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At least 775 records · Page 43Linked to original sources
PubMed1976

Asymetric septal hypertrophy in childhood.

Although considerable information is available concerning the clinical features and natural history of asymmetric septal hypertrophy (ASH) in adults, little is known of this disease in children. The clinical characteristics and course of 46 children with ASH, who were evaluated at the National Heart and Lung Institute, have been analyzed. Twenty-four children had obstruction to ventricular outflow; 22 children had no obstruction to ventricular outflow, including 11 patients without overt manifestations of cardiac disease other than echocardiographic evidence of ASH. Thirty-five of the 46 children have been followed for one to 16 years (average 7.4 years). These latter children represent that subgroup of patients with ASH referred to the National Heart and Lung Institute and diagnosed prior to the general availability of echocardiography. The clinical course of these patients was variable. Fourteen (40%) of the 35 patients improved or remained stable, including four patients who received propranolol. Ten (29%) of the 35 patients deteriorated clinically and 11 (31%) of the 35 patients died suddenly (4% mortality per year). Two of the patients who died suddenly had previously undergone operation (six and 13 years previously) with resultant abolition of the outflow gradient; four others were taking propranolol. Neither symptomatology, electrocardiographic abnormalities, heart size, left ventricular ejection or upstroke time, magnitude of outflow gradient, or left ventricular end-diastolic pressure proved predictive of sudden death. Excluding patients who had previous operation, eight (40%) of 20 patients with obstruction who were followed long term and one (9%) of 11 patients without outflow obstruction died suddenly. Thus, the clinical and hemodynamic spectrum of ASH in childhood is broad. However, deterioration in clinical condition or sudden death has been relatively common in children with overt signs of cardiac disease.

Adolescent↗
PubMed1985

Assessment of aortic blood flow velocities with continuous wave Doppler ultrasound in the neonate and young child.

Aortic flow velocities can be recorded with pulsed or continuous wave Doppler ultrasound. In the absence of obstruction or regurgitation, changes in flow can be assessed and stroke volume obtained. Continuous wave Doppler ultrasound has the advantage that there is no limit to the velocities that can be recorded. In left ventricular outflow obstruction and coarctation, the pressure drop across these can be calculated from increases in maximal velocity using a modification of the Bernoulli equation. Other systolic high velocity jets such as mitral regurgitation or ventricular septal defect may also be recorded with continuous wave Doppler ultrasound from the suprasternal notch, but they can be distinguished from aortic flow velocities by their timing and duration when the flow signals are recorded together with the electrocardiogram and phonocardiogram. In aortic regurgitation, reversal of flow across the aortic valve in diastole can be shown and with high velocity in the regurgitant jet.

Aorta↗
PubMed1991

Surgical treatment of left-ventricular outflow-tract obstruction guided by intraoperative transesophageal echocardiography.

Transesophageal echocardiography may provide additional morphologic information in many cases of cardiovascular disease when compared with the traditional transthoracic approach. In our department 3 male patients underwent surgical treatment with preoperative diagnosis of left-ventricular outflow-tract obstruction. We describe the intraoperative transesophageal echocardiographic findings and in which way they guided the surgical strategy.

Adolescent↗
PubMedDate not supplied

Hypertrophic cardiomyopathy--therapy with slow channel inhibiting agents.

Slow channel inhibiting agents, particularly verapamil, appear to produce beneficial effects in relieving symptoms of dyspnea, chest pain, and syncope or presyncope in over 70% of patients with hypertrophic cardiomyopathy. Symptomatic relief occurs in patients with and without left ventricular outflow obstruction. Exercise hemodynamics, exercise tolerance, and cardiac performance during exercise tend to improve. The mechanisms for this symptomatic improvement, however, are not fully explained. Relief of symptoms is observed irrespective of any changes in the resting or provocable left ventricular outflow gradient. Similarly, changes in left ventricular systolic function, which in general remains unaffected, cannot be the basis for the beneficial response. Slow channel inhibiting agents, however, appear to improve left ventricular diastolic function, the mechanism of which is yet to be elucidated. Nevertheless, improved left ventricular diastolic function may provide an explanation for the relief of some symptoms in patients with hypertrophic cardiomyopathy. The influence of therapy with slow channel inhibiting agents on arrhythmias, sudden death, and on long-term prognosis of patients with hypertrophic cardiomyopathy remains uncertain at the present time and should be the subject of future investigations.

Angiocardiography↗
PubMedDate not supplied

Animal models of primary myocardial diseases.

Feline and canine cardiomyopathies (primary myocardial diseases) were reviewed and divided into three groups based on the clinical, hemodynamic, angiocardiographic, and pathologic findings: (1) feline and canine hypertrophic cardiomyopathy, (2) feline and canine congestive (dilated) cardiomyopathy, and (3) feline restrictive cardiomyopathy. All three groups consisted predominantly of mature adult male cats and dogs. Cardiomyopathy in the hamster and turkey was also reviewed. The most common presenting signs were dyspnea and/or thromboembolism in the cat, systolic murmurs with gallop rhythms on auscultation, cardiomegaly with (groups 1 and 3) or without (group 2) pulmonary edema, abnormal electrocardiograms, elevated left ventricular end-diastolic pressures, and angiocardiographic evidence of mitral regurgitation with left ventricular concentric hypertrophy (group 1), left ventricular dilatation (group 2), or midventricular stenosis (group 3). Some cats in groups 1 and 3 also had evidence of left ventricular outflow obstruction. The principal pathologic findings in all of the cats and dogs were left atrial dilation, hypertrophy, increased septal:left ventricular free wall thickness ratio with disorganization of cardiac muscle cells (group 1); dilatation of the four chambers with degeneration of cardiac muscle cells (group 2); and extensive endocardial fibrosis and adhesion of the left ventricle (group 3). Aortic thromboembolism was commonly observed in the cats of all three groups. These clinical and pathologic findings indicate that cardiomyopathy in the cat or dog is similar to the three forms of cardiomyopathy in humans (hypertrophic, congestive, and restrictive).

Animals↗
PubMed1987

Effects of therapeutic interventions on minimal cardiac transit times and volume parameters in hypertrophic cardiomyopathy.

45 patients with hypertrophic obstructive cardiomyopathy (HOCM) and 18 patients with hypertrophic non-obstructive cardiomyopathy (HNCM) underwent simultaneous measurements of pulmonary artery pressure and minimal transit times (MTTs) of an intravenously injected bolus of indium-113m-EDTA through the heart at rest and during exercise in supine position. At rest, rate-corrected left and right ventricular MTTs were in the lower normal range, whereas left atrial and, to a lesser degree, right atrial MTTs were abnormally prolonged, indicative of high ventricular ejection fractions and impaired atrial ejection. During exercise, ventricular MTTs rose slightly but remained within the normal range, which corresponds to a slight fall in ventricular ejection fractions. Atrial MTTs exhibited, in contrast, a substantial further prolongation. Together with an abnormal increase in pulmonary artery pressure in the majority of patients, these findings suggest an aggravation of inflow impairment to both ventricles during exercise. There was no quantitative difference between HOCM and HNCM patients suggesting that impaired atrial ejection due to impaired diastolic function is of major pathophysiological importance irrespective of a possible additional role of left ventricular outflow obstruction in HOCM. The influence of surgical therapy (transaortal septal myectomy) was studied in 12 patients with HOCM. A significant increase in left ventricular MTTs to the upper normal range, indicative of a depression of left ventricular ejection fractions to the lower normal range, and a significant shortening of left atrial and pulmonary MTTs were observed, whereas corresponding changes in the right heart were not significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1987

Quantitative assessment of pulmonary hypertension in patients with rheumatic heart disease using continuous wave Doppler ultrasound.

The accuracy of Doppler ultrasound in estimating pulmonary arterial systolic pressure non-invasively was evaluated in 50 patients with rheumatic heart disease. In all cases, the maximal velocity of the tricuspid regurgitation jet was measured by continuous wave Doppler ultrasound and the systolic pressure gradient between right ventricle and the right atrium was calculated by the modified Bernoulli equation. There was a close correlation between Doppler estimated and hemodynamically measured transtricuspid systolic gradient (r = 0.86, P less than 0.001). Right ventricular systolic pressure, which equals pulmonary arterial systolic pressure in the absence of right ventricular outflow obstruction, was calculated by adding a constant of 10 to the Doppler gradient and also by using a regression equation. Right ventricular systolic pressure obtained by both of these Doppler methods correlated closely with values at cardiac catheterization (r = 0.82 and 0.83, respectively). Our study suggests that pulmonary arterial systolic pressure can be determined non-invasively with accuracy, by Doppler ultrasound, in patients with rheumatic heart disease.

Adolescent↗
PubMed1981

Double-chambered right ventricle in two dogs.

In 2 dogs (3 and 8 months old), double-chambered right ventricle was diagnosed by selective angiocardiography. In 1 dog, the systolic pressure in the outflow tract portion of the right ventricle and in the main pulmonary artery was 13 mm of Hg, whereas the systolic pressure in the right ventricle proximal to a constricting muscular ring was 80 mm of Hg. The absence of a valvular pressure gradient and the appearance of normal valves at surgery indicated that the right ventricular outflow obstruction was a congenital lesion. The 67-mm of Hg pressure gradient suggested the need for resection of the obstruction. The defect was corrected surgically and the dog was clinically normal when examined 1 1/2 years later. The 2nd dog was not considered for corrective surgery because of a clinically insignificant gradient in the right ventricular outflow tract. When the dog was examined at 11 months of age, the cardiac silhouette was bilaterally enlarged. However, inasmuch as the dog had not experienced any exercise intolerance or weakness and the electrocardiogram was normal, further diagnostic and therapeutic work was not done. When the dog was examined at 20 months of age, it appeared healthy.

Animals↗
PubMed1976

Calcified right ventricular fibroma causing outflow obstruction. Report of a case with successful excision.

A 5-year-old boy with clinical findings of pulmonic stenosis was found to have a large calcified mass in the right ventricular outflow region and a gradient of 120 mm Hg between the right ventricle and the pulmonary artery. At surgery, an ovalshaped tumor attached to the interventricular septum and obstructing the right ventricular outflow tract was removed. The child survived and is doing well. Histologically, the tumor had the characteristics of fibroma. A hemodynamic study three months after surgery showed almost complete abolishment of the gradient. To our knowledge this is the fifth reported case of calcified right ventricular fibroma with successful operation. In childhood intracardiac calcifications, together with obstruction, are highly suggestive of this lesion.

Angiocardiography↗
PubMed1987

Parental genetic contribution to mode of presentation in Pompe disease.

Echocardiograms were performed on parents of five infants with Pompe disease (glycogen storage disease, type II). Three of the infants had presented with congestive cardiomyopathy and two with dynamic muscular subaortic stenosis. No heart murmurs were audible in any of the parents of the five infants. The parents of the three infants without left ventricular outflow tract obstruction had normal echocardiographic results, whereas one parent of each of the infants with left ventricular outflow obstruction had asymmetric septal hypertrophy. The association between left ventricular outflow obstruction and parental asymmetric septal hypertrophy suggests that both septal hypertrophy and glycogen storage disease were inherited by these two infants.

Cardiomyopathy, Hypertrophic↗
PubMedDate not supplied

Hypertrophic cardiomyopathy: a review of etiology and treatment.

Hypertrophic cardiomyopathy (HCM) is a congenital cardiac disease with an estimated prevalence of 1:500 in the population. Individuals with HCM can present with clinical manifestations that include left ventricular outflow obstruction, cardiac dysrhythmias, diastolic heart failure, cardiac angina, and sudden cardiac death. Current treatments include pharmacologic intervention to reduce heart rate and ventricular contractility as well as surgery or septal alcohol ablation to reduce myocardial septal size. Implantable cardiac defibrillators are considered a treatment option in individuals with HCM who are at an increased risk for sudden cardiac death. The identification of persons at risk for complications related to HCM is important for reducing mortality and morbidity in this population. In addition, diagnosis of HCM in an individual allows the healthcare provider caring for these patients to screen, educate, and institute timely preventative measures in other members of the family. The purpose of this review is to provide clinicians caring for cardiac patients with a guide for recognition, diagnosis, prevention, and treatment of HCM.

Cardiomyopathy, Hypertrophic↗
PubMed1986

Familial spontaneous complete heart block in hypertrophic cardiomyopathy.

Two siblings with hypertrophic cardiomyopathy developed spontaneous complete heart block requiring permanent pacemaker implantation at similar ages (29 and 33 years). The clinical, morphological, and haemodynamic expressions of hypertrophic cardiomyopathy differed considerably in these two patients. The sister had severe functional limitation due to dyspnoea, pronounced and diffuse left ventricular hypertrophy (maximum ventricular septal thickness of 41 mm), and left ventricular outflow obstruction (peak subaortic gradient of 75 mm Hg under basal conditions). In contrast the brother was symptom free, had only modest left ventricular hypertrophy which was confined to the anterior ventricular septum (maximal thickness of 16 mm), and had no echocardiographic evidence of subaortic obstruction. These dissimilar findings in siblings with hypertrophic cardiomyopathy suggest that the predisposition to develop complete heart block was probably genetically transmitted, although it was unrelated to the phenotypic and clinical expression of the disease.

Adult↗
PubMed1978

Exercise testing in children and young adults: an overview.

This chapter has demonstrated the diagnostic capability and feasibility of documenting functional abnormalities during dynamic stress in a pediatric population. The overview confirms that a controlled exercise procedure can be performed routinely in ambulatory children with or without cardiovascular disease and should be included in the clinical evaluation of specific lesions. It now appears that the primary indications for noninvasive exercise testing in the pediatric population include the following disorders: 1. Left ventricular outflow obstructions, a. Subvalvar obstructions, b. Valvar obstructions, c. Supravalvar obstructions, d. Idiopathic hypertrophic subaortic stenosis, e. Coarctation of the aorta; 2. Chronic left or right ventricular volume overload, a. Atrioventricular or semilunar valve incompetence, b. Left-to-right shunts; 3. Rhythm and conduction disturbances, a. Postoperative ventriculotomy, b. Bradytachyarrhythmias, c. Arrhythmias in patients with or without symptoms. The role of the exercise procedure is not yet established in the following areas: 1. Patients with family history of premature atherosclerosis or Type II hyperlipoproteinemia; 2. Patients with elevated blood pressure; 3. The evaluation of syncope, chest pain, or atypical findings on physical examinations (especially in athletes). Consequent upon increased interest and improved technology, the role of this technique will soon be established in the invasive and noninvasive evaluation of pediatric patients with or without overt cardiovascular disease.

Adolescent↗
PubMed1999

[Progressive subaortic stenosis caused by accessory mitral valve tissue].

Accessory mitral valve tissue is a rare cause of subaortic obstruction. The reported case correspond to a two days old patient diagnosed by 2D-Echocardiography. Serial doppler flow analysis showed progressive left ventricular outflow obstruction. A cardiac catheterization at the age of 9 months confirmed the obstruction without defining the cause. Five months later, transesophageal echocardiography clearly defined the intraventricular connections of the accessory mitral tissue. At the age of 18 months the patient suffered from cardiac failure and underwent surgery for removing the accessory tissue, assisted by intraoperative transesophageal echocardiography pre and post by-pass. Follow-up echocardiography at 25 months showed no left ventricle outflow obstruction and the patient is now asymptomatic.

Aortic Valve Stenosis↗
PubMedDate not supplied

[Postoperative changes in diastolic function of the left ventricle in patients with aortic valve stenosis].

INTRODUCTION: Diastolic dysfunction in valvular aortic stenosis frequently precedes systolic dysfunction. The purpose of this study was to examine the changes in left ventricular diastolic function after aortic valve replacement. METHODS: Seventy eight patients with significant isolated valvular aortic stenosis were enrolled in the study. The echocardiographic examination was performed with ACUSON-XP 10 imaging system. Complete M-mode, 2-dimensional and Doppler echocardiographic results were obtained. In 48 patients right and left heart catheterisation was performed. Left ventricular diastolic function was evaluated by pulse Doppler recording of inflow velocity on the tips of the mitral valve leaflets. Forty two underwent aortic valve replacement. They were followed up 6-12 months postoperatively. RESULTS: Abnormal patterns of left ventricular diastolic filling were noticed in almost all patients (Table 1). Most prominent changes were found in subjects with marked and diffuse hypertrophy (Table 2). After aortic valve replacement decrease in left ventricular size, mass, pressures and improvement in systolic Function (Table 3). Twelve months after the operation late diastolic filling velocity was lower (A = 64 +/- 15 cm/s, Avti = 7.1 +/- 1.8 cm), early diastolic filling velocity was higher (E = 83 +/- 14 cm/s, Evti = 10.3 +/- 1.4 cm), deceleration time (DT = 123 +/- 14 ms) and isovolumetric relaxation time (IRT = 66 +/- 6 ms) were longer in patients with preoperative moderate hypertrophy (Table 4). In patients with severe left ventricular hypertrophy changes in diastolic function were slower. We found decrease in early diastolic filling velocity (A = 44 +/- 6 cm/s, Avti = 4.6 +/- 04 cm), increase in late diastolic filling velocity (E = 67 +/- 14 cm/s, Evti = 9.4 +/- 1.7 cm), with prolongation of deceleration (DT = 131 +/- 18 ms) and isovolumetric relaxation time (IRT = 94 +/- 23 ms) (Table 5). DISCUSSION: In adults with significant sympthomatic aortic valve stenosis, aortic valve replacement is therapy of choice. Replacement of the diseased aortic valve with a prosthetic valve yields relief of left ventricular outflow obstruction. Myocardial remodeling with regression of mass transpires as the heart adapts to the new level of afterload. In patients with moderate left ventricular hypertrophy improvement in diastolic function during the first year after aortic valve replacement is visible, while in patients with extreme myocardial hypertrophic changes it was slower.

Adolescent↗
PubMed1970

Atrial fibrillation in patients with idiopathic hypertrophic subaortic stenosis.

Atrial fibrillation occurred in 16 (10%) of 167 patients with idiopathic hypertrophic subaortic stenosis. The clinical and haemodynamic findings in these 16 patients are presented. Atrial fibrillation appeared late in the course of the disease, and its occurrence did not seem to be related to the severity of left ventricular outflow obstruction or to the amount of associated mitral regurgitation. In each patient the onset of the arrhythmia was accompanied by severe clinical deterioration, which often necessitated urgent medical treatment. Digitalis was administered to all 16 patients with subsequent clinical improvement in 15. Electrical cardioversion was uniformly successful in restoring sinus rhythm, but atrial fibrillation usually recurred. In each of 8 patients catheterized during atrial fibrillation, cardiac output was strikingly low (average, 1.9 l./min./m.(2)), whereas it was normal in 10 of 13 patients studied in sinus rhythm. The duration of follow-up from the onset of atrial fibrillation has averaged 5 years, and 3 of the 16 patients have died of causes related to their heart disease. Four have suffered cerebral emboli. Only 5 patients are now in stable sinus rhythm; in general, they are less symptomatic than the patients in whom atrial fibrillation has recurred.The unusually severe clinical deterioration at the onset of atrial fibrillation and the low cardiac output measured during catheterization are thought to be related to the loss of the important contribution to ventricular filling of atrial systole in patients with poorly compliant ventricles, and to the effect of an irregular ventricular rhythm on the variable nature of the outflow obstruction.

Adolescent↗
PubMed1976

Familial prevalence of asymmetric septal hypertrophy.

Echocardiography was used to detect the familial prevalence of asymmetric septal hypertrophy in relatives of patients with proven idiopathic hypertrophic subaortic stenosis. Idiopathic hypertrophic subaortic stenosis is only one clinical expression of a cardiomyopathic disease spectrum, including asymptomatic patients having asymmetric septal hypertrophy as a characteristic anatomic marker which can be detected by echo. The validity of previous proposed criteria to detect this marker was checked in our population. Therefore we examined normal subjects, patients with fixed left ventricular outflow obstruction (valvular aortic stenosis), and those with idiopathic hypertrophic subaortic stenosis who served as index cases. A septal thickness exceeding that of the free left ventricular posterior wall by 30% separates patients with a cardiomyopathy from those without this disease. 27 of 73 examined relatives of 14 index cases were found to have asymmetric septal hypertrophy. In those instances where information was available from the parents of the index cases, one parent was found to be affected. When the examined group is considered from a parent-child relationship (including the index case when appropriate), it included 78 children of affected single parents of which 20 males and 19 females had asymmetric septal hypertrophy. The history, clinical examination and electrocardiogram were not useful to detect the disease. The results suggest an autosomal dominant mode of inheritance of asymmetric septal hypertrophy with a high penetrance.

Adolescent↗