Medical Journal of South Punjab

www.mjsp.com OA-91-02/22

Serial measurement of lipid profile in patients with acute myocardial infarction

1. PGR CPEIC, Faisal Ramzan1, Noshad Javed2,Tahir Yasin3, Hafiz Muhammad Hanzlah Shahid4, Ansar Ali Khan5
Multan
2. PGR CPEIC, Abstract… Objective: To investigate the effect of acute myocardial infarction (AMI) on the
Multan levels of lipid profile and inflammatory markers. Study Design: Prospective study. Place of
3. PGR CPEIC, study: Choudhary Pervaiz Ellahi Institute of Cardiology in one-year duration from May 2019
Multan
to May 2020. Methodology: Patients admitted within 24 hours of onset of symptoms were
4. PGR CPEIC,
Multan enrolled in study and their total cholesterol, triglycerides, high density and low density
5. PGR CPEIC, lipoprotein was assessed. SPSS version 23 was used for data analysis. Tests of significance
Multan were applied and p-value less than or equal to 0.05 was taken as significant.
Results: The mean total cholesterol, triglyceride, low-density lipoprotein cholesterol,
high-density lipoprotein cholesterol, TC / HDL-C, LDL-C / HDL-C, high sensitive C-reactive
protein, interleukin-6 and interleukin-10 of the control patients was 169.02±6.69 mg/dl,
152.27±3.59 mg/dl, 108.18±4.22 mg/dl, 50.93±4.81 mg/dl, 3.97±0.49, 2.48±0.64,
0.96±0.48 mg/dl, 14.31±4.68pg/dl, and 13.98±2.53pg/dl, respectively. Conclusion: Early
treatment of lipid changes provides advantages and treatment lines for clinical decisions
and lipid lowering therapy. Therefore, within 24 hours of onset of symptoms serum lipid
values should be assessed.
Cardiovascular diseases, chronic obstructive pulmonary disease, Risk factor

Ramzan F, Javed N, Yasin T, Shahid HMH, Khan AA. Serial

Coronary heart disease is a serious medical condition This study aims to investigate the serum lipid changes in
that may lead to morbidity or mortality in young age. acute myocardial infarction in different time periods.
Among its risk factors dyslipidemia is major risk factor. Study was started after permission from hospital ethical
Epidemiologically low level of high density cholesterol, board and completed at Choudhary Pervaiz Elahi institute
lipoprotein cholesterol of low density and raised total of Cardiology, Multan in one year duration from May 2019
cholesterol are major contributing factors in incidence to May 2020. Informed written consent was obtained from
of coronary heart disease and its mortality rate. patients. Non probability consecutive sampling technique
It is documented that treatment of hyperlipidemia at was used. Suspected patients of acute myocardial
earlier time after acute myocardial infarction gives infarction presented at emergency department were
good advantages and also reduce the risk of morbidity enrolled in study. Patient diagnosed as AMI on baseline
and mortality. During acute illness level of lipid and characteristics. Sampling for lipid profile was done within
protein changes abruptly, which may complicate the 24 hours of onset of symptoms was included in the study.
management. Acute phasic changes during tissue Patients with chronic liver disease, rheumatic heart
necrosis change the lipid profile after coronary artery disease, cancer, renal failure, critical illness from last one
events. month, sepsis, stroke history of last months, surgical
After AMI serum lipid modifications may include procedure in last three months and regularly taking anti
decrease in HDL, LDL and TL in approximately 20% in inflammatory drugs were excluded from the study.
values that reciprocally raised the triglycerides up to Physical examination, clinical history, presence of CVS risk
30%. Number of mechanisms is responsible for this factors, chest pain was monitored and recorded for every
change like up regulation of LDL receptors which is patients. Continuous electrocardiogram and cardiac
associated with acute phase response. Many previous enzymes were recorded. A rise in cardiac biomarkers was
studies concluded hyperlipidemia in acute myocardial labeled as MI and at least one alternation in
infarction and recommended lipid profile assessment electrocardiogram (ST segment change and bundle branch
within 24 hours of AMI. Early duration of hyperlipidemia block). Loss of myocardium on echocardiography,
ensures the medication for lipid lowering.
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diabetic patients were labelled as fasting blood sugar Table. II). Comparison of inflammatory makers and serum
more than 126mg/dl and history of taking anti diabetic. lipid profile of post-acute myocardial infraction at one
Systolic blood pressure more than 140 and diastolic day, two days and seven days were shown in table. III. We
above 90mmhg was labelled as hypertension. Patients set the hypothesis that the mean of serum lipid profile and
of BMI more than was labelled as obese, total inflammatory makers are equal verses at least two means
cholesterol above 200mg/dl labelled as hyperlipidemia. are different. We test this hypothesis by using one way
Lipid profile and inflammatory marker measured within ANOVA. It can be concluded that serum lipid profile and
24 hours of symptoms and then at 2nd and 7th day after inflammatory makers are not equal at day 1 and day 2, day
MI. 1 and day 7, day 2 and day 7, at (p<0.05). (Table. III).
SPSS version 23 was used for data analysis. Mean and Table-I: Demographic and clinical
standard deviation was calculated for numerical data characteristics of both the groups
like age, BMI and hemoglobin. Frequency and
Variable Control AMI patients P-value
percentages were calculated for categorical data like
n=150 (50%) n=150 (50%)
gender, hypertension, diabetes, socioeconomic status,
Age (years) 54.77±5.89 53.28±5.05 0.020
obesity, dyslipidemia and ischemic heart disease. P
Gender
value less than or equal to 0.05 was considered as
Male n=97 (64.7%) n=103 0.462
significant.
(68.7%)
Results Female n=53 (35.3%) n=47 (31.3%)
Three hundred patients were included in this study,
BMI (kg/m2) 25.02±1.98 24.89±2.03 0.566
both genders. The mean age of control patients was
Haemoglobin 12.48±2.34 12.79±2.57 0.271
54.77±5.89 years. There were n=97 (64.7%) males and
g/mL
n=53 (35.3%) females. The mean BMI and hemoglobin of
Hypertension n=62 (41.3%) n=72 (48%) 0.246
control patients was 25.02±1.98 kg/m2 and 12.48±2.34
g/mL, respectively. Hypertension and diabetes were Diabetes n=42 (28%) n=39 (26%) 0.696
noted in n=62 (41.3%) and n=42 (28%), respectively. Smoking n=48 (32%) n=48 (32%) 1.000
n=48 (32%) patients were smokers. While, n=34.7 (52%) Alcohol n=34.7 (52%) n=47 (31.3%) 0.539
patients used alcohol. n=34 (22.7%) patients had family Family history n=34 (22.7%) n=34 (22.7%) 1.000
history. While, the mean age of AMI patients was
53.28±5.05 years. There was n=103 (68.7%) males and Table-II: Comparison of lipid profile and inflammatory in
n=47 (31.3%) females. The mean BMI and hemoglobin of baseline between two groups
AMI patients was 24.89±2.03 kg/m2 and 12.79±2.57 Variable Control AMI patients P-value
g/mL, respectively. Hypertension and diabetes was n=150 (50%) n=150 (50%)
noted in n=72 (48%) and n=39 (26%), respectively. n=48
TC (mg/dL) 169.02±6.69 177.74±5.11 0.000
(32%) patients were smokers. While, n=47 (31.3%)
patients used alcohol. n=34 (22.7%) patients had family TG (mg/dL) 152.27±3.59 160.31±6.54 0.000
history. The age difference was statistically significant, LDL-C 108.18±4.22 115.13±7.25 0.000
(p=0.020). (Table. I). (mg/dL)
The mean total cholesterol, triglyceride, low density
lipoprotein cholesterol, high density lipoprotein HDL-C 50.93±4.81 45.57±3.47 0.000
cholesterol, TC / HDL-C, LDL-C / HDL-C, high sensitive (mg/dL)
C-reactive protein, interleukin-6 and interleukin-10 of
the control patients was 169.02±6.69 mg/dl, TC / HDL-C 3.97±0.49 5.18±2.13 0.000
152.27±3.59 mg/dl, 108.18±4.22 mg/dl, 50.93±4.81 LDL-C / 2.48±0.64 3.03±1.02 0.000
mg/dl, 3.97±0.49, 2.48±0.64, 0.96±0.48 mg/dl, HDL-C
14.31±4.68pg/dl and 13.98±2.53pg/dl, respectively.
While, the mean total cholesterol, triglyceride, low hs-CRP 0.96±0.48 10.48±3.28 0.000
density lipoprotein cholesterol, high density lipoprotein (mg/L)
cholesterol, TC / HDL-C, LDL-C / HDL-C, high sensitive IL-6 14.31±4.68 54.01±4.11 0.000
C-reactive protein, interleukin-6 and interleukin-10 of (pg/mL)
the AMI patients was 177.74±5.11 mg/dl, 160.31±6.54
mg/dl, 115.13±7.25 mg/dl, 45.57±3.47 mg/dl, IL-10 13.98±2.53 11.74±3.19 0.000
5.18±2.13, 3.03±1.02, 10.48±3.28 mg/dl, (pg/mL)
54.01±4.11pg/dl and 11.74±3.19pg/dl, respectively. By
using the independent sample t-test, the differences of
lipid profile and inflammatory in baseline of both
groups were statistically significant at (p˂0.001)
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 Table-III: Comparison of lipid profile and samples.
inflammatory in baseline between two groups In our study we observed HDL-C started decreasing from
Variable Day 1 Day 2 Day 7 day 2 and continue decreasing with passage of time. In a
TC 176.24±7.63 161.53±3.52 167.62±7.93 study by Nigam et al17 reported that HDL C decreased after
(mg/dL) 48 hours of acute attack and this fall in values remain at
TG 160.41±8.02 174.67±6.05 170.03±3.61 lower level after that. Kumar et al 18 conducted a study on
(mg/dL) this topic in 2009 and reported that fall in high density
LDL-C 115.23±6.59 103.09±3.68 104.09±3.52 lipids and cholesterol may be cause of metabolic
(mg/dL) alterations after acute myocardial infarction and enzyme
HDL-C 45.49±4.36 38.29±3.43 38.82±10.36 changes. Both these studies coinside with our findings
(mg/dL) strengthens our conclusion.
TC / 4.72±1.29 5.19±1.36 4.79±1.21 Rosjika et al19 also reported that ideal time for
HDL-C determination of HDL level is first 24 hours after acute
LDL-C / 2.82±0.99 3.01±1.08 2.93±1.36 myocardial attack that reflects the real cause of actual
HDL-C cardiac event. Several quantitative and qualitative effects
hs-CRP 10.37±2.52 17.22±5.72 13.91±3.66 occur on serum HDL level and this event labeled as acute
(mg/L) phase response. Endothelial lipase activity increases on
IL-6 52.21±3.39 67.96±5.89 54.20±6.35 this time that result in decrease of HDL in serum and also
(pg/mL) inflammatory response.
IL-10 12.16±2.49 18.75±6.69 15.02±2.88 Conclusion
(pg/mL) Early treatment of lipid changes provides advantages and
treatment line for clinical decisions and lipid lowering
therapy. Therefore, within 24 hours of onset of symptoms
Discussion serum lipid values should be assessed.
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