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At least 127 records · Page 7Linked to original sources
PubMed1988

Impaired relaxation of the hypertrophied left ventricle in aortic stenosis: effects of aortic valvuloplasty and of postextrasystolic potentiation.

Impaired left ventricular (LV) filling in aortic stenosis (AS) is explained by slow LV pressure decay, which impedes LV inflow. This slow LV pressure decay could be explained by the altered myocardial wall stress pattern of AS or by a failure of inactivation of hypertrophied myocardium. To evaluate whether altered LV loading or impaired myocardial inactivation is the predominant control of LV relaxation and filling in AS, we studied the effects of aortic valvuloplasty (PTAV) and of postextrasystolic potentiation (PESP). LV micromanometer tip pressure recordings and simultaneous LV angiograms were obtained before and after PTAV in 10 patients with AS. PTAV reduced peak-to-peak aortic valve gradient from 101 +/- 7 to 40 +/- 5 mmHg (P less than 0.01), peak LV systolic pressure from 211 +/- 8 to 169 +/- 4 mmHg (P less than 0.01) and LV end-diastolic pressure from 22 +/- 3 to 13 +/- 2 mmHg (P less than 0.01). Despite these large drops of LV loading after PTAV, the time constant, T, of LV pressure decay decreased only slightly from 47 +/- 4 to 44 +/- 4 ms (P less than 0.05) and the LV peak filling rate remained unaltered. The influence of PESP on LV relaxation and filling was investigated in patients with AS using LV micromanometer tip pressures (n = 22) and simultaneous mitral valve Doppler echocardiograms (n = 9). After PESP the time constant, T, of isovolumic LV pressure decay increased from 43 +/- 4 to 54 +/- 4 ms (P less than 0.01).2+ 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Aortic Valve↗
PubMed2004

Should coronary artery bypass graft surgery patients with mild or moderate aortic stenosis undergo concomitant aortic valve replacement? A decision analysis approach to the surgical dilemma.

OBJECTIVES: This study utilizes Markov decision analysis to assess the relative benefits of prophylactic aortic valve replacement (AVR) at the time of coronary artery bypass graft surgery (CABG). Multiple sensitivity analyses were also performed to determine the variables that most profoundly affect outcome. BACKGROUND: The decision to perform CABG or concomitant CABG and AVR (CABG/AVR) in asymptomatic patients who need CABG surgery but have mild to moderate aortic stenosis (AS) is not clear-cut. METHODS: We performed Markov decision analysis comparing long-term, quality-adjusted life outcomes of patients with mild to moderate AS undergoing CABG versus CABG/AVR. Age-specific morbidity and mortality risks with CABG, CABG/AVR, and AVR after a prior CABG were based on the Society of Thoracic Surgeons national database (n = 1,344,100). Probabilities of progression to symptomatic AS, valve-related morbidity, and age-adjusted mortality rates were obtained from available published reports. RESULTS: For average AS progression, the decision to replace the aortic valve at the time of elective CABG should be based on patient age and severity of AS measured by echocardiography. For patients under age 70 years, an AVR for mild AS is preferred if the peak valve gradient is >25 to 30 mm Hg. For older patients, the threshold increases by 1 to 2 mm Hg/year, so that an 85-year-old patient undergoing CABG should have AVR only if the gradient exceeds 50 mm Hg. The AS progression rate also influences outcomes. With slow progression (<3 mm Hg/year), CABG is favored for all patients with AS gradients <50 mm Hg; with rapid progression (>10 mm Hg/year), CABG/AVR is favored except for patients >80 years old with a valve gradient <25 mm Hg. CONCLUSIONS: This study provides a decision aid for treating patients with mild to moderate AS requiring CABG surgery. Predictors of AS progression in individual patients need to be better defined.

Age Factors↗
PubMed1998

Transumbilical venous, anterograde, snare-assisted balloon aortic valvuloplasty in a neonate with critical aortic stenosis.

Balloon aortic valvuloplasty is an acceptable alternative to surgery in the treatment of critical aortic stenosis in the neonate. In this report, we describe a 1-day-old infant with critical aortic stenosis who was successfully treated with an anterograde, transumbilical venous, snare-assisted balloon aortic valvuloplasty. Based on this experience, it is suggested that the anterograde transumbilical venous approach is a feasible and effective alternative to retrograde femoral, carotid, or umbilical arterial and transfemoral venous anterograde routes for performing balloon aortic valvuloplasty in the neonate.

Aortic Valve Stenosis↗
PubMed2001

Valve-sparing operation for balloon-induced aortic regurgitation in congenital aortic stenosis.

OBJECTIVE: Aortic regurgitation after balloon dilation of congenital aortic stenosis may be treated with valve repair as an alternative to replacement. METHODS: Charts and echocardiograms of all patients undergoing aortic valve operations after balloon dilation of congenital aortic stenosis at our institution between January 1988 and December 1999 were reviewed. RESULTS: Twenty-one patients underwent valvuloplasty for predominant aortic regurgitation 9 months to 15 years (mean, 6.1 years) after balloon dilation. The mean +/- SD age at the time of the operation was 11 +/- 7 years. Aortic regurgitation was caused by a combination of commissural avulsion (10), cusp dehiscence with retraction (9), cusp tear (5), central incompetence (2), perforated cusp (1), or cusp adhesion to the aortic wall (1). Repair techniques included commissural reconstruction with a pericardial patch (8), pericardial patch cusp augmentation (6), primary suture repair (6), raphae release and debridement (4), commissurotomy (4), commissural resuspension with sutures (3), and cusp release (1). There were no deaths. At a mean follow-up of 30.1 months (range, 9 months-8 years), all patients were asymptomatic, and the grade of aortic regurgitation had been significantly reduced (P <.001). Left ventricular end-diastolic dimension z scores and proximal regurgitant jet/aortic anulus diameter ratios were significantly reduced (P <.001) and remained so over time. Freedom from reoperation for late failure was 100%, and overall freedom from reintervention was 80% at 3 years. CONCLUSION: Aortic valve repair for balloon-induced aortic regurgitation is reproducible and durable at medium-term follow-up.

Adolescent↗
PubMed2000

Prenatal therapy of non-immunologic hydrops fetalis caused by severe aortic stenosis.

Congenital aortic stenosis is a rare cause of congestive heart failure and hydrops fetalis. This report describes a case of prenatally diagnosed critical aortic stenosis and endocardial fibroelastosis leading to a severe hydrops fetalis at 27 weeks of gestation. Successful transplacental digitalization was performed and all signs of hydrops resolved within 2 weeks. The pregnancy continued with normal development of the fetus and birth was induced at 39 weeks of gestation. After an uneventful vaginal birth, the child was transferred for cardiac catheterization, and balloon dilation of the aortic valve was performed successfully. Follow up at the age of 2 years showed only mild left ventricular cardiac hypertrophy, a moderate elevated pressure gradient of 50 mmHg at the aortic valve and mild aortic and mitral regurgitation. No further interventions were necessary at this point.

Adult↗
PubMed2002

[Specification of rheumatic fever contribution to formation of senile aortic stenosis].

Calcinated aortic stenosis developing in the elderly is erroneously referred to atherosclerotic lesion of the valve or is thought to be rheumatic heart defect undetected previously. The atherosclerotic hypothesis is rejected by foreign investigated while a conception of postrheumatic damage is discussed in the light of immune inflammation found in the calcinated valve. Immunogenetic testing was used for investigation of correlations between senile aortic stenosis and rheumatic fever.

Aged↗
PubMed1977

Minor congenital variations of cusp size in tricuspid aortic valves. Possible link with isolated aortic stenosis.

Clinically isolated aortic stenosis is most commonly caused by a congenitally malformed aortic valve. Many elderly patients with isolated aortic stenosis have a tricuspid aortic valve. It has been suggested in the past that inequalities in individual cusp size could be a factor leading to the development of the stenoses in these cases. In this study the width and height of individual aortic valve cusps were measured at necropsy in 200 hearts of patients without clinical signs of aortic stenosis, though the majority of valves obtained from elderly persons showed some ageing changes. The results were compared with similar measurements in 16 hearts of patients with clinically diagnosed and necropsy proven isolated aortic stenosis. The results show that inequality in cusp size is the rule rather than the exception. Indeed, only 5 of the 200 'normal' tricuspid aortic valves had 3 cusps of identical height and width, and each of the 16 cases with isolated aortic stenosis has cusps of differing size. The results seem to contradict the aforementioned hypothesis. However, the striking similarities between isolated aortic stenosis and the ageing aortic valve, suggest that isolated tricuspid aortic stenosis is an extreme with a spectrum of ageing alterations. Inequality in cusp size, with differences in mechanical tissue stress as a consequence, could then play a role in the pathogenesis of the stenosis by accelerating the ageing process.

Adolescent↗
PubMed1988

Left ventricular systolic function in aortic stenosis.

In aortic valve stenosis, concentric hypertrophy develops which is characterized by a reduced end-diastolic radius-to-wall thickness ratio (r/h) with an essentially normal cavity shape. As long as the product of (r/h) and LV systolic pressure remains constant, hypertrophy is appropriate. An increase in the product, which represents an increase in wall stress signals inadequate LV hypertrophy. Although at first glance, massive LV hypertrophy appears favourable for the maintenance of a normal LV ejection fraction in aortic stenosis, data from 23 studies of the literature have shown an inverse relationship between ejection fraction and LV angiographic mass m-2 (r = -0.59). Both a degree of hypertrophy inadequate to keep systolic wall stress within normal limits and a reduction of LV contractility may explain the depression of ejection fraction when LV angiographic mass is sizeably increased. Conversely, a normal ejection fraction in aortic stenosis may not be indicative of normal systolic myocardial function under all circumstances. In the presence of mildly reduced contractility, a normal ejection fraction may be maintained by the use of preload reserve. Assessment of myocardial structure from LV endomyocardial biopsies revealed no differences in muscle fibre diameter, interstitial fibrosis and volume fraction of myofibrils between patients with aortic stenosis having a normal and those with a depressed ejection fraction. Preoperative ejection fraction is a poor predictor of postoperative survival, whereas markedly increased preoperative angiographic mass and end-systolic volume have been reported to predict an unsatisfactory postoperative outcome characterized by either death or poor LV function.

Aortic Valve↗
PubMed2006

Projected valve area at normal flow rate improves the assessment of stenosis severity in patients with low-flow, low-gradient aortic stenosis: the multicenter TOPAS (Truly or Pseudo-Severe Aortic Stenosis) study.

BACKGROUND: We sought to investigate the use of a new parameter, the projected effective orifice area (EOAproj) at normal transvalvular flow rate (250 mL/s), to better differentiate between truly severe (TS) and pseudo-severe (PS) aortic stenosis (AS) during dobutamine stress echocardiography (DSE). Changes in various parameters of stenosis severity have been used to differentiate between TS and PS AS during DSE. However, the magnitude of these changes lacks standardization because they are dependent on the variable magnitude of the transvalvular flow change occurring during DSE. METHODS AND RESULTS: The use of EOAproj to differentiate TS from PS AS was investigated in an in vitro model and in 23 patients with low-flow AS (indexed EOA <0.6 cm2/m2, left ventricular ejection fraction < or =40%) undergoing DSE and subsequent aortic valve replacement. For an individual valve, EOA was plotted against transvalvular flow (Q) at each dobutamine stage, and valve compliance (VC) was derived as the slope of the regression line fitted to the EOA versus Q plot; EOAproj was calculated as EOAproj=EOArest+VCx(250-Q(rest)), where EOArest and Q(rest) are the EOA and Q at rest. Classification between TS and PS was based on either response to flow increase (in vitro) or visual inspection at surgery (in vivo). EOAproj was the most accurate parameter in differentiating between TS and PS both in vitro and in vivo. In vivo, 15 of 23 patients (65%) had TS and 8 of 23 (35%) had PS. The percentage of correct classification was 83% for EOAproj and 91% for indexed EOAproj compared with percentages of 61% to 74% for the other echocardiographic parameters usually used for this purpose. CONCLUSIONS: EOAproj provides a standardized evaluation of AS severity with DSE and improves the diagnostic accuracy for distinguishing TS and PS AS in patients with low-flow, low-gradient AS.

Aged↗
PubMed2004

Safety and efficacy of angiotensin-converting enzyme inhibitors in symptomatic severe aortic stenosis: Symptomatic Cardiac Obstruction-Pilot Study of Enalapril in Aortic Stenosis (SCOPE-AS).

BACKGROUND: Animal models have demonstrated a benefit of angiotensin-converting enzyme inhibitors (ACEI) in experimental aortic stenosis (AS), and intravenous nitroprusside has shown hemodynamic improvements in AS with left ventricular (LV) dysfunction. Although routinely used in most heart failure situations, ACEI are avoided in AS because of the risk of hypotension. We aimed to determine the clinical tolerance and efficacy of the ACEI enalapril in the setting of symptomatic severe AS. METHODS: Patients with symptomatic severe AS were enrolled in a randomized, double-blinded, controlled trial to enalapril or placebo arms after initial stabilization. Standard antifailure medications were continued. Enalapril was started at 2.5 mg bid and increased to 10 mg bid. The primary end points were development of hypotension and improvements in Borg dyspnea index and 6-minute walk distance at 1 month. Secondary end points were minor ACEI intolerance, cough, presyncope, improvement in New York Heart Association class, and echocardiographic parameters. RESULTS: Fifty-six patients were enrolled (37 in the enalapril arm and 19 in the placebo arm). Enalapril was tolerated without hypotension or syncope when LV systolic function was preserved. Three of 5 patients with LV dysfunction and congestive heart failure had hypotension and were withdrawn. Patients who tolerated enalapril (n = 34) demonstrated significant improvement in NYHA class, Borg index (5.4 +/- 1.2 vs 5.6 +/- 1.7, P =.03), and 6-minute walk distance (402 +/- 150 vs 376 +/- 174, P =.003) compared with control subjects. Within the enalapril group, patients with associated regurgitant lesions improved the most. CONCLUSIONS: ACEI are well tolerated in symptomatic patients with severe AS. Patients with congestive heart failure with LV dysfunction and low normal blood pressure are prone to have hypotension. Enalapril significantly improves effort tolerance and reduces dyspnea in symptomatic AS.

Adult↗
PubMed2003

Low Gradient, Low Ejection Fraction Aortic Stenosis.

Low gradient aortic stenosis can be caused by critical aortic stenosis causing left ventricular impairment or by more moderate aortic stenosis coexisting with another cause of left ventricular impairment. The main challenges are to differentiate these two states and then to determine whether the left ventricle is likely to recover after aortic valve surgery. Exhaustive echocardiography is necessary, including the use of dobutamine stress. Guideline criteria for severe aortic stenosis are given in this article. The most secure criteria are mean transaortic pressure difference greater than 30 mm Hg and effective orifice area less than 1.2 cm(2) during dobutamine stress. However, the presence of left ventricular contractile reserve more closely determines outcome after surgery than do markers of stenosis. Surgery is most clearly indicated if there is severe aortic stenosis and an increase in the systolic velocity integral by greater than 20% during dobutamine infusion. Preoperative catheterization is necessary to determine coronary anatomy, but the aortic valve should not be crossed because of the relatively high risk of death, stroke, pulmonary edema, and cardiogenic shock. In patients judged too ill for immediate surgery, a period of medical resuscitation with diuretics and dobutamine should be considered. Balloon valvotomy is not indicated.

Journal Article↗
PubMedDate not supplied

Pathology of the diffuse variant of supravalvar aortic stenosis.

Supravalvar aortic stenosis is a rare congenital heart anomaly, producing left ventricular outflow tract obstruction. Of the two anatomic variants that have been described, diffuse type is the rarest. We report five such cases in children between two months and nine years of age. None had features of Williams syndrome. The entire aorta was involved in three cases, with abdominal aortic coarctation in two cases. Stenosis was mainly due to involvement of the media, which showed smooth muscle hypertrophy, abnormal elastic fibers, and mild collagenization. Predominant intimal change was seen in one case. Pulmonary, coronary, arch, renal, and common iliac arteries were also involved.

Aorta, Abdominal↗
PubMed2006

Congenital heart disease: Molecular diagnostics of supravalvular aortic stenosis.

Supravalvular aortic stenosis (SVAS) is a congenital heart disease that can occur as an isolated autosomal-dominant condition or as part of the developmental disorder Williams-Beuren syndrome (WBS) and is caused by heterozygous genetic lesions involving the elastin (ELN) gene locus on chromosome 7ql 1.23. SVAS is one of many phenotypic features associated with the contiguous gene microdeletion disorder, WBS, and is caused by deletion of the ELN locus on one chromosome 7 homolog. Point mutations, chromosomal deletions, and translocation involving ELN have also been described in individuals with nonsyndromic SVAS. In addition, ELN is involved in the connective tissue disorder, autosomal-dominant cutis laxa, and has been implicated as a susceptibility gene for hypertension and intracranial aneurysms. The molecular analysis of ELN defects is, therefore, an area of significant interest. Genetic screening can be achieved using a variety of techniques to detect both mutations and gross chromosome rearrangements involving the ELN locus, providing the ability to screen families and individuals with SVAS and associated elastinopathies.

Aortic Stenosis, Supravalvular↗
PubMed2006

Novel mutations in the human elastin gene (ELN) causing isolated supravalvular aortic stenosis.

Supravalvular aortic stenosis (SVAS), an inherited vascular disease, is caused by mutations in the elastin gene (ELN). Our aim was to identify novel mutations of ELN and to determine the expression of ELN in patients with SVAS. For screening mutations in ELN, we performed PCR-directed sequence analysis with genomic DNA isolated from SVAS patients and control subjects. Expression of ELN at the mRNA and protein levels were assessed by real-time PCR and Western blot analyses, respectively, using primary skin fibroblast cultures established from SVAS patients and control subjects. We identified two novel mutations of ELN, G297_A308del and Q700X, in two unrelated Korean patients with isolated SVAS. G297_A308del occurred de novo while Q700X was derived maternally. In the patient with G297_A308, elastin expression was not significantly altered at the mRNA level, but was reduced to approximately 50% of the normal control at the protein level. The elastin expression levels in the patient with Q700X were reduced to <50% of the normal controls at both the mRNA and protein levels. Our findings confirm that functional haploinsufficiency of elastin is responsible for the pathogenesis associated with isolated SVAS across different ethnic backgrounds.

Aortic Stenosis, Supravalvular↗
PubMed2000

Elastin: mutational spectrum in supravalvular aortic stenosis.

Supravalvular aortic stenosis (SVAS) is a congenital narrowing of the ascending aorta which can occur sporadically, as an autosomal dominant condition, or as one component of Williams syndrome. SVAS is caused by translocations, gross deletions and point mutations that disrupt the elastin gene (ELN) on 7q11.23. Functional hemizygosity for elastin is known to be the cause of SVAS in patients with gross chromosomal abnormalities involving ELN. However, the pathogenic mechanisms of point mutations are less clear. One hundred patients with diagnosed SVAS and normal karyotypes were screened for mutations in the elastin gene to further elucidate the molecular pathology of the disorder. Mutations associated with the vascular disease were detected in 35 patients, and included nonsense, frameshift, translation initiation and splice site mutations. The four missense mutations identified are the first of this type to be associated with SVAS. Here we describe the spectrum of mutations occurring in familial and sporadic SVAS and attempt to define the mutational mechanisms involved in SVAS. SVAS shows variable penetrance within families but the progressive nature of the disorder in some cases, makes identification of the molecular lesions important for future preventative treatments.

Alternative Splicing↗
PubMed1990

Echocardiographic evaluation of systolic left-ventricular function in infants with critical aortic stenosis before and after aortic valvotomy.

Infants with critical aortic stenosis may have global or regional left ventricular contraction abnormalities. In order to evaluate the clinical significance of these contraction abnormalities, we examined the systolic left ventricular function before and after aortic valvotomy in 16 infants operated on between 1980 and 1987. Left ventricular free wall and septal motion were studied by cross sectional echocardiography using the apical 4-chamber view. Enddiastolic and endsystolic left ventricular frames were digitized. The relative systolic reduction of the total left ventricular area (reflecting ejection fraction) as well as of 5 left ventricular sectors (reflecting regional wall motion) was calculated and compared to previously established normal values. Before valvotomy, 8 infants had normal and the other 8 impaired left ventricular systolic wall motion. These latter infants showed hypokinesia of the apex and/or the posterolateral left ventricular wall resulting in a decreased systolic reduction of the total left ventricular area. Four of these infants had evidence of myocardial infarction on intraoperative inspection. Early after operation, the systolic reduction of the total left ventricular area was normal in all infants, and the left ventricular apex and poster-lateral wall were either normo- or hyperkinetic. Follow-up studies of all infants more than 10 months and of 7 infants more than 3 years after operation showed that the left ventricular systolic wall motion remained normal in all, irrespective of whether it was normal or abnormal preoperatively. This study suggests that left ventricular contraction abnormalities in infants with critical aortic stenosis may be reversible and thus do not constitute a contraindication against aortic valvotomy.(ABSTRACT TRUNCATED AT 250 WORDS)

Aortic Valve↗