The incidence and mortality of cardiovascular diseases, of which coronary heart disease (CHD) is a significant cardiovascular burden, are on the rise. Pyroptosis as an incipient programmed cell death mediated by inflammasomes can sense cytoplasmic contamination or interference and is typically marked by intracellular swelling, plasma membrane blistering and intense inflammatory cytokine release. As research on pyroptosis continues to progress, there is mounting evidence that pyroptosis is a vital participant in the pathophysiological basis of CHD. Atherosclerosis is the major pathophysiological basis of CHD and involves pyroptosis of endothelial cells, macrophages, vascular smooth muscle cells, and other immune cells, often in association with the release of pro-inflammatory factors. When cardiomyocytes are damaged, it will eventually lead to heart failure. Previous studies have covered that pyroptosis plays a critical role in CHD. In this review, we describe the properties of pyroptosis, summarize its contribution and related targets to diseases involving angina pectoris, myocardial infarction, myocardial ischemia in perfusion injury and heart failure, and highlight potential drugs for different heart diseases.

Background: Women are often neglected in cardiovascular health prevention. Age at menarche (AAM) has been linked to cardiovascular (CVD) disease in women and is potentially identified as one of the significant CVD risk factor. However, there is still limited comprehensive evidence addressing this issue. This systematic review and meta-analysis aimed to investigate how early menarche affects the outcome of all-cause mortality, CVD mortality, total cardiovascular disease event, stroke (ischemic, hemorrhagic, and total stroke), and coronary heart disease (CHD).

Method: The Cochrane Library, MEDLINE, Embase, ScienceDirect, and Google Scholar databases were searched from March 2013 to March 2023 for cohorts investigating the effect of early onset of menarche on CVD events with a minimum follow-up period of 5 years. Studies that observed specific population and/or included women with a history of CVD at baseline were excluded. The Newcastle–Ottawa scale was used for risk of bias assessment for each cohort included. The data were presented as dichotomous measure using risk ratios. I2 statistics were utilized to evaluate the heterogeneity of presented data.

Results: Thirteen cohorts included 18 626 799 female patients with ages ranging from 43 to 62.6 years. These reported 6 estimates each for CHD (5 483 298 patients) and all-cause mortality (1 595 878 patients), 5 estimates each for total stroke (2 941 321 patients) and CVD mortality (1 706 742 patients), 4 estimates each for total CVD events (3 988 311 patients) and ischemic stroke (2 434 580 patients), and 1 estimate for hemorrhagic stroke (66 104 patients). Our study found that events of CHD were significantly lower in early menarche (RR 0.57; 95% CI 0.41-0.78; P <.00001), as well as total stroke (RR 0.51; 95% CI 0.35-0.73; P =.0003), CVD mortality (RR 0.47; 95% CI 0.22-0.98; P =.04), total CVD events (RR 0.44; 95% CI 0.25-0.76; P =.003), ischemic stroke (RR 0.31; 95% CI 0.15-0.61; P <.0008), and hemorrhagic stroke (RR 0.12; 95% CI 0.07-0.20; P <.00001); and insignificantly higher in all-cause mortality (RR 0.90, 95% CI 0.76-1.06, P =.20).

Conclusion: In our study, cardiovascular events are lower in women with early menarche; hence, the later age of menarche is a potential risk factor to be considered when assessing CVD risk in a patient. However, our sample characteristics were heterogenous, and we did not consider other female hormonal factors that might potentially contribute to the CVD outcomes observed; thus, further studies are needed to clarify.

Background: Radial artery cardiac catheterization is a common diagnostic and interventional procedure for cardiovascular conditions. Pain and hemorrhage at the access site can cause patient discomfort and complications. This pilot study investigates the potential of local forearm heating to reduce pain and hemorrhage in patients undergoing radial artery cardiac catheterization.

Methods: We enrolled 100 patients scheduled for radial artery cardiac catheterization and randomly assigned them to the heating or control group. The heating group received local forearm heating before sheath removal, while the control group did not. Pain intensity was assessed with a visual analog scale, and hemorrhage was measured by assessing ecchymosis or hematoma size at the catheterization site. Hemodynamic parameters were also monitored. Statistical analysis compared outcomes between the groups.

Results: Patients who received local forearm heating had significantly lower pain intensity (4.15 ± 2.73) compared to the control group (5.84 ± 3.34) (P =.009). Hemodynamic parameters and the extent of hemorrhage at the catheterization site did not significantly differ between the heating and control groups (P >.05). No adverse effects related to forearm heating were reported.

Conclusion: Local forearm heating is a promising intervention to reduce pain intensity without increasing hemorrhage or affecting hemodynamic parameters during radial artery cardiac catheterization. This simple, noninvasive approach has the potential to enhance patient comfort and safety post procedure.

Background: The aim was to analyze the correlation between serum microRNA (miR)-18a level, endothelial function, and prognosis in female coronary heart disease (CHD) patients.

Methods: One hundred sixtyfemale patients admitted to our hospital for the first occurrences of chest pain and tightness were divided into CHD and non-CHD groups based on the coronary angiography results. Clinical data, laboratory indexes, serum miR-18a level, and endothelial function [flow-mediated dilation (FMD) function, endothelin 1 (ET-1), and nitric oxide (NO)] were compared.

Results: There were no significant differences in clinical data (except CHD family history) between 2 groups. Coronary heart disease group had significantly lower levels of NO and FMD, while significantly higher levels of miR-18a and ET-1 than non-CHD group (P <.05). Pearson correlation showed that serum miR-18a level was positively correlated with ET-1 (r = 0.492, P <.001), and negatively correlated with NO and FMD (r = −0.504, −0.307, P <.001). The receiver operating characteristic) curve showed that the area under the curve of serum miR-18a level in predicting the occurrence of CHD in women was 0.878 (95% CI:  0.828-0.928). Compared with good prognosis group, poor prognosis group had significantly lower NO, and FMD levels, while higher proportions of acute coronary syndrome, multi-vessel disease, miR-18a, and ET-1 levels (P <.05).

Conclusion: The expression of serum miR-18a in female CHD patients was high, which was related to endothelial function. The increase in serum miR-18a level was a risk factor for the occurrence of MACE in female CHD patients during follow-up, and the serum miR-18a level could effectively predict the occurrence of CHD in female patients.

Background: Myocardial ischemia–reperfusion injury (I/R) has been improved with drugs and effective reperfusion, but it still cannot be prevented.

Methods: To investigate whether renal denervation (RDN) reduces cardiomyocyte apoptosis by ameliorating endoplasmic reticulum stress, 60 male specific pathogen-free (SPF) Wistar rats were randomly divided into 6 groups (n = 6). We established the I/R rat model by ligating the left anterior descending artery. The I/R+ angiotensin receptor neprilysin inhibitors (ARNI) group received ARNIs for 2 weeks until euthanasia.

Results: The I/R+RDN and I/R+ARNI groups have significantly ameliorated left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) and reversed expansion of the left ventricular end-systolic diameter (LVSD) and left ventricular end diastolic diameter (LVDD) compared to the I/R group. The levels of norepinephrine (NE), angiotensin II, and aldosterone (ALD) increased significantly in the I/R group, but decreased significantly after RDN and ARNI intervention. In the I/R+RDN and I/R+ARNI groups, the myocardial tissue edema was alleviated. The infarct size was smaller in the I/R+RDN and I/R+ARNI groups compared to the I/R group. Apoptosis of cardiomyocytes and fibroblasts in myocardial tissue increased significantly in the I/R group, which was greatly diminished by RDN and ARNI. The expression of Bax, caspase-3, CHOP, PERK, and ATF4 protein was significantly increased in the I/R group, which compared to other groups, and the level of CHOP, PERK, and ATF4 gene expression increased. After RDN intervention, these expression levels recovered to varying degrees.

Conclusion: The effect of RDN may be associated with regulating the endoplasmic reticulum stress PERK/ATF4 signaling pathway.

Background: Radial angiography, preferred for its safety and comfort in percutaneous coronary interventions, occasionally leads to paresthesia—a tingling or numbing sensation in the hand. This study aimed to investigate the presence of nerve damage in patients experiencing paresthesia post-radial angiography through electrophysiological examination.

Methods: This prospective study involved 77 patients who developed hand paresthesia following radial angiography. Excluded were those with malignancy, pregnancy, pace-makers, or recent angiography. Nerve conduction studies were performed using the Neuropack MEB 9102K EMG device, assessing sensory and motor amplitudes, latencies, and velocities of median, ulnar, and radial nerves.

Results: The study included 77 patients (23 females, 54 males; average age 58.39 ± 10.44 years). In 11 diabetic patients, polyneuropathy was detected. For the remaining 66 patients, electrophysiological evaluations showed no significant pathological findings. Comparative analysis of both upper extremities revealed no significant differences in nerve conduction parameters between the side where angiography was performed and the other side. Despite paresthesia complaints, no electrophysiological evidence of nerve damage was found, suggesting that symptoms might be due to local irritation rather than direct nerve injury. This aligns with the safety profile of radial angiography and underscores the importance of distinguishing between transient paresthesia and serious nerve complications.

Conclusion: Paresthesia post-radial angiography, while clinically notable, is not typically associated with nerve damage. This study is significant as it is the first in the literature to demonstrate that radial angiography does not cause nerve damage.