PubMed · 6656415
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M Ballester Rodés. 1983-11-12. [Functional mitral insufficiency].. https://pubmed.ncbi.nlm.nih.gov/6656415/
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The aim of this study was to determine the prenatal fetal pyelectasis which requires postnatal evaluation. This was a retrospective analysis involving 65 infants with complete urological follow-up; 59 had shown prenatal evidence of pyelectasis using previously published standards. Males were more common in both the normal (75 per cent) and the abnormal (77 per cent) postnatal outcome groups. Unilateral prenatal lesions were less common than bilateral, but had significant postnatal pathology in 47 and 26 per cent, respectively (n.s.). Persistent dilatation was likely to be associated with postnatal pathology. A 6 mm threshold of dilatation predicted the 19 infants with significant postnatal pathology. The majority of fetuses with pyelectasis in the study had normal outcomes, with males often showing 'transitory pyelectasis'. A repeat prenatal scan at 30-40 weeks' gestation is recommended for all fetuses where 6 mm or more of renal pelvic dilatation is detected prior to 28 weeks. Postnatal follow-up is required for persistent pyelectasis.
BACKGROUND: The increasing experience with prenatal ultrasonographic diagnosis allows detection of more and more mild urinary tract anomalies. Thus, the clinical significance of many pyelectasis detected before birth is not known. PATIENTS AND METHODS: From a retrospective study of 78 patients, we determined the positive predictive value (PPV) of prenatal ultrasound findings for urinary tract malformations. RESULTS: This PPV was 27.3% when the prenatal pelvic dilatation was isolated, but grew up to 100% if a caliceal dilatation was associated. Renal pelvic diameter in the third trimester of pregnancy could predict the degree of post-natal renal impairment, as pelvic size was 6.7 +/- 2.15 mm for the post-natal pyelectasis group, significatively smaller than 13.4 +/- 3 mm in the ureteropelvic junction obstruction group (grade 1) and than 17 +/- 9 mm in other pathological renal units. On the other hand, antenatal ultrasound had a bad sensibility for vesico-ureteral reflux detection, four primary reflux among 14 being detected without homolateral antenatal ultrasound anomaly. CONCLUSION: According these results, we propose a post-natal diagnostic strategy. Urological explorations are performed when the prenatal renal pelvic diameter is larger than 10 mm. If the postnatal ultrasound shows an isolated pyelectasis below this level, a clinical follow-up is advised, the parents being informed of the possibility of vesico-ureteral reflux and of the necessity to perform a cytobacteriological exam of urines in case of unexplained fever.
Within a narrow time frame after acute myocardial infarction (AMI), spontaneous or therapeutic reperfusion can lead to myocardial salvage, preservation of left ventricular (LV) function and improved survival. However, several studies have shown that the improvement in prognosis of patients with sustained patency of the infarct-related artery (IRA) is out of proportion to the observed improvement in ventricular function. Also, patients who undergo late thrombolysis (i.e. after the traditional 4- to 6-hour time window for myocardial salvage), show improvements in LV function and prognosis. These observations suggest that other mechanisms contribute to the beneficial effects of reperfusion in addition to the salvage of ischaemic myocardium. Experimental and clinical data support the concept the late reperfusion prevents LV dilatation and improves LV function by limiting infarct expansion and ventricular remodelling. These benefits are independent of any limitation on infarct size. Ventricular remodelling is a dynamic process, starting in the acute phase with infarct expansion, and progressing to LV dilatation and hypertrophy. The remodelling process has regional and global effects on wall thickness, and on chamber size, shape and function. Possible mechanisms by which late reperfusion limits infarct expansion independently of infarct size reduction include accelerated scar formation and healing, increased stiffness of the myocardium due to a blood-filled coronary vascular bed, and preservation of a subepicardial rim of viable cells. Evidence from trials of thrombolytic therapy given both early and late after AMI indicates that patency of the IRA is a critical predictor of progressive remodelling and LV dilatation in the long term. Long-term follow-up studies also show the importance of residual stenosis or reocclusion in this context. Thus, adequacy of reperfusion of the infarct bed may be more important than timing of reperfusion in attenuating LV dilatation. Since the pathogenesis of remodelling is influenced by many factors, the optimal therapeutic approach may involve a combination of treatment modalities targeted at several of the underlying processes. In fact, a variety of interventions show great promise in their ability to influence the remodelling process. In particular, there is increasing evidence that remodelling can be prevented through the use of late reperfusion therapy and therapy aimed at maintaining IRA patency in the long term. Based on current evidence, a rational strategy for the primary prevention of ventricular remodelling should involve intervention starting very early after infarction, spanning the entire healing process and continuing well beyond. Prospective clinical trials are required to evaluate late reperfusion therapy, as well as strategies for reducing residual stenosis, preventing reocclusion, and maintaining IRA patency in the long term.