-
Clinical Cardiology Jul 2024Papillary muscle (PM) infarction (PMI) detected by cardiac magnetic resonance imaging (CMR) is associated with poor outcomes. Whether PM parameters provide more value...
BACKGROUND
Papillary muscle (PM) infarction (PMI) detected by cardiac magnetic resonance imaging (CMR) is associated with poor outcomes. Whether PM parameters provide more value for mitral regurgitation (MR) management currently remains unclear. Therefore, we examined the prognostic value of PMI using CMR in patients with MR.
METHODS
Between March 2018 and July 2023, we retrospectively enrolled 397 patients with MR undergoing CMR. CMR was used to detect PMI qualitatively and quantitively. We also collected baseline clinical, echocardiography, and follow-up data.
RESULTS
Of the 397 patients with MR (52.4 ± 13.9 years), 117 (29.5%) were assigned to the PMI group, with 280 (70.5%) in the non-PMI group. PMI was demonstrated more in the posteromedial PM (PM-PM, 98/117) than in the anterolateral PM (AL-PM, 45/117). Compared with patients without PMI, patients with PMI had a decreased AL-PM (41.5 ± 5.4 vs. 45.6 ± 5.3)/PM-PM diastolic length (35.0 ± 5.2 vs. 37.9 ± 4.0), PM-longitudinal strain (LS, 20.4 ± 6.1 vs. 24.9 ± 4.6), AL-PM-LS (19.7 ± 6.8 vs. 24.7 ± 5.6)/PM-PM-LS (21.2 ± 7.9 vs. 25.2 ± 6.0), and increased inter-PM distance (25.7 ± 8.0 vs. 22.7 ± 6.2, all p < 0.001). Multiple logistic regression analyses identified male sex (odds ratio [OR] = 3.65, 95% confidence interval = 1.881-7.081, p < 0.001) diabetes mellitus (OR/95% CI/p = 2.534/1.13-5.68/0.024), AL-PM diastolic length (OR/95% CI/p = 0.841/0.77-0.92/< 0.001), PM-PM diastolic length (OR/95% CI/p = 0.873/0.79-0.964/0.007), inter-PM distance (OR/95% CI/p = 1.087/1.028-1.15/0.003), AL-PM-LS (OR/95% CI/p = 0.892/0.843-0.94/< 0.001), and PM-PM-LS (OR/95% CI/p = 0.95/0.9-0.992/0.021) as independently associated with PMI. Over a 769 ± 367-day follow-up, 100 (25.2%) patients had arrhythmia. Cox regression analyses indicated that PMI (hazard ratio [HR]/95% CI/p = 1.644/1.062-2.547/0.026), AL-PM-LS (HR/95% CI/p = 0.937/0.903-0.973/0.001), and PM-PM-LS (HR/95% CI/p = 0.933/0.902-0.965/< 0.001) remained independently associated with MR.
CONCLUSIONS
The CMR-derived PMI and LS parameters improve the evaluation of PM dysfunction, indicating a high risk for arrhythmia, and provide additive risk stratification for patients with MR.
Topics: Humans; Mitral Valve Insufficiency; Male; Female; Papillary Muscles; Retrospective Studies; Middle Aged; Magnetic Resonance Imaging, Cine; Myocardial Infarction; Prognosis; Follow-Up Studies; Aged
PubMed: 38953314
DOI: 10.1002/clc.24312 -
International Journal of Nanomedicine 2024Myocardial infarction, usually caused by the rupture of atherosclerotic plaque, leads to irreversible ischemic cardiomyocyte death within hours followed by impaired... (Review)
Review
Myocardial infarction, usually caused by the rupture of atherosclerotic plaque, leads to irreversible ischemic cardiomyocyte death within hours followed by impaired cardiac performance or even heart failure. Current interventional reperfusion strategies for myocardial infarction still face high mortality with the development of heart failure. Nanomaterial-based therapy has made great progress in reducing infarct size and promoting cardiac repair after MI, although most studies are preclinical trials. This review focuses primarily on recent progress (2016-now) in the development of various nanomedicines in the treatment of myocardial infarction. We summarize these applications with the strategy of mechanism including anti-cardiomyocyte death strategy, activation of neovascularization, antioxidants strategy, immunomodulation, anti-cardiac remodeling, and cardiac repair.
Topics: Myocardial Infarction; Humans; Nanomedicine; Animals; Myocytes, Cardiac; Antioxidants; Nanostructures; Neovascularization, Physiologic
PubMed: 38952676
DOI: 10.2147/IJN.S467219 -
Neuroepidemiology Jun 2024Smoking is a well-known risk factor for cardiovascular diseases, including myocardial infarction (MI) and ischemic stroke (IS). While the relationship between smoking...
INTRODUCTION
Smoking is a well-known risk factor for cardiovascular diseases, including myocardial infarction (MI) and ischemic stroke (IS). While the relationship between smoking and the risk of cardiovascular diseases is established, the impact of changing smoking habits post-IS on the risk of subsequent MI remains unclear. This study aims to elucidate the effects of alterations in smoking behavior following an IS diagnosis on the likelihood of experiencing an MI.
METHODS
Utilizing data from the Korean National Health Insurance Services Database, this nationwide population-based cohort study included 199,051 participants diagnosed with IS between January 2010 and December 2016. Smoking status was categorized based on changes in smoking habits before and after IS diagnosis. The association between changes in smoking behavior and the risk of subsequent MI was analyzed using multivariable Cox proportional hazard regression models.
RESULTS
During a median follow-up of 4.17 person-years, a total of 5,734 (2.88%) patients were diagnosed with MI after IS. Smoking quitters (2.93%) or former smokers (2.47%) have a similar or lower rate of MI than the average, even if they have smoked cigarettes, while sustained smokers (3.46%) or new smokers (3.81%) have much higher rates of MI. Among sustained and new smokers, the risk of incident MI were significantly higher than never smokers (new smoker adjusted HR [aHR]: 1.496, 95% CI 1.262-1.774; sustained smoker aHR 1.494, 95% CI 1.361-1.641). Also, among the study participants, approximately two-thirds continued smoking after their IS diagnosis.
CONCLUSION
Changing smoking habits after an IS diagnosis significantly influences the risk of subsequent MI. Specifically, continuing or starting to smoke after an IS diagnosis is associated with a higher risk of MI. These results underscore the importance of targeted smoking cessation interventions for stroke patients to reduce the risk of subsequent myocardial infarction.
PubMed: 38952140
DOI: 10.1159/000540058 -
JMIR Aging Jun 2024
Topics: Humans; Heart Failure; Veterans; Retrospective Studies; Frailty; Aged; Male; Female; Frail Elderly; Aged, 80 and over; Geriatric Assessment; United States
PubMed: 38952001
DOI: 10.2196/56345 -
Clinical Pharmacology and Therapeutics Jul 2024Beta-blockers are widely used medications for a variety of indications, including heart failure, myocardial infarction, cardiac arrhythmias, and hypertension. Genetic... (Review)
Review
Beta-blockers are widely used medications for a variety of indications, including heart failure, myocardial infarction, cardiac arrhythmias, and hypertension. Genetic variability in pharmacokinetic (e.g., CYP2D6) and pharmacodynamic (e.g., ADRB1, ADRB2, ADRA2C, GRK4, GRK5) genes have been studied in relation to beta-blocker exposure and response. We searched and summarized the strength of the evidence linking beta-blocker exposure and response with the six genes listed above. The level of evidence was high for associations between CYP2D6 genetic variation and both metoprolol exposure and heart rate response. Evidence indicates that CYP2D6 poor metabolizers experience clinically significant greater exposure and lower heart rate in response to metoprolol compared with those who are not poor metabolizers. Therefore, we provide therapeutic recommendations regarding genetically predicted CYP2D6 metabolizer status and metoprolol therapy. However, there was insufficient evidence to make therapeutic recommendations for CYP2D6 and other beta-blockers or for any beta-blocker and the other five genes evaluated (updates at www.cpicpgx.org).
PubMed: 38951961
DOI: 10.1002/cpt.3351 -
Journal of Cardiothoracic Surgery Jul 2024In patients with unprotected left main coronary artery disease (ULMCAD), this study compared the long-term prognosis of drug-eluting stent insertion guided by...
BACKGROUND
In patients with unprotected left main coronary artery disease (ULMCAD), this study compared the long-term prognosis of drug-eluting stent insertion guided by intravascular ultrasonography (IVUS) vs. angiography.
PATIENTS AND METHODS
This retrospective consort investigation was performed in December 2021. This analysis included 199 patients who underwent IVUS-guided (IVUS group, n = 81) or angiography-guided (angiography group, n = 118) drug-eluting stent implantation at the Affiliated Hospital of Inner Mongolia Medical University between September 2013 and September 2018. Major adverse cardiac events (MACE) were defined as cardiovascular death, sudden cardiac death, myocardial infarction.
RESULTS
The IVUS group had considerably lower proportions of MACE within 1 year postoperatively (P = 0.002) and cardiac mortality within 3 years postoperatively (P = 0.018) compared to the angiography group. However, after adjusting for confounding variables, the hazard ratio for 3-year cardiac mortality was similar between the two groups (P = 0.28). In the IVUS group, there was considerably greater minimum lumen diameter (MLD) (P = 0.046), and reduced frequencies of target vessel restenosis (P < 0.050) and myocardial infarction (MI) (P = 0.024) compared to the angiography group. Cox regression analysis for 3-year cardiac mortality found that MSD was independently associated with low cardiac mortality (HR = 0.1, 95% CI: 0.01-14.92, P = 0.030).
CONCLUSION
IVUS-guided drug-eluting stent implantation may lead to better long-term prognosis in patients with ULMCAD, and MSD may be a predictor for lower cardiac mortality.
Topics: Humans; Drug-Eluting Stents; Male; Female; Ultrasonography, Interventional; Retrospective Studies; Coronary Artery Disease; Coronary Angiography; Middle Aged; Aged; Percutaneous Coronary Intervention; Treatment Outcome
PubMed: 38951893
DOI: 10.1186/s13019-024-02800-0 -
Journal of Nanobiotechnology Jul 2024Reperfusion therapy is critical for saving heart muscle after myocardial infarction, but the process of restoring blood flow can itself exacerbate injury to the...
Targeting delivery of miR-146a via IMTP modified milk exosomes exerted cardioprotective effects by inhibiting NF-κB signaling pathway after myocardial ischemia-reperfusion injury.
Reperfusion therapy is critical for saving heart muscle after myocardial infarction, but the process of restoring blood flow can itself exacerbate injury to the myocardium. This phenomenon is known as myocardial ischemia-reperfusion injury (MIRI), which includes oxidative stress, inflammation, and further cell death. microRNA-146a (miR-146a) is known to play a significant role in regulating the immune response and inflammation, and has been studied for its potential impact on the improvement of heart function after myocardial injury. However, the delivery of miR-146a to the heart in a specific and efficient manner remains a challenge as extracellular RNAs are unstable and rapidly degraded. Milk exosomes (MEs) have been proposed as ideal delivery platform for miRNA-based therapy as they can protect miRNAs from RNase degradation. In this study, the effects of miR-146a containing MEs (MEs-miR-146a) on improvement of cardiac function were examined in a rat model of MIRI. To enhance the targeting delivery of MEs-miR-146a to the site of myocardial injury, the ischemic myocardium-targeted peptide IMTP was modified onto the surfaces, and whether the modified MEs-miR-146a could exert a better therapeutic role was examined by echocardiography, myocardial injury indicators and the levels of inflammatory factors. Furthermore, the expressions of miR-146a mediated NF-κB signaling pathway-related proteins were detected by western blotting and qRT-PCR to further elucidate its mechanisms. MiR-146 mimics were successfully loaded into the MEs by electroporation at a square wave 1000 V voltage and 0.1 ms pulse duration. MEs-miR-146a can be up-taken by cardiomyocytes and protected the cells from oxygen glucose deprivation/reperfusion induced damage in vitro. Oral administration of MEs-miR-146a decreased myocardial tissue apoptosis and the expression of inflammatory factors and improved cardiac function after MIRI. The miR-146a level in myocardium tissues was significantly increased after the administration IMTP modified MEs-miR-146a, which was higher than that of the MEs-miR-146a group. In addition, intravenous injection of IMTP modified MEs-miR-146a enhanced the targeting to heart, improved cardiac function, reduced myocardial tissue apoptosis and suppressed inflammation after MIRI, which was more effective than the MEs-miR-146a treatment. Moreover, IMTP modified MEs-miR-146a reduced the protein levels of IRAK1, TRAF6 and p-p65. Therefore, IMTP modified MEs-miR-146a exerted their anti-inflammatory effect by inhibiting the IRAK1/TRAF6/NF-κB signaling pathway. Taken together, our findings suggested miR-146a containing MEs may be a promising strategy for the treatment of MIRI with better outcome after modification with ischemic myocardium-targeted peptide, which was expected to be applied in clinical practice in future.
Topics: Animals; MicroRNAs; Myocardial Reperfusion Injury; Exosomes; NF-kappa B; Signal Transduction; Rats; Rats, Sprague-Dawley; Male; Milk; Myocardium; Cardiotonic Agents; Myocytes, Cardiac
PubMed: 38951872
DOI: 10.1186/s12951-024-02631-0 -
Scientific Reports Jul 2024While the efficacy of GpIIb-IIIa-inhibitors during primary PCI (pPCI) for ST-elevated myocardial infarction (STEMI) has previously been demonstrated, its ongoing role... (Comparative Study)
Comparative Study
While the efficacy of GpIIb-IIIa-inhibitors during primary PCI (pPCI) for ST-elevated myocardial infarction (STEMI) has previously been demonstrated, its ongoing role and safety in combination with newer P2Y12-inhibitors is unclear. We therefore sought to compare outcomes between two centers with divergent approaches to the use of GpIIbIIIa antagonists in pPCI. We performed a retrospective chart review of all-comer STEMI patients treated with pPCI at two high-volume Montreal academic tertiary care centers. One center tended to use GpIIb-IIIa-inhibitors up-front in a large proportion of patients (liberal strategy) and the other preferring a bail-out approach (conservative strategy). Baseline patient characteristics and procedural data were compared between the two groups. The main efficacy outcome was rate of no-reflow/slow-reflow and the main safety outcome was BARC ≥ 2 bleeding events. A total of 459 patients were included, of whom 167 (36.5%) were exposed to a GpIIb-IIIa-antagonist. There was a significant overall difference in use of GpIIb-IIIa-antagonist between the two centers (60.5% vs. 16.1%, p < 0.01). Rate of no-reflow/slow-reflow was similar between groups (2.6% vs. 1.4%, p = 0.22). In-hospital rates of unplanned revascularization, stroke and death were also not different between groups. Use of a liberal GpIIb--IIIa-antagonist strategy was however associated with a higher risk of bleeding (OR 3.16, 95% CI 1.57-6.37, p < 0.01), which persisted after adjustment for covariables (adjusted OR 2.85, 95% CI 1.40-5.81, p < 0.01). In this contemporary retrospective cohort, a conservative, bail-out only GpIIb--IIIa-antagonist strategy was associated with a lower incidence of clinically relevant bleeding without any signal for an increase in no-reflow/slow-reflow or ischemic clinical events.
Topics: Humans; Male; Platelet Glycoprotein GPIIb-IIIa Complex; Female; Middle Aged; ST Elevation Myocardial Infarction; Aged; Retrospective Studies; Percutaneous Coronary Intervention; Platelet Aggregation Inhibitors; Treatment Outcome; Hemorrhage
PubMed: 38951544
DOI: 10.1038/s41598-024-64652-x -
Hellenic Journal of Cardiology : HJC =... Jun 2024
PubMed: 38950885
DOI: 10.1016/j.hjc.2024.06.009 -
European Journal of Pharmacology Jun 2024With a global towering prevalence of index acute myocardial infarction (nonrecurrent MI, NR-MI), a high incidence of recurrent MI (R-MI) has emerged in recent decades....
With a global towering prevalence of index acute myocardial infarction (nonrecurrent MI, NR-MI), a high incidence of recurrent MI (R-MI) has emerged in recent decades. Despite the extensive occurrence, the promising predictors of R-MI have been elusive within the cohort of survivors. This study investigates and validates the involvement of distinct gene expressions in R-MI and NR-MI. Bioinformatics tools were used to identify DEGs from the GEO dataset, functional annotation, pathway enrichment analysis, and the PPI network analysis to find hub genes. The validation of proposed genes was conceded by qRT-PCR and Western Blot analysis in experimentally induced NR-MI and R-MI models on a temporal basis. The temporal findings based on RT-PCR consequences reveal a significant and constant upregulation of the UBE2N in the NR-MI model out of the proposed three DEGs (UBE2N, UBB, and TMEM189), while no expression was reported in the R-MI model. Additionally, the proteomics study proposed five DEGs (IL2RB, NKG7, GZMH, CXCR6, and GZMK) for the R-MI model since IL2RB was spotted for significant and persistent downregulation with different time points. Further, Western Blot analysis validated these target genes' expressions temporally. I/R-induced NR-MI and R-MI models were confirmed by the biochemical parameters (CKMB, LDH, cTnI, serum nitrite/nitrate concentration, and inflammatory cytokines) and histological assessments of myocardial tissue. These results underscore the importance of understanding genetic mechanisms underlying MI and highlight the potential of UBE2N and IL2RB as biomarkers for non-recurrent and recurrent MI, respectively.
PubMed: 38950836
DOI: 10.1016/j.ejphar.2024.176795