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Biomedical subjects

J D Thomas

Publications and source records attributed to J D Thomas.

At least 217 records · Page 12Linked to original sources
PubMed1995

Influence of left ventricular hypertrophy on detection of coronary artery disease using exercise echocardiography.

OBJECTIVES: This study examined the influence of left ventricular hypertrophy on the accuracy of exercise electrocardiography and echocardiography for detection of coronary artery disease. BACKGROUND: Electrocardiographic repolarization abnormalities caused by left ventricular hypertrophy compromise the diagnostic accuracy of exercise electrocardiography but not of exercise echocardiography. The relative merits of these investigations are less well defined in patients with hypertrophy but without electrocardiographic (ECG) changes. METHODS: We prospectively evaluated 147 consecutive patients without prior myocardial infarction undergoing both exercise echocardiography and coronary arteriography. Coronary stenoses > 50% diameter were present in 62 patients (42%). Positive test results were defined by a new or worsening wall motion abnormality or > 0.1 mV of ST depression. Echocardiographic left ventricular hypertrophy (mass > 131 g/m2 in men, > 100 g/m2 in women) was identified in 68 patients. A subgroup with clinically suspected hypertrophy was defined according to the presence of ECG evidence of hypertrophy, hypertension or aortic stenosis. RESULTS: The overall sensitivity of exercise echocardiography exceeded that of exercise electrocardiography (71% vs. 54%, p = 0.06). Echocardiographic hypertrophy had no significant effect on the sensitivity of either test. The specificity of exercise echocardiography exceeded that of exercise electrocardiography (91 vs. 74%, p = 0.01). In patients with hypertrophy, the specificity of exercise echocardiography exceeded that of exercise electrocardiography (95% vs. 69%, p < 0.01), whereas among patients without hypertrophy, the specificities (respectively, 87% and 78%) were more comparable. The accuracy of exercise echocardiography exceeded that of the exercise ECG in the overall group (82% vs. 65%, p = 0.002) and in patients with hypertrophy (85% vs. 60%, p = 0.004), but this difference was less prominent in patients without hypertrophy (80% vs. 69%, p = NS). In patients with clinically suspected hypertrophy, exercise echocardiography demonstrated a higher sensitivity, specificity and accuracy than exercise electrocardiography. The cost incurred in the identification of coronary disease was least with a strategy involving use of the exercise echocardiogram instead of routine exercise testing in patients with known or clinically suspected left ventricular hypertrophy. CONCLUSIONS: Exercise echocardiography is more accurate than exercise electrocardiography for the detection of coronary artery disease in patients with known or clinically suspected left ventricular hypertrophy.

Adult↗
PubMed1995

Effect of the implantable left ventricular assist device on neuroendocrine activation in heart failure.

BACKGROUND: The HeartMate left ventricular assist device has been successfully used as a bridge to cardiac transplantation. Because many patients exhibit marked clinical improvement in their heart failure after HeartMate implantation, we studied the physiological effect of this device on the neurohormonal axis. METHODS AND RESULTS: In 13 patients awaiting transplant (mean cardiac index, 1.7 +/- 0.3 L.min-1.m-2) who underwent HeartMate implantation, venous atrial natriuretic peptide, epinephrine, norepinephrine, plasma renin activity, angiotensin, and arginine vasopressin were measured immediately before insertion and at explant/transplantation. Mean time to explant was 86 +/- 40 days. All patients were taken off inotropic medications within 1 month. Mean cardiac index on support before explant was 3.1 +/- 0.9 L.min-1.m-2. Plasma renin activity decreased from 57 +/- 56 ng.mL-1.h-1 at baseline (before insertion) to 3 +/- 3 ng.mL-1.h-1 at explant (mean percent change, 92%; P < .001). Angiotensin II level decreased from 237 +/- 398 U/L at baseline to 14 +/- 14 U/L at explant (mean percent change, 73%; P < .001). Plasma epinephrine level fell from 6800 +/- 1323 pg/mL at baseline to 46 +/- 46 pg/mL at explant (mean percent change, 86%; P < .001). Norepinephrine level decreased from 2953 +/- 1457 pg/mL at baseline to 518 +/- 290 pg/mL at explant (mean percent change, 79%; P < .001). Atrial natriuretic peptide fell from baseline values of 227 +/- 196 to 168 +/- 40 pg/mL at explant (mean percent change, -49%; P = 519); and arginine vasopressin level decreased from 6 +/- 6 pg/mL at baseline to 0.8 +/- 0.5 pg/mL (mean percent change, 69%; P = .002). CONCLUSIONS: We provide data supporting that the neurohormonal axis markedly improves after HeartMate implantation, providing biochemical confirmation of the improvement in hemodynamic status.

Adult↗
PubMed1995

Quantification of mitral regurgitation by the proximal convergence method using transesophageal echocardiography. Clinical validation of a geometric correction for proximal flow constraint.

BACKGROUND: Proximal flow convergence is a promising method to quantify mitral regurgitation but may overestimate flow when the flow field is constrained. This has not been investigated clinically, nor has a correction factor been validated. METHODS AND RESULTS: Eighty-five patients were studied intraoperatively with transesophageal echocardiography and divided into two groups: central convergence (no constraining wall) and eccentric convergence (at least one constraining wall). Regurgitant stroke volume (RSV) and orifice area (ROA) were calculated by ROA = 2 pi r2 Va/Vp and RSV = ROA x VTIcw, where r and va are the radius and velocity of the aliasing contour and vp and VTIcw are the peak and integral of regurgitant velocity. In eccentric convergence patients, convergence angle (alpha) was measured from two-dimensional Doppler color flow maps, and ROA and RSV were corrected by multiplying by alpha/180. For reference, RSV was the difference between thermodilution and pulsed Doppler stroke volumes. In central convergence patients (n = 45), RSV (r = .95, delta = 2.5 +/- 10.8 mL) and ROA (r = .96, delta = 0.02 +/- 0.08 cm2) were accurately calculated, but significant overestimation was noted in the eccentric convergence patients (n = 40, delta RSV = 63.9 +/- 38.0 mL, delta ROA = 0.54 +/- 0.31 cm2), 68% of whom had leaflet prolapse or flail. delta RSV was correlated with alpha (r = -.69, P < .001). After correction by alpha/180, overestimation was largely eliminated (delta RSV = 15.5 +/- 19.3 mL and delta ROA = 0.14 +/- 0.14 cm2) with excellent correlation for the whole group (RSV, r = .91; ROA, r = .95). CONCLUSIONS: A simple geometric correction factor largely eliminates overestimation caused by flow constraint with the proximal convergence method and should extend the clinical utility of this technique.

Case-Control Studies↗
PubMed1995

Determination of left ventricular chamber stiffness from the time for deceleration of early left ventricular filling.

BACKGROUND: A noninvasive measure of left ventricular (LV) chamber stiffness (KLV) would be clinically useful. Our theoretical analysis predicts that KLV can be calculated from the time for deceleration of LV early filling (tdec) by [formula: see text] where p = density of blood, L = effective mitral length, and A = mitral area. METHODS AND RESULTS: We tested this hypothesis in eight conscious dogs instrumented for measurement of LV pressure (P) with use of a micromanometer and volume (V) with use of sonomicrometers. KLV was determined as the slope of the late diastolic portion of the LV P-V loop. KLV was varied from 0.99 +/- 0.35 to 2.58 +/- 0.92 mm Hg/mL with use of three graded doses of phenylephrine. We assumed that p = 1.0 and that L/A = 3.4. Thus, we predicted that KLV = (0.08/tdec)2. The LV filling pattern was determined from the derivative of LV volume (dV/dt). tdec was measured from peak early filling to the end of early filling. Predicted KLV and actual KLV were closely correlated (r = .94, SEE = 0.06 mm Hg/mL, P < .05). The regression line was close to the line of identity (slope = 0.95, intercept = 0.13 mm Hg/mL). Dobutamine did not alter the relation between tdec and KLV.tdec determined from the mitral valve flow velocity measured with Doppler echocardiography correlated well with that measured by dV/dt (r = .89, P < .01) but was 0.02 seconds longer. KLV-calculated tdec from the corrected Doppler tdec provided a good estimate of measured KLV (r = .75, SEE = 0.5 mm Hg/mL, P < .01). CONCLUSIONS: LV chamber stiffness can be determined from the time for deceleration of LV early filling, which can be measured noninvasively.

Animals↗
PubMed1995

Selective vulnerability of late-generated dopaminergic neurons of the substantia nigra in weaver mutant mice.

In homozygous weaver (wv/wv) mutant mice, nearly 50% of the dopaminergic substantia nigra neurons degenerate by postnatal day 20. We have now determined that the total number of dopaminergic neurons in the ventral midbrains of a litter of obligatory homozygous weaver pups and a litter of normal wild-type control pups indicates that no significant differences are present between groups at birth. To test the hypothesis that the subsequent degeneration of these neurons is linked to their time of origin, [3H]thymidine autoradiography was combined with tyrosine hydroxylase immunocytochemistry to construct neurogenetic timetables on postnatal day 20 in wild-type mice and weaver homozygotes. Both groups have the same span of neurogenesis but have statistically different proportions of neurons generated on specific days. In wild-type mice, more than half of the dopaminergic neurons originate on or after embryonic day 12. In contrast, over two-thirds of the surviving dopaminergic neurons in homozygous weaver mice originate on or before embryonic day 11. Our data suggest that the weaver gene does not interfere with the generation of dopaminergic neurons, but it preferentially kills late-generated dopaminergic neurons between birth and postnatal day 20.

Aging↗
PubMed1995

Provocation of latent left ventricular outflow tract gradients with amyl nitrite and exercise in hypertrophic cardiomyopathy.

Amyl nitrite may be used to provoke latent gradients in patients with hypertrophic cardiomyopathy (HC) without significant resting outflow tract gradients, but afterload reduction may not be comparable to a more physiologic stressor such as symptom-limited exercise testing. This study compared the ability of amyl nitrite and exercise testing to provoke outflow tract gradients in 57 patients (40 men and 17 women, mean age +/- SD 49 +/- 16 years) with HC (septal thickness 19 +/- 5 mm, average resting gradient 13 +/- 10 mm Hg) who underwent echocardiography at rest, after amyl nitrite inhalation, and after maximal exercise. No significant gradient (< 50 mm Hg) was induced after either provocation in 26 patients (46%); in 15 patients (26%), inducibility was achieved after both stressors, in 6 (11%) after exercise only, and in 10 (18%) after amyl only. Patients with amyl-induced gradients differed from those in whom gradients were noninducible on the basis of smaller outflow tract dimensions (p < 0.001), larger resting gradients (p < 0.001), and a greater prevalence of "septal bulge" morphology (p = 0.02). Those with exercise-induced gradients were able to attain a greater workload (p = 0.07), have larger resting gradients (p = 0.02), and also tended to have a septal bulge morphology (p < or = 0.01). Although outflow tract obstruction increased to similar levels after amyl nitrite (49 +/- 39 mm Hg) and symptom-limited exercise (47 +/- 39 mm Hg), gradients induced by exercise and amyl correlated poorly (r = 0.54).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMed1995

Systematic differences in time of dopaminergic neuron origin between normal mice and homozygous weaver mutants.

Immunocytochemical labeling for tyrosine hydroxylase and [3H]thymidine autoradiography were combined in wild-type mice and in mice homozygous for the weaver mutant gene (wv) to see whether the neurogenetic patterns of midbrain dopaminergic neurons was normal in the mutants and whether the degeneration of dopaminergic neurons was linked to their time of origin. Dams of wild-type and homozygous weaver mice were injected with [3H]thymidine on embryonic days (E) 11-E12, E12-E13, E13-E14, and E14-E15 to label neurons in the retrorubral field, the substantia nigra pars compacta, the ventral tegmental area, and the interfascicular nucleus as they were being generated. The quantitatively determined time of origin profiles indicated that wv/wv mice have the same time span of neurogenesis as +/+ mice (E10 to E14), but have significant deficits in the proportion of late-generated neurons in each dopaminergic population. In the retrorubral field and substantia nigra, weaver homozygotes had substantial losses of dopaminergic neurons and had a greater deficit in the proportion of neurons generated late while, in the ventral tegmental area and interfascicular nucleus, there were slight losses of dopaminergic neurons and only slight deficits in the proportion of late-generated neurons. These findings lead to the conclusion that the weaver gene is specifically targeting dopaminergic neurons that are generated late, mainly on E13 and E14.

Animals↗
PubMed1995

Anatomic explanation of mobile systolic clicks: implications for the clinical and echocardiographic diagnosis of mitral valve prolapse.

An echocardiogram (echo) is often ordered for suspected mitral valve prolapse (MVP). Using echo as the gold standard, we conducted a meticulous physical examination on 61 patients with this referral diagnosis. Ninety percent of patients with negative physical examination and echo results for MVP had physical examination findings likely to have been misinterpreted as MVP by the referring physician. Redundant portions of the mitral valve apparatus were found in 57% of patients with MVP on our physical examination but not on echo. A carefully performed physical examination (including dynamic auscultation) can exclude MVP. Not all mobile systolic clicks are associated with anatomic echo prolapse; they can be generated by redundant chordae tendineae and, in the absence of echo prolapse, probably by redundant leaflets. Patients with mobile systolic clicks should have an echo to determine the portion of the spectrum of echo prolapse present and to determine risk stratification and management.

Adult↗
PubMed1995

Structural and left ventricular histologic changes after implantable LVAD insertion.

Long-term support on the implantable left ventricular assist device (LVAD) produces structural changes in the recipient's heart. To assess the possibility of heart "recovery" we reviewed the records of 19 HeartMate LVAD recipients to determine structural and left ventricular histologic changes during LVAD support. Intraoperative transesophageal echocardiographic studies were performed in the operating room before LVAD insertion, immediately after LVAD insertion, and at explantation and heart transplantation (mean duration of support, 76 +/- 34 days). The initiation of LVAD pumping led to an immediate decrease (p < 0.001) in left ventricular dimensions, which were not significantly different by the time of device explantation. Left ventricular fractional shortening did not significantly improve during LVAD support (0.07 +/- 0.03 before LVAD; 0.11 +/- 0.10 immediately after LVAD; 0.11 +/- 0.11 before explantation). Histologic specimens showed a significant reduction in the number of wavy fibers, and contraction band necrosis (p < 0.01), both markers of acute myocyte damage. However, myocardial fibrosis increased (p < 0.05). Myocyte diameter increased slightly (p = 0.07). We conclude that implantable LVAD support is associated with immediate changes in ventricular structure. Histologic markers of acute myocyte damage improve, but fibrosis increases. Because the structural changes occur immediately, they do not indicate "recovery" of left ventricular function, but merely changes in loading conditions.

Adult↗
PubMed1995

Initial experience with the Cosgrove-Edwards Annuloplasty System.

BACKGROUND: The mitral valve has a nonplanar shape and a sphincter action. Pathologic dilatation occurs along the posterior annulus. To preserve the physiologic function and correct annular dilatation, we developed an annuloplasty system that is universally flexible and produces a measured plication of the posterior annulus (Cosgrove-Edwards Annuloplasty System). METHODS: The results of 150 consecutive mitral valve repairs using this system were analyzed. Mean age was 58 +/- 13 years; 59% were men. The cause of the valve disease was degenerative in 75% of the patients, rheumatic in 13%, ischemic in 8%, and infectious in 4%. Associated procedures were performed in 61 patients (41%). RESULTS: Echocardiographic mitral regurgitation decreased from 3.7 +/- 0.6 before repair to 0.2 +/- 0.4 after repair (p < 0.0001). There were no hospital deaths and no cases of hemodynamically significant systolic anterior motion or other annuloplasty-related complications. Follow-up was 100% complete at a mean of 3.1 +/- 3.6 months. There were three late deaths, three transient ischemic attacks, and one episode of endocarditis. Five patients (3.3%) have undergone reoperation for recurrent mitral insufficiency; no reoperations were related to the annuloplasty system. At a mean of 9 months, three-dimensional reconstruction of the mitral annulus from multiple echocardiographic images confirmed the nonplanar shape and sphincter mechanism of the annulus. Annular orifice area decreased 19% during the cardiac cycle from a mean of 10.3 cm2 in diastole to 8.6 cm2 in systole. CONCLUSIONS: This annuloplasty system is effective for repair of insufficiency secondary to all causes, preserves physiologic annulus function, and is associated with a low incidence of valve-related complication.

Adult↗
PubMed1995

Progression of aortic stenosis in 394 patients: relation to changes in myocardial and mitral valve dysfunction.

OBJECTIVES: This study reports the results of echocardiographic follow-up in a large cohort of patients with aortic stenosis and correlates the progression of aortic stenosis with changes in the degree of mitral regurgitation and left ventricular hypertrophy and systolic dysfunction. BACKGROUND: Progressive aortic stenosis often causes left ventricular dysfunction and mitral regurgitation. Doppler echocardiography has greatly assisted in the noninvasive evaluation and follow-up of aortic stenosis. Nevertheless, the longitudinal follow-up of patients with Doppler echocardiography for the progression of aortic stenosis and the significance of progressive ventricular hypertrophy and mitral regurgitation have not been reported. METHODS: Serial Doppler echocardiography was performed in 394 consecutive patients with valvular aortic stenosis at baseline and after a mean follow-up period of 37 +/- 16 months. Mean and peak aortic gradients, aortic valve area, left ventricular systolic and diastolic diameters and percent area change (shortening fraction) were expressed as continuous variables, and systolic dysfunction, mitral regurgitation, ventricular hypertrophy and filling properties were tabulated as categoric variables using a semiquantitative grading system. RESULTS: Peak and mean gradients increased by an average of 8.3 and 6.3 mm Hg/year, respectively; end-systolic and end-diastolic diameters increased by 1.9 and 1.6 mm/year, respectively; and aortic valve area decreased by 0.14 cm2/year during the follow-up interval (p < 0.001 for all), indicating progression of aortic stenosis and ventricular dilation. Patients in the lowest quartile of aortic valve area and highest quartiles of mean and peak gradients had the least change compared with those in the highest quartile of aortic valve area and lowest quartile of mean and peak gradients (p < 0.01 for all). Patients with more mitral regurgitation at follow-up than at baseline had higher mean percent increase in mean and peak gradients as well as more progression of ventricular dilation and worsening systolic function compared with those with stable or improving mitral regurgitation (p < 0.05 for all). Similarly, subjects with worsening left ventricular hypertrophy had larger mean percent increase in mean and peak gradients than those with stable left ventricular hypertrophy (p < 0.01) but maintained stable ventricular volumes and systolic function. There was no correlation between the amount of change in mean or peak gradients and degree of deterioration in systolic function. CONCLUSIONS: Aortic stenosis progresses predictably over time; however, systolic dysfunction is an inconsistent marker of the hemodynamic consequences of severe aortic stenosis. As an adaptive response to pressure overload, progressive hypertrophy appears to prevent ventricular dilation and development or worsening of mitral regurgitation. Conversely, progressive mitral regurgitation may be seen as a maladaptive consequence of increasing aortic stenosis.

Aged↗
PubMed1995

Intraoperative validation of mitral inflow determination by transesophageal echocardiography: comparison of single-plane, biplane and thermodilution techniques.

OBJECTIVES: This study investigated the accuracy of mitral inflow quantification using biplane transesophageal echocardiography. BACKGROUND: Mitral stroke volume can be reliably quantified by transthoracic Doppler echocardiography, but previous studies involving monoplane transesophageal echocardiography have yielded mixed results. METHODS: Thirty patients without mitral regurgitation were prospectively examined immediately before cardiovascular surgery. Mitral annulus diameter was measured in the transverse (d1) and longitudinal views (d2) by biplane transesophageal echocardiography. Assuming an elliptic shape, the annular area was calculated as pi d1d2/4; area was also calculated from single-plane data assuming a circular annular shape as pi d2/4. The time-velocity integral of mitral annular Doppler velocity was then multiplied by annular area to yield stroke volume. These data were compared with simultaneous thermodilution measurements by linear regression. RESULTS: Good correlations were observed between thermodilution (x) and Doppler (y) measurements of stroke volume (SV) (r = 0.86, p < 0.01, delta SV [y-x] = 2.64 +/- 9.86 ml for single four-chamber view; r = 0.77, p < 0.01, delta SV = 1.82 +/- 12.59 ml for two-chamber view; r = 0.94, p < 0.001, delta SV = 1.78 +/- 5.90 ml for biplane measurements) with similar data for cardiac output (r = 0.82, r = 0.74 and r = 0.92, respectively). The biplane measurements were most accurate and had less variability in individual patients (p < 0.05). This finding was supported by a numerical model that demonstrated (for an ellipse of eccentricity 1.5:1) that even maximal misalignment of biplane diameters yielded only 8% area overestimation, whereas single-plane calculations assuming a circular shape produced a variation in area of 225%. CONCLUSIONS: This study validates the accuracy of measurements of mitral inflow using biplane transesophageal echocardiography with potential application for quantification of valvular regurgitation in the operating room. The results are further generalizable, indicating that orthogonal biplane measurements are both necessary and sufficient to ensure accuracy in area calculation for any elliptic structure.

Adult↗
PubMed1995

Angiographic and prognostic implications of an exaggerated exercise systolic blood pressure response and rest systolic blood pressure in adults undergoing evaluation for suspected coronary artery disease.

OBJECTIVES: This study was designed to assess the angiographic and prognostic implications of an exaggerated systolic blood pressure response to exercise ("exercise hypertension") in adults undergoing evaluation for suspected coronary artery disease. BACKGROUND: The clinical implications of exercise hypertension are unclear. METHODS: Subjects for this prospective cohort study were derived from a consecutive sample of 9,608 adults who were referred for treadmill testing and who augmented their systolic blood pressure by at least 10 mm Hg. There were 594 subjects who underwent coronary angiography within 90 days of treadmill testing. Exercise hypertension was defined as a peak exercise systolic blood pressure > or = 210 mm Hg in men and > or = 190 mm Hg in women. Severe angiographic coronary disease was defined as left main coronary artery disease (> or = 50% diameter stenosis), three-vessel disease (> or = 70% diameter stenosis) or two-vessel disease with > or = 70% diameter stenosis of the proximal left anterior descending coronary artery. All-cause mortality was assessed during a follow-up period of approximately 2 years. RESULTS: Exercise hypertension was present in 196 subjects (33%). Severe coronary disease was less common in subjects with exercise hypertension (14% vs. 25%, odds ratio 0.51, 95% confidence interval [CI] 0.32 to 0.81, p = 0.004). Exercise hypertension remained associated with a lower rate of severe coronary disease even after adjusting for rest hypertension, age, gender, exercise capacity and other possible confounders. During the follow-up period, there were 23 deaths; only 2 occurred in the group with exercise hypertension. After adjusting for severity of coronary disease, exercise hypertension remained associated with a lower mortality rate (adjusted relative risk 0.20, 95% CI 0.05 to 0.84, p = 0.03). CONCLUSIONS: In adults evaluated for coronary artery disease, exercise hypertension is associated with a lower likelihood of angiographically severe disease and a lower adjusted mortality rate.

Blood Pressure↗
PubMed1995

Exercise echocardiography is an accurate and cost-efficient technique for detection of coronary artery disease in women.

OBJECTIVES: This study compared the accuracy and cost implications of using exercise echocardiography and exercise electrocardiography for detection of coronary artery disease in women. BACKGROUND: The specificity of exercise electrocardiography in women is lower than in men. Exercise echocardiography accurately identifies coronary artery disease in women, but its utility in place of exercise electrocardiography is unclear. METHODS: One hundred sixty-one women without a previous Q wave infarction underwent exercise echocardiography and coronary angiography. Positive findings were a new or worsening wall motion abnormality on the exercise echocardiogram and ST segment depression > 0.1 mV at 0.08 s after the J point on the exercise electrocardiogram (ECG). RESULTS: Coronary artery stenosis > 50% diameter narrowing was present in 59 patients; the sensitivity (mean +/- SD) of exercise echocardiography was 80 +/- 3%. In 48 patients with an interpretable ECG, the sensitivity of exercise echocardiography was 81 +/- 4%, and that of the exercise ECG was 77 +/- 3% (p = 0.50). In 102 patients without coronary artery disease, the overall specificity of exercise echocardiography was 81 +/- 4%. In 70 patients with an interpretable ECG, the specificity of exercise echocardiography (80 +/- 3%) exceeded that of the exercise ECG (56 +/- 4%, p < 0.0004). The accuracy of exercise echocardiography was also greater than exercise electrocardiography (81 +/- 5% vs. 64 +/- 6%, p < 0.005). Exercise echocardiography stratified significantly more patients of intermediate (20% to 80%) pretest disease probability into the high (> 80%) or low (< 20%) posttest probability group. In women without a previous exercise ECG, the specificity of exercise echocardiography continued to exceed that of exercise electrocardiography (80 +/- 3% vs. 64 +/- 3%, p = 0.05). Exercise echocardiography had the best balance between accuracy and cost for the diagnosis of coronary artery disease in women. CONCLUSIONS: Exercise echocardiography is more specific than exercise electrocardiography for diagnosis of coronary artery disease in women and is a cost-effective approach to the diagnosis of coronary artery disease because of the avoidance of inappropriate angiography.

Adult↗