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Results for “AORTIC STENOSIS”

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PubMed1990

Coronary atherosclerosis is associated with left ventricular dysfunction and dilatation in aortic stenosis.

Patients with aortic stenosis develop widely variable patterns of left ventricular hypertrophy and dysfunction. We postulated that coronary atherosclerosis (CAD) may be associated with impaired left ventricular function and chamber dilatation in patients with aortic stenosis. Left ventricular mass and volumes were quantified from two-dimensional echocardiography and correlated with coronary angiography in 78 patients with severe aortic stenosis and no previous myocardial infarction or regional wall motion abnormalities. Eighteen patients (group 1) had smooth coronary arteries, 25 patients had irregular coronary arteries with 50% or less stenosis (group 2), and 35 patients had obstructive CAD (group 3). Even though the calculated valve area was similar in all three study groups, group 1 patients had higher values for ejection fraction (65 +/- 9%, 51 +/- 17%, and 48 +/- 13%; p = 0.0002), systolic mass-to-volume ratio (9.2 +/- 3.9, 5.6 +/- 2.8, and 5.2 +/- 2.2; p = 0.0001), and cardiac index (2.9 +/- 0.7, 2.5 +/- 0.7, and 2.3 +/- 0.6 l/min.min2; p = 0.015) than patients in groups 2 and 3, respectively (mean +/- SD). Mean circumferential wall stress was inversely related to severity of CAD. Multivariate analysis showed that CAD is an independent predictor of ejection fraction and mass-to-volume ratio in this group of patients. Thus, in an elderly population with severe aortic stenosis, patients with both obstructive and nonobstructive CAD have an increased incidence of left ventricular enlargement and systolic dysfunction.

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PubMed1989

Risk of noncardiac surgical procedures in patients with aortic stenosis.

Although severe aortic stenosis has been reported to increase the risk of noncardiac operation, recent advances in anesthetic management may alter this risk. We reviewed the perioperative course of 48 consecutive patients (mean age, 73 years) with significant aortic stenosis who underwent a noncardiac operation or diagnostic procedure between 1985 and 1987. Twenty-five patients had local anesthesia with intravenous sedation, 22 (17 with severe and 5 with moderate aortic stenosis) underwent general anesthesia, and 1 had spinal anesthesia. Of the 48 patients, 36 (75%) had symptoms--congestive heart failure in 24, angina in 19, and syncope in 7. Doppler echocardiography, performed in all 48 patients, revealed a mean peak instantaneous gradient of 76 mm Hg and a calculated aortic valve area (in 22 patients) of 0.61 cm2. In the 20 patients who also underwent preoperative cardiac catheterization, the calculated mean aortic valve area was 0.59 cm2. Seven patients had one or more perioperative events, including intraoperative hypotension in five; all except one of these events were transient and without major sequelae. No intraoperative deaths occurred. Selected patients with severe aortic stenosis can undergo noncardiac procedures at a reasonably low risk with careful monitoring of anesthesia.

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PubMed1986

Resolution of Heyde's syndrome of aortic stenosis and gastrointestinal bleeding after aortic valve replacement.

The observation by Heyde that unexplained gastrointestinal bleeding may be associated with aortic stenosis has been confirmed by many others. It has been suggested that the combination of gastrointestinal bleeding and aortic stenosis be termed Heyde's syndrome. Gastrointestinal bleeding in this syndrome has been attributed to angiodysplasia. Segmental resection of those portions of the gastrointestinal tract containing the angiodysplastic lesions has been considered the definitive treatment for patients with Heyde's syndrome who are symptomatic because of chronic blood loss. However, recent observations suggest that aortic valve replacement with a bioprosthesis is a better therapeutic approach for those patients with severe aortic stenosis. This treatment has been shown to alleviate the symptomatology of both the stenosed aortic valve and the chronically bleeding bowel.

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PubMed1987

Doppler ultrasound in aortic stenosis: in vitro studies of pressure gradient determination.

Torricelli's equation expresses a simple relationship between fluid velocity and pressure gradient in orifice flow and is currently used in conjunction with noninvasive Doppler ultrasound to determine gradients in mitral stenosis, and aortic stenosis, as well as other cardiovascular orifices. In theory, however, the Torricelli equation overestimates the gradient in aortic stenosis and the Borda equation should be more applicable. A brief tutorial derivation of the Borda and Torricelli equations is presented. The applicability of Torricelli's equation in aortic stenosis was studied experimentally with a rigid wall, pulsatile flow analogue. Doppler ultrasound and manometric data were collected simultaneously. Percent stenosis, peak flow rate and fluid viscosity were varied. The results demonstrated that the Torricelli equation consistently overestimated the pressure gradient. At 61% area stenosis, the overestimation exceeded 100%. In vivo studies are required to determine the relevance of the observations to clinical situations.

Aortic Valve Stenosis↗
PubMed1953

AORTIC stenosis.

Explore the source record for details and available documents.

Aortic Valve↗
PubMed1988

Demonstration of an imbalance between coronary perfusion and excessive load as a mechanism of ischemia during stress in patients with aortic stenosis.

Patients with aortic stenosis are susceptible to myocardial ischemia during hemodynamic stress, which may be caused by two mechanisms. First, vascular abnormalities inherent in myocardial hypertrophy may impair coronary vasodilation, limiting the ability to increase coronary blood flow to meet increased metabolic demands. Second, aortic stenosis itself may cause an imbalance between oxygen supply and demand during hemodynamic stress by decreasing aortic pressure (decreasing coronary perfusion or oxygen supply) and increasing left ventricular pressure (increasing oxygen demand). By decreasing aortic valve gradient without immediately altering ventricular hypertrophy, aortic balloon valvuloplasty offers the opportunity to distinguish these mechanisms. We hypothesized that aortic valvuloplasty would improve the balance between myocardial oxygen supply and demand, especially during isoproterenol infusion. Nine patients undergoing aortic balloon valvuloplasty were assessed at baseline and during isoproterenol infusion (5 +/- 2 micrograms/min, mean +/- SD) before and after valvuloplasty. Valvuloplasty increased myocardial oxygen supply. After valvuloplasty, isoproterenol decreased diastolic pressure time index (DPTI) less and increased coronary sinus blood flow more than before valvuloplasty (-630 +/- 367 vs. -292 +/- 224 mm Hg.sec/min, p = 0.02 and 53 +/- 137 vs. 179 +/- 145 ml/min, p = 0.001, respectively). Valvuloplasty also decreased oxygen demand, decreasing systolic pressure time index (SPTI) from 4,135 +/- 511 to 3,021 +/- 492 mm Hg.sec/min (p = 0.0002). Valvuloplasty improved the balance between myocardial oxygen supply and demand, increasing baseline DPTI:SPTI, decreasing aortocoronary sinus oxygen content difference (0.51 +/- 0.15 to 0.68 +/- 0.14, p = 0.005 and 96 +/- 14 to 78 +/- 15 ml O2/l, p = 0.002, respectively), and decreasing myocardial lactate production during isoproterenol infusion (mean lactate extraction fraction, -0.26 +/- 0.40 to 0.14 +/- 0.17; p = 0.01). We conclude that aortic valvuloplasty improves the balance between myocardial oxygen supply and demand during hemodynamic stress induced by isoproterenol infusion. We speculate that the clinical improvement, which often occurs in these patients after valvuloplasty despite persistence of hemodynamically "critical" aortic stenosis, is in part attributable to immediate improvement in the myocardial oxygen supply:demand ratio.

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PubMed1986

Prognostic factors in valvotomy for critical aortic stenosis in infancy.

Aortic valvotomy for critical aortic stenosis in infancy has had a high mortality. To determine the factors that influence survival, we reviewed the cases of 24 infants who underwent aortic valvotomy in the first 6 months of life (mean 4 1/2 weeks) for aortic stenosis from 1978 to 1984. Cardiopulmonary bypass was used in all patients. Operative mortality was 21% (5/24), four of the five deaths occurring from low cardiac output. Analysis of preoperative factors affecting survival versus nonsurvival revealed that low ejection fraction (60% +/- 17% in survivors versus 36% +/- 2% in nonsurvivors), high left ventricular end-diastolic pressure (16 +/- 7 mm Hg in survivors versus 30 +/- 14 mm Hg in nonsurvivors), and presence of endocardial fibroelastosis (25% in survivors versus 100% in nonsurvivors) all were predictive of a poor outcome, although the small sample size indicated caution in interpreting results. Factors that did not appear to influence survival included peak systolic gradient (79 +/- 30 mm Hg in survivors versus 60 +/- 15 mm Hg in nonsurvivors) and left ventricular end-diastolic volume (37 +/- 17 cm3/m2 in survivors versus 36 +/- 7 cm3/m2 in nonsurvivors). Four patients with a left ventricular end-diastolic volume below 26 cm3/m2 survived. Postoperative gradients averaged 25 +/- 21 mm Hg at 3.4 +/- 2 years' follow-up in nine recatheterized patients. Ejection fraction of these patients increased from 45% +/- 10% to 70% +/- 11% and left ventricular end-diastolic volume increased from 37 +/- 17 to 58 +/- 5 cm3/m2. Two of 17 patients have required apical-aortic conduits; all other patients are asymptomatic. We conclude that infants with critical aortic stenosis benefit from valvotomy even with impaired left ventricular function and severely reduced left ventricular dimensions and many have nearly normal hemodynamics on late follow-up.

Age Factors↗
PubMed2004

[New concepts on the physiopathology and therapy of aortic stenosis].

Calcified "degenerative" aortic stenosis is currently the most common valvulopathy in industrialised countries. In the course of the last decade, experimental studies have allowed a better understanding of the physiopathology of this vavlulopathy. The latest development is the evidence for the initiation and progression of this disease, similar to those described for atherosclerosis. Lipid disturbances, in particular hypercholesterolaemia, constitute an important factor in the initiation of valvular lesions, but also in aortic orifice calcification. Certain preliminary clinical studies are in favour of the significance of statins for slowing the progression of aortic stenosis. This potential beneficial effect requires confirmation by randomised prospective studies and raises hopes for medical therapy in order to avoid the evolution of ordinary aortic sclerosis into tight calcified aortic stenosis.

Aortic Valve Stenosis↗
PubMed2003

Acquired von Willebrand syndrome in aortic stenosis.

BACKGROUND: Aortic-valve stenosis can be complicated by bleeding that is associated with acquired type 2A von Willebrand syndrome. However, the prevalence and cause of the hemostatic abnormality in aortic stenosis are unknown. METHODS: We enrolled 50 consecutive patients with aortic stenosis, who completed a standardized screening questionnaire to detect a history of bleeding. Forty-two patients with severe aortic stenosis underwent valve replacement. Platelet function under conditions of high shear stress, von Willebrand factor collagen-binding activity and antigen levels, and the multimeric structure of von Willebrand factor were assessed at base line and one day, seven days, and six months postoperatively. RESULTS: Skin or mucosal bleeding occurred in 21 percent of the patients with severe aortic stenosis. Platelet-function abnormalities under conditions of high shear stress, decreased von Willebrand factor collagen-binding activity and the loss of the largest multimers, or a combination of these was present in 67 to 92 percent of patients with severe aortic stenosis and correlated significantly with the severity of valve stenosis. Primary hemostatic abnormalities were completely corrected on the first day after surgery but tended to recur at six months, especially when there was a mismatch between patient and prosthesis (with an effective orifice area of less than 0.8 cm2 per square meter of body-surface area). CONCLUSIONS: Type 2A von Willebrand syndrome is common in patients with severe aortic stenosis. Von Willebrand factor abnormalities are directly related to the severity of aortic stenosis and are improved by valve replacement in the absence of mismatch between patient and prosthesis.

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