Atrial Component Research Articles

SECOND CARDIAC SOUND ANALYSIS TECHNIQUES AND PERFORMANCE COMPARISON

This paper presents the applications of the spectrogram, Wigner distribution and wavelet transform analysis methods to the second cardiac sound S2 of the phonocardiogram signal (PCG). A comparison between these methods has shown the resolution differences between them. It is found that the spectrogram Short-Time Fourier Transform (STFT) cannot detect the two internals components of the second sound S2 (A2 and P2, atrial and pulmonary components respectively). The Wigner Distribution (WD) can provide time-frequency characteristics of the sound S2, but with insufficient diagnostic information as the two components (A2 and P2) are not accurately detected, appearing to be one component only. It is found that the wavelet transform (WT) is capable of detecting the two components, the aortic valve component A2 and pulmonary valve component P2, of the second cardiac sound S2. However, the standard Fourier transform can display these components in frequency but not the time delay between them. Furthermore, the wavelet transform provides more features and characteristics of the second sound S2 that will hemp physicians to obtain qualitative and quantitative measurements of the time-frequency characteristics.

Participation of the Atrial Components of a Dual-Chamber Cardiac Pacemaker During Ventricular Pacing

A 70-year-old man with coronary artery disease, chronic atrial firillation, and cardiomegaly was scheduled for redo coronary bypass urgery. His initial heart rate was 38 beats/min. Because of the bradyardia and the epicardial scarring expected from the previous surgery, pacing probe was made ready in the right ventricular channel of a aceport pulmonary artery catheter (Edwards Lifesciences, Irvine, CA) nserted via the right internal jugular vein.4,5 After surgical revascularzation (performed with cardiopulmonary bypass and hypothermic poassium cardioplegia), the patient underwent electrical defibrillation, hich restored sinus rhythm with first-degree atrioventricular block. he surgeon attached pairs of epicardial pacing wires to the right trium and the right ventricle. After chest closure, the patient’s rhythm everted to atrial fibrillation. Subsequently, the thresholds for the epiardial ventricular pacing wires increased and then failed to capture at he maximal output (25 mA) of the temporary pacemaker (Medtronic 388, Minneapolis, MN). The endocardial ventricular pacing probe was dvanced 4 cm from its channel, and transvenous pacing was successully instituted with the Medtronic 5388 pacemaker programmed to eliver 15 mA ventricular pulses at 80 beats/min in the demand mode VVI). Interestingly, both demand (VVI) and asynchronous (VOO) transenous ventricular pacing failed whenever the epicardial atrial wires ere detached from the pulse generator. Even though the atrial ortion of the dual-chamber pacer was turned “off,” the atrial ystem participated in ventricular pacing (Fig 1). The circuit is iagrammed in Figure 2. The epicardial atrial wires were no longer required for ventricular acing when the endocardial ventricular pacing probe was advanced to rotrude 6 cm, instead of 4 cm, from the Paceport catheter. The aceport probe is comprised of 2 wires, one of which projects farther han the other. Advancing the probe enabled both wires to make contact ith the right ventricular endocardium. With both Paceport wires in ontact with the right ventricular endocardium, attached atrial wires ere not required for ventricular pacing. However, when only the distal ire of the Paceport probe made contact with the ventricular endocarium, then an effective ventricular pacing circuit was completed by eans of the epicardial atrial wires and the atrial portion of the ual-chamber pacer. By means of an oscilloscope (Tektronix digital model 2430, Beaerton, OR), this unconventional pacing possibility was duplicated in he laboratory. A 500-ohm resistor was run from the V pole of the ulse generator to either the V pole or the A pole. The pacemaker as set to deliver 15 mA pulses at 80/min in the VVI mode, and the otential difference across the resistor was tracked in time. Four edtronic 5388 pacemakers were examined. As expected, the V V rrangement produced strong electrical pulses. The amplitudes were .62 0.12 V, and the widths were 1.52 0.02 milliseconds. Howver, the V A arrangement also produced significant pulses (0.58 .04 V and 1.51 0.04 milliseconds). Significant pulses were also etected in a V A arrangement at higher amperage, but significant ulses were not detected in V A or in V A situations. p

Reconstruction of the Patterns of Gene Expression in the Developing Mouse Heart Reveals an Architectural Arrangement That Facilitates the Understanding of Atrial Malformations and Arrhythmias

Firm knowledge about the formation of the atrial components and of the variations seen in congenital cardiac malformations and abnormal atrial rhythms is fundamental to our understanding of the normal structure of the definitive atrial chambers. The atrial region is relatively inaccessible and has continued to be the source of disagreement. Seeking to resolve these controversies, we made three-dimensional reconstructions of the myocardial components of the developing atrium, identifying domains on the basis of differential expression of myocardial markers, connexin40, and natriuretic precursor peptide A. These reconstructions, made from serial sections of mouse embryos, show that from the outset of atrial development, the systemic and pulmonary veins are directly connected to the atrium. Relative to the systemic junctions, however, the pulmonary venous junction appears later. Our experience shows that three-dimensional reconstructions have three advantages. First, they provide clear access to the combined morphological and molecular data, allowing clarification and verification of morphogenetic concepts for nonmorphological experts and setting the scene for further discussion. Second, they demonstrate that, from the outset, the myocardium surrounding the pulmonary veins is distinct from that clothing the systemic venoatrial junctions. Third, they reveal an anatomical and molecular continuity between the entrance of the systemic venous tributaries, the internodal atrial myocardium, and the atrioventricular region. All these regions are derived from primary myocardium, providing a molecular basis for the observed nonrandom distribution of focal right atrial tachycardias.

Atrial extracellular matrix remodeling and the maintenance of atrial fibrillation.

Remodeling occurs in both ventricle and atrium in dilated cardiomyopathy and heart failure. However, the alteration of atrial extracellular matrix components during remodeling and its effect on the electrical remodeling and atrial arrhythmia have never been explored. Atrial tissue samples of 53 explanted hearts from patients with dilated cardiomyopathy and end-stage heart failure who underwent heart transplantation were examined. Nineteen patients had permanent atrial fibrillation (PmAF), 18 had persistent AF (PsAF), and 16 had no documented AF (NAF). Sixteen donor left atria (LA) were used as controls (CNs). Western Blot analysis revealed a selective downregulation of tissue inhibitor of metalloproteinase (TIMP)-2 in PmAF and PsAF groups compared with the NAF and CN groups and an upregulation of atrial metalloproteinase (MMP)-2 that was most pronounced in the PmAF group followed by the PsAF and NAF groups. Immunofluorescent staining revealed that in the LA, type I collagen volume fraction (CVF-I) increased significantly in the PmAF group followed by the PsAF and NAF groups compared with that in CN. LA CVF-I significantly correlated with LA dimension and TIMP-2 to MMP-2 ratio. In the PsAF group, CVF-I/CVF-III ratio was significantly correlated with AF duration and the frequency of AF recurrence. Atrial extracellular matrix remodeling manifested by the selective downregulation of TIMP-2 along with upregulation of MMP-2 and CVF-I in the atrium is associated with the development of sustained atrial fibrillation in patients with cardiomyopathy and heart failure.

ANATOMY OF THE ATRIOVENTRICULAR NODE AND ATRIOVENTRICULAR CONDUCTION SYSTEM

The anatomy of the atrioventricular conduction system was first described nearly a hundred years ago. Since then, it has been an occasional subject of controversy mainly through a lack of adherence to the original definitions based on histology. The gross landmarks for locating the atrial component of the conduction system are found in the right atrium. The components and structure of the system in human are comparable to that found in commonly used laboratory animals. The conduction system is composed of specialized myocytes. Its atrial component, the atrioventricular node, is in contact with atrial myocardium. Having penetrated the atrioventricular insulating plane, the major ventricular bundles are encased in fibrous sheaths that separate the specialized myocytes from the ordinary myocardium. Only at the distal ramifications of the bundle branches do the fibrous sheaths disappear, allowing continuity with ventricular myocardium. Being the only muscular pathway connecting atrial with ventricular myocardium, knowledge of its structure can help in developing potential therapies for some forms of cardiac arrhythmias.

664 Early diastolic filling dynamics in patients with diastolic dysfunction

0.66, p< 0.05). The normal group did not show a correlation between the acceleration of transmitral flow and mitral annular relaxation velocity (r=0.18, p < 0.22). Those with diastolic dysfunction also had a lower E/A ratio than the normal group (0.7 ± 0.2 vs. 1.9 ± 0.5, p < 0.001), a higher time-velocity integral of the atrial component (11.7 ± 3.2 cm vs. 5.5 ± 2.1 cm, p < 0.0001) and a lower rate of acceleration of blood across the mitral valve (549.2 ± 151.9 cm/sec2 vs. 871 ± 128.1cm/sec2 ,p <.001). Conclusions In diastolic dysfunction where the influence of preload is minimal, recoil and the acceleration of early diastolic blood flow are reduced compared to normals. Also the rate of flow across the mitral valve was found to be strongly related to mitral annular tissue velocity. This relationship reveals the influence of recoil on flow in diastolic dysfunction. However in normal subjects the acceleration of early diastolic blood flow and recoil are not correlated. Recoil in normal provides the potential energy for rapid early diastolic filling and occurs during isovolumic relaxation before filling. Therefore rapid early diastolic filling under the influence of preload occurs after isovolumic relaxation and no relationship exists. This supports the existence of an early diastolic mechanism in normal.

The annular fat stripe as a fluoroscopic guide to anatomic sites during diagnostic and interventional electrophysiology studies.

Few radiographic landmarks are visible during electrophysiology procedures to aid in catheter positioning other than the catheters themselves. In the 35 degrees -45 degrees RAO projection, a linear radio-opacity corresponding to the rings of fat surrounding both annuli can be easily identified. This "fat stripe" can serve as a useful landmark for several important anatomic sites. Intracardiac catheters positioned left of (posterior) the fat stripe lie within an atrial cavity while those positioned to the right (anterior) lie within a ventricular cavity. The superior third of the stripe corresponds to the region of the right and left atrial appendages while the inferior end identifies the site of the coronary sinus os. The middle third serves as a reference for the fast AV nodal pathway and compact AV node. The region corresponding to the slow AV nodal pathway superimposes on the lower third of the fat stripe. Electrophysiological recordings from catheters positioned along the fat stripe always exhibit both an atrial and ventricular component consistent with an annular recording, whether the catheter is septal or free wall in its location. Coronary sinus os engagement and catheterization can be simplified by using the fat stripe as an anatomic guide. In addition to facilitating catheter positioning for evaluating normal AV conduction, the fat stripe can serve as an excellent guide for targeting the majority of structures intended for ablation because of their annular location. These include the compact AV node, the slow AV nodal pathway, the subeustachian isthmus and any accessory pathway. Good ablation catheter tip contact with annular structures is confirmed by observing its movement in unison with the fat stripe.

Molecular diversity of the developing and adult myocardium: implications for tissue targeting.

The heart is the first functional embryonic organ. During embryogenesis the development of the heart and its vasculature is a complex process that give rise to the formation of four-chambered heart with a synchronously contraction, from a single tubular heart with a peristaltic contraction. The spectacular progress of modern developmental biology has marked the beginning of a new era in embryology. Over the last years, several families of genes with restricted cardiac expression have been identified including genes such as those encoding for tissue-specific transcription factors, contractile proteins, as well as, more recently, ion channels. In this review, we illustrate the heterogeneity of the developing and adult myocardium in mice. Looking at the expression profile of transcription factors and contractile proteins, it can be seen that the tubular heart is patterned along the three embryonic axes, antero/posterior, dorso/ventral and left/right, besides having several genes that are expressed homogeneously within the entire myocardium. In the embryonic heart, two new types of pattern arise, chamber-specific and systemic/pulmonary gene expression, while within the foetal and adult heart, a wider heterogeneity is observed, not only between the working myocardium and the specialized cardiac conduction system but also within distinct myocardial chambers, specially in the atrial components. Such heterogeneity is also observed if one looks at the electrophysiological characteristics of the developing myocardium and their underlying molecular components. Several evidences support the notion that the distinct expression profiles observed in mice can be extrapolated to humans. Thus, these data reveal that the molecular diversity of the myocardium should be taken into account on the design of drug targets as well as on gene and cell therapy approaches.

Complete atrioventricular septal defect repair: Simplified single patch technique

Background: There has been a rekindling of interest in alternatives to conventional two patch technique for the repair of complete atrioventricular septal defect in infancy in the recent past. We applied the simplified single patch technique to 15 consecutive infants and herein report our intermediate term results. Methods: Between March 1998 and September 2001, fifteen patients underwent repair of complete atrioventricular septal defect with this technique (mean age 6 months, mean weight 5.4 kg). Downs syndrome was present in 11 patients. Repair was done in all patients by direct suturing of the common atrioventricular valve leaflets to the crest of the ventricular septum irrespective of the size of the ventricular septal component. The cleft in the anterior mitral leaflet was closed in all patients. The atrial septal component was closed by a pericardial patch. Results: There was no mortality. There were no pulmonary arterial hypertensive crises or heart block. The mean follow up was 13.2 months. One patient underwent mitral valve replacement after one year due to severe mitral regurgitation. The remaining fourteen patients had no significant mitral regurgitation, residual ventricular septal defect or left ventricular outflow tract obstruction on echocardiography. Conclusion: Simplified single patch technique is an easily reproducible method for surgical repair of complete atrioventricular septal defect. It is less time consuming and minimises ischaemic time. Atrioventricular valve function is preserved and there is no incidence of obstruction to left ventricular outflow tract. The intermediate term results are encouraging.

Left ventricular long-axis changes in early diastole and systole: impact of systolic function on diastole

Impaired long-axis motion is a sensitive marker of systolic myocardial dysfunction, but no data are available that relate long-axis changes in systole with those in diastole, particularly in subjects with diastolic dysfunction and a 'normal' left ventricular (LV) ejection fraction. A total of 311 subjects (including 105 normal healthy volunteers) aged 20-89 years with variable degrees of systolic function (LV ejection fraction range 0.15-0.84) and diastolic function were studied using tissue Doppler echocardiography and M-mode echocardiography to determine mean mitral annular amplitude and peak velocity in systole and early and late diastole. The LV systolic mitral annular amplitude (S(LAX), where LAX is long-axis amplitude) and peak velocity (S(m)) correlated well with the respective early diastolic components (E(LAX) and E(m)) and late diastolic (atrial) components (A(LAX) and A(m)). A non-linear equation fitted better than a linear relationship (non-linear model: S(LAX) against E(LAX), r(2)=0.67; S(m) against E(m), r(2)=0.60; S(LAX) against A(LAX) and S(m) against A(m), r(2)=0.42). After adjusting for age, sex and heart rate, linear relationships of early diastolic (E(LAX), r(2)=0.70; E(m), r(2)=0.60) and late diastolic (A(LAX), r(2)=0.61; A(m), r(2)=0.64) long-axis amplitudes and velocities with the respective values for S(LAX) and S(m) were found, even in those subjects with apparently 'isolated' diastolic dysfunction. Long-axis changes in systole or diastole did not correlate with Doppler mitral velocities. We conclude that ventricular long-axis changes in early diastole are closely related to systolic function, even in subjects with diastolic dysfunction. 'Pure' or isolated diastolic dysfunction is uncommon.

Multiple transcriptional domains, with distinct left and right components, in the atrial chambers of the developing heart.

During heart development, 2 fast-conducting regions of working myocardium balloon out from the slow-conducting primary myocardium of the tubular heart. Three regions of primary myocardium persist: the outflow tract, atrioventricular canal, and inflow tract, which are contiguous throughout the inner curvature of the heart. The contribution of the inflow tract to the definitive atrial chambers has remained enigmatic largely because of the lack of molecular markers that permit unambiguous identification of this myocardial domain. We now report that the genes encoding atrial natriuretic factor, myosin light chain (MLC) 3F, MLC2V, and Pitx-2, and transgenic mouse lines expressing nlacZ under the control of regulatory sequences of the mouse MLC1F/3F gene, display regionalized patterns of expression in the atrial component of the developing mouse heart. These data distinguish 4 broad transcriptional domains in the atrial myocardium: (1) the atrioventricular canal that will form the smooth-walled lower atrial rim proximal to the ventricles; (2) the atrial appendages; (3) the caval vein myocardium (systemic inlet); and (4) the mediastinal myocardium (pulmonary inlet), including the atrial septa. The pattern of expression of Pitx-2 reveals that each of these transcriptional domains has a distinct left and right component. This study reveals for the first time differential gene expression in the systemic and pulmonary inlets, which is not shared by the contiguous atrial appendages and provides evidence for multiple molecular compartments within the atrial chambers. Furthermore, this work will allow the contribution of each of these myocardial components to be studied in congenitally malformed hearts, such as those with abnormal venous return.

Prediction of mean pulmonary wedge pressure using Doppler pulmonary venous flow variables in hypertrophic cardiomyopathy

We examined whether pulmonary venous flow variables, assessed by transthoracic Doppler echocardiography, could predict mean pulmonary wedge pressure in hypertrophic cardiomyopathy. Forty-four patients with no left ventricular systolic dysfunction (left ventricular fractional shortening ≥25%) were studied. Forty patients with systolic dysfunction (dilated cardiomyopathy group) served as control. Mitral and pulmonary venous flow velocity curves were recorded with the pulsed-Doppler method and were related to mean pulmonary wedge pressure obtained by right heart catheterization. In hypertrophic cardiomyopathy group, the systolic ( r=−0.15, P=0.335) and diastolic ( r=0.35, P=0.022) forward flow velocity were poorly related to mean pulmonary wedge pressure, whereas the velocity of atrial reversal ( r=0.68, P<0.001) correlated well with mean pulmonary wedge pressure. In dilated cardiomyopathy group, the systolic ( r=−0.51, P=0.001) and diastolic ( r=0.60, P<0.001) forward flow velocity were strongly related to mean pulmonary wedge pressure. With the cut-off value set at the velocity of atrial reversal >30 cm/s in hypertrophic cardiomyopathy group, the sensitivity for predicting mean pulmonary wedge pressure >15 mmHg was 79% and the specificity was 73%. In conclusion, the atrial component of the pulmonary venous flow can be used to predict mean pulmonary wedge pressure in hypertrophic cardiomyopathy.

Aortopulmonary window associated with complete atrioventricular septal defect

Aortopulmonary (AP) window and atrioventricular (AV) septal defect are congenital cardiovascular defects that typically occur without major associated cardiac anomalies but in a minority of cases are found in conjunction with a variety of other lesions. We describe the case history of an infant with coexisting AP window and complete AV septal defect who underwent complete primary repair at 3 months of age. To our knowledge, this combination of congenital cardiovascular defects has not previously been described. Clinical summary. The patient was born at 37 weeks’ estimated gestational age by spontaneous vaginal delivery, with a birth weight of 3.0 kg and Apgar scores of 8 at 1 minute and 9 at 5 minutes. At 2 months of age, she was referred for cardiac evaluation because of a cardiac murmur and failure to thrive. She weighed 3.4 kg and was feeding poorly. On evaluation, she was found to be nondysmorphic. Cardiac examination disclosed a grade 3/6 holosystolic murmur, a right ventricular heave, a diastolic rumble over the apex of the heart, and a gallop. The oxyhemoglobin saturation was 97% on room air, and the heart rate and blood pressure were within the normal ranges for age. The electrocardiogram showed a normal sinus rhythm, left axis deviation, right atrial enlargement, biventricular hypertrophy, and nonspecific changes in the ST segment. The echocardiogram demonstrated a Rastelli type C complete AV septal defect with large atrial and ventricular components and moderate regurgitation of the left-sided component of the common AV valve, along with a left-sided superior caval vein draining to the right atrium via an enlarged coronary sinus. The patient was initially managed medically with digoxin and furosemide, but there was little improvement in her growth. At the age of 3 months, a repeat echocardiogram confirmed the prior diagnosis but also revealed a large AP window between the proximal pulmonary trunk and ascending aorta, with continuous left-to-right shunting. Cardiac catheterization was performed to assess her hemodynamic

Anatomy of the human atrioventricular junctions revisited

There have been suggestions made recently that our understanding of the atrioventricular junctions of the heart is less than adequate, with claims for several new findings concerning the arrangement of the ordinary working myocardium and the specialised pathways for atrioventricular conduction. In reality, these claims are grossly exaggerated. The structure and architecture of the pathways for conduction between the atrial and ventricular myocardium are exactly as described by Tawara nearly 100 years ago. The recent claims stem from a failure to assess histological findings in the light of criterions established by Monckeberg and Aschoff following a similar controversy in 1910. The atrioventricular junctions are the areas where the atrial myocardium inserts into, and is separated from, the base of the ventricular mass, apart from at the site of penetration of the specialised axis for atrioventricular conduction. There are two such junctions in the normal heart, surrounding the orifices of the mitral and tricuspid valves. The true septal area between the junctions is of very limited extent, being formed by the membranous septum. Posterior and inferior to this septal area, the atrial myocardium overlies the crest of the ventricular septum, with the atrial component being demarcated by the landmarks of the triangle of Koch. The adjacent structures, and in particular the so-called inferior pyramidal space, were accurately described by McAlpine (Heart and Coronary Arteries, 1975). Thus, again there is no need for revision of our understanding. The key to unravelling much of the alleged controversy is the recognition that, as indicated by Tawara, the atrioventricular node becomes the atrioventricular bundle at the point where the overall axis for conduction penetrates into the central fibrous body. There are also marked differences in arrangement, also described by Tawara, between the disposition of the conduction axis in man as compared to the dog.

How constant anatomically is the tendon of Todaro as a marker for the triangle of Koch?

Although well recognized by anatomists as a border of the triangle of Koch demarcating the location of the AV node, the tendon of Todaro is not visible in the operating room or in the catheterization laboratory. Instead, clinicians use as surrogate a projected line between the eustachian valve and the central fibrous body. The constancy of the tendon of Todaro within this border remains to be determined. We reexamined serial histologic sections from 25 adults and 50 infants and gross dissections in four normal hearts. The tendon of Todaro was identified in all cases and traced to the central fibrous body in all but one case. It tended to be thicker in the hearts of infants cases (0.2 to 0.8 mm vs 0.1 to 0.6 mm). The tendon and the hinge-line of the septal leaflet of the tricuspid valve were consistent as landmarks for location of the compact AV node in all the cases studied by histology. Gross dissections traced the tendon to the free edge of the eustachian valve. The tendon of Todaro is present in hearts obtained from both adults and infants. It, or its surrogate, is a reliable border for the triangle of Koch and serves as a landmark to location of the atrial components of the AV conduction axis.

Simplified single patch technique for the repair of atrioventricular septal defect

Objective: Because of the complexity of traditional 1- and 2-patch techniques for the repair of complete atrioventricular septal defect, we modified our repair technique to avoid the use of any ventricular septal patch material. We report our prospective experience with this simplified 1-patch technique. Method: Forty-seven consecutive patients between May 1995 and August 1998 underwent repair with the use of this technique without modification. Repair was done in all patients by direct suturing of the common atrioventricular valve leaflets to the crest of the ventricular septum. No division of valve leaflets was necessary. A single pericardial patch was used to close the defect in the atrial septal component. Follow-up included electrocardiography and echocardiographic assessment of ventricular function, atrioventricular valve function, and adequacy of the left ventricular outflow tract. Results: There were 2 deaths (4%), only 1 cardiac related, in the series. There were 17 male patients and 30 female patients. Mean age at repair was 5.6 months (median, 3.4 months). Associated lesions were repaired in 19 patients (40%). Mean follow-up was 1.85 years (median, 1.9 years). There was no heart block. There were no significant residual ventricular septal defects detected and no left ventricular outflow tract obstruction seen on echocardiography in any patient to date. Mitral valve status after operation was assessed as no incompetence in 13 patients (28%), minimal in 19 patients (40%), mild in 12 patients (26%), and moderate in 3 patients (6%). Conclusion: The repair of complete atrioventricular septal defect by direct suturing of the atrioventricular valve leaflets to the crest of the ventricular septum with a single-patch technique greatly simplifies the repair and does not lead to left ventricular outflow tract obstruction nor interfere with valve function. (J Thorac Cardiovasc Surg 1999;118:642-7)

Effect of Ovariectomy and Estrogen Replacement on Cardiovascular Disease in Heart Failure-Prone SHHF/Mcc- fa cp Rats

The importance of endogenous and exogenous estrogen levels to the development of cardiovascular disease in women in controversial. The purpose of our study was to examine the effect of estrogen on the development of hypertension, cardiac hypertrophy, ventricular function, and gene expression for atrial natriuretic peptide (ANP) and components of the renin angiotensin system in spontaneously hypertensive heart failure rats (SHHF/Mcc- facp). Development of hypertension was prevented in 3-month-old ovariectomized rats receiving subcutaneous 17 β -estradiol implants (EST) compared to ovariectomized (OVX) and controls (CON). EST had the least left ventricular hypertrophy, CON were intermediate, and OVX had the most (P<0.05), correlating well with systolic blood pressure. OVX had significantly lower percentage V1myosin isoform compared to EST and CON, indicating reversion to a more immature phenotype associated with hypertrophy. Similarly, OVX had decreased percentage left ventricular shortening fraction by echocardiography compared to EST and CON. These changes were not accompanied by alterations in plasma ANP, or in expression of mRNA for left ventricular ANP, renal renin, or hepatic angiotensinogen. Serum angiotensin converting enzyme activity was lower in EST compared to CON or OVX. When 17β -estradiol was given to 17-month-old rats that had naturally ceased estrous cycling, there was no effect on hypertension, progression of cardiac functional decline, or survival. In conclusion, estradiol treatment given prior to the development of hypertension in SHHF prevented left ventricular hypertrophy and hypertension. Development of congestive heart failure was not delayed if 17 β -estradiol was begun in the post-menopausal period. Effectiveness of estrogen therapy may depend on age or whether hypertension is already established at the time treatment is begun.

Cross sectional echocardiographic assessment of the extent of the atrial septum relative to the atrioventricular junction in atrioventricular septal defect

ObjectiveTo study patients with atrioventricular septal defect to determine the pathognomonic morphological features of the lesion and the relation between the septal structures and the atrioventricular junction.SettingTertiary level paediatric cardiology...

Atrial fibrillation after coronary artery bypass grafting. An increase in high-frequency atrial activity in patients with right coronary artery revascularization.

The increase in atrial high-frequency activity has been reported as a marker of the risk of paroxysmal atrial fibrillation. The presence of proximal right coronary artery disease is a predictor of atrial fibrillation after bypass surgery, however, the potential mechanism remains controversial. In this study, high-frequency atrial activity to clarify the electrophysiologic background for the predisposition to have proximal right coronary artery disease leading to atrial fibrillation after coronary revascularization was investigated. Before and soon after coronary revascularization, frequency analyses were performed on the 100 ms segment at the end of signal-averaged P waves in 22 patients with right coronary artery disease as opposed to the 23 patients without disease. Under the spectrum curve, area ratio (AR50) and magnitude ratios (MR) were calculated as follows; AR50 = (area 20-50 Hz/0-20 Hz) x 100, and MR = (magnitude at 20, 30, 40 and 50 Hz, respectively/maximal magnitude) x 100. In patients with proximal right coronary artery disease, high-frequency atrial components increased significantly in the 20 to 50 Hz range after coronary revascularization, and the incidence of postoperative atrial fibrillation was higher than in those without disease. In patients without right coronary artery disease, the frequency distribution of P waves was unchanged. Postoperatively, the two groups showed the same atrial frequency distribution. This data suggests that the increase in high-frequency atrial activity after right coronary artery revascularization might be associated with the pathogenesis of postoperative atrial fibrillation.

Morphologic analysis of animal models of congenital heart disease

Background: The description and analysis of congenitally malformed hearts has provided a fertile ground for arguments and disagreements. It would be unfortunate if those now working in the field of animal models of human congenital hearts were forced to till the same soil, potentially recreating the same controversies. This can be avoided by following a simple but rigorous plan for the analysis of the congenitally malformed heart. Method: The system proposed for analysis depends initially on considering the heart in terms of its atrial, ventricular, and arterial segments. Each segment contains two components, one belonging to the right heart and the other to the left. The next step is to establish ways of distinguishing anatomically these components, and then determining how they are or are not joined together. Thereafter, a catalogue is made of all associated malformations in the heart, and note taken of the arrangement of the other abdomino-thoracic organs. At all stages, care is taken not to define one variable in terms of another feature which is itself variable. Results: The morphologically right and left atrial components are distinguished on the basis of the structure of the appendages, since all other components are variable. Similarly, ventricles are distinguished according to their apical trabeculations, and arterial trunks according to their patterns of branching. There are four possible arrangements of the appendages. The atriums can be connected to the ventricles in biventricular or univentricular fashion, with each group having further subdivisions. Ventricles can be connected to the arterial trunks in concordant, discordant, double outlet or single outlet fashion. This is the basis of analysis which is equally applicable to animal models. Conclusions: By the simple expedient of distinguishing morphologically right from morphologically left features in each of the three cardiac segments, and then determining how the segments are joined together over their junctional areas, it is possible to give a basic account of all congenitally malformed hearts, even if they have not previously been described. This form of analysis is completed by providing a catalogue of all associated malformations. This will provide the basis for description of all congenital cardiac malformations seen in animal models of human disease.