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Introduction: Empagliflozin, a sodium-glucose cotransporter 2 (SGLT2) inhibitor, improves cardiovascular outcomes in heart failure patients, but data regarding the efficacy of empagliflozin in the setting of acute myocardial infarction (AMI) is still unclear. The current study aimed to evaluate whether treatment with empagliflozin before primary percutaneous coronary intervention (PCI) improves parameters associated with patients' outcomes. Methods: We randomly assigned 101 non-diabetic and non-heart failure patients with ST-elevation myocardial infarction (STEMI) who underwent primary PCI to receive either empagliflozin (10 mg before PCI and once daily for 40 days) or placebo, in addition to the standard treatment. The primary outcomes were changes in left ventricular ejection fraction (LVEF) 40 days after PCI, changes in cardiac troponin I (cTnI) and estimates of its area under the curve (AUC) and the peak level, and resolution of ST-segment in > 50% of leads 90 min after PCI. Results: No significant difference was observed in terms of the occurrence of ST-segment resolution > 50% (46.0% versus 45.0%; p = 0.92) and the mean level of cTnI at each time point between the two groups. The estimated mean [standard deviation (SD)] AUC of cTnI was 955.0 (595.7) ng h/ml in the intervention and 999.7 (474.7) ng h/ml in the control groups (p = 0.85) without any significant difference in peak cTnI level. The mean (SD) LVEF 40 days after primary PCI was significantly higher in empagliflozin-treated patients than the placebo group [43.2% (5.8%) versus 39.2% (6.7%); p = 0.002]. Conclusion: In this study, no significant differences were observed across the groups in terms of cTnI levels and ST-segment resolution in patients with STEMI undergoing primary PCI. However, it shed light on the potential benefits of empagliflozin in improving LVEF following STEMI. Registration: Iranian Registry of Clinical Trials Platform (https://irct.behdasht.gov.ir/) identifier number IRCT20111206008307N42. [ABSTRACT FROM AUTHOR]

Introduction: Percutaneous Coronary Intervention (PCI) is a fundamental procedure for coronary artery disease management, yet the risk of adverse events such periprocedural myocardial injury (PMI) persists. This double-blind, randomized clinical trial aims to assess the efficacy of empagliflozin in preventing myocardial injury during PCI procedure. Methods: A total of 90 patients were randomly assigned to two groups A and B; Group A as the intervention group received empagliflozin 25 mg 24 hours before and empagliflozin 10 mg 1-2 hours before coronary intervention and group Bas the control group received placebo at similar intervals. The primary outcome involved comparing baseline, 8-hour, and 24-hour cTnI and baseline and 24-hour hs-CRP levels after PCI in both groups to measure the incidence of periprocedural myocardial injury (PMI) and anti-inflammatory effects of empagliflozin. Results: Baseline cTnI levels with P = 0.955, 8 hours after PCI with P = 0.469, and 24 hours after the intervention with P = 0.980 were not statistically different in the two groups. Baseline levels of hs-CRP in both intervention and control groups were not statistically significantly different (P = 0.982). Also, there was no statistically significant difference in hs-CRP levels 24 hours after PCI in two groups (P = 0.198). Finally, the results showed that MACEs did not occur in any of the groups. Conclusion: The results of this trial could not express the advantages of acute pretreatment with empagliflozin in preventing PCI-related myocardial injury. [ABSTRACT FROM AUTHOR]

Purpose: There is accumulating evidence regarding the potential benefits of empagliflozin in individuals with acute myocardial infarction (MI). Based on the literature, colchicine could also reduce the risk of MI and death in individuals with cardiovascular disease (CVD). However, trials investigating the effects of the combination of empagliflozin with colchicine and high-dose empagliflozin monotherapy in this setting are lacking. Methods: In this trial, 106 non-diabetic participants with reduced left ventricular ejection fraction (LVEF) following recent ST-elevation MI were randomly assigned to empagliflozin 10 mg/day, empagliflozin 10 mg/day plus colchicine 0.5 mg twice daily, or empagliflozin 25 mg/day groups within 72 h after primary percutaneous coronary intervention (PCI). The study's primary outcomes were the changes in New York Heart Association (NYHA) functional class and high-sensitivity C-reactive protein (hs-CRP) over 12 weeks. Results: The baseline characteristics of individuals were statistically similar between the study groups. Changes in NYHA functional class over 12 weeks were not significantly different between the study groups. hs-CRP was significantly reduced in all groups (all P < 0.001); however, there was no significant change between the groups over the study period. Changes in tumor necrosis factor-alpha (TNF-α), LVEF, and left ventricular end-diastolic dimension (LVEDD) during the research period did not differ significantly between groups. Conclusion: This study showed that neither the combination treatment of empagliflozin 10 mg/day with colchicine nor the monotherapy of empagliflozin 25 mg/day was superior to empagliflozin 10 mg/day in terms of changes in clinical, inflammatory, and echocardiographic outcome parameters in patients with recent MI with reduced LVEF over 3 months. Further studies are warranted to confirm the findings. Trial registration: Clinical trial ID: IRCT20111206008307N39. Registration date: 27 October 2022. https://www.irct.ir/trial/66216 [ABSTRACT FROM AUTHOR]

Introduction: It is well-established that oxidative stress is deeply involved in myocardial ischemia-reperfusion injury. Considering the potent antioxidant properties of coenzyme Q10 (CoQ10), we aimed to assess whether CoQ10 supplementation could exert beneficial effects on plasma levels of oxidative stress biomarkers in patients with ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPIC). Methods: Seventy patients with the first attack of STEMI, eligible for PPCI were randomly assigned to receive either standard treatments plus CoQ10 (400 mg before PPCI and 200 mg twice daily for three days after PPCI) or standard treatments plus placebo. Plasma levels of oxidative stress biomarkers, including superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), total antioxidant capacity (TAC), and malondialdehyde (MDA) were measured at 6, 24, and 72 hours after completion of PPCI. Results: The changes in plasma levels of the studied biomarkers at 6 and 24 hours after PPCI were similar in the both groups (P values > 0.05). This is while at 72 hours, the CoQ10-treated group exhibited significantly higher plasma levels of SOD (P value < 0.001), CAT (P value = 0.001), and TAC (P value < 0.001), along with a lower plasma level of MDA (P value = 0.002) compared to the placebo-treated group. The plasma activity of GPX showed no significant difference between the groups at all the study time points (P values > 0.05). Conclusion: This study showed that CoQ10 has the potential to modulate the balance between antioxidant and oxidant biomarkers after reperfusion therapy. Our results suggest that CoQ10, through its antioxidant capacity, may help reduce the reperfusion injury in ischemic myocardium. [ABSTRACT FROM AUTHOR]

Due to the potential benefits of triamterene in diuretic resistance, this study was performed to assess whether triamterene add‐on to the standard treatment of heart failure (HF)‐related diuretic resistance improves outcomes. A randomized clinical trial was performed on 45 hospitalized patients with HF with reduced ejection fraction who had diuretic resistance. Patients were randomized to receive either triamterene 50 mg plus hydrochlorothiazide 25 mg (n = 23) or hydrochlorothiazide 50 mg alone (n = 22) until hospital discharge. The primary outcomes were changes in weight and fluid input‐to‐output ratio. Secondary outcomes were respiratory rate, hospitalization duration, serum sodium and potassium, estimated glomerular filtration rate, creatinine, and blood urea nitrogen levels during the study period. The mean (standard deviation) of weight changes was not significantly different in the intervention and the control groups (−6.3 [4.8] vs −4.8 [2.4] kg, respectively; P =.1). No significant differences were shown in input‐to‐output changes between the 2 groups (208.0 [243.4] in the intervention and 600.2 [250.3] in the control group; P =.4). Although the respiratory rate of triamterene‐treated patients decreased, the difference did not reach statistical significance (P =.2). Other secondary outcomes were also similar in both groups. This study did not support the use of triamterene as an add‐on therapy for patients with HF‐related diuretic resistance. [ABSTRACT FROM AUTHOR]

Introduction: Data has shown that pharmacist-directed health services play a key role in the treatment of hypertension. Aim: We aimed to perform this study to compare two methods of the pharmacist-directed home blood pressure monitoring (HBPM) and the usual care. Methods: A total of 126 patients with uncontrolled blood pressure (BP) were randomized 1:1 into the pharmacist-directed HBPM and the usual care groups. In the intervention group, the patients were trained to measure their BPs and adjust their medications based on the designed protocol under the supervision of a clinical pharmacist. The primary endpoint of the study was the comparison of the BPs at baseline and months 1, 3, and 6. Results: One month after the allocation, the baseline systolic BP (SBP) (150.5 ± 13.1 vs. 149.7 ± 11.2 mm Hg; P = 0.71) and diastolic BP (DBP) (97.2 ± 9.8 vs. 93.6 ± 14.5; P = 0.11) significantly dropped to the control range equally in 85.2% of the patients in two groups (SBP: 128.8 ± 6.4 vs. 125.6 ± 7.1 mm Hg; P = 0.01 and DBP: 89.1 ± 6.2 vs. 81.5 ± 6.0 mm Hg; P = 0.01). This pattern continued during the study period (month 6; SBP: 115.6 ± 10.1vs. 116.1 ± 9.6 mm Hg; P = 0.78; DBP: 79.0 ± 5.0 vs. 77.2 ± 5.8 mm Hg; P = 0.08). Conclusions: In this study, we did not observe any significant difference between the pharmacist-directed HBPM and usual care methods in decreasing BP. [ABSTRACT FROM AUTHOR]

Because of the key role blood viscosity plays in the regulation of blood pressure (BP) and the hemorheological effects of pentoxifylline (PTX), this study was conducted to evaluate whether PTX can reduce BP when added to captopril in patients with stage 1 hypertension. In this randomized clinical trial 62 patients with stage 1 hypertension were entered. The intervention group (n = 30) received 1200 mg PTX in 3 divided doses plus 25 mg captopril 3 times a day, whereas the control group (n = 32) received only 75 mg captopril in 3 divided doses. Measurements of BP were done at baseline and in the first and second months after entering the study. Major adverse cardiac events during this period were recorded. When the systolic BP levels in the intervention and the control groups were compared, no significant differences at baseline (150.4 ± 6.03 versus 150.4 ± 6.2, P =.98) or first (138.4 ± 9.4 versus 142.3 ± 5.6, P =.08) or second (134.6 ± 8.9 versus 137.4 ± 6.0, P =.20) month of the study were noted. Similarly no significant difference was observed in the diastolic BP at baseline (91.7 ± 3.9 versus 92.0 ± 3.7, P =.84) or first (85.5 ± 5.1 versus 86.9 ± 3.8, P =.27) or second (82.6 ± 5.7 versus 84.0 ± 3.5, P =.31) month. Based on the results of present study, adding PTX as a hemorheological agent to captopril could not significantly reduce blood pressure in the patients with stage 1 hypertension. [ABSTRACT FROM AUTHOR]

Cell death following acute myocardial infarction (MI) is the hallmark pathology of cardiovascular disease, leading to considerable mortality and morbidity. Platelet and neutrophil activation and inflammatory cytokines, prominently TNF-α, play an important role in the development of cell death. Because pentoxifylline inhibits platelet and neutrophil activation and reduces TNF-α, this study was performed to assess the potential benefit of pentoxifylline in the reduction of myocardial injury following acute MI. In this randomized clinical trial, 98 patients with acute MI were randomly divided into 2 groups. The intervention group received an oral dose of 1200 mg of pentoxifylline immediately before thrombolytic therapy (TLT). All patients received the same standard protocol for treatment of MI. Cardiac enzymes were checked over 48 hours. ST resolution was measured over 90 minutes. Then all patients were followed up for a 1-month period to assess major adverse cardiac effects (MACEs). There were no significant differences in peak levels of CPK ( P = .18) and CK-MB ( P = .33) between the 2 groups, whereas peak level of troponin I was significantly lower in the pentoxifylline group (16.8 ± 10.4 vs 21.3 ± 11.6; P = .048). No significant change between the groups was observed in biomarkers levels, ST segment resolution, cardiac ejection fraction, and MACEs. The results showed that pentoxifylline significantly reduced the peak value of troponin I in patients with acute MI receiving TLT. No significant change was observed in the other studied parameters. Further outcome-based studies are needed to show the clinical relevance of differences between the groups in troponin peak. [ABSTRACT FROM AUTHOR]

Despite the known role of vitamin D deficiency in development of thrombosis, no studies have evaluated the impact of treating of vitamin D deficiency on the markers of thrombosis. A pilot randomized clinical trial was done on 40 vitamin D-deficient patients with deep vein thrombosis (DVT) or pulmonary embolism (PE). The intervention group received an oral dose of 50,000 IU vitamin D3 every week for 8 weeks, followed by 1 pearl every 2 weeks for 4 weeks (a total of 3 months), while the control group did not receive vitamin D. Then, P-selectin and hs-CRP were measured at baseline and 1 and 3 months after the intervention. There was no significant decrease in hs-CRP in either group after 1 month ( P = .955) or after 3 months ( P = .525). Likewise, there was no significant decrease in P-selectin between the 2 groups after 1 month ( P = .921) or 3 months ( P = .795). The results indicated that treatment of vitamin D deficiency had no significant effect on hs-CRP or P-selectin after 3 months among DVT/PE patients. However, treatment of vitamin D deficiency in these patients resulted in the control of the international normalized ratio (INR) with the lower doses of warfarin. This observation is the first clinical report of enhancement of the anticoagulant effect of warfarin by the supplementing of vitamin D. Larger trials are needed to clearly show the effect of treating of vitamin D deficiency on thrombosis. [ABSTRACT FROM AUTHOR]