Original Research

Association Between Coronary Artery Calcium Score and Left Ventricular Diastolic Dysfunction in Patients with Hypertension

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Background: Left ventricular diastolic dysfunction (LVDD) and coronary artery calcium (CAC) are common in patients with hypertension and are strong predictors of cardiovascular events. Aim: This study aims to investigate the association between CAC and LVDD in patients with hypertension without coronary artery disease (CAD). Methods: Consecutive patients with hypertension who underwent echocardiography and non-contrast coronary CT were studied. CAC was quantified using the Agatston score. Patients with a history of CAD, AF or left ventricular ejection fraction (LVEF) <50% were excluded. Characteristics of patients with and without LVDD were compared and the association between LVDD and CAC was evaluated. Univariable and multivariable analyses were performed to determine the predictors of LVDD and high CAC (>median CAC). A p value of <0.05 was considered statistically significant. Results: A total of 250 patients were included, with a mean age of 64.3 ± 10.1 years, 59% women and 26.4% had diabetes. The prevalence of LVDD was 64.8% (grade I LVDD 48%; grade II LVDD 16.8%) and the median CAC score was 58.2 (interquartile range [IQR] 0.7–349.8). Patients with LVDD had a significantly higher median CAC score than those without LVDD (142.8 [IQR 18.8–514.8] versus 5.0 [IQR 0–64.4]; p<0.001). Multivariable analysis showed that the CAC score was independently associated with LVDD (OR 1.003; 95% CI [1.001–1.004]; p<0.001). Left atrial volume index and E-wave deceleration time were independently associated with high CAC (OR 1.05; 95% CI [1.01–1.09]; p=0.008 and OR 1.008; 95% CI [1.002–1.02]; p=0.01), respectively. Conclusion: CAC scoring was associated with LVDD in patients with hypertension.

Disclosure:The authors have no conflicts of interest to declare.



Published online:

Data Availability Statement:

The datasets used and/or analysed during the current study are available from the corresponding author on reasonable request.

Ethics Approval Statement:

This study was approved by the Siriraj Institutional Review Board (SIRB) (COA no. Si 639/2021), Faculty of Medicine Siriraj Hospital, Mahidol University. The need for consent was waived by the board due to its retrospective nature and as all personal identifying information was obliterated. The study protocol conforms to the Declaration of Helsinki.

Acknowledgements:PK and WL contributed equally.

Author contributions:

Conceptualisation: PK, WL, TB, YK; data curation: PK, WL, YK; formal analysis: PK, WL, TB, YK; funding acquisition: None;
investigation: PK, WL, TB, YK; methodology: PK, WL, TB, YK; project administration: TB, YK; resources: PK, WL, TB, YK; software: PK, WL, TB, YK; supervision: TB, YK; validation: PK, WL, TB, YK; visualisation: PK, WL, TB, YK; writing – original draft preparation: PK, WL, TB, YK; writing – review & editing: PK, WL, TB, YK.

Correspondence Details:Yodying Kaolawanich, Division of Cardiology, Department of Medicine, Faculty of Medicine Siriraj
Hospital, Mahidol University, Bangkok, Thailand 10700 E: yodying.kao@gmail.com

Open Access:

This work is open access under the CC-BY-NC 4.0 License which allows users to copy, redistribute and make derivative works for non-commercial purposes, provided the original work is cited correctly.

Coronary artery calcium (CAC) is an established marker of subclinical atherosclerosis and an independent predictor of future coronary artery disease (CAD).1,2 The CAC score, determined using non-contrast coronary CT (CCT), can assist in cardiovascular (CV) risk assessment and clinical decision-making.3 The presence and extent of CAC are associated with an increased risk of CV events with an incremental value beyond traditional CV risk factors.4 Vascular calcification is an active and regulated process integral to CV disease and is intimately linked to hypertension.5 A study by Grossman et al. showed that the presence of CAC in normotensive healthy subjects can predict the development of hypertension.6

Left ventricular diastolic dysfunction (LVDD) is an alteration of left ventricular (LV) diastolic filling due to decreased myocardial relaxation and increased LV stiffness. Assessment of LV diastolic function is important since most patients with heart failure demonstrate an abnormal diastolic filling pattern due to LVDD. LVDD is common in patients with hypertension and is a predictor of increased adverse CV outcomes.7 Previous studies have revealed the incidence of LVDD between 20–58% in hypertension.8–10 The mechanisms, including increased afterload, myocardial fibrosis and inflammation, would cause LVDD in patients with hypertension.11,12

Given CAC score and LVDD are strong predictors of CV events and share common risk factors, previous studies have shown a relationship between LVDD and CAC score in several patient populations, including asymptomatic patients, elderly patients and patients with diabetes.13–15 However, there is no specific study regarding an association between CAC score and LVDD in patients with hypertension. We hypothesise that patients with hypertension could have a relationship between CAC score and LVDD due to an atherogenic process and inflammation. This study aimed to investigate the association between CAC and LVDD in patients with hypertension.


Study Population

Consecutive patients aged 18 years or older with hypertension who underwent both non-contrast CCT for CAC scoring and resting echocardiography between 2016 and 2020 in a tertiary hospital were studied. Hypertension was defined as a self-reported history of hypertension, the use of antihypertensive medication or a blood pressure (BP) of ≥140/90 mmHg. The grading of hypertension was defined in accordance with the latest European guideline for hypertension. Grade 1 hypertension was classified as a systolic BP of 140–159 mmHg and/or a diastolic BP of 90–99 mmHg. Grade 2 hypertension was characterised by a systolic BP of 160–179 mmHg and/or a diastolic BP of 100–109 mmHg. Grade 3 hypertension was defined as a systolic BP of ≥180 mmHg and/or a diastolic BP of ≥110 mmHg.16 Patients with a history of CAD or MI, prior cardiac surgery or coronary revascularisation, AF, severe left-sided valvular disease, any prosthetic cardiac valve, LV systolic dysfunction with left ventricular ejection fraction (LVEF) of <50%, congenital heart disease, permanent pacemaker, limited or poor-quality echocardiography or incomplete data were excluded.

The protocol for this study was approved by the institutional review board. The requirement to obtain written informed consent was waived due to the retrospective design of the study.

Clinical symptoms, CAD risk factors and details of current medications were obtained from electronic medical records. Diabetes was defined as a self-reported history and/or receiving treatment for diabetes, or a fasting glucose of ≥126 mg/dl. Dyslipidaemia was defined as a total cholesterol level of ≥240 mg/dl, an LDL cholesterol level of ≥130 mg/dl, an HDL cholesterol level of <40 mg/dl, a triglyceride level of ≥200 mg/dl, and/or treatment with a lipid-lowering agent. BP and heart rate data were obtained before CCT. Laboratory results, including serum creatinine, estimated glomerular filtration rate (eGFR), haematocrit, fasting plasma glucose, total cholesterol, HDL cholesterol, LDL cholesterol and triglyceride were obtained from the medical records within 3 months of CCT. The eGFR was calculated using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation.17

CCT Protocols and Echocardiography

CCT was performed using a 256-slice scanner (SOMATOM Definition Flash, Siemens Healthcare) according to established guidelines and institutional protocol at the time of the scan.18 A non-enhanced prospective electrocardiography (ECG)-gated sequential CCT scan was performed to determine CAC scoring using the following parameters: rotation time of 280 ms, slice collimation of 0.6 mm, slice width of 3.0 mm, tube voltage of 120 kV and tube current of 50 mAs. Analysis of CAC images was performed following the standard protocol on a separate workstation (syngo.via, Siemens Healthineers). CAC scans were interpreted according to the Agatston method with a high CAC score defined as greater than median CAC score.19

Echocardiograms were performed by experienced cardiologists. A comprehensive transthoracic echocardiographic examination consisted of 2D, M-mode, Doppler and tissue Doppler imaging (TDI). All echocardiographic measurements were performed according to the standard guidelines with the average of 3–5 consecutive cardiac cycles for the analyses.20 Diastolic function was assessed by pulsed-wave Doppler examination of mitral flow and TDI of the mitral annulus.21 Peak early (E) and late (A) diastolic velocities of mitral inflow and E-wave deceleration time were measured using pulsed-wave Doppler study with the sample volume at the tip of mitral valve. Longitudinal early (e’) and late diastolic myocardial velocities were measured using TDI in apical four-chamber view with the sample volume at the medial and lateral aspects of mitral annulus. The average of medial and lateral e’ was used for the E/e’ ratio.21 Left atrial (LA) volume and LV mass were measured using the recommendations by the American Society of Echocardiography and indexed with body surface area.20 LVDD was diagnosed if three or more of the following parameters met the cut-off values: septal e’ <7 cm/s or lateral e’ <10 cm/s, average E/e’ ratio > 14, left atrial volume index (LAVI) >34 ml/m2 and peak tricuspid regurgitation velocity >2.8 m/s.21

Statistical Analysis

All statistical analyses were performed using SPSS Statistics for Windows version 20.0 (SPSS Inc). Continuous variables with normal distribution were presented as mean (±SD) and continuous variables with non-normal distribution were presented as median and interquartile ranges (IQR). The normality of the distribution of variables was examined by the Kolmogorov-Smirnov test. Categorical variables were present as absolute numbers and percentages. Differences between patient characteristics with and without LVDD as well as high (>median CAC) and non-high CAC (≤median CAC) in terms of baseline and image characteristics were compared using the Student’s unpaired t-test or the Mann-Whitney U-test for continuous variables, while the χ2-square test or Fisher’s exact test was used for categorical variables as appropriate. Normally distributed continuous data of multiple (>2) groups were compared using one-way analysis of variance. Non-normally distributed continuous data of multiple (>2) groups were compared using the Kruskal–Wallis test. Univariable Cox logistic regression analysis was performed to identify significant predictors of LVDD and high CAC. Variables with a p value <0.05 from univariable analysis were entered into Cox logistic regression multivariable analysis. The results of the univariable and multivariable analyses are given as odds ratios along with their respective 95% CI. A p-value <0.05 was considered statistically significant for all tests.

Sample size estimation was performed based on a study by Osawa et al. that examined the association between CAC and LVDD in elderly people.15 The median CAC of patients with LVDD was 91 (IQR 455), while the median CAC of patients without LVDD was 25 (IQR 186). The sample size was determined using the Mann–Whitney test, with a type I error rate of 5% and a test power of 80% to detect an estimated standard deviation from the 10th percentile. Therefore, the total number of patients needed was 242.

Baseline Characteristics of Patients Stratified According to Left Ventricular Diastolic Function

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Study Population

There were 250 patients with hypertension included in the analyses. Table 1 shows baseline characteristics, laboratory data, and CAC scores of all patients as well as the comparisons between patients with and without LVDD. The common primary indications for echocardiography and CCT were dyspnoea (49%) and chest pain (35%). Mean age was 64.3 (±10.1) years (59% women). Eighty-two percent of patients had grade 1 hypertension. The rest had grade 2 hypertension. The average number of antihypertensive drugs was 1.7 (±0.8). LVDD was present in 162 (64%) patients. The median CAC score was 58.2 (IQR 0.7, 349.8) and 191 (76%) patients had a CAC score >0.

Regarding the inclusion criteria, 25 patients reported having hypertension, 209 patients were using antihypertensive medications and 16 patients had a BP of ≥140/90 mmHg without taking medications. There were no significant differences observed in the prevalence of LVDD among these categories. Specifically, the prevalence of LVDD was 44.0% (11 of 25) in the self-report group, 66.9% (140 of 209) in the antihypertensive medication group and 68.7% (11 of 16) in the group with BP ≥140/90 mmHg (p=0.07) (Table 1). Additionally, there were no significant differences in CAC scores between these groups. The median CAC scores were as follows: self-reported group 18.1 (IQR 0, 105.5), hypertensive medication group 69 (IQR 1.9, 379.5), and BP ≥140/90 mmHg group 27.2 (IQR 1.1, 194.9) (p=0.06).

Patients with LVDD were older (67.3 ± 8.7 versus 58.8 ± 10.4; p<0.001) and likely to present with dyspnoea (55.6% versus 38.6%; p=0.01). Compared to those without LVDD, they had a higher severity of hypertension, with higher systolic blood pressure (141.7 ± 18.9 mmHg versus 135.4 ± 13.5 mmHg; p=0.006), higher prevalence of grade 2 hypertension (22.2% versus 8%; p=0.004) and used a greater number of antihypertensive medications (1.8 ± 0.9 versus 1.5 ± 0.7; p=0.002) . Patients with LVDD had higher median CAC scores (142 [IQR 18.8; 514.8] versus 5.0 [IQR 0; 64.4], p<0.001). Figure 1 shows that CAC scores of patients with grade I or grade II LVDD were significantly higher than patients without LVDD (median CAC score; grade I LVDD=127.3 [IQR 17.9; 509.6], grade II LVDD=215.3 [IQR 21.0; 532.3]). However, there was no significant difference in median CAC scores between patients with grade I and grade II LVDD (p=0.59).

Figure 1: The Coronary Artery Calcium Scores of Patients Categorised by Left Ventricular Diastolic Dysfunction Grade

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Echocardiographic Parameters of Patients Stratified According to Median CAC Score

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Echocardiographic Data

Table 2 demonstrates echocardiographic data in all patients as well as the comparisons between patients with and without high CAC scores (>median CAC score of all patients; 58.2). The average LVEF was 66.4% (±8.2) and 48% of patients had grade I diastolic dysfunction and 16.8% had grade II. Patients with high CAC had higher LV mass index, LAVI and greater prevalence of diastolic dysfunction as well as greater severity of diastolic dysfunction. Figure 2 shows diastolic function categories stratified by quartiles of CAC scores. The prevalence of grade I and grade II LVDD progressively increased according to quartiles of CAC scores. Patients with the fourth quartile of CAC score had over double the rates of grade I and grade II LVDD compared to the first quartile. Patients with the first quartile had the highest rate of normal diastolic function (60.3%).

Figure 2: Diastolic Function Categories Stratified by Quartiles of Coronary Artery Calcium Scores

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Univariable and Multivariable Analyses of Factors Associated with Left Ventricular Diastolic Dysfunction

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Univariable and Multivariable Analyses of Factors Associated with High CAC Score

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Multivariable Analyses

Table 3 shows the association between LVDD and clinical variables and CAC score. The univariable analysis indicates that age, systolic BP, the use of angiotensin-converting enzyme inhibitors or angiotensin-receptor blockers, calcium channel blockers, diuretics, eGFR, hematocrit and levels of total and LDL cholesterol as well as CAC scores are associated with LVDD. Multivariable analysis demonstrated age (OR 1.09; 95% CI [1.06–1.13]; p<0.001) and CAC score (OR 1.003; 95% CI [1.001–1.004]; p<0.001) were independently associated with LVDD. Table 4 shows the association between high CAC (>58.2), clinical variables and echocardiographic parameters. Multivariable analysis demonstrated age (OR 1.06; 95% CI [1.02–1.10]; p=0.005), systolic BP (OR 1.02; 95% CI [1.005–1.04]; p=0.01), LAVI (OR 1.05; 95% CI [1.01–1.09]; p=0.008) and E-wave deceleration time (OR 1.008; 95% CI [1.002–1.02]; p=0.01) were independently associated with high CAC score.


The study, conducted in patients with hypertension without CAD who underwent both echocardiography and non-contrast CCT, yielded several key findings. Firstly, it revealed that 64% of the patients had LVDD. Secondly, those with LVDD exhibited higher CAC scores compared to those without LVDD. Thirdly, CAC was independently associated with LVDD. Finally, LAVI and E-wave deceleration time were both independently associated with high CAC scores.

CAC is now established as a reliable tool for estimating the risk of MI, coronary death and all-cause mortality.2,22 Current guidelines endorse using non-contrast CCT to assess CAC in suitable asymptomatic patients to improve clinical risk evaluation.22,23 Previous studies showed CAC was associated with age, CAD risk factors such as hypertension, diabetes, dyslipidaemia and a family history of CAD.24,25 In our study, 76% of the patients had a CAC score over 0. The multivariable analysis showed age and systolic BP were independently associated with high CAC. These were consistent with previous studies.15,24,25

LVDD is associated with increased myocardial fibrosis and ventricular stiffness. Comorbidities associated with LVDD include hypertension, diabetes, obesity, CAD and smoking.26 LVDD has been recognised in several cardiovascular diseases and is associated with worse outcomes, including all-cause mortality.7,11,12,27 The mechanism underlying the association between high CAC scores and LVDD can be explained by several factors.

First, the presence of extensive coronary artery calcification indicates a higher burden of atherosclerosis and plaque formation within the coronary arteries. This can lead to reduced coronary blood flow and impaired perfusion of the myocardium, affecting the overall cardiac function, including diastolic function.28 Second, the accumulation of calcium deposits in the coronary arteries reflects the chronic inflammatory process associated with atherosclerosis. Inflammation can contribute to the development of LVDD by promoting myocardial fibrosis, impaired relaxation and increased stiffness of the LV. Furthermore, coronary artery calcification is closely associated with other cardiovascular risk factors such as hypertension, diabetes and dyslipidaemia. These risk factors can directly influence LVDD through their effects on myocardial remodelling, vascular function and neurohormonal imbalances.

In a study by Osawa et al. on elderly individuals, age, female sex and hypertension were found to be independently associated with LVDD.15 Haddad et al. conducted a large population-based study and found that advanced LVDD (>grade I) was independently associated with age, female sex, being black, lower height, higher body weight, higher pulse pressure, higher HbA1c, lower HDL-C and prevalent CAD.29 Both studies demonstrated that CAC was independently associated with LVDD.15,29 Our study also found that patients with LVDD were older and had a higher hypertension grade, which is consistent with previous studies that have shown an association between LVDD and age and CV risk factors.15,29 Furthermore, our study adds to the existing literature by demonstrating an association between CAC and LVDD in patients with hypertension.

Echocardiography is the main imaging modality for assessment of LV diastolic function. Multiple echocardiographic variables can be used to determine LV diastolic function. Like the previously published data, the present study confirms that patients with a high CAC score had worse diastolic parameters, such as higher A, E-wave deceleration time, E/e’ ratio, LV mass index and LAVI than those with lower CAC.15,29 Furthermore, LAVI and E-wave deceleration time were independently associated with a high CAC score representing the link between LVDD and CAC in patients with hypertension. LA volume is directly related to LV filling pressure and it has been shown to be a predictor of stroke and development of heart failure.27

Nearly half of the patients in this study reported experiencing dyspnoea, especially in patients with LVDD. It has been demonstrated in recent studies that a high CAC score is linked to the history and progression of congestive heart failure.30,31 While our study did not involve patients with overt heart failure, the association between CAC score and LVDD could indicate the occurrence of heart failure events in this population. As LVDD is one of the contributing factors to heart failure, incorporating the CAC score into the risk stratification for heart failure prediction may be beneficial. However, further studies are required to investigate this topic.

Study Limitations

Our analysis has several limitations. First, this study included patients with mixed symptomatic and asymptomatic presentations and the sample size was relatively small. Additionally, the study population predominantly consisted of women. Therefore, the generalisability of our results to the broader population or patients at higher risk may be limited. Second, all analyses were cross-sectional, which complicates the causal interpretation of the associations that were observed. Third, patients with a history of CAD, post percutaneous coronary intervention, coronary artery bypass surgery or AF were excluded from our analysis due to the potential for inaccurate CAC scores and significant artefact from cardiac motion.


This study highlights a significant association between CAC and LVDD in patients with hypertension without CAD. Patients with LVDD had higher CAC scores, and CAC independently predicted LVDD.

Clinical Perspective

  • Left ventricular diastolic dysfunction and coronary artery calcification are common in patients with hypertension.
  • Coronary artery calcium score is independently associated with left ventricular diastolic dysfunction even after adjusting for traditional cardiovascular risk factors.


  1. Budoff MJ, Achenbach S, Blumenthal RS, et al. Assessment of coronary artery disease by cardiac computed tomography: a scientific statement from the American Heart Association Committee on Cardiovascular Imaging and Intervention, Council on Cardiovascular Radiology and Intervention, and Committee on Cardiac Imaging, Council on Clinical Cardiology. Circulation. 2006;114:1761–91.
    Crossref | PubMed
  2. Raggi P, Cooil B, Shaw LJ, et al. Progression of coronary calcium on serial electron beam tomographic scanning is greater in patients with future myocardial infarction. Am J Cardiol 2003;92:827–9.
    Crossref | PubMed
  3. Visseren FLJ, Mach F, Smulders YM, et al. ESC guidelines on cardiovascular disease prevention in clinical practice: developed by the task force for cardiovascular disease prevention in clinical practice with representatives of the European Society of Cardiology and 12 medical societies with the special contribution of the European Association of Preventive Cardiology (EAPC). Eur Heart J 2021;42:3227–337.
    Crossref | PubMed
  4. McClelland RL, Chung H, Detrano R, et al. Distribution of coronary artery calcium by race, gender, and age: results from the Multi-Ethnic Study of Atherosclerosis (MESA). Circulation 2006;113:30–7.
    Crossref | PubMed
  5. Kalra SS, Shanahan CM. Vascular calcification and hypertension: cause and effect. Ann Med 2012;44(Suppl 1):S85–92.
    Crossref | PubMed
  6. Grossman C, Shemesh J, Dovrish Z, et al. Coronary artery calcification is associated with the development of hypertension. Am J Hypertens 2013;26:13–9.
    Crossref | PubMed
  7. Schillaci G, Pasqualini L, Verdecchia P, et al. Prognostic significance of left ventricular diastolic dysfunction in essential hypertension. J Am Coll Cardiol 2002;39:2005–11.
    Crossref | PubMed
  8. Catena C, Verheyen N, Pilz S, et al. Plasma aldosterone and left ventricular diastolic function in treatment-naïve patients with hypertension: tissue-Doppler imaging study. Hypertension 2015;65:1231–7.
    Crossref | PubMed
  9. Catena C, Colussi G, Verheyen ND, et al. Moderate alcohol consumption is associated with left ventricular diastolic dysfunction in nonalcoholic hypertensive patients. Hypertension 2016;68:1208–16.
    Crossref | PubMed
  10. Catena C, Colussi G, Fedrizzi S, Sechi LA. Association of a prothrombotic state with left-ventricular diastolic dysfunction in hypertension: a tissue-Doppler imaging study. J Hypertens 2013;31:2077–84.
    Crossref | PubMed
  11. Drazner MH. The progression of hypertensive heart disease. Circulation 2011;123:327–34.
    Crossref | PubMed
  12. Nadruz W, Shah AM, Solomon SD. Diastolic dysfunction and hypertension. Med Clin North Am 2017;101:7–17.
    Crossref | PubMed
  13. Graça B, Donato P, Ferreira MJ, et al. Left ventricular diastolic function in type 2 diabetes mellitus and the association with coronary artery calcium score: a cardiac MRI study. AJR Am J Roentgenol 2014;202:1207–14.
    Crossref | PubMed
  14. Mansour MJ, Chammas E, Hamoui O, et al. Association between left ventricular diastolic dysfunction and subclinical coronary artery calcification. Echocardiography 2020;37:253–9.
    Crossref | PubMed
  15. Osawa K, Miyoshi T, Oe H, et al. Association between coronary artery calcification and left ventricular diastolic dysfunction in elderly people. Heart Vessels 2016;31:499–507.
    Crossref | PubMed
  16. Williams B, Mancia G, Spiering W, et al. ESC/ESH guidelines for the management of arterial hypertension: the task force for the management of arterial hypertension of the European Society of Cardiology (ESC) and the European Society of Hypertension (ESH). Eur Heart J 2018;39:3021–104.
    Crossref | PubMed
  17. Miller WG, Myers GL, Ashwood ER, et al. Creatinine measurement: state of the art in accuracy and interlaboratory harmonization. Arch Pathol Lab Med 2005;129:297–304.
    Crossref | PubMed
  18. Abbara S, Blanke P, Maroules CD, et al. SCCT guidelines for the performance and acquisition of coronary computed tomographic angiography: a report of the society of cardiovascular computed tomography guidelines committee: endorsed by the North American Society for Cardiovascular Imaging (NASCI). J Cardiovasc Comput Tomogr 2016;10:435–49.
    Crossref | PubMed
  19. Agatston AS, Janowitz WR, Hildner FJ, et al. Quantification of coronary artery calcium using ultrafast computed tomography. J Am Coll Cardiol 1990;15:827–32.
    Crossref | PubMed
  20. Lang RM, Badano LP, Mor-Avi V, et al. Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr 2015;28:1–39.e14.
    Crossref | PubMed
  21. Nagueh SF, Smiseth OA, Appleton CP, et al. Recommendations for the evaluation of left ventricular diastolic function by echocardiography: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr 2016;29:277–314.
    Crossref | PubMed
  22. Alluri K, Joshi PH, Henry TS, et al. Scoring of coronary artery calcium scans: history, assumptions, current limitations, and future directions. Atherosclerosis 2015;239:109–17.
    Crossref | PubMed
  23. Taylor AJ, Cerqueira M, Hodgson JM, et al. ACCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/SCMR 2010 appropriate use criteria for cardiac computed tomography. A report of the American College of Cardiology Foundation appropriate use criteria task force, the Society of Cardiovascular Computed Tomography, the American College of Radiology, the American Heart Association, the American Society of Echocardiography, the American Society of Nuclear Cardiology, the North American Society for Cardiovascular Imaging, the Society for Cardiovascular Angiography and Interventions, and the Society for Cardiovascular Magnetic Resonance. J Am Coll Cardiol 2010;56:1864–94.
    Crossref | PubMed
  24. Cademartiri F, Maffei E, Palumbo A, et al. Coronary calcium score and computed tomography coronary angiography in high-risk asymptomatic subjects: assessment of diagnostic accuracy and prevalence of non-obstructive coronary artery disease. Eur Radiol 2010;20:846–54.
    Crossref | PubMed
  25. Villines TC, Hulten EA, Shaw LJ, et al. Prevalence and severity of coronary artery disease and adverse events among symptomatic patients with coronary artery calcification scores of zero undergoing coronary computed tomography angiography: results from the CONFIRM (Coronary CT Angiography Evaluation for Clinical Outcomes: an International Multicenter) registry. J Am Coll Cardiol 2011;58:2533–40.
    Crossref | PubMed
  26. Pfeffer MA, Shah AM, Borlaug BA. Heart failure with preserved ejection fraction in perspective. Circ Res 2019;124:1598–617.
    Crossref | PubMed
  27. Benjamin EJ, D’Agostino RB, Belanger AJ, et al. Left atrial size and the risk of stroke and death the Framingham Heart Study. Circulation 1995;92:835–41.
    Crossref | PubMed href="https://www.ncbi.nlm.nih.gov/pubmed/7641364">7641364.
  28. Lin FY, Zemedkun M, Dunning A, et al. Extent and severity of coronary artery disease by coronary CT angiography is associated with elevated left ventricular diastolic pressures and worsening diastolic function. J Cardiovasc Comput Tomogr 2013;7:289–96.e1.
    Crossref | PubMed
  29. Haddad F, Cauwenberghs N, Daubert MA, et al. Association of left ventricular diastolic function with coronary artery calcium score: a project baseline health study. J Cardiovasc Comput Tomogr 2022;16:498–508.
    Crossref | PubMed
  30. Kälsch H, Lehmann N, Möhlenkamp S, et al. Association of coronary artery calcium and congestive heart failure in the general population: results of the Heinz Nixdorf Recall study. Clin Res Cardiol 2010;99:175–82.
    Crossref | PubMed
  31. Leening MJ, Elias-Smale SE, Kavousi M, et al. Coronary calcification and the risk of heart failure in the elderly: the Rotterdam study. JACC Cardiovasc Imaging 2012;5:874–80.
    Crossref | PubMed