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Proteoglycans in health and disease: new concepts for heparanase function in tumor progression and metastasis buy generic avana 200mg line. Spontaneous tumorigenicity of primary human oral keratinocytes with human papillomavirus negativity and impaired apoptosis order avana 50 mg without prescription. Potential of Diagnostic Microbiology for Treatment and Prognosis of Dental Caries and Periodontal Disease order avana canada. Toh Y, Oki E, Ohgaki K, Sakamoto Y, Ito S, Egashira, Saeki H, Kakeji Y, Morita M, Sakaguchi Y, Okamura T, Maehara Y. Alcohol drinking, cigarette smoking, and the development of squa- mous cell carcinoma of the esophagus: molecular mechanisms of carcinogenesis. Comporti M , Signorini C , Leoncini S , Gardi C, Ciccoli L , Giardini A , Vecchio D , Arezzini B. Rate-limiting steps of glucose and sorbitol metabolism in Streptococcus mutans cells exposed to air. Carcinogenicity of acetaldehyde in alcoholic beverages: risk assessment outside ethanol metabolism. Afﬁnity of the gastric pathogen Helicobacter pylori for the N-sulphated glycosaminoglycan heparan sulphate. A population based prospective study of Chlamydia trachomatis infection and cervical carcinoma. The phosphoenolpyruvate:sugar phosphotransferase system of oral streptococci and its role in the control of sugar metabolism. Identiﬁcation and characterization of a Candida albicans binding proteoglycan secreted from rat submandibular salivary glands. Conversion of normal to malignant phenotype: telomere shortening, telome- rase activation, and genomic instability during immortalization of human oral keratinocytes. Replicative senescence of normal human oral keratinocytes is associated with the loss of telomerase activity without shortening of telomeres. Koliocytosis: A cooperative interaction between the human papillomavirus E5 and E6 oncoproteins. Passive immunization against dental caries and periodontal disease: development of recombinant and human monoclonal antibodies. Malignant transformation of hpv-immortalized human oral keratinocytes by chemical carcinogens. More clearly accepted as established are the roles of smoking and alcohol consumption in the etiology of oral and oropharyngeal cancers, even with variance in inclusion of sites of head and neck cancers. Yet there is considerable evidence that at the population level, different risk factors have stronger associations with speciﬁc anatomical sites. Assessments are also being made concerning sexual behaviors and risk of head and neck cancers (Heck et al. Speciﬁc attention has been given to the potential for both differences between males and females (Gillison et al. The 13 registries are located in the metropolitan areas of Atlanta, Detroit, Los Angeles, San Jose- Monterey, San-Francisco-Oakland, and Seattle-Puget Sound and the states of Alaska Natives, Connecticut, Hawaii, Iowa, New Mexico, Rural Georgia, and Utah. Relative survival was deﬁned as the observed probability of survival adjusted for the expected survival rate of the U. All races include White, Black, American Indian/Alaskan Native, Asian Paciﬁc Islander, other unspeciﬁed, and unknown race categories. Survival time was calculated from the date of diagnosis to the date of death or last contact. The highest incidence rate is for combined oral cavity and pharynx with Blacks at 11. The Black versus White incidence rate ratio is statistically signiﬁcantly different for all cancer sites with rates for Blacks observed to be lower than Whites for only the lip, tongue and salivary gland. Statistically signiﬁcant increases in incidence rates over the 1992–2008 time frame were found among All races and White for tongue and tonsil, esophagus for White, and anal sites for All races, White and Black groups. The incidence rates between Black and White males statistically signiﬁcantly differ for all cancer sites except for tongue with rates for Blacks lower than those observed for Whites only for lip and salivary gland. Incidence rate increases were found to be statistically signiﬁcant in tongue and tonsil for All races and Whites, esophagus for Whites, and anal sites for All races and Whites. It should be noted that the anal sites rate also approaches signiﬁcance (p value ¼ 0. The highest incidence rate observed is invasive cervix uteri cancer for Blacks at 11. Black and White females differed with observed rates statistically signiﬁcantly lower for blacks than whites for cancers of the lip, tongue, anal sites and vulva but higher for nasopharynx, 112 L. See P-Value bThe rate ratio indicates that the rate is signiﬁcantly different than the rate for White (p < 0. Black:White rate ratios did not differ for the total oral cavity and pharynx, salivary gland, ﬂoor of mouth, or gum and other mouth sites. Statistically signiﬁcant incidence rate increases were only found for tongue in All races and White categories and in the anal sites category for trends in each of the three race groups. Black and White mortality rates statistically differed for all cancer sites presented with Blacks only having lower mortality associated with lip and salivary gland cancers than Whites. Mortality rates increased with statistical signiﬁcance for esophagus for Whites, and anal sites for All races and Whites. See P-Value bThe rate ratio indicates that the rate is signiﬁcantly different than the rate for White (p < 0. In all of the cancer sites of interest, Black and White rates differed at statistically signiﬁcant levels on all mortality rates with lower rates only found for Blacks than Whites in lip and salivary gland cancers. Mortality rates were observed to statistically signiﬁcantly increase for esophageal cancer and anal cancer sites in All races and White male categories. For three sites, the rate of mortality was statistically signiﬁcantly lower in Black than in White females (lip, salivary gland, and vulva). For four cancer sites, there was no signiﬁcant difference between the female Black and White rates (tongue, ﬂoor of mouth, gum and other mouth, and the anal cancer sites). Mortality rates increased statistically signiﬁcantly for the anal sites in the All races and White categories. See P-Value bThe rate ratio indicates that the rate is signiﬁcantly different than the rate for White (p < 0. Figures 1 and 2 depict the 5-year relative survival rates for a subset of cancer sites in combined males and females and separately for males and females, respec- tively. In all of the graphs, the poorest survival is seen for esophagus followed by cancers of the oropharynx. The assess- ment indicates that the best 5-year relative survival outcome is observed for the anal sites among those cancers occurring in both genders. See P-Value bThe rate ratio indicates that the rate is signiﬁcantly different than the rate for White (p < 0. There are shared challenges by health care professionals for examining or screening tissues contained in body cavities, albeit by health care professionals trained in different disciplines. Health disparities are conﬁrmed for many cancer sites for differential incidence, mortality, and trend rate between Blacks and Whites.
It is anticipated that the major insights into causes buy discount avana 50mg on line, pathophysiology generic avana 50mg free shipping, and preventive and management strategies developed during the past few decades will continue to evolve order avana 100mg without a prescription. Definitions Sudden cardiac death is natural death from cardiac causes heralded by abrupt loss of consciousness within 1 hour of the onset of an acute change in cardiovascular status (Table 42. Preexisting heart disease may or may not have been known to be present, but the time and mode of death are unexpected. This definition incorporates the key elements of natural, rapid, and most importantly, unexpected death by a cardiac cause or mechanism. As the epidemiology, clinical expression, causes, and mechanisms began to be understood, these differences merged. To satisfy clinical, scientific, legal, and social considerations, four temporal elements must be considered: (1) prodromes, (2) onset, (3) cardiac arrest, and (4) biologic death (Fig. The 1-hour definition primarily refers to the duration of the “terminal event,” which defines the interval between the onset of symptoms signaling the pathophysiologic disturbance leading to cardiac arrest and the onset of the cardiac arrest itself. Some victims experience no prodromes, with onset leading almost instantaneously to cardiac arrest; others may have an onset that lasts up to 1 hour before clinical arrest. Other patients may live days to weeks after the cardiac arrest before biologic death, often because of irreversible brain damage and dependence on life support. The two most relevant clinical factors are onset of the terminal event and the clinical cardiac arrest itself; legal and social considerations focus on the time of biologic death. The same premonitory signs and symptoms may be more specific for imminent cardiac arrest when they begin abruptly. Sudden onset of chest pain, dyspnea, or palpitations and other symptoms of arrhythmias often precede the onset of cardiac arrest and define the 1- hour onset of the terminal event that brackets the cardiac arrest. The fourth element, biologic death, was an immediate consequence of cardiac arrest in the past and usually occurred within minutes. However, the generally accepted clinical-pathophysiologic definition of up to 1 hour between onset of the terminal event and biologic death requires qualifications for specific circumstances. For example, since the development of community-based interventions and life support systems, patients may now remain biologically alive for a long period after the onset of a pathophysiologic process that has caused irreversible damage and will ultimately lead to death. In this circumstance, the causative pathophysiologic and clinical event is the cardiac arrest itself rather than the factors responsible for the delayed biologic death. Finally, forensic pathologists studying unwitnessed deaths continue to use the definition of sudden death for a person known to be alive and functioning normally 24 hours before, and this remains appropriate within obvious limits. Among the precautions is the recognition that not all sudden deaths are 7 cardiac in origin. There are persisting inconsistencies about the definition and challenges in accessing data and adjudicating individual cases in datasets, in determining pathophysiologic mechanisms, and in making distinctions 8 between population risk and individual risk. The differences between chronic disease evolution and transient events call for different forms of epidemiologic modeling (Table 42. Furthermore, the emerging field of genetic epidemiology adds another dimension for consideration, and there is a need to focus on interventional epidemiology, a term coined to define the population dynamics of therapeutic outcomes. It should not be perceived as limited to anatomic features because risk substrates may exist at a molecular level. In contrast, expression-based risk refers to the identification of mechanisms and pathways that contribute to the clinical manifestation of the risk established by the substrate. This category includes plaque transition and acute coronary syndromes (plaque disruption and thrombogenesis) and their potential for specific expression as an arrhythmic event in susceptible individuals. The arrhythmogenic category of risk can also be viewed to include modifiers of molecular-based risk that drive individual expression. These figures suggest an overall incidence of between one and two deaths per 1000 persons in the general population. Retrospective death certificate studies have demonstrated that a temporal definition of sudden death of less than 2 hours after the onset of symptoms results in 12% to 15% of all natural deaths being defined as “sudden” and almost 90% of all natural sudden deaths having cardiac causes. In contrast, application of a 24-hour definition of sudden death increases the fraction of all natural deaths falling into the sudden category to more than 30% but reduces the proportion of all sudden natural deaths resulting from cardiac causes to 75%. Prospective studies have demonstrated that approximately 50% of all deaths caused by coronary heart disease are sudden and unexpected and occur shortly (instantaneous to 1 hour) after the onset of symptoms. Because coronary heart disease is the dominant cause of both sudden and nonsudden cardiac deaths in the United States, the fraction of total cardiac deaths that are sudden is similar to the fraction of deaths from coronary heart disease that are sudden, although there does appear to be geographic variation 14,15 in the fraction of coronary deaths that are sudden. It is also of interest that the age-adjusted decline in mortality from coronary heart disease in the United States during the past half-century has not changed the 16,17 fraction of coronary deaths that are sudden and unexpected, even though there may be a decline in out- of-hospital deaths relative to emergency department deaths. Furthermore, the decreasing age-adjusted mortality does not imply a decrease in absolute numbers of cardiac or sudden deaths, because of the 14 growth and aging of the U. A, Estimates of incidence (percent per year) and the total number of events per year for the general adult population in the United States and for increasingly high-risk subgroups. With the identification of increasingly powerful risk factors, the incidence increases progressively, but this is accompanied by a progressive decrease in the total number of events represented by each group. The inverse relationship between incidence and the total number of events results from the progressively smaller denominator pool in the highest subgroup categories. In contrast to earlier iterations of this incidence profile, the magnitude of risk in the heart failure category exceeds that in the high-risk post–myocardial infarction and post–primary cardiac arrest groups. Successful interventions in larger population subgroups require identification of specific markers to increase the ability to identify specific patients who are at particularly high risk for a future event. Approximately 50% of all cardiac arrests caused by coronary heart disease occur as the first clinically manifested event, and up to an additional 30% occur in the clinical setting of known disease in the absence of strong risk predictors. Less than 25% of victims have high-risk markers based on arrhythmic or hemodynamic parameters. Because it is impractical to plan an intervention designed for the general population that would be applied to the 999 per 1000 who do not have an event to reach and possibly influence the 1 per 1000 who will experience an event, better risk profiling is needed to identify smaller high-risk subsets in whom interventions are practical. The cost and risk-to-benefit uncertainties 20 limit the nature of such broad-based interventions and demand a higher resolution of risk identification. Two fundamental approaches to this challenge can be followed: (1) a general population strategy targeting prevention of acquired risk factors, such as obesity (primordial prevention), and primary 21 prevention by control of manifest risk factors, and (2) a more focused individual risk strategy based on identification and intervention in small subsets of the general population with a high density of risk (Fig. The mean risk in the general population is demonstrated as a continuum across four decades. Potentially identifiable subgroups with varying risk densities populate each range of risk. The ability to identify high–risk density subgroups within the general population would contribute to better individual risk prediction. The size of the denominator pool, however, remains very large, and implementation of interventions remains problematic, even at this heightened level of risk. Higher resolution is desirable and can be achieved by identification of more specific subgroups. However, the corresponding absolute number of deaths becomes progressively smaller as the subgroups become more focused (see Fig. General patterns of heightened risk during the morning 18 hours, on Mondays, and during the winter months have been described. Both excessive cold 24 and excessive heat have been linked to risk for cardiac arrest, although the studies did not determine whether temperature extremes are associated with ventricular tachyarrhythmias versus other mechanisms of cardiac arrest. Thus, there is a time dependence of risk that focuses the potential opportunity for maximum efficacy of an intervention during the early period after a cardiovascular event. For the latter, however, early nonarrhythmic deaths also contribute a large proportion of the fatal events.
It is the combination of the diverticulum and the ring that causes the airway compression order discount avana on line. Other cases without a diverticulum of Kommerell have a loose vascular ring generic avana 200 mg with amex, made up of the aberrant left subclavian artery and a left ligamentum buy 100 mg avana with amex. Anomalous origin of a right subclavian artery is one of the most common abnormalities of the aortic arch. Although the aberrant right subclavian artery runs posterior to the esophagus, it does not form a vascular ring unless there is an associated right-sided ductus or ligamentum to complete the ring. During adulthood about 5% of patients with an aberrant right subclavian artery (and a left ductus) develop symptoms (usually dysphagia rather than respiratory symptoms) owing to rigidity of the aberrant vessel. In this setting there may be either an ascending left and descending right aorta or an ascending right and descending left aorta. The retroesophageal component of the descending aorta causes esophageal, and sometimes tracheal, compression, in conjunction with the left- or right-sided ligamentum. This is usually made up of the left pulmonary artery arising from the right pulmonary artery, which runs posterior to the trachea but anterior to the esophagus. This is usually seen in isolation and can be associated with significant hypoplasia of the tracheobronchial tree, which is the predominant cause of the airway symptoms. Clinical Features The symptoms produced by vascular rings depend on the tightness of anatomic compression of the trachea and esophagus and consist principally of respiratory difficulties, including stridor and dysphagia. Although most patients with a true ring and some airway compression present early in life, others present later with dysphagia and still others escape diagnosis forever. If there is evidence of a right aortic arch in a symptomatic patient, a vascular ring should be suspected. Prominent posterior indentation of the esophagus is observed in many of the common vascular ring arrangements, although the pulmonary artery vascular sling produces an anterior indentation. This technique has the added advantage of imaging the more posterior structures that run behind the esophagus and trachea. In general, if there is normal branching of the innominate artery, to the right for a left aortic arch and to the left for a right, along with the correct “sidedness” of the descending aorta, then a vascular ring can be excluded. Most cases with a double aortic arch have a dominant right arch, with the descending aorta appearing to dip posteriorly as it runs behind the esophagus. When both arches are patent, a frontal plane sweep from inferior to superior demonstrates both patent arches, as well as their brachiocephalic vessels. A right aortic arch with an aberrant left subclavian artery is suspected when it is not possible to identify normal branching of the left-sided innominate artery. A retroesophageal descending aorta should be suspected when the ascending aorta and its brachiocephalic arteries are readily identified but there is difficulty in identifying the descending aorta as it traverses behind the esophagus. A left pulmonary artery sling is suspected when the normal branching pattern of pulmonary arteries cannot be identified. In this setting color Doppler imaging permits the identification of the left pulmonary artery as it arises from the right pulmonary artery and runs in a posterior and leftward direction. The only disadvantage for infants is that general anesthesia is often required to achieve a successful examination. This latter technique is particularly valuable for patients with a pulmonary artery sling, where the vascular ring often plays a secondary role to the airway abnormalities. The advantages of these techniques are that, unlike echocardiography, they permit a precise assessment of the more posterior vascular structures and their relationships to the esophagus and airways. These techniques are particularly valuable in the more complex forms, such as a retroesophageal descending aorta. Management Options and Outcomes The severity of symptoms and the anatomy of the malformation are the most important factors in determining treatment. Patients, particularly infants, with respiratory obstruction require prompt surgical intervention. A left thoracotomy is the surgical approach in most patients with a vascular ring. Operative repair of the double aortic arch requires division of the minor arch (usually the left) and the ligamentum. Patients with a right aortic arch and a left ductus or ligamentum arteriosum require division of the ductus or ligamentum and/or ligation and division of the left subclavian artery, which is the posterior component of the ring. In patients with a pulmonary artery vascular sling, surgery consists of detachment of the left pulmonary artery at its origin and anastomosis to the main pulmonary artery directly or by way of a conduit with its proximal end brought anterior to the trachea. The addition of tracheal narrowing that requires surgical intervention adds to the mortality rate in this group of patients, as does the association with intracardiac malformations. Pulmonary Stenosis with Intact Ventricular Septum This lesion exists as a continuum, ranging from some patients with an isolated valvular stenosis to others in whom there is complete atresia of the pulmonary outflow tract (Fig. The pulmonary valve may vary from a well-formed trileaflet valve with varying degrees of commissural fusion to an imperforate membrane. The angiogram demonstrates a case before (middle, arrow) and during (right) balloon dilation. At right, successful balloon valvuloplasty shows almost complete disappearance of the stenotic waist (arrow). The supravalvular stenosis is classically at the distal part of the pulmonary valve sinuses, and there is usually no poststenotic pulmonary artery dilation. This entity is associated with Noonan syndrome, which in turn may be associated with hypertrophic cardiomyopathy. In those with isolated pulmonary valvular stenosis who present beyond the neonatal period, the right ventricle and tricuspid valve are usually normal. However, cases with valvular stenosis presenting in the newborn period very often have abnormalities of the tricuspid valve, in particular some leaflet dysplasia and an associated shortened chordal support apparatus. The other group, those with pulmonary valve atresia, have varying degrees of right ventricular hypoplasia, varying from a tripartite right ventricle to conditions with associated infundibular atresia, with intrinsic myocardial abnormalities that persist for life. Those with the smallest right ventricle often have primitive coronary artery–to–right ventricular connections (sometimes termed sinusoids), which in some instances are responsible for myocardial perfusion via the suprasystemic right ventricle (so-called ventricular dependency). The tricuspid valve is invariably abnormal, usually with thickened dysplastic leaflets and varying degrees of leaflet tethering due to a shortened chordal apparatus. The importance of understanding the right ventricular and tricuspid valve abnormalities is that these persist throughout life and have a significant impact on right ventricular and tricuspid valve function in patients who end up with a biventricular circulation. As well, those with the smallest right ventricle may have persistent coronary artery abnormalities that eventually result in both left and right ventricular myocardial perfusion issues. The first mode is seen in patients who present in the neonatal period, usually with associated pathology of the tricuspid valve, right ventricle, and/or coronary arteries. The second mode is seen beyond the neonatal period, when the valvular stenosis is usually isolated. Clinical Features Patients who present beyond the neonatal period with isolated mild to moderate right ventricular outflow tract obstruction of any type usually have no symptoms. Patients with severe right ventricular outflow tract obstruction may present with exertional fatigue, dyspnea, lightheadedness, and chest discomfort (right ventricular angina). Physical examination may reveal a prominent jugular a wave, a right ventricular lift, and possibly a thrill in the second left intercostal space.
Advanced heart failure therapy buy avana 50mg without prescription, including primary prevention implantable cardioverter-defibrillators order avana 200mg otc, is appropriate in patients with cardiomyopathy order 50mg avana amex. Patients with Becker muscular dystrophy with advanced heart failure can undergo cardiac transplantation, with expected outcomes similar to those for non–muscular dystrophy cohorts of age-matched patients with 11 dilated cardiomyopathy. Female carriers of Duchenne and Becker muscular dystrophies do not develop a cardiomyopathy during childhood, and screening can be delayed until later in adolescence. Whether carriers benefit from heart failure pharmacotherapy is unknown, but such treatment would seem reasonable based on shared mechanisms. Myotonic Dystrophies Genetics The myotonic dystrophies are autosomal dominant disorders characterized by myotonia, which is a delayed muscle relaxation after contraction, weakness and atrophy of skeletal muscles, and systemic manifestations, including endocrine abnormalities, cataracts, cognitive impairment, and cardiac involvement (Fig. Whereas unaffected patients have 5 to 37 copies of the repeat, patients with myotonic dystrophy have 50 to several thousand repeats. Cardiac involvement including conduction disease, arrhythmias, and age at cardiovascular death also correlate with the length of repeat expansion (Fig. Typical characteristics of balding, thin face, and distal muscle atrophy are evident. Both congenital presentation and cognitive impairment are lacking in myotonic dystrophy type 2—typically the most severely involved subsets of the type 1 patients. Intergenerational contraction of the repeat expansion has been reported, and there is no apparent relationship between the degree of expansion and clinical severity. Cardiac involvement is related to the resultant dysregulation of multiple cardiac systems, including 12 sarcomeric proteins, calcium handling, and connexins (Fig. Until recently, studies have not genetically differentiated myotonic dystrophy types 1 and 2, so the clinical characteristics described probably are for a mixed group of such disorders. Type 1 is significantly more common than type 2, except possibly in certain areas of northern Europe. The global incidence of myotonic dystrophy type 1 has been estimated to be 1 in 8000, although it is higher in certain populations, such as French Canadians, and lower to nonexistent in other populations, such as African blacks. A congenital presentation is seen in severely affected patients with myotonic dystrophy type 1. Common early manifestations are related to weakness in the muscles of the face, neck, and distal extremities. On examination, myotonia can be demonstrated in the grip, thenar muscle group, and tongue (Fig. The diagnosis when the patient is asymptomatic is possible using electromyography and genetic testing. In general, cardiac symptoms appear after the onset of skeletal muscle weakness but can be the initial manifestation of the disease. Myotonic dystrophy type 2 also manifests with myotonia, muscle weakness, cataracts, and endocrine abnormalities, as in type 1. Cardiovascular Manifestations Cardiac pathology in the myotonic dystrophies involves degeneration, fibrosis, and fatty infiltration preferentially targeting the specialized conduction tissue, including the sinus node, atrioventricular node, and His-Purkinje system (Fig. Degenerative changes are observed in working atrial and ventricular tissue but only rarely progress to a symptomatic dilated cardiomyopathy. It is not clear if there are differences in the cardiac pathology observed between myotonic dystrophy type 1 and 2. Patients with type 2 typically demonstrate cardiac involvement later in life or not at all. A, Fatty infiltration in a specimen from a 57-year-old man (Masson trichrome stain, ×90). Arrows demarcate expected size and shape of the branching atrioventricular bundle (hematoxylin-eosin stain, ×90. Abnormalities included first-degree atrioventricular block in 42%, right bundle branch block in 3%, left bundle branch block in 4%, and nonspecific intraventricular conduction delay in 12%. Electrocardiographic abnormalities are less common in myotonic dystrophy type 2, occurring in approximately 20% of middle-aged patients. Imaging and Heart Failure Left ventricular systolic and diastolic dysfunction, left ventricular hypertrophy, mitral valve prolapse, regional wall motion abnormalities, and left atrial dilatation have been reported in patients with myotonic 14 dystrophy type 1 at moderate prevalence rates. Left ventricular hypertrophy and ventricular dilation have been reported in myotonic dystrophy type 2. Cardiac magnetic resonance imaging is more sensitive than echocardiography for 15 detection of early cardiac involvement. Arrhythmias Patients with myotonic dystrophy type 1 demonstrate a wide range of arrhythmias. At cardiac electrophysiologic study, the most common abnormality found is a prolonged His-ventricular (H-V) interval (see also Chapter 34). Conduction system disease can progress to symptomatic atrioventricular block and necessitate pacemaker implantation. The prevalence of permanent cardiac pacing in patients with myotonic dystrophy type 1 varies widely between studies based on referral patterns and the indications used for implant. Updated practice guidelines have recognized that asymptomatic conduction abnormalities in neuromuscular diseases such as myotonic dystrophy may warrant special consideration 16 for pacing (see also Chapter 41). Atrial arrhythmias, primarily atrial fibrillation and atrial flutter (see also Chapter 37), are the most 13 common arrhythmias observed. Patients with myotonic dystrophy type 1 are at risk for ventricular tachycardia occurring as a consequence of reentry in the diseased distal conduction system, as characterized by bundle branch reentry and interfascicular reentry tachycardia (Fig. Therapy with right bundle branch or fascicular radiofrequency ablation can be curative (see also Chapter 39). A monomorphic ventricular tachycardia is induced with atrial-ventricular (A-V) dissociation and His association, consistent with bundle branch reentry tachycardia. Sudden death is responsible for 18% to 33% of deaths in myotonic dystrophy type 1; presumably, most are due to arrhythmias. The entity of sudden death is second only to respiratory failure as a cause of death. Distal conduction disease producing atrioventricular block can result in the lack of an appropriate escape rhythm and asystole or bradycardia-mediated ventricular fibrillation. Sudden death can occur in myotonic dystrophy type 1 despite pacing, implicating ventricular arrhythmias. Nonarrhythmic causes of sudden death, probably acute respiratory issues, play some role (see also Chapter 42). Arrhythmias and sudden death have been reported in myotonic dystrophy type 2 but seem to be rarer than in type 1. Treatment and Prognosis Neurologists recognize the risk for cardiac issues in the myotonic dystrophies and will refer the patient to a cardiologist. Cardiac manifestations occur in both myotonic dystrophy types 1 and 2, and therefore diagnostic evaluation and therapy should be done in both. Cardiac disease is observed at a younger age in myotonic dystrophy type 1 compared with type 2. Echocardiography or other imaging modalities can determine if structural abnormalities are present.