In 2016, the Lipid Association of India (LAI) developed a cardiovascular risk assessment algorithm and defined low-density lipoprotein cholesterol (LDL-C) goals for prevention of atherosclerotic cardiovascular disease (ASCVD) in Indians. The recent refinements in the role of various risk factors and subclinical atherosclerosis in prediction of ASCVD risk necessitated updating the risk algorithm and treatment goals. The LAI core committee held twenty-one meetings and webinars from June 2022 to July 2023 with experts across India and critically reviewed the latest evidence regarding the strategies for ASCVD risk prediction and the benefits and modalities for intensive lipid lowering. Based on the expert consensus and extensive review of published data, consensus statement IV was commissioned. The young age of onset and a more aggressive nature of ASCVD in Indians necessitates emphasis on lifetime ASCVD risk instead of the conventional 10-year risk. It also demands early institution of aggressive preventive measures to protect the young population prior to development of ASCVD events. Wide availability and low cost of statins in India enable implementation of effective LDL-C lowering therapy in individuals at high risk of ASCVD. Subjects with any evidence of subclinical atherosclerosis are likely to benefit the most from early aggressive interventions. This document presents the updated risk stratification and treatment algorithm and describes the rationale for each modification. The intent of these updated recommendations is to modernize management of dyslipidemia in Indian patients with the goal of reducing the epidemic of ASCVD among Indians in Asia and worldwide.

The association between duration of QRS and myocardial reperfusion is not very well established. Our aim was to assess the relationship between measurements of QRS duration and myocardial blush grade (MBG) in patients with ST-elevation myocardial infarction (STEMI) who were treated with a primary percutaneous coronary intervention (PCI). Between January 2016 and June 2017, 200 patients with STEMI who presented within 12 h of symptom onset and taken up for primary PCI were analyzed with electrocardiogram (ECG) before and after the procedure. Two study groups were then defined on the basis of microvascular perfusion: group A (MBG 0-1) and group B (MBG 2-3). Group A had a total of 80 patients, and group B had 120 patients. The baseline characteristics were similar in the two groups. QRS duration was found to be longer in group A compared with group B at both the immediate ECG (95.5 ± 15.63 vs 80.87 ± 12.80 msec, p < 0.001, respectively) and at the 60th minute ECG (96.95 ± 16.2 vs 78.82 ± 12.08 msec, p < 0.001, respectively) post angioplasty. Significant difference was detected between the two groups post-angioplasty at both the immediate (10.99 ± 10.05 vs -6.64 ± 10.61 msec, p < 0.001) and the 60th minute (13.03 ± 11.64 vs -7.95 ± 11.11 msec, p < 0.001) ECG. Using receiver operator curve analysis, we found that QRS complex narrowing of 4.5 msec post angioplasty was the best cutoff value for predicting reperfusion. QRS duration change post angioplasty is strongly correlated with the myocardial reperfusion in patients presenting with STEMI.

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 × 10⁵) compared to NSTEMI (4.5 ± 5.39 × 10⁵) and unstable angina (3.48 ± 2.83 × 10⁵) (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 × 10⁵ and 4.25 × 10⁵. In NSTEMI, 24.6% presented within 2 h of symptom onset, were troponin-negative, yet had elevated SIIRI. Post-PCI, SIIRI > 4.93 × 10⁵ correlated with increased MACE at 1 year (17.2% vs 5%). Conclusion: NSTEMI and unstable angina patients with SIIRI values >4.80 × 10⁵ and 4.25 × 10⁵ 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.

Background: 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. Case summary: 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. Discussion: 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.