Surgery remains the standard treatment for severe mitral valve regurgitation (MR), but growing evidence highlights the potential role of mitral valve percutaneous edge-to-edge repair (M-TEER). This meta-analysis aims to compare 12-month all-cause mortality between M-TEER and surgical intervention (SMVI). A systematic search (October 2024) of PubMed, Cochrane, Scopus, and Web of Science identified randomized control trials (RCTs) and propensity-matched observational studies comparing 12-month all-cause mortality in MR patients treated with M-TEER or SMVI. An inverse variance random-effects meta-analysis assessed outcomes using risk ratios (RR) and 95% confidence intervals (CI). Two RCTs (MATTERHORN and EVEREST II) and three observational studies totaling 1,782 patients, were included in the final analysis. A non-significant trend of higher mortality at 30 days was observed in the SMVI group (RR: 0.72; CI: 0.26–2.00), along with higher complication rates mainly due to bleeding. At 12 months follow-up, SMVI was associated with a significantly lower risk of all-cause mortality (RR: 1.41; CI: 1.11–1.81), while the M-TEER group had more patients with MR grade 3 or higher (RR: 4.05; CI: 1.54–10.67), with a non-significant trend of higher rate of MR reintervention (RR 2.51; CI 0.83–7.66) at 12 months. Based on current evidence, M-TEER should continue to be reserved for patients with prohibitive high surgical risk. While propensity-matched cohorts were pooled for the study estimates, the limited available data from randomized trials, combined with heterogeneity in patient populations, particularly regarding MR etiology, underscores the need for further studies.
The renin-angiotensin system (RAS) plays a central role in regulating blood pressure and cardiovascular health. Angiotensin-converting enzyme (ACE) facilitates the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor that contributes to hypertension and heart failure. Conversely, ACE2 converts angiotensin II into angiotensin-(1-7), a vasodilator with protective cardiovascular effects. An imbalance between ACE and ACE2 activities has been increasingly associated with the progression of cardiovascular diseases and complications related to COVID-19. This review analyzed 100 relevant studies published up to May 2024, identified through a comprehensive literature search on PubMed and Scopus. The findings highlighted that dysregulation of the ACE/ACE2 axis exacerbates cardiovascular dysfunction. The interaction of SARS-CoV-2 with ACE2 reduces its protective function, intensifying inflammatory responses and leading to complications such as lung injury and heart failure. Additionally, genetic polymorphisms in ACE and ACE2 influence individual susceptibility and severity of COVID-19. Promising therapeutic strategies, including ACE2-based peptides and angiotensin II receptor modulators, are under investigation but require further clinical validation. Targeting the ACE/ACE2 axis could provide effective treatment options for cardiovascular disease and COVID-19-related complications, warranting further in-depth research.
Introduction: The study sought to evaluate changes in left ventricular (LV) strain and native T1/T2 mapping characteristics on cardiac magnetic resonance imaging (CMR) in patients with high-normal blood pressure (HNBP). Methods: A prospective case-control study including 25 cases having HNBP and 25 age- and sex-matched healthy controls was conducted. LV strain was evaluated on CMR using feature tracking and 2-dimensional and 3-dimensional longitudinal, circumferential and radial strain values were calculated. Native T1/T2 mapping values were also calculated. Results: Subclinical impairment of LV mechanics was evident in the form of deranged LV strain parameters in cases with HNBP compared to controls. The two-dimensional global radial (25.34±3.06 vs. 28.52±5.69; P=0.0323), global circumferential (-16.05±1.31 vs. -17.27±2.23; P=0.0241) and global longitudinal strain (-16.33±2.24 vs. -16.49±7.25); P=0.0193) and three-dimensional global circumferential strain (-13.94±10.81 vs. -17.84±2.78; P=0.0133) values were significantly impaired in cases compared to controls. No significant difference was observed in the native T1/T2 mapping parameters. Conclusion: LV strain parameters are significantly deranged in patients with HNBP, compared to healthy controls, in the absence of other morphological changes or interstitial fibrosis. Impaired LV strain parameters can serve as a new marker for detection of subclinical myocardial dysfunction in patients with HNBP having preserved chamber function.
Introduction:Subclinical hypothyroidism (SCH), defined by elevated thyroid-stimulating hormone (TSH) with normal thyroid hormone levels, affects approximately 3-8% of the population. Growing evidence indicates that thyroid-stimulating hormone receptor (TSHR) expression in cardiovascular tissues, together with systemic inflammation (IL-6) and oxidative stress (3-nitrotyrosine), may contribute to cardiovascular dysfunction in SCH. This study aimed to evaluate the association between TSHR gene expression and systemic biomarkers-hormonal, inflammatory, and oxidative-and to assess their predictive value for cardiovascular risk in SCH patients. Methods:A case-control design was adopted involving 150 SCH subjects and 150 age- and sex-matched healthy controls. Demographic and clinical data were collected using structured interviews. Fasting blood samples were analyzed for TSH (CLIA), IL-6, and 3-nitrotyrosine (ELISA), while TSHR gene expression was quantified using real-time PCR with GAPDH as an internal control. Statistical analyses were performed using Stata version 17.0. Results:Compared with controls, SCH patients showed significantly higher levels of TSH, IL-6, 3-nitrotyrosine, and TSHR gene expression (P<0.05). Receiver operating characteristic (ROC) analysis revealed high diagnostic accuracy for these parameters. Although univariate analysis associated TSHR dysregulation with SCH, multivariate regression identified TSH as the only independent predictor of disease status. Oxidative stress demonstrated a significant positive association with TSHR expression, whereas IL-6 showed no independent influence. Conclusion:SCH is characterized by elevated hormonal, oxidative, and inflammatory markers, with oxidative stress contributing to TSHR upregulation. TSH remains the strongest independent predictor, underscoring the hormonal-oxidative interaction in cardiovascular risk among SCH patients.
Mitral valve aneurysm; defined as a bulge of the mitral valve leaflet toward the left atrium is a rare abnormality whose pathophysiology is poorly understood. The weakened aneurysmal wall may rupture and may cause severe mitral regurgitation and life-threatining conditions. In this case report we present a case of mitral anterior leaflet aneurysm rupture in a patient with immun deficiency and chronic renal failure
Introduction: This study investigates the role of the adipokine asprosin in coronary artery disease (CAD) by comparing its levels in epicardial adipose tissue (EAT) and serum between individuals with and without CAD. Asprosin is known to be involved in conditions such as insulin resistance and obesity, both of which are risk factors for CAD. Methods: The study included 25 CAD patients and 25 non-CAD patients undergoing open-heart surgery for valve issues. EAT samples were collected during surgery, and the mRNA levels of the FBN-1 gene were measured using qRT-PCR, while the protein levels of asprosin in both EAT and serum were determined using the ELISA method. Results: The results showed that the mRNA level of FBN-1 in the EAT of CAD patients was significantly higher than that in the control group (P < 0.001). Additionally, asprosin protein levels were significantly elevated in both the EAT (P < 0.003) and serum (P< 0.027) of CAD patients compared to non-CAD individuals. Conclusion: These findings suggest that asprosin may play a critical role in the pathogenesis of CAD, particularly through its increased presence in EAT and serum. The study highlights the potential of asprosin as a biomarker for CAD, though further research is needed to fully understand its mechanisms in the progression of the disease.
Introduction: Thoracic endovascular aortic repair (TEVAR) has become the preferred treatment modality of thoracic aortic pathologies. Since survival outcomes are influenced by disease acuity and pathology, we aim to compare mid-term outcomes of TEVAR in the management of thoracic aortic aneurysms (TAA) vs. Stanford type-B aortic dissections (TBAD). Methods: Patients undergoing TEVAR (2010-2019) in the Vascular Quality Initiative-Medicarelinked database were included in this analysis. Patients were divided into two groups: TAA and TBAD. Postoperative outcomes included 30-day mortality, stroke, myocardial infarction (MI), and spinal cord ischemia (SCI). Mid-term outcomes included 1 and 2-year all-cause mortality, reintervention and rupture. Results: Of the 2105 patients undergoing TEVAR in this analysis, 1,492 (70.9%) had TAA while 613 (29.1%) had TBAD. The TBAD group had a significantly lower 30-day mortality (aOR:0.67,95%Cl:0.46-0.98,P= 0.037), lower 1-year mortality (aHR:0.72,95%CI:0.57-0.90, P= 0.004) and also at 2 years (aHR:0.79,95%CI:0.65-0.95, P= 0.013). Within 1 year, patients with TBAD had a significantly higher incidence of aneurysm related reintervention (18.8% vs. 12.9%, P= 0.003). This finding persisted at 2 years (24.9% vs. 19.7%, P< 0.001). There was no significant difference in rupture between groups at 2 years (4.1% vs. 3.4%, P= 0.40). Conclusion: In this large multi-institutional study, patients undergoing TEVAR for TBAD had significantly lower postoperative mortality but a higher risk of reintervention at one and two years compared to patients with TAA. Additionally, both groups demonstrated a similar risk of rupture at both 1 and 2 years post-TEVAR. The rate of post-TEVAR rupture in both groups underscore the need for careful follow-up and reintervention as needed to maintain the integrity of the repair.
Introduction: The prevalence of obesity is increasing. Eating habits are modifiable factors that may be effective in reducing obesity. We aimed to investigate the relationship between meal frequency and daily breakfast and the presence of obesity. Methods: A total of 4137 overweight and obese individuals registered on IRanian National Obesity Registry (IRNOR) in 2022 were recruited into this cross-sectional study. Individual data was recorded using a self-reported questionnaire. Multivariate logistic and linear regressions were used to evaluate the association between meal frequency, daily breakfast and obesity. Results: There was a lower significant odd of obesity (odd ratio (OR)=0.80, 95% confidence interval (CI): 0.69-0.93; P = 0.004) in people who reported having more than three meals a day. There was a lower odd of obesity (OR = 0.79, 95%CI: 0.69-0.91; P = 0.001) in individuals who had daily breakfast and higher odds of obesity (OR = 1.21, 95%CI: 1.03-1.42; P< 0.01) for individuals who reported dinner as their main meal of the day. There was a significant association between eating frequency and daily breakfast with central obesity in men and in women; there was a significant inverse relationship between eating breakfast and central obesity. Conclusion: Meal frequency and eating breakfast daily as a modifiable eating habits can lead to improvement obesity.
We report a case of a bronchial artery aneurysm accompanied by a bronchial artery to pulmonary artery fistula in which only coil embolization was performed. Post-embolization, the majority of patients face significant metal artifacts from stents or coils during routine CT scans, which can compromise the visibility of the images. In this case, we conducted a spectral CT scan with metal artifact reduction technology postoperatively to clearly visualize the coils and accurately evaluate the treatment's effectiveness.
Transcatheter Aortic Valve Replacement (TAVR) has revolutionized the treatment of severe aortic stenosis, particularly in patients at intermediate or high surgical risk. However, valve selection in individuals with a small aortic annulus remains a clinical challenge. Comparative data on self-expanding (SE) and balloon-expandable (BE) valves are limited, and recent evidence has focused on identifying the optimal prosthesis for this subgroup. This review critically evaluates the comparative outcomes of SE and BE valves in patients with small aortic annuli, emphasizing findings from the Small Annuli Randomized to Evolut or SAPIEN Trial (SMART) and contextualizing them with evidence from major trials including CHOICE, SOLVE-TAVI, SCOPE I, and FRANCE-TAVI. The SMART trial demonstrated that SE valves were non-inferior to BE valves for the composite endpoint of death, disabling stroke, or heart failure rehospitalization at 12 months, while achieving superior valve hemodynamics. SE valves were associated with lower mean gradients, larger effective orifice areas, and reduced rates of prosthesis–patient mismatch and bioprosthetic valve dysfunction. Other clinical studies have shown that BE valves may offer greater procedural precision, better positioning, and lower rates of paravalvular regurgitation. Both SE and BE valves represent effective options for TAVR in patients with small aortic annuli. SE valves provide improved hemodynamic performance, whereas BE valves may offer procedural advantages. Valve selection should be individualized based on anatomical characteristics and operator experience. Long-term studies are required to assess valve durability and late clinical outcomes.
The majority of people experiencing Myocardial Infarction are of working age, which may result in prolonged work disability. This study seeks to consolidate the available evidence regarding the return to work for individuals following a Myocardial Infarction, while also examining its correlation with disease severity, job engagement, and duration of hospitalization. This research is a systematic review. The databases utilized include MEDLINE, Lilacs, Scielo, and Web of Science, with keywords and synonyms sourced from the Health Sciences Descriptors (DeCS), Medical Subject Headings (MeSH), and Embase Subject Headings (Emtree). Data collection took place between November 2023 and June 2024. The studies’ quality was evaluated using the Quality Assessment Tool for Observational Cohort and Cross-Sectional Studies. The search yielded 4,695 articles, from which 12 cohort studies were selected for inclusion, encompassing a total of 83,702 participants. The rate of return to work fluctuated throughout the follow-up period, with a return rate of 21.5% to 41.7% after one month and between 76.9% and 92.7% after one year. Additionally, the studies reported on modifications in work roles, salary reductions, job dismissals, and the incidence of anxiety and depression. All cohort studies were deemed to be of good quality. The rate of returning to work following a Myocardial Infarction is notably high within one year and is associated with physical, psychological, and social factors, highlighting the need for mechanisms that facilitate this return as promptly as possible. However, further research is necessary, particularly involving diverse populations and distinguishing among different professional categories, to gather more extensive data.
Introduction: One of the main causes of illness and death in communities is cardiovascular disease (CVD). Inflammation and oxidative stress are key components in the pathophysiology of CVD. It has been demonstrated that selenium lowers inflammation and oxidative stress. The purpose of this study is to do biochemical assessment of selenium’s cardiovascular protective effects in a lipopolysaccharide (LPS)-Induced damage in rats. Methods: LPS+Selenium (100 µg/kg), LPS (1 mg/kg), LPS+Selenium (200 µg/kg), and Vehicle (instead of both selenium and LPS) were given to the four groups of rats. The rats were sacrificed after 14 days, and the serum, heart, and aorta were examined for the presence of malondialdehyde (MDA), thiol, catalase (CAT), and superoxide dismutase (SOD). Interleukin 6 (IL-6) was also assessed in the tissues of the heart and aorta as an indicator of inflammation. Results: LPS administration raised aortic and cardiac IL-6 levels (P<0.001). In the heart, aorta, and serum, it also raised MDA (P<0.001) and lowered thiol (P<0.001), CAT (P<0.01-P<0.001), and SOD (P<0.001). On the other hand, selenium therapy markedly raised thiol, CAT, and SOD levels (P<0.01-P<0.001) and lowered MDA levels (P<0.05-P<0.001). Furthermore, following selenium delivery, a decrease in the inflammatory marker IL-6 was noted (P<0.01-P<0.001). Conclusion: This study showed that selenium protected the heart, aorta, and serum from oxidative stress brought on by LPS. Additionally, it reduced aortic and cardiac inflammation. These results imply that selenium’s anti-inflammatory and antioxidant properties may help prevent or lower the morbidity and mortality of CVD.
Introduction:Myocardial injury after non-cardiac surgery (MINS), characterized by cardiac troponin (cTn) elevation, is a marker of poor postoperative prognosis. The predictive value of MINS in thoracic oncosurgery remains unclear. The aim of the study was to determine the prognostic value of acute myocardial injury after surgical lung resection for 1-year all-cause mortality in patients with non-small-cell lung cancer (NSCLC). Methods:In this prospective cohort study, 101 consecutive men aged 63.0 (58;67) years who underwent surgical lung resection for NSCLC, were enrolled. Serum cTnI concentration was measured preoperatively and in 24 and 48 hours postoperatively. MINS was defined by at least one postoperative cTnI value that exceeds the 99th percentile upper reference limit, as a result of a presumed ischemic mechanism. The primary endpoint was 1-year all-cause mortality. Results:MINS was diagnosed in 37 patients (36.6%). During the follow-up, three patients were lost, and 28 (27.7%) died. Multivariate Cox regression analysis identified MINS as an independent predictor of all-cause mortality (adjusted hazard ratio [HR] 2.98, 95% confidence interval [CI] 1.29-6.89, P=0.011). The prognostic significance was also revealed for preoperative N-terminal prohormone of brain natriuretic peptide (HR 1.18, 95% CI 1.03-1.34, P=0.014), advanced cancer stage (HR 3.21, 95% CI 1.28-8.04, P=0.013), adjuvant chemotherapy (HR 0.22, 95% CI 0.08-0.57, P=0.002), and aspirin use (HR 0.09, 95% CI 0.01-0.72, P=0.024). Conclusion:Myocardial injury within the first 72 hours after surgical lung resection was found as an independent predictor of 1-year all-cause mortality in patients with NSCLC.
Introduction: Cardio-metabolic disease (CMetD) is a prevalent health issue among healthcare professionals, and suboptimal management of metabolic disorders places a burden on the healthcare system. Methods: The present study aimed to cluster the participants based on risk factors for the CMetDs using Latent Profile Analysis (LPA). This study was conducted on 500 healthcare providers, aged 18 to 75 years at Tabriz University of Medical Sciences, Tabriz, Iran. LPA was used to explore the latent risk profiles based on age, blood pressure (BP), lipid profile, insulin, body mass index (BMI), and waist circumference. Results: The individuals were classified into three LPA-driven profiles: low (42.4%), intermediate (21.8%), and high (35.8%). The high-risk profile found in older age and higher BMI, insulin, fasting blood glucose (FBS), as well as higher levels of high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, total cholesterol, and triglyceride. Furthermore, in the intermediate risk profile, elevated levels of systolic/diastolic BP and waist circumference were associated with higher levels of risk. Haemoglobin and hematocrit levels were significant predictors of low and intermediate latent profiles. Higher levels of hemoglobin and hematocrit were associated with lower odds of being in low and intermediate latent profiles, compared to the high-risk profile (all P< 0.05). Conclusion: LPA-derived latent profiles and the specific predictors of profiles help find control and prevention measures in CMetDs; older individuals with poorer lipid profiles, and, elevated insulin, triglyceride, FBS, BP, and BMI levels should be screened more carefully.
Introduction: Remote ischemic preconditioning (RIPC) is a non-invasive, practically acceptable and applicable conditioning technique reported to confer cardioprotection in myocardial ischemia-reperfusion injury (MIRI). It is documented that cannabinoid B2 receptor (CB2 R) plays crucial role in providing cardioprotection in various cardiovascular pathologies. Methods: MIRI was induced in the isolated hearts of Wistar rats by exposing them to global ischemia of 30 minutes followed by subsequent reperfusion with Kreb’s Henseleit (KH) buffer solution of 120 minutes after mounting on the Langendorff Power Lab apparatus. RIPC was applied by providing four alternate inter-spread cycles of 5 min non-lethal ischemia and 5 min reperfusion by tying the pressure cuff at the hind limb of the rats before isolation of hearts. Results: Ischemia-reperfusion injury (IRI) induced myocardial damage was manifested in terms of significant increase in infarct size, elevated levels of cardiac specific markers i.e. Lactate dehydrogenase-1 (LDH-1), Creatine kinase-MB (CK-MB), Cardiac troponin-I (C-tPn-I), altered hemodynamic parameters i.e. decreased heart rate (HR), coronary flow rate (CFR), left ventricular developed pressure (LVDP), rate pressure product (RPP),+dp/dtmax, and -dp/dtmin and other biochemical markers including increased thiobarbituric acid reactive species (TBARS), decreased glutathione reductase (GSH), and catalase; markers of oxidative stress, increased tumor necrosis factor-α (TNF-α); inflammatory marker, transforming growth factor-β (TGF-β); fibrosis marker, Bax, and caspase-3; markers of apoptosis. RIPC significantly reduced the infarct size, LDH-1, and CK-MB release and C-tPn-I content. Moreover, RIPC significantly improved series of aforementioned hemodynamic as well as biochemical parameters. Pre-administration of AM-630 (selective CB2 R antagonist; 0.5 and 1 mg/kg;i.p.) and BML-275 i.e. AMP activated protein kinase (AMPK) mediated autophagy inhibitor; 1.5 and 3 mg/kg;i.p.) substantially abrogated the cardioprotective response of RIPC. Conclusion: The current findings highlight the pivotal role of CB2 R activation and AMPK activated autophagy in cardioprotective mechanism of RIPC against MIRI.
