Aspirin 75mg / Isosorbide mononitrate 60mg modified-release tablets

<p class="TextAbstract"><strong>Background:</strong> Preeclampsia is a disorder of pregnancy that increases risk for long-term health consequences for both mother and child, and if left untreated is one of the main causes of maternal and fetal mortality. However, delivery of the placenta is the only cure, making prevention options for this condition needed but little consensus exist on their effectiveness. Thus, we conducted a systematic review on the effectiveness of pharmacological and non-pharmacological interventions to prevent preeclampsia. <strong>Methods:</strong> We used MEDLINE and ProQuest to conduct a systematic search for peer-review publications on prevention of preeclampsia. We selected studies conducted in human and published in English from 2010 through 2020 on: i) types of interventions; ii) quality of studies and limitations. We selected 22 articles to be reviewed. <strong>Results:</strong> Eleven types of pharmacological and non-pharmacological interventions were identified. Nitric Oxide-donors with Isosorbide Mononitrate (IMN), and aspirin have been shown to be effective, while selenium, calcium, vitamin D, DHA-rich fish oil-concentrate, copper, phytonutrient, Nitric Oxide-donors with Penthaerythrityl Tetranitrate (PETN), folic acid, vitamins C and E and magnesium have not been proved effective to prevent preeclampsia. Although all studies presented good quality of evidence, they had several limitations, the most common limitations are lack of initial therapy, lack of dosage, and inadequate sample size to detect small effect. <strong>Conclusion:</strong> Despite the growing evidence of treatments to prevent preeclampsia, their effect is not large. More research is needed in the field before prevention treatments are prescribed in clinical settings.</p><p class="TextAbstract"><strong>Keywords</strong><strong>: </strong>prevention; pharmacological; non-pharmacological; Systematic Literature Review; preeclampsia.</p>

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BACKGROUND AND PURPOSE: Endothelial dysfunction is considered an emerging therapeutic target to prevent complications during acute stroke and to prevent recurrent stroke. This review aims to provide an overview of the current knowledge on endothelial dysfunction, outline the diagnostic methods used to measure it and highlight the drugs currently being investigated for the treatment of endothelial dysfunction in acute ischemic stroke. METHODS: The PubMed® and ClinicalTrials.gov electronic databases were searched for eligible articles/studies dealing with endothelial dysfunction and stroke. The references of the articles were screened to identify additional sources. The data were abstracted and summarized. FINDINGS AND DISCUSSION: Endothelial dysfunction can be measured by serum biomarkers as well as by ultrasound or plethysmography techniques. Drugs targeting endothelial dysfunction include widely used agents such as angiotensin-converting enzyme inhibitors or isosorbide mononitrate, but also experimental therapies such as endothelial progenitor cells. CONCLUSION: The role of endothelial dysfunction in acute ischemic stroke has been studied increasingly in recent years. It has been shown that there is a correlation between endothelial dysfunction and parenchymal hematoma after endovascular thrombectomy. Also, early clinical trials are conducted investigating, e.g., endothelial progenitor cells in the treatment of endothelial dysfunction in ischemic stroke. Current research focuses on the integration of novel markers of endothelial dysfunction into routine clinical practice to support decision making in the treatment of acute ischemic stroke.

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Objective: There is a lack of studies investigating the safety of combination regimens specifically for cardiovascular and cerebrovascular diseases. This study aimed to evaluate the safety of combination drugs for cardiovascular and cerebrovascular diseases using real-world data. Methods: We analyzed adverse drug reaction data received by the Hubei Adverse Drug Reaction Center from the first quarter of 2014 to the fourth quarter of 2022. The safety of combined drugs for cardiovascular and cerebrovascular diseases in different people was assessed using the association rule method and Ω shrinkage measurement. Results: A total of 53,038 reports were included in this study, revealing 9 signals of adverse reactions caused by combination drugs. The strongest signal found in this study was jaundice caused by the combination of amlodipine and atorvastatin (Ω 0.025:3.08, lift: 1116.69, conviction: 1.75). Additionally, the combination of aspirin with other drugs was associated with hemorrhaging in various organs. Female patients showed a cold signal when taking vitamin C and vitamin B6 together compared to male patients (Ω 0.025:0.89, lift: 7.15, conviction: 1.12). Patients under 60 years old had a palpitations signal when combining eritrea bei sha Tanzania and felodipine (Ω 0.025:0.41, lift: 14.65, conviction: 3.8), and an erythema signal when combining nifedipine (Ω 0.025:0.23, lift: 8.17, conviction: 1.077). Conclusion: Among the 9 signals identified in this study, 4 were off-label adverse drug reactions that require further clinical research for exploration and confirmation, in order to provide more scientifically informed drug labeling. Five adverse events associated with aspirin-induced bleeding were identified. Notably, different adverse drug reactions were observed in different populations, suggesting the need for future studies to expedite the development of personalized medicine.

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Background Long-acting nitrates are widely prescribed in coronary artery disease (CAD), yet their association with long-term outcomes remains controversial. Whether left ventricular ejection fraction (LVEF) modifies this relationship has not been well characterized. Methods We conducted a single-center retrospective cohort study using the Guizhou Provincial People's Hospital CAD database. Adults (≥18 years) who underwent coronary angiography between July 2012 and September 2016 and met angiographic criteria for CAD (≥50% stenosis in ≥1 proximal epicardial coronary artery) were eligible if LVEF and discharge medications were available. Patients were stratified by LVEF (<45%, 45%–55%, >55%) and by discharge prescription of any nitrate (mononitrate or dinitrate). The primary endpoint was all-cause death. The secondary endpoint was major adverse cardiovascular events (MACE), defined as a composite of cardiovascular death, non-fatal myocardial infarction, and non-fatal stroke. Kaplan–Meier methods and multivariable Cox regression were used to evaluate associations. Results Among 2,404 patients followed for 27.2 ± 13.5 months, 1,153 (48.0%) were discharged on nitrates. In the overall cohort, discharge on nitrates was not associated with all-cause death or MACE. In contrast, among patients with LVEF < 45%, nitrates at discharge were linked to higher cumulative incidences of all-cause death and MACE (log-rank P = 0.024 and 0.029, respectively) and remained independently associated after adjustment [all-cause death: hazard ratio (HR) 2.14, 95% confidence interval (CI) 1.15–3.96; MACE: HR 1.91, 95% CI 1.07–3.43]. No significant associations were observed in the LVEF 45%–55% or >55% strata. Conclusion In this CAD cohort, nitrates were commonly prescribed at discharge. An adverse association with long-term outcomes was confined to patients with reduced LVEF, supporting cautious use in this subgroup and highlighting the need for prospective confirmation.

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BACKGROUND: Fluoropyrimidines, such as 5-fluorouracil (5-FU) and capecitabine, are vital in gastrointestinal cancer treatment but can cause coronary vasospasm (CV). Although calcium channel blockers and nitrates enable rechallenge, the optimal management of patients who cannot tolerate oral medications remains uncertain. CASE PRESENTATION: A 38-year-old man with metastatic gastric adenocarcinoma developed 5-FU-induced CV during 5-FU, leucovorin, oxaliplatin, and docetaxel chemotherapy. Rechallenge with extended-release nifedipine and isosorbide mononitrate was initially successful, but worsening dysphagia precluded oral prophylaxis. Transdermal nitroglycerin was attempted but failed, necessitating 5-FU interruption and sublingual nitroglycerin. Because of inadequate oncologic response and human epidermal growth factor receptor 2 positivity, treatment transitioned to trastuzumab. CONCLUSIONS: This case highlights the challenge of 5-FU rechallenge in patients unable to take oral prophylaxis. Transdermal nitroglycerin monotherapy proved insufficient, suggesting that intravenous prophylaxis may be required. Future studies should determine optimal strategies for preventing CV in patients with a similar presentation.

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