Coriandrum sativum (C. sativum), widely known as coriander, is a herb of global significance, valued for its flavor and therapeutic properties. Originating from the Mediterranean, it has acclimatized to various continents, including Europe, Africa, and Asia. This review article was compiled from the data obtained from Google Scholar, Pub- Med/Medline, ScienceDirect, Hinari, and EBSCO. The herb thrives in areas with favorable agricultural climates, such as India, China, and parts of Europe. The plant's phytochemical spectrum is notably rich, featuring essential oils, flavonoids, phenolic compounds, and fatty acids. The seed oil is predominantly composed of linalool, complemented by γ-terpinene, decanal, and geranyl acetate. Both leaves and seeds are rich in nutrients, including tocopherols, carotenoids, chlorophylls, sugars, ascorbic acid, phenolics, and anthocyanins. C. sativum has shown beneficial effects in easing anxiety, depression, and convulsions, protecting neural health, combating bacteria and fungi, repelling insects, and supporting cardiovascular and diabetic health. These benefits are mainly due to the combined action of its phytochemicals. The toxicity study of this plant revealed that it is safe when administered in single or multiple doses. The essential oils of the herb have also been explored for their repellent and fumigant capabilities. Various clinical trials have been conducted to evaluate its different pharmacological safety profiles and assess its therapeutic potential. This review aimed to discuss the botanical features, chemical constituents, pharmacological properties, toxicity studies, and clinical trials. Further study is needed related to embryonic and other toxicities.

Pulmonary Hypertension (PH) is a significant contributor to cardiac mortality in Dilated Cardiomyopathy (DCM) patients. Inflammatory processes and oxidative stress play pivotal roles in the advancement of Pulmonary Hypertension (PH). The Monocyte-to-High-- Density-Lipoprotein Cholesterol Ratio (MHR), a newly identified biomarker indicative of inflammatory and oxidative stress, has not been extensively researched in the context of pulmonary hypertension, especially within the scope of dilated cardiomyopathy. Given the reason mentioned above, our research explores the correlation between the MHR and the severity of PH in patients suffering from DCM. In this study, we conducted a retrospective review of medical data from 107 individuals diagnosed with non-ischemic DCM, evaluating their clinical profiles, biochemical indicators, MHR, and echocardiographic parameters. We analyzed the relationships between Pulmonary Arterial Systolic Pressure (PASP) and the Ejection Fraction of the Left Ventricle (LVEF). Utilizing logistic regression analysis, we determined the predictors of PH. Findings indicated that the DCM-PH group exhibited a significantly larger male population and elevated New York Heart Association (NYHA) classification scores (both with p-values <0.001 and 0.01, respectively) compared to the DCM-only group. A positive association was observed between the PASP and parameters, such as the Dimensions of the Left Atrium (LAD) and Left Ventricle in Systole (LVDs), Monocyte (M) levels, Direct Bilirubin (DB), and MHR. Conversely, an inverse relationship was noted with serum lipid profiles, including Total Cholesterol (TC), HDL Cholesterol (HDL-c), and apolipoprotein A1. LVEF demonstrated positive linkage with the same lipid profiles and the Left Ventricular Posterior Wall Thickness (LVPWT) yet showed negative correlations with the NYHA classification, Red Blood Cell Distribution Width Standard Deviation (RDW-SD), Total Bilirubin (TB), Direct Bilirubin (DB), and dimensions of the left ventricle in diastole and systole, as well as MHR. Through logistic regression analysis, several factors were recognized as significant predictors for the severity of PH within the DCM cohort, with weight (OR1.20, CI 1.022-1.409, p=0.026), RDW-SD (OR1.988, CI 1.015-3.895, p=0.045), LVPW (OR3.577, CI 1.307-9.792, p=0.013), LVDd (OR1.333, CI 1.058-1.680, p=0.015), MHR (OR3.575, CI 1.502-8.506, p=0.032), and TB (OR1.416, CI 1.014-1.979, p=0.041) showing positive associations, while apoB (OR0.001 CI0.001-0.824, p=0.045) exhibiting negative associations, all with p-values <0.05. Higher MHR and LVD correlate with increased PASP and reduced LVEF in DCMPH patients. MHR and LVPW are independent predictors of PH severity, indicating their potential as novel severity markers in DCM-related PH.

The consumption of tea and coffee as beverages is prevalent worldwide, with each having potential health implications. The study investigated the effect of black tea (BT), green tea (GT), and coffee on blood pressure (BP), heart rate (HR), and blood glucose level (BGL) in healthy females. Forty (40) participants aged 18 to 26 were randomly assigned to four groups: control (250 mL warm water), GT (2 g GT dissolved in 250 mL of hot water), coffee (2 g coffee dissolved in 250 mL of hot water), and BT (2 g BT dissolved in 250 mL of hot water) groups with 10 subjects each. Each group was given its designated drink once a day for three consecutive days. Baseline measurements of BP, HR, and BGL were taken after a 15-minute rest before the consumption of the beverages. Follow-up measurements were taken at 15, 30, 45, and 60 minutes after consumption for cardiovascular indices, and 30 and 60 minutes for BGL. This procedure was repeated for three days. The results showed no significant changes in BP, HR, and BGL in all the experimental groups compared to the control group. Coffee and tea are popular beverages enjoyed worldwide, recognized for their numerous health benefits largely due to their bioactive compounds, particularly polyphenols and caffeine. The different concentrations of polyphenols and caffeine in these drinks can affect various physiological functions in distinct ways. The results of the present study showed no significant changes in blood pressure, heart rate, or blood glucose level among healthy young female participants who consumed green tea, coffee, and black tea, respectively. Although some previous studies have indicated that these beverages can significantly impact these health metrics, other research has shown no notable changes. The lack of significant findings in this study may be attributed to its short duration; a more extended study could potentially uncover significant changes. The findings of this study revealed that green tea, black tea, and coffee have no acute effect on blood pressure, heart rate, and blood glucose levels in healthy female individuals. It can therefore be concluded that green tea, black tea, and coffee have a neutral effect on these physiological parameters, but a more elaborate study is highly recommended.

Chronic renal failure (CRF) triggers chronic systemic inflammation and causes vascular calcification, a prominent contributor to the progression of cardiovascular disease. Adropin and spexin peptides regulate energy balance; also, these peptides trigger anti-inflammatory pathways. Our present study aimed to clarify the potentially protective impact of spexin and adropin peptides on cardiovascular inflammation in an adenine-induced chronic renal failure model. The CRF model in Sprague-Dawley rats was established by the administration of adenine hemisulfate for ten days. Then, rats were treated with saline or adropin, or/and spexin for four weeks. CRP, CK, and CK-MB levels in serum were measured by autoanalyzer. Aortic contraction- relaxation responses were determined by the organ bath system. H&E, PAS, and Masson's trichrome stainings evaluated histopathological alterations in both aorta and cardiac tissue. Gene expression levels of ILs (IL1β, IL10, IL17A, IL18, IL21, and IL33), MMPs (MMP1, MMP2, MMP3, MMP9, MMP13, and MMP14), NGAL, TGFβ1, TIMP1, and TNFα in cardiac tissue were evaluated by real-time PCR. We found increased CK and CK-MB levels by CRF induction. In addition, IL1β, IL17A, IL18, IL21, MMP1, MMP3, MMP13, and MMP14 increased after CRF progression. While adropin has effects on CK levels, spexin decreases CK-MB levels. Also, adropin and spexin had a nitric oxide-dependent impact on vascular reactivity. Besides, spexin downregulated IL1β, IL10, IL17A, TGFβ1, MMP1, MMP3, MMP9, MMP13, MMP14 and NGAL; however, the adropin peptide had a limited effect. These results suggest that adropin and spexin have potential preventive roles on vascular damage in CRF progression via modulation of MMPs and inflammatory genes.

Hypertension, a prevalent cardiovascular condition, increases the risk of strokes and myocardial infarctions by inducing elevated blood pressure. Its prevalence has risen, particularly in low- and middle-income nations. The incidence of hypertension in adults is higher in low- and middle-income countries compared to high-income nations. One significant class of antihypertensive drugs is α1-adrenoceptor antagonists, which inhibit α1-adrenergic receptors and promote vasodilation. Terazosin, doxazosin, tamsulosin, and alfuzosin are examples of α1-adrenoceptor antagonists that have antihypertensive properties; however, they are linked to considerable side effects, including headaches, dizziness, reproductive problems, and postural hypotension. In the last several years, a number of novel α1-adrenergic antagonists have been synthesised by modifications of various pharmacophores such as Isochroman-4-one, Quinazolines, Piperazine, and Quinazoline-triazole, etc. The present review highlights recently synthesized α1-adrenoceptor antagonists for the management of hypertension, and emphasizes their structure-activity relationship and subtype selectivity.

Iron Deficiency (ID) is common in patients with cardiovascular disease. More than 64 million patients are suffering from chronic heart failure. The prevalence of iron deficiency increases with the severity of cardiac and renal dysfunction and is probably more common amongst women. This review article discusses multifactorial pathophysiology, the relationship between clinical characteristics, functional and absolute ID, and the advantages of medicinal intervention in chronic heart failure (CHF). It also covers how iron shortage affects other body parts. The most recent publications that included substantial scientific data on the connection between CHF and ID, with or without anaemia, were selected. Complex physiopathological interactions, including higher hepcidin levels, systemic inflammation, and activation of the renin-angiotensin-aldosterone system, have been identified in these patients. These mechanisms exacerbate the outcomes for patients by amplifying the severity of anemia, chronic heart failure (CHF), and Chronic kidney disease (CKD). Research in this area has been limited and has shown inconsistent findings. Still, it has also examined evidence- based treatment approaches and diagnostic guidelines, especially in relation to iron supplements and erythropoietin-stimulating medications. Anemia is a frequent chronic heart failure consequence and a poor prognostic factor. We still don't completely understand the many complex causes of anemia. Iron deficiency screening is highly recommended for people with cardiac ailments because of its significance for their prognoses. Due to the paucity of research proving its effectiveness, the high incidence of unfavourable gastrointestinal side effects, and the prolonged length of time required for treatment to boost haemoglobin levels, an oral iron supplement is not advised for people with chronic heart failure. An insufficient amount of iron not only impacts the heart but also various other body components.

Approximately 3% of patients treated with heparinoids develop heparin- induced thrombocytopenia (HIT). Although HIT is characterized by thrombocytopenia, type 2 HIT is associated with a high risk of thrombotic events in approximately 30-75% of cases. In some patients, thrombocytopenia represents the primary clinical manifestation of HIT. Early diagnosis of HIT is critical to prevent thrombotic complications by allowing timely replacement of heparin with an alternative anticoagulant. Clinical observations suggest a potential gap in the diagnosis and management of HIT among patients receiving heparinoid therapy in Iran. Hence, this study aimed to compile and analyze published data on the frequency and prevalence of HIT across various provinces in Iran, a representative developing country. The aim of this systematic review was to identify and highlight potential gaps in the diagnosis of HIT within different regions of the country. To investigate this hypothesis, a systematic review was conducted to assess the prevalence of HIT and the adequacy of its detection in the country. Literature searches were performed using PubMed, Google Scholar, Web of Science, and local databases, yielding 81 articles. Following a rigorous evaluation, five studies met the inclusion criteria for the systematic review. The pooled analysis revealed an estimated HIT prevalence of 6.93% among the studied population. The mean age of participants ranged between 58 and 69 years, falling within the late-adolescent to early-elderly spectrum. The overall male-to-female ratio was 175:121 (59.2% male vs. 40.8% female). This study highlights a significant gap in the diagnosis of HIT in the country, suggesting that similar challenges may exist in other developing countries. In conclusion, addressing this issue requires increased clinical awareness and improved diagnostic strategies to mitigate associated risks.

Direct Oral Anticoagulants (DOACs) have transformed the management of thrombotic disorders, offering a more convenient and effective alternative to traditional vitamin K antagonists (VKAs). However, assessing thrombotic risk in patients treated with DOACS remains crucial due to the potential for recurrent events. Current clinical risk scores have limitations in predicting and monitoring venous thromboembolism (VTE) risk in specific DOAC populations. Several emerging biomarkers show promise in assessing thrombotic risk in patients treated with DOACS. Genetic factors like VKORC1 and CYP2C9 variants are well-established determinants of warfarin response, but the genetic landscape for DOAC outcomes appears more complex. Rare variants and polygenic approaches may play a role in personalizing anticoagulation therapy. Elevated factor VIII levels are associated with increased VTE recurrence risk after anticoagulation withdrawal in cancer-associated thrombosis (CAT) patients. In contrast, the circulating tissue factor is not useful for predicting VTE in this setting. Soluble P-selectin has emerged as a good marker of VTE recurrence, and its inclusion in the Vienna CATS risk model improves VTE prediction in cancer patients. While these biomarkers hold promise, larger studies are needed to validate their utility and establish standardized assays. Caution is warranted in patients at high bleeding risk. Integrating clinical factors, genetics, and circulating biomarkers will likely optimize thrombotic risk assessment in patients treated with DOACS. Continued research is crucial to develop personalized anticoagulation strategies to balance thrombosis and bleeding risks.

Myocardial infarction (MI) is a disease characterised by myocardial necrosis due to acute and prolonged ischaemic hypoxia in the coronary arteries. MOTS-c is a mitochondrial- derived peptide that has been reported to have protective effects on cardiac tissue. Although this peptide is thought to be decreased in various diseases and can serve as a potential biomarker, current studies remain limited. This study aimed to evaluate how the post-treatment process affects circulating MOTS- c peptide levels in myocardial infarction patients. For this purpose, patients without obstructive coronary lesions on angiography were included in the control group, while those with significant obstructive coronary lesions on angiography were included in the infarction group. Routine biochemistry tests were performed using an autoanalyzer. Besides, serum MOTS-c levels were measured using ELISA. Our findings showed CRP, ESR, and troponin I levels to be higher in the MI group compared to the control group. Also, there was no significant change in MOTS-c levels between the control and the MI group, while time-dependent changes (day 0, day 3, and day 30) occurred within the MI group. However, a negative correlation was found between MOTS-c and platelet levels in the MI group at day 0 (r: -0.4417, p =0.0450). Similarly, MOTS-c was found to be negatively correlated with troponin I in the MI group at day 3 (r: -0.4571, p =0.0372). The negative correlation of MOTS-c level with both platelet and troponin I has shown that this peptide may contribute to the diagnostic and therapeutic evaluation of the MI process along with other parameters.