Medicinal, Psychological, and Health Research Journal (MPHRJ)

Abstract Introduction: Cardiac surgery is associated with substantial oxidative stress due to surgical trauma, cardiopulmonary bypass, and ischemia–reperfusion injury, which may contribute to postoperative organ dysfunction. Dexmedetomidine has shown potential antioxidative and organ-protective effects. Therefore, this study aimed to systematically review the effect of intraoperative intravenous dexmedetomidine on oxidative stress in patients undergoing cardiac surgery.

Material and methods: This systematic review followed PRISMA guidelines to identify clinical studies on intraoperative intravenous dexmedetomidine and oxidative stress in cardiac surgery. Multiple databases were searched without time limits by two independent reviewers using Boolean-based keywords. Eligible studies were screened, quality-assessed with the Cochrane Risk of Bias tool, and relevant study, patient, intervention, and outcome data were extracted.

Results: Across clinical and experimental cardiopulmonary bypass-related settings, intraoperative intravenous dexmedetomidine showed a broadly protective profile. It attenuated perioperative stress responses, reduced selected markers of myocardial injury and inflammation, improved hemodynamic and recovery outcomes, and lowered postoperative atrial fibrillation. Experimental evidence further indicated direct cardiomyocyte protection through antioxidant, antiapoptotic, autophagy-regulating, electrophysiological, and transcriptional mechanisms.

Conclusion: The available evidence suggests that intraoperative intravenous dexmedetomidine may mitigate oxidative stress-related injury during cardiac surgery through both systemic and cellular mechanisms. Its benefits appear to include attenuation of surgical stress, reduction of selected inflammatory and myocardial injury markers, and improvement in postoperative recovery. These findings support dexmedetomidine as a promising cardioprotective adjunct in cardiac surgical care.

Abstract Introduction: Intravenous dexmedetomidine may influence cardiomyocyte biology through effects on apoptosis, inflammation, oxidative stress, and mitochondrial function, with possible relevance in perioperative and critical care settings. However, available evidence remains heterogeneous and translationally uncertain. This study aims to systematically evaluate its cellular effects on cardiomyocytes and clarify their clinical relevance.

Material and methods: This systematic review followed PRISMA guidelines, searched PubMed, Scopus, Web of Science, and Embase without time restriction using Boolean operators, and included original English studies on intravenous dexmedetomidine and cardiomyocyte biology. Study selection and quality assessment were performed independently by two reviewers, and key methodological and outcome data were extracted from each article.

Results: Dexmedetomidine consistently exerts direct cardiomyocyte-protective effects by attenuating apoptosis, oxidative stress, and inflammation across various stress models. Key mechanisms include activation of antioxidant pathways, enhanced autophagic flux via adrenergic signaling, and epigenetic regulation of anti-inflammatory axes. Additionally, it modulates electrophysiological properties by suppressing sodium and calcium currents, demonstrating a pleiotropic capacity to preserve cellular homeostasis and functional integrity.

Conclusion: Dexmedetomidine functions as a potent pleiotropic modulator of cardiomyocyte biology, providing robust protection against ischemic and oxygen-related stress. Beyond its sedative properties, it directly influences survival signaling, redox balance, and electrophysiology through diverse molecular pathways. These findings underscore its potential as a targeted cardioprotective agent, necessitating further clinical exploration to translate these cellular benefits into perioperative patient care.

Abstract Introduction: Critically ill patients with COVID 19 exhibit a pronounced hypercoagulable state, predisposing them to deep vein thrombosis during ICU admission. Inflammation driven endothelial dysfunction, hypoxia, and immobilization contribute to this elevated risk. Determining the true prevalence of DVT in this population is essential for optimizing thromboprophylaxis strategies and improving clinical outcomes.

Material and methods: This retrospective observational study evaluated critically ill patients with concurrent COVID 19 and active malignancy admitted to a tertiary ICU. Clinical records, laboratory parameters, and imaging confirmed thrombotic events were systematically analyzed. Multivariable logistic regression was applied to identify independent risk factors for vascular thrombosis, providing clinically relevant insights for risk stratification and management in this high risk population.

Results: Thrombotic complications occurred in 28.3% of critically ill ICU patients with concurrent COVID 19 and active malignancy, while 71.7% remained free of thrombosis (P < 0.001). Among affected patients, venous thromboembolism predominated, with lower extremity deep vein thrombosis and pulmonary embolism being the most frequent manifestations, whereas arterial, cerebral, and coronary events were uncommon.

Conclusion: In conclusion, thrombotic complications remain a common and clinically significant problem among ICU patients with concurrent COVID 19 and active malignancy. Venous thromboembolism predominates, and its occurrence is associated with older age, higher BMI, specific cancer types, greater comorbidity burden, prolonged ICU stay, increased need for mechanical ventilation, and higher mortality.

Abstract Introduction: Mechanical prosthetic valve thrombosis is a life threatening complication associated with substantial in hospital mortality, and early prognostic stratification remains clinically challenging. Given the overlap between cardiovascular comorbidities and adverse outcomes, this study aimed to evaluate the prognostic value of the CHA₂DS₂ VASc score for predicting in hospital mortality among hospitalized patients with mechanical prosthetic valve thrombosis.

Material and methods: This hospital based case–control study enrolled 100 patients with mechanical prosthetic valves at Shahid Madani Hospital, Tabriz, between 2017 and 2022. Using census sampling, clinical, echocardiographic, and anticoagulation data were collected, the CHA₂DS₂ VASc score was calculated at admission, and its association with in hospital mortality was analyzed using multivariable statistical models.

Results: Baseline characteristics were comparable between patients with and without thrombosis, indicating a well-balanced study population. The CHA₂DS₂‑VASc score did not differ significantly between thrombotic and non‑thrombotic groups (P = 0.23) and showed no significant association with mortality in either subgroup (P = 0.461 and P = 0.127). ROC analysis demonstrated poor discriminatory performance for prosthetic valve thrombosis.

Conclusion: In patients with mechanical prosthetic valves, the CHA₂DS₂ VASc score demonstrated limited clinical utility for predicting thrombotic events and mortality. Despite its established role in thromboembolic risk stratification for atrial fibrillation, the score failed to effectively discriminate patients at risk for prosthetic valve thrombosis or adverse survival outcomes.

Abstract Introduction: ST-segment elevation myocardial infarction (STEMI) demands rapid risk stratification, often limited by the availability of complex scores. The Modified Shock Index (MSI), derived from routine vital signs, reflects acute circulatory stress. This study aims to determine the predictive correlation between admission MSI values and the underlying angiographic coronary anatomy, specifically the number and type of involved vessels, thereby assessing MSI’s utility as a simple bedside marker for disease complexity in STEMI patients.

Material and methods: This cross-sectional study analyzed 234 consecutive STEMI patients via census sampling at Shahid Madani Hospital in Tabriz between 2018 and 2019. The core procedure involved calculating the Modified Shock Index (MSI) from vital signs recorded at admission. The study then correlated these pre-treatment MSI values with the detailed coronary anatomy determined by subsequent angiography to assess the extent of vessel involvement.

Results: Patients with high MSI (>0.897) were older (61 vs. 57 years, p = 0.002) and had higher rates of hypertension (p = 0.008), diabetes mellitus (p = 0.002), and dyslipidemia (p = 0.009), along with longer chest pain duration (p = 0.004) and elevated WBC (p = 0.001), troponin (p = 0.002), and creatinine levels (p = 0.001). MSI did not differ by number or type of involved vessels (all p > 0.05) but showed moderate predictive value for MACE (pre‑PPCI AUC = 0.677; post‑PPCI AUC = 0.631; both p < 0.001).

Conclusion: In conclusion, this study demonstrates that the Modified Shock Index is closely associated with patient‑level vulnerability and acute disease severity rather than the anatomical extent or distribution of coronary artery involvement in STEMI.

Abstract Introduction: Mechanical mitral valve replacement is associated with a persistent risk of thrombotic complications despite appropriate anticoagulation. Identifying reliable clinical predictors of thrombosis remains a major challenge in this high risk population. This study aimed to evaluate the predictive value of the CHA₂DS₂ VASc score for thrombotic events in patients following mechanical mitral valve replacement.

Material and methods: This case-control study was conducted at Shahid Madani Hospital, Tabriz University of Medical Sciences, from 2017 to 2021. It included 100 consecutive patients who underwent mechanical mitral valve replacement. The primary objective was to evaluate the predictive value of the CHA₂DS₂-VASc score for thrombotic events in this cohort.

Results: In this cohort of 100 patients with mechanical mitral valve replacement, no significant differences were observed between patients with and without thrombosis regarding age (p = 0.148), sex (p = 0.944), comorbidities, valve type, left ventricular ejection fraction (p = 0.723), warfarin dose (p = 0.447), INR levels (p = 0.620), or individual CHA₂DS₂‑VASc components (all p > 0.05).

Conclusion: This study demonstrates that traditional clinical and demographic risk factors, including those incorporated into the CHA₂DS₂ VASc score, do not independently predict prosthetic valve thrombosis in patients with mechanical mitral valves when anticoagulation intensity is considered.

Abstract Introduction: Mechanical aortic valve replacement requires lifelong anticoagulation, yet prosthetic valve thrombosis (PVT) can occur even with therapeutic INR levels, suggesting additional mechanisms beyond standard risk factors. This study aimed to determine whether the CHA₂DS₂ VASc score independently predicts PVT in mechanical aortic valve recipients, providing insight into whether classical thromboembolic predictors apply to this distinct clinical condition.

Material and methods: This case–control study was conducted at Shahid Madani Heart Center, Tabriz, Iran, between 2017 and 2021. Using a census sampling method, 100 patients with mechanical mitral valve replacement were enrolled. Clinical, echocardiographic, and anticoagulation data were retrospectively collected to compare patients with confirmed prosthetic valve thrombosis and matched controls without thrombosis.

Results: After excluding patients with subtherapeutic anticoagulation, 22 patients with prosthetic valve thrombosis and 78 controls were analyzed. Baseline demographic, clinical, and anticoagulation parameters were comparable between groups, with no significant differences observed. The mean CHA₂DS₂ VASc score was numerically higher in the thrombosis group but did not differ significantly between groups (p = 0.23).

Conclusion: In this cohort of patients with mechanical prosthetic valves who maintained therapeutic anticoagulation, traditional clinical and demographic factors were not associated with the development of prosthetic valve thrombosis.