the true goal is to confirm or exclude an ACS [ST elevation myocardial infarction (STEMI), non ST elevation myocardial infarction (NSTEMI) unstable angina (UA)].
Among the causes of chest pain, there are life threatening conditions such as acute aortic syndrome (AAS), pulmonary embolism (PE), and hypertensive pneumothorax.
Aortic dissection and other AASs (aortic ulcer, intramural haematoma) are the causes of chest pain associated with the highest rate of mortality. PE may present with chest pain, dyspnoea, syncope, haemoptysis, cardiac arrest, or a combination of all these symptoms, which may be non-specific, hence the recommendation to use clinical predictive scores such as the Wells Score for PE.9
A missed diagnosis of ACS can occur because uncorrected ECG interpretation, young age of the patient, inexperience of the physician, atypical symptoms presentation, missing ECG at first medical contact (FCM).11
In the absence of ECG abnormalities, the initial anamnestic evaluation also serves to sort the patients into different groups having a lesser or greater likelihood of ACS.
As reported in a meta-analysis of Fanaroff et al.,2 the characteristics of chest pain/discomfort and the associated symptoms can be of used to obtain a probability stratification, but have no significant diagnostic power [LR+(positive likelihood ratio)<3 for all assessed characteristics and for all associated symptoms]. Diaphoresis indicates a slightly higher probability of ACS (LR+1.3–1.4). The presence of symptoms that derive benefit from taking sub-lingual nitrates or from resting is not a predictor of ACS.12
The presentation of symptoms is more atypical in elderly, where dyspnoea tends to dominate over the pain symptom, and also in women and in diabetics.
There are certain scores that integrate anamnesis with ECG and with the results of the first troponin test, introduced initially to assess the prognosis for known ACS: the PURSUIT score,13 the TIMI risk score,14 the HEART score,15 and the GRACE score.16
The physical examination of patients with chest pain/discomfort and suspected ACS is very often normal or almost normal, and if there are signs of haemodynamic instability, or of heart failure, these indicate a particularly severe prognosis. Particular physical signs to look for are those indicating a disease not of myocardial ischaemic origin: pericarditis (pleuritic pain worsening by change in position, pericardial friction rub), PE (sudden onset of dyspnoea and pain, signs of right heart failure), aortic dissection (sudden onset pain often radiating to back, alterations of peripheral pulses) and those suggesting a suspicion of non-cardiac disorders: pneumothorax (abrupt onset of dyspnoea and pain), pneumonia (pleuritic pain, dyspnoea), musculoskeletal (intense fleeting pain), peptic ulcer, and pancreatitis (intense epigastric or substernal pain) diseases.17,18
When a patient has chest pain, 12-lead ECG should be performed within 10min of the FMC. ECG can turn out to be normal in 1/5 of patients with chest pain caused by ACS.19 In terms of electrocardiographic diagnosis, patients affected by ACS can be divided into two categories:
In these cases, only increased biochemical markers of myocardial necrosis will allow a distinction between NSTEMI and UA.
The number of leads involved, the presence and magnitude of ST depression or a transient elevation are all indicative of the extent of the ischaemia and correlated likewise with the prognosis.21
Registry studies show that in 18.5% of cases, the ECG appears normal or doubtful on initial observation, and there is a minimal percentage of patients, with undiagnosed ACS as the result of an ECG having been incorrectly interpreted or badly performed.19 Accordingly, where there is a high likelihood of ACS on the basis of anamnesis, the patient should be monitored continuously or serial 12-lead ECG should be taken. A 12-lead ECG must necessarily be taken in case of symptom recurrence or where symptoms worsen.22 ESC guidelines21 stress the importance of continuous 12-lead monitoring; for certain types of patients, moreover, comparison with previous ECGs is fundamentally important. In the case of left bundle branch block, indications of ischaemic damage will be given by a marked elevation of the ST segment beyond 5mm in the right precordial leads or using the Sgarbossa criteria23: (i) ST elevation more than 1mm and in the same direction (concordant) with the QRS complex, 5 points; (ii) ST depression more than 1mm in leads V1–V3, 3 points; (iii) ST elevation more than 5mm and in the opposite direction (discordant) with the QRS, 2 points. A score of 3 points is required to diagnose an acute myocardial infarction. Similarly, significant ST/T changes accompanying chest pain during right ventricular pacing ECG may be indicative of acute myocardial ischaemia (Figure Figure11).
When there is transmural necrosis of the antero-septal wall in a patient with right bundle branch block, there will be a fall of the R wave in leads V1–V4 with appearance of the Q wave and simultaneous elevation of the ST segment.
If, during an acute episode of chest pain, previously inverted T waves should return to be positive (pseudonormalization), the suspicion of transmural myocardial ischaemia is confirmed.
The need to comparison with previous ECG traces should encourage the use of electronic systems for electrocardiographic archiving. The launch of a national electrocardiography database (https://www.bancadelcuore.it/) by ANMCO is emblematic of the response to this need. With this project, the subject is provided with an electronic card called BancomHeart, allowing remote access to 12-lead electrocardiograms archive stored over time, by way of computer, tablet, and smartphone. An essential characteristic of these databases must be their ease of consultation, hence the possibility of using them via web tools.
For some clinical conditions, the 12-lead ECG can simulate transmural ischaemic myocardial lesion: acute pericarditis, ventricular pre-excitation, Brugada syndrome, early repolarization, electrolytic disorders.
If the 12-lead ECG results normal/non diagnostic, or not ‘definitely ischaemic’, it is better to have the interpretation confirmed as soon as possible by an expert.
Special care must be taken to ensure that the ECG is performed correctly. IEC Standards state that acquisition of the diagnostic ECG signal must be accomplished with a passband of 0.05–150Hz for the diagnosis of ischaemia, infarction, etc. Many other diseases are detectable provided that measures are taken to ensure the quality of the electrical signal, which otherwise could occasion huge diagnostic errors, invalidity and possible legal consequences, as well as considerable ancillary costs. It is also essential that ergometric stress, Holter, telemetry and monitor traces are always ensured compliant with requirements for 12-lead diagnostic ECG, using unreconstructed signals, with a passband of at least 0.05 up to 150Hz. The diagnostic electrocardiography signal must be acquired from 10 electrodes, using 12, simultaneous ECG leads: 6 peripheral, and 6 unipolar precordial.24,25
Many biomarkers are related to diagnostic and prognostic processes associated with acute myocardial infarction. Diagnostic biomarkers for necrosis are creatine-kinase, troponin, Heart-Type Fatty Acid Binding Protein and Copeptin an Arginine Vasopressor Activation. Other biomarkers are related to prognostic process: brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) with biomechamical stress, high sensitive C-reactive protein (Hs-CRP) with inflammation, myeloperoxidase with neutrophilic activation, and endothelin with endothelial activation.26
Abnormal levels of cardiac troponin (cTn), type I (cTn-I) or type T (cTn-T) are considered the standard diagnostic indicator of acute myocardial infarction (AMI).27,28 The third universal definition of myocardial infarction29 considers the raised level of troponin, with a typical curve, as one of the elements indispensable to the diagnosis of AMI.
The elevation of troponin T or I occurs 2–4h following the onset of symptoms.
Laboratory tests of high-analytical sensitivity are used to measure troponin I e T; these employ immunometric methods capable of measuring the 99th percentile of the reference population with an error equal to or less than 10%, as recommended by national guidelines.30
With the ‘new’ troponins, the negative predictive power of a single test is up to 95%, becoming 100% with 2 tests.31 ESC 2015 guidelines on ACS–NSTEMI21 recommend the use of high-sensitivity cardiac troponin (hs-cTn).
The kinetic pattern of hs-cTn is different to that of conventional cTn and consequently the timing of the measurements must be reviewed. Positivity with hs-cTn occurs much earlier than with conventional cTn, and there is evidence32 to show that with this marker, it is possible to rule out AMI within 3h after registration and triage, with a sensitivity and negative predictive values of around 100%.
An increase of cTn indicates only a cardiomyocyte damage and it can occur even in clinical situations other than ACS (Table Table22). Being of lower specificity, these markers can cause a high and growing number of cases involving ‘false positives’, impacting adversely in terms of unsuitability and waste of resources.
An alternative algorithm validated and proposed more recently, of shorter duration with a 0/1hour assessment, is based on a lower and more sensitive cut-off compared to that of the 99th percentile (6ng/L).21 This latter algorithm is based on the fact that hs-cTn is a continuous variable, and as its values increase, so does the probability of AMI. Moreover, this algorithm is based on the assumption that early absolute variations in levels at 1h can be used as surrogates for variations at 3 and 6h, guaranteeing an incremental diagnostic value of the protocol. This protocol has proved useful especially in rule-out procedures, ensuring reliable early discharge of low-risk patients with negative troponin.
To rule out acute infarction of the myocardium, the cTn assay, conducted utilizing methods of the latest generation, though not high sensitivity, should be performed at time 0 and after 6h (considering measurement at 3h as well, however, so as not to miss the peak of the curve). If all the values observed are ≤99th percentile and the variation in concentration is <50% (below the 99th percentile), the patient can be discharged.
If the onset of the symptom was >6h and the patient is asymptomatic, with a GRACE score of <140, and a differential diagnosis can be ruled out, discharge can be allowed possibly after a provocative test, or the test can be performed within a few days following discharge, as will be explained in due course.
Even using hs-cTn, but with tests not directly validated for the 0–1h and 0–3h algorithms, it is advisable to consider application of the 0–6h algorithm.
Among the new biomarkers, copeptin appears to have the most scientific evidence in medical literature.33–37 It represents the C-terminal portion of the pro-hormone of vasopressin secreted from the pituitary gland, and is able to quantify the level of endogenous stress characterizing many clinical conditions, including AMI. Owing to the rapid rise in the level of endogenous stress at the onset of ACS, copeptin immediately becomes positive even as the symptoms are first experienced, hence at the first blood test. A single copeptin assay is therefore sufficient, and this should always be employed in combination with troponin (dual-marker strategy). A patient dischargeable after the first blood test will therefore be one who is troponin-negative and copeptin-negative (<10pmol/L). This combination has a high negative predictive power in respect of AMI (close to 100%) and avoids the need for further troponin tests, thus speeding up management timescales considerably.
There are future developments in this filed. There is an increasing interest in circulating microRNAs, non-coding small ribonucleic acid protein, as potential novel biomarkers for AMI. MicroRNAs increase their plasma levels shortly after the onset of a coronary event and certain isoforms appear exclusively after an AMI. Circulating miRNA seems to improve the diagnostic potential but at the moment the clinical data are very preliminar.38
A maximal exercise test resulting negative for inducible ischaemia can help to avoid needless hospitalizations and allow patient discharge directly from Short-Stay Intensive Observation Unit.40 In certain cases, the exercise test could also be scheduled within a few days following discharge.
The ergometric test (treadmill or bicycle) should be conducted once the patient has been asymptomatic for at least 12h and showing no signs of heart failure for at least 48h. Should the provocative test prove negative, the patient can be discharged directly and considered at low risk.41
The exercise ECG does not reveal high specificity or sensitivity. False responses can be produced in the case of bundle branch blocks or pacing, and reduced specificity of the findings is expected in case of former myocardial infarction. Nonetheless, one study documents a high-negative predictive value (99%) and high confidence in a population with a disease prevalence of 5%.42 On the other hand, the appearance of angina or abnormalities of the ST segment during a low-work load would indicate a high likelihood of critical coronary disease.43
The standard chest X-ray is diagnostic test performed frequently in a critical area on patients presenting with chest pain, especially to rule out pulmonary and vascular disorders.44
ESC guidelines on aortic dissection include the chest X-ray among the diagnostic tests.45
Performing echocardiography quickly in ED was strongly recommended in the ANMCO-SIMEU position paper of 2009,4 especially in cases with a combination of ongoing chest pain, non-diagnostic 12-lead ECG, and haemodynamic instability.46 The latest 2015 ESC guidelines on ACS–NSTEMI21 indicate echocardiography as having an essential role in the diagnosis of acute myocardial ischaemia, as it is able to detect regional wall motion abnormalities of the left ventricle (hypokinesia, akinesia), especially when symptoms are ongoing, and when the differential diagnosis of chest pain are non-coronary cardiovascular (aortic dissection, myocarditis-pericarditis, valve prosthetic dysfunction, etc.).47
Accordingly, an ultrasound scan, exploring not the ‘organ’ (heart, kidney, gall bladder, etc.) but the ‘problem’ (chest pain, haemodynamic instability, dyspnoea, etc.), is frequently performed by a cardiologist, or even by an emergency physician or resuscitator, using echocardiography to investigate not only chest pain but also dyspnoea, transient ischaemic attack (TIA)/stroke to identify cardioembolic sources, low-blood pressure, syncope, etc.48,49
There is still strong debate surrounding the echocardiographic diagnosis of acute myocardial infarction: studies on patients suffering chest pain, observed at a cardiologists-run Chest Pain Unit, showed the usefulness of serial echocardiographic scan of regional left ventricular wall motion in the final diagnosis of acute myocardial infarction, when 12-lead ECG and troponin were still negative. Many other publications insist on the limitations and scant effectiveness of the method in this patient setting.50,51
Stress echocardiography is a technique used for the diagnosis, risk stratification, and prognosis of patients with known or suspected coronary disease employing various stressors that include inotropic drugs (dobutamine) or vasodilators (dipyridamole, adenosine) and also non-pharmacological stressors. Physical exercise is the most physiological stressor and consequently the most utilized and most recommended in literature.52 Assessment is based on abnormalities in regional wall motion of the left ventricle during stress, compared to baseline, and the test is sometimes associated with the assessment of coronary flow reserve (CFR) on the anterior descending artery with adenosine.53
Numerous studies showed that a negative stress echo (using physical or pharmacological stressors) assumes a high negative predictive power and is associated with favourable outcome, as well as demonstrating a higher prognostic value than the ECG ergometric test.54,55
This operator-dependent technique also requires a suitable level of experience and skill which, as suggested by the major European and American scientific societies (European Association of CardioVascular Imaging, American Society of Echocardiography) is obtainable by performing and reporting >100 examinations per year.56
Contrast echocardiography, in a setting of patients with chest pain, serves a dual purpose, allowing: (i) enhancement of the endocardial border during ventricular opacification, significantly improving the analysis of regional wall motion; and (ii) analysis of myocardial perfusion.57
The use of a contrast, which has the effect of enhancing the endocardial border, also increases the sensitivity of the stress echo, improving the assessment of all segments of the left ventricle wall, especially in patients having poor acoustic windows.
For the first time, the 2015 ESC Guidelines on ACS–NSTEMI21 also mention Strain Imaging derived from 2D Speckle-Tracking echocardiography as a possible tool in detecting abnormalities of regional and global systolic function in patients with chest pain.
Coronary computed tomography (CT) using scanners with at least 64 rows of detectors will allow the identification of haemodynamically significant stenosis (>50%), in addition to an already high negative predictive value (higher than 90%) as well as a clear improvement in terms of positive predictive value and specificity.58 This technique should be reserved for an extremely restricted population with a low to intermediate pre-test likelihood, quantifiable at between 20% and 70%.59 This group also includes patients with chest pain not immediately identifiable using the more common diagnostic tools (ECG, biomarkers, blood gas analysis, chest X-ray), or who might be candidates for a triple rule-out (ACS, AAS, and PE) using a single diagnostic test, albeit this approach remains controversial.60 ROMICAT studies61,62 comparing coronary CT with standard assessment procedure in the management of patients with chest pain, found that CT improved clinical decision making, reducing hospitalization time, but was also associated with an increase in downstream testing, exposure to radiation and higher care costs. Consequently, as of today there are no certainties on the real usefulness of coronary CT in decisional algorithms for acute chest pain.
As of today there are no proofs to support the accuracy and the impact of magnetic resonance imaging (MRI) on the management of patients with acute chest pain.
In images obtained during the course of a pharmacological stress test, any myocardial areas with low CFR will show a signal enhancement delayed and attenuated in relation to the surrounding myocardium (hypoperfusion area). A factor of fundamental importance in the interpretation of a myocardial perfusion scan during pharmacological stress is comparison with perfusion images obtained at rest and with delayed-enhancement images.
The capture of diagnostic quality coronary angio-MRI images from the single patient tends not to be constant, and generally will allow the identification of any significant stenoses (>50%) only along the proximal and medial segments of the large epicardial coronary vessels.
A meta-analysis,65 conducted on 37 studies of cardiac MRI involving 2191 patients with known or suspected coronary disease, reported sensitivity, and specificity values of 83% and 86% respectively, in the case of kinematic stress, and of 91% and 81% respectively, in the case of perfusion stress tests. On the basis of these findings, the most recent ESC guidelines on myocardial revascularization indicate recommendation level IA for stress cardiac MRI in the case of symptomatic patients with intermediate pre-test likelihood of obstructive coronary disease, and attribute recommendation class IIB to coronary angio-MRI for the assessment of symptomatic patients examined for obstructive coronary disease.66
Myocardial tomoscintigraphy (SPECT) is used widely for assessing the perfusion of myocardial tissue, the extent of myocardial damage and its impact on cardiac function. In the PROMISE study,67 nuclear tests were the ones most utilized in functional testing arm: 67% as against 22% for stress echo tests and 10% for ergometric tests.
The severity of the patient's illness can influence the result of the test: the number of vessels affected influences results. In effect, sensitivity increases with the rise in the number of vessels affected, from around 85% to 95% if all the 3 main branches are involved. Similarly, the extent of the stenosis is critical in determining positivity. If the stenosis is severe, the test is positive in over 70% of cases. The vessels found most often to be stenotic are the anterior descending and the right coronary artery, on visual inspection, whereas the semi-quantitative method functions better for the right and the circumflex. Indicators of triple vessel disease, in addition to diffuse deficits in the areas involved, include pulmonary capture of the radioactive drug and transient enlargement of the left ventricular lumen. The test should be restricted to those patients presenting with chest pain indicative of coronary disease, but without significant abnormalities on their ECG trace or without biomarker-related abnormalities, making it possible to identify patients at high risk, i.e. those with reversible perfusion defects rather than those who do not have perfusion defects or those who have irreversible perfusion defects as from former necrosis.67,68
The PROMISE study69 was the first to draw a real comparison between anatomical tests (multislice coronary CT) and functional tests (nuclear, stress-echo, ergometric) conducted on patients with chest pain and suspected coronary disease. The primary hypothesis of the study was that cardiac events (combination of death from whatever cause, myocardial infarction, hospitalization for unstable angina, and major peri-procedural complications) at 2 years into follow-up would be fewer in the CT group than in the functional testing group. The study, which enrolled 5000 patients for each arm, showed no difference in predetermined outcomes, legitimating the use of functional tests for the initial diagnosis of symptomatic patients for suspected coronary disease. In short, the study rehabilitated the clinical procedure that had always been practised (and suggested by guidelines) before multislice coronary imaging was made possible by the groundbreaking advent of coronary CT. It is reasonable to concur with Gaibazzi70 in saying that functional tests will never attain the diagnostic accuracy of multislice coronary CT if compared with the gold standard of ‘coronarography’, likewise anatomical, but their capacity for the stratification of patients according to the presence and extent of reversible ischaemia places them notionally on a higher level of usefulness than an anatomical test such as coronary CT.
The paper entitled ‘2015 ACR/ACC/AHA/AATS/ACEP/ASNC/NASCI/SAEM/SCCT/SCMR/SCPC/SNMMI/STR/STS Appropriate Utilization of Cardiovascular Imaging in Emergency Department Patients With Chest Pain’71 provides indications for correct and appropriate use of imaging tests in a setting of patients with chest pain.
It assesses the appropriateness of tests on the basis of four diagnostic entry points: (i) suspected ACS; (ii) suspected PE; (iii) suspected AAS; and (iv) patients for whom it is not possible to establish a probable diagnosis. The grading of tests adopted in the paper is A=appropriate, M=may be appropriate, R=rarely appropriate. Starting from this statement, in this document we report a modified table summarizing the appropriateness of the different non-invasive ultrasound test in the daily management of chest pain patients (Table Table33).
The diagnostic pathway for chest pain patients proposed in this document has the following goals:
The diagnostic pathway proposed in this consensus document will be divided into single steps.
Step 3: diagnostic orientation and in-hospital observation protocol
The main decision-making crossroads coincide with: (i) 12-lead ECG acquiring; and (ii) cardiac troponin dosage.
If the answer to all the above questions is no and there are no signs of haemodynamic instability, a specific diagnostic pathway should be initiated, which will include a troponin assay (Figures Figures44and55).
Small amounts of myocardial damage associated with necrosis can occur in patients with heart failure, kidney failure, myocarditis, arrhythmias, PE, or even during the course of percutaneous coronary or uncomplicated surgical procedures. In these cases, there is no question of infarction, but only of myocardial damage. Accordingly, to have a diagnosis of AMI there must be (even if this alone is not sufficient) a very high initial value of troponin or at least a three-fold increase at the second determination, or, better still, a typical troponin curve showing a rise followed by a fall, and evidence of at least one value higher than the values indicating normality, associated with symptoms or ECG abnormalities suggesting ischaemia, or with positive imaging tests or angiographic data.
A ‘routine’ approach and an unreasoned assessment of troponin plasma levels will result inevitably in:
Figure Figure33 illustrates the decision-making process with regards to selection of the patient who should undergo a troponin assay. The flow chart delineates, first, the assessment of pre-test likelihood of coronary disease (high, intermediate, and low) and thus identifies a subgroup of patients on which the test is not to be performed (low likelihood, atypical symptoms). For this category of patients, if anything, the 0–1h algorithm, indicated in the 2015 ESC guidelines on ACS–NSTEMI, could be applicable.21 For the remaining categories of patients, the 0–3h algorithm with hs-cTn must be integrated with clinical/anamnestic prediction tools such as HEART score or TIMI score.
Values of cTn must be determined on the basis of the 0–3h algorithm (Figure Figure55) in accordance with ESC guidelines. If the high sensitivity test is not available, the 0–6h algorithm can be used. During this period, the patient must be kept under observation by monitoring the 12-lead ECG continuously, or alternatively, by taking serial traces (every hour). It is important that an ECG trace is acquired immediately in case of recurrence/worsening of symptoms. The administration of ASA is advisable.
Where values are above the normality range, the first step is to establish whether or not the increase can be considered typical of ACS (at least a three-fold increase, or a rise/fall type pattern). The delta change depends on the used assay.
If the cTn increase is typical (Figure Figure22), in a patient with a high clinical likelihood of ACS, or an ECG trend appearing positive for ischaemia, or alternatively, an echocardiographic assessment showing positive for left ventricle regional wall motion abnormalities, then a diagnosis of AMI can be given. The inclusion of rest echocardiography in the decision-making pathway is a true novelty in this document.
If the increased troponin level is not typical, other causes of myocardial damage must be considered (heart failure, myocarditis, PE, infection, kidney failure, acute neurological disorder, infiltrative disorders such as amyloidosis, intense physical exercise, etc.).
If a diagnosis of AMI is formulated, the next step in ED (Pathway A, Figure Figure66) is to look for possible factors that might have produced a discrepancy between the demand and supply of O2 (anaemia, hypoxaemia, tachyarrhythmia, etc.). If any one of these factors is found to be present, the diagnosis will be AMI type 2.28 In this case, the possibility of hospitalization in Cardiology ward can be considered especially for a patient with haemodynamic instability or very elevated values of troponin, or persistent ischaemia, or where an extensive ischaemic area is identified (by ECG or echocardiogram). Alternatively, and in the absence of the above criteria, the patient could be hospitalized in an Emergency or Internal Medicine Unit, where steps will be taken promptly to correct the precipitating factors. If factors responsible for the discrepancy between the demand and supply of O2 are not identified, the patient can be diagnosed with myocardial infarction type 1 and must be admitted to a ICU and/or referred to the Cath-lab.
If no diagnosis of myocardial infarction is made (Pathway B, Figure Figure77), and both 12-lead ECG and troponin assays give negative results, the next step in ED is to establish whether or not a clinical diagnosis of unstable angina may be possible. If the answer is yes, the patient should be hospitalized in Cardiology ward. If the answer is no and the patient has had no symptoms for a number of hours (at least 6), given a GRACE score of <140 with cTn and ECG both stable, a provocative test can be performed either immediately or after discharge (within a few days), depending on the case.
If the answer is no but there remains a strong suspicion of non-coronary disease or ACS continues to be suspected or the GRACE score is >140, the patient can be observed for a period (8–12h depending on local logistics) in Short Stay Intensive Observation, Chest Pain Unit or ED. Steps that must be taken during this stage of the pathway include 12-lead ECG monitoring, additional troponin tests if opportune, the administration of aspirin if opportune, and any other diagnostic test (including chest X-ray) that could be of use in formulating a definitive diagnosis. This stage likewise can be concluded with a provocative test before discharge or thereafter (within a few days), depending on the case, favouring a test before discharge if the patient has a history of coronary artery disease.
The management of patients with chest pain in an ED setting needs a close integration and cooperation between emergency physicians and cardiologists, together with nursing staff, especially triage nurses. A prerequisite for such integration is that the organization
should hinge on a shared awareness of the diagnostic pathway. This is the basis for proposing the creation of a Chest Pain Team—comprising an emergency physician, a cardiologist and a triage nurse—in every hospital facility.
Although the many advances and innovations of recent years, the assessment of patients with chest pain continues to be a daily challenge. Given the economic impact and the risk of complications induced by inappropriate tests and examinations carried out on a patient with chest pain, better pathways must be studied, not least in order to avoid pointless examinations and unnecessary hospitalizations.
This document embraces and applies the new proposals offered by medical literature in matters of diagnostic testing and clinical/anamnestic assessment, in seeking to formulate a rule-in/rule-out process for ACS that is both modern and efficient. Above all, the introduction of hs-cTn assays has allowed healthcare professionals to identify a higher number of ACS cases, improving the sensitivity of rule-in/rule-out tests in particular, but has led at the same time to overestimations in diagnosis, and very often to unnecessary hospitalizations, accompanied by a significant waste of economic resources.
The role of this document is to provide operators in the field with guidance on making the right choices, so that the results of different diagnostic tests can be balanced and integrated correctly.
The organization of ED and cardiology departments around a shared diagnostic pathway is the first step in ensuring efficient management of patients with chest pain.
The main purpose of the document is to promote a nationwide standardization of diagnosis and care protocols for patients with chest pain, with the aim of improving outcomes.
Conflict of interest: none declared.
Abrignani Maurizio Giuseppe, Alunni Gianfranco, Amico Antonio, Francesco, Amodeo Vincenzo, Angeli Fabio, Aspromonte Nadia, Audo Andrea, Azzarito Michele, Battistoni Ilaria, Bianca Innocenzo, Bisceglia Irma, Bongarzoni Amedeo, Bonvicini Marco, Calculli Giacinto, Caldarola Pasquale, Capecchi Alessandro, Caporale Roberto,Caretta Giorgio, Carmina Maria Gabriella, Casazza Franco, Casolo Giancarlo, Casu Gavino, Cemin Roberto, Giacomo Chiarandà, Chiarella Francesco, Chiatto Mario, Ciccone Marco Matteo, Cicini Maria Paola, Colivicchi Furio, D’Agostino Carlo, De Luca Giovanni, De Maria Renata, Del Sindaco Donatella, Di Fusco Stefania Angela, Egidy Assenza Gabriele, Egman Sabrina, Enea Iolanda, Fattirolli Francesco, Favilli Silvia, Ferraiuolo Giuseppe, Francese Giuseppina Maura, Gabrielli Domenico, Geraci Giovanna, Giardina Achille, Greco Cesare, Gregorio Giovanni, Iacoviello Massimo, Khoury Georgette, Ledda Antonietta, Luca Fabiana, Lukic Vjerica, Macera Francesca, Marini Marco, Masson Serge, Maurea Nicola, Mazzanti Marco, Mennuni Mauro, Menotti Alberto, Mininni Nicola, Moreo Antonella, Moretti Luciano, Mortara Andrea, Mureddu Gian Francesco, Musumeci Giuseppe, Navazio Alessandro, Nicolosi Gian Luigi, Oliva Fabrizio, Parrini Iris, Patanè Leonardo, Pini Daniela, Pino Paolo Giuseppe, Pirelli Salvatore, Procaccini Vincenza, Pugliese Francesco Rocco, Pulignano Giovanni, Radini Donatella, Rao Carmelo Massimiliano, Riccio Carmine, Roncon Loris, Rugolotto Matteo, Sanna Fabiola, Sauro Rosario, Scherillo Marino, Severi Silva, Silvestri Paolo, Sisto Francesco, Tarantini Luigi, Urbinati Stefano, Vatrano Marco, Vianello Gabriele, Vinci Eugenio.