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At least 217 records · Page 12Linked to original sources
PubMed1996

Aortic valve replacement for aortic stenosis in patients with small aortic root.

BACKGROUND AND AIMS OF THE STUDY: Patients with aortic stenosis and small aortic ostia are getting more and more common in our practice. They now constitute a third of our aortic valve replacement (AVR) material. The patients are usually elderly women with small heart and body dimensions, sometimes making it difficult to implant sufficiently large valve prostheses. MATERIALS AND METHODS: We describe a non-selected series of 254 patients from a geographically defined area who underwent AVR during a six year period (1989-1995) and who were considered to have small aortic annulus, defined as patients receiving 19 and 21 mm prostheses. Mean age was 71 years, 42% were over the age of 75, 88% were women and 32% underwent concomitant coronary artery bypass grafting (CABG). Fifty-nine (23%) required pericardial patch enlargement of the aortic root to accommodate sufficiently large prostheses. Prostheses used included Björk-Shiley Monostrut (n = 54), CarboMedics (n = 58), St. Jude (n = 74), Sorin Bicarbon (n = 2), Mitroflow pericardial (n = 26) and Carpentier-Edwards pericardial valve (n = 40). Pericardial valves were usually employed in patients 75 years and older. RESULTS: Operative mortality was 3.1%. There was no mortality in patients undergoing isolated AVR. Late mortality, after a mean observation period of two years, was 4.9%. At Doppler echocardiography one week postoperatively, 95% had a gradient across the prosthesis that was considered to be within acceptable limits (resting mean gradient < 30 mmHg). In the remaining patients higher gradients indicated some degree of prosthesis-patient mismatch. CONCLUSIONS: To avoid this mismatch the surgical considerations include choosing a prosthesis with a large effective orifice area, using an optimal valve implantation technique (partly or completely supra-annular placement of the prosthesis) and, if this is not enough, enlarging the annulus with an outflow patch.

Aged↗
PubMed1996

Surgical treatment of diffuse supravalvular aortic stenosis.

Diffuse supravalvular aortic stenosis can be treated by a variety of surgical approaches. In this case of severe diffuse supravalvular aortic stenosis in a child, we used the combination of an apicoaortic conduit followed 6 years later by aortic valve replacement, replacement of the ascending aorta and aortic arch, and an ascending to thoracic descending aorta bypass graft.

Adolescent↗
PubMed1997

[Valve replacement in congenital aortic stenosis].

BACKGROUND: Hemodynamically significant congenital aortic stenosis is usually surgically solved by valvotomy, infrequently aortic valve replacement is necessary. The aim of this retrospective study (period 1979-1995) is to find reasons for valve replacement, frequency of these procedures and early and long term results after aortic valve replacement for congenital aortic stenosis. METHODS AND RESULTS: Congenital aortic stenosis was solved by aortic valvotomy in 82 patients and by aortic valve replacement in 18 patients. Aortic valve replacement was performed 6x for congenital valvar aortic stenosis with mean aortic gradient 53.7 +/- 13.9 mm Hg and aortic valve area 0.42 +/- 0.04 cm2/m2 and 4x for valvar and subvalvar stenosis with mean aortic gradient 87.0 +/- 31.3 mm Hg, valve area 0.45 +/- 0.03 cm2/m2 and associated regurgitation 44.7 +/- 25.6%. In the remaining 8 patients aortic valve replacement was performed as reoperation after aortic valvotomy (after 20 +/- 8.4 years). In this group mean aortic gradient was only 32.2 +/- 13.8 mm Hg but regurgitation was 54.0 +/- 15.8%. Infective endocarditis occurred in 8 patients (44.5%) preoperatively. There were two hospital deaths (sudden death and multiorgan failure) and one death 3 years after operation (prosthetic endocarditis). Remaining 15 patients are in very good condition (NYHA I.-II.) 1-13 years after aortic valve replacement. CONCLUSIONS: Severely calcified aortic valve, endocarditis and associated incompetence are indications for valve replacement in patients with congenital aortic valve disease. Prevention of infective endocarditis is necessary pre and postoperatively, too. Long-term results after valve replacement for aortic valve stenosis are very good.

Adult↗
PubMed1977

Rheumatic aortic stenosis in young patients presenting with combined aortic and mitral stenosis.

This report describes 30 patients under the age of 30 years with rheumatic aortic stenosis, presenting with combined aortic and mitral stenosis. Three patients had additional tricuspid stenosis. Twenty-eight patients gave a history of rheumatic polyarthritis. The diagnosis was confirmed by right and left heart catheterisation in all. The murmur of aortic stenosis was not initially present in 8 out of 10 patients in congestive heart failure. Aortic valve calcification was not seen. Cineangiography showed a tricuspid aortic valve in all, unlike congenital aortic stenosis. A unique feature of this group was the raised pulmonary vascular resistance in 87 per cent of the patients. The present study shows that patients in India developing aortic stenosis after rheumatic fever do so early in the natural history of the disease.

Adolescent↗
PubMed2005

[Chlamydia pneumoniae--a new risk factor for calcific aortic stenosis?].

BACKGROUND: Nonrheumatic, calcific aortic stenosis is the main heart valve disease and the main cause of heart valve replacement in the elderly. Recent studies suggest that it is based on a chronic inflammatory process. The pathogenetic mechanisms, however, are unclear. METHODS: A MEDLINE search was conducted for the phrases "chlamydia pneumoniae" and "aortic valve", and all articles published between 1966 and May 2004 were evaluated. Data presented as letter or congress abstract was also included. RESULTS: Clinical and histopathologic studies demonstrate an association of calcific aortic stenosis and cardiovascular risk factors similar to atherosclerosis. As for atherosclerosis, infection with Chlamydia (C.) pneumoniae is also discussed as a further potential risk factor for calcific aortic stenosis. Previous seroepidemiologic and pathologic studies using various detection methods yielded heterogeneous results. CONCLUSION: Thus, data suggesting a pathogenetic association of C. pneumoniae and calcific aortic stenosis should be interpreted cautiously.

Antibodies, Bacterial↗
PubMed1977

Aortic stenosis: echocardiographic cusp separation and surgical description of aortic valve in 22 patients.

Diminished echocardiographic aortic cusp separation is used as one indicator of the severity of aortic stenosis. To test the validity of this index, 22 patients--12 (55 percent) with isolated aortic valve disease and 10 (45 percent) with aortic stenosis associated with mitral or coronary artery disease--underwent M mode echocardiographic examination before aortic valve replacement. Tracings of diagnostic quality were obtained without difficulty from all 22 patients. Cardiac catheterization was performed in 21 patients. Echocardiographic cusp separation was measured from the apparent mid-systolic orifice and from the outer periphery of the anterior cusp to the outer periphery of the posterior cusp (maximal peripheral cusp separation). Mid-systolic cusp separation varied in nearly every patient, depending on the angle of leaflet presentation to the ultrasonic beam. Maximal peripheral cusp separation measured 16 mm in 18 of 22 patients (82 percent); it indicated neither the severity of the aortic stenosis as documented with cardiac catheterization nor the mobility of the cusps seen at operation. The surgical and echocardiographic descriptions of leaflet and aortic root calcification were similar. In situ examination of aortic cusp separation indicated that diseased aortic valves are not comparable with normal valves or valves with uncomplicated congenital obstruction. The aortic leaflets were curled, fused, calcified and deformed from their natural state of coaptation. Abnormal thickening and limited or eccentric mobility of the aortic leaflets were useful indicators of the cause of valve disease, but cusp deformity secondary to aortic stenosis invalidated mid-systolic cusp separation and maximal peripheral cusp separation as indicators of the severity of aortic stenosis.

Adult↗
PubMed1984

Changes in echocardiographic left ventricular minor axis dimensions during exercise in patients with aortic stenosis.

Twelve patients with aortic stenosis (gradient 62 (25) mm Hg), and six normal subjects were examined using M mode echocardiography before and during submaximal bicycle exercise. Normal subjects showed a progressive fall in the end systolic minor axis dimension of the left ventricle and a rise in end diastolic dimension, giving an increase in stroke dimension and shortening fraction of 45% and 37% respectively at peak exercise. Patients with aortic stenosis showed no consistent alteration in either end systolic or end diastolic dimension, and consequently stroke dimension was unchanged during exercise. None of the patients with an abnormal exercise response had evidence of left ventricular failure at rest, and all but one completed the exercise protocol without undue dyspnoea. Non-invasive exercise testing in patients with aortic stenosis may detect abnormalities of left heart function which are not apparent at rest. These abnormalities may provide early evidence either of severe aortic stenosis or of incipient left ventricular failure.

Adolescent↗
PubMed1993

Rapidity of progression of aortic stenosis in patients with congenital bicuspid aortic valves.

The rapidity of progression of aortic stenosis in patients with congenital bicuspid aortic valves, and its relation to aging and valve anatomy are not well known. To elucidate these aspects, 75 patients aged 15 to 76 years were examined by echocardiography. Aortic valve sclerosis began from the second decade, the sclerotic index progressing with age (r = 0.72; p < 0.0001). Aortic valve calcium was noted from the fourth decade. Aortic valve pressure gradient increased approximately 18 mm Hg each decade, concomitant with progression of valve sclerosis (r = 0.78; p < 0.0001). Progression of cusp sclerosis was faster in patients with anteroposteriorly located cusps than in those with right-left-located cusps (p < 0.005), and was faster in those with eccentric cusps (width ratio of major and minor cusps > or = 1.2) than in those with symmetric cusps (p < 0.05). In patients with eccentric and anteroposteriorly located cusps, aortic valve pressure gradient increased 27 mm Hg per decade. In patients with congenital bicuspid aortic valves, the progression of aortic stenosis is rapid, and the rapidity depends to some extent on the position and eccentricity of the cusps.

Adolescent↗
PubMedDate not supplied

Pathophysiology of valvular aortic stenosis in the elderly.

Aortic stenosis in the elderly is related to calcification of either a bicuspid valve or a morphologically normal tricuspid valve. There is increasing evidence that factors relating to atherosclerosis are involved in valvular calcification and that it is an actively regulated process rather than a degenerative one. With severe aortic stenosis left ventricular hypertrophy occurs, decreasing wall stress and supporting the left ventricular ejection fraction. However, with pathologic hypertrophy there is a dropout of myocardial cells, subendocardial ischemia, and fibrosis. Eventually, symptoms of angina, non-Q wave myocardial infarction, exertional syncope, and heart failure occur. Once symptoms begin, the prognosis is poor, with sudden death occurring in about one third of patients who die. In the elderly, symptoms can be recognized very late in the course of the disease since they can be attributed to other problems and since the elderly patient may have reduced physical activity to a minimum. The more comorbidities that exist, the greater the risk of valve replacement. Symptomatic patients with severe aortic stenosis even over age 80 can be operated upon with a relatively low mortality and morbidity. In patients over age 80, prolongation of life for any meaningful length of time is not as important as relief of symptoms and improvement in the quality of life. Thus, it is unlikely that any truly asymptomatic patient over age 80, even with severe aortic stenosis, should be sent to surgery.

Aged↗
PubMed1993

Echocardiographic volume flow and stenosis severity measures with changing flow rate in aortic stenosis.

The anatomy of degenerative valvular aortic stenosis has been poorly represented in animal models, limiting the evaluation of noninvasive echo-Doppler measures of transvalvular volume flow rate and stenosis severity during progressive disease evolution or under conditions of changing volume flow rates. To study these issues, chronic valvular aortic stenosis, characterized by stiff leaflets without commissural fusion, was created in nine adult mongrel dogs by suturing pericardial covered Teflon-felt pads into the sinuses of Valsalva below the coronary ostia during hypothermic cardiac arrest. In the eight surviving dogs, echo-Doppler examinations were performed weekly for up to 8 wk postoperatively. Simultaneous invasive micromanometer pressure data were collected at 2-wk intervals in all subjects, with simultaneous ascending aortic transit time-volume flow measurement in four subjects. Volume flow rates were altered with saline and dobutamine infusions during invasive studies for comparison of echo-Doppler and invasive pressure gradients, volume flow, and valve areas. Serial echo-Doppler follow-up (39 +/- 11 days) demonstrated that, from baseline to final study, mean transvalvular pressure gradient increased (4 +/- 1 to 38 +/- 7 mmHg, P = 0.001), continuity equation aortic valve area decreased (2.06 +/- 0.18 to 0.54 +/- 0.04 cm2, P < 0.0001), and progressive left ventricular hypertrophy developed (62 +/- 6 to 114 +/- 9 g, P = 0.0003). Echo-Doppler and invasive data correlated well for measures of transvalvular pressure gradients (n = 98, maximum instantaneous gradient r = 0.95, mean gradient r = 0.91), volume flow (n = 75, stroke volume r = 0.86, cardiac output r = 0.86), and valve area (n = 73, r = 0.73) despite acute alterations in volume flow and progressive disease evolution. This chronic canine model, with anatomy and hemodynamics similar to clinical degenerative valvular aortic stenosis, should provide a valuable tool for investigating clinically relevant new measures of stenosis severity with use of invasive or noninvasive techniques.

Analysis of Variance↗
PubMedDate not supplied

Failure to detect Chlamydia pneumoniae in senile calcific aortic stenosis or calcified congenital bicuspid aortic valve by immunofluorescence, polymerase chain reaction and electron microscopy.

INTRODUCTION: Chlamydia pneumoniae has been identified in arterial atherosclerosis. Aortic valves affected by senile calcific aortic stenosis (SCAS) or calcification of a congenital bicuspid valve (CCBAV) may have interior environments similar to atherosclerosis. This study aimed to detect C. pneumoniae within either SCAS or CCBAV. METHODS: 60 valves showing either SCAS (n=36) or CCABV (n=22) and control valves (n=2) were studied for the presence of C. pneumoniae by the following three techniques: (1) indirect immunofluorescence (IF) was performed on 36 SCAS valves, 22 CCBAV valves and 2 control aortic valves using a HEp-2 cell line infected with C. pneumoniae as a positive control. Negative controls comprised duplicate slides of the same valves with omission of the primary antibody step. A section of human stomach was also used as a negative control. A semiquantitative scoring method was used to grade positive IF staining. (2) Polymerase chain reaction (PCR) was performed on 30 SCAS valves, 20 CCBAV valves and 1 control valve using C. pneumoniae as a positive control and negative controls comprised a Ureaplasma sp. and human DNA from peripheral blood mononuclear cells. (3) Electron microscopy (EM) was performed upon 13 SCAS, 8 CCBAV and 2 control valves. RESULTS: All three methods failed to detect the presence of C. pneumoniae in any of the 60 aortic valves examined. False positive IF staining was encountered in 81% of test valves and in 76% of negative control valve sections (positive in calcified material due to nonspecific binding of FITC-conjugated secondary antibody). No staining was observed in the negative control stomach sections. CONCLUSIONS: This study failed to detect C. pneumoniae within aortic valves showing SCAS or CCBAV. Studies using IF alone to detect C. pneumoniae in calcified tissues should be interpreted with caution, since nonspecific binding of FITC-conjugated secondary antibody by calcium in the cusps may be misinterpreted as evidence of Chlamydia. The use of appropriate controls and ancillary methods for the identification of C. pneumoniae are important in this regard.

Adult↗
PubMed2005

Analytical modeling of the instantaneous maximal transvalvular pressure gradient in aortic stenosis.

In presence of aortic stenosis, a jet is produced downstream of the aortic valve annulus during systole. The vena contracta corresponds to the location where the cross-sectional area of the flow jet is minimal. The maximal transvalvular pressure gradient (TPG(max)) is the difference between the static pressure in the left ventricle and that in the vena contracta. TPG(max) is highly time-dependent over systole and is known to depend upon the transvalvular flow rate, the effective orifice area (EOA) of the aortic valve and the cross-sectional area of the left ventricular outflow tract. However, it is still unclear how these parameters modify the TPG(max) waveform. We thus derived an explicit analytical model to describe the instantaneous TPG(max) across the aortic valve during systole. This theoretical model was validated with in vivo experiments obtained in 19 pigs with supravalvular aortic stenosis. Instantaneous TPG(max) was measured by catheter and its waveform was compared with the one determined from the derived equation. Our results showed a very good concordance between the measured and predicted instantaneous TPG(max). Total relative error and mean absolute error were on average 9.4+/-4.9% and 2.1+/-1.1 mmHg, respectively. The analytical model proposed and validated in this study provides new insight into the behaviour of the TPG(max) and thus of the aortic pressure at the level of vena contracta. Because the static pressure at the coronary inlet is similar to that at the vena contracta, the proposed equation will permit to further examine the impact of aortic stenosis on coronary blood flow.

Aortic Valve↗
PubMed1996

Correlation of pediatric echocardiographic Doppler and catheter-derived valvar aortic stenosis gradients and the influence of aortic regurgitation.

This report suggests that in the absence of aortic regurgitation, Doppler peak and mean gradients are useful predictors of catheter peak-to-peak aortic stenosis gradients >50 mm Hg; however, in the presence of aortic regurgitation, the predictive value diminishes dramatically, but improves when electrographic data are incorporated. We present potentially useful equations to help predict the need for interventional catheterization for valvar aortic stenosis.

Adolescent↗
PubMed1992

Morphometric investigation of human myocardium in arterial hypertension and valvular aortic stenosis.

UNLABELLED: Both arterial hypertension and aortic stenosis lead to pressure overload of the left ventricle. As intramyocardial vasculature is confronted with pressure overload in hypertension but not in aortic stenosis, structural differences are to be expected in both forms of left ventricular hypertrophy. With the aid of morphometry, we investigated human myocardium from autopsied hearts from six patients with arterial hypertension and 10 controls, as well as myectomy specimens from cardiac surgery from 14 patients with aortic stenosis. Mean left ventricular myocytic diameter was significantly (P less than 0.05) increased compared with controls (12.4 +/- 1.5 microns) during hypertension (+27%) as well as aortic stenosis (+65%) (P less than 0.05). This was combined with a greater volume density of perimyocytic fibrosis (controls = 0.8 +/- 0.4 V upsilon %) during hypertension (+250%) and aortic stenosis (+587%) (P less than 0.05). Walls of intramyocardial arterioles (external diameter 20-40 and 40-80 microns) were thickened to 32% and 44% (P less than 0.05) during hypertension, but not during aortic stenosis. Compared with controls, perivascular fibrosis of these arterioles was increased by +215% and 61% (P less than 0.05), respectively, during hypertension, but not during aortic stenosis. CONCLUSIONS: Myocytic hypertrophy and increased perimyocytic fibrosis accompany intraventricular pressure overload (hypertension and aortic stenosis) in human hearts. Myocardial structure as a result of arterial hypertension, but not aortic stenosis, is also characterized by intramyocardial arteriole wall-thickening and increased perivascular fibrosis. Thus, distinct structural reaction patterns are noted in the cardiac hypertrophy associated with hypertension and aortic stenosis.

Aged↗
PubMed2004

A ventricular-vascular coupling model in presence of aortic stenosis.

In patients with aortic stenosis, the left ventricular afterload is determined by the degree of valvular obstruction and the systemic arterial system. We developed an explicit mathematical model formulated with a limited number of independent parameters that describes the interaction among the left ventricle, an aortic stenosis, and the arterial system. This ventricular-valvular-vascular (V(3)) model consists of the combination of the time-varying elastance model for the left ventricle, the instantaneous transvalvular pressure-flow relationship for the aortic valve, and the three-element windkessel representation of the vascular system. The objective of this study was to validate the V(3) model by using pressure-volume loop data obtained in six patients with severe aortic stenosis before and after aortic valve replacement. There was very good agreement between the estimated and the measured left ventricular and aortic pressure waveforms. The total relative error between estimated and measured pressures was on average (standard deviation) 7.5% (SD 2.3) and the equation of the corresponding regression line was y = 0.99x - 2.36 with a coefficient of determination r(2) = 0.98. There was also very good agreement between estimated and measured stroke volumes (y = 1.03x + 2.2, r(2) = 0.96, SEE = 2.8 ml). Hence, this mathematical V(3) model can be used to describe the hemodynamic interaction among the left ventricle, the aortic valve, and the systemic arterial system.

Aortic Valve Stenosis↗
PubMed1995

Comparison of valvular resistance, stroke work loss, and Gorlin valve area for quantification of aortic stenosis. An in vitro study in a pulsatile aortic flow model.

BACKGROUND: Valvular resistance and stroke work loss have been proposed as alternative measures of stenotic valvular lesions that may be less flow dependent and, thus, superior over valve area calculations for the quantification of aortic stenosis. The present in vitro study was designed to compare the impacts of valvular resistance, stroke work loss, and Gorlin valve area as hemodynamic indexes of aortic stenosis. METHODS AND RESULTS: In a pulsatile aortic flow model, rigid stenotic orifices in varying sizes (0.5, 1.0, 1.5 and 2.0 cm2) and geometry were studied under different hemodynamic conditions. Ventricular and aortic pressures were measured to determine the mean systolic ventricular pressure (LVSPm) and the transstenotic pressure gradient (delta Pm). Transvalvular flow (Fm) was assessed with an electromagnetic flowmeter. Valvular resistance [VR = 1333.(delta Pm/Fm)] and stroke work loss [SWL = 100.(delta Pm/LVSPm)] were calculated and compared with aortic valve area [AVA = Fm/(50 square root of delta Pm)]. The measurements were performed for a large range of transvalvular flows. At low-flow states, flow augmentation (100-->200 mL/s) increased calculated valvular resistance between 21% (2.0 cm2 orifice) and 66% (0.5-cm2 orifice). Stroke work loss demonstrated an increase from 43% (2.0 cm2) to 100% (1.0 cm2). In contrast, Gorlin valve area revealed only a moderate change from 29% (2.0 cm2) to 5% (0.5 cm2). At physiological flow rates, increase in transvalvular flow (200-->300 mL/s) did not alter calculated Gorlin valve area, whereas valvular resistance and stroke work loss demonstrated a continuing increase. Our experimental results were adopted to interpret the results of three clinical studies in aortic stenosis. The flow-dependent increase of Gorlin valve area, which was found in the cited clinical studies, can be elucidated as true further opening of the stenotic valve but not as a calculation error due to the Gorlin formula. CONCLUSIONS: Within the physiological range of flow, calculated aortic valve area was less dependent on hemodynamic conditions than were valvular resistance and stroke work loss, which varied as a function of flow. Thus, for the assessment of the severity of aortic stenosis, the Gorlin valve area is superior over valvular resistance and stroke work loss, which must be indexed for flow to adequately quantify the hemodynamic severity of the obstruction.

Aortic Valve↗
PubMed2002

Comparison of left ventricular geometry and left atrial size and function in patients with aortic stenosis versus those with pure aortic regurgitation.

Chronic aortic valve disease can result in distinct adaptive left ventricular (LV) geometric patterns, which has different effects on LV function and left atrial (LA) performance. In this study we assessed the effect of LV geometry on LA size and function, and we verified the relation between LA size and LV mass in patients with distinct LV overload subsets. We analyzed 183 patients with aortic valve disease who underwent a complete echocardiographic evaluation. Based on the type of valvular dysfunction, patients were classified into 2 groups: 141 patients with aortic stenosis (group AS) and 42 patients with pure aortic regurgitation (group AR). Each of these 2 groups were then divided into those with a concentric LV pattern and those with an eccentric pattern. Both LA size and LA ejection force were significantly greater in group AS than group AR, particularly in patients with a concentric LV pattern. The degree of LA enlargement depended on LV mass in the patients with a concentric LV pattern (group AS r = 0.61, p <0.00001; group AR r = 0.38, p = 0.04). In contrast, no relation was found between LA size and LV mass in the patients with an eccentric pattern, independently of the type of valve dysfunction. Our results indicate that the influence of LV geometry on LA size and function in patients with aortic valve disease is relevant. A concentric LV pattern is associated with greater LA size and higher ejection than an eccentric pattern, suggesting that chronic LV pressure overload more than volume overload has a greater effect on stimulating increases in LA performance. The degree of LA enlargement depends on LV mass in patients with a concentric LV pattern, whereas it was unpredictable in those with an eccentric LV pattern.

Adult↗