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In tissue symptoms 10 weeks pregnant effective mentat ds syrup 100 ml, atrial myocytes are electrically connected via low-resistance gap junctions. Ionic current can flow from cell to cell via this pathway, in addition to the current exchange between intracellular and extracellular spaces through cell membrane proteins. Propagation of the action potential is typically modeled using spatially continuous models that are viewed as resulting from a local spatial homogenization of behavior in tissue compartments (membrane, intracellular and extracellular spaces). The conductivity tensor fields used in these continuous models integrate all the information about the distribution of gap junctions over the cell membranes as well as the fiber, sheet, and other microstructure organization in the atria. Cardiac tissue has orthotropic passive electrical conductivities that arise from the cellular organization of the myocardium into fibers and laminar sheets. Global conductivity values in the atrial or ventricular model are obtained by combining fiber and sheet organization with myocyte-specific local conductivity values. Multiscale models of human heart electrophysiology are typically modular, allowing the use of a variety of cellular ionic models, with different levels of biophysical detail. Animageofthethree-dimensionalgeometricmodelof the patient heart rendered with the epicardium and the infarct border zone semitransparent is shown in the third panel. The right-most panel presents in silico activation map of arrhythmia, revealing reentry on the left ventricular endocardium. Inthisprocess,thematrix of transformation provides the "deformed" fiber orientations, which are the ones matching the patient ventricular geometry. Because the atria are much thinner than the ventricles, image-based models of at least one of the human atrial chambers can further be subclassified into surface and volumetric models. Surface models represent atrial geometry in three dimensions but neglect wall thickness50,51,57,58; the latter is not true for volumetric models. Rule-based approaches have been used to assign fiber orientation consistent with measurements, either manually or using a semiautomatic rule-based approach. Finally, numeric approaches for simulating the electrical behavior of the heart have been described in detail in previous publications, some of which offer comprehensive reviews on the subject. Specifically, modeling work has been conducted to optimize antitachycardia pacing, as reviewed in this section. This criterion is based on the critical mass hypothesis, which postulates that a defibrillation shock is successful if it produces a strong extracellular potential gradient over a large amount of ventricular tissue mass. Optimization of electrode/can placement was also performed in this torso by changing the anatomic relations of electrodes to the heart and by varying the length of the epicardial electrode. The middle graph represents the spatial extent (inred) of the best capture results obtained for eachmodel. In a patient with tricuspid valve atresia, two configurations with epicardial leads were found to have the lowest defibrillation threshold. The study also demonstrated that determining extracellular potential gradients during the shock without actually simulating defibrillation was not sufficient to predict defibrillation success or failure. Research has reported a strong correlation between increased arrhythmia risk and the presence of T-wave alternans. Currently, this trend continues to be strong, with cell-, tissue-, and organ-level studies contributing to major advances in our understanding of heart rhythm and pump dysfunction. In addition, a major thrust in computational cardiac electrophysiology had been to use models as a test bed for evaluation of antiarrhythmic drugs, including testing hypotheses regarding the mechanisms of drug action on the scale of the whole heart; the latter work has the potential to guide the drug development pipeline more effectively, a process that currently has high failure rates and high costs. The use of heart models in personalized diagnosis, treatment planning, and prevention of sudden cardiac death is also slowly becoming a reality. Computer simulations of the function of the individualized diseased heart and its response to electrophysiologic therapies such as pacing and defibrillation represent a profound example of a research avenue in the new discipline of computational medicine, and offer high promise for clinical translation. Vigmond E, Vadakkumpadan F, Gurev V, et al: Towards predictive modelling of the electrophysiology of the heart. Gurev V, Lee T, Constantino J, et al: Models of cardiac electromechanics based on individual hearts imaging data: imagebased electromechanical models of the heart. Nygren A, Fiset C, Firek L, et al: Mathematical model of an adult human atrial cell: the role of K+ currents in repolarization. Clayton R, Bishop M: Computational models of ventricular arrhythmia mechanisms: recent developments and future prospects. Hu Y, Gurev V, Constantino J, et al: Effects of mechano-electric feedback on scroll wave stability in human ventricular fibrillation. Hu Y, Gurev V, Constantino J, Trayanova N: Efficient preloading of the ventricles by a properly timed atrial contraction underlies stroke work improvement in the acute response to cardiac resynchronization therapy. Heijman J, Voigt N, Nattel S, Dobrev D: Cellular and molecular electrophysiology of atrial fibrillation initiation, maintenance, and progression. Ashikaga H, Arevalo H, Vadakkumpadan F, et al: Feasibility of image-based simulation to estimate ablation target in human ventricular arrhythmia. Prakosa A, Malamas P, Zhang S, et al: Methodology for imagebased reconstruction of ventricular geometry for patientspecific modeling of cardiac electrophysiology. Dang L, Virag N, Ihara Z, et al: Evaluation of ablation patterns using a biophysical model of atrial fibrillation. Jacquemet V, Virag N, Kappenberger L: Wavelength and vulnerability to atrial fibrillation: Insights from a computer model of human atria. Ukwatta E, Yuan J, Qiu W, et al: Myocardial infarct segmentation and reconstruction from 2D late-gadolinium enhanced magnetic resonance images. Reumann M, Bohnert J, Seemann G, et al: Preventive ablation strategies in a biophysical model of atrial fibrillation based on realistic anatomical data. Vadakkumpadan F, Arevalo H, Ceritoglu C, et al: Image-based estimation of ventricular fiber orientations for personalized modeling of cardiac electrophysiology. Uldry L, Virag N, Jacquemet V, et al: Optimizing local capture of atrial fibrillation by rapid pacing: study of the influence of tissue dynamics. Uldry L, Virag N, Lindemans F, et al: Atrial septal pacing for the termination of atrial fibrillation: study in a biophysical model of human atria. Eason J, Schmidt J, Dabasinskas A, et al: Influence of anisotropy on local and global measures of potential gradient in computer models of defibrillation. Arevalo H, Rodriguez B, Trayanova N: Arrhythmogenesis in the heart: Multiscale modeling of the effects of defibrillation shocks and the role of electrophysiological heterogeneity. Anderson C, Trayanova N, Skouibine K: Termination of spiral waves with biphasic shocks: role of virtual electrode polarization. Tilg B, Fischer G, Modre R, et al: Model-based imaging of cardiac electrical excitation in humans. Berger T, Fischer G, Pfeifer B, et al: Single-beat noninvasive imaging of cardiac electrophysiology of ventricular preexcitation. Paper presented at Computing in Cardiology (CinC), Krakow, Poland, Sep 9-12, 2012. The sixth publication, dated 1962, is entitled "Complications of an Implantable Cardiac Pacemaker. Since that initial implant, millions of pacemakers have been implanted, saving lives and reducing or even eliminating symptoms. With these undeniable benefits of electronic pacemakers have also come the complications, occurring in 5% to 10% of implant procedures. Long-term management of pacemaker patients is complicated by device and lead failures and a requirement to change out the device when the battery expires. One approach that has been widely publicized over the last few years is the idea of creating a "biological pacemaker" by either gene transfer or cell transplantation methods (Table 23-1). Their delivery method essentially scattered the transgene around the ventricular myocardium. The initial report targeted the left atrium,12 and a subsequent report showed gene transfer to the left bundle branch. The investigators did not report the time course of heart rate increase for the mice, but in the pigs they found a statistically significant increase in heart rate only on the second day postinjection. The usual experience with plasmid-mediated gene transfer is that the effect persists for several weeks or even months after gene transfer. Additional concern is raised when considering possible mechanisms for the increase in heart rate. The mouse study did not target the specialized conducting system, and under ordinary circumstances atrial myocytes should not display automaticity. Increased activity of these calcium-handling proteins could cause automaticity by the calcium clock mechanism, but sustained increase in intracellular calcium would likely be toxic.

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Park J alternative medicine generic 100 ml mentat ds syrup overnight delivery, Lee S, Jeon M: Atrial fibrillation detection by heart rate variability in Poincare plot. Sarkar S, Ritscher D, Mehra R: A Detector for a chronic implantable atrial tachyarrhythmia monitor. Purerfellner H, Pokushalov E, Sarkar S, et al: P-wave evidence as a method for improving algorithm to detect atrial fibrillation in insertable cardiac monitors. Trigano A, Blandeau O, Dale C, et al: Risk of cellular phone interference with an implantable loop recorder. Jekova I, Dushanova J, Popivanov D: Method for ventricular fibrillation detection in the external electrocardiogram using nonlinear prediction. Irusta U, Ruiz J, Aramendi E, et al: A high-temporal resolution algorithm to discriminate shockable from nonshockable rhythms in adults and children. Alonso-Atienza F, Morgado E, Fernandez-Martinez L, et al: Detection of life-threatening arrhythmias using feature selection and support vector machines. Allavatam V, Palreddy S, Sanghera R, Warren J: Inventors; Cameron Health, assignee. Kobe J, Reinke F, Meyer C, et al: Implantation and follow-up of totally subcutaneous versus conventional implantable cardioverter-defibrillators: a multicenter case-control study. Arce-Leon A, Arana-Rueda E, Garcia-Riesco L, et al: Postimplant shocks in a totally subcutaneous defibrillator: what is the mechanism Notably, neuromodulation of the peripheral nervous system has attracted considerable attention because the peripheral nerves are more easily targeted, and they control specific organ functions impacted in chronic diseases. The field of bioelectronic devices is burgeoning with possibilities of developing closed loop pacing systems, where devices will be able to record electrical activity, perform real time analyses, and accordingly modulate the neural signaling via pacing strategies. On the other hand, the autonomic nervous system, which is ubiquitous throughout the body, constitutes a less well understood entity. Dysregulation of the autonomic tone plays a significant role in the pathophysiology and progression of a myriad of disorders, including hypertension, sleep apnea, heart failure, and more. The limited breakthrough advances in the medical therapy on these disease fronts have led to the evolution of innovative nonpharmacologic interventions that can favorably modulate the cardiac autonomic tone. Several new therapeutic modalities that may act at different levels of the autonomic nervous system are being investigated for their role in the treatment of heart failure, arrhythmias, and other cardiovascular disorders. The current chapter examines the role of stimulating these cardiac and extracardiac neural systems that may have a role in clinical electrophysiology. The pelvic visceral organs are innervated by branches of the second to fourth sacral nerves. The ganglia cells are typically clustered within the walls of the viscera, thereby making the parasympathetic postganglionic fibers very short. Cardiac parasympathetic innervation is principally via the tenth cranial nerve, better known as the vagus nerve. The complexity of the cardiac innervation is further enhanced by the presence of intrinsic neurons that form plexuses with the preganglionic nerve terminations and the postganglionic neurons across the cardiac chambers. Notably, the neurons forming this network of connections constitute an intrinsic nerve plexus called the little brain of the heart. These neuronal stations are in constant communication and feedback to each other through cardio-cardiac reflexes, which control spatially organized regions. There are approximately a thousand epicardial ganglia in the human heart and the structural organization of these ganglia and nerves within the subplexuses vary between hearts and with age. Notably, there is a greater concentration of parasympathetic innervation in the atria compared with the ventricles. These paravertebral ganglia are connected via axons of preganglionic neurons, which project rostrally or caudally to terminate on postganglionic ganglia, which may be located some distance away. In this manner the paravertebral ganglia form the sympathetic chain (or sympathetic trunk) bilaterally. Some preganglionic neurons terminate directly on the viscera, such as the adrenal cortex. Preganglionic sympathetic nerves also synapse with ganglia on the heart; sympathetic influence on the heart is primarily through surface synapses. The axons of some postganglionic neurons reenter the spinal nerves after leaving the chain ganglia. Other postganglionic fibers enter the thoracic cavity after leaving the chain and terminate on visceral organs. Cardiac sympathetic fibers travel subepicardially along the main coronary arteries. Cardiovascular reflexes regulate sympathetic outflow to the heart and peripheral tissues. Autonomic fibers carry the afferent limbs of these reflexes, whereas the efferent arms are composed of impulses in either autonomic or somatic nerves. The main reflex responses originate from the baroreceptors of the aortic arch and carotid artery, cardiopulmonary systems (including the Bezold-Jarisch reflex), peripheral chemoreceptors and low-threshold, polymodal receptors. Morphology,distribution,andvariabilityoftheepicardiac neural ganglionated subplexuses in the human heart. For example, afferent signals arise from mechanoreceptors and chemoreceptors in different parts of the circulatory system. Notably, the stress-sensitive baroreceptors (mechanoreceptors) are present in both the high pressure (arterial) and low pressure (venous) sides of the circulatory system. Afferent signals from the carotid sinus receptors are carried by the carotid sinus nerve, which joins the glossopharyngeal nerve (ninth cranial nerve). The axons from the aortic arch receptors constitute an afferent branch of the vagus nerve. The carotid sinus and aortic arch baroreceptors relay their signals and provide feedback for the primary regulation of aortic pressure. The venous mechanoreceptors that are located in the junction of the atria and the pulmonary arteries send their signals via unmyelinated fibers of the vagus nerve as a part of the Bainbridge reflex. These cardiovascular reflex arcs are intimately related to each other with the Bainbridge reflex serving to counterbalance the baroreceptor reflex; the Bainbridge reflex is dominant when blood volume is increased and the baroreceptor reflex is dominant when blood volume is decreased. Afferent signals from carotid sinus chemoreceptors travel via the glossopharyngeal nerve, and signals from the aortic arch chemoreceptors travel via the vagus nerve. The peripheral chemoreceptors predominantly sense arterial oxygen and carbon dioxide concentration, whereas the central receptors sense pH and carbon dioxide concentration. When there is a decrease in blood oxygen, an increase in carbon dioxide, or a decreased pH, the firing rate of the chemoreceptors is decreased. Mixed receptors, which are sensitive to both mechanical and chemical stimuli, are present in the walls of all cardiac chambers. There are five key effects of protein kinase A activation and induced phosphorylations: (1) Ca2+ entry into the cells increases via L-type Ca2+ channels and the ryanodine receptor. This occurs as a result of phosphorylation of troponin I and myosin binding protein C. This is accompanied by altered vagal and sympathetic discharges, both of which may serve as triggers for atrial and ventricular arrhythmias. This is illustrated by the fact that the parasympathetic (vagal) limb is protective in the ventricle,27 while it contributes to the arrhythmogenicity of the atrial substrate. Alterations in the autonomic tone that can be arrhythmogenic could be either systemic via central changes in the tone or locally mediated through regional alterations. In pathologic states such as myocardial ischemia, the cardiac afferent and efferent stimuli from the myocardial region under threat may be altered to promote a proarrhythmic environment, contributing to the risk for sudden cardiac death. Of note, myocardial infarction causes local denervation in the region of the scar,31-33 which when accompanied by nerve sprouting at the edge of the scar,34 results in hypersensitivity to circulating catecholamines. Although modifying the sympathovagal balance through pacing strategies is possible, its role in modifying the risk for arrhythmias in humans needs further study. Microneurography enables quantification of nerve firing within the skin and local vasculature,47,48 but it has low reliability,49 which has precluded its clinical use. Commonly used to measure nerve activity using microelectrode in nerves such as in common peroneal nerve. Additional Information Useful for measuring sympathovagal balance and in risk stratification. Percentage msec/mm Hg Baroreflex sensitivity Cardiovagal baroreflex sensitivity Muscle sympathetic nerve activity Limited availability, but useful in risk stratification and postmyocardial prognostication. Considerable variability in release and uptake of catecholamines in various tissues.

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Thus symptoms 7 dpo bfp cheap mentat ds syrup 100ml with mastercard, the maximum performance that a marathon runner can achieve is directly related to the condition of the cardiovascular system. This explains, in part, why a patient with congestive heart failure may have difficulty in generating enough muscle power to climb out of bed or to walk short distances. Although some of the heat is stored in the body during exercise, most of the heat is dissipated through the skin. Nevertheless, even during normal temperature and humidity conditions, the body temperature may rise from its normal 98. When this happens, a number of signs and symptoms may appear, which collectively are referred to as heat stroke. These signs and symptoms include the following: Profuse sweating, followed by no sweating Extreme weakness Muscle cramping Exhaustion Nausea Headache Dizziness Confusion Staggering gait Altered level of consciousness Unconsciousness Circulatory collapse Heat stroke can be fatal if not treated immediately. Even when the individual stops exercising, the temperature does not readily return to normal because (1) the temperature-regulating mechanism often fails at a very high temperature and (2) the intracellular metabolism is much faster at higher temperatures, which in turn generates still more heat. It provides patients with a process of developing and maintaining a desirable level of physical, social, and psychological well-being. The typical pulmonary rehabilitation team consists of a physician, nurse, respiratory therapist, physical therapist, psychologist or social worker, and dietitian. Pulmonary rehabilitation programs are commonly divided into the following three phases. The patient performs a variety of tests such as pulmonary function studies, stress tests, and 6- to 12-minute walking tests. During this phase, the patient is also evaluated for any nutritional, psychological, lifestyle, and vocational needs. This phase includes patient and family education, group and individual counseling, and group discussion sessions. Educational topics include basic cardiopulmonary anatomy and physiology, breathing techniques, pulmonary hygiene, nutritional guidelines, medications, respiratory therapy equipment, and the importance of exercise. Such exercises include work on the treadmill, air-dyne bike, arm ergometer, and rowing machine plus chest pulleys and steps. The primary objective during this phase is the conditioning of the cardiovascular system (aerobic) and skeletal muscles. During the last portion of this phase, long-term graded exercises are emphasized, such as walking, jogging, stationary bicycling, and/ or swimming. Respiratory muscle training is beneficial-especially when combined with general exercise training. The patient commonly undergoes yearly evaluation, which includes graded exercise testing. Chapter Summary A basic knowledge of the effects of exercise on the cardiopulmonary systems is helpful to the respiratory therapist. Important topics regarding ventilation during exercise include the control of ventilation, alveolar ventilation, oxygen consumption, arterial blood gas values, increased oxygen diffusion capacity, and alveolararterial difference. Topics in this area include sympathetic discharge, cardiac output, arterial blood pressure, pulmonary vascular pressure, and the dilation of muscle capillaries. In addition, a basic understanding of the following should be mastered: the interrelationship among muscle work, oxygen consumption, and cardiac output; the influence of training on the heart and on cardiac output; and the relationship between body temperature and cutaneous blood flow. Finally, the respiratory therapist should know the primary components of the three phases of a pulmonary rehabilitation program. A clinical connection associated with these topics includes the general benefits of exercise. The maximum alveolar ventilation generated during heavy exercise under normal conditions is about what percent of the maximum voluntary ventilation Peripheral vascular system to constrict chapter 18 Exercise and Its Effects on the Cardiopulmonary System 563 3. During exercise, the stroke volume reaches its peak when the cardiac output is at about what percent of its maximum During exercise, the P(A 2 a)O begins to increase when the oxygen consumption reaches about what percent of its maximum Cardiopulmonary Changes Seen at High Altitude the effects of high altitude on the cardiopulmonary system are of interest because better understanding of long-term oxygen deprivation can be applied to the treatment of chronic hypoxia caused by lung disease. Nearly 30 million people live at altitudes greater than 8000 feet-mostly in the Rocky Mountains of North America, the Andes Mountains of South America, the Himalaya Mountains of south central Asia, and the Ethiopian Highlands of East Africa. Unfortunately, these short-term, high-altitude exposures also pose the hazards of acute altitude illnesses. The purpose of this chapter is to review both the normal responses and adaptive processes that occur in response to high altitude. At an altitude of 18,000 to 19,000 feet, the barometric pressure is about half the sealevel value of 760 mm Hg (380 mm Hg). At an altitude of about 65,000 feet, the barometric pressure falls below the pressure of water vapor, and tissue fluids begin to "boil" or "vaporize. When an individual who normally lives near sea level spends a period of time at high altitudes, a number of compensatory responses develop-a process known as acclimatization. For example, it is an interesting fact that after a period of acclimatization, an individual may reach the summit of Mount Everest without supplemental oxygen. However, when an individual is suddenly exposed to the oxygen tension found at the summit of Mount Everest, a loss of consciousness occurs within minutes. The following are some of the primary cardiopulmonary changes seen at high altitude. Because the peripheral chemoreceptors do not acclimate to a decreased oxygen concentration, increased alveolar ventilation will continue for the entire time the individual remains at the high altitude. Pulmonary Function and Mechanics As an individual ascends, the following changes occur in lung function as a result of acute hypoxic exposure: the vital capacity decreases within the first 24 hours. It is believed the causes of the reduced vital capacity include increased interstitial lung fluid-which in turn results in airway narrowing, air trapping, and delayed emptying of alveolar gas-pulmonary vascular engorgement, and decreased respiratory muscle strength. It is interesting to note that the peak expiratory flow rates are actually increased. It is believed that this lower airway resistance is due, in part, to the decreased air density, which works to offset any airway narrowing. Unlike individuals exposed to acute hypoxic environments, long-term high-altitude residents have an increased vital capacity. Research shows a direct relationship to the vital capacity size and the length of time one resides at high altitudes-that is, the more time spent at high altitudes, the larger the vital capacity. People born and raised at high altitudes develop larger vital capacities than those who reside in high altitudes later in life. The increased hemoglobin available in polycythemia is an adaptive mechanism that increases the oxygen-carrying capacity of the blood. In fact, people who live at high altitudes often have a normal, or even above-normal, oxygen-carrying capacity, despite a chronically low PaO and oxygen saturation. Over a 24- to 48-hour period, the renal system tries to 2 568 Section three the Cardiopulmonary System during Unusual Environmental Conditions offset the respiratory alkalosis by eliminating some of the excess bicarbonate. In spite of this mechanism, however, a mild respiratory alkalosis usually persists. In fact, even natives who have been at high altitudes for generations commonly have a mild respiratory alkalosis. It is assumed that respiratory alkalosis may be advantageous for the transfer of oxygen across the alveolar-capillary membrane because alkalosis increases the affinity of hemoglobin for oxygen. In other words, the alkalosis enhances the loading of oxygen to the hemoglobin as desaturated blood passes through the alveolar-capillary system. It is also argued, however, that the increased affinity interferes with the unloading of oxygen at the cells. There is both experimental and theoretical evidence that the increased oxygen affinity at high altitude is beneficial. This is further supported by the fact that a mild respiratory alkalosis usually persists in mountain climbers, high-altitude natives, and even in animals who live in low-oxygen environments. The alkalosis persists even after the kidneys have had more than enough time to fully eliminate the excess bicarbonate. Oxygen Diffusion Capacity In response to short-term exposure to high altitude, there are a number of factors that limit oxygen diffusion.

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On the other hand treatment lung cancer order mentat ds syrup 100ml amex, patients with syncope and bifascicular block represent a different clinical problem. Familial clustering in cases of "idiopathic" conduction system degeneration is consistent with a hereditary basis. Some cases with familiar clustering have an autosomal dominant pattern of inheritance and associated congenital heart malformations and cardiomyopathy. Inherited conduction system disease may be isolated or associated with congenital heart diseases, neuromuscular disorders, and cardiomyopathies. Inherited conduction diseases include developmental transcription factor mutations, cardiac ion channelopathies, and mutations in genes regulating energy metabolism, gap junctions, and structural proteins. All these neuromuscular disorders may be associated with cardiac conduction defects. This autosomal dominant inherited disorder is caused by an expansion of cytosine-thymineguanine repeat on chromosome 19. Of note, there may be a gender difference in the severity of the cardiac phenotypes seen in lamin A/C disease. The channel then becomes inactivated by slow- and fastinactivation conformational changes. This suggests a possible opportunity for early diagnosis of the mutation before development of a clinically significant conduction system defect or cardiomyopathy, even in the absence of a genetic test. Different mutations in the cardiac sodium channel 1-subunits (W179X, E87Q) have also been associated with cardiac conduction disease. This syndrome is characterized by potassium-sensitive periodic paralysis, ventricular arrhythmias, and dysmorphic features. In addition to conduction disease, this phenotype includes atrial or ventricular septal defects. Mutations in the T-box transcription factor Tbx5, which similarly is an important early regulator of cardiac development, cause Holt-Oram syndrome. A mouse model carrying a mutation responsible for the human disease has been generated. Mitochondrial disorders comprise a group of diverse genetic diseases, with cardiac conduction defects reported in 10% to 40% of the patients with these disorders. The conduction defects typically involve the distal His bundle, bundle branches, and infranodal conduction. These causes include atherosclerosis, dilated cardiomyopathy, hypertension, infiltrative cardiomyopathies, inflammatory disorders, and infectious diseases. In most cases the specific etiology is clinically unknown, and with few exceptions. Arrhythmias and other medical conditions that require drug therapy that results in symptomatic bradycardia (level of evidence: C) 3. Documented periods of atrial fibrillation and bradycardia with one or more pauses of at least 5 seconds or longer in awake, symptom-free patients (level of evidence: C) 5. Baerman et al66 investigated the time course of conduction defects after bypass surgery. Surgical technique consisted of cold, hyperkalemic cardioplegia, and conduction defects resolved partially or completely in 50% of patients. Patients with conduction defects generally had longer cardiopulmonary bypass times, longer aortic cross-clamp times, and more vessels requiring bypass. Reasons for conduction abnormalities after cardiac surgery include ischemic injury to the conduction system, direct surgical manipulation or trauma to conduction tissue, traumatic disruption of the distal conduction system, edema, dissecting hematomas, and alterations in conduction caused by cardioplegia. Surgery for correction of valvular heart disease often leads to conduction defects. Conduction disturbances are particularly common both in patients with aortic valve disease and after aortic valve replacement, with 5% to 30% of patients experiencing some conduction abnormality after valve replacement. The incidence of conduction disorders requiring permanent pacing in patients after aortic valve replacement is 3% to 6%. The incidence of permanent pacemaker implantation ranged from 25% in high-risk patients to 3. In most institutions, permanent pacing would be instituted earlier, probably by the fourth to sixth postoperative day. Long-term survival after "ablate and pace" approach has been reported by Ozcan and colleagues. A few cases of persistent heart block requiring permanent pacemaker implantation have been described. The severity of injury does not always correlate with the development of posttraumatic complications, including conduction disorders. The mechanism of conduction defects in this setting may be related to ischemia and infarction of the conduction system. Complete heart block has been described in various infectious diseases, including bacterial, viral, fungal, protozoan, and rickettsial infections. In most infectious diseases, heart block is transient and resolves with treatment of the underlying infection. This is particularly true in patients with entities such as endocarditis, in which a valve ring abscess may erode into the conduction system, and in patients with infections such as Chagas disease. This systemic illness, first described in 1975, was characterized later as an infection caused by a spirochete, Borrelia burgdorferi, which is transmitted to humans by a tick bite. This illness is often characterized by a rash, erythema chronicum migrans, which is followed by cardiac and neurologic abnormalities, and in some cases by arthritis. Cardiac involvement may occur in 8% to 10% of Lyme disease patients, is generally transient, and may consist of a myocarditis or a myopericarditis. Two important axioms worth repeating are that (1) heart block associated with infectious disease usually resolves with appropriate and prompt antibiotic treatment and (2) conduction disease is rarely the only manifesting feature of an infectious illness. Heart block may occur after radiation therapy if radiation is directed at the mediastinum, as for Hodgkin and some non-Hodgkin lymphomas. In general, it is unusual for toxicity to antineoplastic drugs such as doxorubicin to result in damage to the cardiac conduction system. Certain neuromuscular diseases may give rise to progressive and insidiously developing cardiac conduction system disease. The disorders include Duchenne muscular dystrophy, fascioscapulohumeral muscular dystrophy, X-linked muscular dystrophy, myasthenia gravis, myotonic dystrophy, and Friedreich ataxia. His-Purkinje disease can culminate in fatal Stokes-Adams attacks unless anticipated by insertion of a pacemaker. Permanent pacing should be considered early in the course of neuromuscular disease and should be offered to the asymptomatic patient once any conduction abnormality is noted. The majority of patients with sarcoid heart disease have extracardiac involvement that manifests either clinically or on biopsy. Other organ systems involved in sarcoid include the lymph nodes, skin, eyes, and the nervous, musculoskeletal, renal, and endocrine systems. Isolated cardiac involvement in sarcoidosis is less common and usually precedes future systemic sarcoidosis. In Japan, sarcoid heart disease is more common, accounting for up to 85% of mortality from sarcoidosis. Recommendations regarding management are summarized by the recently published sarcoidosis guidelines. In these patients immunosuppressive therapy (methylprednisolone + azathioprine) may normalize rhythm disturbances. In these patients prenatally established structural damage of immune origin appears to be the pathologic basis. Several reports of patients with cardiac asystole after exertion have demonstrated postexercise sinus arrest with ventricular asystole.

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Therefore medicine 319 pill buy mentat ds syrup in india, for the electrode to make contact with the myocardium, the lead must be wedged into the target vein. By comparison, when the pacing electrode is at the tip, the electrode may contact the myocardium without being wedged. There are a variety of approaches to passive fixation, including tines (straight), single curve, double curve (S-shape)58,59 and double cant. Nof and colleagues found no significant differences in success or complication rates among passive fixation leads. If lead selection is limited to one manufacturer, a less desirable target vein or even implantation failure may result. Jude, Biotronik, and Sorin (Milan, Italy) have unique preformed distal shapes intended to promote stability and orient the tip electrodes toward the myocardium. Type, Size, and Personality of Left Ventricular Pacing Lead Each lead has a size, shape, and electrode configuration that produces a "personality" that will have advantages and disadvantages when the lead is used in different veins. The section in this book on commercially available leads gives examples of how changing the method of lead fixation can solve problems of lead instability, high thresholds, and phrenic pacing. Selecting the Shape of the Vein Selector As mentioned previously, the current approach relies on the shape of the vein selector and not the delivery guide for target vein cannulation, which is now possible because of the soft tip on the vein selectors and the delivery guide. The black distal section of the catheter is soft and can be easily straightened as it is advanced over wires into the target vein. Thus, once the ostium of the vein is identified by a puff of contrast, the wire can be advanced followed by the vein selector to add a second wire. The ability of the vein selector to be advanced deep into the vein over the wires allows for the creation of a stable rail over which to advance the delivery guide. Selecting the Lumen Size of the Delivery Guide the size of the lead suitable for the target vein determines the lumen size of the delivery guide to be used. The soft tip section of the delivery guide can be advanced deep into a target vein over the vein selector if needed. As a result, we now rely on the shape of the vein selector and not the shape of the delivery guide to accommodate the takeoffs of various veins. When looking for the target vein with the vein selector, proper interventional technique must be used. Ideally, puffs of contrast are only used to verify position but may be necessary to reveal the target vein location. Remove the Vein Selector Retaining the Wires and Deliver the Lead It is particularly important that the instrument table be perpendicular to the patient table as the vein selector is withdrawn. To prevent the delivery guide from being displaced during the process of removal, it is important not to advance the wires as the vein selector is removed. To maintain wire access in the vein, it is important not to pull the wires out as the vein selector is removed. Keeping the wires in a stable position during the process is best accomplished with the catheters in a straight line resting on the table. Once the lead is in place, it is time to discuss removing the delivery system without displacing the leads. There are several factors that influence the risk of lead dislodgment during removal of the guiding catheter. The use of a delivery guide impacts lead dislodgement via the size and final position of the lead. Use of a delivery guide impacts lead dislodgment via the final position of the stylet. Final Lead Size and Position A delivery guide helps insert a lead that is appropriately sized and positioned in the vein which is less likely to be displaced. With large veins, a 9-Fr delivery guide allow larger (6- to 7-Fr), more stable leads to be placed compared with the smaller, 6- to 7-Fr delivery guides (4- to 5-Fr leads). B, Injection system is attached to the vein selector through a rotating Y-adapter. Again,tousetheveinselector in a safe and effective manner and to reduce contrast use, both handsmustbeonthecatheter. Slicing Versus Peeling for Coronary Sinus Catheter Removal Slicing requires the operator to fix the lead to the slicer, fix the position of the slicer and lead, then pull the catheter straight back over slicer without moving the cutting hand or allowing the lead to lead to buckle or detach from the slicer. A natural tendency is to pull the catheter off to one side, disengaging the blade from the catheter. If the lead is not dislodged as the blade disengages, the motion of trying to reengage the blade into the catheter frequently does dislodge it. If additional lead slack is required to prevent lead dislodgement, it cannot be added (fixed slicing hand position) until the slicing operation has been completed. Before peeling, an assistant stabilizes the lead distally by pinching the walls of the sheath against the lead where the sheath exits the body. With the lead secure, the hub is cracked and the sheath peeled down to the fingers of the assistant. The cycle of withdrawal, pinch, and peel is repeated until the sheath clears the body and the assistant can secure the lead. The sliceable plastic hub is joined to the braided catheter via an overlapping of the plastic and braid. The resistance to cutting increases significantly as the blade reaches the plastic hub and then decreases abruptly as the blade reaches the guide. The telescoping delivery guide supports the lead in the target vein while the angioplasty wire is removed and the stylet is advanced. The importance of using a soft curved stylet becomes apparent once guides and sheaths are removed. Usingthe support provided by the vein selector and wires, the delivery guide is advanced toward the ostium of the target vein. B, Support provided by the extrasupport wire and the delivery guide allows the lead to be advanced deepintothesmallvein. Thesheathdetermines the length of the lead in the body, particularly in the right atrium. Pressure Products achieves this by exposing the catheter when the valve is broken in two pieces. Jude have integrated, slittable hemostatic hubs where the troublesome transition between hub and guide is avoided. Splitting the Hub/Guide Without Grabbing and Displacing the Lead After it is cut, the thick plastic of the hub of the guide can close around the lead. B, Without moving the lead, the operator cuts the third-generation guide down to the SafeSheath hub. The operator removes the lead from the cut guide and secures it to the cutter by placing the lead in the notch of the cutter under thethumb. C D Pinching the lead between the walls of the sheath stabilizes the lead and sheath distally. Because there is no braid, the walls of the sheath can be pinching against the lead reducing blood loss and the risk of air embolization once the valve is removed. It is far more difficult, if not impossible, to effectively pinch a catheter with wire braid incorporated in the wall. After an assistant releases the sheath/lead, the rest of the sheath is drawn back over the lead under fluoroscopic observation. As the tip of the sheath exits the body and the pacing lead becomes visible, the assistant secures the lead position with fingers in the pocket. The two issues of importance are the physical characteristics of the stylet and how the stylet is withdrawn. An unsupported lead with a stylet may result in the tip of the lead withdrawing from the target vein. A softer stylet exerts less displacing force when the shape of the stylet and course of the lead do not match despite the curve. The longer the stylet remains in a position prone to displacing the lead, the more likely the lead will be displaced. To prevent the stylet from displacing the pacing lead when the course of the lead and the shape of the stylet do not match, the stylet is removed quickly (like pulling the cord on a lawn mower). Consider a comparison of the relative risk of arterial to venous system complications.

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Inferiorly symptoms xanax discount mentat ds syrup 100ml fast delivery, the subclavian vein is associated with a depression in the first rib and on the pleura. The brachiocephalic or innominate veins are two large, venous trunks located on each side of the base of the neck. The left innominate vein is larger and longer than the right, passing from left to right for approximately 2. The external jugular vein is a superficial vein of the neck that receives blood from the exterior cranium and face. This vein starts in the substance of the parotid gland, at the angle of the jaw, and runs perpendicular down the neck to the middle of the clavicle. In this course, the external jugular crosses the sternocleidomastoid muscle and runs parallel to its posterior border. At the attachment of the sternocleidomastoid to the clavicle, the external jugular vein perforates the deep fascia and terminates in the subclavian vein just anterior to the scalenus anticus muscle. The external jugular is separated from the sternocleidomastoid muscle by a layer of deep cervical fascia. Superficially, it is covered by the platysma muscle, superficial fascia, and skin. Because of its larger size and deeper and more protected orientation, however, the internal jugular vein is used more frequently than the external jugular vein. The internal jugular vein starts just external to the jugular foramen at the base of the skull. It drains blood from the interior of the cranium, as well as superficial parts of the head and neck. Superiorly, the internal jugular is lateral to the internal carotid and inferolateral to the common carotid. At the base of the neck, the internal jugular vein joins the subclavian vein to form the innominate vein. The internal jugular vein is large and lies in the cervical triangle, defined by the (1) lateral border of the omohyoid muscle, (2) inferior border of the digastric muscle, and (3) medial border of the sternocleidomastoid muscle. The superficial cervical fascia and platysma muscle cover the internal jugular vein, which is easily identified just lateral to the easily palpable external carotid artery. From a venous access perspective, the location of the subclavian vein may vary from a normal lateral course to an extremely anterior or posterior orientation in elderly patients. Byrd51 has described the subclavian venous anatomy of two distinct deformities, both of which make venous access more difficult and hazardous. This is usually seen in patients with chronic lung disease and anteroposterior chest enlargement. Such patients can be identified by the presence of a horizontal deltopectoral groove and the posteriorly displaced clavicle. In this situation, the clavicle is anteriorly bowed or actually displaced anteriorly. It is important that the implanting physician recognize such variations to avoid complications such as pneumothorax and hemopneumothorax when using the percutaneous approach. It is assumed that the implanting physician is also completely familiar with the anatomy of the heart and great vessels. These situations are considered later, in the discussion of ventricular electrode placement. At times, the apex may be located directly anterior to or even to the right of midline. A lack of appreciation of these variations can lead to considerable difficulty in electrode placement. The decision should not be made according to the dominant hand of the implanting physician. It seems to be easier for many right-handed implanters to work on the right side of the patient, and vice versa, but from a surgical point of view, catheter manipulation from the right can be a frustrating experience. The groove can be precisely located by palpating the coracoid process of the scapula. The dermis along the deltopectoral groove is infiltrated with local anesthetic, encompassing the anticipated length of the incision. One can create smooth skin edges by making an initial single stroke that carries through the dermis to each corner of the wound. The subcutaneous tissue is infiltrated with local anesthetic along the edges of the incision. The Weitlaner retractor is applied to the edges of the wound, and the subcutaneous tissue is placed under tension. As the subcutaneous tissue falls away, tension is restored by reapplication of the Weitlaner retractor. At this level, the borders of the pectoral and deltoid muscles forming the deltopectoral groove are identified. Gradual release of the fascial tissue between the two muscle bodies will expose the cephalic vein. In this case, the cephalic vein can be dissected centrally to the axillary vein, and this larger vein can be catheterized. Once the vein to be catheterized is localized, it is freed of all fibrous attachments. The anterior half of the vein at this site is grasped with a smooth forceps, and the vein is gently lifted. The venotomy is held open by any of several means: a mosquito clamp, forceps, or vein pick. Gentle traction is applied on the distal ligature while tension is released on the proximal ligature. This simple approach calls for the percutaneous puncture of the vessel with a relatively long, largebore needle; passage of a wire through the needle into the vessel; removal of the needle; and passage of a catheter or sheath over the wire into the vessel with removal of the wire. An 18-gauge, thin-walled needle 5 cm in length is typically used, although smaller needles are available. These needles come prepackaged with most introducer sets, but an extra supply should be available. Given the previously discussed anatomic variations, the subclavian vein puncture is typically made near the apex of the angle formed by the first rib and clavicle. At this puncture site (and after both skin infiltration with local anesthetic and a 1-cm incision at the site, which generally is 1-2 cm inferolateral to the point where the clavicle and first rib actually cross), the needle is aimed in a medial and cephalic direction. It is important to make the puncture with the patient in a "normal" anatomic position. The infraclavicular space or costoclavicular angle should not be artificially opened by maneuvers such as extending the arm or placing a towel roll between the scapulae. These maneuvers can open a normally closed or tight space and lead to undesirable puncture of the costoclavicular ligament or subclavius muscle, which in turn can result in lead entrapment and crush. With the patient in the normal anatomic position, access to the subclavian window is medial yet usually avoids the costoclavicular ligament. The more medial puncture and needle trajectory of this approach vastly improves the success rate and dramatically reduces the risks of pneumothorax and vascular injury compared with a more lateral approach. With this medial position, the vein is a much larger target and the apex of the lung is more lateral. This safer approach is a departure from the conventional subclavian venous puncture, which calls for introduction of the needle into the middle third of the clavicle. There are legitimate concerns that this medial approach, although safer, results later in higher complication rates and failure rates due to conductor fracture and insulation damage. Occasionally, this binding can even crush the lead, referred to as the subclavian crush phenomenon. This phenomenon is more common in larger, complex leads of the in-line bipolar, coaxial design. With this technique, subclavian vein puncture should never be made outside the safety zone or in violation of the preceding conditions. Byrd also has described a new technique for cannulating the axillary vein that may now be the dominant technique used (see below). As previously mentioned, the axillary vein is actually a continuation of the subclavian vein after it exits the superior mediastinum and crosses the first rib.

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Thus illustrations of the normal cardiac anatomic structures using these techniques are a kind of collateral benefit of the studies medications such as seasonale are designed to purchase generic mentat ds syrup on line. A dedicated algorithm, by increasing the opacity of the intracavitary contrast and, at the same time, reducing the opacity of the myocardium, creates a perfect electronic cast of the cavities. The second is a large triangular pouch that extends laterally and anterosuperiorly, partially covering the anterior aspect of the ascending aorta. These two components are divided externally by a groove filled with fat named the sulcus terminalis. First, the voxel (volume elements) at the base for 3D reconstruction approximates to a small cube of 0. Thus the technique enables the defining of boundaries of two adjacent structures that are close to each other, no less than 0. Second, the ability of the system to "fly around" or "fly through" (in other words, to observe a given organ from different perspectives or to go inside) allows an intuitive perception of three-dimensionality. Indeed, the large difference in acoustic impedance between blood and the internal surface of the wall makes right atrial structures fully visible. Moreover, the capability of displaying these structures from different perspectives permits defining anatomic details with a fidelity that approximates the anatomic specimens. The electrically inert tricuspid hinge line anteriorly, and the eustachian valve and the eustachian ridge posteriorly, clearly delimit this area. Moreover, the wall thickness of the inferior isthmus is thin and presents areas of fatty-fibrous tissue. Both these conditions make the tissue more susceptible to complete transmural ablation. In particular, four anatomic variants of the inferior isthmus may make linear ablation difficult or ineffective, forcing the electrophysiologist to move to the inferolateral or paraseptal isthmus. Subeustachian pouch, which may cause lack of catheter-tissue contact, making the ablation line incomplete. Prominent and rigid eustachian valve, which, acting like a fulcrum, may make the catheter manipulation difficult, requiring tricky catheter angling for obtaining a good tip-tissue contact. When unexpected, these variants may prolong the procedural time, increase the number of radiofrequency applications, or make the ablation inadequate with recurrence of the arrhythmias. Of course, identifying these variants before the procedure may result in precious time saving for electrophysiologists who may be able to minimize difficulties by adapting their strategy and equipment. A preprocedural knowledge of the course of the right coronary artery and its branches (including the nodal arteries) may be particularly useful in some circumstances to avoid damage during ablation. Indeed, especially at the level of the lateral isthmus, the distance between the atrial endocardium may be as short as 5 mm (more or less the distance to obtain a transmural lesion) with a potential risk for right coronary artery injury. First, definition of the eustachian valve or the insertion of the tricuspid valve are not always optimal. Finally, quantitative measurements are possible in either multiplanar imaging format. Moreover, the presence in the electrophysiologic laboratory of both anesthesiologist and expert echocardiographers with a fully equipped echo machine certainly impose additional costs and logistical burdens. Furthermore, the imperceptible difference in attenuation between fat and muscular tissue makes the septum secundum appear as a nearly homogeneous structure. This sequence provides a high signal-to-noise ratio and an optimal blood/myocardial contrast, which allows a precise definition of the endocardial borders. Furthermore, the strength of the signal originating from different tissues in this sequence depends on T1/T2 ratio. Conversely, the muscular tissue has a low T1/T2 ratio and the signal originating from this tissue is weak (represented in the final image in dark gray). The use of a pigtail advanced in the ascending aorta has the advantage of defining with certainty the lowest border of the right aortic sinus and at the same time recording aortic blood pressure. The major tributaries are the lateral veins (anterolateral, midlateral, and posterolateral) and the middle cardiac vein. This latter vein ascends along the interventricular posterior groove parallel to the posterior descending coronary artery. A slight elevation (<3 mm) from the atrioventricular sulcus is present in nearly 10%, a moderate elevation (between 4 and 7 mm) in 50%, and a wide elevation (between 8 and 15 mm) in nearly 20% of the normal hearts. This wall is probably the thinnest area measuring in some areas no more than 2 mm. One of the complications of ablation in this area is injury to the adjacent vessels. The region in between two separate ipsilateral veins is called the intervenous ridge. The pulmonary venous vestibule includes the ipsilateral veins orifices and intervenous ridge. Gadolinium, in fact, does not cross the cellular membrane, remaining in the interstitial space. Due to the reduced clearance and larger interstitial space in the scarred areas, the gadolinium remains entrapped in the regions with fibrosis longer than in the normal myocardium. The presence of gadolinium shortens significantly the local T1 producing a signal of high intensity, which allows a precise delimitation of scarred areas. However, detecting scar in the atrial myocardium remains challenging because thin myocardium produces a low signal-to-noise ratio and scar is less apparent than in the thick ventricular myocardium, making manual quantification highly operator-dependent. Moreover, patients often have an irregular heart rate, making it difficult to acquire good image quality. Nerve bundles, small atrial arteries, and the remnant of the Marshall vein run into the fold. The width of this ridge is not uniform (ranging from 3 to 6 mm) and presents a concave profile with the concavity toward the cavity. The same technique allows precise quantitative measurements either in multiplanar reconstruction. All three imaging techniques are able to illustrate the anatomy of cardiac valves, but each of them has its points of strength and weakness. With this modality, the x-ray source is continuously on, rotating in a spiral fashion around the patient (helical or spiral scanning). This technique has a good temporal resolution, provides a comprehensive evaluation of the valve anatomy with the largest field of view (including also surrounding extracardiac organs and structures), and is not dependent on acoustic windows. In the following paragraphs, we describe the anatomy of the cardiac valves as illustrated by these imaging techniques. A perfect systolic competence of the valve requires a precise temporal and spatial coordination of all the components of the valve apparatus. Any anatomic change or disruption of one or more components inevitably leads to mitral regurgitation. In 1988, Angelini and co-workers found that the arrangement atrial wall-fibrous ring-ventricular wall in the atrioventricular junction is rather rare. Segments of posterior leaflet may therefore be anchored directly to the myocardium without a fibrous support. On the other hand, the anterior annulus described as a fibrous chord that sustains the anterior leaflets does not exist at all. Indeed the anterior mitral leaflet continues imperceptibly with the aortic interleaflet triangle. This anatomic arrangement is known as mitral-aortic continuity, mitral-aortic curtain, or intervalvular fibrosa. At the two ends of this area, near the commissures, two nodules of dense fibrous tissue called trigons delimit the hinge line of the anterior leaflet. A correct definition of the mitral annulus should therefore be the mitral hinge line, which describes the line where both leaflets freely swing regardless if they are anchored on a string of dense connective tissue, directly on the muscular tissue, or connected with the aortic interleaflet triangle. This complex spatial configuration must have had an evolutionary advantage because it is present in all mammals. Moreover, in a saddle-shaped annulus the tension exerted by the intraventricular pressure is equally distributed between anterior and posterior chordae, whereas in a flat annulus the tension should be exerted mainly on anterior chordae. Indeed, the deep incisures (called commissures) that divide the anterolateral (or aortic) leaflet from the posteromedial (or mural) leaflet usually do not reach the annulus, leaving 2 or 3 mm of valvular tissue which ensures the continuity between anterior to posterior leaflet. The posterior leaflet has a more quadrangular shape and covers the remaining two thirds of the annulus.

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Henderson D symptoms narcolepsy mentat ds syrup 100ml discount, Maher M, Johnson D: Pacemaker inhibition due to anodal ring electrode contact. Senzaki H, Kyo S, Matsumoto K, et al: Cardiac resynchronization therapy in a patient with single ventricle and intracardiac conduction delay. Hauser J, Michel-Behnke I, Khazen C, et al: Successful cardiac resynchronization therapy in a 1. Strieper M, Karpawich P, Frias P, et al: Initial experience with cardiac resynchronization therapy for ventricular dysfunction in young patients with surgically operated congenital heart disease. Khairy P, Fournier A, Thibault B, et al: Cardiac resynchronization therapy in congenital heart disease. Jauvert G, Rousseau-Paziaud J, Villain E, et al: Effects of cardiac resynchronization therapy on echocardiographic indices, functional capacity, and clinical outcomes of patients with a systemic right ventricle. Gasparini M, Mantica M, Galimberti P, et al: Is the outcome of cardiac resynchronization therapy related to the underlying etiology Labombarda F, Blanc J, Pellissier A, et al: Health-e-Child project: mechanical dyssynchrony in children with dilated cardiomyopathy. Friedberg M, Silverman N, Dubin A, Rosenthal D: Mechanical dyssynchrony in children with systolic dysfunction secondary to cardiomyopathy: a doppler tissue and vector velocity imaging study. Fauchier L, Marie O, Casset-Senon D, et al: Interventricular and intraventricular dyssynchrony in idiopathic dilated cardiomyopathy: a prognostic study with fourier phase analysis of radionuclide angioscintigraphy. Vogel M, Sponring J, Cullen S, et al: Regional wall motion and abnormalities of electrical depolarization and repolarization in patients after surgical repair of tetralogy of Fallot. Janousek J, Vojtovic P, Hucin B, et al: Resynchronization pacing is a useful adjunct to the management of acute heart failure after surgery for congenital heart defects. Lubiszewska B, Gosiewska E, Hoffman P, et al: Myocardial perfusion and function of the systemic right ventricle in patients after atrial switch procedure for complete transposition: long-term follow-up. Pettersen E, Helle-Valle T, Edvardsen T, et al: Contraction pattern of the systemic right ventricle shift from longitudinal to circumferential shortening and absent global ventricular torsion. Single right ventricles compared with systemic right ventricles in a dual-chamber circulation. Materna O, Kubus P, Janousek J: Right ventricular resynchronization in a child with hypoplastic left heart syndrome. Tzemos N, Harris L, Carasso S, et al: Adverse left ventricular mechanics in adults with repaired tetralogy of Fallot. Amant J, et al: Quality of life in pediatric patients with implantable cardioverter defibrillators. The contribution of new advances has been dramatic in this development, especially over the last 25 years, because of the introduction of electronics and the progress in battery technology. However, the physical structure of the system remained the same: a can containing the battery and the electronic circuit is connected to the heart by one or more leads. The first implantations were surgical with epicardial leads, but the standard procedure fast became endovascular. Since the origins of the art, the implanters have become accustomed to complications related to this hardware, especially those due to the very presence of the case, placed mostly in an infraclavicular subcutaneous position, and those related to the endovenous electrodes. With longer life expectancy, many implanted patients suffer the pangs of chronic complications that are dangerous in themselves and can also affect the success of their treatmentl. Other justifications include the provision of the pacing technique to a larger number of patients. Emerging countries have a very high birth rate and the need for pacemakers will be substantial in the future. In economically developed countries, the population is aging, and pacing indications are also increasing. Therefore solutions that are simpler, less expensive, and quick to set up are needed. This assertion means the development of minimally invasive and safe implant procedures, usable by nonexpert hands in clinics that do not necessarily have high performance equipment. In addition, the proportion of nonresponders to this procedure is far too important and forces us to seek other implantation techniques that are tailored to each patient. However, this line of research is somewhat in contrast with the one of conventional pacing, because the path is much more complex. We must search for and determine the optimal stimulation sites and adapt the implantation technique to each patient. These requirements mean the continuation of intensive research to understand the mechanisms of resynchronization, a research that is far from complete more than 20 years after the first definition of this therapy and its first application. Therefore the objective is different and leads to complex and expensive systems, set up in sophisticated centers, in which we will observe that the energy supply is the most challenging aspect. The first topic will be illustrated by the first data of the validation protocols in progress with leadless pacemakers; the second will explain the principles of cardiac pacing by a capsule receiving its energy from an extrathoracic transmitter. The goal is twofold: diagnostic, to test various pacing modalities before providing implantable cardiac pacing tailored to the individual, and therapeutic, to deliver noninvasive temporary cardiac pacing in emergency situations. This time, the entire system has been redesigned which represents an extraordinary technical and technologic challenge. For a long time, alternative techniques have been sought in order to remove the leads that are at the origin of the most serious long-term complications. Thus as the leads disappear, we must implant the pacemaker directly in contact with the myocardium. The new devices are made of a small cylindrical capsule composed of electronics, a battery, the electrodes, and the fixation system. The miniaturization of the electronic circuit was mandatory and is available today. Space constraints within the capsule required the development of a different way to wind or fold the electronic support. The same applies to communication with the outside, whether this is a programmer for telemetry or a transmitter for telemedicine. The onboard energy is high density, and requires a life at least as long as the one of the conventional pacemakers. The development of those new pacing systems fully benefits from existing advanced techniques sometimes applied to other therapies, such as new materials and processes that allow us to conceive new shapes and fixations applicable to our devices. To implant the prosthesis into the ventricle means the development of new delivery systems. Several transcutaneous therapies have already forced the development of similar systems such as the implantation of a left atrial appendage occluder for permanent foramen ovale or of percutaneous heart valves. The concept is not new, since William Spickler in 19709 described what we have in hand today, including the method to implant the system. It took 45 years for the technology to make available this revolutionary concept, according to current specifications. The fixation mechanism for the Nanostim is a helix and four electrically inactive protractable nitinol tines for Micra. They include a docking button that allows attachment of the device to the catheter for delivery, repositioning, and retrieval. The steroid eluting tip electrode is made of titanium nitride coated platinumiridium and has a surface area of 2 to 2. A dedicated programmer communicates with Nanostim by wireless telemetry, for interrogation and programming. Signal transmission from the programmer to the implanted Nanostim is accomplished by applying subliminal 250-kHz pulses to the skin electrodes. Except for this special type of signal transmission, the programmer obeys the same operating principles as conventional pacemaker programmers. For Micra, the conventional programmer is used with communication through the programmer header. The delivery systems include a steerable catheter with a protective sleeve designed to protect the fixation hardware. Delivery is accomplished by rotation of the Nanostim to secure the helix in the myocardium, and by a simple push of the Micra to engage the tines into the myocardium. Then both devices are undocked from the delivery catheter, but still maintaining a link to the device with a tether when thresholds are measured, without the catheter applying forces to the device. To release the device, the tether is disconnected (Nanostim), or cut (Micra), and removed. Given the structure of these systems and their implementation mode, what can we expect from this new therapeutic modality Only the test of time will accurately determine the benefits and risks of this new method.