Luke K. Hermann

2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with thoracic aortic disease: Executive summary: A report of the american college of cardiology foundation/american heart association task force on practice guidelines, american association for thoracic surgery, american college of radiology, american stroke association

2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the Diagnosis and Management of Patients With Thoracic Aortic Disease A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of Thoracic Surgeons, and Society for Vascular Medicine

2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the Diagnosis and Management of Patients With Thoracic Aortic Disease

It is essential that the medical profession play a central role in critically evaluating the evidence related to drugs, devices, and procedures for the detection, management, or prevention of disease. Properly applied, rigorous, expert analysis of the available data documenting absolute and relative

Sensitivity of the Aortic Dissection Detection Risk Score, a Novel Guideline-Based Tool for Identification of Acute Aortic Dissection at Initial Presentation Results From the International Registry of Acute Aortic Dissection

Background— In 2010, the American Heart Association and American College of Cardiology released guidelines for the diagnosis and management of patients with thoracic aortic disease, which identified high-risk clinical features to assist in the early detection of acute aortic dissection. The sensitivity of these risk markers has not been validated. Methods and Results— We examined patients enrolled in the International Registry of Acute Aortic Dissection from 1996 to 2009. The number of patients with confirmed acute aortic dissection who presented with 1 or more of 12 proposed clinical risk markers was determined. An aortic dissection detection (ADD) risk score of 0 to 3 was calculated on the basis of the number of risk categories (high-risk predisposing conditions, high-risk pain features, high-risk examination features) in which patients met criteria. The ADD risk score was tested for sensitivity. Of 2538 patients with acute aortic dissection, 2430 (95.7%) were identified by 1 or more of 12 proposed clinical risk markers. With the use of the ADD risk score, 108 patients (4.3%) were identified as low risk (ADD score 0), 927 patients (36.5%) were intermediate risk (ADD score 1), and 1503 patients (59.2%) were high risk (ADD score 2 or 3). Among 108 patients with no clinical risk markers present (ADD score 0), 72 had chest x-rays recorded, of which 35 (48.6%) demonstrated a widened mediastinum. Conclusions— The clinical risk markers proposed in the 2010 thoracic aortic disease guidelines and their application as part of the ADD risk score comprise a highly sensitive clinical tool for the detection of acute aortic dissection.

Yield of Routine Provocative Cardiac Testing Among Patients in an Emergency Department–Based Chest Pain Unit

IMPORTANCE The American Heart Association recommends routine provocative cardiac testing in accelerated diagnostic protocols for coronary ischemia. The diagnostic and therapeutic yield of this approach are unknown. OBJECTIVE To assess the yield of routine provocative cardiac testing in an emergency department-based chest pain unit. DESIGN AND SETTING We examined a prospectively collected database of patients evaluated for possible acute coronary syndrome between March 4, 2004, and May 15, 2010, in the emergency department-based chest pain unit of an urban academic tertiary care center. PARTICIPANTS Patients with signs or symptoms of possible acute coronary syndrome and without an ischemic electrocardiography result or a positive biomarker were enrolled in the database. EXPOSURES All patients were evaluated by exercise stress testing or myocardial perfusion imaging. MAIN OUTCOMES AND MEASURES Demographic and clinical features, results of routine provocative cardiac testing and angiography, and therapeutic interventions were recorded. Diagnostic yield (true-positive rate) was calculated, and the potential therapeutic yield of invasive therapy was assessed through blinded, structured medical record review using American Heart Association designations (class I, IIa, IIb, or lower) for the potential benefit from percutaneous intervention. RESULTS In total, 4181 patients were enrolled in the study. Chest pain was initially reported in 93.5%, most (73.2%) were at intermediate risk for coronary artery disease, and 37.6% were male. Routine provocative cardiac testing was positive for coronary ischemia in 470 (11.2%), of whom 123 underwent coronary angiography. Obstructive disease was confirmed in 63 of 123 (51.2% true positive), and 28 (0.7% overall) had findings consistent with the potential benefit from revascularization (American Heart Association class I or IIa). CONCLUSIONS AND RELEVANCE In an emergency department-based chest pain unit, routine provocative cardiac testing generated a small therapeutic yield, new diagnoses of coronary artery disease were uncommon, and false-positive results were common.

The Limited Utility of Routine Cardiac Stress Testing in Emergency Department Chest Pain Patients Younger Than 40 Years

STUDY OBJECTIVE This is a study designed to evaluate the utility of routine provocative cardiac testing in low-risk young adult (younger than 40 years) patients evaluated for an acute coronary syndrome in an emergency department (ED) setting. METHODS This was a retrospective observational study of patients aged 23 to 40 years who were evaluated for acute coronary syndrome in an ED-based chest pain unit from March 2004 to September 2007. All patients had serial cardiac biomarker testing to rule out myocardial infarction and then underwent provocative cardiac testing to identify the presence of myocardial ischemia. Patients were excluded from the study if they had known coronary artery disease, had ECG findings diagnostic of myocardial infarction or ischemia, or self-admitted, or tested positive for cocaine use. RESULTS Of the 220 patients who met inclusion criteria, 6 patients (2.7%; 95% confidence interval 1% to 5.8%) had positive stress test results. Among these 6 patients, 4 underwent subsequent coronary angiography that demonstrated no obstructive coronary disease, suggesting the initial provocative study was falsely positive. For the remaining 2 patients, no diagnostic angiography was performed. Discounting the patients who had negative angiography results, only 2 of 220 study patients (0.9%; 95% confidence interval 0.1% to 3.2%) had a provocative test result that was positive for myocardial ischemia. CONCLUSION In our study, a combination of age younger than 40 years, nondiagnostic ECG result, and 2 sets of negative cardiac biomarker results at least 6 hours apart identified a patient group with a very low rate of true-positive provocative testing. Routine stress testing added little to the diagnostic evaluation of this patient group and was falsely positive in all patients who consented to diagnostic coronary angiography (4 of 6 cases).

Diagnostic value of coronary artery calcium scoring in low-intermediate risk patients evaluated in the emergency department for acute coronary syndrome.

Early and accurate triage of patients with possible ischemic chest pain remains challenging in the emergency department because current risk stratification techniques have significant cost and limited availability. The aim of this study was to determine the diagnostic value of the coronary artery calcium score (CACS) for the detection of obstructive coronary artery disease (CAD) in low- to intermediate-risk patients evaluated in the emergency department for suspected acute coronary syndromes. A total of 225 patients presenting to the emergency department with acute chest pain and Thrombolysis In Myocardial Infarction (TIMI) scores <4 who underwent non-contrast- and contrast-enhanced coronary computed tomographic angiography were included. CACS was calculated from the noncontrast scan using the Agatston method. The prevalence of obstructive CAD (defined from the contrast scan as ≥ 50% maximal reduction in luminal diameter in any segment) was 9% and increased significantly with higher scores (p <0.01 for trend). CACS of 0 were observed in 133 patients (59%), of whom only 2 (1.5%) had obstructive CAD. The diagnostic accuracy of CACS to detect obstructive CAD was good, with an area under the receiver-operating characteristic curve of 0.88 and a negative predictive value of 99% for a CACS of 0. In a multivariate model, CACS was independently associated with obstructive CAD (odds ratio 7.01, p = 0.02) and provided additional diagnostic value over traditional CAD risk factors. In conclusion, CACS appears to be an effective initial tool for risk stratification of low- to intermediate-risk patients with possible acute coronary syndromes, on the basis of its high negative predictive value and additive diagnostic value.

Screening, Evaluation, and Early Management of Acute Aortic Dissection in the ED

Acute aortic dissection (AAD) is a rare and lethal disease with presenting signs and symptoms that can often be seen with other high risk conditions; diagnosis is therefore often delayed or missed. Pain is present in up to 90% of cases and is typically severe at onset. Many patients present with acute on chronic hypertension, but hypotension is an ominous sign, often reflecting hemorrhage or cardiac tamponade. The chest x-ray can be normal in 10-20% of patients with AAD, and though transthoracic echocardiography is useful if suggestive findings are seen, and should be used to identify pericardial effusion, TTE cannot be used to exclude AAD. Transesophageal echocardiography, however, reliably confirms or excludes the diagnosis, where such equipment and expertise is available. CT scan with IV contrast is the most common imaging modality used to diagnose and classify AAD, and MRI can be used in patients in whom the use of CT or IV contrast is undesirable. Recent specialty guidelines have helped define high-risk features and a diagnostic pathway that can be used the emergency department setting. Initial management of diagnosed or highly suspected acute aortic dissection focuses on pain control, heart rate and then blood pressure management, and immediate surgical consultation.

Sensitivity of the Aortic Dissection Detection Risk Score, a Novel Guideline-Based Tool for Identification of Acute Aortic Dissection at Initial Presentation

Background— In 2010, the American Heart Association and American College of Cardiology released guidelines for the diagnosis and management of patients with thoracic aortic disease, which identified high-risk clinical features to assist in the early detection of acute aortic dissection. The sensitivity of these risk markers has not been validated. Methods and Results— We examined patients enrolled in the International Registry of Acute Aortic Dissection from 1996 to 2009. The number of patients with confirmed acute aortic dissection who presented with 1 or more of 12 proposed clinical risk markers was determined. An aortic dissection detection (ADD) risk score of 0 to 3 was calculated on the basis of the number of risk categories (high-risk predisposing conditions, high-risk pain features, high-risk examination features) in which patients met criteria. The ADD risk score was tested for sensitivity. Of 2538 patients with acute aortic dissection, 2430 (95.7%) were identified by 1 or more of 12 proposed clinical risk markers. With the use of the ADD risk score, 108 patients (4.3%) were identified as low risk (ADD score 0), 927 patients (36.5%) were intermediate risk (ADD score 1), and 1503 patients (59.2%) were high risk (ADD score 2 or 3). Among 108 patients with no clinical risk markers present (ADD score 0), 72 had chest x-rays recorded, of which 35 (48.6%) demonstrated a widened mediastinum. Conclusions— The clinical risk markers proposed in the 2010 thoracic aortic disease guidelines and their application as part of the ADD risk score comprise a highly sensitive clinical tool for the detection of acute aortic dissection.

Opiates and acute pulmonary oedema: Addicted to the wrong therapy

We read with interest Dr Sosnowski’s article ‘Lack of effect of opiates in the treatment of acute cardiogenic pulmonary oedema’ in this issue of Emergency Medicine Australasia not only because it helps to dispel the persistent mythology that surrounds the use of i.v. opiates in the treatment of acute pulmonary oedema (APO), but also because it points out several of the fundamental issues that plague the current management of acute decompensated heart failure (ADHF). As is clear from the article, there is a dearth of good evidence to help guide the management of ADHF patients. In the current age of evidence-based medicine, this is worth noting because it places front-line providers in the difficult position of constructing their own treatment algorithms, without the tools typically available to them. Not a small matter given the prevalence and seriousness of the disease in question. Heart failure has reached near epidemic proportions with an estimated 550 000 new cases annually in the United States and a hospitalization rate that has increased 159% during the past decade. Although we have become more successful at treating advanced cardiac disease via aggressive medical and interventional management, we have effectively created a growing population of cardiac cripples, patients who will predictably present with exacerbation of ADHF and APO as their cardiac function progressively declines. Of equal concern, heart failure is a disease with an abysmal prognosis. With mortality rates that exceed those of myocardial infarction at both time points of 30 days and 1 year, there is a strong impetus to continue to improve the ways we provide care for this patient group. Interestingly, despite the tremendous burden heart failure places on the medical system, few prospective randomized trials have been conducted to establish best care. Most of the literature that exists, as reflected in Sosnowski’s current review article, consists of small, poorly designed studies that do little to delineate the true efficacy of individual therapeutic interventions. Given the lack of good evidence to guide their practice, it is not surprising that many clinicians base their treatment decisions on their own experience, as well as the anecdotal reports provided by colleagues and instructors during their training. In this framework, it is understandable that opiates have remained an accepted part of the heart failure treatment regimen, because portions of their therapeutic effect are at least theoretically beneficial in the ADHF/APO patient. The most reasonable argument for using opiates in APO is that they do possess some vasodilatory properties and therefore might potentially improve cardiac output by decreasing preload and afterload. Regardless of whether APO presents in the setting of systolic or diastolic dysfunction, it is a state that is characterized by significant elevation of both systemic vascular resistance (i.e. afterload) and filling pressures (i.e. preload). These altered cardiac loading conditions, in the presence of ventricular dysfunction, prevent adequate forward flow of blood from the left ventricle and result in transmission of elevated pressures into the pulmonary vasculature with the development of pulmonary oedema. As has been increasingly reported, pulmonary oedema might develop with or without significant volume overload, suggesting that the primary issue in APO, and therefore the focus of initial therapy, should

GC1QR: A NOVEL BIOMARKER ASSOCIATED WITH RISK OF CARDIOVASCULAR EVENTS

The gC1qR is a 33KDa protein, which interacts with components of the complement, kinin, and coagulation cascades, and select microbial pathogens. It is highly expressed in atherosclerotic lesions and on a variety of cells, including activated platelets and endothelial cells. Circulating gC1qR has