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Articles by A Roth
Total Records ( 3 ) for A Roth
  P. S Wild , C. R Sinning , A Roth , S Wilde , R. B Schnabel , E Lubos , T Zeller , T Keller , K. J Lackner , M Blettner , R. S Vasan , T Munzel and S. Blankenberg

Echocardiography, the dominant imaging modality for quantification of left ventricular metrics, has undergone continuing development in the past few decades. However, given the lack of population-based data, current guidelines are still based on restricted and small data sets analyzed with methods including expert opinion. This work presents empirically derived reference values from a large-scale, epidemiologic study conducted with state-of-the-art imaging technology and methods.

Methods and Results—

The distribution of echocardiographic measurements of the left ventricle was analyzed in a population-based sample of 5000 mid-Europeans from the Gutenberg Heart Study in Germany. The randomly selected, noninstitutionalized sample provides data on apparently healthy individuals, as well as on those with prevalent disease. Standardized echocardiograms were recorded in a comprehensive data set at a single site with centralized training and certification of sonographers. Sex-specific reference limits and categories indicating the grade of deviation from the reference were calculated, and nomograms were created by quantile regression. Detailed information is given on the association between left ventricular geometry and age.


The rapidly evolving echocardiographic technology with persistent improvements in image quality and new measurement conventions require the evaluation of new reference limits for left ventricular metrics. The present investigation formulates reference limits and nomograms from state-of-the-art technology and methods based on a large population-based data set. The distribution of echocardiographic measures of left ventricular geometry presents, in part, nonlinear associations with age, which should be the subject of future investigations.

  A Halkin , D Fourey , A Roth , V Boyko and S. Behar

Background: The clinical importance of classifying myocardial infarction (MI) into non-Q-wave (NQWMI) vs. Q-wave (QWMI) subsets is controversial and might depend on the therapeutic reperfusion strategy employed. The prognostic implications of NQWMI development following primary percutaneous coronary intervention (PCI) have not been reported.

Aim: To examine the incidence, determinants and prognostic implications of NQWMI vs. QWMI development following primary PCI.

Design: The ACSIS Registry, a 2-month nationwide survey conducted biennially, prospectively collects data from all MI admissions in Israel.

Methods: Outcomes were compared among patients managed by primary PCI who subsequently developed NQWMI vs. QWMI. Independent predictors of Q-wave development and 1-year mortality were determined by multivariate stepwise logistic regression analysis and Cox proportional hazard model, respectively.

Results: Of 4537 MI patients with ST-segment elevation on admission, 1230 (27%) were treated with primary PCI. A discharge diagnosis of NQWMI was made in 259 (21.1%) patients. The baseline features and PCI strategies employed were similar among NQWMI vs. QWMI patients, though peak creatine kinase levels were higher (median 795 U/l vs. 1681 U/l, P = 0.0001) and severe left ventricular ejection fraction (LVEF) impairment (<40%) more frequent (22.6% vs. 43.9%, P < 0.0001), in the latter group. Mortality at 1-year was significantly lower in NQWMI vs. QWMI patients (3.9% vs. 10.8%, P log-rank = 0.001). By Cox proportional hazard analysis, NQWMI vs. QWMI was an independent predictor of freedom from 1-year mortality [HR = 0.34 (95% CI: 0.15–0.79), P = 0.01].

Discussion: The diagnosis of NQWMI after primary PCI is associated with an excellent prognosis independent of established prognosticators, including LVEF.

  A. P Hegle , H Nazzari , A Roth , D Angoli and E. A. Accili

All four mammalian hyperpolarization-activated cyclic nucleotide-modulated (HCN) channel isoforms have been shown to undergo N-linked glycosylation in the brain. With the mouse HCN2 isoform as a prototype, HCN channels have further been suggested to require N-glycosylation for function, a provocative finding that would make them unique in the voltage-gated potassium channel superfamily. Here, we show that both the HCN1 and HCN2 isoforms are also predominantly N-glycosylated in the embryonic heart, where they are found in significant amounts and where HCN-mediated currents are known to regulate beating frequency. Surprisingly, we find that N-glycosylation is not required for HCN2 function, although its cell surface expression is highly dependent on the presence of N-glycans. Comparatively, disruption of N-glycosylation only modestly impacts cell surface expression of HCN1 and leaves permeation and gating functions almost unchanged. This difference between HCN1 and HCN2 is consistent with evolutionary trajectories that diverged in an isoform-specific manner after gene duplication from a common HCN ancestor that lacked N-glycosylation and was able to localize efficiently to the cell surface.

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