Antepartum fetal heart rate monitoring: III. Fetal movements and accelerations in fetal heart rate

This third part of the paper deals with the study of the relationships between fetal movements, fetal heart rate accelerations associated with such movements, fetal heart rate instability and neonatal outcome.No correlation has been found between absence of fetal movements and neonatal distress.A correlation has been found between the lack of fetal heart rate accelerations, the flatness of the record and poor neonatal outcome.In extreme situations (i.e. flatness in less than 10% of the record or in more than 80%) the presence or absence of accelerations does not add further useful information. Such information, however, is gained in the intermediary situations (the ‘combined’ recordings) and particularly when the record is between 51 and 80% flat where there appears to be an 85.6% risk to the fetus.Consequently, when trying to analyse an antenatal record it seems advisable to take primarily into account the percentage of flat recordings (providing the records are numerous enough and of sufficient length). Then, in records between 10 and 50% flat, the presence or the lack of spontaneous decelerations requires consideration whereas, when the record is between 51 and 80% flat, it is the presence or absence of fetal heart rate accelerations which is important.     

α_2受体阻滞后肾上腺素诱导的心衰病人血小板的聚集功能

先前的研究表明血小板α_2受体变化表征交感神经突触前α_2受体的变化。为了解心衰病人血小板α_2受体功能状况,我们观察了10例Ⅲ、Ⅳ级心功能的心衰病人及10例配对正常人由肾上腺素诱导的血小板聚集率在α_2受体阻滞前后的变化。结果表明肾上腺素诱导的血小板聚集率在两组无显著性差异,但应用α_2阻滞剂Rauwolscine(0.25mg/L)后,0.25,0.5,1.0mg/L E诱导的心衰病人血小板聚集率显著低于对照组,提示血小板α_2受体在心衰时有数量的减少或(和)功能的降低,表征交感神经突触前NE释放的负反馈机制被抑制。     

Altered neuropeptide Y Y1 responses in mesenteric arteries in rats with congestive heart failure

The aim of the present study was to elucidate if the potentiating effect of neuropeptide Y on various vasoactive agents in vitro is (1) altered in mesenteric arteries from rats with congestive heart failure and (2) mediated by the neuropeptide Y Y₁ receptor. The direct vascular effects of neuropeptide Y and its modulating effects on the contractions induced by endothelin-1-, noradrenaline-, 5-hydroxytryptamine (5-HT)-, U46619-(9, 11-dideoxy-11, 9-epoxymethano-prostaglandin F₂) and ATP, and acetylcholine-induced dilatations were studied in the presence and absence of the neuropeptide Y Y₁ antagonist, BIBP3226 (BIBP3226{(R)-N2-(diphenylacetyl)-N-[(4-hydroxyphenyl)methyl]- -arginine-amide}). Neuropeptide Y, per se, had no vasoactive effect in the arteries. The potency of endothelin-1 was significantly decreased in congestive heart failure rats. Neuropeptide Y and neuropeptide Y-(13–36) potentiated the endothelin-1-induced contraction in congestive heart failure mesenteric arteries. In 20% of the congestive heart failure rats, sarafotoxin 6c induced a contraction of 31±4%. Neuropeptide Y also potentiated U46619- and noradrenaline-induced contractions but not 5-HT-induced contractions in congestive heart failure arteries. In sham-operated animals neuropeptide Y potentiated noradrenaline- and 5-HT-induced contractions. These potentiations were inhibited by BIBP3226. Acetylcholine induced an equipotent relaxation in both groups which was unaffected by neuropeptide Y. In conclusion, neuropeptide Y responses are altered in congestive heart failure rats. The potentiating effect differs between vasoactive substances. Neuropeptide Y Y₁ and non-neuropeptide Y₁ receptors are involved.     

Regional myocardial oxygen tension: 19F MRI of sequestered perfluorocarbon

A novel noninvasive method of measuring local myocardial oxygen tension (pO₂) In the perfused rat heart using ¹⁹F MRI is demonstrated. Tissue pO₂ was determined on the basis of the ¹⁹F spin-lattice relaxation rate (R1) of perflubron (perfluorooctyl bromide) sequestered in the heart after IV infusion of an emulsion. Spectroscopic measurement of R1 was previously used to measure a global weighted average of oxygen status. ¹⁹F MRI now provides 3D spatial resolution indicating local cardiac pO₂ under normally perfused, globally ischemic, and regionally ischemic conditions.     

Right internal thoracic artery through the transverse sinus in myocardial revascularization

Background. A major concern in evaluating dynamic cardiomyoplasty has been whether the synchronous stimulation of latissimus dorsi muscle is essential for benefit or not. We studied 10 patients to determine the efficacy of the systolic augmentation generated by the synchronous electrical stimulation of the latissimus dorsi muscle.

Methods. Left ventricular ejection fraction, end-systolic and end-diastolic volume indexes, and stroke volume index obtained during resting, peak exercise, and recovery periods (“on” values) were compared with those obtained 1 week after cessation of electrical stimulus (“off” values). Double product and estimated total body oxygen consumption at peak exercise were also calculated and compared.

Results. Higher ejection fractions (0.36 ± 0.07 versus 0.33 ± 0.06 at rest, 0.40 ± 0.07 versus 0.33 ± 0.07 peak exercise, and 0.37 ± 0.06 versus 0.31 ± 0.06 at recovery) and lower end-systolic volume indexes with relatively constant end-diastolic volume indexes were observed with the cardiomyostimulator on. Further, exercise response was better with the cardiomyostimulator on. Double product indirectly reflected better myocardial oxygen supply/demand ratio when on at peak exercise (17 ± 2.2 mm Hg × beats/min × 10⁻³ for on versus 19 ± 2.6 mm Hg × beats/min × 10⁻³ for off). Estimated total body oxygen consumption was improved at peak exercise when the cardiomyostimulator was functional (12 ± 2.7 mL · kg⁻¹ · min⁻¹ versus 11 ± 2.6 mL · kg⁻¹ · min⁻¹).

Conclusions. Current data suggest a true systolic assist during synchronous contractions of the latissimus dorsi muscle. It is thought, therefore, that synchronous electrical stimulation is essential for maximum benefit and all the beneficial effect of cardiomyoplasty certainly cannot be attributed to simple wrapping itself.     

Short and long term effects of exercise training on the tonic autonomic modulation of heart rate variability after myocardial infarction

We studied the effects of cardiac rehabilitation on the sympathovagalcontrol of heart rate variability in 30 patients after a first,uncomplicated myocardial infarction. Twenty-two patients completed8 weeks of endurance training (trained), while eight decidednot to engage in the rehabilitation programme for logisticalreasons, and were taken as untrained controls. Age, site ofinfarction, ejection fraction, ventricular diameter and stresstest duration were similar in the two groups at baseline. Heartrate variability was evaluated 4 weeks after infarction beforestarting rehabilitation, and repeated 8 weeks and one year laterin both trained and untrained patients. Measures of heart ratevariability, obtained from both time- and frequency- domainanalysis of a 15 min ECG recording in resting conditions, wereas follows: mean RR interval and its standard deviation (RRSD),the mean square successive differences (MSSD), the percent ofRR intervals differing >50 ms from the preceding RR (pNTN50),the low and high frequency components of the autoregressivepower spectrum of the RR intervals and their ratio (LF/HF).At baseline, heart rate variability was similar in trained anduntrained patients. In the short term (8 weeks after infarction),training increased RRSD by 25% (P<0·01), MSSD by 69%(P<0·01), pNN50 by 120% (P<0·01), and reducedLF/HF ratio by 30% (P<0·01). The effects persistedafter one year in trained patients. In untrained patients, theautonomic control of heart rate variability did not change 8weeks after myocardial infarction and was only slightly modifiedby time. Thus, exercise training, performed for 8 weeks aftera myocardial infarction, modifies the sympathovagal controlof heart rate variability toward a persistent increase in parasympathetictone, known to be associated with a better prognosis. This maypartly account for the favourable outcome of patients who undergorehabilitation.     

Lipids and lipoproteins as risk factors for coronary heart disease in men with abnormal glucose tolerance: the Honolulu Heart Program

Abstract. Objectives. To evaluate lipids and lipoproteins as risk factors for coronary heart disease (CHD) in older men with non-insulin-dependent diabetes (NIDDM) or abnormal glucose tolerance compared with normoglycaemic men. Design. A prospective, population-based cohort study based on the lipoprotein examination (1970–72) of the Honolulu Heart Program. Follow-up was through to December 1988. Setting. Honolulu, Hawaii. Subjects. Japanese-American men, ages 51–72 at baseline: 2042 with 1 h glucose < 12.5 mmol l^?1 (normal group); 376 on oral hypoglycaemic agents or with 1 h glucose ≥ 12.5 mmol l^?1 after 50 g oral glucose challenge (abnormal glucose tolerance group). None had prevalent coronary heart disease (CHD) or stroke at baseline. Main outcome measures. Incident CHD: definite nonfatal myocardial infarction (MI) or fatal CHD. Results. There were 221 incident cases in the normal group, and 65 in the abnormal glucose tolerance group. Total and high-density lipoprotein (HDL) cholesterol were significant predictors of incident CHD in men with NIDDM or abnormal glucose tolerance after controlling for age, body-mass index, systolic blood pressure, pack-years of cigarettes and alcohol consumption (P < 0.05). Total, low-density lipoprotein (LDL) and very-low-density lipoprotein (VLDL) cholesterol were significant predictors in normal men, and HDL cholesterol was of borderline significance. Conclusions. Abnormal lipids and lipoproteins are significant, independent predictors of CHD in subjects with NIDDM or abnormal glucose tolerance. Attention to lipid and lipoproteins as CHD risk factors should be part of clinical management of these patients.     

Radiologic search for embolized leaflets of prosthetic heart valves: A report of two cases

In a radiologic search for embolized leaflets of Edwards-Duromedics bileaflet valves in 2 patients, the embolized fragments were localized in the iliac vessels using computed tomography. Sonography was successful in one case and standard X-ray films of the abdomen were negative in both cases.In vitro investigations with Björk-Shiley and Edwards-Duromedics leaflets suggested that standard X-ray films of the abdomen and pelvis should be considered as the first investigational technique. If negative, computed tomography of the lower abdomen should be done.     

Holt-Oram syndrome associated with the hypoplastic left heart syndrome

We present the first case of Holt-Oram syndrome associated with the lethal congenital heart defect of hypoplastic left heart syndrome. The possible pathophysiological link is explored and the need for careful genetic and cardiologic evaluation in these patients is reiterated.