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Hirudin is a direct thrombin inhibitor that has several potential advantages over heparin, including efficacy against fibrin clot-bound thrombin. This drug, derived from the saliva of the medicinal leech (Hirudo medicinalis), does not require co-factors and is not inactivated by platelet factor 4 or plasma proteins. As with heparin, these direct thrombin inhibitors have very narrow therapeutic indices. Inogatran (a selective, active-site inhibitor of thrombin), napsagatran (a synthetic direct thrombin inhibitor), argatroban (a direct thrombin inhibitor), tick anticoagulant peptide (a selective factor Xa inhibitor), and tissue factor pathway inhibitor are also under investigation. Bleeding is the major complication of heparin and warfarin therapy (see Chapter 188). The rates of major bleeding in recent trials using heparin by continuous infusion or high-dose subcutaneous injection are less than 5%. Heparin-induced thrombocytopenia (defined as a platelet count less than 150,000/mm3) typically develops 5 or more days after the initiation of heparin therapy, and occurs in 5 to 10% of patients (see Chapter 188); the syndrome is caused by heparin-dependent immunoglobulin (Ig) G antibodies that activate platelets via their Fc receptors. If heparin therapy is instituted for venous thromboembolism and the platelet count progressively decreases to 100,000/mm3 or less, heparin therapy should be discontinued. For example, danaparoid (a heparinoid) has been approved for use in the setting of heparin-induced thrombocytopenia. Bleeding related to warfarin therapy increases with intensity and duration of therapy (see Chapter 188). Warfarin-induced skin necrosis is a rare but serious complication that mandates immediate cessation of the drug; it is related, at least in some patients, to protein C or S deficiency. Warfarin crosses the placenta and may cause fetal malformations if used during pregnancy. The primary indications for filter placement include contraindications to anticoagulation, recurrent embolism while receiving adequate therapy, and significant bleeding complications during anticoagulation. Filters are sometimes placed in the setting of massive pulmonary embolism when it is believed that any further emboli might be lethal, particularly if thrombolytic therapy is contraindicated. A number of filter designs exist, but the Greenfield filter has been most widely used. Thrombolytic Therapy Thrombolytic agents activate plasminogen to form plasmin, which then results in fibrinolysis as well as fibrinogenolysis (see Chapter 188). Because anticoagulants do not actively cause lysis of emboli, thrombolytic agents are considered in certain settings to hasten the reduction in thromboembolic burden. In the 160-patient multicenter, prospective, randomized, Urokinase Pulmonary Embolism Trial, thrombolysis was accelerated in the first 24 hours in patients receiving urokinase compared with those receiving heparin, but thereafter the difference between the two groups diminished; by day 5, the improvement in each group was similar, and no difference was noted in the frequency of recurrent pulmonary embolism or mortality within 2 weeks of treatment. Although no data are available from prospective, randomized, clinical trials to indicate a reduction in mortality from thrombolytic therapy, thrombolytic therapy is often recommended in patients with hemodynamic instability (hypotension) or severely compromised oxygenation. An argument can also be made for thrombolytic therapy when the perfusion defect by lung scan or pulmonary arteriogram is extensive (defect approaching the equivalent of one-half 447 Figure 84-4 An algorithm for the approach to the patient with massive acute pulmonary embolism. Although thrombolytic therapy may result in more rapid improvement of right ventricular function in patients with acute pulmonary embolism, controversy remains as to whether or not patients with echocardiographic right ventricular dysfunction without hypotension or severe hypoxemia should receive this form of treatment. Thrombolytic therapy may also be considered when extensive deep-vein thrombosis accompanies a submassive pulmonary embolism. Coagulation assays are unnecessary during thrombolysis because the approved regimens are administered as fixed doses. Catheter-directed administration of intra-embolic thrombolytic therapy has been utilized in small clinical studies, but data are currently inadequate to recommend this approach. Both lysis of hemostatic fibrin plugs and fibrinogenolysis can lead to bleeding complications, which commonly occur at sites of invasive procedures such as pulmonary arteriography or arterial line placement. The most devastating complication associated with this form of treatment is the development of intracranial hemorrhage, which occurs in fewer than 1% of patients. Retroperitoneal hemorrhage may result from a vascular puncture above the inguinal ligament and may be life-threatening. Absolute contraindications to systemic thrombolytic therapy include intracranial surgery or other intracranial pathologic processes and active or recent internal bleeding, whereas relative contraindications include bleeding diathesis/thrombocytopenia, uncontrolled severe hypertension, recent cardiopulmonary resuscitation, surgery within the previous 10 days, and pregnancy.

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Clinical manifestations include depigmentation of skin and hair, neurologic disturbances, leukopenia, hypochromic microcytic anemia, and skeletal abnormalities. The anemia arises from impaired utilization of iron and is therefore a conditioned form of iron deficiency anemia. Toxicity Toxicity after oral ingestion is uncommon and seems confined to gastric irritation. Airborne exposure may cause contact dermatitis, eczema, skin ulcers, and bronchogenic carcinoma. Assessment of Status Plasma or serum concentrations of chromium are crude indicators of chromium status; they appear to be meaningful when their value is markedly above or below the normal range. It is carried to the liver, where it is bound to ceruloplasmin, which circulates systematically and delivers copper to target tissues in the body. Absorptive and excretory processes vary with the levels of dietary copper and thereby provide a means of copper homeostasis. Copper serves as a component of many enzymes, including amine oxidases, ferroxidases, cytochrome- c oxidase, dopamine beta-hydroxylase, superoxide dismutase, and tyrosinase. Acute copper toxicity has been described after excessive oral intake and with absorption of copper salts applied to burned skin. Milder manifestations include nausea, vomiting, epigastric pain, and diarrhea; coma and hepatic necrosis may ensue in severe cases. Wilson disease is a rare, inherited disease associated with abnormally low ceruloplasmin levels and accumulation of copper in the liver and brain, eventually leading to damage to these two organs (see Chapter 120). Large doses (>2 mg/d in adults) may induce hypothyroidism by blocking thyroid hormone synthesis. Supplementation with >100 mug/day to an individual who was formerly deficient occasionally induces hyperthyroidism. Marked deficiency is reliably detected by diminished serum copper and ceruloplasmin concentrations, as well as by low erythrocyte superoxide dismutase activity. It is incorporated into the crystalline structure of bone, thereby altering its physical characteristics. Estimates of intake or clinical assessment are used because no good laboratory test exists. Iodine Readily absorbed from the diet, concentrated in the thyroid, and integrated into the thyroid hormones thyroxine and triiodothyronine. They modulate resting energy expenditure and, in the developing human, growth and development. In the absence of supplementation, populations relying primarily on food from soil with a low iodine content have endemic iodine deficiency. Maternal iodine deficiency leads to fetal deficiency, which produces spontaneous abortions, still-births, hypothyroidism, cretinism, and dwarfism. Permanent cognitive deficits may also be induced by iodine deficiency during infancy and childhood. In the adult, compensatory hypertrophy of the thyroid (goiter) occurs along with varying degrees of hypothyroidism. Women of childbearing age constitute the highest-risk group because of menstrual blood loss, pregnancy, and lactation. In children, mild deficiency insufficient to cause anemia is associated with behavioral disturbances and poor school performance. The thyroid-stimulating hormone level in the blood is an indirect and therefore not entirely specific means of assessment. Iron Participates in redox reactions in a number of metalloproteins such as hemoglobin, myoglobin, and the cytochrome enzymes. Intestinal absorption is 15-20% for "heme" iron and 1-8% for the iron contained in vegetables. Absorption of the latter form is enhanced by the ascorbic acid in foodstuffs; by poultry, fish, or beef; and by an iron-deficient state; it is decreased by phytate and tannins.

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Familial adenomatous polyposis and Gardner syndrome are inherited as autosomal dominant disorders with incomplete penetrance. Different mutations at that locus may account for the phenotypic differences between the syndromes. Gene abnormalities can be detected by a blood test in 87% of affected individuals, thereby enabling screening within affected families to be much more accurate. Flexible proctosigmoidoscopy should be performed annually in all first-degree relatives, from age 12 years until age 40 years, and every 3 years thereafter. Because gene markers are not yet 100% specific and sensitive, screening is also indicated for those without the mutant gene, although considerably less often. Surveillance with a side-viewing endoscope for gastric and duodenal polyps should begin when the diagnosis of colonic polyposis is made and should continue every 2 to 3 years thereafter, and possibly yearly if prominent lesions are apparent in the duodenum. Total proctocolectomy with conventional ileostomy or ileal pouch-anal anastomosis is more often used as opposed to the older procedure of subtotal colectomy with ileo-rectal anastomosis. Pharmacologic interventions such as the use of cyclooxygenase-2 inhibitors are under study. This definition may be too restrictive, and other variants of this classic pedigree exist. Several adenomas may be present despite the name of the syndrome, but diffuse adenomatosis is not found. The average age at diagnosis of cancer is the mid-40s, and it is characteristic to find multiple synchronous cancers with a majority of lesions proximal to the splenic flexure. Mucocutaneous pigmentation and benign gastrointestinal polyposis are the primary features of the syndrome. The Peutz-Jeghers syndrome is characterized by melanotic spots on the lips, buccal mucosa, and skin, and by multiple hamartomatous polyps throughout the gastrointestinal tract from the stomach to the rectum. It is inherited in an autosomal dominant fashion but it has a variable expressivity. Microscopically, these polyps consist of elongated branching glands lined by benign epithelium native to the location of the polyps. The most distinctive feature is the presence of an arborizing proliferation of smooth muscle in the lamina propria. Rarely, intestinal malignancies have been described, with a preponderance in the small intestine. Other manifestations include ovarian sex cord stromal tumors and polyps of the gallbladder, ureter, and nose. Intestinal symptoms of recurrent, colicky abdominal pain may appear in adolescence, and intussusception may require surgical removal of a polyp. Juvenile polyposis is inherited as an autosomal dominant trait, with an occasional case occurring spontaneously. The number of polyps is less than in familial adenomatous polyposis, averaging 25 to 40. Polyps may be found throughout the gastrointestinal tract or may be restricted to the colon. Symptoms may begin in childhood or adolescence with rectal bleeding, anemia, abdominal pain, or intussusception. A variety of extraintestinal symptoms including congenital abnormalities, and pulmonary arteriovenous malformations have been described in association with juvenile polyposis. The hamartomas of juvenile polyposis are morphologically distinct from those found in Peutz-Jeghers syndrome. Foci of adenomatous epithelium may be present in these polyps, or adenomas may coexist. The true risk of malignancy in these patients is unknown, but carcinoma of the gastrointestinal tract has developed in 10% of reported patients with juvenile polyposis. Subtotal colectomy may occasionally be warranted in those with severely dysplastic adenomas. Cronkhite-Canada syndrome is a nonfamilial disorder of adults characterized by diffuse gastrointestinal polyposis, alopecia, dystrophy of the fingernails, and cutaneous hyperpigmentation. The polyps resemble juvenile polyps and are in greatest density in the stomach and colon. Watery diarrhea, anorexia, abdominal pain, cachexia, protein-losing enteropathy, and carcinoma of the gastrointestinal tract (in up to 14% of cases) have been reported.

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The discovery that spectrin deficiency is the sine qua non of hereditary spherocytic red cells led some to hypothesize that primary defects in spectrin would be found in most cases of hereditary spherocytosis. Surprisingly, mutations in alpha-spectrin (autosomal recessive hereditary spherocytosis) and beta-spectrin (autosomal dominant hereditary spherocytosis) are each present in only about 10% of patients with hereditary spherocytosis. Instead, mutations in ankyrin (autosomal dominant and recessive hereditary spherocytosis; about 40 to 50% of cases) and band 3 (autosomal dominant hereditary spherocytosis; about 20% of cases) are much more common. The severity of hemolysis correlates with the cellular spectrin content in spherocytic red cells, providing strong evidence in support of the pathogenetic mechanisms described above. The clinical manifestations of hereditary spherocytosis can vary from a clinically insignificant hemolytic state that is fully compensated by increased marrow erythropoiesis to a life-threatening hemolytic state that is dependent on red cell transfusion. This variation in clinical phenotype is a reflection of the variation in the molecular consequences of the mutations in spectrin, ankyrin, band 3, or protein 4. In general, an autosomal recessive inheritance pattern is associated with clinically more severe disease whereas an autosomal dominant pattern is associated with a milder phenotype. Although all cases of hereditary spherocytosis are present from birth, the diagnosis can be made at any age. Clinical manifestations common in hereditary spherocytosis include jaundice and splenomegaly (Table 164-1). Decrease in red cell membrane protein(s): Spectrin and/or Ankyrin and/or Band 3 and/or Protein 4. By several months of age, most patients with hereditary spherocytosis achieve a partially compensated hemolytic state characterized by mild to moderate anemia (hemoglobin, 9 to 11. Even in patients with fully compensated hemolysis, states associated with splenic enlargement and/or increased splenic blood flow (such as infectious mononucleosis and, occasionally, intense physical activity) may provoke severe hemolysis and anemia. Previously compensated elderly patients with hereditary spherocytosis may experience more severe anemia with aging because of a decline in compensatory bone marrow activity. Common clinical complications of hereditary spherocytosis include occasional crises and the formation of bilirubinate gallstones. Hemolytic crisis appears to be caused by the increased activity of the mononuclear phagocyte (reticuloendothelial) system associated with many infections; such crises are typified by a small decrease in the hematocrit that is not clinically significant. Aplastic crisis is most often associated with parvovirus B19 infection (see Chapter 160); such crises may be clinically severe and require prompt red cell transfusion. Fortunately, infection with parvovirus B19 generally produces lifelong immunity, so most patients are subjected to no more than one such crisis in a lifetime. Megaloblastic crisis is caused by a relative lack of folic Figure 164-2 Model of the pathophysiology of spherocytosis and hemolysis in hereditary spherocytosis. The increased generation of bilirubin associated with ongoing hemolysis leads to the formation of bilirubinate gallstones in most untreated teenagers and adults with hereditary spherocytosis. The incidence of this complication increases from about 5% in children 0 to 10 years old, to about 45% in patients aged 11 to 50 years, and to about 65% in older patients. Because a large fraction of bilirubinate gallstones are not radiopaque, abdominal ultrasonography is the most reliable imaging method to detect these stones. Relatively rare clinical complications of hereditary spherocytosis in adults include gout, rashes, and ulcers of the lower extremities and extramedullary hematopoietic tumors of the thorax. The gout and lower extremity complications usually disappear after splenectomy (see below), but the tumors commonly undergo fatty change after splenectomy and therefore persist on routine chest film. Several families with hereditary spherocytosis and either spinocerebellar degeneration or cardiomyopathy have been described, perhaps suggesting a common genetic basis for these disorders. Laboratory features common to all cases of hereditary spherocytosis include an elevated reticulocyte count and the presence of spherocytes on the blood smear (Color Plate 5 G). Patients with very mild disease may not be anemic or manifest hyperbilirubinemia, although many patients with hereditary spherocytosis do exhibit mild to moderate anemia and an elevated indirect bilirubin level. The laboratory test most commonly used to confirm the presence of spherocytosis is the osmotic fragility test, which measures the ability of red cells to withstand swelling in solutions of decreasing osmotic strength. Because spherocytes have a decreased ratio of surface area to volume, these cells are less able to swell in a hypotonic environment than normal discocytes are. Thus populations of red cells containing a significant proportion of spherocytes exhibit increased osmotic fragility when compared with normal red cell populations. In some cases of mild hereditary spherocytosis, however, neither striking spherocytosis on the blood smear nor an abnormal osmotic fragility test is apparent.

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These data are not consistent with these reports, which have shown either no change in breast cancer mortality with estrogen use or actually a decrease in mortality. Mortality from stroke has also been shown to decrease by approximately 40% with estrogen use. However, the literature is less consistent about stroke than the effect on ischemic heart disease. In general, the data are consistent in showing decreased mortality and an increased longevity (1 to 2. The benefit is greatest for those with cardiovascular risk factors and is least for those with significant risk factors for breast cancer. Endometrial disease occurs with unopposed estrogen therapy in women who have a uterus. Thus, the risk is far less for endometrial cancer than it is for varying degrees of hyperplasia. One recently conducted study showed that the risk of endometrial hyperplasia was 20% after 1 year of use of 0. In another study, the 3-year postmenopausal Estrogen/Progestin Interventions Trial, this risk was approximately 40% at the end of 3 years. No cancers were reported in either of these two studies, and the addition of a progestin essentially eliminated the hyperplasia. The risk of developing endometrial cancer is the same for a woman taking estrogen and progestin (hormone replacement therapy) as for the general population. The addition of a progestin merely eliminates the excess risk induced by estrogen. Other endometrial cancers occurring in postmenopausal women are not thought to be hormonally related. Although the risk of developing endometrial cancer is increased significantly in estrogen users, the risk of death from this type of endometrial cancer does not increase proportionately. Endometrial cancers associated with estrogen use are thought not to be as aggressive as spontaneously occurring cancers or that tumors in women taking estrogen are likely to be discovered and treated at an earlier stage, thus improving survival rates. Several meta-analyses have suggested either no significantly increased risk, a relative risk hovering around 1. It has also been suggested that there is no additional risk for women with a family history of breast cancer. Admittedly, a slightly increased surveillance bias exists for women who see their doctors regularly. It is also possible that estrogen use causes breast cancer to occur earlier in some women, but it is not clear which women are at greatest risk. However, breast cancer-related mortality has not been shown consistently to be increased, and indeed there are data to suggest that it may be lower among estrogen users. Thus, we are left with the question of whether estrogen use carries any increased relative risk for breast cancer or a real risk that may be relatively small. For moderate doses of estrogen, the risk of breast cancer is probably in the range of 20 to 30% in those women who are susceptible. Recent trends in prescribing have suggested lowering the dose of estrogen for long-term use, as both dose and duration are associated with risk. One of the greatest concerns of women receiving estrogen is the return of menstrual bleeding. Such concerns should be discussed with the patient, and the choice of regimen should remain flexible. Idiosyncratic reactions including hypertension, thrombosis, and allergic manifestations have also been observed in users of estrogen, particularly oral estrogen. Hypertension with estrogen use, the cause of which is not entirely clear, occurs in about 5% of oral contraceptive users. Estrogen usually causes no change in blood pressure; it may actually reduce blood pressure, a finding that has relevance for normotensive as well as hypertensive individuals. Alterations in the route of estrogen administration and dose have resulted in improved blood pressure in such individuals.

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Because most patients with the acquired immunodeficiency syndrome and esophagitis will have candidiasis, an empirical 1- to 2-week course of antifungal therapy may be justified. Those who fail this approach, however, should almost always have an endoscopy and biopsy because each of the common causes requires specific therapy. Dysphagia can often be categorized as oropharyngeal based on the clinical features of nasal regurgitation, laryngeal aspiration, or difficulty in moving the bolus out of the mouth. Although endoscopic examination is considered mandatory in all patients with dysphagia, barium radiography can guide an endoscopy that is anticipated to be difficult. Endoscopic treatment options are available for many causes of esophageal dysphagia. Tumors may be dilated mechanically, ablated by thermal means (cautery or laser), or stented with prosthetic devices; metallic expandable stents have become the palliative procedure of choice for most patients with symptomatic esophageal cancer. Benign lesions of the esophagus, such a strictures or rings, can also be dilated endoscopically, usually with excellent results (Color Plate 1 D). Finally, some motility disturbances such as achalasia are best approached endoscopically with the use of large balloon dilators for the lower esophageal sphincter or sometimes with the local injection of botulinum toxin. Dyspepsia, which is chronic or recurring pain or discomfort centered in the upper abdomen, is seen in approximately 25% of the population and accounts for 2 to 5% of all family practice consultations. Up to 40% of patients with dyspepsia will have a structural lesion such as peptic ulcer (15-25%), reflux esophagitis (5-15%), and, rarely, gastric or esophageal cancer (<2%). Other structural lesions such as gallstones, pancreatic diseases, infiltrative diseases of the stomach or intestines. The optimal diagnostic approach to dyspepsia is somewhat controversial and is still evolving (see. In recent years there has been a move toward empirical approaches to dyspepsia because only a minority of patients with dyspepsia have peptic ulcers and gastric cancer is extremely rare in Western countries. However, dyspepsia is a recurrent condition, and patients who fail to respond to empirical therapy will commonly undergo endoscopy. If a diagnostic test is to be performed, endoscopy, sometimes with biopsies to detect H. Finally, upper gastrointestinal cancers are occasionally associated with significant bleeding. Endoscopy is able to detect and localize the site of the bleeding in 95% of cases and is clearly superior to contrast radiography (with an accuracy of only 75 to 80%). The endoscopic appearance of bleeding lesions can also help predict the risk of rebleeding, thus facilitating the triage and treatment process. Finally, and perhaps most importantly, bleeding can be effectively controlled during the initial endoscopy itself in the majority of cases. In general, endoscopy should be performed only after adequate stabilization of hemodynamic and respiratory parameters. The role of gastric lavage before endoscopy is controversial; some endoscopists prefer that it be done, occasionally even using a large-bore tube, whereas others avoid such preparation because of the fear of producing artifact. The timing of subsequent endoscopy is dependent on two factors: the severity of the hemorrhage and the risk status of the patient (see. Patients with active, persistent, or severe bleeding (>3 units of blood) will require urgent endoscopy. Endoscopy in these patients is best performed in the intensive-care unit because they are at particular risk for aspiration and may require emergent intubation for respiratory protection and ventilation. Patients with slower or inactive bleeding may be evaluated by endoscopy in a "semi-elective" manner (usually within 12-20 hours), but a case can be made to perform endoscopy very early even in these stable patients (perhaps in the emergency department itself) to allow triage decisions to be made more confidently. Most bleeding from upper gastrointestinal lesions can be effectively controlled endoscopically. The endoscopist considers factors such as age (older patients have a higher risk of rebleeding) and the severity of the initial hemorrhage (which has a direct correlation with the risk of rebleeding) in addition to the appearance of the lesion when determining the need for endoscopic therapy. Non-variceal bleeding vessels can be treated with a variety of means including injections of various substances (epinephrine, saline, sclerosants) or thermal coagulation (laser or electrocautery). In the United States, the most popular approach to a bleeding peptic ulcer lesion is a combination of injection with dilute epinephrine and electrocoagulation.

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Thoracic aortic aneurysms are frequently recognized on chest radiographs, often producing widening of the mediastinal silhouette, enlargement of the aortic knob, or displacement of the trachea from midline. Transthoracic echocardiography, which generally visualizes the aortic root and ascending aorta well, is useful for screening patients with Marfan syndrome because this group is at particular risk for aneurysms involving this portion of the aorta. The majority of aneurysms expand over time, and the risk of rupture increases with aneurysm size. The overall mortality in those who rupture an abdominal aortic aneurysm is 80%, including a mortality of 50% even for those who reach the hospital. Similar to what is seen with abdominal aneurysms, the rupture of thoracic aneurysms has a high early mortality of 76% at 24 hours. The goal of medical therapy for patients with aortic aneurysms is to attempt to reduce the risk of aneurysm expansion and rupture. Aortic aneurysms that produce symptoms due to aneurysm expansion, vascular complications, or compression of adjacent structures should be repaired. When aneurysms involve branch vessels, such as renal or mesenteric arteries, these must be reimplanted into the graft. Similarly, when a dilated aortic root must be replaced in the repair of an ascending thoracic aortic aneurysm, the coronary arteries must be reimplanted. In some centers an alternative approach for repair of abdominal aortic aneurysms (and some descending thoracic aneurysms) is the percutaneous placement of an expandable endovascular stent graft inside the aneurysm; however, this technique is usually reserved for high-risk patients. Aortic dissection is a rare but life-threatening condition with an early mortality as high as 1% per hour. However, survival is significantly improved if the diagnosis is made promptly and appropriate medical and/or surgical therapy instituted. Aortic dissection classically begins with a tear in the aortic intima that exposes a diseased medial layer to the systemic pressure of intraluminal blood. The blood then penetrates into the media, cleaving it into two layers longitudinally and producing a blood-filled false lumen within the aortic wall. This false lumen then propagates distally (or sometimes retrograde) a variable distance along the aorta from the site of intimal tear. In Braunwald E [ed]: Heart Disease: A Textbook of Cardiovascular Medicine, 5th ed, p 1555. Two thirds of aortic dissections are type A (proximal) and the other one third is type B (distal). The classification schemes all serve the same purpose, which is to distinguish those dissections that involve the ascending aorta from those that do not. Involvement of the ascending aorta carries a high risk of early rupture and death from cardiac tamponade, so prognosis and management differ according to the extent of aortic involvement. Dissections are also classified according to their duration, with those present for less than 2 weeks considered acute and those present for 2 weeks or more considered chronic. Disease of the aortic media, with degeneration of the medial collagen and elastin, is the most common predisposing factor for aortic dissection. Patients with Marfan syndrome have classic cystic medial degeneration and are at particularly high risk of aortic dissection at a relatively young age. The peak incidence of aortic dissection in patients without Marfan syndrome is in the sixth and seventh decades of life, and men are affected twice as often as women. A history of hypertension is present in the large majority of cases, whereas a bicuspid aortic valve or coarctation of the aorta are less common. Rarely, aortic dissection may occur in a young woman during the peripartum period. Iatrogenic trauma from intra-aortic catheterization procedures or cardiac surgery may also cause aortic dissection. Severe pain, occurring in 74 to 90% of cases, is the most common presenting symptom of aortic dissection. The pain may be retrosternal, in the neck or throat, interscapular, in the lower back, abdominal, or in the lower extremities depending on the location of the aortic dissection.

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The pain usually builds up rapidly within 30 seconds and disappears in decrescendo within 5 to 15 minutes, and more promptly when nitroglycerin is used. Chest pain is variably described but is typically a tightness, squeezing, or constriction; however, some patients describe an ache, a feeling of dull discomfort, indigestion, or burning pain. The discomfort is most commonly midsternal and radiates to the neck, left shoulder, and left arm. It can also be precordial or radiate to the jaw, teeth, right arm, back, and, more rarely, to the epigastrium. Episodes of discomfort that are less than 1 minute or more than 30 minutes in duration are unlikely to be stable angina, but prolonged episodes can be consistent with unstable angina, especially if associated with ischemic electrocardiographic changes. When discomfort is considered clinically typical for angina, about 80% of individuals will have demonstrable coronary artery disease and evidence of myocardial ischemia; however, 20% of patients, including a higher percentage of younger patients without risk factors, will have no evidence of myocardial ischemia despite the typical complaints. The probability of coronary artery disease varies by age range, gender, and characteristics of symptoms (Table 59-1) (Table Not Available). Some patients do not note any pain or discomfort but rather an "anginal equivalent" of shortness of breath, dizziness, or fatigue. The characteristics as well as triggers are variable among patients but usually reproducible in a given patient. Atypical angina describes symptoms that are suggestive of angina but unusual with regard to location, characteristics, triggers, or duration. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Exercise Testing). In women and the elderly, the clinical features of angina may be more atypical, the initial manifestations more subtle, and the various non-invasive tests less reliable indicators of the absence or presence of coronary artery disease. Although coronary disease occurs on average 10 years later in women than in men, the prognosis may be worse. Effort or stress angina is typically associated with a greater than or equal to 75% reduction in the cross-sectional diameter of one or more of the large epicardial coronary arteries, resulting in inadequate myocardial oxygen supply when demands are increased. The severity of angina should be graded by a careful history using a standardized classification system (see Table 38-4). The key clinical feature of unstable angina is rapid aggravation of symptoms, as manifested by more severe, more frequent, or more prolonged pain; pain less promptly relieved with nitroglycerin; or pain occurring at rest or at a decreasing threshold of exercise. It implies a pathophysiologic process related to an abrupt decrease in myocardial oxygen delivery. Unstable angina occurring within 6 months after a percutaneous intervention procedure (see Chapter 61) is considered a different entity because it is most often related to a restenosis at the site of the previous dilatation. One way to categorize unstable angina is to use the Braunwald classification system, which is based on severity, clinical circumstances, associated electrocardiographic changes, and intensity of treatment (Table 59-2) (Table Not Available). These syndromes mark rapid progression in the severity of coronary artery obstruction generally caused by an obstructing intravascular thrombus. It may be a marker of distal embolization with shedding of thrombogenic material from a complex plaque. The episodes of chest pain may be repetitive or intermittent with periods of exacerbation; episodes are promptly relieved by nitroglycerin. Syncope during an episode of chest pain is infrequent but strongly suggestive of the syndrome. Angina may be caused by microvascular dysfunction without detectable lesions or spasm in the large coronary vessels. The chest pain episodes are often triggered by emotional stress and commonly occur in clusters. Myocardial ischemia of a cardiac cause other than atherosclerosis develops in aortic valve stenosis, hypertension with left ventricular hypertrophy, hypertrophic cardiomyopathy, paroxysmal tachycardia, cocaine-induced chest pain, and congenital abnormalities of the coronary circulation. Non-ischemic cardiac causes of chest pain include pericarditis and aortic dissection. Non-cardiac, non-ischemic chest pain includes esophageal reflux and spasm, neuromuscular disorders, bronchopulmonary disease, and psychogenic factors. No historical points, physical examination findings, or tests are faultless in the diagnosis of angina. The likelihood of coronary artery disease is influenced by age, gender, and other coronary risk factors (hyperlipidemia, smoking, hypertension), as well as by the clinical history of chest pain (see Table 59-1) (Table Not Available). The cardiopulmonary physical examination may be totally normal in patients with stable angina, even during an anginal attack.


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