N. Rasarus. Heritage University.
The deliberate killing of a child in the ﬁrst year of life by either act or omission is infanticide buy lamotrigine treatment trichomoniasis. In 1999 order cheap lamotrigine on line shakira medicine, in the United States cheap lamotrigine 25mg free shipping treatment trends, approximately 205 children less than 1 year of age were reported murdered. The most commonly cited weapons used were “personal weapons” — hands, feet ﬁsts etc, — 105 cases. Other weapons or manners were strangulation and asphyxia, 29 cases; blunt objects, ten; ﬁrearms, four cases: and knives and cutting instruments, six cases; other or not stated, 51. Occasionally, she is assisted by a relative or a friend, but usually neonaticide is an act committed by a single individual with no witnesses. Their goal is either to conceal the fact that they gave birth to a child or to dispose of an unwanted child. Finding dead infants in sewers, trash dumps, and public bathrooms is fairly common in large metropolitan areas. If apprehended, her defense is usually that the child was stillborn; she panicked and disposed of the body. Thus, in cases of suspected neonaticide, the ﬁrst fact to establish is whether the child was alive at the time of birth. The presence of milk or any food material in the stomach would indicate that the child was alive. Unfortunately, in cases of neonaticide, the killing usually occurs immediately after birth and one does not ﬁnd milk or food material in the stomach. The standard test to determine if a child has breathed has traditionally been the hydrostatic test. If they sink, the child is presumed to have been stillborn, and if they ﬂoat, the child is presumed to have been born alive. If putrefaction has taken place, then, even in the stillborn, the lungs might ﬂoat. Second, some children who are delivered alive take only a few breaths and do not aerate their lungs enough to ﬂoat. Because of this, physicians have resorted to microscopic examination of the lungs. If the alveoli were collapsed, then it was presumed that the children had not breathed. If they were completely and uniformly distended (presumably by air), then the child obviously had breathed. Unfortunately, microscopic examination is even more inaccurate than the hydrostatic test. If there has been attempted resuscitation, there may be distention of the air passages and alveoli by air and it will not be possible to determine whether the child was alive or stillborn. One of the authors had a case of a child dead 10 h intrau- terine who, on microscopic examination of the lungs, showed uniform dis- tention of all alveoli, which is consistent with a child who has breathed for several hours. We determine if both lungs ﬂoat in toto and then we attempt to ﬂoat sections of the lungs. This, of course, assumes that there has been no attempt at resuscitation and that there is no decomposition. Other ﬁndings used to Neonaticide, Infanticide, and Child Homicide 337 determine whether a child was alive include petechiae of the lungs or heart and air in the stomach on radiological examination. Petechiae are nonspeciﬁc and can occur from intrauterine stress, and gas in the stomach can be due to labored respiratory efforts as the infant is in transit through the birth canal. Once it has been established that a child was born alive, then one has to determine how it was killed. The simplest, most convenient, and probably the most common method of killing infants of this age is by suffocation. This can be accomplished by the direct application of a hand over the face, by obstructing the nose and mouth with an object such as a pillow, or by placing the child in a plastic bag. Less common methods are strangulation, stufﬁng the mouth with rags or toilet paper, drowning the child in a toilet, throwing the child off a building, and abandonment, with death caused by exposure or lack of care. Deaths following abandonment may be unintentional in that the mother places the child in an area where she expects it to be found, but for some reason it is not, or environmental conditions (such as temperature) change radically. Given moderate temperatures, newborns can survive 7–10 days without food or water. This was illustrated in the Mexico City earthquake of September 1985 where 44 newborns were buried beneath tons of debris when a hospital collapsed. Thus, the pathologist can make this diagnosis only if the mother leaves the baby in a plastic bag, leaves toilet tissue in the mouth, or confesses. If the body of a newborn is placed in a warm dry atmosphere, it will frequently undergo mummiﬁcation. Mummiﬁed infants are occasionally found in trunks in attics and beneath ﬂoorboards of old houses. Infanticide and Child Murder Once past the ﬁrst few days of life, the methods used to commit homicide change radically. In addition, the mother is joined by the husband, boyfriend, or babysitter as possible perpetrators. Most child homicides occur in the ﬁrst two years of life, the majority in the ﬁrst year, with a steep decline after the second year. The most commonly used weapons were hands, feet, and ﬁsts, 123 cases; ﬁrearms, 39 cases; blunt objects, 33; asphyxia and stran- gulation, 16 and knives, 10 cases; other or not stated, 59. There is the classical battered child, with its variant the neglected or starved child; the “impulse” or “angry” homicide, with its variant the “punished” child (often a scalded child); and the “gentle” homicide, smothering, with its variant the lethal form of Munchausen’s Syndrome by Proxy. There is also a miscellaneous category for deaths that do not ﬁt into any of these categories. Contrary to what one would conclude from reading the clinical medical literature and the popular press, deaths of children do not usually involve the classical battered baby syndrome, but rather are more likely “impulse” or “angry” homicides. In a series of 184 homicides of children ages 5 years or younger who died of blunt force injuries, in 10% of the cases, the children showed absolutely no external evidence of injury. In others, external injuries were relatively mild and tended to be about the head and neck. If one correlates age with the cause of death: • In children 12 months of age or less, isolated head injuries accounted for 85. Thus, as the age of the child increases, abdominal injuries become more common as a cause of death. In children dying of head injuries, the most common ﬁndings are sub- arachnoid or subdural hematoma with or without a skull fracture. The authors reviewed a series of deaths of young children in which there was epidural, subdural, or subarachnoid hemorrhage or a combination of these. Fractures of the skull seem to be more commonly associated with bilateral subdural hematoma and subarachnoid hemorrhage than sin- gle-sided subdural hematomas. In the children dying of abdominal injuries, 43% showed no external evidence of injury to the abdominal wall, though virtually all showed external evidence of trauma.
Persistent regional downregulation in mitochondrial enzymes and upregulation of stress proteins in swine with chronic hibernating myocardium buy generic lamotrigine 50mg on-line treatment zinc toxicity. The physiological significance of a coronary stenosis differentially affects contractility and mitochondrial function in viable chronically dysfunctional myocardium order lamotrigine 50 mg otc symptoms zollinger ellison syndrome. Reductions in mitochondrial O consumption and preservation2 of high-energy phosphate levels after simulated ischemia in chronic hibernating myocardium buy cheap lamotrigine 50mg line medicine used during the civil war. Revascularization of chronic hibernating myocardium stimulates myocyte proliferation and partially reverses chronic adaptations to ischemia. Hibernating myocardium results in partial sympathetic denervation and nerve sprouting. Dissociation of hemodynamic and electrocardiographic indices of myocardial ischemia in pigs with hibernating myocardium and sudden cardiac death. Regional myocardial sympathetic denervation predicts the risk of sudden cardiac arrest in ischemic cardiomyopathy. Characteristic findings include coagulation necrosis and contraction band necrosis, often with patchy areas of myocytolysis at the periphery of the infarct. All result in myocardial oxygen supply-demand mismatch and can precipitate ischemic symptoms, and all processes, when severe or prolonged, will lead to myocardial necrosis or infarction. The reduction in flow may be caused by a completely occlusive thrombus (bottom half, right side) or by a subtotally occlusive thrombus (bottom half, middle). Of particular concern from a global perspective, the burden of coronary disease 5 in low- and middle-income countries has reached the rate affecting more affluent countries. Models were adjusted for patient demographic characteristics, previous cardiovascular disease, cardiovascular risk factors, chronic lung disease, and systemic cancer. Mortality rates in clinical trial populations tend to be approximately half of those observed in registries of consecutive patients, most likely because of the exclusion of patients with more extensive comorbidities. Cardiovascular risk in post-myocardial infarction patients: nationwide real world data demonstrate the importance of a long-term perspective. The “clinical observation phase” of coronary care consumed the first half of the 20th century and focused on detailed recording of physical and laboratory findings, with little active treatment of the infarction. The “coronary care unit phase” began in the mid-1960s and emphasized early detection and management of cardiac arrhythmias based on the development of monitoring and cardioversion/defibrillation capabilities. The “high-technology phase,” heralded by the introduction of the pulmonary artery balloon flotation catheter, set the stage for bedside hemodynamic monitoring and directed hemodynamic management. Care of another substantial proportion of patients does not meet the recommended door-to- 17 reperfusion time. This gap mandates initiatives to increase timely administration of guideline-directed 18 reperfusion therapy (see Chapter 59). Pathologic Findings Almost all acute coronary syndromes result from coronary atherosclerosis, generally with superimposed 22 coronary thrombosis caused by rupture or erosion of an atherosclerotic lesion (see Chapters 44 and 60). The term Q wave infarction was frequently considered to be virtually synonymous with “transmural infarction,” whereas non–Q wave infarctions were often referred to as “subendocardial infarctions. Current clinical data have challenged the simplistic concept of the ”vulnerable plaque. Thus, equating the lipid-rich, thin- capped plaque with “vulnerability” is a misnomer. Other morphologic characteristics associated with rupture-prone plaque include expansive remodeling that minimizes luminal obstruction (mild stenosis by angiography), neovascularization (angiogenesis), plaque hemorrhage, adventitial inflammation, and a 24 “spotty” pattern of calcification. Lesions that had a larger plaque burden, signifying greater atherosclerotic content, and smaller lumen were at greatest risk for subsequently triggering an acute coronary event. Red indicates necrotic core, dark green indicates fibrous tissue, white indicates confluent dense calcium, and light green indicates fibrofatty tissue. An adequate collateral network that prevents necrosis from occurring can result in clinically silent episodes of coronary occlusion; in addition, many plaque ruptures are asymptomatic if the thrombosis is not occlusive. Characteristically, completely occlusive thrombi lead to extensive injury to the ventricular wall in the myocardial bed subtended by the affected coronary artery (Fig. A new terminology for the left ventricular walls and location of myocardial infarcts that present Q wave based on the standard of cardiac magnetic resonance imaging. Myocardial relaxation-contraction is compromised, and irreversible cell injury begins within as early as 20 minutes. Necrosis is usually complete in 6 hours unless reperfusion occurs or an extensive collateral circulation is present (Fig. The myocardial hemorrhage at one edge of the infarct was associated with cardiac rupture, and the anterior scar (lower left) was indicative of an old infarct. Bottom, The early tissue response to the infarction process involves a mixture of bland necrosis, inflammation, and hemorrhage. Nontransmural infarctions, however, frequently occur in the presence of severely narrowed but still patent coronary arteries, or when the infarcted region has sufficient collateral circulation. Necrosis begins in a small zone of the myocardium beneath the endocardial surface in the center of the ischemic zone. This entire region of myocardium (dashed outline) depends on the occluded vessel for perfusion and is the area at risk. A narrow zone of myocardium immediately beneath the endocardium is spared from necrosis because it can be oxygenated by diffusion from the ventricle. Subsequently, the infarcted myocardium undergoes a sequence of gross pathologic changes (Fig. Top, Schematics of the time frames for early and late reperfusion of the myocardium supplied by an occluded coronary artery. For approximately 30 minutes after the onset of even the most severe ischemia, myocardial injury is potentially reversible; after this point, progressive loss of viability occurs and is complete by 6 to 12 hours. The benefits of reperfusion are greatest when it is achieved early, with progressively smaller benefits occurring as reperfusion is delayed. The pattern of pathologic findings following reperfusion varies depending on the timing of reperfusion, previous infarction, and collateral flow. These histologic sections derived from the heart of a woman who suffered a stuttering reinfarction illustrate the histologic appearance of the injured myocardium and various phases of its healing. Times are estimated based on the clinical history and the typical pathologic findings of myocardial ischemic injury. There is myocardial interstitial edema, and leukocytes have begun to appear in the ischemically injured zone. In the center of this micrograph, a predominantly monocytic leukocyte infiltrate surrounds the debris of dead myocytes. D, At 14 days following an acute ischemic insult, an island of granulation tissue has begun to form. E, At 3 months following the acute ischemic event, an organized scar has formed in the matrix-rich and relatively hypocellular area on the bottom of this micrograph. In experimental infarction, the earliest ultrastructural changes in cardiac muscle after ligation of a coronary artery, noted within 20 minutes, consist of a reduction in the size and number of glycogen granules; intracellular edema; and swelling and distortion of the transverse tubular system, sarcoplasmic reticulum, and mitochondria. Changes after 60 minutes of occlusion include myocyte swelling, swelling and internal disruption of mitochondria, development of amorphous (flocculent) aggregation and margination of nuclear chromatin, and relaxation of myofibrils. After 20 minutes to 2 hours of ischemia, the changes in some cells become irreversible, and progression of these alterations occurs. Patterns of Myocardial Necrosis Coagulation Necrosis Coagulation necrosis results from severe, persistent ischemia and is usually present in the central region of infarcts; it causes arrest of muscle cells in the relaxed state and passive stretching of ischemic muscle cells.
Several important imaging features can predict periprocedural complications generic lamotrigine 200 mg without prescription medications 4 less, including minimum aortoiliac artery diameter less than diameter of external sheath purchase generic lamotrigine canada symptoms during pregnancy, severe calcifications in femoral and superficial femoral arteries buy lamotrigine 25mg overnight delivery treatment anal fissure, “horseshoe” calcifications, and severe aortic atheromatous plaque. Appropriate Use Criteria Multimodality Imaging in Stable Ischemic Heart Disease and Heart Failure James E. The documents encompass patients with stable ischemic heart disease, that is, those with suspected or known coronary 1 2 artery disease (Table 18G. Testing is rated based on the published literature as well as expert opinion, in a well-defined process. Tests are rated using the current nomenclature as 3 “appropriate,” “may be appropriate,” or “rarely appropriate. Newly diagnosed diastolic heart failure M A A A R M M Evaluation of Arrhythmias Without Ischemic Equivalent (No Prior Cardiac Evaluation) 14. Prior Testing Without Intervening Revascularization (If Intervening Revascularization Since Most Recent Test, Refer to Section 2. Abnormal prior stress imaging study (assumes not repeat of same R M M M R A A type of stress imaging) 27. Prior stress imaging study (assumes not repeat of same type of R M M M R A A stress imaging) 32. Coronary stenosis or anatomic abnormality of unclear M A A A R R — significance on previous coronary angiography 2. Last test ≥2 years ago M M M R R R R Abnormal Prior Stress Imaging Study, Asymptomatic or Stable Symptoms 37. Last study ≥2 years ago M M M M R R R Prior Coronary Calcium Agatston Score, Asymptomatic (Without Ischemic Equivalent) or Stable Symptoms 41. Incomplete revascularization M A A M R R R Additional revascularization feasible 66. Determine Exercise Level Prior to Initiation of Exercise Prescription or Cardiac Rehabilitation 4. No prior revascularization A R R R R R R Appropriate Use Key: A = Appropriate; M = May Be Appropriate; R = Rarely Appropriate. Initial Evaluation of Cardiac Structure and Function for Newly Suspected or Potential Heart Failure Newly Suspected or Potential Heart Failure 1. Familial or genetic dilated A M R R A R R R R R R cardiomyopathy in first-degree relative 4. Viability Evaluation (After Ischemic Etiology Determined) Known to Be Amenable to Revascularization With or Without Angina 8. Procedure planning: considerations A R R R A R R R R A R Patient meets all published clinical standards for device Evaluation of myocardial fibrosis/scarring, coronary vein variations, and intracavitary thrombus (for dyssynchrony evaluation) 17. Follow-up late (>6 months) after implantation M R R R R R R R R R R Improved symptoms (i. Appropriate Use Key: A = Appropriate; M = May Be Appropriate; R = Rarely Appropriate. Moreover, a strength of these multimodality documents is that the writing panels had as one of its goals to “identify any and all tests that are considered reasonable for a given clinical 1 indication. Importantly, it is acknowledged that local expertise and quality of testing are additional critical factors in determining test selection. Computed Tomography: Fundamentals, System Technology, Image Quality, Applications. Coronary artery calcium area by electron-beam computed tomography and coronary atherosclerotic plaque area: a histopathologic correlative study. Comparison of different strategies of ivabradine premedication for heart rate reduction before coronary computed tomography angiography. Incidence of contrast-induced nephropathy in patients with chronic renal insufficiency undergoing multidetector computed tomographic angiography treated with preventive measures. Guideline for minimizing radiation exposure during acquisition of coronary artery calcium scans with the use of multidetector computed tomography: a report by the Society for Atherosclerosis Imaging and Prevention Tomographic Imaging and Prevention Councils in collaboration with the Society of Cardiovascular Computed Tomography. Scoring of coronary artery calcium scans: history, assumptions, current limitations, and future directions. Coronary calcium as a predictor of coronary events in four racial or ethnic groups. Coronary artery calcium score and risk classification for coronary heart disease prediction. Coronary risk stratification, discrimination, and reclassification improvement based on quantification of subclinical coronary atherosclerosis: the Heinz Nixdorf Recall Study. Determinants of coronary calcium conversion among patients with a normal coronary calcium scan: what is the “warranty period” for remaining normal? A 15-year warranty period for asymptomatic individuals without coronary artery calcium: a prospective follow-up of 9,715 individuals. Comparison of novel risk markers for improvement in cardiovascular risk assessment in intermediate-risk individuals. Comparison of coronary artery calcium presence, carotid plaque presence, and carotid intima-media thickness for cardiovascular disease prediction in the Multi-Ethnic Study of Atherosclerosis. Coronary artery calcium progression and atrial fibrillation: the Multi-Ethnic Study of Atherosclerosis. Cancer and its association with the development of coronary artery calcification: An assessment from theMulti-Ethnic Study of Atherosclerosis. Coronary calcification and the risk of heart failure in the elderly: the Rotterdam Study. Calcium density of coronary artery plaque and risk of incident cardiovascular events. Role of nonenhanced multidetector ct coronary artery calcium testing in asymptomatic and symptomatic individuals. Relationship between stress-induced myocardial ischemia and atherosclerosis measured by coronary calcium tomography. The incremental value of coronary artery calcium scores to myocardial single photon emission computer tomography in risk assessment. Treatment of asymptomatic adults with elevated coronary calcium scores with atorvastatin, vitamin C, and vitamin E: the St. Utility of nontraditional risk markers in individuals ineligible for statin therapy according to the 2013 American College of Cardiology/American Heart Association cholesterol guidelines. Guideline-based statin eligibility, coronary artery calcification, and cardiovascular events. Diagnostic performance of 64-multidetector row coronary computed tomographic angiography for evaluation of coronary artery stenosis in individuals without known coronary artery disease: results from the prospective multicenter accuracy (Assessment by Coronary Computed Tomographic Angiography of Individuals Undergoing Invasive Coronary Angiography) trial. Diagnostic accuracy of 64-slice computed tomography coronary angiography: a prospective, multicenter, multivendor study. Detection of significant coronary artery disease by noninvasive anatomical and functional imaging. Multidetector computed tomography angiography for assessment of in-stent restenosis: meta-analysis of diagnostic performance.
There are emerging implications that left ventricular volume and other structural evaluations of the left ventricle 55 order genuine lamotrigine on line treatment zinc toxicity,56 (e discount lamotrigine 25 mg without prescription medications reactions. Arrhythmias in the recovery phase purchase discount lamotrigine on-line medicine 4h2 pill, previously thought to be benign, appear to predict higher risk than do arrhythmias in the exercise phase, and there is a gradient of risk with increasing severity of arrhythmias. Other studies have suggested that ambulatory ventricular arrhythmias in patients with heart failure do not specifically predict an increased risk for death. The excess mortality rates may be accounted for by the occurrence of ischemic events in the presence of drug. No adverse effect (other than short-term proarrhythmic risk at initiation of therapy) was observed with the other drug in the study (moricizine), and no long-term benefit emerged with further study. Emerging Markers of Risk for Sudden Cardiac Death Additional risk markers with independent or added predictive power are being studied for risk profiling. Coronary artery disease is also the most common cause in many areas of the world where the prevalence of atherosclerosis is lower. In this regard, it is anticipated that as third-world countries improve access to health care for communicable disease in the earlier years of life, 63 coronary atherosclerosis and its consequences will emerge as a larger problem. Congenital aortic (potentially high risk) or pulmonic (low risk) valve stenosis 1. Congenital septal defects with Eisenmenger physiology thrombosis, spasm, physical stress 1. Chronic atherosclerosis with a change in myocardial substrate, including previous C. Origin of a left coronary artery from the right or noncoronary sinus of Valsalva b. Secondary to fibrosis and calcification of the “cardiac skeleton” (Lev (lower incidence; higher risk) disease) 4. Abnormal native valves or left ventricular mural thrombus (1) Romano-Ward syndrome (without deafness) 4. Prosthetic valve dysfunction Atherosclerotic Coronary Artery Disease The structural and functional abnormalities of the coronary vasculature as a result of coronary atherosclerosis interact with the electrophysiologic alterations that result from the myocardial impact of an ischemic burden (see Chapters 58 to 62). The relationship between the vascular and myocardial components of this pathophysiologic model, as well as its modulation by hemodynamic, autonomic, genetic, and other influences, establishes multiple patterns of risk derived from the fundamental disease 2 state (Fig. Risk is modulated by multiple factors that can be either transient or persistent, and transient modulations may interact with persistent changes. The myocardial component of this pathophysiologic model is not static over time, and the term persistent must be viewed with caution because of the gradual effects of remodeling after an initial ischemic event and the effects of recurrent ischemic episodes. When the anomalous artery passes between the aortic and the pulmonary artery root, the takeoff angle of the anomalous ostium creates a slitlike opening of the vessel that reduces the effective cross-sectional area for blood flow. Coronary artery emboli occur most frequently in aortic valve endocarditis and from thrombotic material on diseased or prosthetic aortic or mitral valves. Emboli can also originate from left ventricular mural thrombi or as a consequence of surgery or cardiac catheterization. Coronary artery dissection, with or without dissection of the aorta, occurs in Marfan syndrome (see Chapter 75) and has also been reported after trauma and in the peripartum period of pregnancy. Scattered fibrosis in the distribution of the affected vessel is typically seen at postmortem examination and suggests a chronic or intermittent ischemic burden over time. Deep bridging seems to be more common in association with hypertrophic cardiomyopathy. Coronary artery spasm is usually associated with some degree of concomitant coronary atherosclerotic disease. Painless myocardial ischemia, associated with either spasm or fixed lesions, is recognized as a mechanism of previously unexplained sudden death. Genetic studies have confirmed autosomal dominant inheritance patterns, but with much allele and phenotypic heterogeneity. Most of the mutations are at loci that encode elements in the contractile protein complex, the most common being beta-myosin heavy chain and cardiac troponin T, which together account for more than half of identified abnormalities. Nonischemic Cardiomyopathy and Systolic and Diastolic Heart Failure The advent of therapeutic interventions that provide better long-term control of congestive heart failure has improved the long-term survival of these patients (see Chapters 21, 25, and 77). However, the proportion of patients with heart failure who die suddenly is substantial, especially among those who 18 appear clinically stable (i. Heart Fail Rev 2002;7:229, with permission from Springer Science and Business Media. Other causes include “idiopathic” fibrosis, alcoholic, and postmyocarditis cardiomyopathies; peripartum cardiomyopathy (see Chapter 90); and the 70 familial pattern of dilated cardiomyopathy, often associated with lamin A/C mutations. A residual group of undefined causes have been classified as “idiopathic myocarditis. The electrophysiologic mechanisms involved may be caused by acute stretching of ventricular myocardial fibers or the His- Purkinje system, based on experimentally demonstrated arrhythmogenic effects. However, the roles of neurohumoral mechanisms and acute electrolyte shifts have not been fully evaluated. Air Force recruits, 8 of 19 victims (42%) had evidence of myocarditis (5 nonrheumatic, 3 rheumatic) at postmortem examination, and 15 of 19 (79%) had their cardiac arrests during strenuous exertion. Giant cell myocarditis and acute necrotizing eosinophilic myocarditis are 71 particularly virulent for both myocardial damage and arrhythmias. In a report of the pathologic findings in nine patients who died of progressive systemic sclerosis, eight who died suddenly had evidence of transient ischemia and reperfusion histologically, thus suggesting that this might represent spasm caused by Raynaud-like involvement of the coronary vessels. The inheritance pattern is autosomal dominant, except in one geographically isolated cluster in which it is autosomal recessive (Naxos disease, plakoglobin locus on chromosome 17). Autosomal dominant mutations have also been identified in the ryanodine receptor locus on chromosome 1 (1q42) (see Chapter 33). Valvular Heart Disease Before the advent of surgery for valvular heart disease, severe aortic stenosis was associated with high risk for mortality. A high incidence of ventricular arrhythmia has been observed during the follow-up of patients with valve replacement, especially those who had aortic stenosis, multiple valve surgery, or cardiomegaly. Sudden death during follow-up was associated with ventricular arrhythmias and thromboembolism. Mitral Valve Prolapse Mitral valve prolapse is prevalent, but probably less so than previously thought, and is associated with a high incidence of annoying low-risk cardiac arrhythmias (see Chapter 69). Endocarditis of the Aortic and Mitral Valves Endocarditis of the aortic and mitral valves may be associated with rapid death resulting from acute disruption of the valvular apparatus (see Chapter 73), coronary embolism, or abscesses of valvular rings or the septum. However, such deaths are rarely true sudden deaths because conventionally defined tachyarrhythmic mechanisms are uncommon. Coronary embolism from valvular vegetations can trigger fatal ischemic arrhythmia on rare occasion. In a later study evaluating the impact of thrombolytic therapy versus the prethrombolytic era experience, the incidence of pure right bundle branch block was higher, but that of bifascicular block was lower, as were late complications and mortality. However, survival appears to depend more on the nature and extent of the underlying disease than on the conduction disturbance itself. Sodium channel gene mutations have been associated with progressive conduction system disturbances, 81 along with aging, and some are variants of Brugada gene expression. Less often, but not rarely, such mutations may occur de novo or may be transmitted from an apparently normal mosaic 84 parent.