In inferior myocardial infarction, neither ST elevation in lead V1 nor ST depression in lead I are reliable findings for the diagnosis of right ventricular infarction.

OBJECTIVE: In the presence of inferior myocardial infarction (MI), ST depression (STD) in lead I has been claimed to be accurate for diagnosis of right ventricular (RV) MI. We sought to evaluate this claim and also whether ST Elevation (STE) in lead V1 would be helpful, with or without STD in V2. METHODS: Retrospective study of consecutive inferior STEMI, comparing ECGs of patients with, to those without, RVMI, as determined by angiographic coronary occlusion proximal to the RV marginal branch. STE and STD were measured at the J-point, relative to the PQ junction. The primary outcomes were sensitivity/specificity of 1) STD in lead I ≥ 0.5 mm and 2) STE in lead V1 ≥ 0.5 mm, stratified by presence or absence of posterior (inferobasal) MI, as determined by ≥0.5 mm STD in lead V2, for differentiating RVMI from non-RVMI. RESULTS: Of 149 patients with inferior STEMI, 43 (29%) had RVMI and 106 (71%) did not. There was no difference in the presence or absence of at least 0.5 mm STD in Lead I between patients with (37/43, 86%) vs. without RVMI (85/106, 80%, p = 0.56). In those with, vs. without, RVMI, (15/43, 35%) had STE in V1, versus (17/106, 16%) (p = 0.015). Specificity of STE in V1 for RVMI was 84%; sensitivity was 35%. Sensitivity was higher without (69%), than with (35%), STD in V2. CONCLUSION: Among inferior STEMI, the presence of any ST depression in lead I does not help to diagnose RVMI. ST elevation ≥0.5 mm in lead V1 is specific for RVMI, and moderately sensitive only if concomitant STD ≥ 0.5 mm in V2 is not present. Although STE in V1 is quite specific, overall the diagnostic characteristics of the standard 12­lead ECG are inadequate to definitively diagnose, or exclude, RVMI, as defined angiographically.

The Pittsburgh Fistula Classification System: a standardized scheme for the description of palatal fistulas.

OBJECTIVE: Vague terminology is a problem in cleft palate research. No classification scheme for palatal fistulas has been proposed to date. Although a well-healed velum is a significant outcome of palatoplasty, it is nearly impossible to compare fistula-related palatoplasty results in the literature or in medical records without a standardized vocabulary. We endeavor to devise a palatal fistula classification system that may have clinical and research applicability. DESIGN: PubMed was searched for definitions and classifications of palatal fistula as well as incidence and recurrence rates of this outcome. Next, a 25-year retrospective review of our Cleft Center's records was performed, and fistulas were identified (n=641 charts reviewed). The fistula descriptions yielded by this chart review were evaluated in the context of anatomical descriptions in the literature, and a clinician-friendly classification scheme was designed. RESULTS: A literature review failed to reveal a standardized fistula classification system. An anatomically based numerical fistula classification system was devised: type I, bifid uvula; type II, soft palate; type III, junction of the soft and hard palate; type IV, hard palate; type V, junction of the primary and secondary palates (for Veau IV clefts); type VI, lingual alveolar; and type VII, labial alveolar. CONCLUSIONS: We propose a standardized numerical classification system for palatal fistulas. Its clinical adoption may prospectively clarify ambiguities in the literature and facilitate future cleft palate research and clinical practice.

A human glucagon-like peptide-1 receptor polymorphism results in reduced agonist responsiveness.

Glucagon-like peptide-1 (GLP-1) and its cognate receptor play an important physiological role in maintaining blood glucose homeostasis. A GLP-1 receptor (GLP-1R) polymorphism in which threonine 149 is substituted with a methionine residue has been recently identified in a patient with type 2 diabetes but was not found in non-diabetic control subjects. We have functionally assessed the recombinant GLP-1R variant after transient expression in COS-7 and HEK 293 cells. Compared to the wild type receptor, the variant GLP-1R showed (i) similar expression levels, (ii) 60-and 5-fold reduced binding affinities, respectively, for two GLP-1R full agonists, GLP-1 and exendin-4, and (iii) markedly decreased potencies of these peptides in triggering cAMP-mediated signaling (despite conserved efficacies). In contrast to full agonists, the efficacy of the primary GLP-1 metabolite/GLP-1R partial agonist, GLP-1 (9-36) amide, was essentially abolished by the T149M substitution. By hydropathy analysis, the polymorphism localizes to transmembrane domain 1, suggesting this receptor segment as a novel determinant of agonist affinity/efficacy. These findings reveal that naturally occurring sequence variability of the GLP-1R within the human population can result in substantial loss-of-function. A genetic link between the T149M variant and increased susceptibility to type 2 diabetes remains to be established.