J Gandhara Med Dent Sci

July - September 2026

FREQUENCY OF LEFT VENTRICULAR DIASTOLIC DYSFUNCTION IN TYPE 2 DIABETES

MELLITUS PATIENTS WITH NON -ALCOHOLIC FATTY LIVER DISEASE

Muhammad Saad

, Fawad Rahim

, Said Amin

, Muhammad Ahmed Yar

, Alina Batool

, Hira Nadeem

Shehriyar Khan

How to cite this article

Saad M, Rahim F, Amin S, Yar MA,

Batool A, Nadeem H, et al. Frequency

of Left V entricular Diastolic

Dysfunction in Type 2 Diabetes

Mellitus Patients with Non-Alcoholic

Fatty Liver Disease. J Gandhara Med

Dent Sci. 2026;13(3): 09-13.

Date Submission: 12-02-2026

Date Revised: 04-06-2026

Date Acceptance: 11-06-2026

Post-Graduate resident, Department

of Medicine, Hayatabad Medical

Complex, Peshawar

Professor, Department of Medicine,

Hayatabad Medical Complex,

Peshawar

Medical Officer, Department of

Medicine, Hayatabad Medical

Complex, Peshawar

Correspondence

Fawad Rahim, Associate Professor,

Department of Medicine, Hayatabad

Medical Complex, Peshawar

drfawadrahim@outlook.com

+92-333-9351983

ABSTRACT

OBJECTIVES

The study aimed to determine the frequency of left ventricular diastolic

dysfunction (LVDD) in type 2 diabetes mellitus (DM) patients with non-

alcoholic fatty liver disease (NAFLD).

METHODOLOGY

This cross-sectional study was conducted in the Department of Medicine at

Hayatabad Medical Complex, Peshawar, Pakistan, between 01.03.2025 and

10.09.2025. The study participants were patients with type 2 DM and

concomitant NAFLD. Patients with a history of hypertension, ischemic heart

disease, and chronic kidney disease were excluded. All patients underwent

echocardiography, and LVDD was diagnosed based on the E/A ratio

reversal. The association between LVDD and its risk factors (age, gender,

body mass index, smoking status) was determined using univariate and

multivariable analyses.

RESULTS

Of the 252 participants, 51 patients (20.2%) were diagnosed with LVDD. It

was more frequent in males (22.4% vs 18.4%), individuals over 60 years of

age (24.6% vs 16.4%), obese patients (21.9% vs 19%), and smokers (30.1%

vs 15.4%). Nevertheless, univariate and multivariable regression analyses

indicated that age, gender, and obesity were not statistically signicant or

independent predictors of LVDD. Conversely, smoking was identied as a

signicant independent risk factor in both univariate (p = 0.006) and

multivariable regression analyses (AOR: 3.865; 95% CI: 1.384–10.793; p =

0.010).

CONCLUSION

A signicant number of patients with type 2 DM and NAFLD showed LVDD.

Smoking is independently linked to LVDD, highlighting the importance of

quitting smoking and performing early cardiovascular screenings to prevent

progression to overt heart failure in this high-risk group.

KEYWORDS: Diabetes Mellitus, Non-alcoholic Fatty Liver Disease,

Metabolically Dysfunctional Liver Disease, Left Ventricular Diastolic

Dysfunction, Pakistan

INTRODUCTION

Non-alcoholic fatty liver disease (NAFLD), recently

redefined as metabolic dysfunction-associated steatotic

liver disease (MASLD), is one of the most common

chronic liver disorders worldwide, with a global

prevalence of approximately 30.05%, and an even

higher burden in South Asia (33.83%).

In Pakistan,

NAFLD prevalence varies by province, being highest in

Punjab (34.03%), followed by Sindh (30.27%) and

Khyber Pakhtunkhwa (25.38%).

Non-alcoholic fatty

liver disease encompasses a spectrum ranging from

simple steatosis to non-alcoholic steatohepatitis, which

may progress to advanced brosis, cirrhosis, and

hepatocellular carcinoma.

Left Ventricular diastolic

dysfunction (LVDD) is an important, yet often

underrecognized, cardiovascular complication

associated with NAFLD. Left Ventricular diastolic

dysfunction, a known precursor of heart failure with

preserved ejection fraction, results from impaired

ventricular relaxation and increased left atrial pressure,

leading to reduced cardiac eciency. Zahra et al. from

Pakistan have reported that 71.42% of NAFLD patients

exhibited LVDD compared to 14.28% of healthy

controls, highlighting a substantial impact of hepatic

steatosis on early cardiac impairment.

Emerging

evidence increasingly supports the association between

NAFLD and LVDD among individuals with type 2

diabetes mellitus (T2DM). Bonapace et al. (2012) from

Italy showed that 64% of patients with T2DM and

NAFLD had LVDD, compared with 36% in patients

with T2DM without NAFLD, and that NAFLD

independently predicted LVDD.

In 2025,

Faramarzpour et al. from Iran showed that 81.1% with

https://doi.org/10.37762/jgmds.13-3.866

ORIGINAL ARTICLE

J Gandhara Med Dent Sci

July - September 2026

T2DM and NAFLD were found to have LVDD.

In a

Korean cohort, Lee et al. (2019) examined 606 T2DM

patients aged ≥50 years and reported a higher

prevalence of LVDD in those with NAFLD (59.7% vs.

49.0%).

Similarly, Mantovani et al. (2012) found

NAFLD as an independent predictor of left ventricular

hypertrophy in hypertensive T2DM patients.

Qureshi et

al. (2016) from Bahawalpur (Pakistan) reported that

LVDD was present in 38.16% of patients with T2DM

with NAFLD, highlighting a substantial burden of

subclinical cardiac dysfunction in the Pakistani diabetic

population.

In Pakistan, the prevalence of both T2DM

and NAFLD is on the rise due to sedentary lifestyles

and dietary habits.

10,11

Although Qureshi et al. have

evaluated the association between NAFLD and LVDD

among diabetic patients in the Punjab province of

Pakistan, data on the prevalence of LVDD in T2DM

patients with NAFLD in the Khyber Pakhtunkhwa

province are lacking.

Considering the distinct genetic

background, unique dietary, cultural, and lifestyle

practices, and dierent body composition of patients

from Khyber Pakhtunkhwa, this study seeks to assess

the prevalence of LVDD among local diabetic patients

with NAFLD. The study will also have implications for

managing NAFLD in patients with T2DM. Pioglitazone

is widely used in patients with T2DM and NAFLD due

to its benecial eects on hepatic steatosis and insulin

sensitivity.

But its use has been associated with uid

retention, which may prove detrimental in the presence

of unrecognized LVDD.

Therefore, identifying the

burden of LVDD and its risk factors in local diabetic

patients with NAFLD will help clinicians make

evidence-based decisions to screen them early and use

alternative agents for managing NAFLD in patients

with concomitant LVDD. In addition, the study results

will ensure that patients from this region of Pakistan are

represented in the pooled data used for systematic

reviews and meta-analyses on the subject.

METHODOLOGY

This cross-sectional study was conducted in the

Department of Medicine, Hayatabad Medical Complex,

Peshawar, Pakistan, from 03/01/2025 to 10/09/2025.

Patients of both genders aged 25-75 years with T2DM

and concomitant NAFLD were eligible for inclusion in

the study. Type 2 diabetes mellitus was dened as

patients already diagnosed with diabetes mellitus and

having glycosylated hemoglobin (HbA1c) greater than

6.5%. Non-alcoholic fatty liver disease was dened as

the presence of hepatic steatosis detected on abdominal

ultrasonography in diabetic patients who had no history

of alcohol consumption and no other known causes of

liver disease (viral hepatitis, drug-induced liver injury)

as per history and review of record. Obesity was

defined as a BMI greater than 30 kg/m

. Patients with

hypertension, chronic kidney disease, and ischemic

heart disease were excluded from the study. A total of

252 patients with T2DM and concomitant NAFLD

were enrolled in the study through convenience

sampling after informed consent, considering a

prevalence of LVDD of 38.16% among T2DM with

NAFLD, a 95% condence level, and an absolute

precision of 6%.

Demographic data, including age,

gender, body mass index (BMI), and smoking history,

were recorded. All study participants underwent

transthoracic echocardiography to assess for LVDD

under the supervision of a consultant cardiologist.

LVDD was diagnosed based on the reversal of the early

diastolic-to-late diastolic velocity ratio (E/A ratio).

Statistical Package for the Social Sciences (SPSS)

version 21 was used for analysis. Age and BMI were

presented as means and standard deviations, while

gender, age groups, obesity, smoking, and the presence

of LVDD were presented as frequencies and

percentages. Based on the presence or absence of

LVDD, the two groups were compared for dierences

in LVDD frequency by gender, age group, obesity

status, and smoking status using the chi-square test. To

minimize confounding, a multivariable regression

analysis including all variables was performed to

identify independent risk factors for LVDD. A p-value

of less than 0.05 was regarded as signicant for all

analyses.

RESULTS

The mean age of the study participants (n = 252) was

60.5 ± 11.5 years. Most participants were female (n =

136, 54%), under 60 years of age (n = 134, 53.2%),

non-obese (n = 147, 58.3%), and non-smokers (n = 169,

67.1%). The prevalence of LVDD was 20.2% (n = 51).

Table 1 summarizes the characteristics of the study

participants.

Table 1: Characteristics of the Study Population (n=252)

Variables Mean ± SD / Freq (%)

Age (Y ears)

60.5 ± 11.5

BMI (kg/m

)

30.1 ± 3.9

Gender, No. (%)

Female 136 (54%)

Male 116 (46%)

Age group, No. (%)

Up to 60 years 134 (53.2%)

More than 60 years 118 (46.8%)

Obesity, No. (%)

Non-obese 147 (58.3%)

Obese 105 (41.7%)

Smoking, No. (%)

No 169 (67.1%)

Yes 83 (32.9%)

LVDD, No. (%)

No 201 (79.8%)

Yes 51 (20.2%)

Frequency of Left Ventricular Diastolic Dysfunction in type 2 Diabetes

J Gandhara Med Dent Sci

July - September 2026

SD: Standard Deviation; LVDD: Left Ventricular

Diastolic Dysfunction

In univariate analysis, LVDD was more frequent in

males (22.4% vs 18.4%), although the dierence was

not statistically signicant (p = 0.427). Similarly,

LVDD was more common in patients over 60 years

(24.6% vs 16.4%, p = 0.108) and in obese patients

(21.9% vs 19%, p = 0.578). Compared to non-smokers,

smokers had a signicantly higher frequency of LVDD

(30.1% vs 15.4%, p = 0.006) (Table 2). After adjusting

for other risk factors in multivariable regression

analysis, smokers were still more likely than non-

smokers to have LVDD (AOR: 3.865; 95% CI: 1.384 –

10.793; p = 0.010) (Table 3).

Table 2: Univariate Analysis of Risk Factors for Left Ventricular

Diastolic Dysfunction in Patients with Diabetes Mellitus and Non-

Alcoholic Fatty Liver Disease

Variables LVDD P-

Value

No (n=201) Yes (n=51)

Gender Female 111 (81.6%) 25 (18.4%) 0.427*

Male 90 (77.6%) 26 (22.4%)

Age

group

Up to 60

years

112 (83.6%) 22 (16.4%) 0.108*

More than

60 years

89 (75.4%) 29 (24.6%)

Obesity Non-obese 119 (81%) 28 (19%) 0.578*

Obese 82 (78.1%) 23 (21.9%)

Smoking No 143 (84.6%) 26 (15.4%) 0.006*

Yes 58 (69.9%) 25 (30.1%)

LVDD: Left ventricular diastolic dysfunction

*Chi-square test

Table 3: Multivariable Regression Analysis of Risk Factors for

Left Ventricular Diastolic Dysfunction in Patients with Diabetes

Mellitus and Non-Alcoholic Fatty Liver Disease

Variables AOR 95%

P-value

Gender

Female*

0.100

Male 0.471 0.166 -

1.339

Age Group

Up to 60

years*

0.309

More than 60

years

1.437 0.715 -

2.888

Obesity

Non-obese*

0.391

Obese 1.344 0.684 -

2.640

Smoking

No*

0.010

Yes 3.865 1.384 -

10.793

*Reference category

AOR: Adjusted odds ratio; CI: Condence Interval

cardiac dysfunction in these patients.

DISCUSSION

This study explored the burden of LVDD among

patients with type 2 DM and NAFLD. This is a high-

risk group, often having subclinical cardiovascular

involvement. The study aimed to detect this early

The results will

ensure representation of the Pakistani population in the

regional and global literature focused on subclinical

cardiac dysfunction in patients with type 2 DM and

concomitant NAFLD. Clinically, early identication of

LVDD and its subsequent management will lead to

better outcomes for these patients. This study yielded

an overall prevalence of LVDD as 20.2% in T2DM

with NAFLD. The LVDD prevalence observed in our

study is considerably lower than that reported in most

international cohorts. Bonapace et al. from Italy (64%),

Lee H et al. from Korea (59.7%), and Faramarzpour et

al. from Iran (81.1%) have consistently shown

substantially higher diastolic dysfunction rates in

T2DM patients with NAFLD.

5,6,14

Mantovani et al.

reported the LVDD prevalence of 82% in T2DM

patients with NAFLD.

A systematic review by Wang

et al. analyzing 1,800 T2DM patients across 10 studies

reported consistently higher LVDD rates in NAFLD

patients compared to non-NAFLD controls.

Regionally, Qureshi et al. from Pakistan documented a

prevalence of 38.16% of LVDD in T2DM with

NAFLD.

Similarly, Sahoo et al. from India reported

that 55.55% of T2DM patients with NAFLD had

LVDD, and NAFLD conferred nearly a two-fold higher

risk of diastolic impairment (OR 1.84).

Several

methodological dierences likely account for the lower

LVDD prevalence observed in this study. A key factor

is the strict exclusion criteria, which systematically

removed patients with hypertension, chronic kidney

disease, and ischemic heart disease-conditions well-

established as independent risk factors for LVDD and

frequently comorbid with T2DM and NAFLD. Many

prior studies either included hypertensive patients (e.g.,

Bonapace et al., Mantovani et al., Sahoo et al. focused

on hypertensive T2DM) or did not explicitly exclude

them, potentially inating LVDD rates due to the

confounding eects of elevated blood pressure on left

ventricular lling pressures and myocardial

stiness.

5,8,16

Bonapace et al.5 had a relatively smaller

sample size of 50, with only 32 subjects having

NAFLD, giving a relatively higher prevalence of

LVDD.

Inclusion of patients with hypertension and

renal impairment in other cohorts may have contributed

to higher prevalences, as these conditions exacerbate

diastolic impairment through mechanisms such as

volume overload, uremic toxins, or subclinical

ischemia. Additionally, in this study, the diagnostic

criterion for LVDD-reversal of the E/A ratio (E/A<1)

represents an earlier and more conservative denition

compared to contemporary guidelines, which often

incorporate multiple parameters, including E/e’, left

atrial volume index, and tricuspid regurgitation velocity

for graded assessment of diastolic dysfunction. Studies

employing tissue Doppler imaging (e.g., Bonapace et

al.

, Lee H et al.) or comprehensive echocardiographic

panels (e.g., Wang et al.) detected subtler impairments

Frequency of Left Ventricular Diastolic Dysfunction in type 2 Diabetes

J Gandhara Med Dent Sci

July - September 2026

(e.g., reduced e’ velocity, elevated E/e’), leading to

higher detection rates.

5,14,15

Our reliance on E/A

reversal alone may have underestimated preclinical or

grade I diastolic dysfunction, capturing primarily more

overt reversal. It was further reported that LVDD was

more frequent in males as compared to females (22.4%

vs 18.4%). Bouthoorn et al. have reported similar

LVDD prevalence between men and women with

T2DM (46% vs 47%).

Similarly, the results of Suresh

et al.(28% vs 22%) also support our ndings.

In this

study, LVDD was reported to be more frequent in those

aged 60 years or older (24.6% vs 16.4%). However, age

did not independently predict LVDD, consistent with

findings from Bonapace et al. (OR 0.95, p=0.58) and

Sahoo et al., where age either showed no eect or was

not reported as signicant.

5,16

This contrasts with Lee et

al., who observed a modest independent eect of age

(OR 1.07 per year, p<0.001), likely due to their larger

cohort (n=606), older population (mean 63 years, all

≥50), and broader age variability, which enhanced the

detection of subtle cumulative age-related changes.

our cohort, the narrower age range and smaller sample

limited variability, reducing the ability to detect a small

age eect. Furthermore, LVDD was found to be present

in obese patients (21.9% vs 19%). However, obesity did

not independently predict LVDD in our study, despite a

higher numerical prevalence in obese participants.

Using a strict obesity cuto (BMI >30 kg/m²) may have

limited the ability to detect obesity’s eect on LVDD,

especially if much of the risk was already explained by

NAFLD. This supports our ndings that NAFLD

contributes to additional cardiac risk beyond obesity

alone. Bonapace et al. found no signicant dierences

in BMI or waist circumference between patients with

and without NAFLD.

By matching the groups for

obesity measures, NAFLD emerged as an independent

factor associated with left ventricular diastolic

dysfunction (LVDD), even after adjusting for

hypertension and other cardiometabolic risk factors.

Similarly, Lee H et al. reported that advanced liver

fibrosis, a marker of non-alcoholic steatohepatitis, was

independently linked to LVDD (OR 1.58) after

accounting for insulin resistance, BMI, and other

factors.

While BMI predicted LVDD in univariate

analysis, it lost signicance in multivariable models,

indicating that NAFLD progression mediates much of

obesity’s eect on diastolic function. Sahoo et al.

observed higher BMI and waist-hip ratios in NAFLD

patients, with strong associations with microvascular

complications and LVDD.

Yet, NAFLD remained

independently associated with LVDD (OR 1.84),

suggesting that hepatic steatosis and brosis contribute

beyond general obesity. Collectively, these ndings

highlight that NAFLD often mediates the pathway from

obesity to LVDD through mechanisms like insulin

resistance, inammation, and lipotoxicity. When

analyses adjust for or match on obesity (Bonapace et

al.) or focus on NAFLD severity (Lee H et al), the

independent eect of obesity on LVDD is reduced.

5,14

However, univariate analysis did not demonstrate that

any of these factors reached statistical signicance.

Additionally, after adjusting for all the other measured

variables in multivariate analysis, age, gender, and

obesity were not shown to be independent predictors of

LVDD. Smoking emerged as the strongest and the only

independent predictor of LVDD in this cohort (AOR

3.865) (p = 0.010), as the smokers were seen to exhibit

nearly a four-fold increase in the odds of LVDD

compared to the non-smokers. This observation thus

suggests that smoking may act as a potent and

modifiable determinant of early myocardial dysfunction

in this metabolically vulnerable population. Although

smoking was considered a covariate in several major

studies, its impact has been inconsistent across

populations. In the Korean study by Lee et al., smoking

did not independently predict LVDD, which may be

explained by the very low prevalence of active smokers

in their older, predominantly female cohort.

contrast, Bonapace et al. from Italy reported a higher

prevalence of smoking among NAFLD patients;

however, it did not remain signicant after adjustment

for metabolic risk factors.

Similarly, Qureshi et al.

from Pakistan noted that smoking was common in their

study population but did not evaluate it as an

independent predictor.

LIMITATIONS

The diagnosis of LVDD was based only on the reversal

of the E/A ratio. Although this is commonly used in

clinical practice, it is not the most sensitive marker of

early LVDD. Similarly, NAFLD was diagnosed using

ultrasound. Recruitment from a single center and the

convenience sampling may have contributed to

selection bias. Some factors, such as diabetes duration

and control, NAFLD severity, medications, and level of

physical activity, were not studied and may have served

as confounders. The cross-sectional design cannot

determine cause-and-eect relationships.

Comprehensive, long-term, prospective, and multi-

center studies would be needed to clarify causality and

disease progression.

CONCLUSIONS

In this study, LVDD was reported in 20.2% of patients

with NAFLD and T2DM. This shows that subclinical

heart dysfunction is fairly common in this group, even

if the prevalence was lower than what some regional

and international studies have reported. Among the risk

factors, smoking was signicantly associated with

LVDD, highlighting its role as a modiable contributor

Frequency of Left Ventricular Diastolic Dysfunction in type 2 Diabetes

J Gandhara Med Dent Sci

July - September 2026

LICENSE: JGMDS publishes its articles under a Creative Commons Attribution Non-Commercial Share-Alike license (CC-BY-NC-SA 4.0).

COPYRIGHTS: Authors retain the rights without any restrictions to freely download, print, share and disseminate the article for any lawful purpose.

It includes scholarlynetworks such as Research Gate, Google Scholar, LinkedIn, Academia.edu, Twitter, and other academic or professional networking sites.

to LVDD. These results emphasize the importance of

encouraging smoking cessation and support the need

for early cardiac assessments in patients with T2DM

and NAFLD in the smoking population.

CONFLICT OF INTEREST: None

FUNDING SOURCES: None

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Muhammad Saad

Concept & Design; Data Acquisition;

Drafting Manuscript;

Critical Revision;

Final Approval

Fawad Rahim -

Concept & Design;

Data

Analysis/Interpretation; Drafting Manuscript; Critical

Revision; Supervision; Final Approval

Said Amin -

Concept & Design;

Data Analysis/Interpretation;

Drafting Manuscript; Critical Revision; Supervision; Final

Approval

Muhammad Ahmed Yar –

Concept &

Design; Data

Acquisition; Drafting Manuscript; Critical Revision;

Final

Approval

Alina Batool -

Concept &

Design; Data Acquisition; Drafting

Manuscript; Critical Revision;

Final Approval

Hira Nadeem -

Concept &

Design; Data Acquisition; Drafting

Manuscript; Critical Revision;

Final Approval

Shehriyar Khan -

Concept &

Design; Data Acquisition;

Drafting Manuscript; Critical Revision;

Final Approval

AUTHORS CONTRIBUTION

The authors accept responsibility for all aspects of the work

and will ensure that any concerns regarding the accuracy or

integrity of any part are properly investigated and resolved.

Frequency of Left Ventricular Diastolic Dysfunction in type 2 Diabetes