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Biomedical subjects

C M Otto

Publications and source records attributed to C M Otto.

At least 55 records · Page 3Linked to original sources

Osteopontin is expressed in human aortic valvular lesions.

BACKGROUND: Nonrheumatic stenosis of trileaflet aortic valves, in which calcification is a prominent feature, has been termed a "degenerative" condition, but it has been demonstrated recently that chronic inflammation is a characteristic feature of the developing lesion of aortic stenosis. This observation raised the possibility that calcification in the aortic valve might be actively regulated. Thus, the present study investigated whether osteopontin, a protein implicated in the regulation of both normal and dystrophic calcification, could be detected in lesions of valvular aortic stenosis. METHODS AND RESULTS: Morphological and immunohistochemical studies were performed on 14 human aortic valves, representing a range of pathology from normal to clinically stenotic. The extent of calcification and macrophage accumulation and their relation to the presence of osteopontin protein were characterized. Highly statistically significant associations were found between the degree of osteopontin expression and the degrees of both calcification and macrophage accumulation in early through late lesions of aortic stenosis. Further, in situ hybridization localized osteopontin mRNA to a subset of lesion macrophages. CONCLUSIONS: These results suggest that, rather than representing a degenerative and unmodifiable process, calcification in aortic stenosis may be, in part, an actively regulated process with the potential for control either through modification of inflammation or synthesis of proteins such as osteopontin, which may modulate calcification in this tissue.

Aortic Valve↗

Tumor necrosis factor production in cats in response to lipopolysaccharide: an in vivo and in vitro study.

Supernatants from feline peritoneal exudate cells (PECs) exposed to lipopolysaccharde (LPS) produced significantly (P < 0.05) more tumor necrosis factor (TNF) activity than supernatants from cells exposed to media. An in vitro LPS response was obtained following incubation of whole blood with 10 micrograms ml-1 LPS for 2 h. Intravenous infusion of LPS (750 micrograms kg-1 rapidly increased plasma TNF activity to a maximum at 60 min after initiation of LPS infusion. By 180 min, TNF activity returned to baseline. Cats produce TNF in response to LPS in a manner similar to other species. Measurement of TNF activity in plasma or in LPS-stimulated whole blood are methods to further characterize the inflammatory response in feline diseases.

Animals↗

Expression of recombinant feline tumor necrosis factor is toxic to Escherichia coli.

The tumor necrosis factor (TNF) genes from cats, horses, and pigs have all been cloned into the pFLAG-1 fusion protein expression vector (International Biotechnologies, Inc., Kodak, New Haven, Conn.). Growth curves for Escherichia coli containing the pFLAG-1 vector alone and the pFLAG-1 vector containing the TNF gene from each species were determined by visible light spectrophotometry (at 600 nm). Porcine TNF, equine TNF, and feline TNF cultures had slower doubling rates than cultures containing the pFLAG-1 vector alone. Cultures of cells transformed with feline TNF reached peak densities at 3 to 4 h and then decreased to near initial densities prior to the recovery of growth. The induction of expression with isopropyl-beta-D-thiogalactopyranoside (IPTG) arrested the growth of fresh feline TNF cultures for 6 h, which was followed by complete recovery. This inhibition occurred in two strains of E. coli (LL308 and JM101). Induced feline TNF cultures expressed the TNF-FLAG fusion protein for the first 6.5 h. Uninduced cultures expressed low levels of fusion protein. The feline TNF-pFLAG-1 vector was purified from cells expressing fusion protein and from cells with recovered growth curves. Sequencing the vector demonstrated the complete feline TNF gene and tac promoter in cells expressing the fusion protein and a deletional mutation of the tac promoter site in recovered cells. In contrast to equine and porcine TNF, the expression of recombinant feline TNF is toxic to E. coli. Alterations in protein folding and the prevention of secretion of the feline protein may explain the toxic effect.

Animals↗

Gender differences in left ventricle geometry and function in patients undergoing balloon dilatation of the aortic valve for isolated aortic stenosis. NHLBI Balloon Valvuloplasty Registry.

BACKGROUND: Gender differences in cardiac size have been described in normal humans and animals and in response to pressure overload. To examine the influence of gender on the left ventricular response to pressure overload, clinical, haemodynamic, and echocardiographic data were analysed in the 232 adults with isolated aortic stenosis enrolled in the Balloon Valvuloplasty Registry. METHODS AND RESULTS: There were 92 men (mean (SD) age 75 (11) years) and 140 women (79 (9) years; P = 0.002). Women had similar symptoms (New York Heart Association class) but lower overall functional status than men (P = 0.008). Catheterisation data showed similar valve area indices (mean (SD) (0.30 (0.09) in men and 0.31 (0.13) cm/m2 in women) but higher peak and mean gradients in women (peak 74 (30) v 63 (22) mm Hg; mean 61 (21) v 54 (18) mm Hg; both P < or = 0.01). On M mode echocardiography women had greater septal and posterior wall thickness but similar cavity diameter, after normalising dimensions to body surface area, resulting in higher relative wall thickness (0.60 (0.20) v 0.50 (0.15); P = 0.0002). Left ventricular mass index was similar in women and men (166 (59) v 159 (50) gm/m2 respectively), however, the prevalence of left ventricular hypertrophy according to sex specific criteria was 54% in men and 81% in women (P = 0.0001). Multiple logistic regression models that adjusted for age, functional status, fractional shortening, and left ventricular systolic pressure found the presence or absence of hypertrophy to be independently associated with gender (P < or = 0.002). Left ventricular systolic function tended to be better in women, who had a higher cardiac index (2.5 (0.8) v 2.3 (0.6) 1/min/m2; P = 0.01), left ventricular peak systolic pressure (211 (36) v 192 (35) mm Hg; P = 0.0001), and echo fractional shortening (32 (13) v 28 (12)%; P = 0.05); however, these differences were reduced when patients with regional wall motion abnormalities were excluded. CONCLUSIONS: In this population of elderly patients undergoing balloon dilatation of isolated aortic stenosis, left ventricular chamber geometry was different in men and women. Because this was a selected population, gender should be further evaluated as a possible determinant of the cardiac adaptation to chronic pressure overload.

Aged↗

Flow dependence of measures of aortic stenosis severity during exercise.

OBJECTIVES: This study was designed to investigate the effect of altering transvalvular volume flow rate on indexes of aortic stenosis severity (valve area, valve resistance, percent left ventricular stroke work loss) derived by using Doppler echocardiography. BACKGROUND: Assessment of hemodynamic severity in aortic stenosis has been limited by the absence of an index that is independent of transvalvular flow rate. The traditional measurement of valve area by the Gorlin equation has been shown to vary with alterations in transvalvular flow. Recently, valve resistance and percent stroke work loss have been proposed as indexes that are relatively independent of flow. Although typically derived with invasive measurements, valve resistance and percent stroke work loss (in addition to continuity equation valve area) can be determined noninvasively with Doppler echocardiography. METHODS: We performed 110 symptom-limited exercise studies in 66 asymptomatic patients with valvular aortic stenosis. Continuity equation valve area, valve resistance (the ratio between mean transvalvular pressure gradient and mean flow rate) and the steady component of percent stroke work loss (the ratio between mean transvalvular pressure gradient and left ventricular systolic pressure) were assessed by Doppler echocardiography at rest and immediately after exercise. RESULTS: Mean transvalvular volume flow rate increased 24% (from [mean +/- SD] 319 +/- 80 to 400 +/- 140 ml/s, p < 0.0001); mean pressure gradient increased 36% (from 30 +/- 14 to 41 +/- 18 mm Hg, p < 0.0001); continuity equation aortic valve area increased 14% (from 1.38 +/- 0.50 to 1.58 +/- 0.69 cm2, p < 0.0001); valve resistance increased 13% (from 137 +/- 81 to 155 +/- 97 dynes.s.cm-5, p < 0.0001); and percent stroke work loss increased 17% (from 17.4 +/- 6.9% to 20.3 +/- 8.5%, p < 0.0001). The effects of flow on valve area, valve resistance and percent stroke work loss were independent of the presence of an aortic valve area < or = or > 1.0 cm2 or reduced transvalvular flow rate (rest cardiac output < 4.5 liters/min). CONCLUSIONS: In patients with asymptomatic aortic stenosis, Doppler echocardiographic measures of valve area, valve resistance and percent stroke work loss are flow dependent. Flow dependence is observed with valve area < or = or > 1.0 cm2 and in the presence of both normal and low transvalvular flow states. The potential effects of transvalvular flow should be considered when interpreting Doppler measures of aortic stenosis severity.

Adult↗

Terfenadine toxicosis in dogs.

Terfenadine is an antihistamine that has been reported to be safe for use in human beings and animals. This report focuses on an index case of terfenadine toxicosis and several cases of terfenadine toxicosis reported to the National Animal Poison Control Center from 1987 through 1992. Adverse effects of terfenadine can be seen with dosages as low as 6.6 mg/kg of body weight. Any accidental exposure to terfenadine should be treated by inducing emesis and by administering activated charcoal, along with supportive care.

Animals↗

Acute aortic dissection: typical and atypical imaging features.

Acute aortic dissection (AAD) is the most common emergency affecting the aorta. Noninvasive imaging allows prompt and reliable diagnosis of AAD and has largely supplanted aortography. However, atypical imaging features and diagnostic pitfalls can delay lifesaving therapy. An intimal flap is the characteristic feature of AAD. If there is flow within both lumina, typical imaging features are probably present. If the false lumen is thrombosed or there is no intimal tear to permit flow through the false lumen, a distinct intimal flap may not be present. Secondary signs of AAD include an intramural or periaortic acute thrombus, which manifests as a high-attenuation cuff or crescent on unenhanced computed tomographic scans. Other conditions that can reduce the conspicuity of the intimal flap include atypical configurations of the flap, such as seen with short dissections or with multiple false channels, in which case the flaps are complex. Finally, aortic anomalies may cause confusion.

Acute Disease↗

Three-year outcome after balloon aortic valvuloplasty. Insights into prognosis of valvular aortic stenosis.

BACKGROUND: To identify predictors of long-term outcome after balloon aortic valvuloplasty, we analyzed data on 674 adults (mean age, 78 +/- 9 years; 56% were women) undergoing this procedure at 24 clinical centers who had a mean initial increase in aortic valve area of 0.3 cm2. METHODS AND RESULTS: Baseline data included clinical, echocardiographic, and catheterization variables. Follow-up data included mortality, cause of death, rehospitalization, 6-month echocardiography, and functional status. Kaplan-Meier curves and log-rank tests were used to evaluate survival in subgroups. Multivariate Cox regression models were used to identify independent predictors of survival. Overall survival was 55% at 1 year, 35% at 2 years, and 23% at 3 years, with the majority of deaths (70%) classified as cardiac by an independent review committee. Rehospitalization was common (64%), although 61% of survivors at 2 years reported improved symptoms. Echocardiography at 6 months (n = 115) showed restenosis from the postprocedural valve area of 0.78 +/- 0.31 cm2 to 0.65 +/- 0.25 cm2 (P < .0001). With stepwise multivariate analysis, sequentially adding clinical, echocardiographic, and catheterization variables, the overall model identified independent predictors of survival as baseline functional status, baseline cardiac output, renal function, cachexia, female gender, left ventricular systolic function, and mitral regurgitation. Baseline and postprocedural variables were examined to identify which subgroup of patients has the best outcome after aortic valvuloplasty. A "lower-risk" subgroup (28% of the study population), defined by normal left ventricular systolic function and mild clinical functional limitation, had a 3-year survival of 36% compared with 17% in the remainder of the study group. CONCLUSIONS: Long-term survival after balloon aortic valvuloplasty is poor with 1- and 3-year survival rates of 55% and 23%, respectively. Although survivors report fewer symptoms, early restenosis and recurrent hospitalization are common.

Adult↗

Dependence of Gorlin formula and continuity equation valve areas on transvalvular volume flow rate in valvular aortic stenosis.

BACKGROUND: Valve areas derived by the Gorlin formula have been observed to vary with transvalvular volume flow rate. Continuity equation valve areas calculated from Doppler-echo data have become a widely used alternate index of stenosis severity, but it is unclear whether continuity equation valve areas also vary with volume flow rate. This study was designed to investigate the effects of changing transvalvular volume flow rate on aortic valve areas calculated using both the Gorlin formula and the continuity equation in a model of chronic valvular aortic stenosis. METHODS AND RESULTS: Using a canine model of chronic valvular aortic stenosis in which anatomy and hemodynamics are similar to those of degenerative aortic stenosis, each subject (n = 8) underwent three studies at 2-week intervals. In each study, transvalvular volume flow rates were altered with saline or dobutamine infusion (mean, 10.3 +/- 5.1 flow rates per study). Simultaneous measurements were made of hemodynamics using micromanometer-tipped catheters, of ascending aortic instantaneous volume flow rate using a transit-time flowmeter, and of left ventricular outflow and aortic jet velocity curves using Doppler echocardiography. Valve areas were calculated from the invasive data by the Gorlin equation and from the Doppler-echo data by the continuity equation. In the 24 studies, mean transit-time transvalvular volume flow rate ranged from 80 +/- 33 to 153 +/- 49 mL/min (P < .0001). Comparing minimum to maximum mean volume flow rates, the Gorlin valve area changed from 0.54 +/- 0.22 cm2 to 0.68 +/- 0.21 cm2 (P < .0001), and the continuity equation valve area changed from 0.57 +/- 0.18 cm2 to 0.70 +/- 0.20 cm2 (P < .0001). A strong linear relation was observed between Gorlin valve area and mean transit-time volume flow rate for each study (median, r = .88), but the slope of this relation varied between studies. The Doppler-echo continuity equation valve area had a weaker linear relation with transit-time volume flow rate for each study (median, r = .51). CONCLUSIONS: In this model of chronic valvular aortic stenosis, both Gorlin and continuity equation valve areas were flow-dependent indices of stenosis severity and demonstrated linear relations with transvalvular volume flow rate. The changes in calculated valve area that occur with changes in transvalvular volume flow should be considered when measures of valve area are used to assess the hemodynamic severity of valvular aortic stenosis.

Animals↗

Characterization of the early lesion of 'degenerative' valvular aortic stenosis. Histological and immunohistochemical studies.

BACKGROUND: Nonrheumatic stenosis of trileaflet aortic valves, often termed senile or calcific valvular aortic stenosis, is considered a "degenerative" process, but little is known about the cellular or molecular factors that mediate its development. METHODS AND RESULTS: To characterize the developing aortic valvular lesion, we performed histological and immunohistochemical studies on Formalin-fixed and methanol-Carnoy's-fixed paraffin-embedded aortic valve leaflets or on frozen sections obtained at autopsy from 27 adults (age, 46 to 82 years) with normal leaflets (n = 6), mild macroscopic leaflet thickening (n = 15), or clinical aortic stenosis (n = 6). Focal areas of thickening ("early lesions") were characterized by (1) subendothelial thickening on the aortic side of the leaflet, between the basement membrane (PAS-positive) and elastic lamina (Verhoeff-van Gieson), (2) the presence of large amounts of intracellular and extracellular neutral lipids (oil red O) and fine, stippled mineralization (von Kossa), and (3) disruption of the basement membrane overlying the lesion. Regions of the fibrosa adjacent to these lesions were characterized by thickening and by protein, lipid, and calcium accumulation. Control valves showed none of these abnormalities. Immunohistochemical studies were performed using monoclonal antibodies directed against macrophages (anti-CD68 or HAM-56), and contractile proteins of smooth muscle cells or myofibroblasts (anti-alpha-actin and HHF-35) or rabbit polyclonal antiserum against T lymphocytes (anti-CD3). In normal valves, scattered macrophages were present in the fibrosa and ventricularis, and occasional muscle actin-positive cells were detected in the proximal portion of the ventricularis near the leaflet base, but no T lymphocytes were found. In contrast, early lesions were characterized by the presence of an inflammatory infiltrate composed of non-foam cell and foam cell macrophages, occasional T cells, and rare alpha-actin-positive cells. In stenotic aortic valves, a similar but more advanced lesion was seen. CONCLUSIONS: The early lesion of "degenerative" aortic stenosis is an active inflammatory process with some similarities (lipid deposition, macrophage and T-cell infiltration, and basement membrane disruption) and some dissimilarities (presence of prominent mineralization and small numbers of smooth muscle cells) to atherosclerosis.

Aged↗

Subacute ventricular free wall rupture complicating myocardial infarction.

Myocardial free wall rupture accounts for between 8% and 17% of mortality after myocardial infarction. In up to 40% of cases death occurs subacutely over a matter of hours, not minutes. Illustrative clinical cases and data suggest that a high degree of clinical suspicion, along with the early use of echocardiography, could significantly reduce mortality resulting from myocardial free wall rupture complicating myocardial infarction. Myocardial free wall rupture should be suspected in patients with recent myocardial infarction who have recurrent or persistent chest pain, hemodynamic instability, syncope, pericardial tamponade, or transient electromechanical dissociation. In this clinical situation, emergent echocardiography showing a pericardial effusion or pericardial thrombus is highly suggestive of free wall rupture. Surgical exploration and rupture repair is the definitive diagnostic and therapeutic procedure.

Aged↗

Delayed hypersensitivity testing as a clinical measure of cell-mediated immunity in the cat.

The purposes of this study were to examine the cell-mediated immune response of the normal cat to the modified live feline viral rhinitis, calicivirus, and parvovirus (FVRCP) vaccine (Felocell CVR, Norden, Lincoln, NE), and to evaluate the intradermal skin test as a clinical measure of the immune response of cats. Vaccine and diluent were injected intradermally on the dorsal pinna of 34 normal adult cats. Skin thickness measurements, lymphocyte counts, and Concanavalin A mitogenesis indices were evaluated in 18 of these cats. Skin biopsies were obtained in 16 cats. In normal cats, the FVRCP vaccine induced a delayed hypersensitivity response characterized by a mononuclear infiltrate most pronounced at 72 h. Five cats with either feline leukemia (FeLV) or feline immunodeficiency virus (FIV) were tested and had a significantly reduced response to the skin test. The skin test provides a clinically useful method of evaluating immune function in cats and may be useful in development of a prognostic index.

Animals↗

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↗

Physiologic changes with maximal exercise in asymptomatic valvular aortic stenosis assessed by Doppler echocardiography.

OBJECTIVES: We hypothesized that the physiologic response to exercise in valvular aortic stenosis could be measured by Doppler echocardiography. BACKGROUND: Data on exercise hemodynamics in patients with aortic stenosis are limited, yet Doppler echocardiography provides accurate, noninvasive measures of stenosis severity. METHODS: In 28 asymptomatic subjects with aortic stenosis maximal treadmill exercise testing was performed with Doppler recordings of left ventricular outflow tract and aortic jet velocities immediately before and after exercise. Maximal and mean volume flow rate (Qmax and Qmean), stroke volume, cardiac output, maximal and mean aortic jet velocity (Vmax, Vmean), mean pressure gradient (delta P) and continuity equation aortic valve area were calculated at rest and after exercise. The actual change from rest to exercise in Qmax and Vmax was compared with the predicted relation between these variables for a given orifice area. Subjects were classified into two groups: Group I (rest-exercise Vmax/Qmax slope > 0, n = 19) and Group II (slope < or = 0, n = 9). RESULTS: Mean exercise duration was 6.7 +/- 4.3 min. With exercise, Vmax increased from 3.99 +/- 0.93 to 4.61 +/- 1.12 m/s (p < 0.0001) and mean delta P increased from 39 +/- 20 to 52 +/- 26 mm Hg (p < 0.0001). Qmax rose with exercise (422 +/- 117 to 523 +/- 209 ml/s, p < 0.0001), but the systolic ejection period decreased (0.33 +/- 0.04 to 0.24 +/- 0.04, p < 0.0001), so that stroke volume decreased slightly (98 +/- 29 to 89 +/- 32 ml, p = 0.01). The increase in cardiac output with exercise (6.5 +/- 1.7 to 10.2 +/- 4.4 liters/min, p < 0.0001) was mediated by increased heart rate (71 +/- 17 to 147 +/- 28 beats/min, p < 0.0001). There was no significant change in the mean aortic valve area with exercise (1.17 +/- 0.45 to 1.28 +/- 0.65, p = 0.06). Compared with Group I patients, patients with a rest-exercise slope < or = 0 (Group II) tended to be older (69 +/- 12 vs. 58 +/- 19 years, p = 0.07) and had a trend toward a shorter exercise duration (5.3 +/- 2.9 vs. 7.3 +/- 4.9 min, p = 0.20). There was no difference between groups for heart rate at rest, blood pressure, stroke volume, cardiac output, Vmax, mean delta P or aortic valve area. With exercise, Group II subjects had a lower cardiac output (7.4 +/- 2.4 vs. 11.5 +/- 4.6 liters/min, p = 0.005) and a smaller percent increase in Vmax (3 +/- 9% vs. 22 +/- 14%, p < 0.0001). CONCLUSIONS: Doppler echocardiography allows assessment of physiologic changes with exercise in adults with asymptomatic aortic stenosis. A majority of subjects show a rest-exercise response that closely parallels the predicted relation between Vmax and Qmax for a given orifice area. The potential utility of this approach for elucidating the relation between hemodynamic severity and clinical symptoms deserves further study.

Adult↗

Methodologic issues in clinical evaluation of stenosis severity in adults undergoing aortic or mitral balloon valvuloplasty. The NHLBI Balloon Valvuloplasty Registry.

Although both catheterization and Doppler measures of valvular stenosis severity have been validated, each has specific advantages and limitations, particularly in the setting of balloon valvuloplasty. Invasive valve area and mean pressure gradient recorded immediately before and after aortic (n = 589) or mitral (n = 608) catheter balloon valvuloplasty were compared with Doppler valve area and mean pressure gradient recorded less than 30 days before and 24 to 72 hours after the procedure. For aortic stenosis, Doppler valve area ranged from 0.1 to 1.4 cm2 before and 0.2 to 2.3 cm2 after catheter balloon valvuloplasty. Doppler and invasive aortic valve areas differed by less than or equal to 0.5 cm2 in 99% and by less than 0.2 cm2 in 92% of patients. Linear correlation was higher before versus after catheter balloon valvuloplasty, for both valve area (r = 0.49 vs r = 0.35, p = 0.01) and mean pressure gradient (r = 0.64 vs r = 0.50, p = 0.01). Group mean invasive valve area was slightly smaller before (0.50 vs 0.59 cm2, p less than 0.0001) but was not different after (0.80 vs 0.78 cm2, p = 0.16) catheter balloon valvuloplasty. Variables affecting the valve area differences were cardiac output, aortic regurgitation, heart rate and blood pressure. Mean pressure gradient differences were related to echo quality, blood pressure and mitral regurgitation. For mitral stenosis, 2-dimensional echocardiographic valve area ranged from 0.4 to 2.8 cm2 before and 0.7 to 3.8 cm2 after catheter balloon valvuloplasty. Two-dimensional echocardiography and invasive mitral valve areas differed by less than or equal to 0.5 cm2 in 96% and by less than 0.2 cm2 in 81% of cases. Linear correlation was not different before versus after catheter balloon valvuloplasty for two-dimensional echocardiographic valve area (r = 0.40 vs 0.36), pressure halftime valve area (r = 0.31 vs 0.32) or mean pressure gradient (r = 0.55 vs r = 0.46). Group mean 2-dimensional echocardiography and pressure halftime valve areas were larger than invasive valve areas before (1.09 vs 1.02 cm2, p = 0.001) and smaller after (1.71 vs 2.02 cm2, p less than 0.0001) catheter balloon valvuloplasty. Important variables affecting the differences were mitral regurgitation, interatrial shunt, cardiac output and heart rate. Nonsimultaneous studies, differing volume flow measurements, and the underlying accuracy of each technique largely account for discrepancies between these methods. The clinical use of each will depend on its ability to predict long-term patient outcome.

Adult↗