Hasan Tokdil

Background and Objectives: Comorbidities, the coexistence of additional conditions with a primary disease, are increasingly prevalent, complicating disease management and clinical outcomes. While CTEPH is a well-studied condition in terms of risk factors and outcomes, the specific impact of comorbidity burden on clinical presentation, treatment decisions, and survival remains insufficiently explored. This study aims to assess the prevalence and burden of comorbidities in CTEPH and to examine their associations with initial clinical characteristics, treatment allocation, and survival, stratified by pulmonary endarterectomy (PEA) status. Materials and Methods: We included 187 CTEPH patients from eight tertiary PH centers (2009–2020). Cardiovascular and non-cardiovascular comorbidities were identified and categorized as 0, 1–2, or ≥3. Their impact on baseline six-minute walk distance (6MWD), hemodynamic parameters, operability decision, and survival was assessed. Results: Comorbidities were prevalent (90%), with 49% of patients having three or more. Hypertension, diabetes, coronary artery disease, and chronic kidney disease (CKD) were associated with lower 6MWD. Hypertension, atrial fibrillation, left heart failure, and CKD were linked to elevated right atrial and pulmonary arterial wedge pressures. Comorbidities rendered 39% of anatomically operable patients ineligible for surgery. No single comorbidity predicted survival. Among PEA patients, those with ≥3 cardiovascular comorbidities had worse survival (p = 0.010). In contrast, the comorbidity burden did not impact survival in non-PEA patients. PEA surgery (HR 0.342, 95% CI 0.130–0.899, p = 0.030) and baseline 6MWD (HR 0.997, 95% CI 0.994–1.000, p = 0.036) were identified as independent predictors of mortality. Conclusions: A high comorbidity burden is common in CTEPH and influences functional status, hemodynamics, and operability decisions. It may worsen long-term outcomes after PEA but appears to be less prognostic in non-operated patients, where disease severity seems to be the primary determinant of outcomes. These findings underscore the importance of careful operability assessment and proactive comorbidity management.

Background and Objectives: The purpose of this study was to determine the factors that cause delay time in patients admitted to the hospital with STEMI. In addition, the effect of this delay on the patient’s prognosis has also been investigated. Materials and Methods: a total of 301 patients diagnosed with STEMI treated with primary percutaneous coronary intervention (pPCI) were included in the study. Reinfarction, revascularization, cerebrovascular event, and cardiac death were determined as major cardiac clinical events. The follow-up period of our study was 475 ± 193 days. Results: Univariate analysis revealed that factors influencing delay time included BMI, hypertension diabetes, smoking habit and variability in pain intensity. In multivariate logistic regression analysis, BMI, diabetes, hypertension, smoking, variation in pain intensity, and infarct-related artery other than the LAD were identified as independent factors associated with increased delay times. We determined the cut-off values predicting the composite endpoint as 122.5 min for patient delay, 95.5 min for system delay, and 371 min for total ischemic time. It was observed that the in-hospital NT pro-BNP values of the patients presenting early were lower (181 vs. 594 pg/mL p < 0.001), had a higher ejection fraction at the first measurement, and even improved at the sixth week of follow-up (p = 0.047). Conclusions: Prolonged ischemia duration was associated with several factors. Early reperfusion in STEMI patients reduces both cardiac death and clinical events. Delays are influenced by patient awareness, emergency care efficiency, and hospital-specific factors. Improving education, response times, and hospital protocols is essential to minimize delays and improve outcomes.

Current guidelines recommend the use of glycoprotein IIb/IIIa (GpIIb/IIIa) inhibitors in patients with ST-segment elevation myocardial infarction (STEMI) only as a bail-out therapy. However, drug penetration to the jeopardised area may not be achieved due to impeded blood flow and increased microvascular resistance. Aim of our study is to investigate the impact of distal intracoronary GpIIb/IIIa inhibitor agent infusion in STEMI patients. Primary endpoints were microvascular obstruction (MVO) and infarct size. Patients with STEMI who have high thrombus burden or slow-flow/NR phenomenon and undergoing primary percutaneous coronary intervention (pPCI) were enrolled. Tirofiban was the preferred GpIIb/IIIa inhibitor. Patients were assigned to the systemic intravenous infusion group and intracoronary infusion group in whom bolus dose of tirofiban was distally infused to the infarct related artery. MVO and size of the infarct size were assessed via cardiac MRI. We prospectively included 75 patients and mean follow-up duration was 383 days. Baseline characteristics were similar between groups except a lower rate of diabetes in distal intracoronary infusion group (p = .006). There was no significant difference in localisation of myocardial infarction, ischaemia duration and preloading of P2Y12 inhibitor between groups. MVO (p = .048) and infarct size (p = .030) were significantly lower in distal intracoronary infusion group. Cardiac MRI based assessment revealed that intracoronary administration of GpIIb/IIIa inhibitors distal to the culprit lesion was associated with reduced MVO and infarct size in high thrombotic risk STEMI patients undergoing pPCI.

Background: Heme oxygenase-1 (HO-1) is known to have anti-inflammatory, antiapoptotic and antioxidant effects in various diseases. In this study, we aimed to investigate whether HO-1 has a protective effect on isoprenaline (IP)-induced acute myocardial infarction (AMI) in rat.Materials and methods: Rats were received 200 mg/kg IP, alone or together with cobalt protoporphyrin (CoPP) and zinc protoporphyrin (ZnPP), an inducer and an inhibitor of HO-1, respectively. Four hours after the IP application, rats were killed. Blood and hearts were removed. Troponin-T (TnT) levels were assayed in serum as an indicator of AMI. Dien conjugate levels, protein carbonyl levels and antioxidant defense system are assayed in heart tissues by spectrophotometric methods. HO-1 protein levels were quantitated by western blot analysis in heart tissues. The results were compared with those obtained from control groups.Results: We confirmed AMI formation with higher serum TnT levels in IP-treated groups comparing to control groups. We found a significant elevation in HO-1 protein levels in IP plus CoPP-treated rats as compared to IP-treated rats, while serum TnT levels were observed to decrease at the same time. Protein carbonyl levels in heart tissues increased significantly in IP-treated groups compared with control groups. But, dien conjugate and antioxidant defense system remained unchanged.Conclusions: As a conclusion, we may suggest that HO-1 induction produces a protective effect against to myocardial damage occured by IP application in rat.