Changes in Coagulation and Fibrinolysis Systems During the Perioperative Period of Acute Type A Aortic Dissection.

BACKGROUND: Acute type A aortic dissection (ATAAD) has a high risk of perioperative bleeding and often requires extensive blood product infusions. Analysis of the changes in coagulation and fibrinolysis is both helpful for proper treatment and an improved prognosis. The present study investigated the changes in the coagulation and fibrinolysis systems during the perioperative period of ATAAD. METHODS: Twenty-two patients with ATAAD were included in this study. After diagnosis, all patients underwent ascending aorta replacement, aortic arch replacement, and implantation of a special stented endovascular graft. The control group included 25 patients undergoing elective aortic surgery. Baseline preoperative, intraoperative, and postoperative data were collected in both groups. Venous blood samples of all subjects were collected at five time points, after admission (T1), before surgery (T2), after protamine reversal (T3), postoperative 6 h (T4), and postoperative 24 h (T5), measuring the concentrations of platelet factor 4 (PF4), prothrombin fragment 1 + 2 (F1+2), tissue factor (TF), tissue factor pathway inhibitor (TFPI), plasminogen activator (PA), plasminogen activator inhibitor-1 (PAI-1) and thrombin antithrombin complex (TAT) by enzyme-linked immunosorbent assays (ELISAs). RESULTS: The average age of the ATAAD group was 49.9±12.5 years old, while that of the control group was 57.0±12.1 years old. There were more patients with a smoking history, and the cardiopulmonary bypass time, aortic cross-clamp time, and preoperative left ventricular ejection fraction were higher in the ATAAD group than in the control group (P < 0.05). Additionally, preoperative fibrin degradation products (FDP) and preoperative D-dimer were higher in the ATAAD group than in the control group (P < 0.05). However, time from onset to operation, intraoperative core temperature, preoperative B-type natriuretic peptide (BNP), and left ventricular end-diastolic diameter in the ATAAD group were lower than those in the control group (P < 0.05). In contrast, however, the proportion of abnormal bicuspid aortic valves in the control group was higher (P < 0.05). TF in the ATAAD group was significantly higher at T1 (7.9±3.7 ng/mL versus 0.9±0.7 ng/mL, P < 0.05). The TFPI in the ATAAD group was higher than that in the control group at T1 and T2 (P < 0.05). Additionally, PA in the ATAAD group was higher than that in the control group at T1, T2, T3, and T5 (P < 0.05), while PA in the control group was significantly higher at T3 than at T1 (P < 0.05). There was no significant difference in PAI-1 between the two groups before surgery (P > 0.05). Nevertheless, both groups reached their peak value at T3. The platelet count and fibrinogen (FBG) in the ATAAD group decreased significantly from T1 to T2 and continued to decrease after cardiopulmonary bypass. F1+2 and TAT in the ATAAD group were higher than in the control group (P < 0.05); however, they peaked at T3. The PF4 in the ATAAD group slightly increased at T1, while PF4 at T3 was significantly higher than at T1 (P < 0.05). CONCLUSION: The changes in coagulation and fibrinolysis in the ATAAD group before surgery were very significant, which caused a large amount of fibrinogen and platelet consumption. Cardiopulmonary bypass (CPB) and a lower intraoperative core temperature exacerbated the coagulation and fibrinolysis disorder, and the pro-coagulant function of the platelets was activated after surgery. Maintaining the normal concentration of fibrinogen was helpful to correct the coagulation function disorder.

Methylation-dependent transcriptional repression of RUNX3 by KCNQ1OT1 regulates mouse cardiac microvascular endothelial cell viability and inflammatory response following myocardial infarction.

Myocardial infarction (MI) is a major contributor to death and disability throughout the world. Increasing evidence shows that long noncoding RNAs (lncRNAs) are involved in the progression of MI. Here, we hypothesized that lncRNA potassium voltage-gated channel subfamily q member 1 overlapping transcript 1 (KCNQ1OT1) could affect the development of MI via regulation of Runt-related transcription factor (RUNX)3 by methylation. Initially, by ligation of the left anterior descending coronary artery, an acute MI (AMI) mouse model was established to collect the cardiac microvascular endothelial cells (CMECs), which revealed a high KCNQ1OT1 expression and a low RUNX3 expression with its high methylation. After that, KCNQ1OT1 knockdown or RUNX3 overexpression were transduced into the CMECs in order to detect their role in CMEC proliferation, apoptosis, and inflammatory response. Moreover, we assessed their interaction with the inflammatory Notch pathway, by determining the expression of Jagged 1, Hey1, Hes1, Notch intracellular domain, and Notch1. It was observed that after KCNQ1OT1 knockdown, the proliferation of AMI-CMECs was promoted, whereas their apoptosis was inhibited, accompanied by reduced level of inflammatory factors. These trends could also be achieved by RUNX3 overexpression via the Notch pathway. Finally, the regulation of DNA methyltransferase (DNMT)1-dependent methylation in RUNX3 by KCNQ1OT1 was determined, suggesting that KCNQ1OT1 could result in down-regulated RUNX3 expression through promoted RUNX3 methylation caused by recruiting DNMT1. Overall, this study demonstrates that KCNQ1OT1 silencing inhibits RUNX3 methylation, thereby offering protection against CMEC injury and inflammatory response in AMI, which may serve as a promising target for the disease treatment. -Wang, Y., Yang, X., Jiang, A., Wang, W., Li, J., Wen, J. Methylation-dependent transcriptional repression of RUNX3 by KCNQ1OT1 regulates mouse cardiac microvascular endothelial cell viability and inflammatory response following myocardial infarction.

Gene expression profiling analysis to investigate the role of remote ischemic postconditioning in ischemia-reperfusion injury in rats.

BACKGROUND: Blood flow restoration is a definitive therapy for salvaging the myocardium following ischemic injury. Nevertheless, the sudden restoration of blood flow to the ischemic myocardium can induce ischemia-reperfusion injury (IRI). RESULTS: Herein, we investigated the cardioprotective effect of remote ischemic postconditioning (RPostC) through our in vivo rat model of myocardial IRI. The study included three groups: the control group, the IRI group, and the IRI + RPostC group. Ischemia-reperfusion treatment led to an increase in the myocardial infarction area, which was inhibited by RPostC. In contrast to that in the control group, the myocardial apoptosis level was enhanced in the IRI group, whereas RPostC treatment decreased IRI-induced cellular apoptosis. Affymetrix Rat Gene 2.0 ST chip data identified a total of 265 upregulated genes and 267 downregulated genes between the IRI and IRI + RPostC groups. A group of differentially expressed noncoding RNAs (ncRNAs), such as MTA_TC0600002772.mm, MTA_TC1300002394.mm, U7 small nuclear RNA (Rnu7) and RGD7543256_1, were identified. Gene Ontology (GO) enrichment analysis indicated that the positive regulation of some molecular functions, such as GTPase activity, GTP binding, cyclic-nucleotide phosphodiesterase activity and cytokine activity, may contribute to the cardioprotective role of RPostC. Moreover, pathway enrichment analysis using the Kyoto Encyclopedia of Genes and Genomes (KEGG) suggested the potential implication of the TNF signaling pathway and Toll-like receptor signaling pathway. Global signal transduction network analysis, co-expression network analysis and quantitative real-time polymerase chain reaction analysis further identified several core genes, including Pdgfra, Stat1, Lifr and Stfa3. CONCLUSION: Remote ischemic postconditioning treatment can decrease IRI-mediated myocardial apoptosis by regulating multiple processes and pathways, such as GTPase activity, cytokine activity, and the TNF and Toll-like receptor signaling pathways. The potential role of the above ncRNAs and core genes in IRI-induced cardiac damage merits further study as well.

Long Period and High Level of D-Dimer after Coronary Artery Bypass Grafting Surgery.

Hyper-coagulation after off-pump coronary artery bypass grafting (OPCAB) is one of the main reasons for graft thrombosis. D-dimer is closely linked to the activation of coagulation. Few studies have reported the variation range and long-term abnormal coagulation after OPCAB in the Chinese population. Our study aimed to determine the characteristics and value of D-dimer after OPCAB.In this prospective study, 265 patients who underwent OPCAB for the first time were recruited from 2011 to 2012. The D-dimer level of the patients was tested before surgery and on the 1st, 4th, and 14th day, and 1st, 2nd, and 3rd month after surgery. Clinical data in the perioperative period and during the one-year follow-up period were recorded.D-dimer level increased from day 4 after OPCAB ([1321.9 ± 36.4] µg/L), peaked at 1 month ([2839.7 ± 101.4] µg/L), and decreased to the baseline ([370.3 ± 260.2] µg/L) 3 months after surgery. No death occurred, but 25 (10%) patients suffered recurrent angina in the one-year follow-up. They had significantly higher D-dimer level at one month after OPCAB than those of patients who did not suffer from angina. Preoperative ejection fraction <50% and D-dimer level >2915 µg/L at one month after surgery were significantly associated the recurrent angina.After OPCAB, patients have a higher level of D-dimer. And this lasts for a long period (about 3 months). It may reflect a certain degree of hypercoagulable and hyperfibrinolytic state after OPCAB.

MiR-144-5p/CCL12 Signaling Axis Modulates Ischemic Preconditioning-Mediated Cardio-protection by Reducing Cell Viability, Enhancing Cell Apoptosis, Fibrosis, and Pyroptosis.

Ischemic postconditioning (IPost) represents short periods of nonlethal ischemia-reperfusion performed at the onset of reperfusion. Studies have shown that IPost involves various biological processes such as cell proliferation, apoptosis, and pyroptosis and can activate complex signaling pathways. CCL12 is a critical mediator in the inflammatory process after tissue injury. In the present study, we examined the potential actions of CCL12-mediated signaling pathways in cardioprotection after IPost using a cardiomyocyte model. By applying the bioinformatics analysis, we found that CCL12 was upregulated in the rat heart tissues after I/R injury, and the expression level of CCL12 was restored in rats with IPost. The in vitro studies showed that CCL12 and CCR2 expression levels were upregulated in the hypoxia/reoxygenation (H/R)-induced H9C2 cells, which was attenuated in the H/R + hypoxia post-conditioning (PostC) group. The functional assays showed that H/R treatment reduced cell viability, increased cell apoptosis, and promoted fibrosis and pyroptosis of H9C2 cells, which was attenuated in the H/R + PostC group. Overexpression of CCL12 impaired the protective action of hypoxia post-conditioning in the H9C2 cells. Further mechanistic studies showed that miR-144-5p could directly target the 3' untranslated region of CCL12. Overexpression of miR-144-5p markedly repressed the expression levels of CCL12 and CCR2 in H9C2 cells, while miR-144-5p inhibition had the opposite effects. Furthermore, the inhibition of miR-144-5p reduced the cell viability, increased cell apoptosis, and enhanced fibrosis and pyroptosis of H9C2 cells after H/R or H/R + PostC treatment. In conclusion, CCL12 was downregulated in cardiomyocytes following ischemic postconditioning, and CCL12 overexpression impaired the cardioprotective actions of ischemic postconditioning by reducing cell viability, enhancing cell apoptosis, fibrosis, and pyroptosis. Further mechanistic evidence revealed that CCL12 was a direct target of miR-144-5p, and miR-144-5p/CCL12/CCR2 signaling may represent a critical pathway in mediating the cardioprotective effects of ischemic postconditioning.

Implication of inhaled nitric oxide for the treatment of critically ill COVID-19 patients with pulmonary hypertension.

AIMS: This study aims to analyse whether inhaled nitric oxide (iNO) was beneficial in the treatment of coronavirus disease 2019 (COVID-19) patients with pulmonary hypertension. METHODS AND RESULTS: Five critically ill COVID-19 patients with pulmonary hypertension designated Cases 1-5 were retrospectively included. Clinical data before and after iNO treatment were serially collected and compared between patients with or without iNO treatment. The five cases experienced pulmonary artery systolic pressure (PASP) elevation (≥50 mmHg) at 30, 24, 33, 23, and 24 days after illness onset (d.a.o), respectively. Cases 1-3 received iNO treatment on the 24th, 13th, and 1st day after the first elevation of PASP, with concentrations varied from 10 to 20 ppm based on the changes of PASP and blood pressure for 10, 9, and 5 days, respectively. Upon iNO treatment, PASP of Cases 1 and 2 returned to normal on the 10th day and 1st day, and maintained between 50 and 58 mmHg in Case 3. Pa02 /Fi02 increased from 88 to 124, 51 to 118, and 146 to 244, respectively. SPO2 increased from 91% to 97% for Case 1 and maintained a high level above 97% for Case 2. Cardiac function remained normal in the three patients after treatment. Moreover, Cases 1 and 3 survived from severe acute respiratory syndrome coronavirus 2 infection, while Case 2 finally died on the 36th day after the first elevation of PASP due to severe complications. Both cases who did not receive iNO treatment experienced a sudden decrease of PASP and Pa02 /Fi02 due to right heart failure and then died. CONCLUSIONS: Inhaled nitric oxide treatment was beneficial in reducing and stabilizing the PASP and might also reduce the risk of right heart failure in COVID-19 with pulmonary hypertension.

Noninvasive Ventilation in Patients With COVID-19-Related Acute Hypoxemic Respiratory Failure: A Retrospective Cohort Study.

Introduction: Noninvasive ventilation (NIV) has been used to alleviate hypoxemia and dyspnea, but there is no consensus on the application of NIV in patients with coronavirus disease 2019 (COVID-19). Some staff use NIV as the rescue therapy which might lead to the adverse outcomes. This study was to identify early factors associated with intubation to help the medical staff select appropriate patients for receiving NIV treatment. Methods: Patients with laboratory-confirmed COVID-19 who were treated with NIV in emergency department or ICU of the Third People's Hospital (the only designated hospital for treating COVID-19 in Shenzhen) between January 1 and August 31, 2020, were retrospectively analyzed. Results: Thirty-nine patients with COVID-19 treated with NIV were included; of them, 16 (41%) received endotracheal intubation and 3 (8%) died. Significant differences were observed between intubated and non-intubated patients in PaO2/FiO2 before NIV initiation, hospitalization duration, NIV as the rescue therapy, and PaO2/FiO2 of ≤200 mmHg after 1-2 h of NIV initiation. Notably, 1-2 h after NIV initiation, a PaO2/FiO2 of ≤200 mmHg (odds ratio [OR], 9.35; 95% confidence interval [CI], 1.84-47.62; P = 0.007) and NIV as the rescue therapy (OR, 5.43; 95% CI, 1.09-27.12; P = 0.039) were the risk factors for intubation. Conclusions: In patients with COVID-19-related acute hypoxemic respiratory failure receiving NIV, close attention should be paid to PaO2/FiO2 after 1-2 h of NIV initiation. Also, using NIV as rescue therapy should draw our awareness that it might delay escalation of respiratory support and lead to adverse outcomes.

Research on clinical characteristics and prognostic analysis of heparin-induced thrombocytopenia after surgery for acute type a aortic dissection.

PURPOSE: The present study aimed to explore the clinical characteristics of heparin-induced thrombocytopenia (HIT) after surgery for acute type A aortic dissection and perform a relevant prognostic analysis. METHODS: After continuous observation and analysis of 204 patients who underwent acute type A aortic dissection, we found that blood platelets decreased significantly after surgery and that these patients can be suspected to suffer HIT based on relevant 4Ts scores. For these suspected HIT patients, a latex particle-enhanced immunoturbidimetric assay was conducted to detect heparin-induced antibodies. Perioperative clinical data of patients in HIT and non-HIT groups were recorded as were blood platelet counts, HIT antibody test results, 4Ts scores, thromboembolic complications, clinical prognosis and outcomes. RESULTS: In the present study, 38 suspected HIT patients, 16 HIT patients and 188 non-HIT patients were selected in the clinical setting. Among them, HIT patients were found to have prolonged cardiopulmonary bypass time (223 min on average vs. 164 min) and delayed aortic cross-clamp time (128 min on average vs. 107 min), and these differences between HIT patients and non-HIT patients were significant (P < 0.05). Additionally, the HIT group required longer operation time and higher dose of heparin, but showing no statistical differences (P > 0.05). The transfusions of blood platelets in the HIT group and non-HIT group were 18.7 ± 5.0u and 15.6 ± 7.34 u, respectively. In the HIT group, the mechanic ventilation time and the length of ICU stay were longer comparing the non-HIT group(P < 0.05), though no significant differences in total length of stay or In-hospital mortality were observed (P > 0.05). The incidence of continuous renal replacement therapy in HIT group was higher than the non-HIT group (P < 0.05). Additionally,there were no significant differences in 24-h postoperative drainage or reoperation for bleeding in both group(P > 0.05). However, the HIT antibody titer in the HIT group was significantly higher than that in the Suspected HIT group (2.7 ± 0.8 U/mL vs. 0.3 ± 0.2 U/mL) (P < 0.05). Among patients diagnosed with HIT, the incidence of thromboembolism reached 31.5%.For example, two HIT patients newly developed thromboembolism in both lower extremities,and three patients experienced cerebral infarction. CONCLUSIONS: After surgery for acute type A aortic dissection, HIT patients developed postoperative complications, the duration of ventilatory support and length of ICU stay were extended, and the incidence of thromboembolism increased. HIT antibody detection and risk classification should be implemented for high-risk patients showing early clinical characteristics.

Hybrid two-stage repair of Stanford A dissection with visceral or peripheral malperfusion.

BACKGROUND: The present study aimed to evaluate the effect of two-stage hybrid aortic repair at the distal aorta of Stanford A dissection with malperfusion. METHODS: This retrospective case series included 20 patients with Stanford A dissection administered two-stage thoracic endovascular aortic repair (TEVAR) about 1 month after central repair because of visceral or limb malperfusion. The patients were examined by computed tomography (CT) angiography at 3, 6, 12 and 24 months after operation. Recovery of malperfusion and true lumen index were evaluated during follow-up. RESULTS: Twenty patients underwent two-stage hybrid aortic repair, including 11 males and 9 females. The follow-up time was 24 ± 7 months. No intervention-related complications were observed, including stent graft-induced new re-entry tears, death, stroke and spinal cord injury. Malperfusion in all cases was corrected. The true lumen was not enlarged enough 1 month after the first surgery. Thrombosis of the false lumen was observed around the elephant trunk at the carina level and the celiac artery. Three months after second stage TEVAR, the false lumen thrombosis was resorbed; in addition, the trunk was fully expanded at the carina level, and the true lumen was enlarged at the celiac artery. CONCLUSIONS: Two-stage hybrid aortic repair for residual true lumen in the distal aorta 1 month after initial surgery is helpful for descending aorta remodeling and effective in treating malperfusion. This procedure may be a good option for patients suffering from Stanford A dissection with small true lumen in the distal aorta and malperfusion.

99-Case Study of Sporadic Aortic Dissection by Whole Exome Sequencing Indicated Novel Disease-Associated Genes and Variants in Chinese Population.

BACKGROUND: In this study, the whole exome sequencing in human aortic dissection, a highly lethal cardiovascular disease, was investigated to explore the aortic dissection-associated genes and variants in Chinese population. METHODS: Whole exome sequencing was performed in 99 cases of aortic dissection. All single nucleotide polymorphisms (SNPs), insertions/deletions (InDels), and copy number variations (CNVs) were filtered to exclude the benign variants. Enrichment analysis and disease-gene correlation analysis were performed. RESULTS: 3425873 SNPs, 685245 InDels, and 1177 CNVs were identified, and aortic dissection-associated SNPs, InDels, and CNVs were collected. After the disease correlation analysis, 20 candidate genes were identified. Part of these genes such as MYH11, FBN1, and ACTA2 were consistent with previous studies, while MLX, DAB2IP, EP300, ZFYVE9, PML, and PRKCD were newly identified as candidate aortic dissection-associated genes. CONCLUSION: The pathogenic and likely pathogenic variants in most of AD-associated genes (FBN1, MYH11, EFEMP2, TGFBR2, FBN2, COL3A1, and MYLK) were identified in our cohort study, and pathogenic CNVs involved in MYH11, COL family, and FBN were also identified which are not detectable by other NGS analysis. The correlation between MLX, DAB2IP, EP300, ZFYVE9, PML, PRKCD, and aortic dissection was identified, and EP300 may play a key role in AD.

Monitoring bronchoalveolar lavage with electrical impedance tomography: first experience in a patient with COVID-19.

OBJECTIVE: Patients with the novel coronavirus disease (COVID-19) often have airway secretions that severely compromise ventilation. This study investigates electrical impedance tomography (EIT) monitoring of a therapeutic bronchoalveolar lavage (BAL) in a patient with COVID-19. APPROACH: A patient with COVID-19 developed acute respiratory distress syndrome requiring mechanical ventilation. He received regional BAL to remove mucus in the small airways (20 ml × 5). Regional ventilation changes before BAL, 30 min after and in the following days, were monitored with EIT. MAIN RESULTS: Regional ventilation worsened shortly after BAL and improved in the following days. The improvement of the oxygenation did not exactly match the ventilation improvement, which indicated a possible ventilation/perfusion mismatch. SIGNIFICANCE: Therapeutic BAL might improve regional ventilation for COVID-19 and EIT could be a useful tool at the bedside to monitor the ventilation treatment of COVID-19.

Arterial stiffness is associated with target organ damage in subjects with pre-hypertension.

INTRODUCTION: Present study was to evaluate whether increased arterial stiffness was associated with target organ damage in pre-hypertensive subjects. MATERIAL AND METHODS: Pre-hypertensive subjects enrolled and echocardiography was used to evaluate left ventricular hypertrophy (LVH) and the first morning urine was collected to evaluate albumin and creatinine ratio (ALB/Cr ratio). Carotid-femoral pulse wave velocity (cf-PWV) was measured. RESULTS: A total of 420 subjects were recruited and mean age was 42.6 years. Mean systolic/diastolic blood pressure (SBP/DBP) were 130 ±9 mm Hg and 85 ±4 mm Hg. The prevalence of albuminuria and left ventricular hypertrophy was 8.6 % and 11.7 %. Mean cf-PWV was 9.2 ±1.0 m/s, with arterial stiffness prevalence was 8.8%. Subjects with arterial stiffness had higher cf-PWV value (10.6 ±0.4 m/s vs. 8.7 ±0.6 m/s, p < 0.05), and ALB/Cr ratio (28.3 ±13.2 µg/mg vs. 23.1 ± 11.4 µg/mg, p < 0.05). Overall, with multivariate regression analysis, aging and arterial stiffness were significantly associated with pre-hypertension. With stepwise adjusted for potential covariates including age, male gender, fasting plasma glucose, presence of current cigarette smoking, dyslipidemia, statins and SBP, increased cf-PWV remained independently associated with left ventricular hypertrophy and albuminuria, with an increased odds of 41 % and 24 % (p < 0.05), respectively. CONCLUSIONS: In pre-hypertensive subjects, arterial stiffness is independently associated with LVH and albuminuria and cf-PWV may be a useful marker to identify target organ damage in pre-hypertensive subjects.

[Acidic fibroblast growth factor promotes the growth of skeletal muscle satellite cells: experiment with rabbits].

OBJECTIVE: To explore if human recombinant acidic fibroblast growth factor (rhaFGF) can promote the proliferation of skeletal muscle satellite cells (MSCs). METHODS: MSCs were obtained from rabbits and cultured, and divided into 2 groups: rhaFGF group, treated with rhaFGF of the concentrations of 0, 5, 10, 20, 40, 60, and 80 microg/L, and rhaFGF + low molecular weight heparin (LMWH) group, treated with rhaFGF of different concentrations and LMWH of the terminal concentration of 10 mg/L. MTT method was used to observe the proliferation of the MSCs so as to determine the appropriate concentration to be used in the next experiment. Other MSCs were cultured and treated with the rhaFGF of the appropriate concentration and then LMWH of the terminal concentration of 10 mg/L was added to be co-cultured for 3 days. Flow cytometry was used to observe the cell cycle of the MSCs. RESULTS: rhaFGF of the concentrations 20 approximately 60 ng/ml promoted the proliferation of MSCs, and 40 ng/ml was selected as the best concentration to be used in the next experiment. Treated with the rhaFGF of the concentration of 40 ng/ml and LMWH for 3 days, the proportion of MSCs at the stage G(0)/G(1) was significantly lower and those at the stage S significantly higher in comparison with the control group (both P < 0.01), however, not significantly different from those of the rhaFGF group. CONCLUSION: rhaFGF promotes the proliferation of MSCs.

[The effects of 40 mg atorvastatin on serum lipids, inflammatory markers and clinical events in ACS patients post PCI].

OBJECTIVE: To assess the safety and effects of 40 mg atorvastatin on serum lipids, inflammatory markers and clinical events in ACS patients post PCI. METHODS: A total of 92 patients with ACS post successful PCI were randomly divided into atorvastatin 10 mg/d (group A) and atorvastatin 40 mg/d (group B) on top of the standard medical therapy. Blood were taken at baseline, 4, 12 and 24 weeks for serum alanine aminotransferase (ALT), lipids, high-sensitive C-reactive protein (hs-CRP) and matrix metalloprotease-9 (MMP-9) measurements. The major adverse cardiac events (MACE) were also observed. RESULTS: There was no significant difference in medication withdrawn (2 vs. 3 cases) due to increased ALT (3 times higher than normal) and incidence of MACE (5 vs. 7 cases) between the groups. TC and LDL were significantly reduced in both groups 4 weeks and thereafter post medication compared to pre-treatment (P < 0.05) and the reduction was more significant in group B than that in group A at 24 weeks post medication (P < 0.05) while TG and HDL remained unchanged. hs-CRP was significantly reduced at 12 and 24 weeks in both groups compared to baseline and the reduction was more significant in group B than that in group A at 24 weeks. MMP-9 was significantly reduced in both groups 4 weeks and thereafter post medication compared to pre-treatment (P < 0.05) and the reduction was more significant in group B than that in group A at 12 weeks post medication (P < 0.05). CONCLUSION: Both atorvastatin doses significantly reduced TC, LDL, hs-CRP and MMP-9 in ACS patients post PCI and the reduction was more significant in high dose atorvastatin group at 24 weeks while the MACE and drug withdraw rates were similar between the groups.