European Journal of Cardiovascular Medicine

Background: This study is done to compare the biomarkers CRP(c reactive protein) and NLR (Neutrophil lymphocyte ratio) in predicting the severity of acute pancreatitis. Here 92 patients were enrolled in the study spanning over a period of 4 months from January to April 2025 in Victoria hospital Bangalore. Out of the 92 patients 57 patients were of mild and moderate severity and rest 35 were of severe cases according to CTSI (Computerised tomography severity index). The CRP and NLR was sent at the time of admission (0hrs) and at 48hrs of admission (48hrs) and CECT (Contrast enhanced computerised tomography) scan was done . The admitted patients was treated according to their severity and the outcome and complications documented. The correlation of CTSI was done with CRP and NLR values at 0hrs and 48hrs and results were drawn. ANOVA shows significant changes in both CRP(0 hrs: F = 25.689, p = 0.0005; 48 hrs: F = 29.574, p = 0.0005) and NLR(0 hrs: F = 34.830, p = 0.0005; 48 hrs: F = 54.330, p = 0.0005) at 0hrs and 48hrs indicating both CRP and NLR to be valuable in predicting the severity of the disease. Paired t test shows NLR to have significant change from 0 hrs to 48hrs(7.85 ± 3.11 to 8.84 ± 3.83)  as compared to CRP(185.33 ± 109.08 to 186.65 ± 104.10) with confidence interval of 95% (–1.35 to –0.62) implying NLR better in determining prognosis of the patient. Logistic regression implies CRP to be better at time of diagnosis and NLR is better at predicting the prognosis of the patient. Hence both CRP and NLR are independent in predicting the severity of pancreatitis, but NLR shows a better predilection in determining the prognosis of the patient.

Background: Differentiating uncomplicated from complicated acute appendicitis remains a significant clinical challenge despite advances in diagnostic imaging. Recent evidence suggests that hyponatremia may serve as a reliable biomarker of severe intra-abdominal inflammation. This study aimed to evaluate the diagnostic role of serum sodium in predicting complicated appendicitis. Methods: A comparative observational study was conducted in 80 patients clinically diagnosed with acute appendicitis. Serum sodium levels were measured at admission, and patients were categorized into uncomplicated and complicated groups based on intraoperative and histopathological findings. Statistical analysis included Student’s t-test, chi-square test, odds ratio estimation, and ROC curve analysis. Results: Serum sodium levels were significantly lower in complicated appendicitis (132.4 ± 3.1 mEq/L) compared to uncomplicated cases (136.8 ± 2.9 mEq/L; p<0.001). Hyponatremia (<135 mEq/L) was present in 70% of complicated versus 15% of uncomplicated cases (p<0.001). Hyponatremia increased the odds of complicated appendicitis by more than fivefold (OR 5.32; 95% CI 2.10–13.47). ROC analysis showed good discriminatory ability (AUC 0.84), with an optimal cut-off of 134 mEq/L yielding 82.5% sensitivity and 75% specificity. Conclusion: Hyponatremia is strongly associated with complicated appendicitis and demonstrates excellent diagnostic accuracy. Serum sodium is an inexpensive, readily available biomarker that can enhance early risk stratification and support timely surgical decision-making. Its integration into routine evaluation may improve clinical outcomes.

Background: Recurrent stroke is associated with higher mortality, greater functional disability, and increased healthcare burden compared with first‑ever stroke, yet many contributory lifestyle and clinical risk factors remain suboptimally controlled in routine practice. This study aimed to evaluate the influence of lifestyle and clinical determinants on outcomes after recurrent stroke in a tertiary care centre.Methods: A hospital‑based prospective study was conducted over one year among 104 patients presenting with second or subsequent ischemic or intracerebral haemorrhagic stroke, confirmed on neuroimaging. Detailed history, clinical examination, and investigations (including vascular imaging, cardiac evaluation, and laboratory tests) were recorded using a structured proforma. Lifestyle factors (smoking, alcohol use, physical inactivity, obesity) and clinical risk factors (hypertension, diabetes, dyslipidaemia, cardiac disease, atrial fibrillation, medication non‑adherence) were documented. Functional outcome was assessed using the modified Rankin Scale (mRS) at admission, discharge, and 3‑month follow‑up. Data were analysed using chi‑square test for categorical variables and Student’s t‑test for continuous variables, with p<0.05 considered statistically significant. Results: Of the 104 patients, 86.5% had recurrent ischemic stroke and 13.5% had recurrent haemorrhagic stroke, with a male predominance and mean age around 60 years in both groups. Hypertension (66.3%) and dyslipidaemia (63.5%) were the most prevalent risk factors and showed significant association with haemorrhagic recurrence, while diabetes, smoking, and alcohol use were more frequent in ischemic events but without statistical significance. A majority of patients (over two‑thirds) experienced recurrence more than 12 months after the index stroke, indicating gaps in long‑term secondary prevention. At admission, 81.7% had poor functional status (mRS 3–6); this improved to 53.8% with good outcome at discharge and 88.5% with good outcome at 3 months, although overall mortality remained 4.8% and was higher in the haemorrhagic group. Conclusion: Lifestyle and clinical risk factors, particularly uncontrolled hypertension and dyslipidaemia, play a pivotal role in determining the pattern and outcome of recurrent stroke in this tertiary care setting. Despite substantial functional recovery by 3 months in most survivors, the high burden of modifiable risk factors and delayed recurrence beyond one year highlight the need for sustained, intensive secondary prevention, patient education, and long‑term follow‑up to reduce recurrent events and improve prognosis.

Introduction: Amiodarone, a class III antiarrhythmic agent, is widely employed in the management of supraventricular and ventricular tachyarrhythmias. While hepatotoxicity related to chronic oral administration is a well-recognized complication, acute hepatic injury following intravenous (IV) amiodarone is exceedingly rare and potentially fatal. The mechanism is multifactorial, often attributed to the solvent polysorbate 80, which may induce mitochondrial dysfunction and hepatic ischemia. We present a case of acute, reversible hepatocellular injury following IV amiodarone infusion, successfully managed with early discontinuation of the drug and administration of intravenous N-acetylcysteine (NAC). Case Presentation: A 74-year-old male with a history of hypertension and dyslipidemia presented with acute abdominal pain and was diagnosed with a perforated duodenal ulcer. Following emergency laparotomy and primary repair, the patient developed postoperative respiratory failure requiring ICU care and mechanical ventilation. During his ICU stay, he developed new-onset atrial fibrillation with rapid ventricular response, for which IV amiodarone was initiated (150 mg loading followed by continuous infusion). Within 24 hours, the patient reverted to sinus rhythm but exhibited a sharp rise in hepatic transaminases   AST 5024 U/L, ALT 1393 U/L   with mild hyperbilirubinemia (1.6 mg/dL) and normal alkaline phosphatase levels. No hypotension, hypoxia, or exposure to other hepatotoxic drugs was noted. Viral and autoimmune hepatitis panels were negative, and abdominal ultrasound revealed normal hepatic architecture. The diagnosis of IV amiodarone-induced acute hepatocellular injury was made based on clinical chronology and exclusion of alternative causes. Amiodarone was discontinued, and IV N-acetylcysteine was initiated using a standard 5-day infusion protocol (150 mg/kg loading dose followed by 50 mg/kg and 100 mg/kg maintenance doses). Remarkable biochemical improvement occurred within 48 hours, with normalization of liver enzymes by day five. The patient recovered completely and was discharged in stable condition, maintaining sinus rhythm on oral beta-blocker therapy. Discussion: Acute hepatocellular injury following IV amiodarone infusion is rare but potentially severe, with an onset typically within hours of drug administration. The hepatotoxic component is likely related to polysorbate 80, an emulsifying agent in the IV formulation, which induces mitochondrial damage, circulatory collapse, and hepatic ischemia. The biochemical pattern of massive aminotransferase elevation with mild bilirubin rise mimics ischemic hepatitis but in the absence of hypotension. N-acetylcysteine, originally developed for acetaminophen toxicity, has demonstrated efficacy in non-acetaminophen acute liver failure by replenishing glutathione stores, scavenging reactive oxygen species, and improving hepatic microcirculation. In this case, early NAC administration led to rapid enzyme normalization and clinical recovery, supporting its hepatoprotective role in IV amiodarone-induced hepatic injury. Conclusion: This case highlights that intravenous amiodarone can cause acute, severe but reversible hepatocellular injury even in patients with normal baseline liver function. Early recognition, immediate discontinuation of the drug, and timely administration of N-acetylcysteine can result in complete hepatic recovery and prevent progression to acute liver failure. Vigilant monitoring of liver function tests within the first 24 hours of infusion is crucial to ensure patient safety.