ABSTRACT
Background: There is an increasing prevalence of coronary artery disease (CAD) in younger individuals. Lipid biomarkers such as lipoprotein-a (Lp-a), Apo A1, Apo B and Paraoxonase-1 (PON1) serve as important risk predictors for development of CAD. There is little evidence regarding the role of lipid biomarkers and their genetic polymorphisms in young (<50 years) ST-segment elevation myocardial infarction (STEMI) patients. Methods: This study included 110 young (18e50 years) STEMI patients and 110 healthy controls. Serum levels of Apo A1, Apo B, Paraoxonase-1 (PON-1) and Lipoprotein-associated phospholipase A2 (Lp-PLA2) were estimated for both patients as well as controls. Additionally, genetic polymorphisms in the Apo A1 (75G/A) and the PON1 (Q192R) genes were evaluated. Results: Serum levels of apo B (101.31 ± 27.58 vs 75.31 ± 18.77 mg/dl; p < 0.0001), Lp(a) [87.56 ± 74.28 vs 25.81 ± 24.66 mg/dl, p < 0.0001] and Lp-PLA2 [5.97 ± 1.39 vs 3.49 ± 1.27 ng/mL, p < 0.0001] were significantly higher in patients as compared to controls. Serum levels of Apo A1 [44.76 ± 35.65 vs 95.97 ± 29.89; p < 0.0001] and PON1 [2.63 ± 1.5 vs 3.87 ± 1.47 ng/mL, p < 0.0001] were significantly lower in cases as compared with controls. Additionally, patients with genetic polymorphisms in the Apo A1 (75G/A) and the PON1 (Q192R) gene had an increased risk of STEMI. Conclusion: Lipid biomarkers such as Apo A1, Apo B and PON1 and their genetic polymorphism are associated with the susceptibility for STEMI in young individuals.
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Background: Genetic polymorphism in MMPs are associated with multiple adverse CV events. There is little evidence regarding role of MMPs and their genetic polymorphisms in young (<50 years) STsegment elevation myocardial infarction (STEMI) patients. Methods: This study included 100 young (18e50 years) STEMI patients and 100 healthy controls. Serum levels of MMP-3, MMP-9 and TIMP were estimated for both patients as well as controls. Additionally, genetic polymorphisms in the MMP-9 gene (_x0001_1562 C/T and R279Q) & MMP-3 gene (5A/6A-1612) was evaluated. All these patients were followed up for one year and major adverse cardiac events (MACE) were determined. Results: Serum levels of MMP-3 (128.16 ± 115.81 vs 102.3 ± 57.28 ng/mL; P ¼ 0.04), MMP-9 (469.63 ± 238.4 vs 188.88 ± 94.08 pg/mL; P < 0.0001) and TIMP (5.84 ± 1.93 vs 2.28 ± 1.42 ng/mL; P < 0.0001) were significantly higher in patients as compared to controls. Additionally, patients with genetic polymorphisms in the MMP genes (5A/5A, 6A/6A and the AG genotypes) had an increased risk of STEMI. Patients with MACE had significantly higher levels of MMP-9 (581.73 ± 260.93 vs 438.01 ± 223.38 pg/mL; P ¼ 0.012). A cutoff value of 375.5 pg/mL of MMP-9 was best able to discriminate patients with STEMI and MACE with sensitivity of 77.3% and specificity of 57%. Conclusion: Novel biomarkers such as MMP-3, MMP-9 and TIMP and their genetic polymorphism are associated with the susceptibility for STEMI in young individuals. Higher MMP-9 levels in STEMI patients with MACE suggests its potential role in predicting cardiac remodeling and left ventricular dysfunction
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Background: Overt left ventricular (LV) dysfunction and congestive heart failure are known entities in Takayasu arteritis (TA). Subclinical LV dysfunction may develop in these patients despite normal LV ejection fraction (LVEF). Moreover, effect of treatment of aortic or renal artery narrowing in such patients is unknown. Methods: This study included 15 angiographically confirmed TA patients undergoing aortic and/or renal intervention. A comprehensive clinical, biochemical and echocardiographic (2-dimensional, speckle tracking and tissue doppler imaging) evaluation were done at baseline, 72 h, and six months post intervention. Results: Six patients (40%) had reduced LVEF (<50%) at baseline while rest 9 (60%) patients had reduced global longitudinal strain (GLS) but normal EF. Diastolic filling pattern was abnormal in all the patients. In patients with baseline reduced EF, mean EF improved from 24.62 ± 12.14% to 45.6 ± 9.45% (p ¼ 0.001), E/ e’ ratio decreased from 15.15 ± 3.19 to 10.8 ± 2.56 (p ¼ 0.005) and median NT pro BNP decreased from 1673 pg/ml (970e2401 pg/ml) to 80 pg/ml (40e354 pg/ml) (p ¼ 0.001) at 6 months after interventional procedure. In patients with baseline normal EF, median NT pro BNP decreased from 512 pg/ml (80 e898.5 pg/ml) to 34 pg/ml (29e70.8 pg/ml) (p < 0.01), mean GLS improved from 8.80 ± 0.77% to 16.3 ± 0.78% (p < 0.001) and mean E/e’ decreased from 12.93 ± 2.63 to 7.8 ± 2.73 (p ¼ 0.005) at 6 months follow up. Conclusion: LV dysfunction is common in patients with TA and obstructive lesions in aorta or renal arteries. GLS can be used to assess subclinical systolic dysfunction in these patients. Timely intervention can improve LV dysfunction and can even reverse the subclinical changes
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Background CHA2DS2-VASc score, used for atrial fibrillation to assess the risk of embolic complications, have shown to predict adverse clinical outcomes in acute coronary syndrome (ACS), irrespective of atrial fibrillation. This study envisaged to assess the predictive role of CHA2DS2-VASc score for contrast-induced nephropathy (CIN) in patients with ACS undergoing percutaneous coronary intervention (PCI). Methods A total of 300 consecutive patients with ACS undergoing PCI were enrolled in this study. CHA2DS2-VASc score was calculated for each patient. These patients were divided into two groups as Group 1 (with CIN) and Group 2 (without CIN). CIN was defined as increase in serum creatinine level ≥0.5 mg/dL or ≥25% increase from baseline within 48 h after PCI. After receiver operating characteristic curve analysis, the study population was again classified into two groups: CHA2DS2-VASc score ≤3 group (Group A) and score ≥4 group (Group B). Results CIN was reported in 41 patients (13.6%). Patients with CIN had a higher frequency of hypertension, diabetes mellitus, and had a lower left ventricular ejection fraction and baseline estimated glomerular filtration rate. Receiver operating characteristic curve analysis showed good predictive value of CHA2DS2-VASc score for CIN (area under the curve 0.81, 95% CI 0.73–0.90). Patients with a CHA2DS2-VASc score of ≥4 had a higher frequency of CIN as compared with patients with score ≤3 (56.8% vs 4.8%; p = 0.0001) with multivariate analysis demonstrating CHA2DS2-VASc score of ≥4 to be an independent predictor of CIN. Conclusion In patients with ACS undergoing PCI, CHA2DS2-VASc score can be used as a novel, simple, and a sensitive diagnostic tool for the prediction of CIN