The Role of Aortic Stiffness Parameters in Evaluating Myocardial Ischemia.
Aortic stiffness
Exercise ECG
Myocardial ischemia
Journal
Cardiology research
ISSN: 1923-2829
Titre abrégé: Cardiol Res
Pays: Canada
ID NLM: 101557543
Informations de publication
Date de publication:
Oct 2020
Oct 2020
Historique:
received:
27
06
2020
accepted:
07
07
2020
entrez:
28
8
2020
pubmed:
28
8
2020
medline:
28
8
2020
Statut:
ppublish
Résumé
Arterial stiffness is a process resulting in deterioration of hemodynamic function of the aorta, a decrease in its compliance and elasticity, caused by the proportional change of components of the extracellular matrix. Although many researches have been done to determine the etiologies of myocardial ischemia in the absence of obstructive coronary artery disease, none of them has investigated the relation between the parameters of aortic stiffness and the myocardial ischemia documented by the exercise stress test. The present cross-sectional study aimed to investigate the difference of aortic stiffness parameters between the groups separated by exercise stress test result as positive and negative ischemic findings in the absence of obstructive coronary artery disease. The present study included 79 patients who were admitted to Istanbul Faculty of Medicine, Department of Cardiology with complaint of chest pain. Forty patients (21 women and 19 men) have ischemic findings on the exercise electrocardiography (ECG) test and 39 patients (20 women and 19 men) have normal exercise ECG results. The patients who have positive exercise ECG findings underwent coronary angiography and all the patients had non-obstructive coronary artery disease. Demographic features (age, sex and comorbidities) were statistically similar between the groups. Aortic stiffness measurements (pulse wave velocity, pulse pressure, aortic augmented pressure, augmentation index, systolic pressure-time index, diastolic pressure-time index and subendocardial viability ratio) were done with tonometric methods. There was no significant difference between the two groups in terms of the aortic stiffness parameters. Systolic blood pressure (P = 0.33), diastolic blood pressure (P = 0.24), pulse pressure (P = 0.60), systolic pressure-time index (P = 0.10), diastolic pressure-time index (P = 0.91), subendocardial viability ratio (P = 0.19), aortic augmented pressure (P = 0.87), augmentation index (P = 0.58) and pulse wave velocity (P = 0.56) were detected between the two groups. Biochemical parameters were found similar between the two groups. Only low-density lipoprotein levels were slightly higher in patients with negative exercise stress test result (139 vs. 123 mg/dL, P = 0.02). There is no finding supporting that the aortic stiffness identifies the patients with non-obstructive coronary artery disease but with signs of myocardial ischemia and further investigation of other causes of myocardial ischemia is required.
Sections du résumé
BACKGROUND
BACKGROUND
Arterial stiffness is a process resulting in deterioration of hemodynamic function of the aorta, a decrease in its compliance and elasticity, caused by the proportional change of components of the extracellular matrix. Although many researches have been done to determine the etiologies of myocardial ischemia in the absence of obstructive coronary artery disease, none of them has investigated the relation between the parameters of aortic stiffness and the myocardial ischemia documented by the exercise stress test. The present cross-sectional study aimed to investigate the difference of aortic stiffness parameters between the groups separated by exercise stress test result as positive and negative ischemic findings in the absence of obstructive coronary artery disease.
METHODS
METHODS
The present study included 79 patients who were admitted to Istanbul Faculty of Medicine, Department of Cardiology with complaint of chest pain. Forty patients (21 women and 19 men) have ischemic findings on the exercise electrocardiography (ECG) test and 39 patients (20 women and 19 men) have normal exercise ECG results. The patients who have positive exercise ECG findings underwent coronary angiography and all the patients had non-obstructive coronary artery disease. Demographic features (age, sex and comorbidities) were statistically similar between the groups. Aortic stiffness measurements (pulse wave velocity, pulse pressure, aortic augmented pressure, augmentation index, systolic pressure-time index, diastolic pressure-time index and subendocardial viability ratio) were done with tonometric methods.
RESULTS
RESULTS
There was no significant difference between the two groups in terms of the aortic stiffness parameters. Systolic blood pressure (P = 0.33), diastolic blood pressure (P = 0.24), pulse pressure (P = 0.60), systolic pressure-time index (P = 0.10), diastolic pressure-time index (P = 0.91), subendocardial viability ratio (P = 0.19), aortic augmented pressure (P = 0.87), augmentation index (P = 0.58) and pulse wave velocity (P = 0.56) were detected between the two groups. Biochemical parameters were found similar between the two groups. Only low-density lipoprotein levels were slightly higher in patients with negative exercise stress test result (139 vs. 123 mg/dL, P = 0.02).
CONCLUSION
CONCLUSIONS
There is no finding supporting that the aortic stiffness identifies the patients with non-obstructive coronary artery disease but with signs of myocardial ischemia and further investigation of other causes of myocardial ischemia is required.
Identifiants
pubmed: 32849968
doi: 10.14740/cr1125
pmc: PMC7430893
doi:
Types de publication
Journal Article
Langues
eng
Pagination
328-336Informations de copyright
Copyright 2020, Kumrular et al.
Déclaration de conflit d'intérêts
None to declare.
Références
Am Heart J. 1999 Sep;138(3 Pt 2):220-4
pubmed: 10467216
Circulation. 2017 Mar 14;135(11):1075-1092
pubmed: 28289007
Am J Hypertens. 2005 Feb;18(2 Pt 1):249-60
pubmed: 15752954
Int J Clin Pract. 2012 May;66(5):477-92
pubmed: 22512607
Circulation. 2015 Mar 24;131(12):1044-6
pubmed: 25712204
Eur Heart J. 2011 Feb;32(4):404-11
pubmed: 21169615
Am J Hypertens. 2007 Apr;20(4):378-84
pubmed: 17386343
J Am Coll Cardiol. 2011 Apr 5;57(14):1511-22
pubmed: 21453829
Eur Heart J. 2020 Jan 14;41(3):407-477
pubmed: 31504439
Hypertension. 2006 Mar;47(3):365-70
pubmed: 16432047
Circ Cardiovasc Imaging. 2016 Dec;9(12):
pubmed: 27956408
J Appl Physiol (1985). 2018 Dec 1;125(6):1871-1880
pubmed: 30359540
Circ Res. 2017 Sep 1;121(6):695-710
pubmed: 28860319
Glob Heart. 2012 Dec 1;7(4):315-329
pubmed: 23682350
Am J Hypertens. 2005 Jan;18(1):50-5
pubmed: 15691617
J Hypertens. 2015 Sep;33(9):1767-71
pubmed: 26244626
Am J Hypertens. 2005 Jul;18(7):930-4
pubmed: 16053989
Clin Hypertens. 2016 Jul 12;22:16
pubmed: 27413538
J Am Coll Cardiol. 1995 Apr;25(5):1000-9
pubmed: 7897108
Circulation. 2008 Mar 25;117(12):1526-36
pubmed: 18347213
JACC Cardiovasc Interv. 2014 May;7(5):453-63
pubmed: 24746648
J Cardiovasc Transl Res. 2012 Jun;5(3):243-55
pubmed: 22447229
Curr Cardiol Rev. 2010 Feb;6(1):71-81
pubmed: 21286281
Clin Exp Pharmacol Physiol. 2009 Apr;36(4):413-8
pubmed: 19018798
J Am Coll Cardiol. 2002 Aug 21;40(4):773-9
pubmed: 12204510
J Am Coll Cardiol. 2010 Mar 30;55(13):1318-27
pubmed: 20338492
J Hum Hypertens. 2012 Jan;26(1):64-70
pubmed: 21228823
J Am Heart Assoc. 2016 Mar 25;5(3):e002693
pubmed: 27016574
Cardiol Res Pract. 2011;2011:263585
pubmed: 21845218
J Cardiol. 2008 Oct;52(2):67-78
pubmed: 18922380
Curr Atheroscler Rep. 2007 Aug;9(2):139-44
pubmed: 17877923
Hypertens Res. 2004 Nov;27(11):851-7
pubmed: 15824467
Atherosclerosis. 2013 Dec;231(2):359-64
pubmed: 24267252
Rom J Intern Med. 2017 Mar 1;55(1):8-13
pubmed: 27490029
J Hypertens. 2013 Jul;31(7):1447-54; discussion 1454-5
pubmed: 23615325
J Am Coll Cardiol. 2010 Mar 9;55(10):1032-7
pubmed: 20202520
Eur Heart J. 2006 Nov;27(21):2588-605
pubmed: 17000623
Integr Blood Press Control. 2014 May 23;7:29-34
pubmed: 24910511
J Am Coll Cardiol. 2002 Oct 16;40(8):1531-40
pubmed: 12392846