L. David Hillis

ACC/AHA 2004 guideline update for coronary artery bypass graft surgery: summary article. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1999 Guidelines for Coronary Artery Bypass Graft Surgery).

The American College of Cardiology (ACC)/American Heart Association (AHA) Task Force on Practice Guidelines regularly reviews existing guidelines to determine when an update or full revision is needed. This process gives priority to areas where major changes in text, particularly recommendations, are mentioned on the basis of new understanding of evidence. Minor changes in verbiage and references are discouraged. The ACC/AHA Guidelines for Coronary Artery Bypass Graft Surgery published in 1999 have now been updated. The full-text guidelines incorporating the updated material are available on the Internet (www.acc.org or www.americanheart.org) in both a version that shows the changes from the 1999 guidelines in track changes mode, with strike-through indicating deleted text and underlining indicating new text, and a “clean” version that fully incorporates the changes. This article describes the major areas of change reflected in the update in a format that we hope can be read and understood as a stand-alone document. Please note we have changed the table of contents headings in the 1999 guidelines from roman numerals to unique identifying numbers. Interested readers are referred to the full-length Internet version to completely understand the context of these changes. Classification of Recommendations and Level of Evidence are expressed in the ACC/AHA format as follows: ### Classification of Recommendations ### Level of Evidence

1999 Update: ACC/AHA guidelines for the management of patients with acute myocardial infarction: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Acute Myocardial Infarction)

Executive Summary andListing of Recommendations These guidelines are intended for physicians, nurses, and allied healthcare personnel who care for patients with suspected or established acute myocardial infarction (MI). These guidelines have been officially endorsed by the American Society of Echocardiography, the American College of Emergency Physicians, and the American Association of Critical-Care Nurses. This executive summary and listing of recommendations appears in the November 1, 1996, issue of Circulation. The guidelines in their entirety, including the ACC/AHA Class I, II, and III recommendations, are published in the November 1996 issue of the Journal of the American College of Cardiology. Beginning with these guidelines, the full text of ACC/AHA guidelines will be published in one journal and the executive summary and listing of recommendations in the other . Reprints of both the full text and the executive summary with its listing of recommendations are available from both organizations. Each year 900 000 people in the United States experience acute MI. Of these, roughly 225 000 die, including 125 000 who die “in the field” before obtaining medical care. Most of these deaths are arrhythmic in etiology. Because early reperfusion treatment of patients with acute MI improves left ventricular (LV) systolic function and survival, every effort must be made to minimize prehospital delay. Indeed, efforts are ongoing to promote rapid identification and treatment of patients with acute MI, including (1) patient education about the symptoms of acute MI and appropriate actions to take and (2) prompt initial care of the patient by the community emergency medical system. In treating the patient with chest pain, emergency medical system personnel must act with a sense of urgency. When the patient with suspected acute MI reaches the emergency department (ED), evaluation and initial management should take place promptly, because the benefit of reperfusion therapy is greatest if therapy …

ACC/AHA Guidelines for the Management of Patients With Acute Myocardial Infarction

The American College of Cardiology and the American Heart Association request that the following format be used when citing this document: Ryan TJ, Antman EM, Brooks NH, Califf RM, Hillis LD, Hiratzka LF, Rapaport E, Riegel B, Russell RO, Smith EE III, Weaver WD. ACC/AHA guidelines for the management of patients with acute myocardial infarction: 1999 update: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Acute Myocardial Infarction). Available at http://www.acc.org/clinical/guidelines and http://www.americanheart.org. Accessed on [insert date].

2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines

L. David Hillis, MD, FACC, Chair†; Peter K. Smith, MD, FACC, Vice Chair*†; Jeffrey L. Anderson, MD, FACC, FAHA*‡; John A. Bittl, MD, FACC§; Charles R. Bridges, MD, SCD, FACC, FAHA*†; John G. Byrne, MD, FACC†; Joaquin E. Cigarroa, MD, FACC†; Verdi J. DiSesa, MD, FACC†; Loren F. Hiratzka, MD, FACC, FAHA†; Adolph M. Hutter, Jr, MD, MACC, FAHA†; Michael E. Jessen, MD, FACC*†; Ellen C. Keeley, MD, MS†; Stephen J. Lahey, MD†; Richard A. Lange, MD, FACC, FAHA†§; Martin J. London, MD ; Michael J. Mack, MD, FACC*¶; Manesh R. Patel, MD, FACC†; John D. Puskas, MD, FACC*†; Joseph F. Sabik, MD, FACC*#; Ola Selnes, PhD†; David M. Shahian, MD, FACC, FAHA**; Jeffrey C. Trost, MD, FACC*†; Michael D. Winniford, MD, FACC†

2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery

Alice K. Jacobs, MD, FACC, FAHA, Chair Jeffrey L. Anderson, MD, FACC, FAHA, Chair-Elect Nancy Albert, PhD, CCNS, CCRN, FAHA Mark A. Creager, MD, FACC, FAHA Steven M. Ettinger, MD, FACC Robert A. Guyton, MD, FACC Jonathan L. Halperin, MD, FACC, FAHA Judith S. Hochman, MD, FACC, FAHA

Hemorrhagic events during therapy with recombinant tissue-type plasminogen activator, heparin, and aspirin for acute myocardial infarction : results of the thrombolysis in myocardial infarction -TIMI), phase II trial

OBJECTIVES To assess the effects of invasive procedures, hemostatic and clinical variables, the timing of beta-blocker therapy, and the doses of recombinant plasminogen activator (rt-PA) on hemorrhagic events. DESIGN A multicenter, randomized, controlled trial. SETTING Hospitals participating in the Thrombolysis in Myocardial Infarction, Phase II trial (TIMI II). INTERVENTIONS Patients received rt-PA, heparin, and aspirin. The total dose of rt-PA was 150 mg for the first 520 patients and 100 mg for the remaining 2819 patients. Patients were randomly assigned to an invasive strategy (coronary arteriography with percutaneous angioplasty [if feasible] done routinely 18 to 48 hours after the start of thrombolytic therapy) or to a conservative strategy (coronary arteriography done for recurrent spontaneous or exercise-induced ischemia). Eligible patients were also randomly assigned to either immediate intravenous or deferred beta-blocker therapy. MEASUREMENTS Patients were monitored for hemorrhagic events during hospitalization. MAIN RESULTS In patients on the 100-mg rt-PA regimen, major and minor hemorrhagic events were more common among those assigned to the invasive than among those assigned to the conservative strategy (18.5% versus 12.8%, P less than 0.001). Major or minor hemorrhagic events were associated with the extent of fibrinogen breakdown, peak rt-PA levels, thrombocytopenia, prolongation of the activated partial thromboplastin time (APTT) to more than 90 seconds, weight of 70 kg or less, female gender, and physical signs of cardiac decompensation. Immediate intravenous beta-blocker therapy had no important effect on hemorrhagic events when compared with delayed beta-blocker therapy. Intracranial hemorrhages were more frequent among patients treated with the 150-mg rt-PA dose than with the 100-mg rt-PA dose (2.1% versus 0.5%, P less than 0.001). The extent of the plasmin-mediated hemostatic defect was also greater in patients receiving the 150-mg dose. CONCLUSIONS Increased morbidity due to hemorrhagic complications is associated with an invasive management strategy in patients with acute myocardial infarction. Our findings show the complex interaction of several factors in the occurrence of hemorrhagic events during thrombolytic therapy.

Potentiation of Cocaine-Induced Coronary Vasoconstriction by Beta-Adrenergic Blockade

STUDY OBJECTIVE To determine whether beta-adrenergic blockade augments cocaine-induced coronary artery vasoconstriction. DESIGN Randomized, double-blind, placebo-controlled trial. SETTING A cardiac catheterization laboratory in an urban teaching hospital. PATIENTS Thirty clinically stable patient volunteers referred for catheterization for evaluation of chest pain. INTERVENTIONS Heart rate, arterial pressure, coronary sinus blood flow (by thermodilution), and epicardial left coronary arterial dimensions were measured before and 15 minutes after intranasal saline or cocaine administration (2 mg/kg body weight) and again after intracoronary propranolol administration (2 mg in 5 minutes). MEASUREMENTS AND MAIN RESULTS No variables changed after saline administration. After cocaine administration, arterial pressure and rate-pressure product increased; coronary sinus blood flow fell (139 +/- 28 [mean +/- SE] to 120 +/- 20 mL/min); coronary vascular resistance (mean arterial pressure divided by coronary sinus blood flow) rose (0.87 +/- 0.10 to 1.05 +/- 0.10 mm Hg/mL.min); and coronary arterial diameters decreased by between 6% and 9% (P less than 0.05 for all variables). Subsequently, intracoronary propranolol administration caused no change in arterial pressure or rate-pressure product but further decreased coronary sinus blood flow (to 100 +/- 14 mL/min) and increased coronary vascular resistance (to 1.20 +/- 0.12 mm Hg/mL.min) (P less than 0.05 for both). CONCLUSIONS Cocaine-induced coronary vasoconstriction is potentiated by beta-adrenergic blockade. Beta-adrenergic blocking agents probably should be avoided in patients with cocaine-associated myocardial ischemia or infarction.

Limitations of qualitative angiographic grading in aortic or mitral regurgitation

This study was performed to assess the accuracy of qualitative angiographic grading in persons with aortic regurgitation (AR) or mitral regurgitation (MR) and to determine the factors that may influence the reliability of such grading. In 230 patients (152 men, 78 women, aged 52 +/- 14 years) with AR or MR, forward cardiac index was measured by the Fick and indicator dilution techniques and left ventricular (LV) angiographic index by the area-length method, from which the regurgitant volume index was calculated. In 124 other patients (89 men, 35 women, aged 52 +/- 11 years) without regurgitation, there was good agreement between forward and angiographic cardiac indexes (r = 0.87, p less than 0.001). In the 83 patients with AR, the regurgitant volume indexes in those with 1+ (0.87 +/- 0.57 liters/min/m2) and 2+ (1.72 +/- 1.19 liters/min/m2) angiographic regurgitation were not significantly different from one another, but were significantly different from those with 3+ (3.0 +/- 1.42 liters/min/m2) and 4+ (4.80 +/- 2.25 liters/min/m2) regurgitation; at the same time, the regurgitant volume indexes of patients with 3+ and 4+ AR were not significantly different from one another. In the 147 patients with MR, the regurgitant volume indexes in patients with 1+ regurgitation (0.61 +/- 0.64 liters/min/m2) were significantly lower than other grades, but the regurgitant volume indexes of 2+ (1.14 +/- 0.85 liters/min/m2) vs 3+ (2.14 +/- 1.37 liters/min/m2) and of 3+ vs 4+ (4.60 +/- 2.31 liters/min/m2) were not significantly different. With AR and MR, regurgitant flow within each angiographic grade varied widely, especially in grades 3+ and 4+, and there was considerable overlap of regurgitant volume indexes between grades.(ABSTRACT TRUNCATED AT 250 WORDS)

The Eisenmenger Syndrome in Adults

In 1897, Vicktor Eisenmenger described a patient with cyanosis and dyspnea since infancy who died of massive hemoptysis at 32 years of age. Postmortem examination showed a ventricular septal defect and severe pulmonary vascular disease [1]. In 1958, Paul Wood coined the term Eisenmenger complex to describe pulmonary hypertension at the systemic level due to a high pulmonary vascular resistance, with reversed or bidirectional shunting through a large ventricular septal defect [2]. Subsequently, the term Eisenmenger syndrome has been used to describe pulmonary vascular disease and cyanosis resulting from any systemic-to-pulmonary circulation connection (such as an atrial septal defect, ventricular septal defect, patent ductus arteriosus, or aortopulmonary window). Pathophysiology We reviewed the literature on the pathophysiology, clinical features, natural history, prognosis, and management of the Eisenmenger syndrome in adults. English-language articles from 1966 to the present were identified through a search of the MEDLINE database by using the terms Eisenmenger, congenital heart disease, and pulmonary hypertension. We also included selected cross-referenced articles. Articles on the pathophysiology, clinical presentation, evaluation, natural history, complications, and treatment of the Eisenmenger syndrome in adults were selected, and descriptive and analytical data relevant to the practicing physician were manually extracted. In patients with intracardiac shunting, blood initially shunts from the systemic to the pulmonary circulation (so-called left-to-right shunting) because the resistance in the former is higher. If the defect is large and the left-to-right shunting is sustained (for example, over months to years), exposure of the pulmonary vasculature to systemic arterial pressure or increased blood flow leads to progressive morphologic changes in the microvasculature (Figure 1), including arteriolar medial hypertrophy, intimal proliferation and fibrosis, and capillary and arteriolar occlusion. Eventually, plexiform lesions and necrotizing arteritis occur [3], with resultant obliteration of pulmonary arterioles and capillaries and increased pulmonary vascular resistance. Finally, pulmonary vascular resistance and pulmonary arterial pressure approach systemic vascular resistance and systemic arterial pressure, and the shunt reverses. Figure 1. Pathophysiology of the Eisenmenger syndrome. The pathophysiologic mechanisms responsible for the development of pulmonary microvascular changes in patients with the Eisenmenger syndrome are not completely known. In experimental animals, pulmonary microvascular injury stimulates the production of elastase enzymes and growth factors (that is, insulin-like growth factor I and transforming growth factor), which may cause medial hypertrophy, cellular intimal proliferation, progressive occlusion, and eventual destruction of small arterioles [4-6]. Endothelium-dependent pulmonary arteriolar relaxation is impaired, pulmonary endothelin production is increased, and plasma thromboxane B2 concentrations are elevated in patients with the Eisenmenger syndrome, suggesting that endothelial dysfunction or platelet activation may play a causative role in this condition [7-11]. Clinical Presentation Patients with the Eisenmenger syndrome often have a history of transient pulmonary congestion in infancy as a result of a substantial pulmonary blood flow caused by a large left-to-right intracardiac shunt. Later in infancy or in early childhood, as pulmonary vascular resistance increases, pulmonary blood flow declines, and symptoms of pulmonary congestion abate. When the shunt reverses (that is, when right-to-left shunting occurs), cyanosis and erythrocytosis develop. Less commonly, patients develop the Eisenmenger syndrome in adulthood without obvious symptoms during childhood and seek medical attention because of progressive fatigue, dyspnea, or cyanosis. Eventually, most patients with the Eisenmenger syndrome have one or more of the following conditions: 1) symptoms of a low systemic output [such as dyspnea on exertion, fatigue, or syncope], 2) subtle neurologic abnormalities [such as headache, dizziness, or visual disturbances] due to erythrocytosis and hyperviscosity, or 3) symptoms of congestive heart failure. In addition, arrhythmias and hemoptysis are common, and the former may lead to sudden death. Hemoptysis is caused by pulmonary infarction; rupture of a pulmonary artery dilated by aneurysm or a thin-walled pulmonary arteriole; or bleeding diathesis, which often manifests initially as mucosal (that is, epistaxis or gingival) bleeding. Cerebrovascular accidents frequently occur as a result of hyperviscosity, paradoxical embolism, or a cerebral abscess. Physical Examination Physical examination of the patient with the Eisenmenger syndrome reveals central cyanosis and clubbing of the nail bed. If systemic vascular resistance falls, as may occur with hot weather, exercise, fever, or systemic infection, the magnitude of right-to-left shunting and cyanosis increases. Patients with a patent ductus arteriosus may have normal, pink nail beds on the right hand and cyanosis and clubbing of the nail beds on the left hand and both feet (so-called differential cyanosis). This occurs because venous blood shunts through the ductus and enters the aorta distal to the right subclavian artery. The jugular venous pressure may be normal or elevated, with a prominent V wave if tricuspid regurgitation is present. The arterial pulse is usually diminished or normal [2]. Signs of pulmonary hypertension, including a right parasternal heave, a palpable pulmonary valve closure, a right-sided fourth heart sound, and a loud pulmonic component of the second heart sound, are uniformly present. The second heart sound may be single (such as with ventricular septal defect) or widely split (such as with atrial septal defect). A high-pitched, diastolic, decrescendo murmur of pulmonic regurgitation (Graham Steell murmur) is often audible, and a holosystolic murmur of tricuspid regurgitation may occur when right heart failure intervenes. In many patients, a pulmonary ejection click and soft systolic ejection murmur are audible and are attributable to dilation of the main pulmonary artery. Murmurs usually associated with ventricular septal defect or patent ductus arteriosus are absent. The lung fields are clear, and peripheral edema is absent unless right ventricular systolic dysfunction ensues. Noninvasive and Invasive Evaluation In patients with the Eisenmenger syndrome, 12-lead electrocardiography shows right atrial enlargement and right ventricular or biventricular hypertrophy. Atrial arrhythmias are often present, especially in patients with atrial septal defects. Chest radiography usually reveals prominent, dilated central pulmonary arteries with a reduction in the size and number of peripheral vessels. Calcification of the pulmonary arteries or ductus arteriosus, signifying atherosclerosis, may be visualized. Patients with the Eisenmenger syndrome who have ventricular septal defect or patent ductus arteriosus usually have a normal or minimally increased cardiothoracic ratio, whereas most patients with the syndrome who have atrial septal defect have cardiomegaly [12] with dilation attributed to right ventricular enlargement caused by previously increased flow [2]. Two-dimensional echocardiography is helpful in visualizing intracardiac defects and identifying associated cardiac or valvular abnormalities. Color flow Doppler imaging usually can detect intracardiac shunting. However, because the pulmonary and systemic arterial pressures are similar in patients with the Eisenmenger syndrome, the pressure gradient and flow across the intracardiac defect may be small and therefore difficult to visualize by color flow Doppler imaging [13]. In such patients, contrast echocardiography should be performed. An intravenously injected contrast agent (such as agitated normal saline, indocyanine green, or hydrogen peroxide) quickly appears in the left heart chambers when a right-to-left intracardiac shunt is present; the magnitude of intracardiac right-to-left shunting can be assessed qualitatively as small, moderate, or large but cannot be quantitated precisely [14, 15]. Transesophageal echocardiography can be performed safely in patients with the Eisenmenger syndrome and is superior to the transthoracic approach for detecting atrial septal abnormalities or patent ductus arteriosus [13, 16]. It is valuable for evaluating patients with unexplained pulmonary hypertension. Transesophageal echocardiography should be performed in patients with the Eisenmenger syndrome who are being considered for lung transplantation because it provides additional diagnostic information (such as the presence of additional unsuspected intracardiac defects, unrecognized intracardiac shunts, or proximal pulmonary artery thrombus) that may alter surgical intervention in approximately 25% of patients [16, 17]. Magnetic resonance imaging can identify intracardiac defects and patent ductus arteriosus and is particularly useful in patients with previous cardiac surgery in whom echocardiographic evaluation is technically difficult [18-21]. Although this test provides excellent visualization of the pulmonary and systemic arterial systems and cardiac chambers, it is limited in its ability to identify structural valvular abnormalities. Cine magnetic resonance imaging can detect right-to-left or bidirectional intracardiac shunting but has not yet proven useful in assessing the magnitude of shunting. In patients suspected of having the Eisenmenger syndrome, cardiac catheterization should be performed to detect, localize, and quantitate intracardiac shunting and to determine the severity of pulmonary vascular disease [15]. The assessment of pulmonary vascular resistance before and after administration of a pulmonary arteriolar vasodilator (that is, 100% oxygen o

Coronary-artery vasoconstriction induced by cocaine, cigarette smoking, or both

BACKGROUND In humans, the use of cocaine and cigarette smoking each increase the hearts metabolic need for oxygen but may also decrease the supply of oxygen. As cocaine abuse has proliferated, cocaine-associated chest pain, myocardial infarction, and sudden death have occurred, especially among smokers. We assessed the influence of intranasal cocaine and cigarette smoking, alone and together, on myocardial oxygen demand and coronary arterial dimensions in subjects with and subjects without coronary atherosclerosis. METHODS In 42 smokers (28 men and 14 women; age, 34 to 79 years; 36 with angiographically demonstrable coronary artery disease), we measured the product of the heart rate and systolic arterial pressure (rate-pressure product) and coronary arterial diameters before and after intranasal cocaine at a dose of 2 mg per kilogram of body weight (n = 6), one cigarette (n = 12), or intranasal cocaine at a dose of 2 mg per kilogram followed by one cigarette (n = 24). RESULTS No patient had chest pain or ischemic electrocardiographic changes after cocaine use or smoking. The mean (+/- SE) rate-pressure product increased by 11 +/- 2 percent after cocaine use (n = 30, P < 0.001), by 12 +/- 4 percent after one cigarette (n = 12, P = 0.021), and by 45 +/- 5 percent after both cocaine use and smoking (n = 24, P < 0.001). As compared with base-line measurements, the diameters of nondiseased coronary arterial segments decreased on average by 7 +/- 1 percent after cocaine use (P < 0.001), by 7 +/- 1 percent after smoking (P < 0.001), and by 6 +/- 2 percent after cocaine use and smoking (P < 0.001). The diameters of diseased segments decreased by 9 +/- 2 percent after cocaine use (n = 18, P < 0.001), by 5 +/- 5 percent after smoking (n = 12, P = 0.322), and by 19 +/- 4 percent after cocaine use and smoking (n = 12, P < 0.001). The increase in the rate-pressure product and the decrease in the diameters of diseased segments caused by cocaine use and smoking together were greater (P < 0.001 and P = 0.037, respectively) than the changes caused by either alone. CONCLUSIONS The deleterious effects of cocaine on myocardial oxygen supply and demand are exacerbated by concomitant cigarette smoking. This combination substantially increases the metabolic requirement of the heart for oxygen but simultaneously decreases the diameter of diseased coronary arterial segments.