If there is no indication of a uterus by examination or lower abdominal ultra- Screen for Eating Disorders sound purchase clozapine us anxiety treatment centers, a karyotype is needed to determine the con- If you suspect anorexia nervosa or bulimia clozapine 25mg on line depression executive dysfunction, administer genital disorder purchase cheap clozapine line depression symptoms lump in throat. A referral to an endocrinologist or a screening instrument to help determine the diagnosis. About half of any abdominal male gonads, which would be a risk of the females with eating disorders will have short for cancerous degeneration. Chapter 5 • Amenorrhea 55 Calculate the Body Mass Index production, there is no ovulation; anovulatory cycles Seventeen percent body fat is needed for most females are amenorrheic. Also look for Turner syndrome to be menarchal, and about 22% body fat is necessary stigmata—webbed neck and low-set ears (other signs for ovulation. Palpate the Thyroid Gland and Lymph Nodes Obesity causes amenorrhea secondary to ovarian Palpate the thyroid gland for diffuse enlargement, dysfunction. Assess for supraclavicular cell stroma convert androstenedione to estrogen (es- and infraclavicular lymphadenopathy or carcinogenic trone) as the body fat increases. Obesity also increases masses of the sternal notch and abdomen, which could sex hormone binding globulin, thereby increasing free arise from a tumor of germ cell, adrenal, or pituitary steroid levels. Perform Clinical Breast Examination Examine the Skin and Hair Physical examination verifes sexual maturation level. Observe for signs of thyroid dysfunction or adrenal The growth spurt occurs before breast development excess. Features of hypothyroidism include dry, (thelarche), which is followed by the appearance of coarse, faky skin; coarse hair that tends to break; and axillary hair. More than by fne, warm skin that is hyperpigmented at pressure 95% of adolescents are menarchal 1 year after they points. A congenital problem Perform a Head and Neck Examination might manifest as vaginal or uterine agenesis, and is During the head and neck examination note any visual identifed by the absence of a vagina, cervix, or uterus. Take menses behind an obstructed outfow tract needs im- that number (product) and divide by the patient’s height in mediate intervention to prevent infammatory changes inches. Needle aspiration is not recom- Example: Weight 5 75 pounds; height 5 4 feet 2 inches mended because it might potentiate infection. Vaginal walls that are pale and dry, have few rugae, 56 Chapter 5 • Amenorrhea and are friable are estrogen defcient. Pelvic Ultrasound and Vaginal Ultrasound Prolactin Levels Pelvic and vaginal ultrasound studies are used to deter- About one-third of women with no obvious cause of mine the presence of a uterus, the anatomical size and amenorrhea will have an elevated prolactin level. Ultrasound is used to measure reference range, less than 50 ng/mL, a progesterone ovarian size, to identify cysts, and to evaluate follicular challenge test is indicated. In primary amenorrhea, ultrasound is is high, greater than 50 ng/mL, or if the patient has helpful in assessing müllerian agenesis and gonadal galactorrhea, a cone-down view of the sella turcica is dysgenesis, because there could be internal organs and taken to rule out a pituitary adenoma. One-third of these patients than 200 ng/mL, is highly suggestive of a prolacti- also have urinary tract abnormalities; therefore an noma. A prolactin elevation less than 100 ng/mL, but abdominal ultrasound can be obtained at the same time higher than normal, is most frequently caused by pre- to evaluate that system. The hyperprolactinemia usually subsides a few weeks after stopping the offending Progesterone Challenge Test drug. Serum Follicle-Stimulating Hormone Levels The patient should respond to the medication within Ovarian failure, which causes a low estradiol secretion, 2 to 7 days. This demonstrates that there are Chapter 5 • Amenorrhea 57 suffcient endogenous estrogens to prepare the endo- cells, 40% intermediate cells, and 60% superfcial metrium and confrms that there is a functioning cells. Low estrogen effect is forms of progesterone can be used: micronized proges- demonstrated by the predominance of intermediate cells. A no menstrual fow, administer the regimen a second value greater than 3 ng/mL is found with ovulation. A positive test denotes that there is inadequate estrogen production either Pregnancy is the most common reason for amenor- from inadequate functional ovarian follicles, or from rhea in women of childbearing age. Chromosome Analysis (Karyotyping) Constitutional Problems Karyotyping is done to delineate probable chromo- somal abnormalities. It is used in the workup for Delayed Puberty ambiguous genitalia, primary amenorrhea, oligomen- A pituitary adenoma must be ruled out for all patients orrhea, delayed puberty, or abnormal development at with delayed puberty. Endometrial Biopsy Endometrial biopsy can be used to show the hormonal Anorexia Nervosa and Bulimia response of the uterine endometrium. Affected women have such a fear Basal Body Temperature Charting of being fat that they do not eat or they purge after A woman can take her awakening body temperature eating. Often these women are overachievers and have each day and chart it to determine if ovulation is oc- low self-esteem. If this increase in temperature occurs, ovulation has occurred and a Exercise-Induced Amenorrhea positive estrogen component is inferred. This amenorrhea is common in competitive athletes, but exercise can also cause skipped menses in the ca- Maturation Index sual trainer. Gymnasts, ballerinas, and long distance The maturation index indicates the degree of maturation runners are at high risk, especially if they started their of the vaginal epithelium and provides an objective as- training at a very early age. Body fat of 17% is needed sessment of vaginal hormone response as well as overall for menarche, whereas 22% body fat is necessary for hormonal environment. The index is read Congenital or Chronic Disorders from left to right and refers to the percentage of parabasal, intermediate, and superfcial squamous cells appearing on Turner Syndrome a smear, with the total of all three values equaling 100%. The typical features are short 58 Chapter 5 • Amenorrhea stature, webbed neck, shieldlike chest, and delayed or curettage. The average age of menopause in the a moon face, acne, hirsutism, kyphosis, purplish striae United States is 51 years. Clinical symptoms are hot fashes, night Thyroid Dysfunction sweats, insomnia, mood changes, and amenorrhea Amenorrhea from thyroid dysfunction subsides as for 12 months. If this occurs before age 40 years, it is soon as serum thyroid levels return to normal. Common causes of premature thyroidism frequently causes amenorrhea and is char- ovarian failure include genetic and enzyme disorders, acterized by fatigue, constipation, cold intolerance, immune disturbances, and chemotherapy. Offending drugs are primarily dopamine antagonist agents, estrogens, and Uterine and Outfow Tract Problems marijuana. Imperforate Hymen The woman with an imperforate hymen could present Chest Wall or Nipple Stimulation with a painful, bulging perineum. The higher the prolactin level, the Cervical Os Stenosis greater the likelihood that the patient will be amen- Stenosis of the cervical os can be the cause for either orrheic. Stenosis is often caused by therapeutic procedures of the cervix such Pituitary Adenoma as cryotherapy or cone biopsies. These procedures Pituitary macroadenomas and microadenomas should cause scarring and stenosis of the os, obstructing the be suspected if the prolactin level is greater than outfow tract. Patients with Asherman Syndrome pituitary adenomas should be referred to an endocri- Asherman syndrome occurs when the uterine endome- nologist. Patients with prolactin levels exceeding trial lining is denuded or scarred, usually by infection 1000 ng/mL probably have an invasive tumor. Deligeoroglou E, Tsimaris P: Menstrual disturbances in puberty, Current evaluation of amenorrhea, Fertil Steril 90:S219–225, 2008.
Glycerophospholipids are constituents of all cellular membranes and consist of a glycerol molecule linked to two fatty acids (designated R and R ; 1 2 see Fig buy generic clozapine 25mg line postpartum depression definition dsm iv. The third carbon of the glycerol backbone carries a phosphate group linked to one of four molecules: choline (phosphatidylcholine purchase clozapine canada depression and alcohol, also called lecithin) purchase clozapine 25mg free shipping anxiety service dog, ethanolamine (phosphatidylethanolamine), serine (phosphatidylserine), or inositol (phosphatidylinositol). Another phospholipid, sphingomyelin, has special functions in the plasma membrane in the formation of membrane microdomains such as rafts and caveolae. Phospholipids are polar molecules, more water soluble than triglycerides or cholesterol or its esters. The phosphorylation of phosphatidylinositol contributes critically to membrane and cell organelle signaling and transport. Lipoproteins, Apolipoproteins, Receptors, and Processing Enzymes Lipoproteins are complex macromolecular structures coated by a water-compatible envelope of phospholipids, free cholesterol, and apolipoproteins covering a hydrophobic core of cholesteryl esters and triglycerides. Lipoproteins vary in size, density in the aqueous environment of plasma, and lipid and apolipoprotein content (Fig. The classification of lipoproteins reflects their density in plasma (the density of plasma is 1. Phospholipids are oriented with their polar group toward the aqueous environment of plasma. Apolipoproteins are involved in the secretion of lipoprotein, provide structural integrity, and act as cofactors for enzymes or as ligands for various receptors. Many proteins regulate the synthesis, secretion, and metabolic fate of lipoproteins; their characterization has provided insight into molecular cellular physiology and targets for drug development (Table 48. Macrophages express receptors that bind modified (especially oxidized) lipoproteins. Lipoprotein Metabolism and Transport The lipoprotein transport system has two major roles: (1) efficient transport of triglycerides from the intestine and liver to sites of utilization (fat tissue or muscle) and (2) transport of cholesterol to peripheral tissues for membrane synthesis and steroid hormone production or to the liver for bile acid synthesis (Fig. The human body derives from the diet essential fatty acids that it cannot make (linoleic acid, from which arachidonic acid is derived, and linolenic acid, which leads to the formation of eicosapentaenoic acid). For an individual consuming 2000 kcal/day, with 30% in the form of fat, this represents approximately 66 g of triglycerides and 250 mg (0. The intestine has very efficient fat absorption mechanisms, probably evolved to maximize provision of the organism with nutrients under circumstances of limited or irregular availability of food. The mechanism of micelle uptake by intestinal brush border cells still engenders debate. After uptake into intestinal cells, fatty acids undergo re-esterification to form triglycerides and packaging into chylomicrons inside the intestinal cell and enter the portal circulation (Fig. This mechanism involves a cytosine deaminase and leads to a termination codon at residue 2153 and a truncated form of apo B. Adipose cells can store triglycerides made from fatty acids for energy utilization, a process that requires insulin. Hepatic Pathway (Very-Low-Density Lipoprotein to Intermediate-Density Lipoprotein). This exchange constitutes a major part of the “reverse cholesterol transport pathway. This internalized particle then fuses with lysosomes whose hydrolytic enzymes (cholesteryl ester hydrolase, cathepsins) release free cholesterol and degrade apo B. In conditions of cholesterol sufficiency, the cell can decrease cholesterol synthesis. Lipoprotein Disorders Definitions Time and new knowledge have stimulated changes in the classification of lipoprotein disorders. The original classification of lipoprotein disorders by Fredrickson, Lees, and Levy (1967) depended on analysis of lipoprotein patterns by ultracentrifugation or electrophoresis and has fallen into disuse (see prior editions of this textbook for details). Most clinicians now classify lipoprotein disorders by which specific lipoprotein lipid is elevated and, when carefully characterized, by the genetic defect (e. The clinical usefulness of apolipoprotein levels has stirred debate (see Chapter 45). Taken as a single measurement, the apo B level provides information on the number of potentially atherogenic particles and can be used as a goal of lipid-lowering therapy. Genetic Lipoprotein Disorders Understanding of the genetics of lipoprotein metabolism has expanded rapidly. Classification of genetic lipoprotein disorders usually requires a biochemical phenotype in addition to a clinical phenotype. With the exception of familial hypercholesterolemia, monogenic disorders tend to be infrequent or very rare. Disorders considered heritable on careful family study may be difficult to characterize unambiguously because of age, sex, penetrance, and gene-gene and environmental interactions. Most common lipoprotein disorders encountered clinically result from the interaction of increasing age, lack of physical exercise, weight gain, and a suboptimal diet with individual genetic makeup. In adulthood, clinical manifestations include corneal arcus, tendinous xanthomas over the extensor tendons (metacarpophalangeal joints, patellar, triceps, and Achilles tendons), and xanthelasmas. Remarkably, prompt recognition in childhood or early adulthood and treatment (statins) can normalize life 24 expectancy. Apo B truncated close to its amino terminus loses the ability to bind lipids and produces a syndrome similar to abetalipoproteinemia, a rare recessive lipoprotein disorder of infancy that causes mental retardation and growth abnormalities. The resulting lack of apo B–containing lipoproteins in plasma causes a lack of fat-soluble vitamins (A, D, E, and K) that circulate in lipoproteins. In turn, this deficiency result in mental and developmental impairment in affected children. Premature atherosclerosis, often apparent clinically well before adulthood, occurs in patients with sitosterolemia. Diagnosis requires specialized analysis of plasma sterols documenting an elevation in sitosterol, campesterol, cholestanol, sitostanol, and campestanol. A defect in either of the genes inactivates this transport mechanism, and net accumulation of plant sterols (because of impaired elimination) ensues. The apo (a) moiety consists of a protein with a high degree of homology with plasminogen. Plasma Lp(a) levels depend almost entirely on genetics and correlate inversely with the number of kringle repeats and therefore with the molecular weight of apo (a). Lp(a) concentrations follow a skewed distribution in the population, and black Americans tend to have higher Lp(a) levels than do other ethnic groups in the United States. The pathogenesis 37 of Lp(a) may result from an antifibrinolytic potential and ability to bind oxidized lipoproteins. Severe elevation of plasma triglycerides can result from genetic disorders of the processing enzymes or apolipoproteins and poorly controlled diabetes. The disorder clusters in first-degree relatives but varies phenotypically depending on sex, age, hormone use (especially estrogens), and diet. Alcohol intake potently stimulates hypertriglyceridemia in these patients, as does caloric or carbohydrate intake. Depending on the criteria used, the prevalence of familial hypertriglyceridemia ranges from 1 in 100 to 1 in 50. This highly heterogeneous disorder probably results from several genes, as well as a strong environmental 40 influence. An unrelated X-linked genetic disorder, familial glycerolemia, may mimic familial hypertriglyceridemia because most measurement techniques for triglycerides use the measurement of glycerol after enzymatic hydrolysis of triglycerides.
This approach creates a proximal attachment zone that can be extended distally with an endovascular graft to complete the aneurysm repair order 25 mg clozapine fast delivery anxiety zoloft. Bypasses to all the aortic arch branches can also be performed from the proximal ascending aortic arch in select patients order 100 mg clozapine fast delivery anxiety questionnaire for adults, with a healthy portion left in the ascending aorta for attachment and seal of an endovascular graft order clozapine 50mg on-line anxiety low blood pressure. Branched devices developed to manage patients with complex thoracic and thoracoabdominal aneurysms are undergoing early evaluation. Spinal cord dysfunction with the development of paraparesis or paraplegia is a major source of morbidity. Endoleaks are the most common 17 complication of endovascular repairs and occur in 10% to 20% of patients. The rate of freedom from reintervention on the aortic segment treated was 85% at 10 years. After discovery of an aneurysm, patients should be reevaluated in 6 months to assess the aneurysm status. For relatively small 17 aneurysms that are stable from year to year, imaging may be performed every 2 to 3 years. Avoidance of strenuous physical activity, especially isometric 34,35 exercise and weightlifting, is important and may impact work-related recommendations. In the absence of an identified mutation, first-degree relatives should have evaluation and imaging. If a first-degree relative has thoracic aortic disease, 17 second-degree relatives should also be screened. In 80% to 90% of acute aortic syndromes, classic aortic dissection is present, with intimal disruption leading to a dissection plane in the media that may propagate anterograde (or less often retrograde) throughout the length of the aorta (see Video 63. Adventitial disruption may lead to rupture, or more frequently, a distal tear(s) results in blood reentering the aortic lumen. In classic aortic dissection an intimal flap exists between the two lumens (true and false lumens). There is a tear in the intima with blood entering the media and a dissecting cleavage plane propagating for variable distances anterograde (and occasionally retrograde) throughout the aortic wall. A spontaneous hemorrhage of the vasa vasorum leads to bleeding within the media in the absence of an intimal tear or intimal flap. An ulcerated aortic plaque ruptures into the media, leading to an outpouching or ulceration in the aortic wall. Ascertaining the exact incidence of aortic dissection is difficult as many patients die before the condition is recognized. In Sweden the incidence of dissection in men is reported to be 16 per 100,000 17 yearly. Patients with acute aortic dissection have very high early mortality, with up to 1% per hour reported in the first 24 hours before surgery for type A 17,36 dissection. Type A aortic dissection occurs most often in individuals age 50 to 60 years, with type B dissection more at a peak of 60 to 70 years. There are two main hypotheses for acute aortic dissection: (1) a primary tear in the aortic intima with blood from the aortic lumen penetrating into the diseased media and leading to dissection and creation of the true and false lumens and (2) primary rupture of the vasa vasorum leading to hemorrhage in the aortic wall, with subsequent intimal disruption creating the intimal tear and aortic dissection. Distention of the false lumen with blood causes the intimal flap to compress the true lumen and narrow its caliber and may lead to malperfusion syndromes. Classification The two major classification schemes for aortic dissection, DeBakey and Stanford, are based on the location of the dissection (Fig. The ascending aorta is proximal to the brachiocephalic artery, and the descending aorta begins distal to the left subclavian artery. DeBakey type I dissections originate in the ascending aorta and extend at least to the aortic arch and often to the descending aorta—frequently all the way to the iliac arteries. The Stanford classification categorizes dissections into type A and type B based on whether the ascending aorta is involved. Type A dissections involve the ascending aorta, with or without extension into the descending aorta. Thus, dissections that involve the aortic arch but not the ascending aorta are characterized as type B in the Stanford classification. DeBakey classification: Type I dissection originates in the ascending aorta and extends at least to the aortic arch and often to the descending aorta (and beyond). Stanford classification: Type A dissection involves the ascending aorta (with or without extension into the descending aorta). Stanford Classification A Dissection involves the ascending aorta (with or without extension into the descending aorta). Most type A dissections begin within a few centimeters of the aortic valve, and most type B dissections begin just distal to the left subclavian artery. Approximately 65% of intimal tears occur in the ascending aorta, 30% in the descending aorta, less than 10% in the aortic arch, and approximately 1% in the abdominal aorta. Treatment depends on the site, with emergency surgery being recommended for acute type A dissections and initial medical therapy recommended for type B dissections. Aortic dissection is also classified according to its duration, with the classic definition of “acute” when present for less than 2 weeks and “chronic” when present for longer than 2 weeks. Others classify dissections as acute (<2 weeks), subacute 17 (2 to 6 weeks), or chronic (>6 weeks) (Table 63. Kaplan-Meier survival curves for type A dissection (A) and type B dissection (B) stratified by treatment type. Guidelines for the diagnosis and management of patients with thoracic aortic disease: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of Thoracic Surgeons, and Society for Vascular Medicine. Cause and Pathogenesis Several conditions predispose the aorta to dissection (Table 63. Hypertension may affect the elastic properties of the arterial wall and increase stiffness, predisposing to aneurysm or dissection. However, hypertension alone is not usually associated with significant aortic dilation, and the vast majority of hypertensive patients never have aortic dissection. Genetically triggered aortic syndromes, congenital heart diseases, inflammatory vascular diseases, and cocaine and methamphetamine use are also risk factors for aortic dissection. Recognition of genetic mutations as a cause of aortic aneurysms and 6,12 dissections has increased. Aortic dissection is also associated with Noonan syndrome, unicuspid aortic valve, supravalvular aortic stenosis, aberrant right subclavian artery (Kommerell diverticulum), right-sided 1,17 aortic arch, polycystic kidney disease, and Alport syndrome (in males). Nonspecific aortitis, Takayasu arteritis, IgG4 disease, and Behçet syndrome all are associated with aortic dissection. Cocaine use accounts for less than 2% of cases of aortic 41 dissection, more often presenting with hypertension and small aortic diameters. Underlying elastic medial abnormalities and the biomechanical stress related to hypertension and tachycardia may play a role. Aortic dissection may also occur with intense weightlifting, but generally in the setting of an underlying aortopathy.
After a long course generic 25mg clozapine depression test for loved ones, the distal portion of these fibers buy discount clozapine 50mg on-line depression symptoms after quitting smoking, which conducts rapidly generic clozapine 50mg free shipping anxiety upset stomach, inserts into the distal right bundle branch or the apical region of the right ventricle. No preexcitation is generally apparent during sinus rhythm, but it can be exposed by premature or rapid right atrial stimulation. The delta wave represents ventricular activation from input over the accessory pathway. The extent of the contribution to ventricular depolarization by the wavefronts over each route depends on their relative activation times. Such a transformation occurred repeatedly in this patient and was associated with quickening of the ventricular rate. Pacing the atrium at rapid rates, at premature intervals, or from a site close to the atrial insertion of the accessory pathway accentuates the anomalous activation of the ventricles and shortens the H-V interval even more (His activation may become buried in the ventricular electrogram, as shown in Fig. T wave abnormalities can occur after the disappearance of preexcitation, with orientation of the T wave according to the site of preexcitation (T wave memory). D, Orthodromic tachycardia with a slowly conducting accessory pathway (arrowhead). In both tachycardias the accessory pathway is an obligatory part of the reentrant circuit. Usually, a posteroseptal accessory pathway (most often right ventricle but other locations as well) that conducts very slowly, possibly because of a long and tortuous route, appears to be responsible. Although anterograde conduction over this pathway has been demonstrated, the long anterograde conduction time over the accessory pathway usually prevents the electrocardiographic manifestations of accessory pathway conduction during sinus rhythm. Premature ventricular stimulation (arrowhead) occurs at a time when the His bundle is refractory from depolarization during the tachycardia (second labeled H). The rhythm strips below (lead I) indicate that whenever a nonconducted P wave occurs, the tachycardia always terminates, only to begin again after several sinus beats. Recognition of Accessory Pathways When retrograde atrial activation during tachycardia occurs over an accessory pathway that connects the left atrium to the left ventricle, the earliest retrograde activity is recorded from a left atrial electrode usually positioned in the coronary sinus (see Fig. When retrograde atrial activation during tachycardia occurs over an accessory pathway that connects the right ventricle to the right atrium, the earliest retrograde atrial activity is generally recorded from a lateral right atrial electrode. Participation of a septal accessory pathway creates the earliest retrograde atrial activation in the low right portion of the atrium situated near the septum, anterior or posterior, depending on the insertion site. Recording electrical activity directly from the accessory pathway obviously provides precise localization. Some accessory pathways can conduct anterogradely only; more often, pathways conduct retrogradely only. If the pathway conducts only anterogradely, it cannot participate in the usual form of reciprocating tachycardia (see Fig. Some data suggest that the accessory pathway demonstrates automatic activity, which could conceivably be responsible for some cases of tachycardia. Clinical Features The reported incidence of preexcitation syndrome depends in large measure on the population studied and varies from 0. Left free wall accessory pathways were most common, followed in frequency by posteroseptal, right free wall, and anteroseptal locations. The prevalence is higher in men and decreases with age, apparently because of loss of preexcitation. Most adults with preexcitation syndrome have normal hearts, although various acquired and congenital cardiac defects have been reported, including Ebstein anomaly, mitral valve prolapse, and cardiomyopathies. Patients with Ebstein anomaly often have multiple right- sided accessory pathways, either in the posterior septum or in the posterolateral wall, with preexcitation localized to the atrialized ventricle (see Chapter 75). For most patients with recurrent tachycardia, the prognosis is good, but sudden death does occur rarely, with an estimated frequency of 14 0. Before invasive testing, patients and parents/guardians should undergo counseling to discuss the risks and benefits of proceeding with invasive ‡ studies, the risks associated with observation only, and risks related to the medication strategy. Relatives of patients with preexcitation, particularly those with multiple pathways, have an increased prevalence of preexcitation, thus suggesting a hereditary mode of acquisition. Some children and adults can lose their tendency for the development of tachyarrhythmias as they grow older, possibly as a result of fibrotic or other changes at the site of insertion of the accessory pathway. Tachycardia still present after 5 years of age persists in 75% of patients, regardless of the location of the accessory pathway. These approaches are relatively specific but not very sensitive, with low positive predictive accuracy. Patients with asymptomatic intermittent ventricular preexcitation do not require further 14 evaluation or therapy and should simply be observed. Young patients (8 to 21 years of age) who have only persistent electrocardiographic abnormalities, without tachyarrhythmias or a history of palpitations, should undergo stress testing to determine whether abrupt loss of preexcitation occurs. For patients with frequent episodes of symptomatic tachyarrhythmia, therapy should be initiated. Verapamil and propranolol do not directly affect conduction in the accessory pathway, and digitalis has had variable effects. An external cardioverter-defibrillator should be immediately available if necessary. In many patients, particularly those with a very rapid ventricular response and any signs of hemodynamic impairment, electrical cardioversion is the initial treatment of choice. For patients with frequent symptomatic arrhythmias not fully controlled by drugs, those who are drug intolerant, or those who choose not to take drugs, ablation is advisable. This option should be considered early in the course of treatment of a symptomatic patient because of its high success rate, low frequency of complications, and potential cost-effectiveness. Even though transvenous catheter ablation is generally effective, epicardial ablation through a pericardial approach or surgical interruption of the accessory pathway may be necessary in rare cases. Drug therapy is an alternative to ablation or is used in rare cases of failed ablation attempts, but it is not always possible to predict which drugs may be most effective for an individual patient. Oral administration of two drugs, such as flecainide and propranolol, to decrease conduction capability in both limbs of the reentrant circuit can be beneficial. Depending on the clinical situation, empiric drug trials or serial electrophysiologic drug testing can be used to determine optimal drug therapy for patients with reciprocating tachycardia. Patients who have accessory pathways with very short refractory periods may be poor candidates for drug therapy because the refractory periods may be insignificantly prolonged in response to the standard agents. Very long-term outcome of catheter ablation of post-incisional atrial tachycardia: role of incisional and non-incisional scar. Recurrent spontaneous clinical perimitral atrial tachycardia in the context of atrial fibrillation ablation. Atrial flutter: clinical risk factors and adverse outcomes in the Framingham Heart Study. Contemporary utilization and safety outcomes of catheter ablation of atrial flutter in the United States: analysis of 89,638 procedures.