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Cardiovascular disease is the leading cause of death in the United States. Coronary artery disease, which is responsible for more than 50% of all cardiovascular disease–related deaths, was expected to account for more than $80 billion in direct costs in 2010. In the United States, approximately 1 million people sustain an acute myocardial infarction (MI) every year because of atherosclerotic coronary disease. Although recent advances in percutaneous intervention have reduced the number of referrals for surgical intervention, coronary artery bypass grafting (CABG) still remains one of the most effective treatments for coronary artery disease and is the most commonly performed open cardiac procedure in the United States.
CORONARY ARTERY ANATOMY AND PHYSIOLOGY Anatomic Considerations
The coronary arteries are the predominant blood supply con-duits to the heart. The coronary arteries arise from the sinuses of Valsalva, which are elastic saccular bulges of the aortic root. The coronary arteries are the first arterial branches of the aorta and usually two are present. They are designated as right and left according to the embryologic chamber that they predomi-nantly supply. The left coronary artery (LCA) arises from the left coronary sinus, which is located posteromedially, whereas the right coronary artery (RCA) arises from the right coronary sinus, which is located anteromedially. The LCA, also called the left main coronary artery , averages approximately 2 to 3 cm in length and courses in a left posterolateral direction, winding behind the main pulmonary artery trunk and then splitting into the left anterior descending (LAD) and left circumflex arteries. The LAD courses in an anterolateral direction to the left of the pulmonary trunk and runs anteriorly over the interventricular septum. The diagonal branches of the LAD supply the antero-lateral wall of the left ventricle. The LAD is considered the most important surgical vessel because it supplies more than 50% of the left ventricular mass and most of the interventricular septum. The LAD has several septal perforating branches that supply the interventricular septum from the anterior aspect. The LAD extends over the interventricular septum up to the apex of the heart, where it may form an anastomosis with the posterior descending artery (PDA), which is typically a branch of the right coronary system (Fig. 60-1).
The circumflex artery passes through the atrioventricular groove (AV) and follows a clockwise course. Where the circum-flex artery courses through the AV groove, it gives off branches in a perpendicular fashion that extend toward, but do not quite reach, the apex of the heart. These branches are designated the obtuse marginal braches and are designated numerically from proximal to distal. The circumflex coronary artery usually ter-minates as the left posterolateral branch after taking a perpen-dicular turn toward the apex.
The term ramus intermedius is used to designate a dominant epicardial coronary vessel that arises from the occasional trifurca-tion of the left main coronary artery. The ramus typically emerges from under the left atrial appendage, which is used as a landmark for identifying this branch and courses over the anterolateral wall of the left ventricle. This branch can be intramyocardial and difficult to locate at times.
The RCA supplies most of the right ventricle, as well as the posterior part of the left ventricle. The RCA emerges from its ostium in the right coronary sinus, passes deep in the right AV groove, and then proceeds over the anterior surface of the heart. At the superior end of the acute margin of the heart, the RCA turns posteriorly toward the crux and usually bifurcates into the PDA over the posterior interventricular sulcus and right postero-lateral artery. The RCA also supplies multiple right ventricular branches (acute marginal branches). Occasionally, the PDA arises from both the RCA and LCA and the circulation is con-sidered to be codominant. The AV node artery arises from the RCA in approximately 90% of patients. The sinoatrial node artery arises from the proximal RCA in 50% of patients. Other prominent branches arising from the RCA include the acute marginal artery and anterior ventricular branches. Although the
source of the PDA is often used clinically to define dominance
ACQUIRED HEART DISEASE: CORONARY INSUFFICIENCY
Raja R. Gopaldas, Danny Chu, and Faisal G. Bakaeen
Acquired HeArt diseAse: coronAry insufficiency Chapter 60 1651
systems—the coronary sinus and its tributaries, the anterior right ventricular veins, and the thebesian veins. The coronary sinus predominantly drains the left ventricle and receives 85% of coronary venous blood. It lies within the posterior AV groove and empties into the right atrium. The anterior right ventricular veins travel across the right ventricular surface to the right AV groove, where they enter directly into the right atrium or form the small cardiac vein, which enters into the right atrium directly or joins the coronary sinus just proximal to its orifice. The the-besian veins are small venous tributaries that drain directly into the cardiac chambers and exit primarily into the right atrium and right ventricle. Understanding the anatomy of the coronary sinus is essential for placing the retrograde cardioplegia cannula during cardiopulmonary bypass.
Physiology and Regulation of Coronary Blood Flow
Aortic pressure is a driving force in the maintenance of myocar-dial perfusion. During resting conditions, coronary blood flow is maintained at a fairly constant level over a wide range of aortic perfusion pressures (70 to 180 mm Hg) through the process of autoregulation.
Because the myocardium has a high rate of energy use, normal coronary blood flow averages 225 mL/min (0.7 to 0.9 mL/g of myocardium/min) and delivers 0.1 mL/g/min of oxygen to the myocardium. Under normal conditions, more than 75% of the delivered oxygen is extracted in the coronary capillary bed, so any additional oxygen demand can only be met by increasing the flow rate. This highlights the importance of unobstructed coronary blood flow for proper myocardial func-tion. Box 60-1 summarizes the unique features of coronary blood flow.
In response to increased load, such as that caused by strenu-ous exercise, the healthy heart can increase myocardial blood flow fourfold to sevenfold. Increased blood flow occurs through several mechanisms. Local metabolic neurohumoral factors cause coronary vasodilation when stress and metabolic demand increase, thereby lowering the coronary vascular resistance. This results in increased delivery of oxygen-rich blood, mimicking the phenomenon of reactive hyperemia. When a transient occlu-sion to the coronary artery is released (e.g., during the perfor-mance of a beating heart operation), blood flow immediately rises to exceed the normal baseline flow and then gradually returns to its baseline level. The autoregulatory mechanism responsible is guided by several metabolic factors, including CO 2, O 2 tension, hydrogen ions, lactate, potassium ions, and adenosine. Of these, adenosine is one of the leading candidates in the autoregulatory mechanism. Adenosine, a potent vasodila-tor and a degradation product of adenosine triphosphate (ATP),
of circulation in the heart, anatomists define it according to where the sinoatrial node artery arises. Table 60-1 summarizes the hierarchy of the coronary artery anatomy.
All the epicardial conductance vessels and septal perforators from the LAD give rise to a multitude of branches, termed resistance vessels, which traverse perpendicularly into the ven-tricular wall. These vessels play a crucial role in oxygen and nutrient exchange with the myocardium by forming a rich plexus capillary network. The rich capillary plexus offers a low-resistance sink to allow for unimpeded increase of arterial blood flow when oxygen demand rises. This is important because the myocardial vascular bed extracts oxygen at its full capacity, even in low-demand circumstances, thereby allowing no margin for further oxygen extraction when demand is high.
An intricate network of veins drains the coronary circula-tion and the venous circulation can be divided into three
FIGURE 60-1 Anatomy of normal coronary artery vasculature.
RC
PD
Acute
LM CA
LAD Diag.
OM
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Epidemiologic evidence suggests that coronary artery ath-erosclerosis is closely linked to the metabolism of lipids, specifi-cally LDLc. The development of lipid-lowering drugs has resulted in a significant reduction in mortality. In one observa-tional study of patients who received statin therapy and were known to have coronary artery disease (CAD), statin treatment was associated with improved survival in all age groups.1 The greatest survival benefit was found in those patients in the highest quartile of plasma levels of high-sensitivity C-reactive protein (hs-CRP), a biomarker of inflammation and CAD.2 Animal and human studies have demonstrated that statin therapy also modifies the lipid composition within plaques by lowering the amount of LDLc and stabilizing the plaque through various mechanisms, including reduction in macro-phage accumulation, collagen degradation, reduction in smooth muscle cell protease expression, and decrease in tissue factor expression.
Pathogenesis
The primary cause of atherosclerotic coronary disease is endo-thelial injury induced by an inflammatory wall response and lipid deposition. There is evidence that an inflammatory response is involved in all stages of the disease, from early lipid deposition to plaque formation, plaque rupture, and coronary artery throm-bosis. Vulnerable or high-risk plaques that are prone to rupture are characterized by the following:1. A large, eccentric, soft lipid core 2. A thin fibrous cap
3. Inflammation within the cap and adventitia
4. Increased plaque neovascularity
5. Evidence of outward or positive vessel remodeling
Thinner fibrous caps are at a higher risk for rupture, prob-ably because of an imbalance between the synthesis and degrada-tion of the extracellular matrix in the fibrous cap that results in an overall decrease in the collagen and matrix components (Fig. 60-2). Increased matrix breakdown caused by matrix degrada-tion by an inflammatory cell-mediated metalloproteinase or
accumulates in the interstitial space and relaxes vascular smooth muscle. This results in vasomotor relaxation, coronary vasodila-tion, and increased blood flow. Another substance that plays an important role is nitric oxide (NO), which is produced by the endothelium. Without the endothelium, coronary arteries do not autoregulate, suggesting that the mechanism for vasodilation and reactive hyperemia is endothelium-dependent.
Extravascular compression of the coronaries during systole also plays an important role in the regulation of blood flow. During systole, the intracavitary pressures generated in the left ventricular wall exceed intracoronary pressure and blood flow is impeded. Hence, approximately 60% of the coronary blood flow occurs during diastole. During exercise. increased heart rate and reduced diastolic time can compromise flow time but this can be offset by vasodilatory mechanisms of the coronary vessels. Buildup of atherosclerotic plaques and fixed coronary occlusion significantly impair coronary blood compensatory mechanisms during increased heart rates. This forms the basis for exercise-induced stress tests, in which increased activity or exercise unmasks underlying coronary disease.
HISTORY OF CORONARY ARTERY BYPASS SURGERY
One of the first attempts at myocardial revascularization was made by Dr. Arthur Vineberg from Canada. He operated on a series of patients who presented with symptoms of myocardial ischemia and implanted the left internal mammary artery into the myocardium by creating a pocket. The operation did not entail a direct anastomosis to any coronary vessel and was performed on a beating heart through a left anterolateral thora-cotomy. Dr. Michael DeBakey performed a successful aortocoro-nary saphenous vein graft in 1964. Dr. Mason Sones, who is credited with inventing cardiac catheterization, helped establish coronary artery bypass surgery as a planned and consistent therapy in patients with angiographically documented coronary artery disease.
The development of the heart-lung machine and demon-stration of successful clinical use by Dr. John Heysham Gibbon in the 1950s and the advancement of cardioplegia techniques in later years by Dr. Gerald Buckberg allowed surgeons to perform coronary anastomosis on an arrested (nonbeating) heart with a relatively bloodless field, thus increasing the safety and accuracy of the coronary bypass. In the 1990s, the advent of devices that could atraumatically stabilize the heart provided another pathway for the development of off-pump techniques of myocardial revascularization. T oday, an armamentarium of techniques, ranging from conventional on-pump CABG to minimally inva-sive robotic and percutaneous approaches, is available to manage coronary artery disease. Table 60-2 summarizes the timeline of major historical events in the development of surgery for myo-cardial revascularization.
ATHEROSCLEROTIC CORONARY ARTERY DISEASE Coronary atherosclerosis is a process that begins early in the patient’s life. Epicardial conductance vessels are the most suscep-tible and intramyocardial arteries, the least. Risk factors for atherosclerosis include elevated plasma levels of total cholesterol and low-density lipoprotein cholesterol (LDLc), cigarette smoking, hypertension, diabetes mellitus, advanced age, low plasma levels of high-density lipoprotein cholesterol (HDLc), and a family history of premature coronary artery disease.
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CLINICAL MANIFESTATIONS AND DIAGNOSIS OF CORONARY ARTERY DISEASE
Clinical Presentation
The most common presenting symptom of CAD is angina. It may be accompanied by dyspnea or mistaken for a gastrointes-tinal disturbance. The symptoms typically are exacerbated or incited by effort but subsequently resolve with rest. Unstable angina encompasses resting angina, new-onset angina, and accel-erated angina and is usually indicative of severe ischemia and impending MI. However, not all cases of angina are necessarily indicative of CAD, because disease processes from other systems can closely mimic those of angina. Approximately 15% of patients with CAD do not present with angina.
The term acute coronary syndrome (ACS) has evolved to refer to a constellation of clinical symptoms that represent myo-cardial ischemia. It encompasses both ST-segment elevation MI (STEMI) and non–ST-segment elevation MI (NSTEMI). MI often presents as crushing chest pain that may be associated with nausea, diaphoresis, anxiety, and dyspnea. Symptoms of hypo-perfusion may also include dizziness, fatigue, and vomiting. Heart rate and blood pressure may be initially normal, but both increase in response to the duration and severity of pain. Loss of blood pressure is indicative of cardiogenic shock and indicates a poorer prognosis. At least 40% of the ventricular mass must
reduced production of extracellular matrix results in thinner fibrous caps. Not all plaque ruptures are symptomatic; whether they are is dependent on the thrombogenicity of the plaque’s components. Tissue factor within the lipid core of the plaque, secreted by activated macrophages, is one of the most potent thrombogenic stimuli. Rupture of a vulnerable plaque may be spontaneous or caused by extreme physical activity, severe emotional distress, exposure to drugs, cold exposure, or acute infection.
Fixed Coronary Obstructions
More than 90% of patients with symptomatic ischemic heart disease have advanced coronary atherosclerosis caused by a fixed obstruction. Atherosclerotic plaques of the coronary arteries are concentric (25%) or eccentric (75%). Eccentric lesions compro-mise only a portion of the lumen; through vascular remodeling, the arterial lumen may remain patent until late in the disease process. The impact of an arterial stenosis on coronary blood flow can be appreciated in the context of Poiseuille’s law. Reduc-tions in luminal diameter up to 60% have minimal impact on flow but when the cross-sectional area of the vessel has decreased by 75% or more, coronary blood flow is significantly compro-mised. Clinically, this loss of flow often coincides with the onset of exertional angina. A 90% reduction in luminal diameter results in resting angina.
FIGURE 60-2 components of atherosclerotic plaque. thinning of the fibrous cap eventually results in plaque rupture with extrusion of highly thrombogenic lipid laden material into the coronary artery. this causes an acute occlusion of the coronary artery resulting in myocardial infarc-tion. (Adapted from choudhury rP, fuster V, fayad ZA. Molecular, cellular and functional imaging of atherothrombosis. nature rev drug discov 3:913–925, 2004.)
Modality Target
Process MRI
Ultrasound PET ++––++++Flow-mediated vasodilation Endothelial dysfunction
Adhesion molecules Endothelial activation
++++Macrophages
Inflammation +–++++++++++
MMPs Cathepsin +±––Lipid core Fibrous cap
αv β3 integrin
Fibrin
Platelets αIIb β3 integrin Tissue factor Proteolysis Apoptosis
Angiogenesis
Thrombosis Thrombus
Fibrous cap
Lipid-rich necrotic core
Monocyte recruitment
↓NO production
Angiogenesis
Internal elastic
lamina
LDL
Foam cell Fibrin Endothelial cell VCAM1, ICAM, selectins
Collagen fibril Smooth muscle cell
Apoptotic cell Platelet
MMP
Approximate American Heart
Association lesion stage I II III IV V VI
αv β3 integrin
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Chest Radiography
The chest radiograph is helpful in identifying causes of chest discomfort or pain other than CAD. Chest radiography does not detect CAD directly; it only identifies sequelae, such as cardiomegaly, pulmonary edema, and pleural effusions, that are indicative of heart failure. Evidence of calcification in the coro-nary arteries, although suggestive of CAD, is not reflective of the severity of the disease.
Resting Electrocardiography
A 12-lead resting electrocardiogram (ECG) should be obtained in patients suspected of having CAD or its sequelae. The ECG is evaluated for evidence of left ventricular hypertrophy, ST-segment depression or elevation, ectopic beats, or Q waves. In addition, arrhythmias (atrial fibrillation or ventricular tachy-cardia) and conduction defects (left anterior fascicular block, right bundle branch block, left bundle branch block) are sug-gestive of CAD and MI. Persistent ST-segment elevation or an evolving Q wave is consistent with myocardial injury and ongoing ischemia. Fifty percent of patients have normal electro-cardiographic results despite having significant CAD, and 50% of ECGs obtained during chest pain at rest will be normal, indicating the inaccurate nature of the test.
Risk Stratification and Further Testing
Based on age, clinical history, symptomatology, physical signs, and diagnostic tests, CAD patients are classified as low, interme-diate, or high risk. Such stratification enables the clinician to determine the intensity of medical therapy and timing of coro-nary angiography.
Low- to intermediate-risk patients treated early and with a conservative strategy may undergo stress testing for further risk stratification. The choice to conduct stress testing depends on the patient’s resting ECG and ability to perform exercise.
An exercise stress ECG is helpful in unmasking underlying CAD and is a more reliable screening test than a resting ECG in patients older than 40 years. The Bruce protocol is the most commonly used standardized treadmill exercise protocol. The protocol involves five 3-minute bouts of treadmill exercise, each designed to elicit greater myocardial oxygen demand than the last, to determine the patient’s ischemic threshold. A typical protocol requires the patient to expend about 12 metabolic equivalents (METs) of energy to ensure a complete test. A posi-tive exercise ECG may show progressive flattening of the ST segment or ST-segment depression as exercise progresses. During the recovery phase, ST depression may persist, with downslop-ing segments and T wave inversion. Additional findings associ-ated with an adverse prognosis and the presence of multivessel occlusive disease include a duration of symptom-limited exercise of less than 6 METs, the failure of systolic blood pressure to increase to more than 120 mm Hg, and the appearance of ven-tricular arrhythmias. For detection of CAD, the sensitivity and specificity of an exercise ECG approach 70% and 80%, respec-tively (Box 60-3).
Conditions that preclude accurate interpretation of the stress ECG include digoxin therapy, widespread resting ST- segment depression (≥1 mm), left ventricular hypertrophy, left bundle branch block, and other conduction abnormalities. For patients with these conditions and those unable to exercise, a pharmacologic stress test with an imaging modality using a radionuclide agent such as thallium or sestamibi, multiple-gated
be involved for cardiogenic shock to occur. The first manifesta-tion of CAD in 40% of patients is sudden onset of a nonper-fusing ventricular rhythm, such as ventricular tachycardia or fibrillation.
The prehospital mortality rate for an acute MI (AMI) is approximately 50%. Of those patients who reach the hospital, another 25% die during the hospital stay and another 25% die in the first year afterward.3,4 Mechanical complications of MI include acute ventricular septal defect (VSD), papillary muscle rupture, and free ventricular rupture. They usually occur approx-imately 7 to 10 days after the initial MI.
Physical Examination
Some clinical findings are generic and are related to the systemic manifestations of atherosclerosis. Eye examination may reveal a copper wire sign, retinal hematoma or thrombosis secondary to vascular occlusive disease, and hypertension. Corneal arcus and xanthelasma are features noticed in cases of hypercholesterol-emia. Other clinical manifestations are caused by sequelae of CAD, as noted in Box 60-2.
A thorough vascular evaluation is essential for any patient who presents with coronary disease because atherosclerosis is a systemic process. In addition, if surgery is being planned, the extremities should be evaluated for any previous surgical scars or fractures that could potentially preclude vein harvest.Diagnostic Testing
Biochemical Studies
Patients suspected of having an ACS should undergo appropri-ate blood testing. Levels of creatinine kinase muscle and brain subunits (CK-MB) and troponin T or I should be assessed at least 6 to 12 hours apart. Additional laboratory tests include a complete blood count (CBC), comprehensive metabolic panel, and lipid profile (total cholesterol, triglycerides, LDLc, HDLc). Elevated brain natriuretic peptide (BNP) and CRP levels suggest a worse outcome.
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Multidetector Computed Tomography
Multidetector computed tomography (MDCT), one of the most recent imaging modalities, allows imaging of the coronary arter-ies, especially of coronary artery bypass grafts. Studies have indicated that the sensitivity and specificity MDCT approach or exceed those of other noninvasive methods of visualizing the coronary artery anatomy.5 MDCT is especially useful for imaging proximal CAD and coronary artery bypass grafts. More recent technology improves on conventional MDCT by adding more arrays to the imaging process; 128-slice MDCT arrays are cur-rently available. These scanners can acquire myocardial images within 1 second while exposing the patient to less radiation than traditional scanners. Although it is still preferable that patients have relatively low heart rates during imaging (to reduce arti-fact), the technology has significantly advanced and produces images on par with those generated by the gold standard, con-ventional angiography.6
Magnetic Resonance Imaging and Gadolinium Magnetic Resonance Imaging
Myocardial first-pass perfusion magnetic resonance imaging (MRI) has been considered a good alternative to nuclear cardiac ischemia and viability testing. However, the procedure has not gained widespread popularity because special training and exper-tise are required to perform this type of imaging and interpret the results.
Cardiac Catheterization and Intervention
Cardiac catheterization remains the gold standard for evaluating the anatomy of the coronary arteries. High-quality coronary angiography is essential for identifying CAD and assessing its extent and severity.
Cardiac catheterization is commonly performed by insert-ing a short, self-sealing vascular sheath into either femoral artery. Vascular access may also be obtained via a brachial or radial artery. Angiography is done by using hollow preshaped catheters (5 or 6 Fr), which are placed under fluoroscopic guidance ret-rograde through the aorta into the ostia of the coronary arteries and coronary bypass grafts. A solution of radiographic contrast material is injected through the catheter to opacify the lumen. Images are recorded in rapid succession onto film or in a digital format. The surgeon typically uses the coronary angiography images to determine the number and location of coronary targets where bypass anastomoses are to be constructed (Figs. 60-3, 60-4, and 60-5).
Other information obtained from cardiac catheterization includes coronary and aortic calcification, ventricular function, and, if ventriculography is performed, mitral regurgitation. Injection of contrast into the aortic root provides useful root and ascending aortic images when indicated.
Right heart catheterization is used to measure central venous, right atrial, right ventricular, pulmonary artery, and pulmonary wedge pressures, as well as cardiac output. It can also be used to identify intracardiac shunts, assess arrhythmias, and initiate temporary cardiac pacing. Preoperative right heart catheterization is used selectively and is generally not necessary unless right ventricular dysfunction or pulmonary vascular disease is suspected.
Percutaneous coronary intervention (PCI) techniques in current use include balloon dilation, stent-supported dilation, atherectomy, and plaque ablation with a variety of devices,
acquisition [MUGA] scanning, or positron emission tomogra-phy (PET) should be considered. Echocardiography may be considered as an alternative. Pharmacologic stress agents include adenosine, dobutamine, and dipyridamole.
Echocardiography
Many patients undergoing CABG also undergo transthoracic echocardiography by the evaluating cardiology team to estimate ventricular wall abnormalities and the ejection fraction. Common indications for a resting echocardiogram include heart murmurs and a suspicion of a structural problem, such as aortic stenosis or insufficiency, hypertrophic cardiomyopathy, mitral valve stenosis or regurgitation, and congestive heart failure. Ven-tricular dilation and wall thinning are other features noted on the echocardiogram in patients with chronic ischemic CAD or prior infarcts.
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insignificant problems, the greatest cause of lumen loss in stented coronary arteries is neointimal hyperplasia. This is the principal mechanism of in-stent stenosis and results from inappropriate cell proliferation—hence, the advent of cytotoxic drug-eluting stents.
INDICATIONS FOR CORONARY ARTERY REVASCULARIZATION
Box 60-4 summarizes the indications for myocardial revascular-ization. The first four indications are managed preferably by PCI, whereas indications 5 through 7 are managed preferably by surgical revascularization. The last two indications constitute surgical emergency. Although this stratification is broad and provides a bird’s eye view of the management approach, each patient should be risk-stratified before an appropriate strategy is initiated. When possible, proper risk stratification is absolutely essential to determine the balance of risks and benefits of medical management, PCI, and CABG.
Chronic Stable Angina
Cardiovascular risk reduction strategy is essential to treating patients with chronic stable angina. In the 2007 focused update of the 2002 American Heart Association (AHA)/American College of Cardiology (ACC) guidelines 7 for managing chronic stable angina, cardiovascular risk reduction strategies included
FIGURE 60-3 Left coronary angiogram demonstrating hemodynami-cally severe lesions in the left anterior descending artery (small arrow) and the circumflex artery (large arrow).
FIGURE 60-4 right coronary angiogram demonstrating hemodynam-ically significant lesions (arrow). the right coronary artery terminates
as a posterior descending artery in the right dominant system.
thrombectomy with aspiration devices, specialized imaging, and physiologic assessment with intracoronary devices.
Coronary artery stents were the first substantial break-through in the prevention of restenosis after angioplasty. Although stent recoil or compression are not completely
FIGURE 60-5 coronary angiogram demonstrating critical left main coronary artery stenosis (arrow).。