Background

Polycystic ovary syndrome (PCOS) is the most prevalent heterogeneous syndrome that potentially has an impact on multiple aspects of a woman’s overall health, particularly during her reproductive years [1,2]. Women with PCOS are identified by chronic anovulation, which occurs along with excess androgen, hyperinsulinemia, insulin resistance (IR), and changes in gonadotropin secretion [3,4]. In addition to the heightened risk of reproductive abnormalities associated with PCOS, most women with this condition also experience metabolic dysfunction [5] and an increased risk of developing cardiovascular risk factors, including marked IR [6], type 2 diabetes mellitus [7], coronary artery disease (CAD) [8], atherogenic dyslipidemia [9], cerebrovascular morbidity [10]. There is a significant positive correlation between peripheral insulin levels and ovarian androgens [11]. In simpler terms, PCOS has been identified as a type of metabolic syndrome [12], and as a result, researchers are now focusing more on understanding the metabolic mechanisms that contribute to the condition’s clinical symptoms [13,14]. Echocardiography, including both conventional and tissue Doppler techniques, is frequently used to evaluate left ventricular (LV) systolic and diastolic function. Studies have demonstrated that diastolic dysfunction, which can be identified through echocardiography, can serve as an early predictor of CAD [15]. Subclinical LV diastolic dysfunction is a prevalent problem in the community [16]. It is considered an important predictor of heart disease [17], and associated with long-term mortality [18]. The latest guidelines on heart failure emphasize the importance of identifying asymptomatic LV dysfunction and its primary risk factors as early as possible [19]. The echocardiographic assessment of PCOS has yielded conflicting results. While some studies have observed notable alterations indicative of diastolic dysfunction in individuals with PCOS, other studies have found no significant differences when compared to control groups.

Objectives

The primary objective of this systematic review and meta-analysis was to compare echocardiographic measures of LV systolic and diastolic function between women with PCOS and healthy women serving as a control group. The aim was to determine whether there is evidence of impaired LV function in women with PCOS, independent of other known cardiovascular risk factors.

Material and methods

This systematic review and meta-analysis adheres to the PRISMA guidelines and includes the PRISMA checklist (Document S1, Supplemental digital content 1, https://links.lww.com/CAEN/A46) in the supporting information. The research protocol was registered with the International Prospective Register of Systematic Reviews (PROSPERO) and assigned the identifier CRD42022340972.

Eligibility criteria

To be considered for inclusion, published studies had to meet the following criteria: (1) report original data using a cross-sectional, cohort, or case-control study design, (2) identify PCOS cases using any of the diagnostic criteria for PCOS, including the Rotterdam, National Institutes of Health (NIH), and Androgen Excess PCOS (AEPCOS) criteria, (3) report at least one echocardiographic parameter measuring LV systolic and/or diastolic function, (4) present data as means and standard deviations, (5) include appropriately matched control participants and evaluate the relevant parameters in both the PCOS cases and controls, (6) include women of reproductive age with or without PCOS, and (7) exclude individuals with known cardiovascular disease, thyroid disease, neoplasms, pregnancy or lactation, smoking, chronic alcohol consumption, diabetes mellitus, hypertension, and renal impairment.

The meta-analysis had the following general exclusion criteria: (1) studies reported as abstracts, case reports, case series, reviews, editorials, or practice guidelines, (2) studies that included women in menopausal or postmenopausal stages, both with and without PCOS, (3) studies that evaluated left heart function using any other cardiac imaging technique other than echocardiography.

Information sources

A thorough search was conducted in the PubMed, Scopus, Web of Science, and Cochrane databases to locate relevant studies published until August 2022. Additionally, a manual search of the reference lists of the identified articles was carried out.

Search strategy

The search strategy of Scopus was conducted as follows: ((ALL (‘echocardiograph*’ OR ‘tissue doppler imaging’ OR ‘tissue doppler echocardiograph*’ OR ‘tde’ OR ‘tdi’)) OR(TITLE-ABS-KEY ((‘left ventric*’ OR ‘left cardiac*’ OR ‘left heart*’ OR atri* OR myocardi* OR diastol* OR systol*) PRE/ 1 (diastol* OR systol* OR dysfunction OR function OR remodeling OR hypertroph* OR active* OR volume OR mass* OR dimension* OR diameter OR thickness OR index* OR ‘ejection time’ OR ‘ejection fraction’))) OR (ALL (‘lvef’ OR ‘lved’ OR ‘lvdd’ OR ‘lvsd’ OR ‘lvedd’ OR ‘lvesd’ OR ‘lvd’ OR ‘lavi’ OR ‘e/em ratio’ OR ‘e/a ratio’ OR ‘lvmi’ OR ‘lvm’))) AND (TITLE-ABS-KEY (‘polycystic ovar* syndrome’ OR ‘polycystic ovar* disease’ OR ‘stein leventhal syndrome’ OR ‘pcos’ OR ‘sclerocystic ovar*’)).

The search strategy employed for PubMed, Web of Science, and the Cochrane Library was similar to that used for Scopus (refer to S1 Table, Supplemental digital content 2, https://links.lww.com/CAEN/A47). Furthermore, two researchers independently reviewed the reference lists of systematic reviews and selected studies to ensure that all pertinent articles were included in the analysis.

Study selection

Six reviewers independently assessed each title and abstract, and if the articles fulfilled the inclusion criteria, the full text was reviewed. Three reviewers evaluated the full texts of the selected articles to verify their eligibility for inclusion. Any discrepancies were resolved through discussion with a fourth reviewer. The study selection process was summarized using the PRISMA flow diagram.

Data extraction

Three reviewers extracted data, which was collected using Microsoft Excel spreadsheets. The following data were collected: study characteristics (study design, year of publication, and first author), type of PCOS diagnostic criteria, number of individuals in each study population (PCOS cases and matched controls), baseline characteristics (age, BMI, impaired glucose tests, and androgen profile). If the laboratory units of parameters differed, online laboratory unit converters were used to standardize the units for analysis. Echocardiographic parameters were extracted and divided into two groups based on conventional echocardiographic and tissue Doppler echocardiographic values. A fourth investigator independently reviewed the data to ensure accuracy.

Outcome definition

The objective of this meta-analysis was to determine the difference in the mean change in echocardiographic parameters between the PCOS cases and control group. The echocardiographic parameters that were included are as follows:

Conventional echocardiography LVM and LVMI

The measurement of LV mass (LVM) typically involves calculating the difference between the volume of the epicardium and the volume of the LV chamber, which is then multiplied by an estimate of myocardial density [20]. LV mass index (LVMI) is the short term for the LV mass indexed to body surface area [21]. Both LVM and LVMI are considered independent indicators of LV hypertrophy and are recognized as risk factors for predicting cardiac morbidity and mortality [22,23].

Interventricular septal thickness and posterior wall thickness

Interventricular septal thickness (IVST) at end-diastole and posterior end-diastolic wall thickness (PWT) are both used to identify LV hypertrophy, with a normal range of 6–11 mm for each parameter [24,25]. These measurements are typically obtained as the distance between the endocardial and epicardial surfaces during the end-diastolic phase [26].

Left ventricular ejection fraction

LV ejection fraction (LVEF) is a fundamental measure of LV function during the systolic phase. It represents the proportion of the chamber volume that is expelled during systole relative to the volume of blood in the ventricle at the end of diastole [27].

Isovolumic relaxation time and isovolumic contraction time

The isovolumic relaxation time (IVRT) is the duration between the closure of the aortic valve and the subsequent opening of the mitral valve [28]. The isovolumic contraction time (IVCT) is defined as the time interval between the closure of the mitral valve and the opening of the aortic valve [29].

Peak E and A wave, and E/A ratio

The E wave represents the maximum velocity of blood flow resulting from LV relaxation during early diastole, while the A wave represents the peak velocity of flow in late diastole due to atrial contraction. The E/A ratio is a meaningful marker of LV function [30].

Deceleration time

Deceleration time (DT) refers to the duration between the onset of the peak E-wave and its projected baseline. The DT reflects the time required for the pressure difference between the left atrium and the left ventricle to be equalized [31].

Left ventricular end-diastolic diameter and left ventricular end-systolic diameter

LV end-diastolic diameter (LVEDD) represents the end-diastolic dimension of the left ventricle, while LV end-systolic diameter (LVESD) indicates the end-systolic dimension of the left ventricle. For women, the cutoff values for LVEDD and LVESD are 52.5 mm and 46.5 mm, respectively [32].

Left atrial diameter

Left atrial diameter (LAD) is independently associated with all-cause mortality in both men and women, as well as with ischemic stroke in women. A normal LAD is less than 3.9 cm in women [33].

Tissue Doppler echocardiography Mitral annular peak diastolic velocities

Early diastolic mitral annular velocity (E’) is an echocardiographic measure that reflects myocardial relaxation in the long-axis direction. It can be measured at either the interventricular-septal annulus (septal E’), lateral annulus (lateral E’), or as the mean value of both (septal-lateral E’) [34].

Mitral annular peak systolic velocities

The mitral annular peak systolic velocity (S’) is an echocardiographic measure that reflects longitudinal LV systolic function. It can be measured at either the interventricular-septal annulus (septal S’), lateral annulus (lateral S’), or as the mean value of both (septal-lateral S’) [35].

Quality assessment

Before being included in the review, eligible studies were subject to quality appraisal by three independent reviewers using appraisal instruments from the Joanna Briggs Institute (JBI) for cross-sectional and case-control studies, as well as other comparative studies (S2 Document, Supplemental digital content 3, https://links.lww.com/CAEN/A48).

Synthesis methods

For data analysis, the RevMan software (version 5.3) was used with the random effects model. When data were reported as median and interquartile range, they were converted to mean and SD using the Hozo formula [36] so that they could be included in the meta-analysis. Mean differences were pooled for the data, with 95% confidence intervals (CIs) also calculated. The level of statistical heterogeneity for each pooled estimate was calculated using Cochran’s chi-squared test and presented with the I2 statistic. I2 values of 25%, 50%, and 75% were considered to represent low, moderate, and high levels of heterogeneity, respectively. To assess the possibility of small study effects, comparison-adjusted funnel plots were visually examined for each outcome. Funnel plots were created for all comparisons of the differences in echocardiographic changes between PCOS cases and controls. Additionally, Begg’s test was performed using Comprehensive Meta-analysis (version 3) software to further evaluate the presence of small-study effects. To conduct subgroup analysis, the data were re-analyzed based on study designs, which included cross-sectional and case-control methodologies. The results of the subgroup analysis were documented in separate tables and included in the supporting information section for reference. To conduct sensitivity analysis, a second analysis was performed excluding cases with obesity, and the results were labeled with a ‘2’ next to each outcome name (e.g. LVMI-2). The main results were labeled with a ‘1’ (e.g. LVMI-1). This approach allowed for the assessment of the impact of obesity on the overall findings and helped determine the robustness of the results.

Main results Study selection

The flowchart of the study is presented in Fig. 1, which indicates that our search strategy identified a total of 1160 studies. After deleting duplicate records, 964 studies underwent title review. Out of these, 126 studies met the requirements for abstract review. Following the abstract review, 40 studies were selected for full-text evaluation. Eventually, 30 studies were deemed eligible for inclusion in this systematic review and meta-analysis, while 10 studies did not meet the criteria for inclusion. The specific reasons for their exclusion are provided in Table S2, Supplemental digital content 4, https://links.lww.com/CAEN/A49. Due to an unclear definition of the PCOS population in a study conducted by Prelevic et al. [37](1995), it was deemed inappropriate to completely exclude it. Consequently, we have chosen to include it for thorough methodological appraisal.

Fig. 1:

The PRISMA flow diagram illustrates the process employed for identifying relevant studies.

Study characteristics

Table 1 displays the characteristics of the 29 studies included in the analysis. The search yielded 29 studies, of which 17 had a cross-sectional study design, 11 had a case-control design, and 1 had a cohort study design. Most of the studies used the Rotterdam criteria for the diagnosis of PCOS, while some employed the NIH or AEPCOS diagnostic criteria. One study diagnosed PCOS based on all three diagnostic criteria, including hyperandrogenism, polycystic ovarian morphology, and oligo-anovulation (classic phenotype). The majority of the studies included PCOS cases who were over 18 years old, while 3 studies focused on adolescent cases (Zachurzok-Buczynska et al. [38], Çetin et al. [39], Patel et al. [40]). Six studies included obese PCOS cases with a BMI above 30 (De Jong et al [41], Patel et al. [40], Tasolar et al. [42], Rees et al. [43], Zehir et al. [44] and Zimmermann et al. [45]). One study (Yildirim et al. [46]) divided PCOS cases into four groups based on four PCOS phenotypes. To ensure consistency with the other included studies, we separated this study into four distinct studies, each with a common healthy control group. Another study (Tasolar et al. [42]) evaluated lean and obese PCOS cases, which we also divided into two separate groups marked as Tasolar et al. [1] for obese PCOS and Tasolar et al. [2] for lean cases. All studies reported at least one conventional echocardiographic value, while only 13 studies used TDI in combination with conventional echocardiography. Among these 13 studies, three (De Jong et al [41], Gazi et al [47] and Tasolar et al [42]) excluded TDI analysis, and one (De Jong et al [41]) did not specify which side of the mitral annulus was used for TDI assessment. Two studies (Gazi et al [47] and Tasolar et al [42]) reported their TDI parameters as the average of the lateral mitral, septal, and anterior mitral annuli. The main findings of each study, along with the echocardiographic results, are presented in Table 2.

Table 1 - Study characteristics First author and year of publication Study design Country No. PCOS No. Controls Age (mean ± SD) BMI (mean ± SD) PCOS diagnosis criteria Conventional echocardiography TDIEchocardiography Baseline characteristics Major findings Zachurzok-Buczynska et al [38] Cross-sectional Poland 34 17 P = 16 ± 1.3
C = 16.2 ± 1.3 P = 24.6 ± 2.3
C = 23.4 ± 2.3 AEPCOS LVEDD, LVESD, LVEF, E wave, A wave, E/A, IVRT, IVST, PWT, LVM, LVMI _ Age, BMI, Testosterone, Androstenedione, DHEAS, FAI, HOMA-IR 1) Increased LVEDD, LVESD in PCOS cases, 2) significant correlations between BMI z-score and LVM, LVEDD, LVESD, and IVST. Çetin et al [39] Cross-sectional Turkey 30 30 P = 15.98 ± 0.27
C = 15.46 ± 0.24 P = 22.07 ± 0.09
C = 20.46 ± 0.61 Rotterdam LVEDD, LVESD, E wave, A wave, E/A, IVRT, IVCT, DT, PWT, IVST Lateral E’, Lateral A’, Lateral S, Lateral E/E’ Age, BMI, Testosterone, Androstenedione, DHEAS, HOMA-IR Presence of diastolic dysfunction in PCOS. Patel et al [40] Case-control USA 36 17 P = 14.81 ± 1.56
C = 13.94 ± 1.75 P = 35.60 ± 3.66
C = 32.16 ± 2.57 NIH LVMI _ Age, BMI, Testosterone, FAI, FBS, F-insulin 1) No significant echocardiographic changes between two groups of PCOS and controls 2) increased carotidintima–media thickness, higher carotid artery beta stiffness index and lower carotid artery compliance. De Jong et al [41] Cross-sectional Australia and Germany 24 29 P = 39.35 ± 2.06
C = 38.43 ± 1.34 P = 35.56 ± 1.52
C = 36.23 ± 1.78 Rotterdam LVEDD, LVESD, IVST, PWT, LVEF, E wave, A wave, E/A, LVM, LVMI, LAD, DT E/E’ and E’ (The analysis did not incorporate these measurements because it remains unclear from which side of the mitral annuli they were obtained) Age, BMI, FBS 1) Increased LVM, 2) concentric hypertrophy in PCOS cases, that was not accompanied by the presence of diastolic dysfunction. Tasolar et al(1) [42] Case-control Turkey 25 obese PCOS 25 P = 29.7 ± 3.5
C = 29.3 ± 4.1 P = 21.7 ± 1.4
C = 22.5 ± 1.6 Rotterdam LVED, LVSD, LVEF, PWT, IVST, DT, LAD, A wave, E wave, E/A, IVRT E’, A’, S, E/E’ (The analysis did not include these values, which were reported as the combined values of the lateral mitral annuli, septal mitral annuli, and tricuspid annuli) Age, BMI, FBS, F-insulin, HOMA-IR, Testosterone 1) LV diastolic parameters were impaired in PCOS, 2) increased atrial electromechanical delay in PCOS. Tasolar et al(2) [42] Case-control Turkey 25 lean PCOS 25 P = 29.7 ± 2.6
C = 29.3 ± 4.1 P = 32.7 ± 2.0
C = 22.5 ± 1.6 Rotterdam LVEDD, LVESD, LVEF, PWT, IVST, DT, LAD, A wave, E wave, E/A, IVRT E’, A’, S, E/E’ (The analysis did not include these values, which were reported as the combined values of the lateral mitral annuli, septal mitral annuli, and tricuspid annuli) Age, BMI, FBS, F-insulin, HOMA-IR, Testosterone 1) LV diastolic parameters were impaired in PCOS, 2) increased atrial electromechanical delay in PCOS. Rees et al [43] Cross-sectional UK (69 Caucasian, 7 Asian, 4 Afro-Caribbean, 2 mixed races, 2 Arab) 84 95 P = 29.8 ± 6.7
C = 32.6 ± 7.9 P = 33.3 ± 7.8
C = 27.6 ± 6.3 Rotterdam LVEDD, IVST, PWT, LVEF Septal-Lateral E’, Septal-Lateral S Age, BMI, HOMA-IR, Testosterone No significant differences in central arterial stiffness and diastolic dysfunction between young women with PCOS and controls, after adjustment for age and BMI, whereas they are associated with insulin resistance and abdominal obesity. Zehir et al [44] Case-control Turkey 51 48 P = 30.2 ± 3.4
C = 31.0 ± 3.2 P = 31.8 ± 2.4
C = 31.2 ± 2.5 Rotterdam LVEDD, LVESD, LVEF, PWT, IVST, DT, LAD, A wave, E wave, E/A _ Age, BMI, Testosterone, DHEAS, FBS, HOMA-IR, 1) Significantly increased A wave, and DT in PCOS compared to controls, 2) Increased atrial electromechanical conduction delay in PCOS. Zimmermann et al [45] Case-control Canada (Caucasian or Caribbean) 14 18 P = 30 ± 1
C = 31 ± 1 P = 31 ± 2
C = 30 ± 2 NIH LVM _ Age, BMI, Testosterone, Androstenedione, DHEAS, FBS, F-insulin No significant difference in LVM and arterial pressure between PCOS and controls. Yildirim et al(1) [46] Cross-sectional Turkey 41 52 P = 23.9 ± 3.6
C = 27.2 ± 6.1 P = 25.6 ± 4.1
C = 23.5 ± 3.1 Rotterdam LVEDD, IVST, PWT, LVEF, E wave, A wave, E/A, LVM, LVMI, LAD Lateral E’, Lateral E/E’ Age, BMI, FBS, F-insulin, HOMA-IR, Testosterone, Androstenedione, DHEAS, FAI 1) Decreased E/A ratio, 2) increased LVMI, 3) significant difference in LVEF with controls and other phenotypes. Yildirim et al(2) [46] Cross-sectional Turkey 20 52 P = 24.9 ± 4.4
C = 27.2 ± 6.1 P = 24.2 ± 2.7
C = 23.5 ± 3.1 Rotterdam LVEDD, IVST, PWT, LVEF, E wave, A wave, E/A, LVM, LVMI, LAD Lateral E’, Lateral E/E’ Age, BMI, FBS, F-insulin, HOMA-IR, Testosterone, Androstenedione, DHEAS, FAI 1) Decreased E/A ratio, 2) increased LVMI. Yildirim et al(3) [46] Cross-sectional Turkey 25 52 P = 22.5 ± 2.6
C = 27.2 ± 6.1 P = 25.7 ± 4.3
C = 23.5 ± 3.1 Rotterdam LVEDD, IVST, PWT, LVEF, E wave, A wave, E/A, LVM, LVMI, LAD Lateral E’, Lateral E/E’ Age, BMI, FBS, F-insulin, HOMA-IR, Testosterone, Androstenedione, DHEAS, FAI Decreased E/A ratio. Yildirim et al(4) [46] Cross sectional Turkey 27 52 P = 24.7 ± 4.3
C = 27.2 ± 6.1 P = 23.8 ± 3.3
C = 23.5 ± 3.1 Rotterdam LVEDD, IVST, PWT, LVEF, E wave, A wave, E/A, LVM, LVMI, LAD Lateral E’, Lateral E/E’ Age, BMI, FBS, F- insulin, HOMA-IR, Testosterone, Androstenedione, DHEAS, FAI Decreased E/A ratio. Gazi et al [47] Cross-sectional Turkey 48 38 P = 24 ± 4
C = 30 ± 7 P = 25.4 ± 5.4
C = 22.5 ± 3.4 AEPCOS LVEDD, LVESD, LVEF, DT, LAD, A wave, E wave, E/A, IVRT, IVCT
(due to inappropriate reporting of this value, we did not include it in the meta-analysis) E’, E/E’ (The analysis did not include these values, which were reported as the combined values of the lateral mitral annuli, septal mitral annuli, and tricuspid annuli) Age, BMI, Testosterone, FBS, HOMA-IR, F-insulin 1) Significantly decreased E/A in PCOS, 2) increased inter- and intra-atrial conduction delays, decreased LA passive Empting volume and fraction. Rashid et al [48] Cross-sectional India 260 250 P = 28.08 ± 4.18
C = 29.44 ± 6.74 P = 24.43 ± 4.15
C = 23.93 ± 4.21 Rotterdam LVMI, LVM, LVEDD, IVST, PWT _ Age, BMI, F-Insulin, HOMA-IR, FBS, Testosterone 1) Significantly increased IVST, PWT, LVDD, LVM, and LVMI in women with PCOS compared to controls, 2) positive correlation between LVMI with IR and markers of inflammation but not with hyperandrogenism. Demirelli et al [49] Cross-sectional Turkey 31 32 P = 24.6 ± 4.8
C = 22.5 ± 3.6 P = 23.3 ± 4.8
C = 22.3 ± 3.0 Rotterdam LVEF, E wave, A wave, E/A, DT, IVRT, LAD, IVSD Septal E’,
Septal S Age, BMI, FBS, F-insulin, HOMA-IR 1) Significantly higher A wave, DT, IVRT and significantly lower E’ and E/A ratio in PCOS cases, 2) strong negative correlations between GLS (Global longitudinal strain), and both the fasting insulin and DT, significant, moderate correlation between GLS and HOMA-IR, significant weak, negative correlation between GLS and IVRT. Özkan et al [50] Cross-sectional Turkey 60 60 P = 26.4 ± 7.1
C = 30.5 ± 6.6 P = 25.84 ± 5.4
C = 24.02 ± 3.3 Rotterdam LVEDD, LVESD, LVEF, PWT, IVST, LAD _ Age, BMI, DHEAS,
HOMA-IR No significant difference in cardiac chamber dimensions between PCOS cases and controls. Aldrighi et al(1) [51] Cross-sectional Brazil 18 11 P = 25 ± 8
C = 28 ± 6 P = 29 ± 4
C = 23 ± 2 Rotterdam LVEDD, IVST, PWT, LVEF, LAD _ Age, BMI, FBS, F-insulin, Testosterone, Androstenedione, DHEAS No significant difference in cardiac chamber dimensions between PCOS cases and controls. Aldrighi et al(2) [51] Cross-sectional Brazil 26 11 P = 29 ± 6
C = 28 ± 6 P = 24 ± 3
C = 23 ± 2 Rotterdam LVEDD, IVST, PWT, LVEF, LAD _ Age, BMI, FBS,
F-insulin, Testosterone, Androstenedione, DHEAS,
No significant difference in cardiac chamber dimensions between PCOS cases and controls. Deveer et al [52] Cross-sectional Turkey 25 25 P = 27.24 ± 5.34
C = 31.8 ± 8.11 P = 25.86 ± 4.61
C = 25.44 ± 5.10 Rotterdam LVMI Lateral-Septal E/E’ Age, BMI, Testosterone, FBS, HOMA-IR, F- insulin No significant difference in echocardiographic indices and carotid intima–media thickness between PCOS and controls. Erdogan et al [53] Cross-sectional Turkey 40 46 P = 25.45 ± 6.72
C = 26.76 ± 6.04 P = 28.1 ± 7.8
C = 26.8 ± 4.5 Rotterdam LVEDD, LVESD, LVEF, DT, LAD, A wave, E wave, E/A, IVRT, IVCT _ Age, BMI, FBS, F- insulin, HOMA-IR 1) Increased IVRT and DT in PCOS, 2) P wave dispersion was significantly correlated with WHR, DT, E/A ratio and DBP. Celik et al [54] Cross-sectional Turkey 30 30 P = 22 ± 3.48
C = 24.75 ± 3.76 P = 24.6 ± 6.5
C = 20.15 ± 1.5 Rotterdam LVEF, LVM, PWT, IVST, IVRT, DT, LAD _ Age, BMI, Testosterone, DHEAS, FBS, F-insulin, HOMA-IR 1) Increased PWT and LVM in PCOS, 2) a positive correlation between LVM and HOMA-IR, 3) a positive correlation between PWT and fasting insulin, HOMA-IR. Kosmala et al [55] Cross-sectional Australia 52 54 P = 30.0 ± 6.2
C = 32.1 ± 5.2 P = 38.1 ± 9.5
C = 36.1 ± 5.5 Rotterdam LVEDD, IVST, PWT, LVMI, LVEF, LAD, E/A, DT Septal E/E’ Age, BMI, Testosterone, DHEA-S, FBS, F-insulin, HOMA-IR Impaired LV systolic and diastolic function in PCOS cases with IR, as compared with women with normal insulin sensitivity. Erdoğan et al [56] Cross-sectional Turkey 30 30 P = 25.9 ± 6.5
C = 26.1 ± 4.5 P = 29.4 ± 8.5
C = 28.2 ± 4.1 Rotterdam LVEDD, LVESD, IVST, PWT, LAD, LVEF, LVM, LVMI, E wave, A wave, E/A ratio, DT, IVRT, IVCT Septal E’
Septal E/E’ Age, BMI, FBS, F-insulin, HOMA-IR Prolonged DT and IVRT, lower E’ and higher E/E’ ratio in PCOS cases. Akdag et al [57] Cross-sectional Turkey 82 74 P = 25.9 ± 5.7
C = 26.4 ± 6.8 P = 26.4 ± 4.1
C = 25.9 ± 5.9 Rotterdam LVEDD, LVESD, LVEF, DT, LAD, A wave, E wave, E/A, IVRT _ Age, BMI, Testosterone, FBS 1) No significant changes in echocardiographic measures between PCOS and control groups, 2) increased atrial conduction time in PCOS.