Cardiovascular & Hematological Agents in Medicinal Chemistry - Volume 23, Issue 3, 2025

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.

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.

This report discusses a rare case involving a patient with high-risk (HR) Del(5q) myelodysplastic syndrome (MDS) who achieved a long-term response to lenalidomide after having received six cycles of azacytidine. The latter treatment led to the clearance of blast cells from the bone marrow (BM).

As per current clinical practice, patients with HR MDS receive azacytidine continuously until the disease progresses or the occurrence of unmanageable side effects. However, in this case, the patient decided to interrupt hypomethylation therapy. Due to the patient's preference for oral therapy at home, the absence of blast cells, the ongoing need for transfusions, and a cytogenetic abnormality-predictive response to lenalidomide, the choice of the latter agent allowed for a sustained response lasting up to 68 months.

Our observations suggest that further studies could explore the sequential use of azacytidine followed by lenalidomide after achieving BM blast clearance in patients with HR MDS with del(5q).