Paula Vesterinen

Magnetocardiographic Assessment of Healed Myocardial Infarction

Background: We evaluated the capability of multichannel magnetocardiography (MCG) to detect healed myocardial infarction (MI).

Temporal Analysis of the Depolarization Wave of Healed Myocardial Infarction in Body Surface Potential Mapping

Background: We studied the ability of different time segments of the depolarization wave recorded with body surface potential mapping (BSPM) to detect and localize myocardial infarction (MI).

Practical implications of novel serum ELISA-assay for matrix metalloproteinase-8 in acute cardiac diagnostics

Matrix metalloproteinases (MMPs) play a major role in inflammatory processes as they degrade extracellular proteins and modify immune responses. Inflammation is the driving factor in atherogenesis and MMPs, particularly MMP-8, has been linked to atherosclerotic plaque progression. MMP-8 is shown to be strongly associated with cardiovascular diseases (CVDs) and its complications thus providing a potential marker to identify patients at risk. Previously, laborious and expensive immunofluorometric assay (IFMA) was needed to reliably detect MMP-8 levels in serum. In this study, we compared a novel in-house ELISA-assay, dentoELISA, to the standard IFMA in determination of serum MMP-8 concentrations. As a cheaper and non-laborious assay, ELISA proved to be diagnostically as sensitive and specific as the IFMA. ROC statistics showed highly similar areas under the curve for both assays (0.779 versus 0.781). Furthermore, the concentrations measured by ELISA correlated significantly with concentrations determined with IFMA (r = 0.881, P < 0.001). In our study population, MMP-8 levels were significantly higher in the acute coronary syndrome patients (n = 2071) in comparison to reference population without significant coronary artery disease (n = 653). With this background, MMP-8-ELISA could provide interesting new approaches to novel CVD diagnostics.

Serum IgG2 Concentration Is Associated with Gm-Allotypes of IgG2 But Not with the R131H Polymorphism of Human Fcγ Receptor Type IIa

Serum concentrations of immunoglobulins IgG, IgG1, and IgG2 were determined in 62 Finnish subjects who were also typed for Gm(n) allele of IgG2 and R131 and H131 alleles of the Fcγ receptor IIa. Statistically significant G2m-allotype-associated differences in serum concentrations of IgG2 were found; the mean concentration of IgG2 was high in Gm(n)-positive homozygotes (3.9 g/liter) and low in Gm(n)-negative individuals (2.6 g/liter; P = 0.0036), which is in accordance with previous reports. Contrary to an earlier report, no statistically significant R131/H131-allotype-associated differences were found in serum concentrations of IgG2, not even in the case where the IgG2 concentration was calculated relative to the IgG1 or IgG concentration (IgG2/IgG1 or IgG2/IgG). The gene frequencies of R131 and H131 alleles were 0.516 and 0.484, respectively, which did not differ significantly from those reported earlier for Finnish or other Caucasian populations.

Low MMP-8/TIMP-1 reflects left ventricle impairment in takotsubo cardiomyopathy and high TIM P-1 may help to differentiate it from acute coronary syndrome

Background Matrix metalloproteinase 8 (MMP-8) is the most potent type-I collagen protease. Such collagen mainly constitutes the transient fibrosis in takotsubo cardiomyopathy (TTC) endomyocardial biopsies. High MMP-8 and tissue-inhibitor of matrix metalloproteinase-1 (TIMP-1) levels are implicated in acute coronary syndrome (ACS). We compared MMP-8 and TIMP-1 levels in consecutive TTC and ACS patients, and their association to TTC severity. Methods and results In 45 acute serum samples of TTC, 2072 ACS and 1000 controls, TIMP-1 differed between ACS 146.7ng/mL (115.0–186.3) (median (interquartile range)), TTC 115.7 (94.3–137.7) and controls 80.9 (73.2–90.4), (p<0.0001). MMP-8 levels were similar between ACS and TTC. In receiver-operating characteristics analysis, TIMP-1 differentiated TTC from ACS with an area under the curve (AUC) of 0.679 (p<0.0001) surpassing troponin T (TnT) at 0.522 (p = 0.66). Compared to other differing factors (age, sex, smoking), TIMP-1 improved diagnostic specificity and sensitivity from AUC of 0.821 to 0.844 (p = 0.007). The MMP8/TIMP-1 molar ratio differentiated normal ejection fraction (EF) at 0.27 (0.13–0.51) from decreased EF<50% at 0.08 (0.05–0.20), (p = 0.04) in TTC, but not in ACS. Conclusions Even with other differing factors considered, TIMP-1 differentiated TTC from ACS better than TnT. In TTC, the low MMP-8/TIMP-1 molar ratio may reflect decreased proteolysis and increased transient fibrosis, perhaps in part explaining the left-ventricle impairment.

Single-Lead Electrocardiographic Variables in the Detection of Prior Myocardial Infarction with Respect to Q-Wave Status and Infarct Age

Objectives: Conventionally, the detection of prior myocardial infarction (MI) is based on QRS abnormalities, which may ignore non-Q-wave MI (NQMI). We aimed at finding automatically applicable quantitative ECG variables for diagnosing prior MI. Methods: Body surface potential mapping (BSPM) was registered and automatically analyzed in 144 patients with prior MI and in 75 healthy controls. The MI was defined according to its age as recent or old, and Q-wave status as Q-wave MI (QMI) or NQMI. Results: The QRSSTT integral, the STT integral and the T-wave apex amplitude applied in single, selected leads were found to be the optimal parameters in the detection of prior MI. The areas under the receiver-operating characteristic curves (AUC) were 89% for each, and detection was equal in old and recent MI (AUCs from 87 to 90%), and in QMI and NQMI (AUCs from 88 to 90%). Conclusions: The quantitative, automatically applicable single-lead variables comprising ventricular repolarization was effective in detecting prior MI, irrespective of the time elapsed from MI or the Q-wave status. These variables could be suitable for population studies and health screening purposes and are applicable to automatic ECG diagnostics of prior MI.

Contents Vol. 109, 2008

E. Abadie, Saint Denis C.W. Akins, Boston, Mass. J.S. Alpert, Tucson, Ariz. E.A. Amsterdam, Sacramento, Calif. J.J. Badimon, New York, N.Y. A. Battler, Petah Tikva R. Becker, Durham, N.C. G.A. Beller, Charlottesville, Va. P.C. Block, Atlanta, Ga. R.O. Bonow, Chicago, Ill. J. Camm, London B. Carabello, Houston, Tex. K. Chatterjee, San Francisco, Calif. P.F. Cohn, Stony Brook, N.Y. M.H. Crawford, San Francisco, Calif. H. Cuénoud, Worcester, Mass. J.E. Dalen, Tucson, Ariz. S. Dalla Volta, Padova P.C. Deedwania, Fresno, Calif. A.N. De Maria, San Diego, Calif. P.S. Douglas, Durham, N.C. J.A. Eleft eriades, New Haven, Conn. U. Elkayam, Los Angeles, Calif. G. Ewy, Tucson, Ariz. M. Ezekowitz, Wynnewood, Pa. R. Ferrari, Milan G. Filippatos, Athens G.I. Fishman, New York, N.Y. K. Fox, London G.S. Francis, Cleveland, Ohio V. Fuster, New York, N.Y. B.J. Gersh, Rochester, Minn. W. Gersony, New York, N.Y. J. Gold, Toledo, Ohio R. Goldberg, Worcester, Mass. S. Goldberg, Philadelphia, Pa. M. Goldman, New York, N.Y. P.J. Goldschmidt, Miami, Fla. J. Gore, Worcester, Mass. T.H. Haghfelt, Odense J.L. Halperin, New York, N.Y. C.L. Hanis, Houston, Tex. S. Haunsø, Copenhagen Z.-X. He, Beijing