Chest pain centers: moving toward proactive acute coronary care

Ischemic heart disease is the major cause of death, disability and lost productivity in the developed countries of the world. The evolution of cardiac care units has improved patient survival from myocardial infarctions, but requires a high-tech, very expensive treatment facility. Chest pain centers, located in emergency departments, present an efficient alternative to triage patients with chest pain, providing prompt and accurate diagnosis, risk evaluation and appropriate treatments. Hospitals benefit from this cost-effective approach as resources are used more efficiently, and patients benefit from a supportive treatment facility that focuses on early intervention. Early recognition of prodromal unstable angina symptoms and intercession with newly developed treatment can help move the cardiologist toward a more proactive role that minimizes or avoids myocardial infarctions rather than reacting to the acute event.     

Chest pain units. Organization and protocol for the diagnosis of acute coronary syndromes

The two main goals of chest pain units are the early, accurate diagnosis of acute coronary syndromes and the rapid, efficient recognition of low-risk patients who do not need hospital admission. Many clinical, practical, and economic reasons support the establishment of such units. Patients with chest pain account for a substantial proportion of emergency room turnover and their care is still far from optimal: 8% of patients sent home are later diagnosed of acute coronary syndrome and 60% of admissions for chest pain eventually prove to have been unnecessary.We present a systematic approach to create and manage a chest pain unit employing specialists headed by a cardiologist. The unit may be functional or located in a separate area of the emergency room. Initial triage is based on the clinical characteristics, the ECG and biomarkers of myocardial infarct. Risk stratification in the second phase selects patients to be admitted to the chest pain unit for 6-12 h. Finally, we propose treadmill testing before discharge to rule out the presence of acute myocardial ischemia or damage in patients with negative biomarkers and non-diagnostic serial ECGs.     

Chest pain syndromes in pregnancy

Chest pain syndromes in pregnancy include numerous catastrophic cardiovascular events. Acute myocardial infarction, aortic dissection, pulmonary embolism, and amniotic fluid embolism are the most important causes of nonobstetric mortality and morbidity in pregnancy. Each of these could result in poor maternal and fetal outcomes if not diagnosed and treated in a timely fashion. However, their diagnosis and management is limited by fetal risks of diagnostic procedures, dangers of pharmacotherapy and interventions that have neither been widely studied nor validated. This article reviews the current literature on epidemiology, risk factors, pathogenesis, diagnosis, and management of 4 potentially lethal chest pain syndromes in pregnancy.     

Coverage of pointed acute coronary syndromes in the general hospital centers

This study presents data on the management of acute coronary syndromes collected in a national registry organized by the french Collège national des cardiologues des h?pitaux généraux in September 2000. In all 86 institutions participated and data from 607 patients (mean age: 67 years; 413 men) were analysed. The final diagnosis was unstable angina in 38%, non-Q wave myocardial infarction in 21% and Q-wave myocardial infarction in 40.5%. Median time to admission was 4 h. At symptom onset, patients called their general practitioners in 46% of cases, emergency ambulatory units in 31% of cases and arrived to the hospital on their own in 23% of cases. Observance of the European Society of Cardiology guidelines was good for patients without ST segment elevation. In patients with ST segment elevation, 9% had pre-hospital thrombolysis, 28% hospital thrombolysis, and 27% had angioplasty within 48 h of admission, including 9% with rescue angioplasty. Overall, 57% of patients with ST segment elevation received reperfusion therapy. In hospital mortality was 6% for the whole cohort, and 11% for patients with acute myocardial infarctions. By multivariate analysis, predictors of in-hospital mortality were age, type of acute coronary syndrome, absence of beta-blocker therapy, and absence of coronary angiography.     

Chest pain: coronary or esophageal?

Although it is often relatively easy for the clinician to differentiate between the heart and the esophagus as sources of chest pain, there remains a substantial minority of patients in whom this task is difficult. We have attempted to review points of differential significance which can be elicited through assessment of the patient's symptoms. Diagnostic studies for the detection of esophageal disorders have been reviewed, and the relative usefulness of these studies has been emphasized. As the result of advancements in diagnostic techniques as well as better understanding of esophageal pathophysiology, the clinician is now capable of accurately identifying the esophagus as the source of chest pain.     

Cardiac markers in the diagnosis of acute coronary syndromes

Evolution of the role of cardiac markers has ranged from the diagnosis of acute myocardial infarction in patients with nondiagnostic electrocardiograms to prognostic risk stratification and to guide therapy. The technology to provide rapid, real time measurements by immunoassay has provided the laboratory and clinician with a range of test options. The principal changes have been the use of rapid serial marker measurements of well-recognized cardiac markers, and the development of immunoassays for the cardiac structural proteins. Measurement of cardiac troponins has generated a new diagnostic paradigm in patients with suspected acute coronary syndromes. There is now a new gold standard biochemical test for myocardial infarction. A range of interventions can be guided by troponin measurement. The use of troponin measurements is central to management of patients with suspected acute coronary syndromes. Future developments in this field will focus on the role of existing and novel markers of inflammation and ischemia.     

Primary angioplasty in acute coronary syndromes with ST-segment elevation: experience of three Alsacian centers

The guidelines of the European Society of Cardiology, published in 2003, consider primary angioplasty as the preferred treatment strategy in acute coronary syndromes with ST-segment elevation, if the procedure can be performed within 90 min after first medical contact. We report the experience of three Alsacian centers running a common prospective registry with 2504 consecutive patients enroled between January 1999 and December 2004. The average age of the patients was 62 years with a proportion of 24% women. The time delay "pain to admission" was > or =3 hours in 55.9% of the cases. The treatment delay "door to catheterisation needle" was 59 min and the mean delay "door-to-reperfusion" was 79 min. The study population was representative of the real world including subsets of patients with a particulary high risk profile: age > or =70 years in 33%, a Killip grade > or =3 in 11.5%, rescucitated sudden death in 6.6% and cardiogenic shock in 10.9% of the patients respectively. The immediate procedural success rate (Timi 3 flow) in the treated coronary artery was 96.5%. The overall inhospital mortality-rate was 9.3%. The combinations of rescucitated sudden death--cardiogenic shock or age > or =75 years--cardiogenic shock were associated with a poor clinical outcome and mortality rates of 69% and 72.6% respectively, where as in the absence of abovementioned clinical high risk settings, the mortality rate was as low as 1.4%. The overall bleeding complication rate was 1.4%. The policy of systematic primary angioplasty in acute coronary syndromes with ST-Segment elevation appears to be coherent. The procedural complications and the in-hospital mortality rates were low, except in the presence of above mentioned clinical high risk settings.     

Acute ischemic syndromes. Chest pain center concept

CPCs have been developed to meet the clinical challenge posed by the diverse group of patients presenting to the ED with findings suggestive of a coronary event. Using a protocol-driven approach, high- and low-risk patients can be identified on presentation, facilitating urgent therapy in the former and triage of the latter to more deliberate management. Most CPCs focus on low-risk patients who are being increasingly managed by accelerated diagnostic protocols. These methods comprise systematic strategies that include innovative diagnostic approaches during a 6 to 12 hour period of observation with serial ECGs, continuous monitoring and cardiac biomarker measurements. A negative evaluation is usually followed by predischarge stress testing, and positive findings mandate admission. An essential aspect of the CPC strategy is continuity of care for patients with negative cardiac evaluations. Current data indicate that management of low-risk patients with chest pain in a CPC is safe accurate, and appears to be cost-effective.     

Chest pain after coronary interventional procedures

Chest pain following successful percutaneous coronary interventions is a common problem. Although the development of chest pain after coronary interventions may be of benign character, it is disturbing to patients, relatives and hospital staff. Such pain may be indicative of acute coronary artery closure, coronary artery spasm or myocardial infarction, but may also simply reflect local coronary artery trauma. The distinction between these causes of chest pain is crucial in selecting optimal care. Management of these patients may involve repeat coronary angiography and additional intervention. Commonly, repeat coronary angiography following percutaneous transluminal coronary angioplasty (PTCA) in patients with chest pain demonstrates widely patent lesion sites suggesting that the pain was due to coronary artery spasm, coronary arterial wall stretching or was of non-cardiac origin. As reported by the National Heart, Lung and Blood Institute PTCA Registry, 4.6% of patients after angioplasty have coronary occlusions, 4.8% suffer a myocardial infarction, and 4.2% have coronary spasm. The frequency of chest pain after new device coronary interventions (atherectomy and stenting) seems to be even higher. However, only the minority of patients with post-procedural chest pain have indeed an ischemic event. Therefore, the vast majority of patients have recurrent chest pain without any signs of ischemia. There is some evidence that non-ischemic chest pain after coronary interventions is more common after stent implantation as compared to PTCA (41% vs. 12%). This may be due to the continuous stretching of the arterial wall by the stent as the elastic recoil occurring after PTCA is minimized. In conclusion, chest pain after coronary interventional procedures may potentially be hazardous when due to myocardial ischemia. However, especially after coronary stent placement, cardiologists must consider "stretch pain" due to the overdilation and stretching of the artery caused by the stent in the differential diagnosis. Clinically, it is, therefore, important to recognize that in addition to ischemia-related chest pain other types of chest pain do exist with cardiac origin.     

Current management of acute coronary syndromes in Australia: observations from the acute coronary syndromes prospective audit

Background: Acute coronary syndromes (ACS) management is now well informed by guidelines extrapolated from clinical trials. However, most of these data have been acquired outside the local context. We sought to describe the current patterns of ACS care in Australia. Methods: The Acute Coronary Syndrome Prospective Audit study is a prospective multi‐centre registry of ST‐segment elevation myocardial infarction (STEMI), high‐risk non‐ST‐segment elevation ACS (NSTEACS‐HR) and intermediate‐risk non‐ST‐segment elevation ACS (NSTEACS‐IR) patients, involving 39 metropolitan, regional and rural sites. Data included hospital characteristics, geographic and demographic factors, risk stratification, in‐hospital management including invasive services, and clinical outcomes. Results: A cohort of 3402 patients was enrolled; the median age was 65.5 years. Female and non‐metropolitan patients comprised 35.5% and 23.9% of the population, respectively. At enrolment, 756 (22.2%) were STEMI patients, 1948 (57.3%) were high‐risk NSTEACS patients and 698 (20.5%) were intermediate‐risk NSTEACS patients. Evidence‐based therapies and invasive management use were highest among suspected STEMI patients compared with other strata (angiography: STEMI 89%, NSTEACS‐HR 54%, NSTEACS‐IR 34%, P < 0.001) (percutaneous coronary intervention: STEMI 68.1%, NSTEACS‐HR 22.2%, NSTEACS‐IR 8.1%, P < 0.001). In hospital mortality was low (STEMI 4.0%, NSTEACS‐HR 1.8%, NSTEACS‐IR 0.1%, P < 0.001), as was recurrent MI (STEMI 2.4%, NSTEACS‐HR: 2.8%, NSTEACS‐IR 1.2%, P = 0.052). Conclusion: There appears to be an ‘evidence‐practice gap’ in the management of ACS, but this is not matched by an increased risk of in‐hospital clinical events. Objective evaluation of local clinical care is a key initial step in developing quality improvement initiatives and this study provides a basis for the improvement in ACS management in Australia.