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J Arce

Publications and source records attributed to J Arce.

12 recordsLinked to original sources

Norethindrone acetate and estradiol-induced endometrial hyperplasia.

OBJECTIVE: To identify the lowest effective continuous dose of norethindrone acetate that significantly reduces 12-month incidence of endometrial hyperplasia associated with unopposed 17beta-estradiol (E2), 1 mg. METHODS: In a double-masked, randomized, multicenter study, 1176 healthy postmenopausal women 45 years of age or older without evidence of endometrial abnormalities were given 12 months of treatment with unopposed E2, 1 mg, or continuous-combined regimens of E2, 1 mg, and norethindrone acetate, 0.1 mg, 0.25 mg, or 0.5 mg. Endometrial histology was evaluated at the end of the treatment period. RESULTS: Continuous-combined E2-norethindrone acetate regimens significantly reduced 12-month incidence of endometrial hyperplasia compared with unopposed E2 1 mg (P <.001). Endometrial hyperplasia occurred in 14.6% of women treated with unopposed E2 1 mg, whereas in all continuous-combined groups, the rate decreased to less than 1%. Among patients who received E2-norethindrone acetate 0.1 mg, incidence was 0.8%; among those who received 0.25 mg and 0.5 mg, it was 0.4%. CONCLUSION: Continuous norethindrone acetate at doses as low as 0.1 mg combined with E2 1 mg effectively negated risk for endometrial hyperplasia associated with unopposed E2 1 mg, at least for the first year of therapy.

Climacteric↗

Initial 17beta-estradiol dose for treating vasomotor symptoms.

OBJECTIVE: To compare the efficacy of different doses of 17beta-estradiol (E2) for relief of vasomotor symptoms in menopausal women. METHODS: This was a randomized, double-masked, placebo-controlled, 12-week study in which 333 menopausal women with moderate or severe hot flushes were assigned to treatment with 0.25 mg, 0.5 mg, 1 mg, or 2 mg oral micronized 17beta-E2, or placebo. The number and severity of hot flushes were recorded daily. RESULTS: There was a significant linear correlation between increased dosage of 17beta-E2 and decreased moderate to severe hot flushes per week (P <.001). Rapid reduction in moderate to severe hot flushes was only achieved with 1 and 2 mg, showing a significant difference from placebo at week 4 (P <.05). At week 4, half the women on placebo had reduced moderate to severe hot flushes of at least 52%; the corresponding figures were 56%, 69%, 86%, and 91% for 0.25, 0.5, 1, and 2 mg, respectively. At week 12, all doses except 0.25 mg were significantly better than placebo for reducing moderate to severe hot flushes (P <.001). Although there were no significant differences, twice as many women in the 2-mg group discontinued treatment due to adverse events, compared with the placebo group. CONCLUSION: Oral micronized 17beta-E2 showed a dose-response effect for reducing moderate and severe hot flushes in menopausal women. 17beta-E2 1 mg appeared to be the most useful initial dose.

Administration, Oral↗

The transesophageal echocardiographic diagnosis of left atrial myxoma simulating a left atrial thrombus in the setting of mitral stenosis.

We report a case of left atrial myxoma simulating a thrombus on transthoracic echocardiography, but correctly diagnosed using transesophageal echocardiography. As this tumor is usually fatal unless surgically resected, a correct diagnosis is essential. Myxomas which do not prolapse between the mitral valve leaflets and coexist with mitral stenosis may be difficult to diagnose accurately using transthoracic echocardiography. The advantages of transesophageal compared with transthoracic echocardiography in the diagnosis of nonclassical left atrial myxoma are discussed.

Aged↗

Two-dimensional transesophageal echocardiographic determination of aortic valve area in adults with aortic stenosis.

To determine if aortic stenosis severity could be accurately measured by two-dimensional transesophageal echocardiography (TEE), 62 adult subjects (mean age 66 +/- 12 years) with aortic stenosis had their aortic valve area (AVA) determined by direct planimetry using TEE, and with the continuity equation using combined transthoracic Doppler and two-dimensional echocardiography (TTE). Eighteen subjects had AVA calculated by the Gorlin method during catheterization. An excellent correlation (r = 0.93, SEE = 0.17 cm2) was found between AVA determined by TEE (mean 1.24 +/- 0.49 cm2; range 0.40 to 2.26 cm2) and TTE (mean 1.23 +/- 0.46 cm2; range 0.40 to 2.23 cm2). The absolute (0.13 +/- 0.12 cm2) and percent (10.8 +/- 8.9%) differences between AVA determined by TEE versus TTE were small. Excellent correlations between AVA by TEE and TTE were also found in subjects with normal systolic function (r = 0.95, SEE = 0.14 cm2; n = 38) and impaired function (r = 0.91, SEE = 0.21 cm2; n = 24). AVA determined by catheterization correlated better with AVA measured by TEE (r = 0.91, SEE = 0.15 cm2) than AVA measured with TTE (r = 0.84, SEE = 0.19 cm2). These data demonstrate that AVA can be accurately measured by direct planimetry using TEE in subjects with aortic stenosis. TEE may become an important adjunct to transthoracic echocardiography in the assessment of aortic stenosis severity.

Adult↗

Noninvasive assessment of left ventricular diastolic function by pulsed Doppler echocardiography in patients with hypertrophic cardiomyopathy.

Hypertrophic cardiomyopathy is a primary myocardial disease in which symptoms may frequently result from impaired left ventricular relaxation, filling and compliance. In the present investigation, Doppler echocardiography was utilized to measure transmitral flow velocity and thereby assess left ventricular diastolic performance noninvasively in a group of 111 patients representative of the broad clinical spectrum of hypertrophic cardiomyopathy. In patients with hypertrophic cardiomyopathy, all Doppler indexes of diastolic relaxation and filling differed significantly (p less than 0.001) from those obtained in 86 control subjects without heart disease, namely, prolongation of isovolumic relaxation (94 +/- 24 versus 78 +/- 12 ms) and of the early diastolic peak of flow velocity (244 +/- 55 versus 220 +/- 28 ms), as well as slower deceleration (3.4 +/- 1.4 versus 4.9 +/- 1.3 m/s2) and reduced maximal flow velocity in early diastole (0.5 +/- 0.2 versus 0.6 +/- 0.1 m/s). As an apparent compensation for impaired relaxation and early diastolic filling, the atrial contribution to left ventricular filling was increased, as shown by increased late diastolic flow velocity (0.4 +/- 0.3 versus 0.3 +/- 0.1 m/s) and reduced ratio of maximal flow velocity in early diastole to that in late diastole (1.4 +/- 0.8 versus 2.1 +/- 0.9). The vast majority of patients with hypertrophic cardiomyopathy (91 [82%] of 111) showed evidence of impaired left ventricular diastolic performance, as assessed from the Doppler waveform. Abnormal Doppler diastolic indexes were identified with similar frequency in patients with (78%) or without (83%) left ventricular outflow obstruction, as well as in patients with (84%) or without (80%) cardiac symptoms. However, patients with nonobstructive hypertrophic cardiomyopathy showed more severe alterations in the Doppler indexes of diastolic function than did patients with obstruction. Thus, abnormal diastolic performance as assessed by Doppler echocardiography was apparent in the vast majority of the study patients with hypertrophic cardiomyopathy, independent of the presence or absence of cardiac symptoms or a subaortic pressure gradient. The high frequency with which diastolic abnormalities are identified in asymptomatic patients with hypertrophic cardiomyopathy suggests that impaired diastolic performance may be present at a time in the natural history of the disease when functional limitation is not yet evident.

Adolescent↗

Development and progression of left ventricular hypertrophy in children with hypertrophic cardiomyopathy.

Whether the magnitude and distribution of left ventricular hypertrophy in patients with hypertrophic cardiomyopathy are established at birth, or whether they evolve during the first years of life, is unknown. Accordingly, we conducted serial echocardiographic studies in 39 children with a family history or morphologic evidence of hypertrophic cardiomyopathy. The patients were initially evaluated at 4 to 15 years of age (mean, 11) and most recently at 9 to 20 years (mean, 16). During a follow-up period of 2.5 to 6.8 years (mean, 4), the magnitude and extent of preexisting left ventricular hypertrophy markedly increased in 17 patients and the morphologic appearance of the heart evolved from normal to hypertrophic in 5 others. In these 22 patients the left ventricular wall thickness increased strikingly (by 6 to 23 mm, a change of 101 +/- 62 percent); these increases significantly exceeded those expected as a consequence of normal growth (13 +/- 10 percent; P less than 0.001) and were not associated with symptomatic deterioration or related to subaortic obstruction. We conclude that left ventricular hypertrophy may develop or progress spontaneously in patients with hypertrophic cardiomyopathy during childhood, when body growth is considerable. Since echocardiograms may be normal during childhood--before the morphologic features of hypertrophic cardiomyopathy develop--a single echocardiographic examination of young relatives of patients with hypertrophic cardiomyopathy may not exclude this disease.

Adolescent↗

Dynamic subaortic obstruction in hypertrophic cardiomyopathy: analysis by pulsed Doppler echocardiography.

To determine whether true obstruction to left ventricular ejection exists in patients with hypertrophic cardiomyopathy and a subaortic gradient, pulsed Doppler echocardiography was used to analyze the patterns of left ventricular emptying in 50 patients with hypertrophic cardiomyopathy (20 with and 30 without evidence of obstruction) and in 20 normal subjects. In obstructive hypertrophic cardiomyopathy, left ventricular ejection was characterized by early and rapid emptying (76 +/- 14% of aortic flow velocity in the initial one-third of systole). The proportion of forward flow velocity occurring before initial mitral-septal contact (and hence, by inference before the onset of the subaortic gradient) was variable, but averaged 58%. In contrast, the proportion of forward flow velocity occurring after mitral-septal contact (and, therefore, concomitant with the gradient and increased intraventricular pressure) was considerable, averaging over 40%. Mid-systolic impedance to left ventricular outflow was suggested by the rapid deceleration in aortic flow velocity concomitant with mitral-septal contact and premature partial aortic valve closure. Furthermore, left ventricular ejection was prolonged (384 +/- 40 ms) and the ventricle continued to empty and shorten during the period when both the pressure gradient and markedly increased intraventricular pressures were present. In 16 of 20 patients, a relatively small second peak in flow velocity appeared in late systole. Since marked systolic anterior motion of the mitral valve was still present, the late systolic portion of forward flow velocity also appeared to be largely ejected during imposition of a mechanical impediment to outflow. In contrast, patients with nonobstructive hypertrophic cardiomyopathy showed no evidence of impedance to left ventricular ejection. Aortic flow velocity waveforms were similar to those of normal subjects, with flow persisting to aortic valve closure; significant mitral systolic anterior motion and partial mid-systolic aortic valve closure were absent, and the systolic ejection period was normal (303 +/- 27 ms).(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗

Prenatal diagnosis and management of nonimmunologic hydrops fetalis.

As problem pregnancies are increasingly subjected to ultrasound evaluation, the prenatal diagnosis of hydrops fetalis is being made more and more frequently. The authors encountered 5 cases of this disorder in 12,830 deliveries (1:2566) and made the diagnosis prior to delivery in 4 of the 5 cases. Amniocentesis and amniotic fluid bilirubin determination have been performed in association with ultrasound scan and a battery of other diagnostic tests, and the results have been correlated with fetal outcome. In general the combination of fetal ascites and increased amniotic fluid bilirubin denotes a poor fetal prognosis. Unless there are other mitigating circumstances, a conservative course of management is recommended.

Adolescent↗

[Not Available].

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Allergy and Immunology↗