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Reassessing Cardiovascular Risk in Patients With Peripheral Artery Disease Undergoing Myocardial Perfusion Imaging
Canadian Journal of Cardiology, Volume: 41, Issue: 10, Pages: 1936 - 1945
Swansea University Authors:
Julian Halcox , Monica Casanova da Silva Martins
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© 2025 The Authors. Published by Elsevier Inc. on behalf of the Canadian Cardiovascular Society. This is an open access article under the CC BY-NC-ND license.
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DOI (Published version): 10.1016/j.cjca.2025.05.002
Abstract
Background: Coronary artery disease (CAD) and peripheral artery disease (PAD) are often regarded as analogous risk factors for major adverse cardiovascular events (MACE), given their shared pathophysiology. We aimed to investigate whether the elevated MACE risk in PAD is driven by myocardial perfusi...
| Published in: | Canadian Journal of Cardiology |
|---|---|
| ISSN: | 0828-282X 1916-7075 |
| Published: |
Elsevier BV
2025
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| URI: | https://cronfa.swan.ac.uk/Record/cronfa70098 |
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2025-08-04T16:01:54Z |
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2025-10-24T07:52:44Z |
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<?xml version="1.0"?><rfc1807><datestamp>2025-10-22T12:19:06.3249522</datestamp><bib-version>v2</bib-version><id>70098</id><entry>2025-08-04</entry><title>Reassessing Cardiovascular Risk in Patients With Peripheral Artery Disease Undergoing Myocardial Perfusion Imaging</title><swanseaauthors><author><sid>3676f695eeda169d0f8c618adf27c04b</sid><ORCID>0000-0001-6926-2947</ORCID><firstname>Julian</firstname><surname>Halcox</surname><name>Julian Halcox</name><active>true</active><ethesisStudent>false</ethesisStudent></author><author><sid>53b42665a15b52c5b961969b11f522c0</sid><firstname>Monica</firstname><surname>Casanova da Silva Martins</surname><name>Monica Casanova da Silva Martins</name><active>true</active><ethesisStudent>false</ethesisStudent></author></swanseaauthors><date>2025-08-04</date><deptcode>MEDS</deptcode><abstract>Background: Coronary artery disease (CAD) and peripheral artery disease (PAD) are often regarded as analogous risk factors for major adverse cardiovascular events (MACE), given their shared pathophysiology. We aimed to investigate whether the elevated MACE risk in PAD is driven by myocardial perfusion abnormalities or through other PAD-specific mediators. Methods: We analyzed 45,252 patients from an international, multicentre registry who underwent SPECT myocardial perfusion imaging, excluding those with early coronary revascularization (< 90 days). Myocardial perfusion abnormalities were quantified using total perfusion deficit (TPD). MACE was defined as all-cause mortality, unstable angina admission, myocardial infarction, or late coronary revascularization. PAD was defined using questionnaires or review of electronic medical records. Propensity-score matching was used to select balanced groups of patients with and without PAD. Results: During a median follow-up of 3.6 years (interquartile range [IQR]: 2.6-4.8 years), 5932 patients (13.7%) experienced at least 1 MACE. Compared with patients with neither disease, isolated history of CAD (adjusted hazard ratio [aHR], 1.92; 95% confidence interval [CI], 1.80-2.05) conferred a similar MACE risk as concomitant history of CAD and PAD (aHR, 1.57; 95% CI, 1.44-1.71) and greater risk than isolated history of PAD (aHR, 1.20; 95% CI, 1.09-1.32; P < 0.001). After propensity-score matching, history of PAD alone was not independently associated with increased MACE risk (P = 0.064). Conclusions: Although patients with PAD often have concomitant CAD and greater myocardial perfusion abnormalities, PAD itself was not linked to higher risk of MACE after adjusting for these factors. These findings highlight the importance of assessing myocardial ischemic burden in PAD for risk stratification and prompt initiation of disease-modifying therapies.</abstract><type>Journal Article</type><journal>Canadian Journal of Cardiology</journal><volume>41</volume><journalNumber>10</journalNumber><paginationStart>1936</paginationStart><paginationEnd>1945</paginationEnd><publisher>Elsevier BV</publisher><placeOfPublication/><isbnPrint/><isbnElectronic/><issnPrint>0828-282X</issnPrint><issnElectronic>1916-7075</issnElectronic><keywords/><publishedDay>12</publishedDay><publishedMonth>5</publishedMonth><publishedYear>2025</publishedYear><publishedDate>2025-05-12</publishedDate><doi>10.1016/j.cjca.2025.05.002</doi><url/><notes/><college>COLLEGE NANME</college><department>Medical School</department><CollegeCode>COLLEGE CODE</CollegeCode><DepartmentCode>MEDS</DepartmentCode><institution>Swansea University</institution><apcterm>Another institution paid the OA fee</apcterm><funders>This research was supported in part by grants R01HL089765 and R35HL161195 from the National Heart, Lung, and Blood Institute at the National Institutes of Health (PI: Dr Slomka).</funders><projectreference/><lastEdited>2025-10-22T12:19:06.3249522</lastEdited><Created>2025-08-04T09:32:42.5563580</Created><path><level id="1">Faculty of Medicine, Health and Life Sciences</level><level id="2">Swansea University Medical School - Health Data Science</level></path><authors><author><firstname>Kaiming</firstname><surname>Wang</surname><order>1</order></author><author><firstname>Tali</firstname><surname>Sharir</surname><order>2</order></author><author><firstname>M. Timothy</firstname><surname>Hauser</surname><order>3</order></author><author><firstname>Sharmila</firstname><surname>Dorbala</surname><order>4</order></author><author><firstname>Marcelo Di</firstname><surname>Carli</surname><order>5</order></author><author><firstname>Mathews B.</firstname><surname>Fish</surname><order>6</order></author><author><firstname>Terrence D.</firstname><surname>Ruddy</surname><order>7</order></author><author><firstname>Timothy</firstname><surname>Bateman</surname><order>8</order></author><author><firstname>Andrew J.</firstname><surname>Einstein</surname><order>9</order></author><author><firstname>Philipp A.</firstname><surname>Kaufmann</surname><order>10</order></author><author><firstname>Edward J.</firstname><surname>Miller</surname><order>11</order></author><author><firstname>Albert J.</firstname><surname>Sinusas</surname><order>12</order></author><author><firstname>Wanda</firstname><surname>Acampa</surname><order>13</order></author><author><firstname>Julian</firstname><surname>Halcox</surname><orcid>0000-0001-6926-2947</orcid><order>14</order></author><author><firstname>Monica</firstname><surname>Casanova da Silva Martins</surname><order>15</order></author><author><firstname>Joanna X.</firstname><surname>Liang</surname><order>16</order></author><author><firstname>Valerie</firstname><surname>Builoff</surname><order>17</order></author><author><firstname>Damini</firstname><surname>Dey</surname><order>18</order></author><author><firstname>Daniel S.</firstname><surname>Berman</surname><order>19</order></author><author><firstname>Robert J.H.</firstname><surname>Miller</surname><order>20</order></author><author><firstname>Piotr J.</firstname><surname>Slomka</surname><order>21</order></author></authors><documents><document><filename>70098__35438__7847572824754e24819dfd3952d6786b.pdf</filename><originalFilename>70098.VOR.pdf</originalFilename><uploaded>2025-10-22T11:40:24.5382807</uploaded><type>Output</type><contentLength>2145925</contentLength><contentType>application/pdf</contentType><version>Version of Record</version><cronfaStatus>true</cronfaStatus><documentNotes>© 2025 The Authors. 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| spelling |
2025-10-22T12:19:06.3249522 v2 70098 2025-08-04 Reassessing Cardiovascular Risk in Patients With Peripheral Artery Disease Undergoing Myocardial Perfusion Imaging 3676f695eeda169d0f8c618adf27c04b 0000-0001-6926-2947 Julian Halcox Julian Halcox true false 53b42665a15b52c5b961969b11f522c0 Monica Casanova da Silva Martins Monica Casanova da Silva Martins true false 2025-08-04 MEDS Background: Coronary artery disease (CAD) and peripheral artery disease (PAD) are often regarded as analogous risk factors for major adverse cardiovascular events (MACE), given their shared pathophysiology. We aimed to investigate whether the elevated MACE risk in PAD is driven by myocardial perfusion abnormalities or through other PAD-specific mediators. Methods: We analyzed 45,252 patients from an international, multicentre registry who underwent SPECT myocardial perfusion imaging, excluding those with early coronary revascularization (< 90 days). Myocardial perfusion abnormalities were quantified using total perfusion deficit (TPD). MACE was defined as all-cause mortality, unstable angina admission, myocardial infarction, or late coronary revascularization. PAD was defined using questionnaires or review of electronic medical records. Propensity-score matching was used to select balanced groups of patients with and without PAD. Results: During a median follow-up of 3.6 years (interquartile range [IQR]: 2.6-4.8 years), 5932 patients (13.7%) experienced at least 1 MACE. Compared with patients with neither disease, isolated history of CAD (adjusted hazard ratio [aHR], 1.92; 95% confidence interval [CI], 1.80-2.05) conferred a similar MACE risk as concomitant history of CAD and PAD (aHR, 1.57; 95% CI, 1.44-1.71) and greater risk than isolated history of PAD (aHR, 1.20; 95% CI, 1.09-1.32; P < 0.001). After propensity-score matching, history of PAD alone was not independently associated with increased MACE risk (P = 0.064). Conclusions: Although patients with PAD often have concomitant CAD and greater myocardial perfusion abnormalities, PAD itself was not linked to higher risk of MACE after adjusting for these factors. These findings highlight the importance of assessing myocardial ischemic burden in PAD for risk stratification and prompt initiation of disease-modifying therapies. Journal Article Canadian Journal of Cardiology 41 10 1936 1945 Elsevier BV 0828-282X 1916-7075 12 5 2025 2025-05-12 10.1016/j.cjca.2025.05.002 COLLEGE NANME Medical School COLLEGE CODE MEDS Swansea University Another institution paid the OA fee This research was supported in part by grants R01HL089765 and R35HL161195 from the National Heart, Lung, and Blood Institute at the National Institutes of Health (PI: Dr Slomka). 2025-10-22T12:19:06.3249522 2025-08-04T09:32:42.5563580 Faculty of Medicine, Health and Life Sciences Swansea University Medical School - Health Data Science Kaiming Wang 1 Tali Sharir 2 M. Timothy Hauser 3 Sharmila Dorbala 4 Marcelo Di Carli 5 Mathews B. Fish 6 Terrence D. Ruddy 7 Timothy Bateman 8 Andrew J. Einstein 9 Philipp A. Kaufmann 10 Edward J. Miller 11 Albert J. Sinusas 12 Wanda Acampa 13 Julian Halcox 0000-0001-6926-2947 14 Monica Casanova da Silva Martins 15 Joanna X. Liang 16 Valerie Builoff 17 Damini Dey 18 Daniel S. Berman 19 Robert J.H. Miller 20 Piotr J. Slomka 21 70098__35438__7847572824754e24819dfd3952d6786b.pdf 70098.VOR.pdf 2025-10-22T11:40:24.5382807 Output 2145925 application/pdf Version of Record true © 2025 The Authors. Published by Elsevier Inc. on behalf of the Canadian Cardiovascular Society. This is an open access article under the CC BY-NC-ND license. true eng http://creativecommons.org/licenses/by-nc-nd/4.0/ |
| title |
Reassessing Cardiovascular Risk in Patients With Peripheral Artery Disease Undergoing Myocardial Perfusion Imaging |
| spellingShingle |
Reassessing Cardiovascular Risk in Patients With Peripheral Artery Disease Undergoing Myocardial Perfusion Imaging Julian Halcox Monica Casanova da Silva Martins |
| title_short |
Reassessing Cardiovascular Risk in Patients With Peripheral Artery Disease Undergoing Myocardial Perfusion Imaging |
| title_full |
Reassessing Cardiovascular Risk in Patients With Peripheral Artery Disease Undergoing Myocardial Perfusion Imaging |
| title_fullStr |
Reassessing Cardiovascular Risk in Patients With Peripheral Artery Disease Undergoing Myocardial Perfusion Imaging |
| title_full_unstemmed |
Reassessing Cardiovascular Risk in Patients With Peripheral Artery Disease Undergoing Myocardial Perfusion Imaging |
| title_sort |
Reassessing Cardiovascular Risk in Patients With Peripheral Artery Disease Undergoing Myocardial Perfusion Imaging |
| author_id_str_mv |
3676f695eeda169d0f8c618adf27c04b 53b42665a15b52c5b961969b11f522c0 |
| author_id_fullname_str_mv |
3676f695eeda169d0f8c618adf27c04b_***_Julian Halcox 53b42665a15b52c5b961969b11f522c0_***_Monica Casanova da Silva Martins |
| author |
Julian Halcox Monica Casanova da Silva Martins |
| author2 |
Kaiming Wang Tali Sharir M. Timothy Hauser Sharmila Dorbala Marcelo Di Carli Mathews B. Fish Terrence D. Ruddy Timothy Bateman Andrew J. Einstein Philipp A. Kaufmann Edward J. Miller Albert J. Sinusas Wanda Acampa Julian Halcox Monica Casanova da Silva Martins Joanna X. Liang Valerie Builoff Damini Dey Daniel S. Berman Robert J.H. Miller Piotr J. Slomka |
| format |
Journal article |
| container_title |
Canadian Journal of Cardiology |
| container_volume |
41 |
| container_issue |
10 |
| container_start_page |
1936 |
| publishDate |
2025 |
| institution |
Swansea University |
| issn |
0828-282X 1916-7075 |
| doi_str_mv |
10.1016/j.cjca.2025.05.002 |
| publisher |
Elsevier BV |
| college_str |
Faculty of Medicine, Health and Life Sciences |
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|
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facultyofmedicinehealthandlifesciences |
| hierarchy_top_title |
Faculty of Medicine, Health and Life Sciences |
| hierarchy_parent_id |
facultyofmedicinehealthandlifesciences |
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Faculty of Medicine, Health and Life Sciences |
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Swansea University Medical School - Health Data Science{{{_:::_}}}Faculty of Medicine, Health and Life Sciences{{{_:::_}}}Swansea University Medical School - Health Data Science |
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| description |
Background: Coronary artery disease (CAD) and peripheral artery disease (PAD) are often regarded as analogous risk factors for major adverse cardiovascular events (MACE), given their shared pathophysiology. We aimed to investigate whether the elevated MACE risk in PAD is driven by myocardial perfusion abnormalities or through other PAD-specific mediators. Methods: We analyzed 45,252 patients from an international, multicentre registry who underwent SPECT myocardial perfusion imaging, excluding those with early coronary revascularization (< 90 days). Myocardial perfusion abnormalities were quantified using total perfusion deficit (TPD). MACE was defined as all-cause mortality, unstable angina admission, myocardial infarction, or late coronary revascularization. PAD was defined using questionnaires or review of electronic medical records. Propensity-score matching was used to select balanced groups of patients with and without PAD. Results: During a median follow-up of 3.6 years (interquartile range [IQR]: 2.6-4.8 years), 5932 patients (13.7%) experienced at least 1 MACE. Compared with patients with neither disease, isolated history of CAD (adjusted hazard ratio [aHR], 1.92; 95% confidence interval [CI], 1.80-2.05) conferred a similar MACE risk as concomitant history of CAD and PAD (aHR, 1.57; 95% CI, 1.44-1.71) and greater risk than isolated history of PAD (aHR, 1.20; 95% CI, 1.09-1.32; P < 0.001). After propensity-score matching, history of PAD alone was not independently associated with increased MACE risk (P = 0.064). Conclusions: Although patients with PAD often have concomitant CAD and greater myocardial perfusion abnormalities, PAD itself was not linked to higher risk of MACE after adjusting for these factors. These findings highlight the importance of assessing myocardial ischemic burden in PAD for risk stratification and prompt initiation of disease-modifying therapies. |
| published_date |
2025-05-12T05:28:45Z |
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1851369692354052096 |
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11.089572 |

