Currently, brain natriuretic peptide (BNP) and N-terminal proBNP (NT-proBNP) are widely used as diagnostic biomarkers for heart failure (HF) and cardiac dysfunction in clinical medicine. They are also used as postmortem biomarkers reflecting cardiac function of the deceased before death in forensic medicine. Several previous studies have reviewed BNP and NT-proBNP in clinical medicine, however, few articles have reviewed their application in forensic medicine. The present article reviews the biological features, the research and application status, and the future research prospects of BNP and NT-proBNP in both clinical medicine and forensic medicine, thereby providing valuable assistance for clinicians and forensic pathologists.

Mn(III) ortho‐N‐alkyl‐ and N‐alkoxyalkyl porphyrins (MnPs) were initially developed as superoxide dismutase (SOD) mimics. These compounds were later shown to react with numerous reactive species (such as ONOO^-, H₂O₂, H₂S, CO₃^•-, ascorbate, and GSH). Moreover, the ability of MnPs to oxidatively modify activities of numerous proteins has emerged as their major mechanism of action both in normal and in cancer cells. Among those proteins are transcription factors (NF‐κB and Nrf2), mitogen‐activated protein kinases, MAPKs, antiapoptotic bcl‐2, and endogenous antioxidative defenses. The lead Mn porphyrins, namely, MnTE‐2‐PyP⁵⁺ (BMX‐010, AEOL10113), MnTnBuOE‐2‐PyP⁵⁺ (BMX‐001), and MnTnHex‐2‐PyP⁵⁺, were tested in numerous injuries of normal tissue and cellular and animal cancer models. The wealth of the data led to the progression of MnTnBuOE‐2‐PyP⁵⁺ into four Phase II clinical trials on glioma, head and neck cancer, anal cancer, and multiple brain metastases, while MnTE‐2‐PyP⁵⁺ is in Phase II clinical trial on atopic dermatitis and itch.

Biomarkers such as B-type natriuretic peptide (BNP), N-terminal pro-BNP (NT-proBNP), cardiac troponin (cTn), and CK-MB contribute significantly to the diagnosis of cardiovascular disease (CVD). Recent studies have demonstrated that suppression of tumorigenicity 2 (ST2) is associated with CVD, but a meta-analysis of ST2 levels in different CVDs has yet to be conducted. Therefore, the present study aimed to investigate soluble ST2 (sST2) levels in patients with ischemic heart disease (IHD), myocardial infarction (MI), and heart failure (HF). A total of 1,425 studies were searched across four databases, of which 16 studies were included in the meta-analysis. The Newcastle–Ottawa Quality Assessment Scale (NOS) values of all 16 studies were ≥7. The meta-analysis results indicated that the sST2 level was not correlated with IHD (standard mean difference [SMD] = 0.58, 95% confidence interval [95% CI] = 0.00 to 1.16, p = 0.05) or MI (weighted mean difference [WMD] = 0.17, 95% CI = −0.22 to 0.55, p = 0.40) but was significantly associated with HF (WMD = 0.21, 95% CI = 0.04 to 0.38, p = 0.02; I² = 99%, p < 0.00001). sST2 levels did not differ significantly between patients with IHD or MI and healthy individuals; however, we believe that ST2 could be used as an auxiliary diagnostic biomarker of HF.

The functions of the brain and heart, which are the two main supporting organs of human life, are closely linked. Numerous studies have expounded the mechanisms of the brain‐heart axis and its related clinical applications. However, the effect of heart disease on brain function, defined as the heart‐brain axis, is less studied even though cognitive dysfunction after heart disease is one of its most frequently reported manifestations. Hypoperfusion caused by heart failure appears to be an important risk factor for cognitive decline. Blood perfusion, the immune response, and oxidative stress are the possible main mechanisms of cognitive dysfunction, indicating that the blood‐brain barrier, glial cells, and amyloid‐β may play active roles in these mechanisms. Clinicians should pay more attention to the cognitive function of patients with heart disease, especially those with heart failure. In addition, further research elucidating the associated mechanisms would help discover new therapeutic targets to intervene in the process of cognitive dysfunction after heart disease. This review discusses cognitive dysfunction in relation to heart disease and its potential mechanisms.

Background: Cardiac troponin I (cTn I) and cardiac troponin T (cTn T) are currently widely used as diagnostic biomarkers for myocardial injury caused by ischemic heart diseases in clinical and forensic medicine. However, no previous meta-analysis has summarized the diagnostic roles of postmortem cTn I and cTn T. The aim of the present study was to meta-analyze the diagnostic roles of postmortem cTn I and cTn T for cardiac death in forensic medicine, present a systematic review of the previous literature, and determine the postmortem cut-off values of cTn I and cTn T. Methods: We searched multiple databases for the related literature, performed a meta-analysis to investigate the diagnostic roles of postmortem cardiac troponins, and analyzed the receiver operating characteristic (ROC) curve to determine their postmortem cut-off values. Results and Conclusions: The present meta-analysis demonstrated that postmortem cTn I and cTn T levels were increased in pericardial fluid and serum in cardiac death, especially in patients with acute myocardial infarction (AMI). We determined the postmortem cut-off value of cTn I in the pericardial fluid at 86.2 ng/mL, cTn I in serum at 9.5 ng/mL, and cTn T in serum at 8.025 ng/mL.