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J D Thomas

Publications and source records attributed to J D Thomas.

At least 253 records · Page 14Linked to original sources

Independent impact of thrombolytic therapy and vessel patency on left ventricular dilation after myocardial infarction. Serial echocardiographic follow-up.

BACKGROUND: It has been shown that successful reperfusion of the infarct-related artery by thrombolysis can prevent left ventricular dilation after acute myocardial infarction; these beneficial effects were detected from several days to several months after infarction. To date, however, no study has shown that these effects can be demonstrated within hours after the onset of infarction. Furthermore, data are scarce on the independent impact of thrombolytic therapy and late vessel patency on ventricular volume and function. The aim of this study was to assess separate effects of thrombolysis and patency of the infarct-related artery on left ventricular size and function by serial two-dimensional echocardiographic examinations. METHODS AND RESULTS: We evaluated 131 consecutive patients with first acute myocardial infarction by two-dimensional echocardiography in the following sequence: days 1, 2, 3, 7, and after 3 and 6 weeks. Intravenous streptokinase was administered in 81 patients, and 50 patients were treated without thrombolysis. Left ventricular end-diastolic volume, end-systolic volume, and ejection fraction were determined from apical two- and four-chamber views using the Simpson biplane formula and normalized to body surface area. Coronary angiography was performed in 107 patients after a mean of 26.0 +/- 20.2 (mean +/- SD) days after infarction. Patency of the infarct-related artery was assessed using TIMI criteria, with 54 considered patent (TIMI 3) and 53 with TIMI grade < 3. On day 1, end-systolic volume was significantly higher in patients not receiving thrombolysis (37.7 +/- 15.3 versus 33.0 +/- 10.6 mL/m2, P = .045). End-systolic volume (ESVi) was significantly higher in patients treated without thrombolysis throughout the study, whereas significant differences in end-diastolic volume (EDVi) were detected from day 3 (P = .041) onward and in ejection fraction (EF) from day 2 (P = .025) onward, all differences becoming progressively more significant with time (6-week values: EDVi, 78.8 +/- 25.4 versus 65.9 +/- 15.7 mL/m2, P = .001; ESVi, 45.4 +/- 22.6 versus 33.9 +/- 15.1 mL/m2, P = .002; EF, 45.1 +/- 11.6% versus 50.2 +/- 10.1%, P = .018). Patients with an occluded infarct-related artery (TIMI < 3) demonstrated highly significant differences at 6 weeks compared with patients with patent vessels (EDVi, 76.8 +/- 24.7 versus 65.2 +/- 15.6 mL/m2, P = .006; ESVi, 44.6 +/- 23.3 versus 31.9 +/- 12.2 mL/m2, P = .001; EF, 45.0 +/- 11.6% versus 52.1 +/- 9.0%, P < .001), but these differences developed more slowly than that seen among the thrombolytic subgroups. Indeed, multivariate analysis demonstrated that thrombolysis was the major determinant of initial volumes (P = .08, .02, and .08 for EDVi, ESVi, and EF, respectively), while vessel patency was the overwhelming determinant of subsequent changes (P = .0033, .0002, and .0024 for EDVi, ESVi, and EF, respectively). Additionally, ventricular volumes were significantly higher and ejection fractions lower in patients with anterior versus inferior infarction, but even adjusting for these differences as well as those associated with age, sex, and initial ventricular volume, the additive and independent impact of thrombolysis and infarct vessel patency persisted. CONCLUSIONS: These data indicate that the beneficial effect of thrombolysis on left ventricular size and function can be demonstrated in the earliest phases of acute myocardial infarction and that subsequent changes are mediated primarily through patency of the infarct-related artery. Thrombolytic therapy and late vessel patency thus have an additive and complementary impact in reducing ventricular dilation after myocardial infarction.

Coronary Vessels↗

Intracardiac ultrasound measurement of volumes and ejection fraction in normal, infarcted, and aneurysmal left ventricles using a 10-MHz ultrasound catheter.

BACKGROUND: Our objective was to examine the accuracy of intracardiac ultrasound (ICUS) measurement of left ventricular (LV) volumes and ejection fraction (EF) using a 10-MHz ultrasound catheter. ICUS can image the LV in cross sections at all levels along the long axis with a transducer mounted on the tip of a catheter. Sequential serial LV cross-sectional images can be obtained during cardiac catheterization and used to calculate LV volumes by Simpson's rule. This technique may be an alternative to contrast LV angiography. METHODS AND RESULTS: A beating-heart in vivo model was created to measure LV volume directly and continuously with an intracavity high-compliance latex balloon connected to a calibrated extracardiac reservoir in eight dogs in 35 experimental stages. A 10F ICUS catheter with a 10-MHz single-element transducer was introduced retrogradely via the aortic valve to the apex. Series of sequential LV cross-sectional images were recorded from the apex to the base during a calibrated pullback of the catheter. At each 5-mm interval, the LV cross section was traced at end diastole and end systole. LV volume was calculated by Simpson's rule by integrating all segmental areas multiplied by segmental height. The effect on accuracy of selecting 5-, 10-, or 15-mm heights or a single section at the midventricular level for measurement was assessed. The influence of distorted ventricular shape on the accuracy of ICUS measurements of LV volume was evaluated. This method was applied in 19 experimental stages in 10 intact dogs and pigs catheterized via the femoral artery. In the in vivo canine model, LV end-diastolic volume, end-systolic volume, and EF determined by ICUS using 5-, 10-, or 15-mm segments were not different from the actual measurements. But correlation and agreement between ICUS end-diastolic volume and direct measurements for 5- and 10-mm segments were significantly better than for 15-mm segments or a single section. Similar excellent correlations and agreement were observed for actual and ICUS-derived end-systolic volumes using 5-, 10-, or 15-mm segments. The ICUS-derived EF correlated very well with actual EF with a small measurement error of 3.91 +/- 2.59% for 5-mm or 4.13 +/- 2.79% for 10-mm segments but a significantly greater measurement error for 15-mm segments (5.35 +/- 3.76%) or single sections (14.8 +/- 12.2%). The presence of LV infarction or aneurysm did not significantly influence the accuracy of ICUS calculations for segmental heights < or = 10 mm. Application in intact animals demonstrated a good correlation between stroke volume measured by ICUS and by thermodilution or flowmeter. ICUS-derived LV volumes correlated well with biplane angiographic volumes, with a tendency toward underestimation. There was no significant difference between ICUS-determined LV EF and EF determined by angiography. CONCLUSIONS: Intracardiac echocardiography accurately measures LV volumes and global systolic function in both regularly shaped and distorted left ventricles. This technique directly and continuously visualizes circumferential LV endocardium and wall thickness without contrast agents or geometric assumptions for calculation of LV volume. Thus, it should be particularly useful in patients at high risk for contrast-related complications or distorted LV shapes in which geometric assumptions may not be valid.

Animals↗

Prognosis of patients with left ventricular dysfunction, with and without viable myocardium after myocardial infarction. Relative efficacy of medical therapy and revascularization.

BACKGROUND: The uptake of F-18 deoxyglucose into dysfunction segments after myocardial infarction identifies metabolically active (FDG+) or inactive (FDG-) myocardium. Although patients with FDG+ segments have been found to be at risk for adverse events, the prognostic significance of viable myocardium in relation to other influences on postinfarction prognosis, including revascularization, remain ill defined. The purpose of this study was to investigate the relative prognostic significance of FDG+ tissue and to establish whether myocardial revascularization in patients with viable tissue attenuates the risk of adverse outcome. METHODS AND RESULTS: One hundred thirty-seven patients with left ventricular dysfunction and resting perfusion defects after myocardial infarction underwent positron emission tomography with both dipyridamole stress Rb-82 perfusion imaging and FDG imaging. After the exclusion of 4 patients proceeding to transplantation, 2 with uninterpretable scans and 2 lost to follow-up, 129 patients were followed clinically for 17 +/- 9 months. Four groups were defined: patients with FDG+ dysfunctional myocardium who were revascularized (n = 49) or treated medically (n = 21) and those with FDG- segments who were revascularized (n = 19) or treated medically (n = 40). The groups of patients with FDG+ or FDG- findings, with and without revascularization, did not differ with respect to known determinants of postinfarction prognosis: age, left ventricular ejection fraction, or the prevalence of multivessel disease. Nonfatal ischemic events occurred in 48% of medically treated FDG+ patients compared with 8% of revascularized patients with FDG+ tissue (P < .001) and 5% of patients with FDG- myocardium (P < .001). Thirteen patients died from cardiac causes; 11 (85%) had a left ventricular ejection fraction of < 30%, and these patients were evenly distributed between FDG+ and FDG- groups. Using Cox's proportional hazards model, only the presence of FDG+ myocardium (odds ratio, 12.9; P < .001) and the absence of revascularization (odds ratio, 5.8; P = .002) independently predicted ischemic events, while only age (P = .02) and ejection fraction (P < .001) but not the presence of viable myocardium were predictive of death. CONCLUSIONS: Residual viable myocardium after myocardial infarction may act as an unstable substrate for further events unless it is revascularized. Despite this association, age and left ventricular dysfunction remained the strongest predictors of cardiac death after myocardial infarction in these patients with a spectrum of left ventricular dysfunction.

Aged↗

Correlated quantitative studies of the neostriatum, nucleus accumbens, substantia nigra, and ventral tegmental area in normal and weaver mutant mice.

Normal mice (+/+) and homozygous weaver mutant mice (wv/wv) at 1 year of age were used for three-dimensional computer-aided reconstructions of the nucleus accumbens (NA) and neostriatum (ST) and for quantitative estimations of the total number of medium-sized neurons in the NA and ST, and for the total number of tyrosine hydroxylase (TH)-containing neurons in the ventral tegmental area (VTA) and substantia nigra (SN). The three-dimensional reconstructions showed that the weaver NA and ST are smaller than they are in +/+. Quantitative volumetric measurements of the NA and ST showed wv/wv were smaller than +/+ by nonsignificant differences of 14% and 13%, respectively. The wv/wv group showed statistically significant depletion of neurons in all four structures. On average, NA neurons are reduced by 27%, ST neurons by 22%, VTA-TH neurons by 40%, and SN-TH neurons by 79%. In wv/wv animals, there was a high positive correlation (r = 0.836) between the numbers of SN-TH neurons and ST neurons and a moderate positive correlation (r = 0.534) between the numbers of SN-VTA neurons and NA neurons. The nuclei in TH-containing neurons in wv/wv and +/+ had the same diameters, but in all animals, the SN-TH neurons contained larger nuclei than the VTA-TH neurons. Cytoarchitectonic measurements in control and weaver NA and ST were also similar. In all animals, the NA contains more densely packed neurons with smaller nuclei than those in the ST.

Aging↗

[The use of the proximal acceleration method in cases of incompetence of the right atrioventricular valve].

BACKGROUND: Quantitation of valvular regurgitation remains an important goal in cardiology. It has been described previously that using color Doppler flow mapping, measurements of apparent jet size do not correlate always closely with quantitative regurgitant indexes. Recently the proximal flow convergence method has been proposed to quantify valvular regurgitation by analysis of the converging flow field proximal to a regurgitant lesion. Assuming hemispherical convergence, peak flow rate Qp can be calculated as Qp = 2 pi r2Va, where Va is the aliasing velocity at a distance r from the orifice. For maximal accuracy, previously validated correction factors must be used to account for the flattening effect of the isovelocity contours close to the orifice and for the actual sector angle subtended by the valve leaflets (alpha) to yield a flow rate formula Qp = 2 pi r2Va (Vp/Vp-Va) (alpha/180), where Vp is the orifice velocity obtained by continuous wave Doppler. METHODS: In 45 patients (35 in sinus rhythm, 10 with atrial fibrillation) with tricuspid regurgitation, regurgitant stroke volume, regurgitant flow rate were calculated using the proximal flow convergence method and compared with values obtained by the Doppler two-dimensional echocardiographic method. RESULTS: Regurgitant stroke volumes (SV) calculated by the proximal flow convergence method correlated very closely with values obtained by the Doppler two-dimensional method with r = 0.95 (y = 0.94x + 0.99) and delta SV = -0.3 +/- 5.2 cm3. Regurgitant flow rates (Q) calculated by both methods showed a similar correlation: r = 0.96 (y = 0.97x + 45) and delta Q = 1.6 +/- 4.29 cm3/min. All correlations were slightly better for the group of patients in sinus rhythm. CONCLUSION: This study demonstrates that the proximal flow convergence method is an accurate and reproducible technique for quantifying tricuspid regurgitation. While improvements of this method are to be expected, flow calculations based on the proximal flow field show excellent results and appear appropriate for clinical use.

Adult↗

[A description of a new method of quantifying the regurgitant flow in patients with an incompetent mitral valve].

BACKGROUND: It has been shown previously that using color Doppler flow mapping, simple measurements of apparent jet size do not correlate closely with regurgitant flow rate and regurgitant fraction. Recently the proximal flow convergence method has been proposed to quantify valvular regurgitation by analysis of the converging flow field proximal to a regurgitant lesion. Flow rate Q can be calculated as Q = 2 pi r2va where va is the aliasing velocity at a distance r from the orifice. PATIENTS AND METHODS: In 54 patients (43 in sinus rhythm, 11 with atrial fibrillation) with at least mild mitral regurgitation by semi-quantitative assessment, regurgitant stroke volume, regurgitant flow rate, and regurgitant fraction were calculated using the proximal flow convergence method and compared with values obtained by the Doppler/two-dimensional echocardiographic method. RESULTS: Regurgitant stroke volumes (VL) calculated by the proximal flow convergence method correlated very closely with values obtained by the Doppler-2D method with r = 0.93 (y = 0.95x + 0.55) and delta VL = -0.3 +/- 4.0 cm3. Regurgitant flow rates (Q) calculated by both methods showed a similar correlation: r = 0.93 (y = 0.95x + 54) and delta Q = -34 +/- 284 cm3/min. The correlation for regurgitant fraction (RF) calculated by both techniques showed r = 0.89 (y = 0.98x + 0.006) and delta RF = -0.005 +/- 0.06. All correlations were slightly better for the group of patients in sinus rhythm compared with the study group in atrial fibrillation. CONCLUSION: This study demonstrates that the proximal flow convergence method is an accurate and reproducible technique to quantify mitral regurgitation. This approach is easy and less time-consuming than the Doppler-echocardiographic method. While future improvements of this method are to be expected, flow calculations based on the assumption of simple hemispheric symmetry of the proximal flow field appear suitable for clinical application at the present time.

Adult↗

Which physical factors determine tricuspid regurgitation jet area in the clinical setting?

The visual assessment of jet area has become the most common method used in daily clinic practice to evaluate valvular regurgitation. Despite the high prevalence of tricuspid regurgitation, however, few studies have systematically compared TR jet areas with a quantitative standard. To evaluate this, 40 patients in sinus rhythm with tricuspid regurgitation were analyzed: 16 with centrally directed free jets and 24 with impinging wall jets. The size of the maximal planimetered color jet area (cm2) was compared with parameters derived using the pulsed Doppler 2-dimensional echocardiographic method: regurgitant fraction and the flow convergence method (peak flow rate, effective regurgitant orifice area and momentum). Mean tricuspid regurgitant fraction averaged 33 +/- 15%, peak flow rate 76 +/- 54 cm3/s, effective regurgitant orifice area 27 +/- 21 mm2 and momentum 21,717 +/- 15,014 cm4/s2. An average of 4-chamber, and long- and short-axis areas in free jets correlated well with regurgitant fraction (r = 0.81, p < 0.001), better with peak flow rate (r = 0.94, p < 0.001), effective regurgitant orifice (r = 0.92, p < 0.001) and momentum (r = 0.94, p < 0.001). The correlation was worse, but still significant, in wall jets. For the same peak flow rate, wall jets were 75% of the size of a corresponding free jet. Jet area measurement is a good semiquantitative tool to measure tricuspid regurgitation in free jets, which correlates well with regurgitant fraction and better with new parameters available from analysis of the proximal acceleration field. In patients with eccentrically directed wall jets the correlation with planimetered jet area was worse, but still significant.

Adult↗

Colocalization of X-linked agammaglobulinemia and X-linked immunodeficiency genes.

Mice that bear the X-linked immunodeficiency (xid) mutation have a B lymphocyte-specific defect resulting in an inability to make antibody responses to polysaccharide antigens. A backcross of 1114 progeny revealed the colocalization of xid with Bruton's agammaglobulinemia tyrosine kinase (btk) gene, which is implicated in the human immune deficiency, X-linked agammaglobulinemia. Mice that carry xid have a missense mutation that alters a highly conserved arginine near the amino-terminus of the btk protein, Btk. Because this region of Btk lies outside any obvious kinase domain, the xid mutation may define another aspect of tyrosine kinase function.

Agammaglobulinaemia Tyrosine Kinase↗

The sugar chemoreception niches of Bulinus (physopsis) globosus (Morelet) and Bulinus rohlfsi (Clessin), the two most important snail hosts of Schistosoma haematobium (Bilharz) in west Africa.

1. The behavioural responses of two species of freshwater pulmonate snails [Bulinus (P.) globosus and Bulinus rohlfsi] to sugar gradients were investigated by means of diffusion olfactometers. 2. Both snail species proved to be very discriminating in their responses. Of the 17 sugars tested, 35.3%, namely D(-)glucuronic, maltotriose, maltose, cellobiose, D(-)arabinose, D(+)mannose proved to be statistically significant attractants or arrestants to B. rohlfsi. Only 23.5% of these sugars (maltotriose, maltose), D(+) mannose and D(+) xylose were significant attractants or arrestants to B. (P.) globosus. 3. Glucuronic acid was a significant repellent to B. rohlfsi but none of the sugars was a repellent to B. (P.) globosus. 4. The results are compared with those obtained for other snail species and their relevance to the ecology and control of the snails are discussed.

Animals↗

Automated flow rate calculations based on digital analysis of flow convergence proximal to regurgitant orifices.

OBJECTIVES: The purpose of the study was to develop and validate an automated method for calculating regurgitant flow rate using color Doppler echocardiography. BACKGROUND: The proximal flow convergence method is a promising approach to quantitate valvular regurgitation noninvasively because it allows one to calculate regurgitant flow rate and regurgitant orifice area; however, defining the location of the regurgitant orifice is often difficult and can lead to significant error in the calculated flow rates. To overcome this problem we developed an automated algorithm to locate the orifice and calculate flow rate based on the digital Doppler velocity map. METHODS: This algorithm compares the observed velocities with the anticipated relative velocities, cos psi/2 pi r2. The orifice is localized as the point with maximal correlation between predicted and observed velocity, whereas flow rate is specified as the slope of the regression line. We validated this algorithm in an in vitro model for flow through circular orifices with planar surroundings and a porcine bioprosthesis. RESULTS: For flow through circular orifices, flow rates calculated on individual Doppler maps and on an average of eight velocity maps showed excellent agreement with true flow, with r = 0.977 and delta Q = -3.7 +/- 15.8 cm3/s and r = 0.991 and delta Q = -4.3 +/- 8.5 cm3/s, respectively. Calculated flow rates through the bioprosthesis correlated well but underestimated true flow, with r = 0.97, delta Q = -10.9 +/- 12.5 cm3/s, suggesting flow convergence over an angle > 2 pi. This systematic underestimation was corrected by assuming an effective convergence angle of 212 degrees. CONCLUSIONS: This algorithm accurately locates the regurgitant orifice and calculates regurgitant flow rate for circular orifices with planar surroundings. Automated analysis of the proximal flow field is also applicable to more physiologic surfaces surrounding the regurgitant orifice; however, the convergence angle should be adjusted. This automated algorithm should make quantification of regurgitant flow rate and regurgitant orifice area more reproducible and readily available in clinical cardiology practice.

Algorithms↗

Toward the quiescent coronary plaque.

The treatment of coronary atherosclerosis requires an understanding of the pathophysiology of plaque rupture. The rupture of lipid-laden, macrophage-rich plaques initiates unstable angina, acute myocardial infarction and sudden cardiac death. Plaque rupture occurs when the circumferential tension on a plaque exceeds its tensile strength, an event that cannot be predicted by coronary angiography. The incidence of plaque rupture appears to be reduced in patients receiving cholesterol-lowering therapy, beta-adrenergic blocking agents and, possibly, angiotensin-converting enzyme inhibitors and antioxidants. Not all ruptured coronary plaques produce an acute coronary syndrome. The consequences of plaque rupture depend on the extent of thrombus formation over the fissured plaque. This is determined by flow characteristics within the vessel as well as the activity of the thrombotic and fibrinolytic systems. Recent advances in cardiovascular molecular biology, coronary diagnostic techniques and cardiac therapeutics have opened windows of opportunity to study and modify the factors leading to plaque rupture. The local modification of gene expression to alter plaque composition and to elucidate and subsequently inhibit the prothrombotic and fibrinolytic defects that promote coronary thrombosis may, in future, prevent plaque rupture and its consequences. The application of such a concerted interdisciplinary approach promises a paradigm shift in the management of coronary artery disease toward the prevention of plaque rupture and its sequelae.

Adrenergic beta-Antagonists↗

Reliability of echocardiographic measurements of myocardial perfusion using commercially produced sonicated serum albumin (Albunex).

OBJECTIVES: The purpose of this study was to assess the reproducibility and pitfalls of intracoronary and aortic root sonicated albumin injections, using time-intensity curves, in a large sample of normal dogs. BACKGROUND: The utility of a new myocardial contrast echocardiographic agent, sonicated serum albumin (Albunex), is currently under investigation. However, the reproducibility, injection techniques and general pitfalls of this contrast agent have not been well characterized. METHODS: We administered sequential intracoronary and aortic root injections (518 injections) of sonicated albumin in 25 closed chest normal dogs to measure the effectiveness and reproducibility of this product. Time-intensity curves, as a measure of myocardial perfusion, were derived and quantified using an on-line videodensitometric analysis system and two-dimensional echocardiography. Measurements included peak intensity, area under the curve, half-time of descent, alpha-parameter and transit time within a 31- x 31-pixel "region of interest" in the anterior septum. Analyses provided 80% power and a type I error protection of 95%. RESULTS: The best reproducibility of the variables was half-time of descent for aortic root injections (coefficient of variation [CV] 20%) and peak intensity for intracoronary injections (CV 25%), whereas aortic root area under the curve showed the most variability (CV 41%). Analysis of variance for repeated measures of serial intracoronary and aortic root injections showed no significant systematic variability within subjects for the measured variables. In a comparison between intracoronary and aortic root injection sites, paired t tests showed no significant difference for mean values between these two techniques. There was also no statistically significant difference between manual versus power intracoronary injections. Finally, there was no significant difference among three injection rates (1, 2 and 3 ml/s) in paired intracoronary injections, nor was there a difference among injection rates in paired aortic root injections, except for a lower peak intensity with a 1-ml/s injection rate compared with a 2-ml/s injection rate (p = 0.01). Potential pitfalls include preparation of sonicated albumin, delivery techniques and measurement variables. CONCLUSIONS: We conclude that the results of serial injections of sonicated albumin show no systemic change or trend in normal dogs. Both intracoronary and aortic root injections at standard injection rates by hand or power injector can be used to quantify time-intensity curves, as measure of myocardial perfusion, with similar variability ranging from 20% to 41%. These results are important in the human model, especially after coronary interventions.

Albumins↗

Application of color Doppler flow mapping to calculate effective regurgitant orifice area. An in vitro study and initial clinical observations.

BACKGROUND: Analogous to stenotic valve area in the assessment of valvular stenosis, regurgitant orifice area (ROA) represents a fundamental parameter to assess valvular insufficiency. However, this parameter has not been routinely available up to now. In this study, we introduce the concept and provide the methodology to calculate regurgitant orifice area noninvasively, based on the analysis of the proximal flow convergence zone. METHODS AND RESULTS: In an in vitro study, we showed the feasibility and the accuracy of calculating effective ROA by the proximal flow convergence method throughout a range of driving pressures. The calculated and true ROA showed an excellent correlation with r = .992, delta ROA = -1.4 +/- 2.9 mm2. We then applied this concept clinically in 77 patients with mitral regurgitation and showed a very good correlation between effective ROA calculated by the proximal flow convergence method and calculated by the Doppler echocardiographic method: r = .95, delta ROA = -0.2 +/- 3.9 mm2. The ROA also correlated very well with Doppler echocardiographic-derived regurgitant stroke volume (r = .93) and regurgitant fraction (r = .82). In a subgroup of 20 patients who underwent invasive evaluation, the calculated effective ROA also correlated well with the angiographic grade of mitral regurgitation (rho = .81). CONCLUSIONS: We conclude that effective ROA represents unique information on the severity of a regurgitant lesion and can easily be calculated by the proximal flow convergence method. This new parameter should enhance our understanding and improve the serial assessment of valvular regurgitation.

Blood Flow Velocity↗

Validation of the proximal flow convergence method. Calculation of orifice area in patients with mitral stenosis.

BACKGROUND: It has been proposed recently that measuring the flow convergence region proximal to an orifice by Doppler flow mapping can provide a means of calculating regurgitant flow rate. Although verified in experimental models, this approach is difficult to validate clinically because there is no ideal gold standard for regurgitant flows in patients. However, this method also can be used to derive cardiac output or flow rate proximal to stenotic orifices and therefore to calculate their areas by the continuity equation (area = flow rate/velocity). Applying this method in mitral stenosis would provide a unique way of validating the underlying concept because the predicted areas could be compared with those measured directly by planimetry. METHODS AND RESULTS: We studied 40 patients with mitral stenosis using imaging and Doppler echocardiography. Doppler color flow recordings of mitral inflow were obtained from the apex, and the radius of the proximal flow convergence region was measured at its peak diastolic value from the orifice to the first color alias along the axis of flow. Flow rate was calculated assuming uniform radial flow convergence toward the orifice, modified by a factor that accounted for the inflow funnel angle formed by the mitral leaflets. Mitral valve area was then calculated as peak flow rate divided by peak velocity by continuous-wave Doppler. The calculated areas agreed well with those from three comparative techniques over a range of 0.5 to 2.2 cm2: 1) cross-sectional area by planimetry (y = 1.08x-0.13, r = .91, SEE = 0.21 cm2); 2) area derived from the Doppler pressure half-time (y = 1.02x-0.14, r = .89, SEE = 0.24 cm2); and 3) area calculated by the Gorlin equation in the 26 patients who underwent catheterization (y = 0.89x + 0.08, r = .86, SEE = 0.24 cm2). Agreement with planimetry was similar for 22 patients with mitral regurgitation and 18 without it (P > .6), as well as for 6 in atrial fibrillation (P > .2). CONCLUSIONS: These results validate the proximal flow convergence concept in the clinical setting and also demonstrate that it can be extended to orifice area calculation using the continuity equation.

Atrial Fibrillation↗