The biochemical assessment of coronary artery disease in patients of mental depression

 

Kavita Jaiswal¹, Debjit Mitra^2*

 

¹Assistant Professor, ²Associate Professor, Department of Biochemistry, M. G. M Medical College and L.S.K. Hospital Kishangnaj. Bihar, INDIA.

Email: drmitra45@gmail.com

 

Abstract               Problem Statement: Mental depression as such though a social problem but its complications share a good number of morbidity and mortality. Various reports have suggested that mental depression can lead to coronary artery disease and obesity which are independently morbidity factors. These mental depressive patients are presenting with multifaceted problems and complications- including diabetes mellitus, hypertension, atherosclerotic cardiovascular, dyslipidemia, obesity, etc. Methods: The cases and controls both were selected by simple random sampling method done in one year from March 2016 to January 2017. The patients are categorized as per ‘Center of Epidemiologic Study of Depression’ scaling according to their depressive severity. The patients selected from the psychiatric OPD, and the biochemical investigation was done in Dept of Biochemistry M.G.M. Medical College and L.S.K. Hospital. Kishanganj, Bihar. Total 50 patients were taken between the age group of 15 to 50 years. 50 patients of same age group taken as control irrespective whether suffering from CAD, dyslipidemia, obesity but without clinical evidence of mental depression. Results: Compared the control with the CES-D A, B, C and D group. We found that HOMA- IR significantly raised in D group over control, A, B, C group.TG level was significantly raised in D group compared to control, A and B group. In C group the rise of TG level is not significant but has raised to 120% over the Group D. Cholesterol level is significantly raised (p value <0.05) in group D over control and group A, B, C. The HDL value is significantly lowered in group B compared to control, A, B, and C values but group C has shown decrease in HDL value of about 38.6%(mean) over group B value. Group B also shows 79.17% lower than that of group A. It denotes that mental depression has such caused the lowering of HDL and increase of atherogenesis stage by stage in a matched age group patients irrespective of the antipsychiatric treatment they have received.

Key Wodrs: Mental Depression, Hypertension, Atherosclerotic Cardiovascular, Coronary artery disease.

 

 

 

INTRODUCTION

R.V. Kanel et al noted that depression is an independent risk factor for coronary artery disease¹. Post MI patients with clinically depressive disorder Cary 2- 2.5 fold increase risk of neocardiovascular events and cardiac mortality². The event of incidence of depression was even stronger after adjustment for confounding factors – (like recent life stressors, psychiatric illness, smoking, alcohol intake etc). However the mechanism underlying the association between depression and cardiovascular diseases is unclear. The author hypothesized that cardiac mortality and morbidity after depression in late life is mediated by subclinical atherosclerosis and is thus confined to ischemic heart disease. Depressions do not discriminate any age, sex, profession. It can strike a debt ridden farmer to young children even housewife. The situation in India is far worse than many other countries because of stigma associated with mental illness and the lack of trained professionals who can help. NIMH (National Institute of Mental Health ) study shows⁴ about 6% people between the age group of 9-17 years and 10% between the age of 18 and above suffers from depression in every year⁵. The causes of depression are currently a matter of intense research. An interaction between genetic predisposition and life history appears to determine a person’s level of risk. Episodes of depression may then be triggered by stress, difficult life events side effects of medications or other environmental factors⁵.

 

MATERIAL AND METHODS

The clinically diagnosed mental depression patients and controls. The cases and controls both were selected by simple random sampling method done over one year. The patients are categorized as per CES-D scaling according to their depressive severity. Controls of same number and matched age group, preferably of both sex distribution were taken without having any mental illness or any complications to show the comparison between mentally ill or non ill persons. These patients may suffer from diabetes mellitus, coronary artery disease, dyslipidemia or obesity but without mental depression. The patients selected from the psychiatric OPD, and the biochemical processing was done in Dept of Biochemistry. The mentally depressed patients taken within 15-50 years (irrespective of sex) attending with various symptoms of mental depression. The categorization of the patients has been done on the basis of CES-D scaling. Within short span of time approximately 50 mentally depressed patients with or without complications were processed along with 50 patients of same age group taken as control irrespective whether suffering from DM, CAD, dyslipidemia, obesity but without clinical evidence of mental depression.

Physical parameters: Body weight, BP, height, abdominal-circumference, BMI.

Biochemical parameters: Blood sugar (fasting, post prandial), glycosylated hemoglobin, Serum urea, creatinine, LFT –Bilirubin, Total protein, SGOT, SGPT, ALP. Serum triglyceride, cholesterol, HDL.

RESULTS

Table 1: Clinical history chart of depressive patients: -

• Receiving antidepressant therapy – 67%
• Antidiabetic therapy -34%
• Antihypertensive (calcium channel blocker/ACE inhibitors /β blockers) –56%
• Patients complaining of chest pain and c/o cardiac illness – 24%

Table 1: Mean, SD, se values of different parameters: - (according to CES-D scale).

 

Table 2:

 

Table 3:

 

Table 4:

 

Table 5:

DISCUSSION

Overweight and obesity are associated with insulin resistance and the metabolic syndrome. However, the presence of abdominal obesity is more highly correlated with metabolic risk factors than an elevated BMI. Therefore the simple measure of waist- circumference is recommended to identify the BMI component of metabolic syndrome. The distribution of adipose tissue in different anatomic depots also has substantial implications for morbidity. Specially intraabdominal and abdominal subcutaneous fat have more significant than subcutaneous fat present in the buttocks and lower extremities. This distinction is most easily made by determining waist-hip ratio, with a ratio >0.9 in women and >1.0 in men being abnormal. Many of the most important complications of obesity such as insulin resistance, diabetes, hypertension, hyperlipidemia and hyperandrogenism in women are linked more strongly to intraabdominal and or upper body fat than to overall adiposity. The mechanism underlying this association is unknown but may relate to the fact that the intraabdominal adipocytes are more lipolytically active than those from other depots. Release of free fatty acids into portal circulation has adverse metabolic actions specially on the liver⁵. In our study there is a increase in abdominal-circumference in depressive patients (mean of depressive patients is- 104 cm including both sexes, and in control groups78 cm in female and 87.8 in male ) and also a variation in different groups according to gradation of depressions (like in CES-D-A 80 cm in female and86 cm in male, CES-D B 85 cm in female and 89 cm in male, CES-D C 86.9 cm in male and 103.17 cm male. CES-D D - 89.4 cm in female and 105.6 cm in male). But some male patients can develop metabolic risk factors when the waist-circumference is only marginally increased, eg 94- 102 cm (37-39 inch). Such patients have strong genetic contributions to insulin resistance. They should benefit from life-style changes, similarly to men with categorical increases in waist-circumference. We found that in A category (CES-D scale) the HOMA-IR was 4.118, in -B category 11.245, in C category 13.99, in –D category 18.13. But in control patients it approximately 1.92. These values showing rise in insulin resistance and corroborate the findings of the study of Anderson and R.J. Last (6,7).In these group of patients the blood glucose level also varies ( in A – 89.97mg/dl, in B- 98.76 mg/dl,in C 128.78 mg/dl, in -D 136.67 mg/dl) These depressive patients has also different HbA1c level (like- A 5.31%, B 5.72 %, C 6.05%, D 6.89%)in comparison to control groups (3.60% ).The measurement of glycated hemoglobin is the standard method for assessing long term glycemic control. When plasma glucose is consistently elevated, there is an increase in nonenzymatic glycation of hemoglobin; and these alteration reflects the glycemic history over the past 2-3 months, since erythrocytes has an average life span of 120 days. Depending on the assay methodology, haemoglobinopathies, anemia, and uremia may interfere the HbA1c results. In standardized assays the HbA1c approximates the plasma glucose values - (A1C of 6% is 7.5 mmol/L (135mg/dl), 7%- 9.5 mmol/L (170 mg/dl), 8% -11.5 mmol/L (205 mg/dl) etc. [A 1% rise in A1C translates into 2.0 mmol/L - 35 mg /dl increase in blood glucose]. In those groups of depressive patients the blood lipid profile also varies. The triglyceride level is raising according to the degree of severity of depression. The mean value of triglyceride level is in -A - 159.272 mg/dl, in B - 170 mg/dl, 183.68 mg/dl in C, 227.175 mg/dl in D and 115.69mg/dl in control groups. Whereas blood cholesterol is 152 mg/dl in A, 179.02 mg/dl in - B, 211.37 mg/dl in C,230.08 mg/dl in D and 107.38 mg/dl in control groups. The HDL level also varies, but instead of rising the blood HDL level it is in declining pattern. It is 40mg/dl in -A, 38 mg/dl in - B, 34.78 mg/dl - in C, 28 mg/dl in - D and 44.95 mg/dl in control groups. Gluecket al (1994)⁸ has demonstrated that high TG and high cholesterol and low HDL level were the sole causative factor in mild to severe depression. Our study also shows the gradual increase of TG, CHOL, and gradual lower value of HDL in A-D categories of mental depressive patients. This acknowledges the findings of Gluek and probably the high viscosity of blood resulting in sluggishness of oxygen supply to the brain leads to organic brain syndrome like- mental depression.

 

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