European Journal of Molecular & Clinical Medicine

Background:Acute myocardial infarction (AMI) is one of the leading causes of all acute emergencies and is becoming an important public health problem in the developing countries. The present study was conducted to assess complications and mortality in ST-segment elevation acute myocardial infarction in diabetic and non-diabetic patients.
Materials & Methods: 80 consecutive patients of diabetic (group I) and non-diabetic (group II) having acute ST-segment elevation myocardial infarction (STEMI) of both genders were included. Different treatment was given to all patients.
Results: Age group <40 years had 12 diabetic and 14 non- diabetic, 40-55 years had 25 diabetic and 22 non- diabetic, 55-70 years had 15 diabetics and 18 non- diabetics and >70 years had 28 diabetics and 26 non- diabetics. The difference was non- significant (P> 0.05). Site of AMI was anterior in 30 and 20, inferior in 20 and 40, inferior+ right ventricular in 20 and 10 and lateral in 10 and 5 in group I and II respectively. Mortality was seen in those in which streptokinase was given in 6 and 3 and streptokinase not given in 14 and 8 in group I and group II respectively (P< 0.05). Type of treatment given was beta- blockers in 82, ACE inhibitors in 105, streptokinase in 96, aspirin in 154, statins in 128 and diuretics in 44 patients. The difference was significant (P< 0.05).
Conclusion: In diabetic and in non- diabetic, reduction in mortality rate was seen with the streptokinase administration. However, diabetics not on streptokinase had higher mortality as compared to non- diabetics

Statin can increase the risk of interstitial cystitis. Recently, the exact mechanism is yet known. We hypothesize that cellular senescence, particularly in the detrusor muscle cells contributes to the mechanism. In this study, we aim to investigate the effect of simvastatin on bladder detrusor senescence activity in the protamine sulfate-induced interstitial cystitis rat model. Thirty-seven female Wistar rats aged 6-8 weeks old were included and divided into three groups. They were treated with simvastatin 10 mg/kg BW (n=12), simvastatin 50 mg/kg BW (n=13), and the solvent carboxymethylcellulose (CMC) 0.5% (n=12) by oral gavage for 30 days. Each group was then equally subdivided into three groups: control, IC day-0, and IC day-3. The IC rat group was induced by protamine sulfate, while the control group was treated with buffered saline intravesical treatment. In less than three hours after intravesical treatment, all animals in the control and IC day-0 group were sacrificed to collect their bladder tissue. Otherwise, animals in the IC day-3 group were sacrificed three days after intravesical treatment. All collected tissue was measured for senescence marke β-Galactosidase 1 (GLB1) expression by immunohistochemistry procedure. In the control group, the GLB1 expression in rat treated with simvastatin 50 mg/kg BW was 20.12 ± 5.77 % and highest than the rat treated with other treatment, although the difference not significant (p=0.812). In the IC day-0 and IC day-3 group, the GLB1 expression in rat treated with simvastatin 10 mg/kg BW and CMC 0.5% were higher than in the control group, otherwise, the GLB1 expression in rat treated with simvastatin 50 mg/kg BW was lower than in the control group, although not significant (p>0.05). We conclude that a higher dose of simvastatin can increase the bladder detrusor senescence expression along with their apoptotic activity in the presence of urinary leakage.