AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Intervention
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Intervention
• Multimedia
• References

Background

Coronary artery disease (CAD) is a complex disease that causes reduced or absent blood flow in 1 or more of the arteries that encircle and supply the heart. The disease may be focal or diffuse. Apart from rare congenital anomalies (birth defects), CAD is usually a degenerative disease, uncommon as a clinical problem before the age of 30 years and common by the age of 60 years.

Lesions that cause blockages may be stable or unstable (unstable lesions activate blood clotting).

For excellent patient education resources, see eMedicine's Cholesterol Center. Also, visit eMedicine's patient education articles Chest Pain, Coronary Heart Disease, and Heart Attack.

Severity of CAD

The severity of CAD is defined several ways: (1) anatomically, by visualizing the blood vessel branches and any blockages to blood flow along the pathways; (2) functionally, by estimating blood delivery to tissue supplied by each branch vessel; and (3) clinically, by determining what symptoms correspond to inadequate blood delivery, what level of activity causes them, what relieves them, and what the pattern of occurrences is. Such patterns are described as stable or not, with variable or accelerating frequency, with variable or increasing severity or other character of symptoms, with a variable or decreasing exercise threshold. Also noted is whether symptoms are reliably relieved by rest or nitroglycerine within 5 minutes or if it lasts longer than 5 minutes.

In addition, one examines the consequences, including the location and extent of reversible and of permanent impairment, motion, and thickening of affected segments of the heart to determine whether the damage is causing or sustaining life-threatening arrhythmias. One also evaluates the patient's overall cardiac performance, which is typically expressed as the ejection fraction (EF), or percentage of the contents the left ventricle pumps forward in a heartbeat.

Imaging of CAD

At present, achieving the best resolution on images of the coronary arteries requires catheterization, injection of an iodinated contrast agent, and use of an x-ray technique. As an alternative, multidetector-row CT (MDCT) or MRI may be used to clarify coronary anatomy and to determine whether a vessel is occluded. Stress imaging has a complementary role in depicting zones with inducible ischemia (blood supply inadequate for the demands of the tissue). Stress may be produced with exercise, an infusion of a medication that increases the strength of cardiac contractions (eg, dobutamine), or an infusion of a medication (eg, adenosine, dipyridamole) that dilates the vessels and thereby reduces the delivery of blood diseased branches.

More than a decade ago, MRI was shown to be capable of imaging the coronary arteries and demonstrating stenoses without catheterization or injection of contrast material.¹ More recently, MDCT is proving to be a fast and accurate alternative for defining the coronary anatomy.² MRI takes more time than MDCT and generally provides less detail of the coronary anatomy, but it avoids ionizing radiation and the use of iodinated contrast agent.

Advances in MRI and CT have markedly improved the speed and resolution of imaging, making these modalities useful in the clinical evaluation of CAD and improving their safety and convenience. In addition to defining the anatomy, both MRI and CT can be used to identify zones of impaired blood supply by timing of the arrival of contrast agent–labeled blood.

In addition, MRI is useful in identifying the location and thickness of myocardial scars. Although neither MRI nor CT has replaced x-ray angiography as the clinical standard for the diagnosis of coronary stenosis, interest in their use in determining if a vessel is open is increasing. Recently, 64-slice multidetector-row CT angiography (CTA) has shown promise as an alternative to x-ray angiography for the identification of coronary blockages.³

Assessment of tissue viability

The amount of impairment or damage caused by stenosis obstructing a coronary artery depends on how much of the myocardium the vessel supplies, the severity of the stenosis and any superimposed spasm, the level of demand in the tissue it supplies, and the condition of the tissue it supplies.

When demand exceeds supply, the tissue becomes ischemic, a term which describes the condition of insufficient blood supply to maintain normal metabolism. Myocardial ischemia may cause chest pain, fatigue, shortness of breath, or another form of reduced exertion tolerance. It may be detected impaired contractile function (wall motion or wall-thickening abnormality on dynamic cardiac imaging series), it may be detected because of interference with the movement of ions (resulting in depolarization and repolarization abnormalities on ECGs as ST-segment shifts, changes in ST and T waves, and/or rhythm abnormalities), and/or it may be detected when a blood test shows a release of enzymes (creatine kinase-MB [CK-MB], troponin-I, troponin-T) from the heart muscle.

Ischemia may deplete high-energy phosphate carriers (eg, creatine, adenosine) that are needed for muscle contraction. Depletion may occur to the point that impaired motion may persist even when ischemia is relieved. Transiently impaired contractile function of muscle that persists after the relief from ischemia is called stun, and long-term dysfunction of viable muscle is called hibernation.

Dead tissue converted to scar likewise loses contractile function. Therefore, a key issue when a region of heart wall shows loss of function is the determination of whether the myocardium is still viable. Persistent wall-motion abnormality at rest shown by using any imaging modality (echocardiography, MRI, CT, x-ray angiography) raises the issue of tissue viability and, therefore, whether repairing a blockage in the blood supply is beneficial.

If a region is thin and akinetic (no motion), it is more likely to scar (dead myocardium) that if it is not. However, when in doubt, viability tests are appropriate. For example, viability can be identified by performing phosphorus-31 MRI and by reporting for each region the relative concentrations of creatine phosphate; inorganic phosphate; and adenosine monophosphate, diphosphate, and triphosphate.

Although MRI of phosphorylated metabolites and positron emission tomography (PET) of metabolic activity (to assess glucose utilization) can be used to assess tissue viability, an alternative method of equal clinical value is imaging to examine wall motion at rest and with light stress. Dobutamine stress imaging may be performed with MRI or echocardiography. Dobutamine stress tests are used to detect viability by demonstrating dose-related increases in contractility if the tissue is viable. An increase in the dose of dobutamine may elicit a decline in contractility associated with induced ischemia, that is, a biphasic response indicating threatened but viable myocardium.

MRI scar mapping is the determination of the fraction of wall thickness that retains gadolinium-based contrast agent 10-20 minutes after a bolus infusion of 20 mL/75 kg. The result is an excellent predictor of potential for functional recovery. If the scar is less than one third the thickness of the wall, improvement with revascularization is likely. However, if the scar is more than two thirds the thickness of the wall, improvement after revascularization is unlikely. MRI scar maps depict contrast retention due to cell disruption. Although acute injury results in slightly enlarged zones of retained contrast agent on MRI after a week, the defined zone appears the same months to years later. Therefore, MRI scar mapping appears to be reproducible and reliable.

Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have recently been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see the eMedicine topic Nephrogenic Fibrosing Dermopathy. The disease has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance MRI or MRA scans. As of late December 2006, the FDA had received reports of 90 such cases. Worldwide, over 200 cases have been reported, according to the FDA. NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or dark patches on the skin; burning, itching, swelling, hardening, and tightening of the skin; yellow spots on the whites of the eyes; joint stiffness with trouble movingorstraightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle weakness. For more information, see the FDA Public Health Advisory or Medscape.

Pathophysiology

Injury and inflammation

Injury to the endothelial lining of arteries, active uptake by the vascular wall of cholesterol esters, inflammatory reaction, thrombosis, calcification, and hemorrhage all contribute to arteriosclerosis or scarring of an artery wall. Levels of the acute-phase reactants C-reactive protein and serum amyloid-A protein are elevated in patients with unstable angina, and inflammatory cells, including abnormal T-lymphocytes, are seen during autopsy in patients with coronary disease or inflammatory diseases.

Whether inflammation causes and/or promotes the disease or whether it is merely a consequence and marker for a poor prognosis is not entirely clear. In a study of 121,700 women, those with rheumatoid arthritis has twice as many heart attacks as did women without inflammatory disease.⁴ Inflammation has also been implicated in elevating the risk of coronary in association with metabolic syndrome (obesity, hypertension, insulin resistance, and dyslipidemia). Hostility (presumably because of changes in hormone levels) is another risk factor.⁵

Platelets and lipoproteins

In a study of patients with a heart attack who underwent coronary angiography within the previous year, one half of the culprit lesions were narrowed less than 70%. A lesion causing mild stenosis may rupture suddenly and cause bleeding into the wall of the vessel (plaque hemorrhage), promoting occlusion of the vessel because of thrombosis. The final step explains why antiplatelet medications, such as aspirin, can help in preventing heart attack (Thrombotic occlusion of the vessel occurs when platelets stick together to form an obstructive plug; therefore, the inhibition of platelet adhesion by aspirin prevents thrombosis.) Cholesterol-lowering medications work by reducing or reversing the balance of lipid deposition into the arterial wall in areas of flow stress, and many also have anti-inflammatory effects.

Lipid levels can be improved by decreasing the amount of circulating low-density lipoprotein cholesterol (LDL-C, "bad" cholesterol) by changing the person's diet, by inhibiting the production of LDL-C in the liver, and/or by decreasing the absorption of LDL-C in the intestines. Furthermore, the rate of uptake of LDL-C into the vessel wall is sensitive to oxidation status, because oxidized LDL-C has a 50-fold increased rate of uptake. Therefore, antioxidants have been suggested as a means to slow the process. In the Women's Health Initiative, patients who took vitamin C supplements had nearly one third fewer heart attacks than those who did not (relative risk of 0.72 and 95% confidence interval of 0.61-0.86 after adjustments were made for age, smoking, and other risk factors).⁶ Consuming omega-3 fatty acids and drinking a glass of grape juice or red wine a day may help avert heart attacks by similar means.

High-density lipoprotein cholesterol (HDL-C, "good" cholesterol) transports lipids from the body back to the liver. Exercise that keeps a heart rate above 130 bpm for at least 10 minutes every other day increases HDL-C levels. Niacin also helps elevate HDL-C values. A new class of medication, cholesteryl ester transfer protein (CETP) inhibitors (eg, torcetrapib), was specifically designed to elevate HDL-C concentrations.⁷

Calcification and angina

Chronic lesions may become calcified and therefore provide evidence of the disease process, as seen on CT or electron-beam tomography (EBT). However, the calcification does not necessarily indicate the lesions that pose the greatest risk. In fact, calcified lesions may be more stable than noncalcified ones. However, evidence also suggests that a soft plaque has an increased capacity to remodel outward; therefore, calcification of a vessel is a significant risk factor. Once the degree of narrowing exceeds 50%, stable narrowing of an artery typically results in exercise limitations, which is often experienced as a squeezing chest tightness that may radiate to the jaw or left arm. This tightness (Heberden angina) is predictable at a specific level of activity.

As an alternative, angina pectoris may have a variable threshold because of changes in muscle tone and spasm of the vessel. The lack of a predictable relationship to exertion often leads to misinterpretation of the symptoms as heartburn. Severe spasm may produce angina at rest in a patient with good exercise tolerance and may produce a distinctive change in ECG (transient ST elevations during angina instead of usual ST depressions). On occasion, the obstruction is not in the vessel. Instead, an external strand of muscle obstructs blood flow in the coronary artery (myocardial bridge), or the proximal portion of a coronary artery may be pinched between the great vessels (anatomic variant).

Patients with diabetes or those who are older than 60 years commonly have no chest pain during ischemia but instead have impaired wall function, which may result in shortness of breath or changes in rhythm, which may remain unnoticed or which may cause palpitations or syncope. Therefore, stress imaging may help in identifying exercise-inducible ischemia with no symptoms.

Angina lasting more than 10 minutes may actuate a heart attack (by producing ischemia sufficient to cause permanent damage, whereby scar replaces the heart muscle). A threatened heart attack is an emergency because it is life threatening and because may be reversible with prompt appropriate intervention. The diagnosis should be achieved as quickly as possible. At the early stages, simply chewing an aspirin tablet and/or taking nitroglycerin can often stop the immediate threat.

When symptoms suggestive of a possible threatened heart attack are present (persisting chest pain or pressure radiating to 1 or both arms or jaw, or unexplained shortness of breath, weakness, sudden sweating, or a serious arrhythmia), an ECG should be obtained promptly, with continual monitoring for arrhythmia or ischemia (impaired blood supply).

Appropriate and timely treatment

For the reasons mentioned above, ambulances have both ECG and monitoring equipment, as do emergency departments. Emergency departments have additional medications that can stop a threatened heart attack (eg, intravenous nitrates, beta-blockers, thrombolytics, anticoagulants), and/or they can promptly transport the patient to the catheterization laboratory for definitive diagnosis and treatment. Experienced cardiac catheterization laboratories are prepared to repair coronary arteries typically within an hour any time day or night on an emergency basis.

If threatened heart attack is untreated, the tissue that depends on the interrupted blood supply eventually dies, and progressive amounts of irreversible damage accrue. The damaged area is typically small even after occlusion if it is effectively treated within an hour. Delay of more than an hour after occlusion is sufficient to produce life-threatening permanent damage to the heart wall, yet some benefit can still be obtained after 6 hours, or longer if the damage is incomplete. Even if revascularization does not prevent damage, it may improve repair in terms of the strength of the scar and the quality of heart remodeling to compensate for the damage (open-artery hypothesis). The duration of chest pain, the timing and pattern of ECG changes, and the timing and area under the curve of enzyme elevation are clues to duration of ongoing damage.

Frequency

United States

CAD accounts for more than 650,000 deaths per year in the United States, including more than 25% of deaths in persons older than 35 years. Each year, 1.25 million acute myocardial infarctions (MIs) occur. Of these, more than one half occur without previously recognized symptoms. Cardiovascular disease is responsible for more than 3 times as many lives than the all forms of cancer combined. In the United States, spending on CAD exceeds $80 billion per year. One third of people who have a heart attack and who do not receive immediate medical attention die.

International

CAD is the leading cause of death in developed countries. The incidence is rising in Central Europe and in Eastern Europe, but it is low in Japan. Epidemiologic studies of differences among countries and regions revealed dietary and environmental factors that contribute to disease (eg, saturated fat, cholesterol, abdominal obesity, smoking, exposure to second-hand smoke) and also factors that protect against it (eg, fish oils, vitamin C and other antioxidants, red wine or grape juice, anti-inflammatory agents).

Mortality/Morbidity

In one half of the population, the first recognized symptom of CAD is MI, which is fatal in nearly one half of patients. Taking aspirin at the onset of a heart attack reduces mortality rates.

For individuals who arrive awake at a hospital, short-term survival is good, but long-term survival depends on the anatomy of the coronary arteries and on treatment. Survival after a heart attack has been continually improving over the last 30 years, but the incidence of new heart attacks has recently stabilized.

With the obstruction of 3 vessels, the left main coronary artery, or the equivalent combination of proximal anterior descending and circumflex disease plus reduced heart function (abnormal EF), bypass surgery may provide a survival benefit. However, similarly good results may be achievable with drug-eluting stents and complete revascularization by percutaneous intervention (PCI, catheterization).

With 1- or 2-vessel disease that is not equivalent to involvement of the left main coronary artery, medical treatment and catheter interventions are equally good, except in patients with diabetes, in whom surgery has provided the best long-term results. At some centers, catheter intervention may be used to manage 3-vessel disease (eg, with normal function). However, when catheter intervention is used in an acutely ill patient, the focus is on the culprit lesion, and repair of other blockages is deferred.

Morbidity depends on the patient's exercise tolerance and on the amount of damage, which is commonly assessed by using the EF. An EF below 40% typically limits a person's activity, an EF below 30% results in severe limitations plus significantly increases the risk of deadly arrhythmias, and an EF below 20% causes problems at rest.

In patients in whom damage is severe enough to cause clinically significant congestive heart failure, one half die within 5 years. The outlook is improving with rapid access to healthcare and with advancements in treatment. As shown in experimental studies, injected muscle precursor cells may be able to repair dead regions.⁸ In clinical studies, implantation of an automated defibrillator prolonged life, reducing the post-MI mortality rate by 31% in patients with persistently low EF.⁹

Race

Mortality rates from CAD declined between 1987 and 1994 in both whites and African Americans, but the decline was less significant in African Americans. Mortality rates in men do not differ by race, but African-American women have the highest risk of death from heart disease, and their rate of heart attacks is increasing. Native Americans, particularly those living in North Dakota and South Dakota, also have a higher risk for heart disease than do whites. Hispanics have the lowest risk for heart disease compared with all these groups.

African Americans have particular biologic and social risks, including the following:

• High prevalence of diabetes and hypertension





• Poor diet





• High stress levels



• Poor access to health care





• Possible genetic trait that increases the danger of triglycerides, especially in women





• Possibly decreased production of nitric oxide (which is critical for increasing blood flow) in response to stress

To study the effect of discrimination, actors portrayed patients presenting with symptoms of heart disease in 1 study.¹⁰ African-American women were 60% less likely to receive aggressive (and expensive) diagnostic tests than African-American men or whites. More recently, referral rates for intervention were similar for white or black individuals, but African-American patients accepted surgery less often than white patients.¹¹

African Americans account for 13% of the United States population but only 2-9% of control subjects in most major research trials. Therefore, major studies have been focused more on the treatment of white patients than on black patients, and knowledge of what is best for patients of other races is limited.

Sex

In individuals younger than 65 years who do not smoke, CAD is primarily a disease of men. The difference is attributed to the protective effects of estrogen. Risk factors for significant coronary obstructions that affect both men and women are smoking; exposure to second-hand smoke; diabetes; poor diet; elevated levels of homocysteine, LDL-C, or triglycerides; low HDL-C levels; hypertension; use of birth control pills; and a sedentary lifestyle.

Because more research has been completed in men than in women, less is known about the reliability of screening women. In addition, vascular tone or spasm may play a larger role in women than in men. Therefore, many recommend a decreased threshold for imaging of the coronary arteries in any woman who complains of chest pain, without a consideration of whether the pain is predictable at a particular level of exercise.

Case-fatality rates are higher in women than men. Noninvasive testing in women has been controversial because of a perception of diminished accuracy, limited female representation, and technical limitations (eg, breast artifact). Exercise treadmill testing has an improved accuracy when multiple risk parameters (eg, ST deviation, chest pain, exercise time) are included in the interpretation. For women, a low-risk Duke treadmill score is predictive of a 5-year survival rate of 97%, and fewer than 20% of patients have obstructive disease.

Calcium scoring in women has a sensitivity of 88% and specificity of 49%; values for exercise echocardiography are 86% and 79%, respectively. A quantitative evaluation of perfusion may improve the precision of risk assessment.

Age

• Fatty streaks in vascular walls are observed in people of all ages, even infants. Children may have cardiac ischemia as a result of a stenotic or acutely angled origin of a vessel or another anomaly, such as a vessel pinched between the aorta and pulmonary artery or trapped under a myocardial bridge.
• In an autopsy series of 19-year-old soldiers, coronary lesions were prevalent but amounted to only mild stenosis.
• After the age of 35 years, clinically significant CAD is prevalent in men. Serious disease at that age typically results from cocaine use; smoking; or exposure to second-hand smoke, diabetes, or other predisposing factors. The lifetime incidence of CAD after the age of 35 years exceeds 1 in 4 people. Autopsy series revealed that 25% of men younger than 25 years and 75% of men older than 25 years have a clinically significant coronary lesion. One in every 4 adults has clinically significant atherosclerotic disease.

Anatomy

CAD may affect a large coronary artery near the vessel origin at the aortic root (proximal segment) or a small branch vessel far from its origin (distal segment). CAD may affect all 3 of the major supply arteries to the heart: the left anterior descending (LAD) artery, the left circumflex artery (LCX), and the right coronary artery (RCA). Therefore, a simple ranking of disease severity is 1-, 2-, or 3-vessel disease. For this purpose, disease is defined as the presence of 1 or more areas of narrowing of a vessel or major branch by 50% or more from its expected normal diameter (eg, compared with a nearby proximal normal segment without intervening branches). Therefore, 50% narrowing in the LAD, LCX, and RCA is considered 3-vessel disease comparisons of surgery, medical therapy, and catheter interventions.

A 50% reduction in vascular diameter is a reasonable definition of a clinically significant lesion because lesions with 50% or greater stenosis are commonly responsible for heart attacks. The definition is imperfect in that an unstable lesion with only 30% stenosis can also cause a heart attack, and lesions that cause angina are typically stenoses of 70% or greater. It is also imperfect in that stenosis based on diameter does not account for the length of the lesion or its entrance and exit effects (funnel versus abrupt), all of which affect flow reduction. Therefore, clinical judgment is also need in assessing the clinical significance of a lesion, such as whether it supplies a territory with demonstrated jeopardy on stress testing or perfusion assessment. In addition, a Doppler flow wire or intravascular ultrasonography (IVUS) may be applied and/or flow reserve may be estimated to assess the hemodynamic significance of a coronary lesion.

In most people, the LAD and LCX have a common origin from the left coronary sinus of the aortic root, a short vessel called the left main coronary artery. A third of the population has a third artery between these 2 called the ramus intermedius. In uncommon cases, the LAD and LCX have separate origins, both of which arise from the left coronary sinus or, in rare cases (1 in 1000 people), the LCX may originate in another sinus. In as many as 20% of individuals, the origins are higher than usual, at the junction with the tubular portion of the aorta (sinotubular junction, or STJ). The RCA has a separate origin in the right coronary sinus, but sometimes its origin is at the sinotubular junction (9%) or higher (1%). The aortic cusps corresponding to the coronary arteries normally arise are anterior and face the pulmonary valve. The third cusp (posterior cusp) just above the aortic valve typically has no arterial branch, but in a quarter of the population, it gives rise to the right conus artery, a smallvessel that is usually the highest branch of the right coronary artery. Anatomic variants are common.

The branches of the LAD are called diagonals and successively labeled D1, D2, and so on. The portion from left main coronary artery to the first diagonal is called the proximal segment of the LAD. The portion between D1 and D2 is the middle segment, and that beyond D2 is called the distal segment. The distal segment typically covers the anterior aspect of the apex of the left ventricle (LV). However, in 12% of the population, it wraps around to cover the inferior surface of the apex as well (wrap-around LAD). In addition to diagonal branches, the LAD gives off numerous, small septal perforators that supply the anterior two thirds of the intraventricular septum.

The branches of the LCX are called obtuse marginal branches and numbered sequentially (OM1, OM2, etc). The LCX often courses around the base of the heart near the atrioventricular (AV) groove. In 20% of patients, the LCX reaches the crux, where the AV groove meets the posterior interventricular septum and turns to supply the inferior surface of the heart as the posterior descending artery, also known as the posterior interventricular artery. In 85% of people, this artery is a distal continuation of the RCA. If the posterior descending artery stems from the RCA, the circulation is described as right dominant, and if the it comes from the LCX, the supply system is called left dominant. In about 5% of patients, both the RCA and the LCX contribute to the PDA territory, a condition described as codominance. The dominant artery is delivers blood to the posterior one third of the septum and the AV node, which penetrates into the center of the heart from the crux.

The proximal RCA usually (in 60%) supplies the sinoatrial note via a branch that runs between the aortic root and the superior vena cava. In a third of the population, the sinuatrial node comes from the left, and in some individuals, it is supplied form both right and left. The RCA courses near the AV groove, extending inferiorly to the right toward the crux (the intersection of the AV groove and the interventricular). The RCA gives off a large branch called the acute marginal branch before it reaches the crux. The RCA may continue in the AV groove past the crux with LV extension branches, or it may terminate short of the crux. The proximal RCA branches typically include the left atrial artery, the conus artery, the sinuatrial node artery (in 55% of the population), the right atrial artery, and the right or acute marginal artery.

Clinical Details

Risk factors for CAD are classified as modifiable or unmodifiable.

Modifiable risk factors include smoking, exposure to second-hand smoke, hypertension, hyperlipidemia, high cholesterol (total or LDL-C) levels, low HDL-C) levels, high triglyceride levels, diabetes, abdominal obesity, sedentary lifestyle, high homocysteine levels, and high levels of C-reactive protein (which indicates inflammation). For patients with a triglyceride concentration of less than 400 mg/dL ( <4.5 mmol/L), the LDL-C value can be estimated by using the following equation: LDL-C concentration = Total-cholesterol concentration - HDL-C concentration - (triglyceride concenration/5).

Treatment before evidence of disease appears is called primary prevention; treatment afterward is called secondary prevention.

Target levels for LDL-C have been lowered from 160 mg/dL to <100 mg/dL. Recently, a target of <70 mg/dL has proved advantageous in preventing the recurrence of a heart attack (O'Keefe, 2004). Cholesterol synthetase inhibitors confer a benefit even in patients with normal LDL-C levels, possibly because of an anti-inflammatory effect. The target level for HDL is >40 mg/dL (>1 mmol/L), the achievement of which may require vigorous exercise and high-dose niacin. Skin flushing may limit the use of niacin; effects may be lessened if niacin is taken half an hour after aspirin or if slow-release preparations are used. A new agent, torcetrapib,⁷ raises HDL-C levels by inhibiting CETP. It promotes reverse transport of lipids from soft plaque back to the liver, potentially reversing atherosclerosis.

Unmodifiable risk factors include age, male sex, and family history. Aggressive lowering of cholesterol levels has reduced individual morbidity and mortality rates in some groups but not the cardiovascular death rate for the overall population.

CAD should be suspected in a patient with any symptoms that may represent cardiac ischemia, such as an ache, pressure, pain, other discomfort, or possibly just decreased activity tolerance due to fatigue, shortness of breath or palpitations. Discomfort or pressure is especially suggestive when it occurs in the chest, left arm, jaw, or upper abdomen and particularly if it is triggered by exertion, exposure to cold, or shaving and if it relieved by rest or nitrates. The symptom often radiates from 1 location to another, eg, from behind the sternum to down the left arm. Nausea, diaphoresis, and a duration longer than 10 minutes suggest that the episode is turning into a heart attack (cell death).

Cardiac ischemia without chest pain represents a defective warning system regarding angina; this presentation is not uncommon in people older than 60 years or in those with diabetes. Patients may have only decreased exertion tolerance, dyspnea, or palpitations triggered by exertion. Although a timely ECG may show silent ischemia, some areas of the heart are electrically silent, which means that they are not represented on the ECG. Perfusion or wall-motion imaging can help in identifying the problem.

Preferred Examination

If a patient has symptoms, suggestive ECG findings, or imaging results that indicates a need for intervention, x-ray angiography by means of catheterization is currently the preferred examination for identifying the culprit lesions and, often, for providing an interventional remedy during a single session.

The patient's clinical history (age, symptoms, risk factors) provide an estimate of disease likelihood. The basic screening test is stress ECG, which increases predictive accuracy to provide different levels of confidence depending on the pretest likelihood of disease. If the patient's resting and stress ECGs are normal, his or her risk of mortality in the next year is low. However, the predictive accuracy of stress ECG overall is not good, as one half of all cases of disease are missed. The simple addition of stress testing of B-type natriuretic peptide (BNP) levels in the blood markedly improves the predictive accuracy.¹² Other ways to improve accuracy are nuclear imaging, echocardiography, MRI, or CT.

Stress nuclear imaging is widely used to assess the patient's exercise tolerance and to identify zones of inducible ischemia (jeopardized myocardium), which is useful information, even after x-ray angiography is performed. PET offers similar rest-stress data and is superior for identifying viable myocardium. Jeopardy and viability are important issues because, if the myocardium is not at risk or if it is not viable, revascularization (bypass or angioplasty) will not help that part of the heart.

Recently, MRI and CT have achieved markedly improved the ability to depict zones of impaired blood supply and to display the coronary anatomy. MRI and CT do not require stress, they offer sensitivity and specificity similar to those of nuclear imaging, they achieve resolution better than that of nuclear imaging, and they can demonstrate the 3-dimensional (3D) coronary anatomy.¹³ Therefore, MRI and CT complement the combination of stress test and catheterization, and in some settings, MRI and/or CT may replace them (eg, by demonstrating normal results).

EBT offers similar value. EBT is a form of CT in which an electron beam, rather than the entire x-ray source, is rotated around the patient. Also, EBT and CT have been used as a screening test to screen for calcifications in the coronary arteries as a marker for risk of coronary disease in young patients.

To monitor angiogenesis, collateral-sensitive and delayed-arrival MRI appear to be far more sensitive than any other technique. Collateral-sensitive MRI generates a dark flare of susceptibility effect due to sparse neovascular development at an early stage while suppressing a similar effect from the LV. This finding is a strong predictor (r = 0.93) of improved blood delivery.

Data from quantitative studies of the extent of delayed arrival in humans and from double-blind postmortem evaluations in porcine models of chronic myocardial ischemia and angiogenesis have validated this method.¹⁴ This finding clearly distinguishes angiogenic treatment from control at 4 weeks after treatment, and the benefit is followed by improvements in wall motion (serial motion assessment by reference tracking [SMART] measurements).¹⁵

Limitations of Techniques

X-ray angiography is considered the criterion standard for evaluating coronary artery stenosis. Flow limitations may be estimated by using the Thrombolysis in Myocardial Infarction (TIMI) score and confirmed by using a flow wire or by performing IVUS.¹⁶ If x-ray angiography fails to depict a culprit lesion and if cardiac ischemia is inducible, the patient may have syndrome X (microvascular disease).

X-ray angiography requires the use of iodine, which may cause serious allergic reactions, including anaphylaxis, and also renal failure. Use of large volumes of saline and the antioxidant acetylcysteine may help prevent renal failure. The catheterization procedure can induce vessel spasm and/or tear the lining of a vessel, resulting in occlusion and, possibly, death in a patient who may not have had CAD. The procedure can also result in embolism, which may cause stroke or limb loss. Nerve damage, infection, and other complications are possible as well. The death rate is approximately 0.1%.

Nuclear imaging produces low-resolution images that may depict an apparent defect resulting from breast tissue, hiccoughs, paradoxical septal motion, or other confounding factors. Nuclear imaging may fail to depict disease because of submaximal stress. Tomographic imaging, attenuation correction or PET substantively eliminate the problems resulting from breast attenuation. The newer combinations of nuclear imaging with CT enable the most accurate correction of nuclear event maps for attenuation by overlying tissues.

MRI requires special precautions in patients with pacemakers or recently placed aneurysm clip. Patients with claustrophobia require premedication, mirrors, and/or an open magnet. Many magnets do not accommodate patients who weigh more than 300 lb. Arrhythmias commonly lower image quality.

CT contrast agents usually contain iodine, which may cause an allergic reaction and possibly anaphylaxis. Nonionic contrast material reduces the risk of harm, as does pretreatment with steroids. Gadopentetate dimeglumine, the contrast agent used for MRI, may be used for CT if patients are allergic to iodine-based media. CT uses X-rays typically equivalent to the dose needed for about 200 chest radiographs. A single routine CT study in a child increases his or her lifetime risk of cancer by 0.35% per scan.¹⁷ In adults, the lifetime risk of cancer may be as high as 2% with annual CT screening.

DIFFERENTIALS

Section 3 of 11  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Intervention
• Multimedia
• References

RADIOGRAPH

Section 4 of 11  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Intervention
• Multimedia
• References

Findings

Coronary angiography shows where vessels originate, how they branch, whether they have obstructions or dissections or thrombi, the degree of any obstructions, and which territories they supply. Some key questions answered during an examination of the anatomy include the following:

• Does a coronary artery pass between the aorta and pulmonary artery where it may get pinched?



• Does a segment tunnel under a myocardial bridge?



• Which pathway supplies the posterior surface? Is it the right, left circumflex, or both? That is, is it right dominant, left dominant, or co-dominant?



• Does the LAD wrap around the apex to supply the distal diaphragmatic surface?



• What vessel supplies the AV node? Is its blood supply impaired?



• If an infarct is present, which is the infarct-related artery?



• If abnormal wall motion is seen, which branch obstruction accounts for it?



• Are any bypass-graft vessels present? If so, where do they originate (left internal mammary, saphenous vein graft from anterior aortic root)? Are they long or short, where do they connect, and how (end to side, side to side)?

The caliber of vessels may be estimated by comparing them with the known diameter of the catheter if it appears on the image. The reviewer should take into account the fact that magnifications differ at different distances from the source to the intensifier with x-ray projection angiography.

After describing the anatomy, note the location, percent narrowing, and character of all focal obstructions (stenoses).

• For each lesion, is it concentric (symmetric) or eccentric (1 sided)?



• Is it long or short?



• Does it abut a branch vessel (which may be lost after intervention)?



• Is it calcified?



• Is any thrombus demonstrated?



• Is evidence of intimal tear demonstrated?



• Is evidence of vessel spasm demonstrated?



• Is diffuse narrowing demonstrated?

The flow of contrast agent–labeled blood offers useful information. TIMI criteria may be applied to determine whether the distribution of contrast material is TIMI 0 (incomplete, fails to fill branches and distal part of the vessel), TIMI 1 (slow but complete), or TIMI 2 (brisk and complete). When imaging is performed at a rate of 30 frames per second, the number of frames it takes for a vessel to completely fill may be assessed. The normal number is approximately 21 frames. Filling takes longer in patients with disease than in healthy people, not only in the diseased vessel but also in normal vessels.

Consider how findings may affect possible interventions and report them accordingly. Clinically significant narrowing in the left main coronary artery is a medical emergency because of the amount of myocardium at risk. Other patterns of disease can pose similar risk; examples are proximal disease in both the LAD and a dominant right or left circumflex vessel.

• What is the caliber of distal vessels that may support a bypass graft?



• Are they calcified?



• Is any stenosis near a branch point (such that balloon angioplasty of the lesion may obstruct a branch artery)?



• How long is the left main coronary artery?



• How much myocardium is at risk?

Examine images for ancillary findings.

• Which calcifications move with the heart?



• Is the mitral valve annulus calcified?



• Is the aortic root or the aortic valve calcified?



• Are valve rings, bypass vessel rings or clips, stents, sternal wires, or other evidence of prior surgeries noted?



• If pacer wires are noted, where do they end?



• Does evidence exist of chamber enlargement, aneurysm, cardiac displacement, abnormal pulmonary venous return, unusual persistence of fetal structures, or other variants?

If left ventriculography is performed, examine LV function for the EF, regional wall-motion abnormalities, and valve integrity. Hypokinesis indicates educed motion, akinesis indicates no motion, and dyskinesis indicates reversed motion ie, ballooning outward during systole. Note any leakage of contrast material back into the left atrium and any restriction of the valve leaflets.

At the time of coronary angiography, the same set of tools can be used to examine other vessels (eg, renal arteries, carotids).¹⁸

Degree of Confidence

X-ray angiography is the standard for identifying the coronary anatomy and stenoses. In select cases, alternative imaging may appear superior, but be careful to distinguish between high-quality or good-looking pictures and the reliability of the results.

False Positives/Negatives

Balloon angioplasty can disrupt an obstruction so that the vessel appears to recover its full diameter when, in fact, the cross-sectional area is improved only minimally and insufficiently. 3D imaging can be used to examine contrast-agent attenuation and the percentage narrowing. On occasion, this condition may be identified by looking at the lesion on different views or by performing IVUS or optical CT.

The introduction of a catheter or a wire can cause intimal dissection (a tear in the lining of a vessel), which may be mistaken for vascular spasm, thrombosis, or a long stenosis on cursory examination. A tissue flap in the endothelial lining may alternate between an open position and an obstructive one, mimicking a spasm; however, it is not responsive to nitrates. The distinction may be a matter of life or death. If clinically significant, stent placement, bypass, placement of a perfusion catheter, or other emergency treatment is typically required to treat a dissection. Sudden obstruction due to a dissection can be deadly, and it does not respond to medications.

Myocardial bridges, or small bands of muscle overlying a vessel, may be mistaken for stenoses; however, these are not amenable to angioplasty. The obstruction from a myocardial bridge is smooth and eccentric. Observation throughout the cardiac cycle shows that the obstruction occurs during systole.

CT SCAN

Section 5 of 11  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Intervention
• Multimedia
• References

Findings

CT imaging of the coronary arteries is achievable with fast CT and EBT systems triggered or gated by ECG to accumulate data when the heart is in diastole. 64-section multidetector-row CT is the newest technology.

With a section thickness of 1 or 0.5 mm or less, the coronary anatomy is laid out in a 3D volume. Image processing can greatly facilitate visualization of the course of vessels and branches and the presence and degree of stenoses. The coronary-artery tree may be viewed as a solid rendering of the surface of the heart, but portions may be obstructed from view.

Proper viewing of each coronary-artery branch should include clean views in which the LV blood pool, aortic root, and all extracardiac structures are removed, and vascular projections are limited to the zones that include the vessel of interest and a margin for partial-volume effects. Do not rely on threshold-based renderings, which can cause false-stenosis and false-obstruction and which can cause an intravascular thrombus to be missed. The use of a pair of volumes before and after the administration of contrast material for elastic matching¹⁹ greatly facilitates the evaluation by automatically isolating the coronary tree without thresholding.¹³

CT also enables superb evaluation of blood delivery. In principle, CT combined with catheterization permits accurate definition of the extent of collateral-dependent myocardium.¹³

Degree of Confidence

The ability of MRI and CT to depict the anatomy and the absence of notable obstructions is improving rapidly, but it is not uniform. The value of MRI and CT must be assessed in a truly double-blind fashion for each center until standardized reliable methods are widely established. Whether MRI and CT results match in terms of the percentage of stenosis is relatively unimportant. Most important is whether MRI and CT reliably depict normal tissue and culprit lesions, and then, whether they establish the severity and the territories supplied by the culprit vessel. Both MRI and CT offer the significant advantage of direct assessment of the zones of impaired blood delivery.

False Positives/Negatives

MRI shows calcifications as black or signal voids, whereas CT shows calcifications as white and similar to contrast-filled blood. These appearances can influence the estimation of stenoses. Heavy calcification causes a beam-hardening artifact on CT that can interfere with visualization. Stents cause a local disturbance stronger on MRI than on CT. Also, with 3D MRI or CT, be certain to understand how the images account for local curvature in and out of the imaging planes. In finding the best plane to show a vessel, radiologists can mistake a local curve that is out of plane for an apparent stenosis. Proper image processing resolves this problem.

MRI

Section 6 of 11  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Intervention
• Multimedia
• References

Findings

Coronary MRI may be performed by using a 3D volume, but the trade off in time and resolution favors imaging in selective planes that address each branch of interest. As a 3D volume, MRIs may show the coronary tree in a way similar to the methods described for CT. Background tissue may be suppressed with fat saturation, tissue saturation, magnetization transfer, and/or T2 preparation (90°-180°-180°- ... -180°-90°).

The vessel-plane approach is as follows: Any desired target plane can be obtained by specifying 3 points to include in the plane, by drawing the lines of intersection with 2 previous images at different angles, or (commonly) by drawing a single line of intersection with a previous image that is perpendicular to the desired view. For example, to obtain a short-axis view of the coronary sinus, first obtain a long-axis view of the LV parallel to the septum and perpendicular to the AV groove, then prescribe a plane in the AV groove perpendicular to that view passing through the 2 observed points of intersection on the first view with the coronary sinus, seen as bright dots anterior and posterior to the mitral valve.

Other points regarding MRI to evaluate CAD are the following:

• A transverse stack of images covering the aortic root depicts the origin of the RCA and the left main coronary artery. The typical section thickness should be 3 mm or less. A bright- or dark-blood technique can be applied with the use of single frames or with a dynamic movie series.

• An additional distal transverse image shows a cross-section of the RCA, LAD, and LCX.

• From 2 points along the proximal vessel and from 1 point from the distal vessel, a plane that captures the desired segment is selected. The plane may be adjusted to be thick enough to encompass out-of-plane bends. As an alternative, it may be subdivided into a stack of thin imaging planes for a localized 3D stack of images.

• The course of the RCA in the AV groove can quickly be ascertained from a 4-chamber long-axis view of the heart by obtaining 1 preliminary image perpendicular to the AV groove and parallel to the septum through the mid RV. This provides 2 points of intersection with the RCA: 1 anterior and 1 posterior in the AV groove. Prescribing a plane through those 2 points from the long axis image gives the desired view.

• The posterior descending artery requires a different imaging plane, as do the LAD, LCX, and major branches. The course of the LCX in the AV groove is assessed in a way similar to that use to image the RCA, by acquiring a scout image parallel to the septum to identify 2 points to include in one final short-axis image. However, in this case, the scout image should be laterally displaced to the outer third because the distal LCX is often hard to identify.

• The present authors routinely identify the proximal course of the coronary arteries in young patients who have had syncope to look for aberrant origins. A complete absence of abnormalities suggests a good prognosis.

• Apparent stenosis must be distinguished from an out-of-plane bend.

• A signal void from flow disturbance may exaggerate apparent stenosis.

• MRI is well established as a means to assess the patency of a bypass graft.

Degree of Confidence

MRI offers high sensitivity to changes in wall function, eg, wall thickening and radial motion.¹⁵ MRI may be useful in identifying and quantifying impaired blood delivery and wall function in response to interventions.^{20, 21, 22, 23, 24, 25, 14, 26} Such applications are perhaps more vital than visualizing the percentage of stenosis.

Confidence in the data depends on the speed and quality of the imaging method, the cooperation of the patient (shallow regular breathing or several matching breath holds), the accuracy of ECG triggering or gating, and the anatomic knowledge and judgment of the person directly supervising data collection.

Cardiac MRI with the vessel-chasing approach requires highly informed decision making as the data are being acquired. If the operator acquiring the data understands what the x-ray angiogram demonstrates, the views may be manipulated for the best match. This consideration is not necessary positive because the operator may exaggerate the agreement.

The ability of MRI and CT to identify anatomy and the absence of clinically significant obstructions is improving rapidly, but it is not uniform. The value of MRI and CT must be assessed in a truly double-blind fashion for each center until standardized and reliable methods are widely established. Whether MRI and CT results match in terms of the percentage of stenosis is relatively unimportant. Most important is whether MRI and CT reliably depict normal tissue and culprit lesions, and then, whether they help in establishing their severity and in depicting the territories supplied by the culprit vessel. Both MRI and CT offer the notable advantage of enabling direct assessment of the zones with impaired blood delivery.

False Positives/Negatives

In an apparent stenosis, be certain that it is not a partial-volume artifact or a velocity-shear effect. Because local differences in velocity can cause a signal void, estimates of stenosis may be exaggerated.

Magnetic susceptibility artifacts may produce signal voids. Stents, clips, and wires cause local disturbances.

The presence of pacemaker wire is considered a relative contraindication to MRI because the rapidly changing magnetic fields may induce a voltage that can trigger an arrhythmia, induce a burn, or shorten the battery life. Also, when the patient enters and leaves the magnet, the magnetic reed switch on most pacemakers will switch it to fixed mode, and the temperature may rise in metal devices. For example, a pacemaker generator may warm by 1-2°C. However, with informed consent, careful pulse monitoring, and a readiness to promptly abort a pulse sequence if an arrhythmia is induced, patients with pacers have undergone MRI with no apparent consequence and no change in their pacer thresholds. In the dozen reports of mishaps related to pacemakers and MRI, none were caused by MRI.

On MRIs, calcification is depicted as a black area or signal void, whereas CT shows calcifications as white, similar to blood filled with contrast agent. These appearances can influence the estimation of stenoses. Also, with 3D MRI or CT, be certain to understand how the images account for local curvature in and out of the imaging planes. In finding a best MRI plane for showing a vessel, radiologists can mistake a local curve that is out of plane for an apparent stenosis. Proper image processing resolves this problem.

With MRI, flow disturbances that cause velocity shear (range of phases in each picture element or pixel resulting from different rates of motion of blood) cause a local decrease in signal intensity, which may create or exaggerate an apparent stenosis.

ULTRASOUND

Section 7 of 11  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Intervention
• Multimedia
• References

Findings

Echocardiography can be used to identify the left main coronary artery. In some patients, much of the RCA and LAD can be viewed; however, in most patients, the imaging window is inadequate for useful coronary imaging from outside the chest.

In the catheterization laboratory, IVUS may be performed to examine the coronary arteries from the inside and to characterize plaque. However, the diameter of the device limits the ability to pass through tight stenoses. Also, the injection of a sonographic contrast agent (eg, agitated Renografin) into the coronary arteries, combined with transthoracic or esophageal ultrasonography, can be useful in identifying perfusion territories.

NUCLEAR MEDICINE

Section 8 of 11  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Intervention
• Multimedia
• References

Findings

Nuclear medicine study does not depict the coronary arteries, but it does demonstrate various metabolites useful in identifying perfusion defects and tissue viability. Thallium-201 and technetium-99m sestamibi are widely used and may be combined to shorten the study of myocardial uptake of radioactive tracer at rest and during stress. Although a rest-and-stress thallium study takes more than 4 hours, a combined study performed with thallium and sestamibi may be completed in less than 2 hours.

By using PET, a rest-and-stress study with rubidium-82 may be completed in 30 minutes, because the agent has a half-life of less than 5 minutes. A defect during stress that is not evident at rest indicates a zone of induced ischemia. A defect at rest and also during stress indicates persisting metabolic dysfunction, either from infarction (scar) or hibernation (prolonged dysfunction). PET with ammonia, fluorinated glucose, or other agents may be used to determine if the tissue with a defect at rest is viable.

Degree of Confidence

Nuclear medicine tests for CAD improve the predictive accuracy over that of stress tests alone, to approximately 90%. The utility of these tests depends on the previous probability of disease and on whether they are being used to identify CAD or to clarify the pathophysiology of known disease.

False Positives/Negatives

Breast attenuation may cause an apparent defect on radionuclide images. Attenuation correction and multiplanar imaging mitigate the problem.

Unusual motion, such as that from a bundle branch block or coughing during imaging, may cause false-positive results. A persisting defect is commonly interpreted as a fixed defect or a scar, but it may represent prolonged yet still-reversible ischemic impairment of tracer uptake.

The low resolution of nuclear medicine studies compared with that of other modalities may result in false-negative results. Also, global disease may be missed because defects are generally identified by comparing them to regions with high uptake of the tracer.

INTERVENTION

Section 9 of 11  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Intervention
• Multimedia
• References

Imaging guidance of interventional procedures

X-ray angiography is widely used to guide interventions, such as balloon angioplasty, atherectomy, laser treatment, stent placement, and other procedures. Current practice indicates the use of x-ray angiography in patients with potentially treatable lesions to confirm the findings and to perform interventions. Both tasks may be accomplished in a single procedure.

Cardiac catheterization is recommended for patients with mild angina (class I or II) plus an EF of less than 45%, including patients with noninvasive test results indicating a high risk, those with an uncertain diagnosis after noninvasive testing, patients with serious ventricular arrhythmias, and those who survive an episode of sudden death. The only indication with submaximal support is mild angina with reduced EF; this is a class IIa recommendation. The classification of indications by the American College of Cardiology indicates the weight of evidence in support of the recommendation. Mild angina with no reduction in EF might be managed with medication as a therapeutic trial.

As an experiment, MRI, CT, or echocardiography may be used to guide interventional procedures. MRI does not involve ionizing radiation; therefore, imaging may be active throughout the procedure. However, special guidewires and other equipment compatible with the magnet and the rapidly changing magnetic field must be used, and staff must be trained to ensure that no magnetic objects are brought near the magnet.

CT uses ionizing radiation and is slower than x-ray angiography, but it provides 3D information that may facilitate localization, especially for newer interventions such as the intramyocardial injection of angiogenic growth factors or stem cells. 3D ultrasonography similarly facilitates accurate injections, with convenience of portability and without a need for lead shielding from x-rays. The use of CT, MRI, and 3D ultrasonography for these purposes is experimental.

Prevention, treatment, repair, and new therapies

Prevention aims to slow or reverse the process that causes disease, for example, by lowering serum LDL-C levels (with statins), by increasing HDL-C levels (with exercise, niacin, or torcetrapib), by lowering homocysteine levels (with folate and B vitamins), and by counteracting the oxidation of LDL-C that accelerates wall uptake of the lipid (with vitamin C and selenium). Vigorous exercise every other day promotes overall health and the development of new vessels.

High levels of homocysteine are associated with the rapid development of disease. High homocysteine levels are as important as high cholesterol levels, and they can be treated by simply administering supplemental doses of folate, adjusted to effect. Patients sometimes also require B vitamin supplements. One area of study is how specific growth factors, such as basic fibroblast growth factor 1 (bFGF1), basic fibroblast growth factor 2 (bFGF2), and vascular endothelial growth factor (VEGF) may stimulate the development of new vessels. These factors are administered either directly or by means of DNA-based therapies.

Medical treatments aim to improve the blood supply as needed by dilating the vessels, typically with nitrates, and/or by decreasing the demand, typically with beta-blockers. Other medical treatments include thrombin inhibitors, IIb/IIIa inhibitors, and high-dose statins.

Repair aims to crack or crush a lesion (with angioplasty), remove a portion of the obstruction (with atherectomy or laser treatment), remove clot (with thrombectomy, passage of a wire, or thrombolysis), hold the vessel open at an increased diameter (with stent placement), apply local medication (with drug-eluting stent placement), provide new pathways (with bypass surgery), and/or stimulate the growth of new vessels (with therapeutic angiogenesis).

New site-specific drug-eluting stents chemically inhibit the reactive endothelial growth that causes early restenosis after angioplasty. The failure of vein grafts after mechanical intervention continues to pose a challenge. New devices (eg, Front Runner and Safe-Cross devices). have been developed to improve the ability to open totally occluded vessels, even chronic occlusions. One area of investigation is the protection of the distal vessel from debris during the treatment of acute MI or degenerating vein grafts. A current trend is to use PCI and complete revascularization, even in high-risk elderly patients.²⁷

Medical/Legal Pitfalls

• Failure to perform timely screening and/or catheterization in a patient referred for evaluation may create liability for the physician if the patient subsequently has a cardiovascular event that might have been prevented if the disease had been discovered earlier.
• Other pitfalls are listed below:
• • Performing a routine stress test in a patient with symptoms from severe aortic stenosis
  • Giving nitrates to a patient in the upright position who is taking Viagra or Cialis without also giving intravenous saline, performing careful BP monitoring, and advising the patient about a possible life-threatening hypotension
  • Failure to obtain promptly an ECG or otherwise properly evaluate and treat a patient with an angina-equivalent condition or silent MI who presents with painless shortness of breath, fatigue, or other painless angina-equivalent symptom
  • Failure to promptly relieve ischemia by applying the relevant treatment options
  • Misinterpreting intimal dissection as stenosis or thrombosis, which may result in the avoidable death of a patient
  • Failure to identify spasm and to promptly initiate appropriate treatment
  • Failure to treat stenosis of the left main coronary artery or its equivalent with appropriate urgency and use of precautionary measures
  • Complications from performing an intervention in a nonculprit lesions in an acute setting

MULTIMEDIA

Section 10 of 11  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Intervention
• Multimedia
• References

Media file 1:  Selective injection image of the left coronary arteries. D1 = first diagonal, LAD = left anterior descending artery, LCX = left circumflex, LM = left main coronary artery, and OM1= first obtuse marginal.
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Media type:  X-RAY

Media file 2:  MRIs of the coronaries can be used to build 4-dimensional images (3-dimensional beating heart). These images show a single frame, including a cutaway view to show the cardiac interior, the outer surface (no thresholding), and the extracted coronary artery tree including the aortic root.
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Media type:  MRI

Media file 3:  Elastic-match imaging automatically identifies differences between image volumes. The acquisition of 1 set of contrast-enhanced chest CT images via the coronaries and a nonenhanced set provides a 3-dimensional view of the coronary-artery tree. The nonenhanced volume data were rendered as holographic projections to provide the anatomic context, and the elastic-match coronary tree was overlaid. In addition to automation, this method avoids thresholding so that small branches and filling defects, if present, are represented properly.
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Media type:  CT

Media file 4:  Elastic-match imaging can be used to identify collateral-dependent myocardium. Left and middle images are baseline and peak-arrival collateral-sensitive MRIs demarcating microvascular development. Right image, based on CT imaging of the heart, was obtained with and without back pressure to nullify collateral-dependent perfusion; white volume on represents collateral-dependent myocardium. The extent of collateral-dependent myocardium corresponds well on MRI and CT (r = 0.95).
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Media type:  CT

Media file 5:  Contrast-labeled blood to the heart is used to identify the territory at risk. The results of this assessment of the delayed arrival compares favorably to the findings of radionuclide stress imaging, and stress induction of ischemia is not required to identify the zone at risk.
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Media type:  MRI

Media file 6:  Space-time maps show the history of blood arrival to all layers of myocardium on a 2-dimensional map. The indentation indicates the severity of the defect in blood delivery, and the length indicates the size as a percentage of the myocardium, without the need for stress induction of ischemia. In addition to the safety advantage, this method is also more reproducible than stress testing, which is useful in assessing the effect of therapy.
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Media type:  MRI

Media file 7:  Compared with radionuclide images of blood delivery, MRIs and CT scans improve resolution, depiction of the functional effect and the relationship to the coronary supply, and identification of the area at risk without stress. The advantage of radionuclide imaging is primarily its predictive value; stress echocardiography has similar predictive value. MRI and CT have been less available than other studies; therefore, data on their value are relatively limited.
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Media type:  X-RAY

Media file 8:  X-ray angiography is the criterion standard for delineating the coronary anatomy, but it is inferior to MRI and CT in identifying myocardium with impaired blood delivery, in assessing the functional consequences, and in identifying the development of microvascular collaterals.
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Media type:  X-RAY

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Intervention
• Multimedia
• References

1. Pearlman JD. NMR imaging and spectroscopy studies of the coronary arteries: II. 3-D reconstruction of in vivo coronary arteries. In: Sideman S, Beyar R, eds. Image Analysis and Simulation of the Cardiac System: Proceedings of 5th Henry Goldberg Workshop on Analysis. London, England: Freund;. 1990: 451-64.
2. Aviram G, Finkelstein A, Herz I, et al. Clinical value of 16-slice multi-detector CT compared to invasive coronary angiography. Int J Cardiovasc Intervent. 2005;7(1):21-8. [Medline].
3. Flohr T, Stierstorfer K, Raupach R, et al. Performance evaluation of a 64-slice CT system with z-flying focal spot. Rofo. Dec 2004;176(12):1803-10. [Medline].
4. Solomon DH, Karlson EW, Rimm EB, et al. Cardiovascular morbidity and mortality in women diagnosed with rheumatoid arthritis. Circulation. Mar 11 2003;107(9):1303-7. [Medline].
5. Todaro JF, Con A, Niaura R, et al. Combined effect of the metabolic syndrome and hostility on the incidence of myocardial infarction (the Normative Aging Study). Am J Cardiol. Jul 15 2005;96(2):221-6.