Evidence for this analysis is not strong. There are no randomized studies that demonstrate that this test is beneficial in assigning therapy. Epidemiologic literature has demonstrated an inverse relationship between levels of high-density lipoprotein (HDL) and cardiovascular risk, indicating that HDL may have a protective role against cardiovascular disease. HDL particles exhibit considerable heterogeneity, and it has been proposed that various subclasses of HDL may have a greater role in protection from atherosclerosis. HDL contains 2 associated apolipoproteins, i.e., AI and A2. HDL particles can also be classified on whether they contain apolipoprotein A-1 only or whether they contain both apolipoprotein A-1 and A-2. An alternative to measuring the concentration of subclasses of HDL, such as HDL2 and HDL3, is direct measurement of HDL particle size and/or number. Several commercial labs offer these measurements of HDL particle size and number. Recently, measurement of apo A-I has used measurement of HDL particle number as a surrogate, based on the premise that each HDL particle contains one apo A-I molecule. Direct measurement of apo A-I has been proposed as more accurate than the traditional use of HDL level in evaluation of the cardioprotective, or “good,” cholesterol. In addition, the ratio of apo B/apo A-I has been proposed as a superior measure of the ratio of proatherogenic (i.e., “bad”) cholesterol to anti-atherogenic (i.e., “good”) cholesterol.

Traditional lipid risk factors such as total HDL and low-density-lipoprotein cholesterol (LDL-C), while predictive on a population basis, are weaker markers of risk on an individual basis. Only a minority of subjects with elevated LDL and cholesterol levels will develop clinical disease, and up to 50% of cases of coronary artery disease (CAD) occur in subjects with “normal” levels of total and LDL cholesterol. Thus, there is considerable potential to improve the accuracy of current cardiovascular risk prediction models and they are n0t a universallya ccepted test. There is good epidemiological evidence but no prospective studies.Framingham and other studies showed how diet adn exrcize can change HDL levels, which are presumed, but not proven to improve health. The same can be said of drug induced changes in HDL and LDL, where there is evidence that supports it prospectively. However, for the fractionated HDL test, no such evidence currenlty exists.
Chapman M, Assmann G, Fruchart J, Shepherd J, Sirtori C. Raising high-density lipoprotein cholesterol with reduction of cardiovascular risk: the role of nicotinic acid – a position paper developed by the European Consensus Panel on HDL-C. Cur Med Res Opin. 2004 Aug;20(8):1253-68.

Reducing risk by raising HDL-cholesterol: the evidence. # European Heart Journal Supplements Vol 8 Suppl F p. F23-F29

Cardiac output  can be used to evaluate global cardiac function. Changes in cardiac output may be used to identify a change in the hemodynamic status of a patient or to evaluate the success of a treatment and to monitoor  critically ill patients over time or perioperatively.

Currently, the most widely accepted methods for the determination of cardiac output are Fick oximetry, thermodilution catheterization (TDC), and indicator dilution using dye or a radioisotope. All of these techniques are invasice and require placing a catheter.

Transthoracic electric bioimpedance (TEB), also called plethysmography or impedance cardiography (ICG), is a noninvasive measurement of cardiac output. Bioimpedance is performed by applying a small electrical current to the chest, and through electrodes placed on the neck and sides and calculating cardiac output from the impedance waveform. Changes in the impedance of the transthoracic electric current are measured electronically, processed by a computer to calculate blood flow, and displayed in real time. The computer software typically displays cardiac data collected over the preceding seconds or minutes, which allows continuous monitoring of alterations in heart rate, cardiac output, and other cardiovascular functions.

This measurment can be perfrmed in office or ER settingsm where catheter placement is impractical or not possible. The difference in time to start bioimpedance monitoring is an advantage over TDC.

A number of studies have been performed. They provide some support for the technique. However, a number of factors can interfere with the accuracy of electrical bioimpedance measurements, and absolute values of cardiac output may not be accurate. Moreover, patient selection criteria have not been clearly and questions remain regarding the appropriate role for cardiac output measurement in patient management and its impact on clinical outcomes.

Agency for Healthcare Research and Quality (AHRQ published a technology assessment on thoracic electrical bioimpedance. The assessment concluded that there was insufficient evidence for meaningful conclusions on the accuracy or clinical usefulness of electrical bioimpedance. The data provided in the available studies suggested that electrical bioimpedance measurements generally correlated similarly with measurements obtained by other testing modalities. Limitations were noted in most reported studies with a scarcity of articles reporting patient outcomes.

WH Wilson Tang,MD Measuring Impedance in Congestive Heart Failure: Current Options and Clinical Applications
Journal article,American heart, May 2009

Centers for Medicare & Medicaid Services (CMS). Technology Assessment for Thoracic Electrical Bioimpedance. Agency for Health Care Research and Quality. November 2002. Available at:http://www.cms.hhs.gov/mcd/viewtechassess.asp?where=search&tid=14&basket=ta:14:Thoracic+Electrical+Bioimpedance.

Stout CL, Van de Water JM, Thompson WM et al.. Impedance cardiography: can it replace thermodilution and the pulmonary artery catheter? Am Surg. 2006 Aug;72(8):728-32; discussion 733-4.

In the United States, LDL apheresis is approved for homozygous familial hypercholestrolemia (FH) patients with an LDL cholesterol level ≥ 500 mg/dL. For patients with heterozygous FH, LDL apheresis may be offered if their LDL is ≥ 300 mg/dL, or ≥ 200 mg/dL with known coronary artery disease, despite maximum medical treatment.  The available LDL apheresis methods differ with respect to acute relative reductions of LDL cholesterol; mean values after the LDL apheresis treatments are not different. Serum triglycerides, HDL-cholesterol, and lipoprotein(a) are also acutely reduced. Cardiovascular events are clearly reduced by the LDL apheresis methods.

Satoshi Morimoto Efficacy of Low-Density Lipoprotein Apheresis in Patients with Peripheral Arterial Occlusive Disease Undergoing Hemodialysis Treatment Nephrology Vol. 27, No. 6, 2007

Puja K. Mehta, Jefferson Baer, Christine Nell and Laurence S. Sperling Low-density lipoprotein apheresis as a treatment option for hyperlipidemia
Journal Current Treatment Options in Cardiovascular Medicine
Volume 11, Number 4 / August, 2009
Pages 279-288, July 14, 2009

Julius U, Frind A, Tselmin S, Kopprasch S, Poberschin I, Siegert G.Comparison of different LDL apheresis methods. Expert Rev Cardiovasc Ther. 2008 Jun;6(5):629-39.

Millman considers a one day admission appropriate for acute coronary syndrome. This is an umbrella term used to cover any group of clinical symptoms compatible with acute myocardial ischemia.  Patients with unstable angina, ECG changes, or both should be admitted to a telemetry bed. A certain subset of patients with stable angina may be treated as outpatients with antianginal agents, but close follow-up is necessary. Patients with chronic stable angina may be considered for discharge from the ER  after occurrence of the following:
◦Symptom duration is brief and identical to symptoms experienced in the past.
◦ECG is normal or unchanged.
◦Patient has access to timely follow-up with a primary care provider.
•When in doubt, admit. The usual reason for a patient with chronic stable angina to present to the ED is a change in pattern or severity of symptoms, which makes their angina unstable.

The necessasry length of stay is determined by response to therapy. In many cases, next day discharge is possible; in others, thrombolysis or percutaneous intervention may be considered.

Millman, Chest Pain,  Angina/Acute Coronary Syndrome

Ryan RJ, Lindsell CJ, Hollander JE, O’Neil B, Jackson R, Schreiber D, et al. A multicenter randomized controlled trial comparing central laboratory and point-of-care cardiac marker testing strategies: the Disposition Impacted by Serial Point of Care Markers in Acute Coronary Syndromes (DISPO-ACS) trial. Ann Emerg Med. Mar 2009;53(3):321-8. [Medline].

Fesmire FM, Decker WW, Diercks DB, Ghaemmaghami CA, Nazarian D, Brady WJ, et al. Clinical policy: critical issues in the evaluation and management of adult patients with non-ST-segment elevation acute coronary syndromes. Ann Emerg Med. Sep 2006;48(3):270-301. [Medline].

Harrington RA, Becker RC, Cannon CP, Gutterman D, Lincoff AM, Popma JJ, et al. Antithrombotic therapy for non-ST-segment elevation acute coronary syndromes: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest. Jun 2008;133(6 Suppl):670S-707S. [Medline].
Storrow AB, Apple FS, Wu AH, Jesse R, Francis G, Christenson RH. Use of cardiac biomarkers for acute coronary syndromes. In: Laboratory medicine practice guidelines: evidence-based practice for point-of-care testing. Washington (DC): National Academy of Clinical Biochemistry (NACB). 2006;13-20.

Chest pain accounts for approximately 6 million annual visits to emergency departments (ED) in the United States (US), making chest pain the second most common complaint.  ED evaluation focuses on distinguishing and admission of life-threatening causes of chest pain; others can be worked up on the outpatient basis.

The published guidelines of the American College of Emergency Physicians, the American Heart Association, and the American College of Cardiology suggest that, for all adult patients complaining of nontraumatic chest pain, a cardiac etiology for their presentation should be considered. History, physical examination, electrocardiogram, chest radiography, and to a lesser extent laboratory results can help differentiate ACS from other emergent diagnoses, e.g., aortic dissection, esophageal rupture, pulmonary embolus, pneumothorax, pneumonia, and pericarditis. No single feature of a patient’s history, physical examination, or diagnostic test results can diagnose ACS to the exclusion of other causes of chest pain. Based on a general impression, patient history, risk factors, ECG and levels of myocardial infarction markers it is decided whether or not to admit the patient for clinical observation.

A recent guideline says this: “Management of patients with definite ACS

Admit and immediately treat patients with new ST segment elevation or new LBBB and a history compatible with ACS, with the intent of re-establishing perfusion.1
Admit and immediately treat patients with a history and ECG (without ST segment elevation) compatible with ischemia, plus either elevated cardiac biomarkers (>99th percentile) or hemodynamic compromise (hypotension or electrical instability), for acute myocardial ischemia.
B. Management of patients with possible ACS

It is recommended that patients with a compatible history and a non-diagnostic initial ECG and cardiac biomarkers, be observed in the ED and be re-assessed at six or more hours after the initial testing with an ECG and cardiac biomarkers. Patients with a compatible history without elevated cardiac biomarkers at 6 or more hours, and an ECG not diagnostic of ischemia are considered to be at a low or intermediate short-term risk for non fatal MI or death.
For low-risk patients without an obvious alternative explanation for the chest pain an out-patient stress test within 72 hours and out-patient physician follow-up is recommended.1
When possible, discuss intermediate-risk patients with an internist or cardiologist. A stress test prior to discharge is recommended.
For both low and intermediate risk groups:
If the patient’s resting ECG is abnormal, a routine stress test will be non-diagnostic. In this scenario, stress myocardial perfusion imaging or stress echocardiography is required to detect ischemia. Therefore, referral to a facility capable of stress myocardial perfusion imaging or stress echocardiography is recommended for such patients. ”

In selected low-risk patients with pulmonary embolism, outpatient care can safely and effectively be used in place of inpatient care.

Aujesky D, Roy PM, Verschuren F, Righini M, Osterwalder J, Egloff M, Renaud B, Verhamme P, Stone RA, Legall C, Sanchez O, Pugh NA, N’gako A, Cornuz J, Hugli O, Beer HJ, Perrier A, Fine MJ, Yealy DM. Outpatient versus inpatient treatment for patients with acute pulmonary embolism: an international, open-label, randomised, non-inferiority trial. Lancet. 2011 Jul 2;378(9785):41-8.

Lindsell, CJ, Anantharaman, V, Diercks, D, et al. The Internet Tracking Registry of Acute Coronary Syndromes (i*trACS): a multicenter registry of patients with suspicion of acute coronary syndromes reported using the standardized reporting guidelines for emergency department chest pain studies. Ann Emerg Med 2006; 48:666.

Ringstrom, E, Freedman, J. Approach to undifferentiated chest pain in the emergency department: a review of recent medical literature and published practice guidelines. Mt Sinai J Med 2006; 73:499.

http://www.bcguidelines.ca/gpac/guideline_chestpain.html

The scientific literature documents that some of the benefits of participation in a cardiac rehabilitation program after myocardial infarction include decreased symptoms of angina pectoris, dyspnea, and fatigue, and improvement in exercise tolerance, blood lipid levels, and psychosocial well-being, as well as a reduction in weight, cigarette smoking and stress.  The efficacy of modification of risk factors in reducing the progression of coronary artery disease and future morbidity and mortality has been established.  Meta-analysis of data from random controlled studies indicates a 20% to 25% reduction in mortality in patients participating in cardiac rehabilitation following myocardial infarction as compared to controls.

There is less literature on rehab after dissection and since it is much rarer, less literature is expected but there is registry data that supports its use.

Corone S, Iliou MC, Pierre B, Feige JM, Odjinkem D, Farrokhi T, Bechraoui F, Hardy S, Meurin P; Cardiac Rehabilitation working Group of the French Society of CardiologyFrench registry of cases of type I acute aortic dissection admitted to a cardiac rehabilitation center after surgery.Eur J Cardiovasc Prev Rehabil. 2009 Feb;16(1):91-5.

Christoph A. Nienaber, and Kim A. Eagle
Aortic Dissection: New Frontiers in Diagnosis and Management: Part II: Therapeutic Management and Follow-Up
Circulation 108: 772-778, 2003

Over the past decade, electron beam computed tomography (CT) and multidetector CT have increasingly been used to identify and measure coronary artery calcification. Calcification levels can be related to the extent and severity of underlying atherosclerosis and can potentially improve cardiovascular risk prediction. However, broad use of these methods for screening is controversial. The American Heart Association (AHA) has released guidelines for the use of cardiac CT when evaluating patients for coronary artery disease.

Asymptomatic patients at low or high risk of cardiovascular disease do not benefit from coronary calcium measurements. However, these measurements may benefit asymptomatic, intermediate-risk patients by refining the risk assessment and prompting lifestyle changes and pharmacologic therapy. Coronary calcium measurements may be reasonable in some symptomatic patients, especially to determine the etiology of cardiomyopathy, to assess patients who have equivocal treadmill or functional test results, and to assess patients with chest pain who have equivocal or normal echocardiography findings and negative cardiac enzyme test results.

http://radiology.rsnajnls.org/cgi/reprint/235/3/723.pdf

Amber Huntzinger AHA guidelines on cardiac CT for assessing coronary artery disease
American Family Physician,  March 1, 2008

Lipoprotein-associated phospholipase A2 (Lp-PLA2) is an enzyme that is produced by inflammatory cells, co-travels with circulating low-density lipoprotein (LDL), and hydrolyzes oxidized phospholipids in LDL. Its biological role has been controversial with initial reports purporting atheroprotective effects of Lp-PLA2 thought to be a consequence of degrading platelet-activating factor and removing polar phospholipids in modified LDL. Recent studies, however, focused on pro-inflammatory role of Lp-PLA2 mediated by products of the Lp-PLA2 reaction (lysophosphatidylcholine and oxidized nonesterified fatty acids). These bioactive lipid mediators, which are generated in lesion-prone vasculature and to a lesser extent in the circulation (eg, in electronegative LDL), are known to elicit several inflammatory responses. The proinflammatory action of Lp-PLA2 is also supported by a number of epidemiology studies suggesting that the circulating level of the enzyme is an independent predictor of cardiovascular events, despite some attenuation of the effect by inclusion of LDL, the primary carrier of Lp-PLA2, in the analysis.

Ascribing a role for Lp-PLA2, an enzyme that is produced by inflammatory cells, is transported on circulating LDL and hydrolyzes oxidized phospholipids in LDL, has been controversial. A growing number of epidemiological studies suggest that Lp-PLA2 is an independent predictor of cardiovascular events, despite some attenuation of this relationship by LDL, the primary carrier of Lp-PLA2. These observations strengthen the rationale to explore causal links between Lp-PLA2 and plaque vulnerability. The connection to cardiovascular diseae and Alzheimer’s remain unproven; neither are the effects of  interventions to reduce the level of this marker known. Empire considers this test to be be not medically necessary.

A.-L. Levonen, E. Vahakangas, J. K. Koponen, and S. Yla-Herttuala
Antioxidant Gene Therapy for Cardiovascular Disease: Current Status and Future Perspectives
Circulation, April 22, 2008; 117(16): 2142 – 2150.

W. Koenig
Cardiovascular Biomarkers: Added Value With an Integrated Approach?
Circulation, July 3, 2007; 116(1): 3 – 5.

A. Oldgren, S. K. James, A. Siegbahn, and L. Wallentin
Lipoprotein-associated phospholipase A2 does not predict mortality or new ischaemic events in acute coronary syndrome patients
Eur. Heart J., March 2, 2007; 28(6): 699 – 704.