Literature DB >> 22459303

Coronary microvascular function and cortical pain processing in patients with silent positive exercise testing and normal coronary arteries.

Antonino Di Franco1, Gaetano A Lanza, Antonio Di Monaco, Alfonso Sestito, Priscilla Lamendola, Roberto Nerla, Pierpaolo Tarzia, Daniela Virdis, Catello Vollono, Massimiliano Valeriani, Filippo Crea.   

Abstract

ST-segment depression during exercise stress testing in asymptomatic subjects showing normal coronary arteries is considered a "false-positive" result. Coronary microvascular dysfunction, however, might be a possible cause of ST-segment depression in these cases. We assessed the coronary blood flow response to adenosine and to cold pressor test in the left anterior descending artery, using transthoracic Doppler echocardiography in 14 asymptomatic subjects with exercise-induced ST-segment depression and normal coronary arteries (group 1), 14 patients with microvascular angina (group 2), and 14 healthy subjects (group 3). Flow-mediated dilation was assessed in the brachial artery. Central pain processing was assessed using cortical laser evoked potentials during chest and right hand stimulation with 3 sequences of painful stimuli. The coronary blood flow response to adenosine was 1.8 ± 0.4, 1.9 ± 0.5, and 3.1 ± 0.9 in groups 1, 2, and 3, respectively (p <0.001). The corresponding coronary blood flow responses to the cold pressor test were 1.74 ± 0.4, 1.53 ± 0.3, and 2.3 ± 0.6 (p <0.001). The flow-mediated dilation was 5.5 ± 2.3%, 4.6 ± 2.4%, and 9.8 ± 1.2% in the 3 groups, respectively (p <0.001). The laser evoked potential N2/P2 wave amplitude decreased throughout the 3 sequences of stimulation in groups 1 and 3 but not in group 2 (chest, -19 ± 22%, +11 ± 42% and -36 ± 12%, p <0.001; right hand, -22 ± 25%, +12 ± 43% and -30 ± 20%, p = 0.009; in groups 1, 2, and 3). In conclusion, exercise stress test-induced ST-segment depression in asymptomatic subjects with normal coronary arteries cannot be considered as a simple false-positive result, because it can be related to coronary microvascular dysfunction. The different symptomatic state compared to patients with microvascular angina can, at least in part, be explained by differences in cortical processing of neural pain stimuli.
Copyright © 2012 Elsevier Inc. All rights reserved.

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Year:  2012        PMID: 22459303     DOI: 10.1016/j.amjcard.2012.02.012

Source DB:  PubMed          Journal:  Am J Cardiol        ISSN: 0002-9149            Impact factor:   2.778


  5 in total

Review 1.  Diagnosis of coronary microvascular dysfunction - Present status.

Authors:  S R Mittal
Journal:  Indian Heart J       Date:  2015-11-06

Review 2.  Targeting the dominant mechanism of coronary microvascular dysfunction with intracoronary physiology tests.

Authors:  Hernán Mejía-Rentería; Nina van der Hoeven; Tim P van de Hoef; Julius Heemelaar; Nicola Ryan; Amir Lerman; Niels van Royen; Javier Escaned
Journal:  Int J Cardiovasc Imaging       Date:  2017-05-13       Impact factor: 2.357

Review 3.  Etiopathogenesis of microvascular angina: caveats in our knowledge.

Authors:  S R Mittal
Journal:  Indian Heart J       Date:  2014-11-04

4.  Pain Tolerance in Persons With Recognized and Unrecognized Myocardial Infarction: A Population-Based, Cross-Sectional Study.

Authors:  Andrea Milde Øhrn; Christopher Sivert Nielsen; Henrik Schirmer; Audun Stubhaug; Tom Wilsgaard; Haakon Lindekleiv
Journal:  J Am Heart Assoc       Date:  2016-12-21       Impact factor: 5.501

5.  Evaluation of non-invasive imaging parameters in coronary microvascular disease: a systematic review.

Authors:  F Groepenhoff; R G M Klaassen; G B Valstar; S H Bots; N C Onland-Moret; H M Den Ruijter; T Leiner; A L M Eikendal
Journal:  BMC Med Imaging       Date:  2021-01-06       Impact factor: 1.930

  5 in total

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