Parjanya Bhatt

Atrial fibrillation (AF) is the most prevalent sustained arrhythmia and is increasingly driven by cardiometabolic disease, including type 2 diabetes mellitus (T2DM), obesity, and insulin resistance. These conditions promote atrial electrical instability and a permissive substrate through mitochondrial dysfunction, oxidative stress, inflammation, calcium-handling abnormalities, and profibrotic signaling, culminating in atrial fibrosis and conduction heterogeneity. Metformin, the foundational glucose-lowering therapy for T2DM, exerts pleiotropic actions that intersect with these upstream pathways. Beyond glycemic control, metformin induces mild mitochondrial complex I modulation with reduction of reverse electron transfer-derived reactive oxygen species, activates adenosine monophosphate (AMP) activated protein kinase, and attenuates nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)-mediated cytokine signaling; experimental data further suggest favorable effects on adiponectin–sarcoendoplasmic reticulum calcium adenosine triphosphatase (SERCA) 2a-dependent calcium cycling, connexin expression, small-conductance Ca²⁺-activated K+ channel remodeling, lipid handling, and transforming growth factor-β (TGF)-β-associated fibrotic remodeling. Observational cohort studies have reported associations between metformin exposure and a modest reduction in incident AF, particularly with longer treatment duration and in higher-risk metabolic phenotypes; device-based surveillance cohorts support a preventive association for new-onset AF rather than reduction of established AF burden. Data after catheter ablation suggest improved freedom from recurrence in metformin-treated patients, whereas evidence in postoperative AF is largely neutral, likely reflecting distinct acute mechanisms. Collectively, metformin may be best conceptualized as a potential substrate-modifying, upstream therapy candidate; however, confounding, exposure misclassification, and heterogeneity in comparators limit causal inference, underscoring the need for prospective randomized trials with AF endpoints. In practice, integration with comprehensive risk-factor modification (blood pressure, weight, sleep apnea, and glycemic optimization) remains essential when considering AF prevention strategies.

Aim: To study the relationship between the location of chest pain (topography) and site of coronary artery involvement in patients of Acute coronary syndrome (ACS) undergoing percutaneous transluminal coronary angioplasty (PTCA). Materials and Method: This observational study analyzed 589 angina topographic sites in 411 consecutive patients hospitalized for Acute Coronary syndrome (ACS) who underwent PTCA at a tertiary care center between January 2017 and December 2019. All parameters including the characteristics and site of the anginal pain, Electrocardiogram (ECG), and Coronary angiography (CAG) findings were recorded and analyzed for their topographical correlation with site of culprit vessel involvement. Result: Out of 411 patients, 337 were Males (82.0%) and 74 (18.0%) were females with 589 topographic sites of angina. The mean age of the study subject was 57.03± 11.28 years. In both ST elevation Myocardial Infarction (STEMI) and Non-ST-elevation Myocardial Infarction (NSTEMI), the Left anterior descending (LAD) was the most affected vessel in 201(63.4%) and 49(53.3%) respectively. The correlation coefficient for LAD occlusion was 0.298 (p=0.001) for the Retrosternal site. The Left Circumflex (LCX) artery showed a positive correlation of 0.647 (p= 0.001) for Jaw with Neck pain and of 0.585 (p=0.001) for Backache with Shoulder pain. The Right Coronary Artery (RCA) showed a positive correlation of 0.713 (p=0.001) for Retrosternal plus Jaw and Neck pain and of 0.719 (p=0.001) for Retrosternal plus Backache. Conclusion: The study reveals a significant correlation between chest pain topography and site of coronary artery involvement. It provides a basis for future research to develop tools that help healthcare professionals quickly identify culprit artery in ACS.

The current coronavirus disease 2019 (COVID-19) pandemic is one example of the scores of zoonotic diseases responsible for various outbreaks resulting in the deaths of millions of people for centuries. The COVID-19 pandemic has broken the age-old healthcare infrastructure and led to utter chaos. In the shadow of this pandemic, other zoonotic infections like the nipah virus, monkeypox, and langya virus, to name a few, have been neglected. Hence, outbreaks caused by such zoonotic viruses are rising in their endemic areas, like the Indian subcontinent. The mortality and morbidity due to such zoonoses are greater than usual due to the shortage of healthcare professionals caused by the COVID-19 crisis. Due to the lack of vaccines and therapeutics directed against this viral infection, treatment of patients is limited to supportive management and prevention, making preparedness for these potential zoonotic viral outbreaks essential. This paper highlights some of these zoonotic infections, which perpetuated and wreaked havoc while the world was occupied with containing the COVID-19 pandemic.

Self-medication is the use of drugs to treat self-diagnosed ailments without the use of a formal prescription. Self-medication is defined by the World Health Organization as the use of medications to address self-diagnosed diseases or symptoms. Over-the-counter (OTC) pharmaceuticals are medications that can be sold without a prescription directly to the client in accordance with the laws of each nation. During the COVID-19 pandemic, an increasing tendency in the use of OTC and self-medication was seen, with the situation in India particularly deteriorating due to lax regulatory restrictions. This has resulted in a slew of problems, ranging from a lack of drugs to severe responses due to overdosage and drug-drug combinations. There is an urgent need for more tangible regulatory control over self-medication and OTC medications to safeguard the uninformed populace from harm.