The Effect of Rosuvastatin Treatment on Fasting Triglyceride Levels, Non Fasting Triglyceride

Levels and hsCRP

Abdulkadir Çakmak ,
1 İlyas Atar ,
1 Ercan Türk ,
1 Cihan Altın ,
1 Emir Karaçağlar 1, Alp Aydınalp ,
1 Bülent Özin1, Haldun Müderrisoğlu .
1

1 University of Başkent Faculty of Medicine, Departments of Cardiology, Ankara, Turkey.

BACKGROUND RESULTS RESULTS

The relationship of hypertriglyceridemia and the risk for coronary heart disease (CHD) has been an issue of Patients’ demographic data, medical history, cardiovascular and biochemical tests were recorded. (Table 1-2)
After one month rosuvastatin treatment, fasting TG levels were significantly decreased according to
great interest and controversy.
their baseline levels (respectively 20%). (Table 4)
Hypertriglyceridemia correlates strongly with the presence of small, dense particles of low density lipoprotein
(LDL) cholesterol and reductions of high density lipoprotein (HDL) cholesterol, both of which are known to be
associated with premature CHD. Age (years) 54.3±11.6 Table 4: Baseline and after treatment, fasting triglyceride and hsCRP levels
Some prospective studies and case-control studies demonstrated a relationship between nonfasting triglyceride Female (n,%) 26 (%50.9)
(TG) levels and cardiovascular disease.
Body mass index (kg/m2) 28.1 ±4.1 Baseline After treatment P value
.
Metabolic sendrom 40 (%78.4) fasting levels fasting levels
Previous coronary heart disease 12 (%23.5) n: 49 n: 49
OBJECTIVES 192±42 SD 154±51 SD
Obesity 19 (%37.3) TG (mg/dL) <0.001
We aimed to show the effect of rosuvastatin treatment on fasting TG levels, non fasting TG levels and an
inflammatory parameter high sensitive C reactive protein (hsCRP). Hypertension (n,%) 33 (%64.7)
HsCRP (mg/L) 5,5±5 SD 5,0±4,9 SD 0,306
Smoking (n,%) 17 (%33.3)
Alcohol use 3 (%5.9)
Coronary heart disease in family (n,%) 6 (%18)
Regular exercise 11 (%21.6)
METHODS Sedantary lifestyle 36 (%70.6)
Study Population
A total of 51 patients who were admitted to our outpatient cardiology clinic were included in the study. After one month rosuvastatin treatment, non fasting TG levels were significantly decreased according
Exclusion criteria: Table 1: Demographic data and medical history of the study population to their baseline levels (respectively 23.5%). (Table 5)
 Age younger than 18 or older than 75 years
 Triglyceride lower than 150 mg/dl or higher than 300 mg/dl Table 5: Baseline and after treatment non fasting triglyceride and hsCRP levels
 LDL-c lower than 100 mg/dl or higher than 160 mg/dl
 Acute myocardial infarction or unstabil angina pectoris Baseline After treatment P value
Table 2: Biochemical parameters of the study population
 Diabetes Mellitus non fasting levels non fasting levels
 Chronic kidney or liver disease n: 49 n: 49
BUN (mg/dl) 15.3 ± 4.3
 Acute or chronic pancreatitis TG (mg/dL) 339±118 SD 259±96 SD <0.001
Creatinine (mg/dl) 0.8 ± 0.2
 Hypothyroidism or hyperthyroidism
Sodium (mEq/L) 139.1 ± 2.5
HsCRP (mg/L) 6±5,2 SD 4,8±4,7 SD 0,135
Potassium (mEq/L) 4.2 ± 0.4
Study Protocol Hemoglobine (g/dl) 14.5 ± 1.3
Oral lipid loading was used in order to measure postprandial TG (PPTG) levels after 12 hours of fasting state.
 All subjects received a breakfast consisting 60% of fat, 16.8% of protein and 23.2% of carbohydrates, with a WBC (K/mm³) 7.354 ± 1.620
total of 891 kcal. Platelet (K/mm³) 285.333 ± 51.690
After rosuvastatin therapy, the decreasing at non fasting TG levels was significantly higher compare
 In the fasting state and after the lipid rich breakfast (at 4th hour), triglyceride, LDL cholesterol, HDL cholesterol, AST (U/L) 22.2 ± 5.7 to fasting TG levels
total cholesterol and hsCRP levels were measured at beginning and after the one month 10 mg/day rosuvastatin ALT (U/L) 24.1 ± 9.2
therapy.
CK 65.3 ± 26.2
TSH 2.1 ± 1.0

Table 6: Comparison of changing difference of fasting and non fasting TG levels

Biochemical analyses
Serum total cholesterol and triglyceride were assayed by enzymatic colorimetric tests, using a Roche/Hitachi
Baseline Level Difference at P value
Modullar PP Analyzer according to the manufacturer’s specifications (Roche).
level after treatment decrease of TG
Serum LDL- cholesterol and HDL- cholesterol were assayed by homogeneous enzymatic colorimetric methods, PPTG levels were significantly increased after lipid loading according to baseline TG levels. (Table 3) levels
using a Hitachi Modullar PP Analyzer according to the manufacturer’s specifications (Roche Diagnostics GmbH,
Mannheim, Germany). n: 49 n: 49 n: 49
Serum hsCRP was measured by an ultrasensitive latex-enhanced immunoassay method, using CRP Ultra Fasting 192±42 SD 154±51 SD 38.3±45.9 <0.001
reagent (Sentinel Diagnostics, Milan, Italy) in an Abbott Architect C8000 Analyzer according to the manufacturer’s Table 3: Baseline fasting and non fasting triglyceride and hsCRP levels
specifications. The detection limit was 0,1 mg/L.
Non fasting 339±118 SD 259±96 SD 80.7±104.3 <0.001
Fasting Non fasting P value
levels levels Difference of 42.4±46.2 <0.001
n: 49 n:49 difference
TG (mg/dL) 192±42 SD 339±118 SD <0.001

HsCRP (mg/L) 5.5±5 SD 6±5.2 SD 0.268

CONCLUSION
Triglyceride levels were significantly increased after fat loading compared to baseline levels in patients
There were no significant changes in hsCRP levels at the beginning.
After one month rosuvastatin treatment, fasting TG levels and non fasting TG levels were significantly
decreased according to their baseline levels but no significant change was observed in hsCRP levels.
After rosuvastatin therapy, the decreasing at non fasting TG levels was significantly higher compare to
fasting TG levels.