PubMed · 4029985
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T E Samdarshi, A K Thakur. Echo visualisation of pacemaker lead.. https://pubmed.ncbi.nlm.nih.gov/4029985/
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In conclusion, ventricular volume calculation from 2DE is feasible in the human fetus and improves the ability to calculate fetal ventricular size and ejection fraction. The right ventricle is clearly dominant at midgestation, but approaches left ventricular size at term. Calculation of the ventricular output from 2DE volume measurements is an accurate alternative to Doppler measurements.
The correlation between episodes of ST-segment elevation on Holter monitoring, clinical characteristics, left ventricular function, exercise testing, and long-term prognosis was determined in 123 consecutive patients 55 +/- 8 years old (mean +/- SD) with a first acute myocardial infarction (AMI). During 36 hours of Holter recording 11 +/- 5 days after AMI, 11 patients (9%) had 91 episodes of ST-segment elevation (group 1), whereas 112 patients had no such episodes (group 2). Most episodes of ST-segment elevation occurred in leads with pathologic Q waves or small, indistinct R waves. Large, anterior Q-wave AMIs were more prevalent in group 1 than in group 2, and in-hospital heart failure also occurred more frequently in group 1 patients (82% vs 23%; p < 0.0005). Regional and global left ventricular function was reduced in group 1 compared with group 2: ejection fraction 33 +/- 11% vs 50 +/- 11% (p = 0.0001). All episodes of ST-segment elevation were asymptomatic and did not correlate with different indicators of myocardial ischemia. Indeed, exercise-induced ST-segment depression was more prevalent in group 2 than in group 1: 57 vs 18% (p < 0.035). Over a mean of 5 years (range 4 to 6) of follow-up, an association between episodes of ST-segment elevation on Holter monitoring and (1) cardiac death (Kaplan-Meier analysis; p < 0.005), and (2) cardiac death and nonfatal reinfarction (Kaplan-Meier analysis; p < 0.025) was found.(ABSTRACT TRUNCATED AT 250 WORDS)
BACKGROUND: Isolated case reports that suggest the potential for development of left heart hypoplasia late in gestation provide the only information about the in utero natural history of left heart obstructive lesions. METHODS AND RESULTS: We reviewed the prenatal and postnatal echocardiograms of 21 fetuses with left heart obstructive lesions, including 15 with serial antenatal study, to elucidate the antenatal natural history of this spectrum of disease and to identify features indicative of postnatal disease severity. Ventricular, atrioventricular valve, and great artery dimensions were measured and growth curves were developed with comparisons to data from 47 normal fetuses. Fetuses were divided into groups according to whether postnatally the left heart was capable (group 1, n = 10) or incapable (group 2, n = 7) of supporting the systemic circulation in the presence of a patent aortic valve. Group 3 (n = 4) included fetuses with aortic atresia. At the initial examination (21.7 +/- 3.4 weeks' gestation), left heart dimensions were normal or reduced, with the most diminutive measurements in group 3. Three fetuses in group 2 and most in group 1 had normal initial left heart dimensions. Subsequent growth of left heart structures either paralleled normal growth or was reduced, the latter resulting in the development or progression of left heart hypoplasia. All left heart dimensions grew more slowly in group 2 and group 3 than in group 1 (P < .05). Other prenatal features observed only in groups 2 and 3 included reversed (n = 10) or bidirectional (n = 1) foramen ovale flow and retrograde distal arch flow (n = 9). Initial midtrimester mitral valve and ascending aorta z scores and the growth rates of all left heart structures correlated strongly with postnatal left ventricular end-diastolic dimension (P = .0007 to .03, r = .57 to .82) and could be additional indicators of postnatal disease severity. One group 1 fetus developed severe aortic stenosis late in gestation. CONCLUSIONS: The potential for the in utero development or progression in severity of left heart obstruction and hypoplasia in left heart obstructive lesions necessitates serial prenatal study in affected fetuses carried to term.