A: Identical His potentials are clearly seen from the ablation catheter (retrograde approach through the aortic valve) and from the His catheter (in a usual position) just prior to initiation of cryomapping discount 140mg malegra fxt erectile dysfunction nursing interventions. Other minor complications have included Doppler detectable increases in valvular regurgitation discount malegra fxt uk erectile dysfunction treatment aids, minor vascular injury trusted 140mg malegra fxt new erectile dysfunction drugs 2014, and minor skin burns at the reference electrode skin site (5,21). Follow-up studies have revealed no evidence of new coronary arterial abnormalities by traditional angiography at 1 to 6 months postablation (5,170), and no significant increase in ventricular arrhythmias as late as 2 to 3 years. Importantly, however, acute coronary arterial injury may not resolve (127) and animal studies have revealed coronary intimal thickening in arteries near the ablation site (66,131). Also, the increasing prevalence of adults with congenital heart disease provides a potential change in patient population and arrhythmia substrate. Finally, the pronounced growth of quality improvement aspects to all aspects of medical practice has prompted new approaches to data elements, analysis and patient- centered care. The initial goal was to create a registry upon which meaningful ongoing quality improvement and research will be conducted. One of the patient-centered outcome measures will be a symptoms severity survey as a basic outcome measure. Following the trend of other modern procedural registries, a clinical complexity score for electrophysiology procedures will be included. Special Considerations for Pediatrics Age (Infants) There are three special considerations in infants which make their management different from the older patient when considering catheter ablation. Finally, the known risks of any catheterization, combined with the specific risks of catheter ablation in this age group (58,62,273,274,275), suggest that pharmacologic control should be aggressively pursued prior to ablation. In humans, myocardial cell division probably occurs through approximately 6 months of age (276). In addition, in contrast to mature ablation scars from adult animals, late lesions from the neonatal lambs and swine often were invasive and poorly demarcated histologically from the surrounding tissue (65,116). An echocardiogram from the infant at the time of a brief resuscitation, and autopsy findings, revealed relatively large lesions extending into the left ventricle from the intended mitral groove ablation site. Although most reports of coronary arterial damage have been limited to the posterior septum or a nondominant right coronary artery (66,67,69), complete occlusion of the left circumflex artery has been reported in a 5-week-old, 5. Until accurate methods are available to assess lesion size in real time, alternative methodologies should be used in all infants. Data on the effects of cryotherapy suggest that this form of energy may be much less harmful to coronary arteries, even when in very close contact (101,111,280), due to the differing effects of cold and heat on connective tissue and the vascular inflammatory response. The future development of real-time ultrasonographic or other modality monitoring of lesion size may also help reduce the procedural risks (283). Size Patient size by itself does not appear to affect the success rate of catheter ablation, but has distinctly influenced the catheter approach, and was a determinant of procedure and fluoroscopy times in the pediatric ablation registry (284). Most clinicians, including our own groups (5), have worried about producing inadvertent ventricular lesions and have found that manipulation of the ablation catheter inside small ventricles is more difficult, leading to the use of the transseptal approach to all left-sided pathways, as described above. Regardless of the technique that is used first, it is always important for the electrophysiologist to consider switching techniques during the procedure if success is not being achieved. Options such as the use of a sheath, or a change in the sheath, catheter or approach should all be considered when the desired result is not forthcoming. Preexcitation Syndromes in Patients with Structural Congenital Heart Disease Though not only a pediatric issue, the combination of structural heart disease and arrhythmias will clearly be encountered often by the pediatric electrophysiologist, occurring in approximately 10% of ablation cases (284,290). Of course, preexcitation also occurs in other patients with congenital heart disease, but with an incidence not statistically higher than the general population. The mitral valve and the anterior leaflet of the tricuspid valve are fully delaminated early in development; however, the posterior and septal leaflets of the tricuspid valve are not even fully formed by 3 months of gestation (295). Ebstein disease appears to occur when there is arrested development of tricuspid valve formation sometime between delamination of the anterior and the posterior leaflets. In fact, multiple pathways are common in these patients, often with a combination of a posteroseptal pathway and one or more additional freewall pathways. However, the physiologic and clinical implications of the tachycardia may be markedly different in patients with congenital heart disease. Abnormal hemodynamics, increased incidence of isolated atrial and ventricular ectopy, sometimes poor tolerance of antiarrhythmic therapy, and the need for surgical repair which accompanies congenital heart disease all contribute to an increased need for aggressive arrhythmia management in this patient population. However, abnormal anatomy and atypical conduction systems may also enhance the difficulty and risks of either surgical or catheter ablation. Multiple pathways are extremely common in this group, occurring in 30% to 80% of patients (170,296,297,298,300) compared with 5% to 10% of patients without congenital heart disease (170,195,301,302,303). Some aspects of the procedure in patients with Ebstein malformation are of special note. Use of a right coronary electrode wire can be considered (301,307), but may be difficult due to a diminutive right coronary artery, and may need to be in place for long periods when multiple pathways are present. A safer recommended alternative is continual display of the relevant coronary angiogram using a real-time biplane image storage and display system. Catheter stabilization for freewall pathways in the largest hearts is difficult and is not sufficiently improved through the use of a long sheath or a variety of approaches (5) (see prior section). One observation that is difficult to prove statistically is that the smaller chamber size in smaller patients with structural heart disease is a technical asset in catheter ablation. Electrograms A through F were recorded with the distal pair of an ablating catheter very near the point of successful ablation shown in F. Electrograms in D and E were not significantly different, but E had transient success. F, the point of permanent success, probably has the earliest activation, however, the differences are much clearer in retrospect. As expected, it appears to be impossible to approach the ventricular side of the tricuspid valve in patients with Ebstein malformation. No specific reports have noted the use of nonstandard ablation technologies for the patient with this condition, but a few observations can be made. Consequently, despite the tendency to use higher-power active or passive cooling ablation systems for difficult cases, such technologies should only be employed when an adequate distance between the catheter tip and the artery has been documented. The definition of “adequate” depends on the size of the nearby coronary artery—the larger the size, the safer the ablation. Furthermore, strong consideration should be given to the use of cryotherapy, at least as a mapping tool. Safety will be enhanced and adhesion of the catheter may be particularly useful in the larger patients. When multiple pathways are present, persistence may be the electrophysiologist best weapon for successful ablation. However, recurrence rates have been reported to be as high as 40%, particularly if multiple pathways are present (170,193,297,298). The decapolar catheter (bottom white arrow in B) was advanced from the left-sided inferior vena cava across the mitral valve and positioned with the second pair of electrodes at the His bundle. The mapping catheter (black arrow in A, upper white arrow in B) was advanced from the inferior vena cava across the atrial septum to the right-sided (anatomic) left atrium and positioned at the location of the accessory pathway, which in this case was at the superior and anterior portion of the left-sided tricuspid valve.
Each aortic valve cusp is traditionally referred to according to its corresponding sinus of Valsalva purchase malegra fxt 140 mg on line erectile dysfunction without pills, that is cheap malegra fxt 140mg line erectile dysfunction drugs lloyds, as the right-coronary discount malegra fxt 140mg mastercard erectile dysfunction in 40s, left- coronary, or noncoronary artery cusp (Fig. Autopsy studies have revealed that while cusps are generally similar in size to each other, there is often minor variation in cusp size within a “normal” valve (24). Each aortic valve cusp is composed of three layers of extracellular matrix surrounded by a thin layer of valve endothelial cells (19). The first layer beneath the endothelium on the aortic surface of the valve is the fibrosa, which is comprised of fibroblasts and circumferentially arranged collagen fibers. In between the fibrosa and the ventricularis is the spongiosa, a compressible layer of fibroblasts, proteoglycans, and mesenchymal cells. By far the most common congenital abnormality of the aortic valve is partial or complete fusion of two of the valve cusps, P. In 95% of cases, the cusps of a bicuspid valve are unequal in size (25), with a raphe frequently present in the larger, fused cusp (Fig. In most instances (70% to 85%) fusion occurs between the right- and left-coronary cusps (8,25,26). Fusion between the right and the noncoronary cusp is next most common, while fusion between the left and the noncoronary cusp is quite rare. A bicuspid valve is most often hemodynamically insignificant at birth, and only ∼2% of bicuspid valves develop clinically significant stenosis or insufficiency by adolescence (27). The development of clinical disease is correlated with valve cusp morphology, with fusion of the right and noncoronary cusps entailing more than twice the risk of significant aortic stenosis or insufficiency compared to the more common intercoronary cusp fusion (8). Much less common than a bicuspid aortic valve is a unicuspid aortic valve, characterized by complete or partial fusion of two (unicuspid, unicommissural) or all three commissures (unicuspid, acommissural) (28). In cases of a unicuspid, unicommissural valve, a single, posteriorly oriented commissure is most commonly seen (Fig. Not surprisingly, given the more abnormal valve morphology, unicuspid aortic valves tend to develop clinically significant disease earlier in life compared with bicuspid valves (30) and are often seen in cases of severe, ductal-dependent aortic stenosis during the neonatal period. Regardless of cusp number, valvar aortic stenosis is generally due to incomplete opening of a “doming” valve resulting in a reduced effective valve orifice (Fig. This is generally seen in the setting of additional left-sided anomalies along the spectrum of hypoplastic left heart syndrome. Calcific aortic stenosis, of either bicuspid or tricuspid aortic valves, is a common disease in adulthood but rarely seen in pediatric patients. Calcification of a bicuspid aortic valve does not generally begin until the fourth decade of life, while sclerosis can be seen as early as the second decade in otherwise asymptomatic valves (31). In the most common cases, there is fusion of the right (R) and left (L) coronary cusps with a thickened raphe at the site of the intracoronary commissure. The patient is a 3-year-old girl with Turner syndrome status post coarctation repair. Dilation of the ascending aorta or aortic root is commonly seen in association with bicuspid aortic valves with or without significant stenosis (Fig. At least mild dilation of the ascending aorta occurs in approximately 50% of pediatric and young adult patients with a bicuspid aortic valve, while at least mild dilation of the aortic root is found in 22% of this population (32). Moderate or severe dilation of the ascending aorta or aortic root is present in 16% and 5% of the patients, respectively. Significant stenosis does not appear to increase the risk of significant aortic dilation, and in fact, valves with moderate or greater aortic stenosis have been associated with less dilation of the aortic root than those with milder stenosis (32). The patient is a 22-year-old young man with a bicuspid aortic valve status post surgical valvotomy. Valvar aortic stenosis is associated with additional anomalies in up to 25% of published cases series, with coarctation of the aorta, patent ductus arteriosus, and ventricular septal defect being the most common (33). The association between coarctation of the aorta and bicuspid aortic valve has been well described, with a bicuspid valve being identified in 20% to 85% of cases of isolated coarctation (31). Concentric left ventricular hypertrophy is the physiologic response to left ventricular outflow tract obstruction, and is often observed in association with hemodynamically significant stenosis. In cases of severe neonatal aortic stenosis, obstruction to left ventricular outflow in utero often leads to the development of endocardial fibroelastosis, a diffuse thickening and scarring of the left ventricular endocardium (34,35). The thin membrane, indicated with an arrow, is located 3 mm below the aortic valve. Subvalvar Aortic Stenosis The pathology of subvalvar aortic stenosis is polymorphic in nature. The most common form, accounting for 70% to 80% of cases, is membranous subaortic stenosis, characterized by a thin, fibrous membrane just proximal to the aortic valve (Fig. The membrane is generally very thin (1 to 2 mm), located within several millimeters of the aortic valve, and is often circumferential, including attachments to the anterior leaflet of the mitral valve (12,13,35). The second most common type of subaortic stenosis involves a fibromuscular ridge, thicker than the membrane and frequently located slightly more inferior to the aortic valve (Fig. Both of these types of discrete subaortic stenosis are rarely present in infancy and are often considered acquired conditions. While their pathogenesis is incompletely understood, there is evidence that certain anatomic substrates create abnormal flow patterns and shear stresses within the left ventricular outflow tract that lead to endothelial damage, cellular proliferation, and collagen deposition resulting in the formation of the fibrous membrane or ridge. An abnormally small angle between the muscular and conal septae may also be a contributing factor to the necessary abnormalities in flow, and the presence of a perimembranous ventricular septal defect likely also predisposes to membrane formation (38,39,40,41,42). As the fibrous deposition becomes prominent enough to cause significant obstruction, the resultant left ventricular hypertrophy can cause the septum to further impinge on the left ventricular outflow tract leading to a self-sustaining cycle of obstruction and hypertrophy. The patient is a 4-year-old boy with a bicuspid aortic valve, history of coarctation repair, and prior resection of a thin, subvalvar membrane. The patient is a 13-year-old girl with a history of previous subaortic stenosis resection. On the most severe end of the subaortic stenosis disease spectrum is “tunnel-type” obstruction, characterized by muscular hypertrophy and narrowing of the left ventricular outflow tract that extends for several centimeters below the valve (Fig. While tunnel type obstruction can present de novo (12,13), it is most commonly diagnosed in patients who have undergone prior congenital heart surgery (44). The most common primary diagnosis was double outlet right ventricle, while interrupted aortic arch, membranous subaortic stenosis, and Shone complex were also significant contributors. As with membranous subaortic stenosis, it is likely that abnormal flow patterns and shear stresses caused by even mild residual postoperative subaortic obstruction result in proliferation and hypertrophy leading to the tunnel-like obstruction. It may be that anatomic narrowing of the left ventricular outflow tract, as with posterior deviation of the infundibular ventricular septum in patients with interrupted aortic arch, may predispose to long segment stenosis as opposed to the more common discrete membranous stenosis. Decreased effective size of the ventricular septal defect, related either to shrinkage of intracardiac baffle material or fibrous deposition within a baffle, has also been proposed as an etiology of left ventricular outflow tract obstruction after repairs requiring construction of a left ventricle to aorta baffle (45). Other etiologies of subaortic obstruction include anomalous insertions of mitral valve chordae or accessory atrioventricular valve tissue (often in the setting of a cleft mitral valve or complete atrioventricular septal defect), the left ventricular outflow tract “goose-neck deformity” P. Another important associated finding is aortic insufficiency, which develops in up to 70% of patients with subaortic stenosis over time (36,48) ( Videos 44. While in some cases aortic insufficiency is related to previous balloon or surgical intervention on the aortic valve (37), insufficiency may also develop in patients with isolated, discrete subvalvar stenosis (13,49). In these cases, the aortic regurgitation may be secondary to valve damage from long-standing exposure to the high-velocity jet caused by the subvalvar membrane. Consistent with this hypothesis, a higher peak echocardiographic Doppler gradient is the strongest independent risk factor for aortic insufficiency in patients with discrete subvalvar stenosis (37).
Cardiac magnetic resonance imaging for accurate diagnosis of aortic arch anomalies in patients with 22q11 order malegra fxt 140mg with amex erectile dysfunction treatment testosterone replacement. Williams-Beuren syndrome: a 30-year follow-up of natural and postoperative course discount 140mg malegra fxt overnight delivery erectile dysfunction facts. Three decades of follow-up of aortic and pulmonary vascular lesions in the Williams-Beuren syndrome discount malegra fxt impotence beavis and butthead. The elastin gene is disrupted by a translocation associated with supravalvular aortic stenosis. Elastin point mutations cause an obstructive vascular disease, supravalvular aortic stenosis. An elastin gene mutation producing abnormal tropoelastin and abnormal elastic fibres in a patient with autosomal dominant cutis laxa. High frequency of submicroscopic genomic aberrations detected by tiling path array comparative genome hybridisation in patients with isolated congenital heart disease. Cryptic chromosomal abnormalities identified in children with congenital heart disease. De novo copy number variants identify new genes and loci in isolated sporadic tetralogy of Fallot. Arteriohepatic dysplasia: familial pulmonary arterial stenosis with neonatal liver disease. Hepatic ductular hypoplasia associated with characteristic facies, vertebral malformations, retarded physical, mental, and sexual development, and cardiac murmur. Cytologically balanced t(2;20) in a two-generation family with alagille syndrome: cytogenetic and molecular studies. Deletions of 20p12 in Alagille syndrome: frequency and molecular characterization. Construction of an integrated physical and gene map of human chromosome 20p12 providing candidate genes for Alagille syndrome. Outcomes of liver transplantation for patients with Alagille syndrome: the studies of pediatric liver transplantation experience. Vascular anomalies in Alagille syndrome: a significant cause of morbidity and mortality. The clinical and genetic spectrum of the Holt-Oram syndrome (heart-hand syndrome). Chamber-specific cardiac expression of Tbx5 and heart defects in Holt-Oram syndrome. Holt-Oram syndrome is a genetically heterogeneous disease with one locus mapping to human chromosome 12q. Protein-tyrosine phosphatase, nonreceptor type 11 mutation analysis and clinical assessment in 45 patients with Noonan syndrome. Phenotypic and genotypic characterisation of Noonan-like/multiple giant cell lesion syndrome. Congenital heart disease and other heterotaxic defects in a large cohort of patients with primary ciliary dyskinesia. Novel copy-number variants in a population-based investigation of classic heterotaxy. Infants of diabetic mothers are at increased risk for the oculo-auriculo-vertebral sequence: A case-based and case-control approach. A mouse model of human congenital heart disease: high incidence of diverse cardiac anomalies and ventricular noncompaction produced by heterozygous Nkx2–5 homeodomain missense mutation. Temporal variability in birth prevalence of congenital heart defects as recorded by a general birth defects registry. Total is more than the sum of the parts: phenotyping the heart in cardiovascular genetics clinics. A population-based study of extra-cardiac anomalies in children with congenital cardiac malformations. Goodwin Introduction The structure and function of the myocardium undergoes dramatic changes during fetal life and in postnatal maturation to adulthood. The postnatal period is marked by extensive physiologic and metabolic remodeling with dynamic changes as the fetal heart adapts to birth and converts to adult function (1). These processes are regulated by a number of hormones, neurotransmitters, growth factors, and mechanical forces. The coronary circulation is tightly coordinated with myocardial growth to ensure an adequate supply of oxygen and metabolic substrates. A complete understanding of the physiologic processes that regulate myocardial structure and function is a necessary prerequisite to understand the pathogenesis of congenital and acquired heart disease. While Chapter 1 in this volume provides a comprehensive discussion of the molecular and genetic determinants of heart development, this chapter describes the developmental and postnatal changes in cardiac structure, metabolic regulation, excitation– contraction (E-C) coupling, and growth/regeneration. Postnatal changes in hemodynamic load, autonomic innervation, and hormonal status are summarized. The effects of these changes on myocardial systolic and diastolic dysfunction are also discussed. The majority of studies on developmental changes in myocardial structure and function has been performed in zebrafish, chick embryos, and rodents, with some additional data taken from higher mammals and humans. While the process of E-C coupling is very similar, there is significant spatiotemporal variability in structural development among the different model species. Unless otherwise noted, the majority of the developmental changes described in this chapter will focus on data from rodent models and humans. Myocardial Structure The heart begins functioning as a simple tube composed of only cardiac myocytes and endocardial cells. However, it quickly becomes a complex organ comprising multiple cell types that can be grouped into conducting, supporting, and functional cells (Fig. The cellular constituents of the heart include cardiac myocytes, cardiac fibroblasts, endothelial cells, and vascular smooth muscle cells. The sinoatrial nodes are specialized myocytes responsible for action potential generation. The conducting cells, also derived from cardiac myocytes are mainly Purkinje fibers. While cardiac myocytes are responsible for the mechanical function of the heart, they comprise only ∼30% of the total number of cells. Cardiac fibroblasts predominate in conferring structural integrity to the heart (5). Cardiac Fibroblasts and the Extracellular Matrix The cardiac fibroblast is the most abundant cell type present within the postnatal mature heart. Cardiac fibroblasts are derived from different cell lineages at different developmental stages.
Diastole is defined as the time between aortic valve closure (arrow 140mg malegra fxt with visa erectile dysfunction drugs in bangladesh, top left) and mitral valve closure (arrow purchase 140 mg malegra fxt overnight delivery erectile dysfunction treatment ayurvedic, bottom right) cheap malegra fxt 140mg mastercard erectile dysfunction causes diabetes. The timing and rate of ventricular relaxation are dependent on preload, afterload, myocardial relaxation, and 2+ mechanical synchrony. Development of the sarcoplasmic reticulum and calcium handling in the myocyte is an age-dependent process that is relatively immature in the fetus and neonate. Age will therefore impact the rate of ventricular relaxation and the observed Doppler variables describing this phenomenon (61). The rate of relaxation will also be influenced by the degree of systolic shortening in the preceding cardiac cycle as well as by elastic recoil in early diastole from forces created in systole. In addition, the myocardium has viscous properties that require greater force to induce rapid expansion than more gradual expansion. These properties are likely most important when rapid filling occurs in early diastole and during atrial systole. Passive filling is impacted by atrial pressure, heart rate, and the elastic properties of the ventricle. The degree of ventricular filling during atrial systole is further modified by ventricular compliance and atrial function. In turn, ventricular filling pressures are influenced not only by ventricular or myocardial properties, but by a variety of additional factors. This complicates isolated assessment of ventricular and myocardial diastolic properties by echo. Therefore, growth and its associated change in heart rate will influence diastole and its assessment by echo. Using Doppler echocardiography, they demonstrated that diastolic dysfunction occurred in progressive sequence that could be characterized by Doppler echocardiography analysis of transmitral and pulmonary venous flow profiles. In adults, ventricular diastolic dysfunction has been classically described as progressing along a spectrum of increasing severity, divided into three main stages. In mild (stage I) diastolic dysfunction, the predominant abnormality is impaired ventricular relaxation. A fourth stage of irreversible restrictive physiology is also considered and portrays worse prognosis. Whether this paradigm of progressive diastolic worsening through these defined stages holds true for children is still under investigation. Our impression is that it is less common to see isolated stage 1 diastolic dysfunction in children, except in specific circumstances such as some children with ventricular hypertrophy secondary to hypertrophic cardiomyopathy or systemic hypertension (67,68). Rather, we often note concomitant abnormalities of relaxation and compliance, with predominance of decreased compliance. Nonetheless, the adult paradigm of staged progression currently provides the best working framework to assess and report diastolic dysfunction and its severity (69). As no single echo index adequately describes diastolic dysfunction, a comprehensive examination is needed incorporating multiple parameters with interpretation and integration of the information by the echocardiographer. Transmitral Doppler Flow Evaluation Transmitral flow is obtained using a 1- to 2-mm pulsed Doppler sample placed between the tips of the mitral leaflets. Therefore, an increase or decrease in filling pressures will shorten or lengthen the E-wave deceleration time, respectively. E-wave deceleration occurs after most early filling has occurred and is largely influenced by ventricular compliance. After cessation of the E wave, there is a period of diastasis (“separation” in ancient Greek), where little or no flow is seen. Although not commonly assessed, some authors advocate for measurement of the mitral flow velocity at the onset of atrial contraction. This “E at A” velocity affects the peak velocity and duration of the mitral A wave and hence important parameters such as the E/A ratio, the duration of pulmonary A-wave reversal relative to mitral A-wave duration. Due to the fast heart rate, there is no diastasis and the E and A waves begin to overlap. This is the point where the E and A waves merge when the E wave does not reach the baseline. In adults, a reduced S wave compared to the D wave would be abnormal and suggestive of delayed relaxation. The duration and peak velocity of this flow reversal are measured as indirect indicators of ventricular compliance. Pulmonary Venous Doppler Flow Analysis Pulmonary venous flow is usually assessed from the apical four-chamber view by placing a 5-mm pulsed Doppler sample volume in the right pulmonary vein. The pulmonary venous flow features a low velocity phasic flow pattern consisting of a systolic S wave, an early diastolic D wave, and a late diastolic reversal during atrial systole (A-wave reversal). During a comprehensive diastolic function assessment, the peak S- and D-wave velocities and the duration and peak velocity of the pulmonary venous A wave are measured, and the S-wave/D- wave velocity ratio is calculated (Fig. Of these, the duration of the A-wave reversal relative to the mitral inflow A-wave duration is considered most useful as an indicator of ventricular compliance and reflects filling pressures in adults and in children (70). Of note, in the largest study of pediatric echo Doppler diastolic values to date, a small, but important, number of normal children were found to have increased duration of pulmonary vein A-wave reversal (70). Data in healthy infants and young children are limited to a small number of children (71). This is in contrast to blood flow velocities, for which high-velocity and low-amplitude signals require different Doppler settings (Fig. Color tissue Doppler is derived from mean velocities and values are approximately 20% lower than the peak values depicted by pulsed tissue Doppler. Color (A) and pulsed (B) tissue Doppler sampled at the basal interventricular septum. Note that tissue velocity directions are a mirror image of atrioventricular valve inflow. Typically, the peak tissue E-wave (Ea[E′]) and A-wave (Aa[A′]) velocities are measured. While the peak E′/A′-wave velocity ratio can be calculated, most research has focused on the utility of the early diastolic velocity (E′). Tissue velocities are influenced by afterload, and although they are also influenced by preload, they are less so than mitral inflow velocities. As abnormal loading is a hallmark of many types of congenital heart disease, thereby complicating interpretation of diastolic function through mitral inflow patterns alone, tissue Doppler velocities may play a useful adjunctive role. However, it should be noted that tissue Doppler velocities are less influenced by loading when ventricular relaxation is impaired. In the presence of normal relaxation, loading will have a greater influence on diastolic tissue velocities. In adults, of all echo indices, E′ is one of the best discriminators between normal and abnormal. It should also be remembered that the E′ is sampled at a specific location, but is used to reflect on “global” ventricular properties, which may not hold true in all individuals. High temporal resolution ensures that peak velocities are captured even when heart rates are high. Measurement of longitudinal velocities partly overcomes tethering effects as longitudinal motion is less affected by tethering. These characteristics should be taken into account when interpreting E′ peak values in children.
V. Steve. Millersville University.