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Table of Contents
ORIGINAL ARTICLE
Year : 2019  |  Volume : 9  |  Issue : 2  |  Page : 95-99

Role of Vitamin D deficiency among patients with acute coronary syndrome


Department of Cardiology, Faculty of Medicine, Zagazig University, Zagazig, Egypt

Date of Web Publication23-Sep-2019

Correspondence Address:
Dr. Ahmed Shawky Shereef
Department of Cardiology, Faculty of Medicine, Zagazig University, Zagazig
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/JICC.JICC_22_19

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  Abstract 


Background: Previous studies demonstrated that low Vitamin D levels are associated with hypertension, obesity, dyslipidemia, and diabetes mellitus, reflecting an increased cardiovascular (CV) risk burden. However, high levels can be associated with increased total and CV mortality. Hence, we aimed to evaluate the prevalence of Vitamin D deficiency and if it has a role in the occurrence of acute coronary syndrome (ACS). Patients and Methods: This study was carried out on 71 patients presented with ACS, undergoing coronary angiography at the cardiology department, Zagazig university hospitals. Exclusion Criteria: Disorders causing Vitamin D deficiency. Methods: All our patients were subjected to (1) careful history-taking; (2) thorough clinical examination; (3) resting electrocardiogram; (4) routine laboratory investigations beside thyroid, parathyroid hormone, Mg, Ph, and Vitamin D levels; (5) echocardiography; and (6) coronary angiography. Results: In the present study, receiver-operating characteristic curve analysis shows that the serum Vitamin D has a cutoff value ≤41.5 nm/L to predict ACS with 94.4% sensitivity and 83% specificity, a cutoff value ≤41.5 nm/L to predict unstable angina with 97.3% sensitivity and 83% specificity a cutoff value ≤52.625 nm/L to predict ST-elevation myocardial infarction (STEMI) with 100% sensitivity and 76.6% specificity, and a cutoff value ≤41 nm/L to predict non-STEMI with 100% sensitivity and 83% specificity. Conclusion and Recommendations: Vitamin D deficiency and insufficiency are common in patients with ACS. Further, larger multicenter studies are needed to assess Vitamin D level in ACS patients and to investigate its relationship with long term prognosis.

Keywords: Acute coronary syndrome, Vitamin D deficiency, unstable angina, STEMI, NSTEMI


How to cite this article:
Shereef AS, Kandeel NT. Role of Vitamin D deficiency among patients with acute coronary syndrome. J Indian coll cardiol 2019;9:95-9

How to cite this URL:
Shereef AS, Kandeel NT. Role of Vitamin D deficiency among patients with acute coronary syndrome. J Indian coll cardiol [serial online] 2019 [cited 2019 Oct 22];9:95-9. Available from: http://www.joicc.org/text.asp?2019/9/2/95/267490




  Introduction Top


Vitamin D and polyunsaturated fatty acids have been found to be inversely related to cardiovascular disease. Low Vitamin D levels have been associated with hypertension, obesity, dyslipidemia, and diabetes mellitus, reflecting an increased CV risk burden. However, high levels can be associated with increased total and CV mortality, as described by a U-shape or reverse J-curve.[1] Naesgaard et al. in 2013[2] have shown that 2–5-year total and cardiac mortality is decreased in the highest as compared to the lowest quartile of Vitamin D in a coronary chest pain population living at altitudes exceeding 1000 m in Subtropical Northern Argentina, and this relationship is stronger in females than in males. Hence, we aimed to evaluate the prevalence of Vitamin D deficiency and if it has a role in the occurrence of acute coronary syndrome (ACS).


  Patients and Methods Top


This cross-sectional study was conducted on 71 patients who are presented with ACS, undergoing coronary angiography at the Cardiology Department at Zagazig University Hospitals between August 30, 2017, and March 30, 2018, to evaluate the prevalence of Vitamin D deficiency and its role in ACS patients.

Exclusion criteria

Disorders causing Vitamin D deficiency (cystic fibrosis, celiac disease, Whipple's disease, Crohn's disease, liver failure, nephrotic syndrome, chronic kidney disease, hyperphosphatemia, rickets, tumor-induced osteomalacia, primary hyperparathyroidism, hyperthyroidism, sarcoidosis, and tuberculosis).

Methods

All patients in the study were subjected to the following:

  • Detailed history-taking
  • Careful clinical assessment
  • Resting electrocardiogram (ECG) data analysis: A 12-lead resting ECG was performed on admission and ECG monitoring was also done. All ECGs were viewed for evidence of ischemia, infarction, or any abnormality, serial ECG tracing was recorded, and continuous ECG monitoring was conducted during stay in the cardiac care unit, patients were divided into three groups: ST-elevation myocardial infarction (STEMI), non-STEMI, and unstable angina (UA)
  • Laboratory investigations including lipid profile, liver function test (SGOT, SGPT, GGT, direct and indirect bilirubin), complete and differential blood count, serum creatinine, serum electrolytes (Na, K, Ca, Mg, and P) troponin, thyroid functions, and parathyroid hormone level
  • Bedside screening ECHO was done with special attention given to measure left ventricular end systolic and diastolic diameters (LVESD, LVEDD), ejection fraction (EF)by modified Simpson method and resting wall motion abnormalities
  • Coronary angiography: Quantitative coronary angiography was performed using the Judkin's technique and interpreted by two experienced interventional cardiologists unaware of the clinical and laboratory results of the patients. Significant CAD was defined as >50% stenosis in the left main and >70% in other coronaries, at least one coronary artery. Each coronary lesion producing a ≥50% luminal obstruction in vessels ≥1.5 mm was separately scored and added to provide the vessel SYNTAX score (SX)
  • Measurement of Vitamin D using commercial enzyme-linked immunosorbent assay kits
  • Expected values:


    • Normal range: 25(OH) D was defined as 76–100 nm/L
    • Insufficiency: 25(OH) D was defined as 51–75 nm/L
    • Deficiency: 25(OH) D was defined as a50 nm/L.[3]


Ethical considerations

All the participants were requested to sign written informed consent regarding the procedure according to the study protocol, and no harm to the patients would be allowed.


  Results Top


Our study was performed in the Cardiology Department at Zagazig University Hospitals. We recruited 71 patients with ACS who had been admitted to our Cath Laboratory for coronary angiography.

We found the following results:

[Table 1] and [Figure 1] show that 41 (57.75%) patients had Vitamin D deficiency, 17 (23.94%) patients had a normal Vitamin D level, and 13 (18.31%) patients had Vitamin D insufficiency out of total samples.
Table 1: The distribution of Vitamin D among our studied population

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Figure 1: Vitamin D among the studied population

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[Table 2] shows the clinical presentation of our patients sample, we found 37 (52.1%) had UA, 19 (26.8%) had STEMI, 15 (21.1%) had NSTEMI.
Table 2: Clinical presentation of the studied population

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[Table 3] and [Figure 2] show the relationship between Vitamin D level and studied population subgroups and we found that the mean value of Vitamin D according to subgroups of ACS (unstable, STEMI and NSTEMI) was 21.80, 22.54, and 17.69, respectively; there was no statistically significant difference between ACS subgroups regarding Vitamin D level (P > 0.05).
Table 3: Relationship between Vitamin D level and studied subgroups

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Figure 2: Vitamin D level in studied population subgroups

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The receiver-operating characteristic (ROC) curve analysis in [Table 4] and [Figure 3] shows that the serum Vitamin D has the best cutoff value to predict ACS if it is ≤41.5 nm/L with 94.4% sensitivity and 83% specificity.
Table 4: Receiver operating characteristic curve for Vitamin D in acute coronary syndrome patients

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Figure 3: Receiver operating characteristic curve for Vitamin D in acute coronary syndrome patients

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The ROC curve analysis in [Table 5] and [Figure 4] shows that the serum Vitamin D has the best cutoff value to predict UA if it is ≤41.5 nm/L with 97.3% sensitivity and 83% specificity.
Table 5: Receiver operating characteristic curve for Vitamin D in unstable angina patients

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Figure 4: Receiver operating characteristic curve for Vitamin D in unstable angina patients

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The ROC curve analysis in [Table 6] and [Figure 5] shows that the serum Vitamin D has the best cutoff value to predict STEMI if it is ≤52.625 nm/L with 100% sensitivity and 76.6% specificity.
Table 6: Receiver operating characteristic curve for Vitamin D in ST-elevation myocardial infarction patients

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Figure 5: Receiver operating characteristic curve for Vitamin D in ST-elevation myocardial infarction patients

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The ROC curve analysis in [Table 7] and [Figure 6] shows that the serum Vitamin D has the best cutoff value to predict NSTEMI if it is ≤41 nm/L with 100% sensitivity and 83% specificity.
Table 7: Receiver operating characteristic curve for vitamin D in non-ST-elevation myocardial infarction patients

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Figure 6: Receiver operating characteristic curve for Vitamin D in non-ST-elevation myocardial infarction patients

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We classified our patients according to the troponin into two groups: Group 1 (positive troponin) and Group 2 (negative troponin). In [Table 8], we found the mean value of Vitamin D in Group 1 was 20.41 ± 11.96 and the mean value of Vitamin D in Group 2 was 21.8 ± 11. There is no statistically significant difference between both groups regarding Vitamin D (P > 0.05).
Table 8: The relation between Vitamin D and troponin

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[Table 9] shows the correlation between Vitamin D and both SX and EF, and we found that there is no statistically significant correlation between Vitamin D and both SX and EF (P > 0.05).
Table 9: Correlation between Vitamin D and both syntax score and ejection fraction

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  Discussion Top


This cross-sectional study was conducted to evaluate the role of Vitamin D in ACS.

It was carried out in the Cardiology Department at Zagazig University Hospitals on 71 patients who presented with ACS, undergoing coronary angiography.

The majority of the patients (76.06) were either Vitamin D deficient (57.75%) or insufficient (18.31%); similarly, Naesgaard et al.[2] confirmed high Vitamin D deficiency among ACS patients.

Luis et al. in 2013[4] confirmed high Vitamin D deficiency among ACS patients (98%). In addition, Karur et al. in 2014[5] stated that 67.5% of the patients enrolled in their study were 25-hydroxy-vitamin D deficient and 16% insufficient for a total of 83.5% of patients with abnormally low 25-vitamin-D level. In our study, there was no statistically significant difference between ACS subgroups (UA, STEMI, and NSTEMI) regarding Vitamin D level.

Litvac et al. in 2011[6] evaluated the association between serum Vitamin D levels and ACS. They concluded that hypovitaminosis D is associated with increased risk for ACS, even after adjustment for traditional risk factors for IHD. There is an association between hypovitaminosis D and NSTEMI rather than with UA or STEMI patients.

In our study, ROC curve analysis showed that serum Vitamin D has the best cutoff value to predict ACS if it is ≤41.5 nm/L with 94.4% sensitivity and 83% specificity. It has the best cutoff value to predict UA if it is ≤41.5 nm/L with 97.3% sensitivity and 83% specificity. Furthermore, it has the best cutoff value to predict STEMI if it is ≤52.6 nm/L with 100% sensitivity and 76.6% specificity and has the best cutoff value to predict NSTEMI if it is ≤41 nm/L with 100% sensitivity and 83% specificity.

DeLuca in 2004[7] found that there is a wide distribution of Vitamin D receptors in the CV system, gastrointestinal tract, muscles, endocrine system, and others; hence, Vitamin D deficiency could participate in the pathogenesis of many diseases including vascular disorders.

Satish et al. in 2014[7] stated that no significant heterogeneity was observed between age or gender subgroups; however, 25(OH) D deficiencies were more commonly seen in those with lower socioeconomic status, lower activity levels, hypercholesterolemia, and hypertriglyceridemia. They also noted that Vitamin D level is lower in diabetic patients.

Wang et al. in 2008[8] evidenced that Vitamin D deficiency is associated with atherosclerosis and CV adverse events in the general population. In prospective Framingham offspring study, Vitamin D deficiency was associated with incident CV first event.

Timms et al. in 2003[9] found that Vitamin D status was the sole determinant of circulating MMP9 (inversely) and an independent determinant of CRP (inversely). Vitamin-D insufficiency is associated with increased circulating MMP2,9 and CRP, Significant reductions in MMP9 (-68%), TIMP-1 (-38%) and CRP (-23%) concentrations followed vitamin-D supplementation.

Dror et al. in 2013[10] examined the safe limits of Vitamin D blood levels and the cutoff points, below and above which the risk for mortality or ACS rises. They concluded that Vitamin D in the 20–36 ng/mL range was associated with the lowest risk for mortality and morbidity. The hazard ratio below and above this range increases significantly.

De Metrio et al. in 2015[11] determined the clinical implications of 25(OH) D levels in an unselected cohort of ACS patients at hospital admission, and their possible association with in-hospital and 1-year morbidity and mortality. They demonstrated the presence of an association between Vitamin D deficiency and poor in-hospital and 1-year outcomes in patients with ACS. The correction of Vitamin D deficiency and maintenance of an optimal status may be a promising approach for acute treatment and secondary prevention of ACS.

Gondim et al. in 2016[12] measured Vitamin D status (serum 25-OHD concentration) in diabetic patients with ACS and its association with the severity of the disease. They concluded that Vitamin D deficiency is associated with more severe ACS and is a predictor of more extensive coronary lesions in patients with T2DM.

Regarding SX, in our study, we found that there was no statistically significant correlation between Vitamin D and SX and this is not compatible with Baktır et al. in 2017,[13] who found that 25(OH) D levels are significantly lower in the group with a high SX than in the group with a low SX, and this difference may be due to our patients were relatively younger (mean age 55 ± 9 vs. 63 ± 3 years); our sample was smaller (113 vs. 71 patients) beside that he did not include patients with UA in his sample.

Limitations of the study

  • On top of the small size of our sample, we could not control multiple confounders such as sun exposure and social status. Vitamin D level may decrease in acute illnesses (as reflected by the high level of CRP and low serum albumin)
  • 25(OH) D levels were measured only once on admission. This single measurement may not reflect the Vitamin D status for a lifetime.



  Conclusion and Recommendations Top


Vitamin D deficiency and insufficiency are common in patients with ACS but has no role in its severity, and this may be explained as:

The role of hypovitaminosis-D is in the development of atherosclerosis, so we recommend for further larger multicenter studies to assess Vitamin D level in ACS patients and to investigate its relationship with long-term prognosis.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Kunadian V, Ford GA, Bawamia B, Qiu W, Manson JE. Vitamin D deficiency and coronary artery disease: A review of the evidence. Am Heart J 2014;167:283-91.  Back to cited text no. 1
    
2.
Naesgaard PA, León de la Fuente RA, Nilsen ST, Woie L, Aarsland T, Staines H, et al. Vitamin D predicts all-cause and cardiac mortality in females with suspected acute coronary syndrome: A comparison with brain natriuretic peptide and high-sensitivity C-reactive protein. Cardiol Res Pract 2013;2013:398034.  Back to cited text no. 2
    
3.
Scharla SH. 25-OH Vitamin D EIA kit. Osteoporos Int 1998;8 Suppl 2:S7-12.  Back to cited text no. 3
    
4.
Luis CL, Fabio's, Guilherme G, Sabino M, Brito M, Kalil F, et al. Relation of Severe Deficiency of Vitamin D to Cardiovascular Mortality During Acute Coronary Syndromes. Am J Cardiol 2013;111:324-7.  Back to cited text no. 4
    
5.
Karur S, Veerappa V, Nanjappa MC. Study of Vitamin D deficiency prevalence in acute myocardial infarction. Int J Cardiol Heart Vessel 2014;3:57-9.  Back to cited text no. 5
    
6.
Litvac S, Katz A, Yosefey C, Schlacover V, Fytlovich S, Gefel E. 25-hydroxyvitamin D serum levels and acute coronary syndromes: A pilot study. www.his-files.com/pdf/annual2012/EC1_3.pdf.  Back to cited text no. 6
    
7.
Satish K, Virupakshappa V and Manjunath CN. Study of vitamin D deficiency prevalence in acute myocardial infarction. IJC Heart & Vessels 2014;3:57-9.  Back to cited text no. 7
    
8.
Wang TJ, Pencina MJ, Booth SL, Jacques PF, Ingelsson E, Lanier K, et al. Vitamin D deficiency and risk of cardiovascular disease. Circulation 2008;117:503-11.  Back to cited text no. 8
    
9.
Timms PM, Mannan N, Hitman GA, Noonan K, Mills PG, Syndercombe-Court D, et al. Circulating MMP9, Vitamin D and variation in the TIMP-1 response with VDR genotype: Mechanisms for inflammatory damage in chronic disorders? QJM 2003;95:787-96.  Back to cited text no. 9
    
10.
Dror Y, Giveon SM, Hoshen M, Feldhamer I, Balicer RD, Feldman BS, et al. Vitamin D levels for preventing acute coronary syndrome and mortality: Evidence of a nonlinear association. J Clin Endocrinol Metab 2013;98:2160-7.  Back to cited text no. 10
    
11.
De Metrio M, Milazzo V, Rubino M, Cabiati A, Moltrasio M, Marana I, et al. Vitamin D plasma levels and in-hospital and 1-year outcomes in acute coronary syndromes: A prospective study. Medicine (Baltimore) 2015;94:e857.  Back to cited text no. 11
    
12.
Gondim F, Caribé A, Vasconcelos KF, Segundo AD, Bandeira F. Vitamin D deficiency is associated with severity of acute coronary syndrome in patients with type 2 diabetes and high rates of sun exposure. Clin Med Insights Endocrinol Diabetes 2016;9:37-41.  Back to cited text no. 12
    
13.
Baktır AO, Doǧan Y, Şarlı B, Şahin Ö, Demirci E, Akpek M, et al. Relationship between serum 25-hydroxyvitamin D levels and the SYNTAX score in patients with acute coronary syndrome. Anatol J Cardiol 2017;17:293-7.  Back to cited text no. 13
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8], [Table 9]



 

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