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Heightened awareness of the characteristic patterns of ST-segment depression and T-wave inversion is paramount to quickly identifying life-threatening disorders. This paper reviews how to distinguish the various causes of these abnormalities.

The purpose of the present study was to determine the extent to which bacteria not detected by culture contribute to the microbial flora of the bowel of preterm infants with and without neonatal necrotizing enterocolitis (NEC). Fecal samples from 32 preterm infants in special care baby units including samples from 10 infants with NEC were examined by culture and PCR amplification of the 16S rRNA gene (rDNA). The 16S rDNA V3 region was amplified with eubacterial primers, and the amplification products derived from the fecal sample DNA were compared with the products from individual cultured isolates by PCR and denaturing gradient gel electrophoresis (PCR-DGGE), allowing the DNA from uncultured bacteria to be identified. For the 22 infants without NEC weekly samples were examined for a mean of 5.3 postnatal weeks. The total number of types detected by culture combined with PCR-DGGE was 10.1 per infant, of which PCR-DGGE contributed 10.4% of the types identified. Additional types detected by PCR-DGGE were found in 14 (63.6%) of the 22 infants. The majority of the sequences associated with uncultured bacteria showed >90% 16S rDNA sequence identity with sequences from culturable human enteric flora, and all were found in single infants with the exception of sequences indistinguishable by DGGE from seven infants. These sequences showed >90% sequence identity with the 16S rDNA of Streptococcus salivarius and may have been derived from upper gastrointestinal or respiratory tract flora. In the present study uncultured bacteria detected by PCR-DGGE were no more frequent in fecal samples from infants with NEC than in samples from infants without NEC, although these findings do not exclude the possibility of unrecognized bacteria associated with the mucosa of the small intestine of infants with NEC.

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The differential diagnosis of ST-segment elevation includes four major processes: ST-segment elevation myocardial infarction (STEMI); early repolarization; pericarditis; and ST elevation secondary to an abnormality of the QRS complex (left bundle branch block, left ventricular hypertrophy, or preexcitation). Other processes that may be associated with ST elevation include hyperkalemia, pulmonary embolism, and Brugada syndrome. The clinical setting and specific electrocardiographic criteria often allow identification of the cause. This article reviews ST-T and QRS configurations specific to each diagnosis.

Atrial fibrillation occurred in 16 (10%) of 167 patients with idiopathic hypertrophic subaortic stenosis. The clinical and haemodynamic findings in these 16 patients are presented. Atrial fibrillation appeared late in the course of the disease, and its occurrence did not seem to be related to the severity of left ventricular outflow obstruction or to the amount of associated mitral regurgitation. In each patient the onset of the arrhythmia was accompanied by severe clinical deterioration, which often necessitated urgent medical treatment. Digitalis was administered to all 16 patients with subsequent clinical improvement in 15. Electrical cardioversion was uniformly successful in restoring sinus rhythm, but atrial fibrillation usually recurred. In each of 8 patients catheterized during atrial fibrillation, cardiac output was strikingly low (average, 1.9 l./min./m.(2)), whereas it was normal in 10 of 13 patients studied in sinus rhythm. The duration of follow-up from the onset of atrial fibrillation has averaged 5 years, and 3 of the 16 patients have died of causes related to their heart disease. Four have suffered cerebral emboli. Only 5 patients are now in stable sinus rhythm; in general, they are less symptomatic than the patients in whom atrial fibrillation has recurred.The unusually severe clinical deterioration at the onset of atrial fibrillation and the low cardiac output measured during catheterization are thought to be related to the loss of the important contribution to ventricular filling of atrial systole in patients with poorly compliant ventricles, and to the effect of an irregular ventricular rhythm on the variable nature of the outflow obstruction.

GLANCY. Serial echocardiographic and clinical evaluation of valvular regurgitation before, during, and after treatment with fenfluramine or dexfenfluramine and mazindol or phentermine. Obes Res. 1999;7:3 13-322. Objective: The prevalence of cardiac valvular regurgitation demonstrated by echocardiography in patients who took appetite-suppressant medication for weight loss has been assessed at 5%-30%. We studied 86 patients who had echocardiograms before treatment with appetite suppressants to determine the incidence of new cases and to evaluate the clinical implication of the echocardiographic findings. Research Methods and Procedures: We studied 69 men [Meandtandard Deviation (S) age 49281 and 17 women (mean2S age 50+7) who had 233 echocardiograms before, during, and after a weight-loss program that used predominantly fenfluramine (or dexfenfluramine) with mazindol (or phentermine). Mean drug exposure was 17 months. Blinded echocardiographic readings were performed to identify and grade aortic regurgitation (AR) or mitral regurgitation (MR).Results: Seven of 86 patients (8%) had pre-existing regurgitation with five (6%) meeting our case definition. Thirteen (16.5%) of initially normal patients developed valvular regurgitation and were new cases. Of the new cases, 12 were grade IAV AR and one was both grade II/III MR and IIDV AR. All 13 patients were asymptomatic, and only two aortic insufficiency murmurs could be auscultated. There was significantly greater risk for developing valvulopathy for those who took medications longer than 6 months (p = 0.03), and no new cases were observed in patients exposed for less than 8 months. No increased risk associated with age, presence of hypertension, or exposure to fenfluraminephentermine combination was demonstrated. Although there was a higher incidence of new regurgitation in women (31% vs. 13% for men), this was not statistically significant (p = 0.093). Discussion: Some patients who had normal echocardiograms at baseline developed cardiac valvular regurgitation after exposure to fenfluramine or dexfenfluramine with mazindol or phentermine. The development of valvulopathy was significantly correlated with duration of exposure. The clinical implications of echocardiographically demonstrated regurgitation are uncertain, since there were only two audible murmurs and no other clinically relevant signs or symptoms among the patients.