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Research article · 2019 · Full text

International Journal of Advanced Biochemistry Research

A study on correlation between fasting & post-prandial serum triglycerides and severity of stroke-at a tertiary care hospital

Mohd Azam Hyder

Volume 3(2) · Pages 21–25 · DOI: 10.33545/26174693.2019.v3.i2a.37 ↗

Research areasPharmacy and Medical PracticesNeurological Disease Mechanisms and Treatments

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Abstract

Author-written

Aim & Objective of the study: The aim of this study is to investigate if serum TG levels predict stroke severity on admission with correlation of fasting and post-prandial serum TG levels Results: Of the 80 patients studied, 54 were males and 26 were females. Among the males, 42 had FTG≤2.3mmol/l and 12 had FTG levels >2.3mmol/l & 27 had PPTG≤2.3mmol/l and 27 had PPTG levels >2.3mmol/l. Of the 26 females 18 had FTG≤2.3mmol/l and 8 patients had FTG levels >2.3mmol/l & 15 had PPTG≤2.3mmol/l and 11 had PPTG levels >2.3mmol/l. In this study the number of patients with severe stroke (SSS≤25) were 20 of which 15 had F TG≤2.3mmol/l and only 5 patient had F TG>2.3mmol/l & 9 had PPTG≤2.3mmol/l and 12 had PPTG>2.3mmol/l. Out of 80 patients, 44 were hypertensive and 32 had FTG≤2.3mmol/l and 12 had FTG>2.3mmol/l & 19 had PPTG≤2.3mmol/l and 25 had PPTG>2.3mmol/l of the remaining 36 non hypertensive patients, 30 had FTG≤2.3mmol/l and 6 had FTG>2.3mmol/l & 25 had PPTG≤2.3mmol/l and 11 had PPTG>2.3mmol/l. 16 were IHD patients of which 12 had FTG≤2.3mmol/l and 4 had FTG>2.3mmol/l & 8 had PPTG≤2.3mmol/l and 8 had PPTG>2.3mmol/l & of the remaining 64 patients, 50 had FTG≤2.3mmol/l and 14 had FTG>2.3mmol/l & 30 had PPTG≤2.3mmol/l and 34 had PPTG>2.3mmol/l. The levels of serum FTG were not influenced by hypertension, IHD, age and sex of an individual but the level of serum PPTG were influenced by HTN. Conclusion: 1 In this study, mean serum fasting & post prandial serum triglyceride levels were not significantly associated with the severity of the stroke. As per this study hypertension, IHD, age and sex of an individual do not influence levels of serum fasting triglyceride levels but the serum post prandial triglyceride level were influenced by HTN.

Summary

Source-checked

Plain-language reading of the full paper, prepared with AI and checked against the text. Each point links to the authors' own words.

  1. Why it matters

    • Stroke is the most frequent and important neurologic disease in adult life, representing up to 20% of all central nervous system disorders in urban India. View evidence ↗

      Why it matters

      Stroke is the most frequent and important neurologic disease in adult life, representing up to 20% of all central nervous system disorders in urban India.

      In the paper's own words

      “Among all the neurologic diseases of adult life, the stroke clearly rank first in frequency and importance accounting upto 20% of all central nervous system disorders, in the urban sectors of India.”

      Page 1

      Found in: Introduction

      Read it in the full textOpen PDF at page 1 ↗
    • Recent research suggests that postprandial triglyceride levels may be more strongly associated with metabolic syndrome and cardiovascular events than fasting triglyceride levels. View evidence ↗

      Why it matters

      Recent research suggests that postprandial triglyceride levels may be more strongly associated with metabolic syndrome and cardiovascular events than fasting triglyceride levels.

      In the paper's own words

      “Recent studies indicate postprandial triglyceride (TG) had a better association with cardiovascular events and metabolic syndrome than fasting TG.”

      Page 1

      Found in: Introduction

      Read it in the full textOpen PDF at page 1 ↗
    • Because humans spend the majority of their time in a postprandial state, their arteries are primarily exposed to postprandial plasma. View evidence ↗

      Why it matters

      Because humans spend the majority of their time in a postprandial state, their arteries are primarily exposed to postprandial plasma.

      In the paper's own words

      “Humans spend most of their time in a postprandial state, not in a fasting state, and their arteries are thus exposed to postprandial plasma most of the time.”

      Page 1

      Found in: Introduction

      Read it in the full textOpen PDF at page 1 ↗
  2. The question

    • The study aimed to determine if fasting and postprandial serum triglyceride (TG) levels could predict the severity of stroke upon admission. View evidence ↗

      The question

      The study aimed to determine if fasting and postprandial serum triglyceride (TG) levels could predict the severity of stroke upon admission.

      In the paper's own words

      “The aim of this study is to investigate if serum TG levels predict stroke severity on admission with correlation of fasting and post-prandial serum TG levels”

      Page 1

      Found in: Introduction

      Read it in the full textOpen PDF at page 1 ↗
  3. What they did

    • Stroke severity was measured using the Scandinavian Stroke Scale (SSS), with patients categorized as having severe stroke (SSS ≤ 25) or mild/moderate stroke (SSS > 25). View evidence ↗

      What they did

      Stroke severity was measured using the Scandinavian Stroke Scale (SSS), with patients categorized as having severe stroke (SSS ≤ 25) or mild/moderate stroke (SSS > 25).

      In the paper's own words

      “Stroke severity on admission was assessed using Scandinavian stroke scale (SSS). The patients were divided into 2 groups: those with severe stroke (SSS ≤ 25) and those with mild/moderate stroke (SSS >25).”

      Page 2

      Found in: Method of Collection of Data

      Read it in the full textOpen PDF at page 2 ↗
    • Fasting and postprandial serum triglyceride levels were measured using commercial kits between 12 and 36 hours after the onset of the stroke. View evidence ↗

      What they did

      Fasting and postprandial serum triglyceride levels were measured using commercial kits between 12 and 36 hours after the onset of the stroke.

      In the paper's own words

      “fasting serum triglyceride level and post prandial serum triglyceride level were measured between 12 and 36 hours after stroke onset using commercially available kits.”

      Page 2

      Found in: Method of Collection of Data

      Read it in the full textOpen PDF at page 2 ↗
    • Hypertriglyceridemia was defined as a triglyceride level greater than 2.3 mmol/l. View evidence ↗

      What they did

      Hypertriglyceridemia was defined as a triglyceride level greater than 2.3 mmol/l.

      In the paper's own words

      “Hypertriglyceridemia was diagnosed if TG >2.3mmol/l.”

      Page 2

      Found in: Method of Collection of Data

      Read it in the full textOpen PDF at page 2 ↗
  4. What they found

    • There was no statistically significant association (at the 5% level) between fasting triglyceride (FTG) or postprandial triglyceride (PPTG) levels and stroke severity as measured by the SSS. View evidence ↗

      What they found

      There was no statistically significant association (at the 5% level) between fasting triglyceride (FTG) or postprandial triglyceride (PPTG) levels and stroke severity as measured by the SSS.

      In the paper's own words

      “In the present study, there is no association between FTG & PPTG Level and SSS at 5% level of significance.”

      Page 2

      Found in: Fasting & post prandial triglycerides levels and severity of stroke

      Read it in the full textOpen PDF at page 2 ↗
    • A statistically significant association (at the 5% level) was found between postprandial triglyceride (PPTG) levels and hypertension. View evidence ↗

      What they found

      A statistically significant association (at the 5% level) was found between postprandial triglyceride (PPTG) levels and hypertension.

      In the paper's own words

      “There is an association between PPTG Level and hypertension (HTN) at 5% level of significance.”

      Page 3

      Found in: Hypertension and Triglyceride Levels

      Read it in the full textOpen PDF at page 3 ↗
    • While fasting triglyceride (FTG) levels were not influenced by age, sex, ischemic heart disease (IHD), or hypertension, postprandial triglyceride (PPTG) levels were influenced by hypertension. View evidence ↗

      What they found

      While fasting triglyceride (FTG) levels were not influenced by age, sex, ischemic heart disease (IHD), or hypertension, postprandial triglyceride (PPTG) levels were influenced by hypertension.

      In the paper's own words

      “The levels of serum FTG were not influenced by hypertension, IHD, age and sex of an individual but the level of serum PPTG were influenced by HTN.”

      Page 1

      Found in: Fasting & post prandial triglycerides levels and severity of stroke

      Read it in the full textOpen PDF at page 1 ↗
    • No statistically significant association was observed between the sex of the individual and either fasting or postprandial triglyceride levels. View evidence ↗

      What they found

      No statistically significant association was observed between the sex of the individual and either fasting or postprandial triglyceride levels.

      In the paper's own words

      “In the present study, there is no association between FTG & PPTG Level and Sex of an individual at 5% level of significance.”

      Page 3

      Found in: Age and fasting & post prandial triglyceride levels

      Read it in the full textOpen PDF at page 3 ↗
    • No statistically significant association was found between age and either fasting or postprandial triglyceride levels. View evidence ↗

      What they found

      No statistically significant association was found between age and either fasting or postprandial triglyceride levels.

      In the paper's own words

      “From the results there is no association between FTG & PPTG Level and age at 5% level of significance.”

      Page 3

      Found in: Fasting & post prandial triglycerides levels and severity of stroke

      Read it in the full textOpen PDF at page 3 ↗
  5. What it means

    • The authors conclude that postprandial serum triglyceride levels should be measured when assessing stroke severity. View evidence ↗

      What it means

      The authors conclude that postprandial serum triglyceride levels should be measured when assessing stroke severity.

      In the paper's own words

      “we conclude that post prandial serum triglyceride level should also be measured to assess the severity of stroke.”

      Page 4

      Found in: Conclusion

      Read it in the full textOpen PDF at page 4 ↗
    • Because patients with hypertension showed higher postprandial triglyceride values and an increased risk for stroke, the authors recommend encouraging dietary and lifestyle modifications. View evidence ↗

      What it means

      Because patients with hypertension showed higher postprandial triglyceride values and an increased risk for stroke, the authors recommend encouraging dietary and lifestyle modifications.

      In the paper's own words

      “In this study patients with HTN have higher PPTG value and has increased risk for stroke. So dietary and lifestyle modifications should be encouraged.”

      Page 4

      Found in: Conclusion

      Read it in the full textOpen PDF at page 4 ↗

Visual summary

3 visuals

Illustrations explain the paper; charts are replotted from the paper's own table values.

AI-generated illustration
AI-generated conceptual illustration (human brain and blood vessels). It explains the idea and does not show study data.↗ Enlarge
Study Variable Relationship Map
AI-generated conceptual illustration (human brain and blood vessels). It explains the idea and does not show study data.

AI-generated conceptual illustration (human brain and blood vessels). It explains the idea and does not show study data.

Open full-size image ↗

Study Variable Relationship Map

AI-generated conceptual illustration (human brain and blood vessels). It explains the idea and does not show study data.

View source evidence ↗
Replotted from source data
Replotted from Table 11 (page 3) of the original paper. Every bar is the paper's own table value.↗ Enlarge
<2.3 and >2.3: No vs Yes
Replotted from Table 11 (page 3) of the original paper. Every bar is the paper's own table value.

Replotted from Table 11 (page 3) of the original paper. Every bar is the paper's own table value.

Open full-size image ↗

<2.3 and >2.3: No vs Yes

Replotted from Table 11 (page 3) of the original paper. Every bar is the paper's own table value.

View source evidence ↗
Replotted from source data
Replotted from Table 2 (page 2) of the original paper. Every bar is the paper's own table value.↗ Enlarge
≤25 and >25: ≤2.3 vs >2.3
Replotted from Table 2 (page 2) of the original paper. Every bar is the paper's own table value.

Replotted from Table 2 (page 2) of the original paper. Every bar is the paper's own table value.

Open full-size image ↗

≤25 and >25: ≤2.3 vs >2.3

Replotted from Table 2 (page 2) of the original paper. Every bar is the paper's own table value.

View source evidence ↗

Figures & tables

From the original paper
Association between Age and SSSTable 1Page 2Association between FTG and SSSTable 2Page 2Association between PPTG and SSSTable 3Page 2Association between FTG Level and ageTable 4Page 2Association between PPTG Level and ageTable 5Page 3Association between PPTG Level and HTNTable 11Page 3Association between IHD and SSSTable 12Page 3Association between SEX and SSSTable 6Page 3Association between FTG Level and IHDTable 13Page 3Association between F TG Level and Sex of an individualTable 7Page 3Association between PPTG Level and IHDTable 14Page 3Association between PP TG Level and Sex of anTable 8Page 3Association between HTN and SSSTable 9Page 3Association between FTG Level and HTNTable 10Page 3Shows the Study population and FTGTable 15Page 4
FULL TEXT Original article · reflowed for reading

Introduction

Among all the neurologic diseases of adult life, the stroke clearly rank first in frequency and importance accounting upto 20% of all central nervous system disorders, in the urban sectors of India. Stroke is defined as an abrupt neurologic deficit that is attributable to focal vascular cause. Risk factors for stroke include hypertension, carotid stenosis, atrial myxomas, smoking, hyperlipidemia, diabetes, myocardial infarction and atrial fibrillation. The link between hyperlipidemia and stroke, was more difficult to establish. The difficulty arose in part because of the heterogeneous nature of stroke. To investigate a possible etiologic relationship between hyperlipidemia and stroke, it became essential to distinguish ischemic from hemorrhagic stroke. It now appears likely that hyperlipidemia is an independent risk factor for ischemic stroke. Humans spend most of their time in a postprandial state, not in a fasting state, and their arteries are thus exposed to postprandial plasma most of the time. One would thus surmise that postprandial lipid values would correlate better with prognosis than fasting values.

Postprandial TG has been suggested as an independent risk factor for cardiovascular disease (CVD) in healthy subjects [1][2][3] . Several studies support the hypothesis postprandial TG is correlated with carotid IMT and waist circumference (WC), and furthermore superior to fasting TG in association with metabolic syndrome [4][5][6] . However, the potential effects of postprandial hypertriglyceridemia on the development of atherosclerosis are still controversial in subjects with type 2 diabetes (T2D) [7] . This study is undertaken to correlate fasting and postprandial serum triglyceride levels with severity of stroke as measured by Scandinavian stroke scale.

Materials and Methods

Materials and Methods

Source of Data

Eighty consecutive patients presenting with acute ischemic stroke, occurring within 24 hours, confirmed by CT scan admitted in Bhaskar Medical College & General Hospital from January 2018 to June 2019 were included in this study and in each patient fasting and post prandial serum TG levels were estimated.

Inclusion Criteria

Patients with first attack of ischemic stroke occurring within 24 hours, confirmed by CT scan, admitted to Bhaskar Medical College, RR District, Telangana, India.

Exclusion Criteria

Patients admitted to the hospital >24 hours after stroke onset. Previous history of stroke. Previous history of transient ischemic attack. Haemorrhagic stroke. Patients with space occupying lesions. Patients with CVT.

Method of Collection of Data

A CT scan head (MRI brain where required) was taken within 24 hours after stroke onset for all patients with first ever stroke admitted in Bhaskar Medical College and hospital. Stroke severity on admission was assessed using Scandinavian stroke scale (SSS). The patients were divided into 2 groups: those with severe stroke (SSS ≤ 25) and those with mild/moderate stroke (SSS >25). Arterial hypertension was diagnosed when at least 2 readings of blood pressure were ≥ 140 mm Hg (systolic) or ≥ 90mm Hg (diastolic) after the acute phase of stroke. Ischemic heart disease was diagnosed when a history of angina pectoris or myocardial infarction was present. In addition to routine investigations as per standard protocol in the evaluation of stroke patient, fasting serum triglyceride level and post prandial serum triglyceride level were measured between 12 and 36 hours after stroke onset using commercially available kits. Hypertriglyceridemia was diagnosed if TG >2.3mmol/l. Patients were followed up till they were discharged from the hospital.

Parameters

The following parameters were tested 1) Age 2) Sex

3) Hypertension 4) IHD

3) Hypertension 4) IHD

Statistical Methods

1. Descriptive statistical analysis has been carried out in the present study. Significance is assessed at 5% level of significance.

Procedure

A detailed history, clinical examination and relevant laboratory investigations were done as per proforma.

Fasting serum triglyceride levels and post prandial serum triglyceride levels were estimated in patients, quantitatively by GPO-TRINDER method based on the method of Wako and the modifications by McGOWAN et al. [8] .

The kit used was Triglycerides Kit: Ortho Clinical Diagnostics Rochester, NY, USA.

Results

The following tables show association between the fasting & post prandial triglyceride levels and severity of stroke based on SSS scale and their influence based on risk factorsage, sex, hypertension, IHD.

Discussion

Discussion

Fasting & post prandial triglycerides levels and severity of stroke

The present study involved 80 patients of acute ischemic stroke. Serum triglyceride levels are generally increased for 3-6 h after a meal [9] . Once postprandial hypertriglyceridemia occurs, it is exacerbated by the next meal and persists for the entire day. The most common pattern of dyslipidemia in type 2 diabetic patients is elevation of triglyceride levels and a decrease in HDL cholesterol levels. Therefore, measuring postprandial values for evaluation of hypertriglyceridemia in patients with diabetes is important. However, to our knowledge, the association between postprandial triglyceride (PPTG) levels and atherosclerosis has not been investigated. One would thus surmise that postprandial lipid values would correlate better with Prognosis than fasting values. This has indeed been shown in recent epidemiologic studies. Bansal and colleagues [10] analyzed the prognostic value of fasting and nonfasting triglyceride levels in a cohort of 26,509

healthy women enrolled in the Women's Health Study. After 11.4 years of follow-up, PPTG but not fasting Triglycerides in the upper tertile of the distribution were associated with an almost 2-fold increase in cardiovascular disease even after adjustment for age, blood pressure, smoking, use of hormone therapy, total and high-density lipoprotein cholesterol, diabetes mellitus, body mass index, and highsensitivity C-reactive protein.

It is important, however, not to dismiss triglyceride elevations in individuals who forget to fast for their regular blood draw. Such an elevation should prompt discussion with the patient about the link between such triglyceride elevations and insulin resistance, future cardiovascular disease, and the importance of lifestyle modifications (quality and quantity of food, weight management, physical activity) [11] .

Postprandial remnant particles of triglyceride-rich lipoproteins have also been found to be an independent risk factor for early atherosclerosis and may be responsible for the increased rate of carotid intima-media thickness in these subjects. The difference in the results of these studies may be related to measurement of triglycerides in the fasting versus postprandial state. Hypertriglyceridemia may also contribute to cerebrovascular disease through its effects on thrombosis. This effect is produced by thrombogenic alterations of the coagulation system as well as elevations in plasma viscosity. Previous study reported that 18 patients with severe hypertriglyceridemia (mean fasting plasma triglyceride level 504.4 mg/dl) had higher concentrations of plasma fibrinogen, lower fibrinolytic activity and higher levels of clotting factor Xc compared to normolipidemic controls [11] . Several studies have not found triglycerides to be an independent risk factor for IS [12] . For example, Bowman et al. [12] Conducted a prospective, randomized, nested casecontrol study among patients from the Physician Health Study, which included 296 fatal and nonfatal IS in white male physicians and an equal number of controls. Another study consisting of 121 consecutive acute ischemic stroke patients showed that a higher (≥1.70 mmol/l) fasting serum triglyceride level (within 24h after admission) was associated with a lower infarct volume (p = 0.014) [13] . The biological mechanism responsible for association between TG level and stroke severity is unknown. Low TG level may reflect poor nutritional status of the patient. [15] and others 863 patients 1.4 ± 0.6 1.7 ± 1.3

In both the studies, the level of serum triglyceride was lower in patients with severe stroke as compared to the levels in mild/moderate stroke patients, which was statistically not significant.

Age and fasting & post prandial triglyceride levels

Triglycerides increase gradually in men until about age 50 years and then decline slightly but in women, they continue to increase with age. The prevalence of mild hypertriglyceridemia is slightly more in men beginning at age 30 years and women starting at age 60 years. Fasting triglycerides gradually increase in age<65 years and severity of stroke is less (SSS<25). Post-prandial triglycerides gradually increase in age<65 years and severity of stroke is more when compared to age >65 years. The present study did not show any statistically significant association between FTG & PPTG Level and age. However, in the present study no statistically significant association between FTG & PPTG level and sex of an individual could be noticed.

IHD and Triglyceride Levels

The role of triglycerides as a risk factor of ischemic heart disease (IHD) remains controversial. In the Copenhagen Male Study on 2906 white men who were initially free of overt cardiovascular disease, an 8-year follow-up period showed that a clear gradient of risk of IHD was found with increasing triglyceride levels within each level of HDL cholesterol, including high HDL cholesterol levels, which are thought to provide protection against IHD. However, the present study did not show any significant association between FTG & PPTG Level and IHD.

Hypertension and Triglyceride Levels

Essential hypertension is frequently associated with metabolic abnormalities including glucose intolerance, hypertriglyceridemia and enhanced postprandial lipemia [14] . In this study there is statistically significant association between PPTG level and hypertension.

Conclusion

In this study, based on our review of the existing evidence, we conclude that post prandial serum triglyceride level should also be measured to assess the severity of stroke. In this study patients with HTN have higher PPTG value and has increased risk for stroke. So dietary and lifestyle modifications should be encouraged. To assess the benefit of pharmacologic and dietary TG reduction with respect to primary and secondary prevention of ischemic stroke.

Acknowledgement

AcknowledgmentThe author thankful to management of Bhaskar Medical College & General Hospital for providing all the facilities to carry out this work.

Figures and tables from the paper

Table 1. Association between Age and SSS
SSS—————
AGE AGE≤25>25TotalX2 Value
≤651540550.133
>65131225
Total285280

Table text extracted from the original PDF; superscript letters are shown inline. The original table image is below.

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Table 1
Association between Age and SSS

Association between Age and SSS

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Original paper tableSource PDF · page 2 ↗
Table 2. Association between FTG and SSS
SSS—————
FTG≤25>25TotalX2 Value
≤2.31550790.647
>2.351021
Total206080

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Table 2
Association between FTG and SSS

Association between FTG and SSS

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Original paper tableSource PDF · page 2 ↗
Table 3. Association between PPTG and SSS
SSS—————
PPTG≤25>25TotalX2 Value
≤2.3934430.548
>2.3122537
Total215980

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Table 3
Association between PPTG and SSS

Association between PPTG and SSS

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Table 4. Association between FTG Level and age
FTG Level (mmol/l)—————
Age<2.3>2.3TotalX2 Value
<654210520.827
>6523528
Total651580

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Table 4
Association between FTG Level and age

Association between FTG Level and age

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Table 5. Association between PPTG Level and age
PPTG Level (mmol/l)—————
Age<2.3>2.3TotalX2 Value
<652528530.231
>65151227
Total404080

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Table 5
Association between PPTG Level and age

Association between PPTG Level and age

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Table 11. Association between PPTG Level and HTN
PPTG Level (mmol/l)—————
HTN<2.3>2.3TotalX2 Value
No2511360.031
Yes192544
Total443680

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Table 11
Association between PPTG Level and HTN

Association between PPTG Level and HTN

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Table 12. Association between IHD and SSS
Association between IHD and SSS↗ Enlarge
Table 12
Association between IHD and SSS

Association between IHD and SSS

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Table 6. Association between SEX and SSS
Association between SEX and SSS↗ Enlarge
Table 6
Association between SEX and SSS

Association between SEX and SSS

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Table 13. Association between FTG Level and IHD
FTG Level (mmol/l)—————
IHD<2.3>2.3TotalX2 Value
No5014640.245
Yes12416
Total621880

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Table 13
Association between FTG Level and IHD

Association between FTG Level and IHD

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Table 7. Association between F TG Level and Sex of an individual
FTG Level (mmol/l)—————
Sex<2.3>2.3TotalX2 Value
Male4212540.857
Female18826
Total602080

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Table 7
Association between F TG Level and Sex of an individual

Association between F TG Level and Sex of an individual

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Table 14. Association between PPTG Level and IHD
PPTG Level (mmol/l)—————
IHD<2.3>2.3TotalX2 Value
No3034640.645
Yes8816
Total384280

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Table 14
Association between PPTG Level and IHD

Association between PPTG Level and IHD

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Table 8. Association between PP TG Level and Sex of an
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Table 8
Association between PP TG Level and Sex of an

Association between PP TG Level and Sex of an

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Table 9. Association between HTN and SSS
SSS—————
HTN≤25>25TotalX2 Value
No1224360.648
Yes133144
Total255580

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Table 9
Association between HTN and SSS

Association between HTN and SSS

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Table 10. Association between FTG Level and HTN
FTG Level (mmol/l)—————
HTN<2.3>2.3TotalX2 Value
No306360.645
Yes321244
Total621880

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Table 10
Association between FTG Level and HTN

Association between FTG Level and HTN

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Table 15. Shows the Study population and FTG
Shows the Study population and FTG↗ Enlarge
Table 15
Shows the Study population and FTG

Shows the Study population and FTG

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Original paper figureSource PDF · page 4 ↗

References

15 in the original paper
  1. Stalenhoef AF, De Graaf J. Association of fasting and nonfasting serum triglycerides with cardiovascular disease and the role of remnant-like lipoproteins and small dense LDL. Curr Opin Lipidol. 2008; 19:355-61.
  2. Bansal S, Buring JE, Rifai N, Mora S, Sacks FM, Ridker PM. Fasting compared with nonfasting triglycerides and risk of cardiovascular events in women. JAMA. 2007; 298:309-16.
  3. Nordestgaard BG, Benn M, Schnohr P, Tybjaerg-Hansen A. Nonfasting triglycerides and risk of myocardial infarction, ischemic heart disease, and death in men and women. JAMA. 2007; 298:299-308.
  4. Ryu JE, Howard G, Craven TE, Bond MG, Hagaman AP, Crouse JR. 3rd. Postprandial triglyceridemia and International Journal of Advanced Biochemistry Research http://www.biochemjournal.com carotid atherosclerosis in middle-aged subjects. Stroke 1992; 23:823-8.
  5. Oka R, Kobayashi J, Miura K, Nagasawa S, Moriuchi T, Hifumi S et al. Difference between fasting and nonfasting triglyceridemia: the influence of waist circumference. J Atheroscler Thromb. 2009; 16:633-40.
  6. Rector RS, Linden MA, Zhang JQ, Warner SO, Altena TS, Smith BK et al. Predicting postprandial lipemia in healthy adults and in at-risk individuals with components of the cardio metabolic syndrome. J Clin. Hypertens (Greenwich). 2009; 11:663-71.
  7. Enkhmaa B, Ozturk Z, Anuurad E, Berglund L. Postprandial lipoproteins and cardiovascular disease risk in diabetes mellitus. Curr Diab Rep. 2010; 10:61-9.
  8. Gowenlock AH. Lipids and lipoproteins; Varley's practical clinical biochemistry. 6th Edn. New Delhi: CBS publishers and distributors, 1988, 464-466.
  9. Bjorkegren J, Karpe F, Milne RW, Hamsten A. Differences in apolipoprotein and lipid composition between human chylomicron remnants and very low density lipopro-teins isolated from fasting and postprandial plasma. J Lipid Res. 1998; 39:1412-1420.
  10. Bansal S, Buring JE, Rifai N, Mora S, Sacks FM, Ridker PM. Fasting compared with nonfasting triglycerides and risk of cardiovascular events in women. JAMA. 2007; 298:309-316.
  11. National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). Third report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report. Circulation. 2002; 106:3143-3421.
  12. Hackman A, Abe Y, Insull W Jr, Pownall H, Smith L, Dunn K et al. Levels of soluble cell adhesion molecules in patients with dyslipidemia. Circulation. 1996; 93:1334-1338.
  13. Pikija S, Milevcić D, Trkulja V, Kidemet-Piskac S, Pavlicek I, Sokol N. Higher serum triglyceride level in patients with acute ischemic stroke is associated with lower infarct volume on CT brain scans. Eur. Neurol. 2006; 55(2):89-92.
  14. Venkatesan A, Hemalatha A, Zachariah B, Selvaraj N, Sathiyapriya. Effect of smoking on lipid profile and lipid peroxidation in normal subjects. Indian J Physiol Pharmacol. 2006; 50(3):273-278.
  15. Tomasz D, Agnieszka S, Elzbieta AG, Szczudlik A. Lower serum triglyceride level is associated with increased stroke severity. Stroke. 2004; 35:e151-e152.