Chronic stable angina overview: Difference between revisions
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Coronary artery bypass surgery, also coronary artery bypass graft (CABG, pronounced "cabbage") surgery, and colloquially heart bypass or bypass surgery is a surgical procedure performed to relieve [[angina]] and reduce the risk of death from [[Coronary heart disease|coronary artery disease]]. [[artery|Arteries]] or [[vein]]s from elsewhere in the patient's body are [[medical grafting|grafted]] to the [[coronary artery|coronary arteries]] to bypass [[atherosclerosis|atherosclerotic]] [[stenosis|narrowings]] and improve the [[blood]] supply to the [[coronary circulation]] supplying the [[myocardium]] (heart muscle). This surgery is usually performed with the heart stopped, necessitating the usage of [[cardiopulmonary bypass]]; techniques are available to perform CABG on a beating heart, so-called "off-pump" surgery. | |||
==References== | ==References== | ||
Revision as of 21:28, 25 January 2013
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Chronic stable angina Microchapters | ||
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Classification | ||
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Differentiating Chronic Stable Angina from Acute Coronary Syndromes | ||
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Diagnosis | ||
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Alternative Therapies for Refractory Angina | ||
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Discharge Care | ||
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Guidelines for Asymptomatic Patients | ||
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Case Studies | ||
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Chronic stable angina overview On the Web | ||
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Risk calculators and risk factors for Chronic stable angina overview | ||
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [3]; Associate Editor(s)-In-Chief: Maheep Singh Sangha, M.B.B.S.; Cafer Zorkun, M.D., Ph.D. [4]
Overview
Angina pectoris, commonly known as angina, is chest pain[1] due to ischemia (a lack of blood and subsequent lack of oxygen supply) of the heart muscle. It is most often due to obstruction or spasm of the coronary arteries (the heart's blood vessels). Coronary artery disease, also referred to as atherosclerosis of the coronary arteries, is the most common cause of angina. The term derives from the Greek ankhon ("strangling") and the Latin pectus ("chest") meaning "a strangling feeling in the chest". In angina pectoris, symptomatic onset may include chest discomfort indicated by a feeling of tightness, heaviness, or pain in the chest cavity.
Historical Perspective
Chronic stable angina is a form of chest pain characterized by an insufficient blood flow to the myocardium of the heart to match myocardial energy demands (ischemia). The term angina was originally derived from the Greek word ankhon and the Latin word pectus, which when combined, loosely translates as "a strangling feeling in the chest". Attempts to classify this disease state began as early as the 4th century B.C., when Lucius Annaeus Seneca first described the symptoms he was experiencing as "to have any other malady is to be sick; to have this is to be dying". Throughout history many renowned researchers and health care professionals have contributed to the understanding, definition, and recognition of angina.
Classification
Chronic Stable Angina
Angina pectoris is a sensation of chest discomfort that is often described as: a feeling of tightness, heaviness, or pain. Angina pectoris is a characteristic of coronary heart disease. When it occurs chronically, this is referred to as stable angina.
Walk Through Angina
Walk through angina is the appearance of anginal chest discomfort early in the course of exertion which subsequently subsides despite continued exertion.
Mixed Angina
Mixed or variable threshold angina pectoris is a syndrome in which there is substantial variation in the magnitude of physical activity that induces anginal chest pain.
Nocturnal Angina
Nocturnal angina is the occurrence of anginal discomfort either during the first hours of sleep or during the early morning hours. It is speculated that discomfort caused during the first hours of sleep is due to increased venous return, whereas the discomfort caused during the early morning hours is due to increased vascular tone.
Postprandial Angina
Postprandial angina pectoris is anginal chest discomfort that occurs following meals. It is thought to be due to an increase in vascular tone or a reduction in coronary blood flow.
Syndrome X
Syndrome X may refer to cardiac syndrome X, metabolic syndrome and single X syndrome, where an individual has a single X chromosome, typically described as turner syndrome. The otherwise unidentifiable rare disease afflicting Brooke Greenberg and only about half a dozen other people in the world.
Vasospastic Angina
Coronary vasospasm is a multi-factorial, transient, and abrupt reduction of luminal diameter of an epicardial coronary artery due to inappropriate constriction of coronary smooth muscle that can generate distal ischemia. This may occur spontaneously or in the context of angioplasty, particularly if denudation of the endothelium or dissection occurs. In addition, the vasospasm can either be focal or multifocal (which compromises more than one vessel).
Differentiating Chronic Stable Angina from Urgent Conditions
Stable angina must be differentiated from unstable angina and acute coronary syndromes. If the pattern of angina is stable, this is termed chronic stable angina. If the magnitude, threshold or frequency of chest pain accelerates, this is termed an acute coronary syndrome.
Pathophysiology
The primary causes of myocardial ischemia in chronic stable angina are: fixed epicardial stenosis, spasm of the epicardial artery and/or microvascualar disease. The causation of angina is not mutually exclusive. Two or more causes may coexist in the same patient.
Epidemiology and Demographics
Coronary artery disease (CAD) remains the single leading cause of death in the United States. Stable angina is the initial manifestation of ischemic heart disease in approximately 50% of these patients.
Risk Stratification
The average mortality in patients with stable angina ranges from 1-3%. However, the prognosis varies widely depending on various factors such as: the duration and severity of symptoms, resting ECG abnormalities, abnormal left ventricular function and associated comorbidities.[2]
Pretest Probability
Pretest probability is defined as the probability of the target disorder before the result of a diagnostic test is known. A number of studies have emphasized the importance of pretest probability of coronary artery disease (CAD).[3] Once a thorough patient history and physical examination is complete, it is important to assess the probability of underlying CAD, as this helps both the physician and the patient to determine the next step in the diagnosis and treatment. In patients with chronic stable angina, the strongest predictors contributing to underlying significant CAD include: the age, gender and type of pain (typical, atypical) experienced.[3]
Prognosis
Ischemic heart disease remains as the number one cause of mortality in developed countries. The prognosis of stable angina varies widely depending on severity of symptoms, extent of atherosclerosis and presence of other risk factors and co-morbidities. The presence of impaired left ventricular function is associated with a poor prognosis. Reduced LV function, number and location of stenoses, workload in METs calculated using Duke score are the strongest predictors of survival in patients with chronic stable angina.
Diagnosis
History and Symptoms
The name 'angina pain' can be thought of as a misnomer as patients often describe the sensation as discomfort rather than physical pain. The best method to characterize this discomfort/pain is through the 'PQRST system'.
Physical Examination
Among patients with chronic stable angina, the physical examination may be asymptomatic or characteristically normal. Patients that present with left ventricular dysfunction are associated with a poorer prognosis than patients who do not present with dysfunction. All patients should be examined carefully for the presence of rales and other signs of heart failure.
The majority of patients present with history of either, chest pain or discomfort categorized as: typical or atypical. Typical presentation would include pain or discomfort in the front or anterior precordium. Atypical presentation can be more convoluted in presentation and involve a wide range of symptoms. For example, an atypical patient may present with dyspnea instead of chest pain and this is termed an angina equivalent.
In addition to the historical presentation of chest pain or discomfort, the patient history should be extensively evaluated to include an assessment of cardiovascular risk factors. Physical examination may be normal or asymptomatic. In some cases, a physical examination may reveal heart failure. Additional findings can be important in understanding the onset of the condition. For instance, the presence of peripheral vascular disease may be associated with an increased risk of coronary artery disease (CAD).
Test Selection Guideline for the Individual Basis
Criteria for test selection hinges largely on the current disease state of the individual patient and subsequent level of fitness for testing. Potential diagnostic testing modalities include: exercise ECG, ECG at rest, exercise echocardiography, echocardiography at rest, and stress scintigraphy.
Laboratory Findings
In patients with chronic stable angina, initial laboratory investigations are used to: identify potential causes of ischemia, establish risk factors, and determine the overall prognosis for the patient. An initial laboratory test can provide a wide variety of clinical information. For instance, low hemoglobin levels can cause ischemia. Therefore, assessing hemoglobin as a part of complete blood count provides prognostic information.[4] Biomarkers, such as troponin and CK-MB, are used to exclude myocardial injury. In assessment for risk factor stratification, all patients with ischemic heart disease are recommended to have a a standard round of blood work conducted including fasting plasma glucose levels and a complete lipid profile. Serum creatinine[5] is used to assess renal dysfunction[6] due to associated hypertension or diabetes and remains a negative prognostic factor. In patients with chronic stable angina, an elevation in fasting glucose[7] independently predicts the adverse outcome. Recent research on NT-pro-BNP has demonstrated the ability to predict long-term mortality in patients with chronic stable angina independent of age, ventricular ejection fraction and other risk factors.[8]
Electrocardiography
A resting 12-lead ECG is performed and recorded in all patients with suspected angina pectoris. However, a normal resting ECG does not exclude the diagnosis of ischemia. Abnormalites commonly observed on resting ECG include: ST-segment changes, left ventricular hypertrophy (LVH), left branch bundle blockage (LBBB), signs of coronary artery disease (CAD) such as previous myocardial infarction (MI) or abnormal repolarization patterns.[9] An ECG recorded during pain helps to identify an underlying vasospasm.
Exercise EKG
In patients with chronic stable angina, exercise ECG is more sensitive and specific to identify inducible ischemia and to diagnose coronary artery disease.[10] ECG abnormalities associated with MI include: down sloping of ST-segment depression or elevation, accompanying angina that occurs at a low workload during early stages of exercise and persistent for more than 3-minutes after exercise. The reliability of diagnosis is shown to improve with the evaluation of ST changes in relation to heart rate.[11] Bruce protocol or treadmill (expressed in terms of METs) or bicycle ergometer (expressed in terms of watts) are used to detect MI. Exercise ECG test must be terminated on the achievement of maximal predicted heart rate and/or if the patient becomes symptomatic or develops pain with significant ST-segment changes. Exercise ECG test also provides prognostic stratification to evaluate the response to medical therapy or revascularization.[12]
Chest X-Ray
Routine chest x-ray examination is important in the evaluation of patients with signs or symptoms of congestive heart failure,[13] valvular heart disease, pericardial disease, or aortic dissection/aneurysm. The presentation of cardiomegaly, characterized by pulmonary congestion on a chest x-ray, is indicative of a poor prognosis for the patient.[14]
Myocardial Perfusion Scintigraphy with Pharmacologic Stress
Pharmacologic stress testing using myocardial perfusion scintigraphy or echocardiography can be employed in patients with known or suspected angina pectoris who are unable to perform adequate exercise tests. These patients often owe their ineligibility status to associated conditions such as: peripheral vascular disease, musculoskeletal disorders, diseases of the lower extremities, severe obesity, or deconditioning. Pharmacologic stress testing is achieved with the infusion of either dobutamine in incremental dose, which acts by increasing myocardial oxygen consumption and thereby mimic effect of exercise, or with the use of coronary vasodilators such as adenosine or dipyridamole, which acts by differentiating regions based on perfusion. Stress imaging is of great value in the evaluation of patients with low pretest probability of CAD.[15] However, in patients with LBBB, perfusion scintigraphy is shown to have poor diagnostic accuracy.[16]
Myocardial Perfusion Scintigraphy with Thallium
In patients with baseline ECG abnormalities,a myocardial perfusion test can be used to localize the region of ischemia. Thallium-201 and technetium-99m are the two radio-labeled agents that are frequently used for the assessment of myocardial perfusion. Myocardial uptake of thallium-201 chloride is directly proportional to the regional myocardial blood flow and is dependent on the presence of viable myocardium. In patients with known CAD, a normal thallium stress test without a perfusion defect is indicative of a benign process and associated with excellent prognosis. Patients with a normal thallium scan are at low risk for CAD and subsequent coronary angiography is indicated only if the patient has a high probabilty Duke treadmill score. Contraindications for thallium stress test include the presence of arrhythmia, acute myocarditis, severe aortic stenosis and acute MI within the past 2 days.
Echocardiography
Echocardiography is useful to evaluate ventricular function[17] and detect ischemia induced regional wall motion abnormality that occurs at rest, during exercise or with pharmacologic stress test. As a testing modality, two-dimensional echocardiography is often coupled with other testing modalities to detect regional wall motion abnormalities that most frequently occur during induced myocardial ischemia associated with coronary artery disease (CAD). Potential paired testing modalities include: upright treadmill exercise, supine bicycle ergometry, pacing, and pharmacologic stress, particularly with dobutamine. Patients with CAD may respond more adversely to testing modalities than their counterparts. Often, an adverse outcome such as the inability to perform a bicycle ergometry test or exercise treadmill protocol can be characterized as a poor prognostic factor.
Exercise Echocardiography
Stress echocardiography is echocardiography that is paired with different forms of stressors, such as exercise or pharmacological. Exercise stress echocardiography is the preferred stress echocardiography modality. However, it is not suitable for all patients and may not be feasible in populations that do not meet a minimum level of fitness. In patients who are ineligible for exercise stress echocardiography, pharmacological stress echocardiography can be a useful alternative. Common pharmacological stressors include: adenosine, dipyridamole, and dobutamine. As a testing modality, exercise echocardiography is noted as more sensitive, more specific and has a higher predictive value than exercise ECG. Exercise echocardiography can be helpful in the evaluation of regional wall motion response, location and extent of ischemia during stress in patients with MI. During exercise, the normal myocardium is hyperdynamic while in patients with MI, the ischemic myocardium is either akinetic or hypokinetic.
Positron Emission Tomography
Positron emission tomography is of particular value in the assessment of regional coronary blood flow reserve, myocardial perfusion, and the presence and extent of hibernating myocardium.
Ambulatory ST Segment Monitoring
Ambulatory ECG monitoring (Holter monitor) is used to detect major arrhythmias and myocardial ischemia occurring during normal activities. Ambulatory ECG monitoring adds very little prognostic value in patients with chronic stable angina, however, does play a role in the detection of major arrhythmias in patients with chronic stable angina and suspected vasospastic angina.
Electron Beam Tomography
The extent of coronary artery calcification directly correlates to the area of atheromatous plaque.[18] Hence in patients with chest pain, coronary artery calcium (CAC) scoring is one of the factor to be considered in the risk assessment for coronary artery disease. The methods used for detection and quantification of CAC include electron beam computed tomography (EBCT) and multi-detector computed tomography (MDCT).[19] Agatston score is a computed software that is commonly used to measure CAC based on the density and area of calcified plaques.[20]
Cardiac Magnetic Resonance Imaging
Cardiac magnetic resonance imaging (CMRI) is a non-invasive test that is useful in the evaluation of overall coronary anatomy and function. CMRI also helps in the identification of inflammation,[21] neovascularization[22] and fibrous cap,[23] It, therefore, holds the potential for plaque characterization.
Coronary Angiography
Coronary angiography is a gold standard test in the evaluation of severity of coronary artery disease and the possibility for revascularization. Coronary angiography is indicated in patients with a high pretest probability of CAD and in symptomatic patients with inconclusive initial noninvasive tests. Provocative testing with ergonovine during angiography may be useful in patients with vasospastic angina. Major complications such as death, MI and stroke associated with routine angiography is as low as 0.1% - 0.2%.[24]
Treatment
- Treatment for chronic stable angina includes:
- Lifestyle modification
- Pharmacotherapy
- Revascularization procedures (percutaneous coronary intervention (PCI), coronary artery bypass surgery (CABG)).
- It is also important to identify any exacerbating factors like anemia, thyrotoxicosis, valvular heart disease or decompensated heart failure and treat them.
- Smoking cessation counseling, diet and weight management, promoting physical exercise, blood pressure and diabetes control are all components of risk factor modifications and should be stressed at each clinic visit.
- Specific medical therapy includes antiplatelets (like ASA, clopidogrel), antianginals (like nitrates, beta blockers, calcium channel blockers, lipid-lowering agents, ACE inhibitors and angiotensin receptor blocking agents).
- Coronary revascularization is recommended when optimal medical therapy has failed to reduce symptoms or severe atherosclerotic disease or high risk criteria on noninvasive testing.[25]
- Options available for revascularization include: percutaneous coronary intervention PCI and coronary artery bypass grafting CABG.
- In patients with chronic stable angina, the factors influencing the choice of coronary revascularization therapy (percutaneous coronary intervention or coronary artery bypass surgery) are varied and complex. The severity of symptoms, lifestyle, extent of objective ischemia, and underlying risks must be weighed against the benefits of revascularization and the patient’s preference, as well as local availability and expertise.
- Evidence from randomized trials and large revascularization registers can guide these decisions.
- In the past decade there has been significant improvements in medical treatment, bypass surgery and percutaneous coronary intervention.
Treatment of chronic stable angina aims at minimizing symptoms, reducing recurrent ischemia, improving the quality of life and improving prognosis by preventing MI and death. Treatment options include lifestyle modification, pharmacotherapy and revascularization that help in slowing the disease progression, preserving the endothelial function and preventing thrombosis.
Patients with single-vessel CAD may be started on initial pharmacologic therapy and if non-responsive or symptomatic despite on therapy, PCI may be a preferred alternative.
Patients with double-vessel CAD and with normal LV function may be started on initial medical management and in non-responders, PCI may be considered. However, the decision of PCI versus CABG depends on the coronary anatomy, LV function and the need for complete revascularization.
Patients with triple-vessel CAD or left main disease or reduced left ventricular function, CABG is the mainstay of management. However, in cases of mild symptoms or preserved LVEF in patients with triple-vessel disease, initial pharmacologic therapy or PCI may be tried.
Pharmacotherapy
The goal of the management of chronic stable angina is to improve the quality of life by decreasing the severity and frequency of symptoms and to decrease premature cardiovascular death caused by myocardial infraction or development of heart failure. The mainstays of the treatment of chronic stable angina are patient education, lifestyle changes and medical therapy.[26] In patients with chronic stable angina, immediate symptomatic relief is achieved with short-acting sublingual nitrates and long term symptom relief is achieved with beta blockers as first line therapy, or calcium channel blockers and long-acting nitrates when beta blockers are contraindicated. Drugs that improve the quality of life and are associated with a better prognosis include: low dose aspirin, beta-blockers and ACEIs.
Anti-platelet Agents
Aspirin
In patients with ischemic heart disease, prophylactic low dose aspirin prevents arterial thrombosis by irreversible inactivation of platelet aggregation.[27][28][29][30]
Dipyridamole
Dipyridamole is a pyrimidopyrimidine derivative with poor anti-thrombotic efficacy and therefore not recommended for anti-platelet therapy in patients with chronic stable angina.[30] Dipyridamole may also exacerbate anginal symptoms due to coronary steal phenomenon.[31]
Clopidogrel
Thienopyridines, such as clopidogrel and ticlopidine, selectively inhibit ADP-induced platelet aggregation and are used as an alternative to aspirin in patients with significant risk of arterial thrombosis.
Anti-anginal Agents
Nitrates
In patients with chronic stable angina, nitrates remain the mainstay of therapy. Organic nitrates are therapeutic precursors of endothelium-derived relaxing factor that produce their beneficial effects both, by decreasing myocardial oxygen requirements and by improving myocardial perfusion. The most commonly used nitrates are nitroglycerin, isosorbide dinitrate and isosorbide mononitrate. Short acting nitrates, such as sublingual nitroglycerin, are best suited to treat acute episodes of angina and are effective when used for situational prophylaxis. Long-acting nitrates help to reduce the frequency and severity of angina and may increase exercise tolerance in patients with stable angina.[32][33][34] Nitrates at therapeutic doses do not affect coronary vascular resistance, thereby reducing the risk of myocardial ischemia due to coronary steal phenomena that is consistent with the use of dipyridamole and other short acting dihydropyridines.
Beta Blockers
In patients with stable angina, beta blockers are used as a first line of therapy for both, symptomatic relief[35][36][37] and the prevention of ischemic events.[38] The physiologic mechanism of benefit of this therapy is a marked reduction in myocardial oxygen consumption by reducing the heart rate and myocardial contractility. Selective beta-1 blockers are preferred to non-selective beta-blockers due to fewer associated side effects.[34] The most commonly used selective beta-1 blockers are metoprolol, atenolol, and bisoprolol.
Calcium Channel Blockers
Calcium channel blockers (CCBs) consist of three sub-classes namely, dihydropyridines (e.g., nifedipine), phenylalkylamines (e.g., verapamil) and modified benzothiazepines (e.g., diltiazem). The beneficial anti-anginal effects of CCB include: reduction in the afterload consequent to systemic vasodilation as well as epicardial vessel vasodilation, enhancement of the coronary collateral flow with subsequent sub-endocardial perfusion due to the inhibition of calcium influx via L-type channels.[39] Long-acting calcium channel blockers are an effective antianginal agent and are considered to be the first choice in post-MI patients with a contraindication to beta-blocker.[40] Long-acting CCBs are also specifically used to control symptoms in patients with vasospastic angina.[41] However short-acting CCBs, such as nifedipine, are avoided due to an increased risk of myocardial infarction and mortality.[42][36][37]
Potassium Channel Openers
Nicorandil has both, anti-anginal effects due to nitrate-like and ATP-sensitive potassium channel activating properties and provides cardio-protective effects as well. Therefore, nicorandil usage in addition to standard anti-anginal therapy may be indicated in patients who are intolerant to beta-blocker therapy or in whom CCB monotherapy or combination therapy CCB is unsuccessful.[43][44][45]
Newer Anti-anginal Agents
Ranolazine is a one of the newer FDA approved anti-anginal medication for management of chronic stable angina. Perhexiline is another anti-anginal, primarily used in Australia and New Zealand, being studied for use in the United States and UK. In patients with chronic stable angina, other effective agents with anti-anginal and anti-ischemic properties are ivabradine, trimetazidine and molsidomine.
ACEI/RAAS Blockers
Patients diagnosed with syndrome X and hypertension may have microvascular angina characterized by a reduced coronary vasodilator reserve and increased sympathetic drive. ACE inhibition in such patients may attenuate sympathetic coronary vasoconstriction, normalize thallium perfusion defects and reduce exercise-induced ischemia with subsequent increased myocardial oxygen supply.[46][47] Based on the recent AHA and ESC guidelines, the recommended goal blood pressure in patients with atherosclerotic coronary vascular disease is less than 130/80 mm Hg.[48][45][49]
Anti-lipid Agents
Statins by inhibiting HMG-CoA reductase subsequently reduce serum cholesterol levels and have been shown to be effective in the primary prevention of various hyperlipidemias and secondary prevention of ischemic heart disease.[50][51] The most commonly used statins are simvastatin, atorvastatin, pravastatin and rosuvastatin. The incidence of major cardiovascular mortality was reduced by 30% with the use of simvastatin[50] and pravastatin[52][53] in patients with coronary artery disease and therefore may be used for both primary and secondary prevention.[54][55][56][57] However, there are no trials specifically performed on patients with stable angina but they form a significant portion in other major trials studying the efficacy of lipid-lowering drugs on the overall mortality from cardiovascular events.[58] In patients with low HDL and high triglycerides as an adjunctive to statin therapy, fibrates or niacin may be used.[59]
Revasularization
The goal of the treatment of chronic stable angina is to reduce the symptoms, delay the progression of atherosclerosis, and prevent cardiovascular events. In order to achieve these goals, lifestyle modifications and medical therapy are the first line treatment. Revascularization is done to increase survival in specific conditions where the stenosis of the coronary arteries is anatomically and functionally significant and the symptoms are refractory to medical therapy. There are currently two well-established revascularization approaches for the treatment of chronic stable angina caused by coronary atherosclerosis: CABG and PCI. Since the introduction of coronary artery bypass surgery in 1967 and percutaneous transluminal coronary angioplasty (PTCA) in 1977, research has supported the effective usage of both strategies for treatment of patients with chronic stable angina. However, as with any treatment method, both methodologies have weaknesses. The choice between PCI and CABG is based upon anatomy and other factors such as left ventricular function and the presence or absence of diabetes. In general, PTCA is reserved for single or some cases of two vessel disease, while CABG is reserved for patients with two or three vessel disease or left main disease. With the availability of drug-eluting stents, PCI is increasingly being performed for many lesions including more complex ones.
PCI
Percutaneous coronary intervention for coronary artery disease first began in 1977, as a valuable mode of revascularization, wherein at the point of coronary stenosis a catheter-borne balloon is inflated to relieve the stenosis.
CABG
Coronary artery bypass surgery, also coronary artery bypass graft (CABG, pronounced "cabbage") surgery, and colloquially heart bypass or bypass surgery is a surgical procedure performed to relieve angina and reduce the risk of death from coronary artery disease. Arteries or veins from elsewhere in the patient's body are grafted to the coronary arteries to bypass atherosclerotic narrowings and improve the blood supply to the coronary circulation supplying the myocardium (heart muscle). This surgery is usually performed with the heart stopped, necessitating the usage of cardiopulmonary bypass; techniques are available to perform CABG on a beating heart, so-called "off-pump" surgery.
References
- ↑ "MerckMedicus : Dorland's Medical Dictionary". Retrieved 2009-01-09.
- ↑ Daly CA, De Stavola B, Sendon JL, Tavazzi L, Boersma E, Clemens F et al. (2006) Predicting prognosis in stable angina--results from the Euro heart survey of stable angina: prospective observational study. BMJ 332 (7536):262-7. DOI:10.1136/bmj.38695.605440.AE PMID: 16415069
- ↑ 3.0 3.1 Diamond GA, Forrester JS (1981) Improved interpretation of a continuous variable in diagnostic testing: probabilistic analysis of scintigraphic rest and exercise left ventricular ejection fractions for coronary disease detection. Am Heart J 102 (2):189-95. PMID: 7258092
- ↑ Horne BD, Anderson JL, John JM, Weaver A, Bair TL, Jensen KR et al. (2005) Which white blood cell subtypes predict increased cardiovascular risk? J Am Coll Cardiol 45 (10):1638-43. DOI:10.1016/j.jacc.2005.02.054 PMID: 15893180
- ↑ Shlipak MG, Stehman-Breen C, Vittinghoff E, Lin F, Varosy PD, Wenger NK et al. (2004) Creatinine levels and cardiovascular events in women with heart disease: do small changes matter? Am J Kidney Dis 43 (1):37-44. PMID: 14712425
- ↑ Fried LF, Shlipak MG, Crump C, Bleyer AJ, Gottdiener JS, Kronmal RA et al. (2003) Renal insufficiency as a predictor of cardiovascular outcomes and mortality in elderly individuals. J Am Coll Cardiol 41 (8):1364-72. PMID: 12706933
- ↑ Arcavi L, Behar S, Caspi A, Reshef N, Boyko V, Knobler H (2004) High fasting glucose levels as a predictor of worse clinical outcome in patients with coronary artery disease: results from the Bezafibrate Infarction Prevention (BIP) study. Am Heart J 147 (2):239-45. DOI:10.1016/j.ahj.2003.09.013 PMID: 14760320
- ↑ Kragelund C, Grønning B, Køber L, Hildebrandt P, Steffensen R (2005) N-terminal pro-B-type natriuretic peptide and long-term mortality in stable coronary heart disease. N Engl J Med 352 (7):666-75. DOI:10.1056/NEJMoa042330 PMID: 15716560
- ↑ Kléber AG (2000) ST-segment elevation in the electrocardiogram: a sign of myocardial ischemia. Cardiovasc Res 45 (1):111-8. PMID: 10728321
- ↑ Ashley EA, Myers J, Froelicher V (2000) Exercise testing in clinical medicine. Lancet 356 (9241):1592-7. DOI:10.1016/S0140-6736(00)03138-X PMID: 11075788
- ↑ Elamin MS, Boyle R, Kardash MM, Smith DR, Stoker JB, Whitaker W et al. (1982) Accurate detection of coronary heart disease by new exercise test. Br Heart J 48 (4):311-20. PMID: 6127094
- ↑ Mark DB, Shaw L, Harrell FE, Hlatky MA, Lee KL, Bengtson JR et al. (1991) Prognostic value of a treadmill exercise score in outpatients with suspected coronary artery disease. N Engl J Med 325 (12):849-53. DOI:10.1056/NEJM199109193251204 PMID: 1875969
- ↑ Chakko S, Woska D, Martinez H, de Marchena E, Futterman L, Kessler KM et al. (1991) Clinical, radiographic, and hemodynamic correlations in chronic congestive heart failure: conflicting results may lead to inappropriate care. Am J Med 90 (3):353-9. PMID: 1825901
- ↑ Hemingway H, Shipley M, Christie D, Marmot M (1998) Cardiothoracic ratio and relative heart volume as predictors of coronary heart disease mortality. The Whitehall study 25 year follow-up. Eur Heart J 19 (6):859-69. PMID: 9651709
- ↑ Shaw LJ, Hachamovitch R, Redberg RF (2000) Current evidence on diagnostic testing in women with suspected coronary artery disease: choosing the appropriate test. Cardiol Rev 8 (1):65-74. PMID: 11174875
- ↑ Vigna C, Stanislao M, De Rito V, Russo A, Santoro T, Fusilli S et al. (2006) Inaccuracy of dipyridamole echocardiography or scintigraphy for the diagnosis of coronary artery disease in patients with both left bundle branch block and left ventricular dysfunction. Int J Cardiol 110 (1):116-8. DOI:10.1016/j.ijcard.2005.05.068 PMID: 16002158
- ↑ Cheitlin MD, Alpert JS, Armstrong WF, Aurigemma GP, Beller GA, Bierman FZ et al. (1997) ACC/AHA guidelines for the clinical application of echocardiography: executive summary. A report of the American College of Cardiology/American Heart Association Task Force on practice guidelines (Committee on Clinical Application of Echocardiography). Developed in collaboration with the American Society of Echocardiography. J Am Coll Cardiol 29 (4):862-79. PMID: 9091535
- ↑ Rumberger JA, Simons DB, Fitzpatrick LA, Sheedy PF, Schwartz RS (1995) Coronary artery calcium area by electron-beam computed tomography and coronary atherosclerotic plaque area. A histopathologic correlative study. Circulation 92 (8):2157-62. PMID: 7554196
- ↑ Greenland P, Bonow RO, Brundage BH, Budoff MJ, Eisenberg MJ, Grundy SM et al. (2007) ACCF/AHA 2007 clinical expert consensus document on coronary artery calcium scoring by computed tomography in global cardiovascular risk assessment and in evaluation of patients with chest pain: a report of the American College of Cardiology Foundation Clinical Expert Consensus Task Force (ACCF/AHA Writing Committee to Update the 2000 Expert Consensus Document on Electron Beam Computed Tomography) developed in collaboration with the Society of Atherosclerosis Imaging and Prevention and the Society of Cardiovascular Computed Tomography. J Am Coll Cardiol 49 (3):378-402. DOI:10.1016/j.jacc.2006.10.001 PMID: 17239724
- ↑ Agatston AS, Janowitz WR, Hildner FJ, Zusmer NR, Viamonte M, Detrano R (1990) Quantification of coronary artery calcium using ultrafast computed tomography. J Am Coll Cardiol 15 (4):827-32. PMID: 2407762
- ↑ Ruehm SG, Corot C, Vogt P, Kolb S, Debatin JF (2001) Magnetic resonance imaging of atherosclerotic plaque with ultrasmall superparamagnetic particles of iron oxide in hyperlipidemic rabbits. Circulation 103 (3):415-22. PMID: 11157694
- ↑ Kerwin W, Hooker A, Spilker M, Vicini P, Ferguson M, Hatsukami T et al. (2003) Quantitative magnetic resonance imaging analysis of neovasculature volume in carotid atherosclerotic plaque. Circulation 107 (6):851-6. PMID: 12591755
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