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.This study included 110 young (18-50 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.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.Lipid biomarkers such as Apo A1, Apo B and PON1 and their genetic polymorphism are associated with the susceptibility for STEMI in young individuals.
BackgroundPatients with severe mitral stenosis (MS) in normal sinus rhythm (NSR), presenting with left atrial appendage (LAA) inactivity and associated left atrial spontaneous echo contrast (LASEC), are prone to left atrial (LA) or LAA thrombus formation. But unlike atrial fibrillation (AF), oral anticoagulants (OAC) are not commonly prescribed for this patient subset. This study aimed to compare the levels of procoagulants and fibrinogen in both local (LA) and systemic contexts between patients with severe MS in NSR and healthy controls.MethodsThe study involved 35 patients with severe MS in NSR with LAA inactivity and LASEC eligible for balloon mitral valvuloplasty and 35 controls. All patients underwent transthoracic and trans-esophageal echocardiography to assess MS severity, LAA activity, and LASEC grade, with blood samples analysed for procoagulant levels.ResultsResults showed comparable baseline characteristics between groups, with most patients in NYHA II or III functional classes and varying LASEC grades. Patients exhibited significantly higher levels of prothrombin fragment 1+2 {patient vs control, 9017(6228.0-10963.5)pg/mL vs 1790(842.3-2712)pg/mL, p<0.0001)}, thrombin-antithrombin III {patient vs control, 39(5.45-74.85)ng/ml vs 2.80(1.6-6.5)ng/mL, p<0.0001}, plasminogen activator inhibitor-1 {patients vs controls, 26.09±8.18ng/mL vs 8.05±3.53ng/mL, p<0.0001)}, and fibrinogen (3.48±0.89g/L vs 3.01±0.53g/L, p=0.029) in the LA of patients compared to controls. Systemic procoagulant levels were also elevated in patients, but D-dimer levels were similar between the two groups.ConclusionThe findings suggest a hypercoagulable state in patients similar to those with AF. The study advocates for consideration of OAC in these patients until LA and LAA function improve to mitigate thrombus formation.
Abstract Background Patients of severe mitral stenosis (MS) in normal sinus rhythm (NSR) with left atrial appendage (LAA) inactivity and associated left atrial spontaneous echo contrast (LASEC) develop left atrial (LA) or LAA thrombus. But unlike atrial fibrillation (AF), oral anticoagulants (OAC) are not routinely prescribed in this subset of patients. Aim To assess local (LA) and systemic levels of procoagulants (PF1+2: prothrombin fragment 1+2; TAT-III: thrombin antithrombin III), PAI-1 (plasminogen activator inhibitor-1) and fibrinogen, in patients of severe MS in NSR with LAA inactivity and associated LASEC with healthy controls. Methods 35 patients of severe MS with valve suitable for balloon mitral valvuloplasty, along with 35 healthy volunteers were enrolled. All patients underwent transthoracic and transesophageal echocardiography to assess severity of MS, LAA activity, grade of LASEC, and exclude the presence of LA or LAA clot. Peripheral venous and LA blood samples were analysed for levels of procoagulants. Results Baseline characteristics like age and sex were comparable in both groups. Most of the patients in our study were either in NYHA II (n=13, 37.1%) or NYHA III functional class (n=21, 60%) and had grade 3+ (n=17;48.57%) or grade 4+ (n =15;42.86%) LASEC. Levels of PF1+2 {patient vs control, 9017(6228-10963.5) pg/mL vs 1790(842.3-2712) pg/mL, p<0.0001)}, TAT-III {patient vs control, 39(5.45-74.85) ng/ml vs 2.80(1.6-6.5) ng/mL, p<0.0001}, PAI-1 {patient vs control, 26.09±8.18 ng/ml vs 8.05 ± 3.53ng/ml. p<0.0001)}and fibrinogen (3.48± 0.89g/L vs 3.01± 0.53g/L, p=0.029) were significantly higher in LA of patients as compared to controls. Similarly, systemic levels of PF1+2, TAT-III, PAI-1 and fibrinogen were significantly higher in patients as compared to controls. However, systemic level of D-dimer was similar in both groups. Conclusion Both local and systemic levels of procoagulants were significantly raised in patients of severe MS in NSR with LAA inactivity and associated grade 3+ or 4+ LASEC, suggestive of a hypercoagulable state similar to that reported in patients of AF. Hence, we feel that OAC should be administered routinely in this subgroup of patients to prevent thrombus formation until there is improvement in LA and LAA function following valvuloplasty or mitral valve surgery. Clinical Perspective What’s new? Patients of severe MS in NSR with LAA inactivity and associated LASEC are prone to develop LA or LAA thrombus. However, the ACC/AHA 2020 guidelines on valvular heart disease still do not recommend oral anticoagulants in this subset of patients. We carried out an adequately powered study to assess the level of procoagulants in patients of severe MS in NSR with associated LASEC (LASEC being a marker of stasis). What are the clinical implications? Both local and systemic levels of procoagulants were significantly raised in patients of severe MS in NSR with LAA inactivity and associated grade 3+ or 4+ LASEC as compared to controls, suggestive of a hypercoagulable state similar to that reported in patients of AF. We feel that OAC should be administered routinely in this subgroup of patients of rheumatic MS in NSR to prevent thrombus formation until there is improvement in LA and LAA function following valvuloplasty or MV surgery.
Coronavirus disease (COVID-19) is a systemic illness characterized by raging impact of cytokine storm on multiple organs. This may trigger malignant ventricular arrhythmias and unmask a clinically silent cardiomyopathy.A 57-year-old gentleman, known case of hyperthyroidism and diabetes, was referred to our emergency department with history of two ventricular tachycardia (VT) episodes requiring direct current cardioversion in last 3 h followed by another episode in our emergency department that was cardioverted. There was no past history of cardiac illness. His 12-lead electrocardiogram (during sinus rhythm) along with screening echocardiography suggested Arrhythmogenic right ventricular cardiomyopathy (ARVC). He was coincidentally found to be COVID-19 positive by reverse transcription-polymerase chain reaction (RT-PCR) as part of our routine screening. However, he had no fever or respiratory complaints. We noted raised systemic inflammatory markers and cardiac troponin T which progressively increased over the next 4 weeks paralleled by an increase in ventricular premature contraction burden and thereafter started decreasing and returned to baseline by 6th week when the patient became COVID-19 negative by RT-PCR. Subsequently, a single-chamber automated implantable cardioverter-defibrillator implantation was done following which there was a transient increase in these biomarkers that subsided spontaneously. The patient is asymptomatic during 6 weeks of follow-up.COVID-19-associated cytokine surge triggering VT storm and unmasking a clinically silent ARVC has not yet been reported. The case highlights a life-threatening presentation of COVID-19 and indicates a probable link between inflammation and arrhythmogenicity.
Background Different treatment approaches exist for non-ST elevation acute coronary syndrome (ACS) patients. This study assessed the systemic immune inflammatory response index (SIIRI) for its prognostic value and incremental clinical utility in determining optimal timing for percutaneous coronary intervention (PCI) in non-ST elevation myocardial infarction (NSTEMI) patients, particularly when troponin levels are initially negative. Methods This study included 1270 ACS patients: 437 STEMI, 422 NSTEMI, and 411 unstable angina. Patients were stratified by SIIRI levels measured at admission, and coronary artery disease severity was evaluated using the SYNTAX score. The primary endpoint was major adverse cardiovascular events (MACE), including cardiovascular death, non-fatal myocardial infarction, stroke, and revascularization. Secondary endpoints encompassed individual MACE components and heart failure hospitalisations. Results The mean age was 54.93 years (83% male). SIIRI levels were significantly higher in STEMI patients (6.83 ± 6.43 × 10 5 ) compared to NSTEMI (4.5 ± 5.39 × 10 5 ) and unstable angina (3.48 ± 2.83 × 10 5 ) ( P < 0.001). Area under the curve for SIIRI distinguished NSTEMI and unstable angina from STEMI (0.81 and 0.80), with optimal cut-off points of 4.80 × 10 5 and 4.25 × 10 5 . In NSTEMI, 24.6% presented within 2 h of symptom onset, were troponin-negative, yet had elevated SIIRI. Post-PCI, SIIRI > 4.93 × 10 5 correlated with increased MACE at 1 year (17.2% vs 5%). Conclusion NSTEMI and unstable angina patients with SIIRI values >4.80 × 10 5 and 4.25 × 10 5 respectively, may require urgent intervention (<2 h). SIIRI can be of significant utility in patients of NSTEMI who present earlier with negative troponins. SIIRI can also aid in identifying high-risk individuals post-PCI, providing a valuable tool for early and accurate assessment.
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) ST-segment elevation myocardial infarction (STEMI) patients.This study included 100 young (18-50 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 (-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.Serum levels of MMP-3 (128.16 ± 115.81 vs 102.3 ± 57.28 ng/mL; P = 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 = 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%.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.
Abstract Background Acute fracture of a left main (LM) stent during angioplasty is a rare complication. Cardiologists should be aware of the risk of stent fracture (SF) following kissing balloon inflation (KBI) even if the effective diameter of the balloons does not exceed the recommended expansion limits of stents. Case summary A 64-year-old female with hypertension and dyslipidaemia presented with crescendo angina since three months in spite of optimal medical therapy. Coronary angiogram showed a distal LM bifurcation lesion. The patient was admitted for LM bifurcation stenting by upfront two-stent technique (inverted double-kissing Culotte technique). Following first KBI of the stent placed from left circumflex artery (LCX) to LM, there was stent deformation in the LM shaft. As we had planned the Culotte technique, we decided to exclude the fractured segment by stenting from left anterior descending artery (LAD) to LM. The stent from LAD–LM successfully excluded the fractured part of the first stent from the lumen of LM. Optical coherence tomography done after final KBI from LCX–LM revealed successful exclusion of the deformed segment of the LCX stent with mild malapposition at the site of the deformed stent. A follow-up angiogram after six months showed normal in-stent flow with no evidence of restenosis or pseudoaneurysm. Discussion Acute LM SF during coronary intervention can occur even if the effective cumulative diameter of the inflated balloons does not exceed the mentioned expansion limit of stents. Intravascular imaging is a helpful modality to define type of SF and its management.
Efficacy of balloon mitral valvuloplasty (BMV) in low gradient severe rheumatic mitral stenosis (MS) is not very well defined. This study was undertaken to evaluate the outcomes of BMV in low gradient severe rheumatic MS.
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