Value of Posterior and Right Ventricular Leads in Comparison to the Standard 12-Lead Electrocardiogram in Evaluation of ST-Segment Elevation in Suspected Acute Myocardial Infarction

In this multicenter prospective trial, we studied posterior (V₇ to V₉) and right ventricular (V₄R to V₆R) leads to assess their accuracy compared with standard 12-lead electrocardiograms (ECGs) for the diagnosis of acute myocardial infarction (AMI). Patients aged >34 years with suspected AMI received posterior and right ventricular leads immediately after the initial 12-lead ECG. ST elevation of 0.1 mV in 2 leads was blindly determined and inter-rater reliability estimated. AMI was diagnosed by World Health Organization criteria. The diagnostic value of nonstandard leads was determined when 12-lead ST elevation was absent and present and multivariate stepwise regression analysis was also performed. Of 533 study patients, 64.7% (345 of 533) had AMI and 24.8% received thrombolytic therapy. Posterior and right ventricular leads increased sensitivity for AMI by 8.4% (

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) but decreased specificity by 7.0% (

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). The likelihood ratios of a positive test for 12, 12 + posterior, and 12 + right ventricular ECGs were 6.4, 5.6, and 4.5, respectively. Increased AMI rates (positive predictive values) were found when ST elevation was present on 6 nonstandard leads (69.1%), on 12 leads only (88.4%), and on both 6 and 12 leads (96.8%; p <0.001). Treatment rates with thrombolytic therapy increased in parallel with this electrocardiographic gradient. Logistic regression analysis showed that 4 leads were independently predictive of AMI (p <0.001): leads I, II, V₃, V₅R; V₉ approached statistical significance (

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). The standard ECG is not optimal for detecting ST-segment elevation in AMI, but its accuracy is only modestly improved by the addition of posterior and right ventricular leads.In this multicenter prospective trial, 0.1 mV of ST-segment elevation in posterior (V₇ to V₉) and right ventricular (V₄R to V₆R) leads was found to increase the sensitivity of the electrocardiogram for acute myocardial infarction by 8.4% (

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), but decrease specificity by 7.0% (

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); logistic regression analysis showed that 4 leads were predictive of AMI at p <0.001: I, II, V₃, V₅; V₉ approached statistical significance (

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). The standard electrocardiogram is not optimal for detecting ST elevation in acute myocardial infarction, but its accuracy is only modestly improved by the addition of posterior and right ventricular leads.     

Diurnal variations of cardiac rhythm,arterial pressure,and urinary catecholamines in borderline and established essential hypertension

Ambulatory continuous ECG and arterial pressure (BP) were recorded simultaneously (Delmar Avionics Pressurometer II) for 24 hours in 13 age-matched normotensive subjects, 11 patients with borderline hypertension (HBP), and in 10 patients with uncomplicated established essential HBP. Urinary concentrations of epinephrine, norepinephrine, and dopamine were simultaneously collected over four successive 4-hour periods and one 8-hour period. Prevalence and total number of ventricular and supraventricular ectopic beats was low and not affected by arterial BP. Twenty-four-hour heart rate (HR) and 4-hourly excretion of epinephrine, norepinephrine, and dopamine were comparable between normotensive and HBP persons and no correlation between urinary catecholamines and arterial BP (systolic, diastolic, or mean), HR, or prevalence of ectopic beats was found in any of the three groups or in the total study population. We conclude that HBP patients without ECG evidence of left ventricular hypertrophy do not have a higher prevalence of supraventricular or ventricular ectopic beats. Urinary catecholamines are not related to circadian fluctuations or variability in arterial BP, HR, or prevalence of ectopic beats.     

Interferon Messenger RNA: Translation in Heterologous Cells

A viral inhibitor with the characteristics of mouse interferon is produced by avian and simian cells preincubated with RNA extracted from interferon-producing mouse cells. Similarly, RNA extracted from interferon-producing monkey cells induces a monkey interferon-like substance in avian cells and also in a line of simian cells, VERO, which normally lacks the capacity to produce its own interferon. In both cases, the RNA effect is inhibited by treatment of the receptor cells by cycloheximide, but not by actinomycin D. We conclude that interferon messenger RNA has been translated in the receptor cells. Thus, the production of interferon in heterologous cells can be used as a sensitive assay of interferon messenger RNA.     

Structural and Functional Analysis of the Pig-a Protein That is Mutated in Paroxysmal Nocturnal Hemoglobinuria

ABSTRACT: There is now convincing evidence that thePig-agene is mutated in patients with paroxysmal nocturnal hemoglobinuria (PNH), a disease in which one or more clones of hematopoietic cells have incomplete assembly of glycosylphosphatidylinositol (GPI) anchors and absence of GPI-linked protein expression on the cell surface. Little is known, however, about the Pig-a protein product that is necessary for GPI anchor bioassembly. Relatively few substitution (missense)Pig-agene mutations have been identified, but we noted two apparent clusters at codons 128-129 and 151-156 and hypothesized that these might represent critical regions of the Pig-a protein. We therefore used site-directed mutagenesis to create conservative mutations in the Pig-a protein, then performed structural and functional analysis. EachPig-amutation generated a Pig-a protein of normal size and stability, but certain mutations had substantial deleterious effects on protein function. Conservative mutation of codons histidine 128 (H128), serine 129 (S129), and serine 155 (S155) had greatly diminished function, while mutations of flanking residues had no effect on function. Our results represent the first structure/function analysis of the Pig-a protein, and suggest that codons H128, S129, and S155 represent critical regions of the Pig-a protein. Our results also suggest a means by which transgenic mice with a “partial knock-out” of Pig-a function could be generated, which would allow investigation of PNH in an animal model.     

Prostaglandin prevents alterations in DNA,RNA, and protein in damaged gastric mucosa

Fasted rats were given either 16,16-dimethyl-PGE2 (dmPGE2) (1 microgram/kg) or normal saline subcutaneously followed by the oral administration of 1 ml of 100% ethanol or saline 30 min later. At 1, 3, 6, and 24 hr later, animals were sacrificed, their stomachs examined for necrotic ulcerations, and the incorporation of [3H]thymidine into DNA as well as tissue levels of DNA, RNA, and protein content of glandular mucosa determined. Compared with control animals, severe ulcerations of 70-80% of the glandular mucosa were observed in rats given 100% ethanol at all time periods. Accompanying these ulcerations were marked depressions in tissue levels of DNA and RNA at 1, 3, 6, and 24 hr after exposure to ethanol, and protein at 1, 3, and 6 hr following ethanol. In rats pretreated with dmPGE2 before ethanol administration, these alterations in tissue levels of DNA, RNA, and protein were prevented as were ulcerations of the glandular stomach at each time period. Synthesis of mucosal DNA was not significantly different from control rats in any of the groups studied. It is concluded that (1) gastric mucosal damage by alcohol is associated with a decrease in tissue levels of DNA, RNA, and protein; (2) dmPGE2 maintains normal tissue levels of DNA, RNA, and protein by preventing the shedding of mucosal cells by alcohol; and (3) the ability of dmPGE2 to prevent gastric damage by alcohol is not mediated through stimulation of DNA synthesis.