Anatolian Journal of Cardiology最新文献

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: 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.

Mendelian forms of renin-angiotensin-aldosterone system (RAAS)-related hypertension, commonly referred to as monogenic hypertension, represent a rare but significant subset of hypertensive disorders characterized by genetic mutations that disrupt the normal physiological mechanisms of blood pressure regulation. This review focuses on elucidating the germline mutations affecting RAAS pathways that lead to distinct forms of heritable hypertension. By understanding the pathophysiological basis of conditions such as Gordon's syndrome, Liddle syndrome, congenital adrenal hyperplasia, and familial hyperaldosteronism types, this review aims to highlight the unique clinical features, diagnostic challenges, and therapeutic implications associated with these disorders. Recognizing specific clinical presentations and family histories indicative of monogenic hypertension is crucial for diagnosis, particularly as it often manifests as early-onset hypertension, abnormalities in potassium and blood pH, and occasionally, abnormal sexual development or related syndromes. Therefore, employing a targeted diagnostic approach through next-generation sequencing is essential to pinpoint the responsible genetic mutations, enabling accurate and individualized treatment plans. The critical importance of certain readily available specific channel blockers, such as thiazides or low-dose corticosteroids, in managing these disorders must be emphasized, as they play a key role in preventing serious complications, including cerebrovascular events. As advancements in genetic and molecular sciences continue to evolve, a deeper comprehension of the mechanisms underlying RAAS-related monogenic hypertension promises to revolutionize the management of this complex disorder, offering hope for more effective and individualized treatment options.

Background: Atrial fibrillation (AF) and heart failure (HF) are prevalent cardiovascular conditions in East Asia, with a complex interrelationship. The directionality of the causal impact of AF on HF risk remains uncertain. This study employs Mendelian randomization (MR) to investigate the potential causal effect of AF on HF.

Methods: Utilizing summary data from genome-wide association studies (GWAS) within the Medical Research Council Integrative Epidemiology Unit open GWAS database, we analyzed 8180 AF cases and 28 612 controls, alongside 9413 HF cases and 203 040 controls, all of East Asian descent. We conducted MR analysis using the inverse variance weighted (IVW) method, complemented by various sensitivity analyses, including bidirectional MR to assess causality in the reverse direction.

Results: Genetically predicted AF was found to be causally associated with an increased risk of HF in East Asian populations (odds ratio = 1.14, 95% CI: 1.10-1.19, P <.001) as per the IVW method. These findings were consistent across multiple MR methods. Sensitivity analyses revealed no significant heterogeneity or pleiotropy. Notably, bidirectional MR analysis showed no causal effect of HF on the risk of developing AF.

Conclusions: The MR analysis supports a unidirectional causal relationship between AF and increased HF risk in East Asian individuals. The absence of a reverse causal effect reinforces the importance of maintaining sinus rhythm to mitigate HF risk. Further research is warranted to corroborate these findings and to explore their clinical implications in depth.

Premature ventricular contractions (PVCs) are a common finding in clinical practice, requiring a full diagnostic work-up in order to exclude an underlying cardiomyopathy. Still, in a substantial proportion of patients, these investigations do not identify any substrate, and the PVCs are labelled as idiopathic. Cardiac magnetic resonance (CMR) has proven in the last decades as the method of choice for the exploration of patients with cardiomyopathies, since it can identify subtle changes in the myocardial tissue and help with risk stratification. In patients with idiopathic PVCs and a high PVC burden, several studies report the presence of late gadolinium enhancement (LGE) at CMR, which can offer additional diagnostic and prognostic benefits, as well as assistance in catheter ablation procedures, as the risk for adverse cardiac and risk for arrhythmic events events is higher compared to patients without scar. This paper focuses on the impact of the presence of LGE in patients with idiopathic PVCs, reviewing all the relevant studies published so far, including randomized controlled clinical trials, prospective or retrospective cohort studies, case series and case reports as well as systematic reviews.