Cardiology Research and Practice最新文献

Background: Long QT syndrome (LQTS) is an inherited cardiac channelopathy marked by QT interval prolongation and increased risk of life-threatening arrhythmias. While variants in KCNQ1, KCNH2, and SCN5A explain most cases, many remain genetically unexplained. This study emphasizes the value of genetic testing in diagnosis and individualized therapy. Methods: A 9-year-old boy with recurrent syncope was evaluated for LQTS. Clinical workup included history, physical exam, ECG, echocardiography, exercise testing, electrophysiology studies (EPS), Holter monitoring, and cardiac MRI. Family history was assessed. Genetic testing involved whole-exome sequencing (WES) and Sanger confirmation, followed by bioinformatic pathogenicity analysis. Results: The boy's ECG showed a QTc of 470 ms, extending to 500 ms during EPS. No structural cardiac defects were detected. WES revealed a heterozygous missense variant, NM_001035.2:c.12370A > C (p.Ser4124Arg), in the RYR2 gene. In silico tools predicted it to be pathogenic, and Sanger sequencing confirmed it. The variant was also identified in the patient's mother, who had a history of syncope, but not in the father. The patient responded well to propranolol and remained symptom-free for 18 months. Conclusion: Identification of a pathogenic RYR2 variant expands the known genetic spectrum of LQTS. The patient's clinical and familial findings highlight the need to consider RYR2 in genetic testing panels, especially for atypical LQTS cases. Continued research is essential to further clarify the genetics of LQTS and guide targeted management.

Background: Ischemia-reperfusion (IR) injury, a process involving the disruption and subsequent restoration of blood flow, is a significant contributing factor to both cardiovascular diseases and broader tissue damage. Carnosine, a natural dipeptide notably abundant in muscle tissue and recognized for its antioxidant attributes, may offer protective benefits against the deleterious effects of IR injury. Methods: A total of 24 rats were randomly allocated into four distinct groups: control, carnosine control, IR, and Carnosine + IR. The IR and Carnosine + IR groups underwent a simulated blood flow blockage lasting 120 min, followed by 120 min of reperfusion. Animals in the carnosine-treated groups received 250 mg/kg of carnosine via intraperitoneal injection prior to the experimental procedure. Muscle tissue samples were subsequently analyzed to quantify markers indicative of oxidative stress, inflammation, and cellular demise. Results: Our findings demonstrated that, when compared to control groups, the IR group exhibited a significant elevation in key markers of oxidative stress (total oxidant status [TOS], Oxidative Stress Index [OSI]), inflammation (myeloperoxidase [MPO]), and cell death (TUNEL, Necrosis, Edema). Specifically, the IR group presented with a TOS of 8.72 ± 0.97 μmol/L, an OSI of 2.03 ± 0.18, and an MPO level of 75.93 ± 5.72 U/L, contrasting with control values of 4.23 ± 0.56 μmol/L, 1.01 ± 0.13, and 43.26 ± 5.7 U/L, respectively. Histopathological assessments corroborated these findings, revealing severe necrosis (2.50 ± 0.55), edema (2.00 ± 0.63), and notable inflammatory cell infiltration (2.67 ± 0.52) within the IR group. Furthermore, apoptosis (quantified by TUNEL assay) was significantly increased to 18.83 ± 1.47% in the IR group. Carnosine administration in the Carnosine + IR group led to a substantial reduction in all these adverse markers, bringing their levels closer to those observed in the control groups. For instance, in the Carnosine + IR group, TOS decreased to 5.63 ± 0.87 μmol/L, OSI to 1.24 ± 0.25, and MPO to 55.91 ± 3.45 U/L. Similarly, histopathological scores for necrosis, edema, and inflammatory cell infiltration were markedly lower in the Carnosine + IR group. Conclusion: Our experimental findings strongly suggest that exogenously administered carnosine significantly reduces oxidative stress, suppresses inflammation, and attenuates cell death in skeletal muscle subjected to IR injury. These results highlight carnosine's promising therapeutic potential as a pharmacological agent for mitigating tissue damage in ischemic conditions.

Background: Heart failure (HF) is a major cause of morbidity and mortality in low-resource settings like Ethiopia. This study aimed to assess time to mortality and identify key predictors among adult HF patients at Jimma Medical Center (JMC). Methods: A retrospective cohort study was conducted on 356 adult HF patients admitted to JMC between 2022 and 2023. Survival probabilities were estimated using the Kaplan-Meier method, and Cox proportional hazard regression was used to identify mortality predictors. Results: Among 356 HF patients, 15.7% (95% CI: 12.2%-19.8%) died during the study period. The median hospital stay was 11 days (IQR: 7-17), and the median age was 55 years (IQR: 38-65). Key predictors of higher mortality included hypertension (AHR: 4.6, 95% CI: 1.88-11.61, p < 0.001), pneumonia (AHR: 4.3, 95% CI: 1.15-15.78, p = 0.031), anemia (AHR: 3.3, 95% CI: 1.17-9.06, p = 0.023), acute myocardial infarction (AMI) (AHR: 4.4, 95% CI: 1.9-10.09, p < 0.001), and hyponatremia (AHR: 2.9, 95% CI: 1.44-5.99, p = 0.003). Each unit increase in systolic blood pressure (SBP) and diastolic blood pressure (DBP) was linked to a 7% and 4% lower mortality risk, respectively (p = 0.035). A higher pulse rate was associated with a 4% increased mortality risk. Patients with heart failure with reduced ejection fraction (HFrEF) had a six-fold higher mortality risk compared to those with preserved ejection fraction (HFpEF) (AHR: 6.1, 95% CI: 1.79-24.4, p = 0.008). Conclusion: This study identifies key mortality predictors for HF patients in a resource-limited setting, including hypertension, pneumonia, anemia, AMI, and hyponatremia. The findings emphasize the need for targeted interventions, improved management strategies, and policies to reduce HF mortality in low-resource environments. Further research is needed to refine these findings and enhance care for HF patients in such settings.

Objective: To identify risk factors for contrast-induced acute kidney injury (CI-AKI) post-PCI in coronary heart disease (CHD) patients, analyze novel inflammatory markers, and develop a predictive model. Methods: CHD patients admitted to Northern Jiangsu People's Hospital in Yangzhou, Jiangsu Province, China, from January 1, 2019, to December 31, 2022, were selected, and a total of 628 patients were included in this study by collecting the general information, past history, and relevant laboratory test results of all patients and excluding those with imperfect relevant medical records, including 142 cases in the CI-AKI group and 486 cases in the non-CI-AKI group. According to the ratio of 7:3, they were randomly divided into a training group (n = 439) and a validation group (n = 189). Independent risk factors for the occurrence of postoperative CI-AKI were screened by unifactorial and multifactorial logistic regression analyses in the training group, a clinical prediction model was established, and the prediction efficiency and applicability of the prediction model were analyzed by ROC curves, DCA curves, and H-L curves in the two groups. Results: Regression analysis suggested that neutrophil count, low-density lipoprotein, and PLR were independent risk factors for CI-AKI (p < 0.05); a model for predicting CI-AKI was established based on the above indexes, and the areas under the ROC curves of the model in the training and validation groups were 0.73 (0.67-0.78) and 0.71 (0.62-0.79), respectively; the H-L curve suggests that the predicted situation of the model is consistent with the actual occurrence, and the DCA curve suggests that patients in the training group and the validation group will have the greatest clinical benefit when the thresholds for the occurrence of postoperatively induced acute kidney injury are 0.26-0.82 and 0.30-0.97, respectively. Conclusion: This CI-AKI prediction model demonstrates good accuracy and clinical applicability, aiding early high-risk patient identification and intervention. Trial Registration: Chinese Registry of Clinical Trials: ChiCTR2500099751.

[This corrects the article DOI: 10.1155/2022/1910841.].

Aim: Left ventricular dysfunction, disturbed mitophagy, and persistent oxidative stress after myocardial infarction (MI) are critical drivers of myocardial injury and cardiac remodeling. Exercise-based cardiac rehabilitation (CR) is a cornerstone of post-MI treatment and management, yet its mechanistic effects on myocardial repair remain incompletely elucidated. This study aimed to the effect of exercise-based CR on the left ventricular dysfunction, mitophagy, and oxidative stress post-MI. Methods: Mendelian randomization analysis elucidated causal relationship between six physical activities and MI. Subsequently, 70 MI patients were randomized to control or exercise-based CR groups (moderate-to-vigorous physical activity intensity, 3 days/week, 10-50 min/day, 12 weeks); left ventricular function, cardiopulmonary function, and SF-36 quality of life scale were assessed pre-/postintervention using standardized protocols. Additionally, 21 rats were allocated to Sham, MI, or MI + treadmill running groups (high-intensity interval exercise training, 5 days/week, 30-50 min/day, 10-25 m/min, 4 weeks); left ventricular function, mitophagy, and oxidative stress were detected postintervention. Results: Genetically predicted moderate-to-vigorous intensity physical activity was significantly associated with lower risk of MI (IVW OR = 0.66, 95% CI: 0.54-0.81), with no causal links for other activities. Critically, clinical and animal studies demonstrated that exercise-based CR improved left ventricular systolic function (LVEF) after MI. Four-week exercise in MI rats enhanced mitophagy levels (LC3, FUNDC1, PINK1, and Parkin) and attenuated oxidative injury (MDA, GSH, SOD2, and GPX4) post-MI. Additionally, exercise-based CR also improved cardiopulmonary function (peak VO₂/kg, peakVO₂/pred%, and MET) in patients with MI and ameliorated mitochondrial damage in MI rats. However, GLS, secondary cardiopulmonary parameters (Wmax, HRR1min, peakVO₂/HR, and peakVO₂/HRpred%), and SF-36 (PCS and MCS) showed no significant changes, which may be associated with shorter duration of exercise intervention. Conclusion: Exercise-based CR significantly ameliorated left ventricular dysfunction, enhanced mitophagy levels, and attenuated oxidative stress post-MI, establishing its role in critical pathological mechanisms. Future studies should validate long-term sustainability of exercise-based CR and explore the interaction mechanism between mitophagy and oxidative stress in cardiac remodeling, providing personalized and precise exercise protocols for people at high risk of exercise.

Background: The relationship between nutritional status at the start of treatment for acute myocardial infarction (AMI) and the onset of acute kidney injury (AKI) remains unclear. This study aimed to clarify the association between nutritional status, as assessed by the controlling nutritional status (CONUT) score before catheter treatment, and the development of AKI in patients with AMI. Methods: This retrospective study included AMI patients treated with percutaneous coronary intervention (PCI) immediately after admission at our institution between 2014 and 2018. Patients undergoing chronic hemodialysis were excluded. Nutritional status was evaluated using the CONUT score derived from blood tests at admission, with scores below 5 indicating good nutrition and scores of 5 or above indicating malnutrition. The two groups were compared retrospectively. Results: A total of 211 AMI patients were included, with a median age of 68 years (59-79), and 156 (74%) were male. The median door-to-balloon time was 74 min (59-94). There were 180 patients in the good nutrition group and 31 in the malnutrition group. The malnutrition group exhibited significantly higher mortality (1.1% vs. 12.9%, p < 0.001) and a higher incidence of AKI (19% vs. 52%, p < 0.001). Multivariable logistic regression analysis identified lactic acid (odds ratio [OR] = 1.570 and 95% confidence interval [CI] 1.310-1.882), baseline creatinine (OR = 7.403 and 95% CI 1.852-29.59), and malnutrition (OR = 3.715 and 95% CI 1.278-10.80) as independent risk factors for AKI. Conclusions: Malnutrition, assessed by the CONUT score before treatment, may be associated with an increased risk of AKI in AMI patients.

Electroacupuncture (EA) therapy combines electrical stimulation with traditional acupuncture therapy and is widely used as a physical therapy in various fields. Coronary heart disease (CHD) is a prevalent cardiovascular condition. Applying EA in the treatment of CHD patients has proven to effectively enhance therapeutic outcomes and improve prognosis. This paper summarizes the potential mechanisms of EA in the treatment of CHD, its therapeutic effects on CHD patients, and analyzes the current bottlenecks in the application of EA therapy for CHD. Furthermore, it discusses potential future directions for EA in CHD management.

Background: Increased level of high-sensitivity C-reactive protein (hs-CRP) is associated with no-reflow phenomenon. Therefore, even when timely coronary revascularization is performed through the primary percutaneous coronary intervention (pPCI), the process can induce reperfusion injury. Purpose: We evaluated the influence of hs-CRP level on the no-reflow phenomenon in patients with ST-segment elevation myocardial infarction (STEMI). Methods: In this study, we included one hundred and eighty-two consecutive patients with STEMI of onset < 12 h, who underwent pPCI. The levels of creatine kinase (CK), the MB fraction of creatine kinase (CK-MB), troponin I, hs-CRP, and other routine laboratory parameters were measured. Measurement of hs-CRP was done on the day of admission by Cobas assay (particle-enhanced immunoturbidimetric assay) on Cobas c501 (Roche). Thereafter, patients were divided in two groups according to the thrombolysis in myocardial infarction (TIMI) flow grade. Results: From a total of 182 STEMI patients who underwent pPCI, the median value of hs-CRP of the patients with TIMI grade flow 3 (successful reperfusion) was 8.5 (0.4-268) and of the patients with no-reflow phenomenon (unsuccessful reperfusion, TIMI flow grade ≤ 2) was 37.90 (1.8-271.20), p < 0.0001. Receiver operating characteristics (ROC) curve of hs-CRP plots the true positive rate against the false positive rate at different cutoff points, AUC = 0.73 (95% CI, 0.64-0.81), and the cutoff value for the hs-CRP was 18.0 mg/L, p=0.0001. Conclusions: hs-CRP may be associated with no-reflow phenomenon in STEMI patients. The cutoff value for hs-CRP may be used to identify patients at risk for reperfusion injury.

Objectives: This study systematically reviewed and meta-analyzed randomized controlled trials (RCTs) evaluating the efficacy and safety of acupuncture in myocardial ischemia/reperfusion (I/R) injury. Methods: A comprehensive literature search was conducted in PubMed, Cochrane Library, Web of Science, Chinese National Knowledge Infrastructure, China Science and Technology Journal Database, and Wanfang from database inception to November 3, 2024. Eligible RCTs assessing acupuncture for myocardial I/R injury were included. Statistical analyses were performed using Review Manager 5.3 and Stata 16. Results: A total of 26 RCTs of moderate methodological quality were included. Acupuncture significantly reduced myocardial enzyme levels compared to controls. Inflammatory markers (hs-CRP, TNF-α, IL-6, IL-8, and IL-1) were suppressed, while anti-inflammatory and immunoregulatory factors (IL-10 and IL-2) increased. Oxidative stress parameters showed improvements, with reductions in MDA and SOD levels. Echocardiographic findings demonstrated enhanced cardiac function, reflected by increased LVEF and LVESV, along with reductions in LVFS, LVEDD, LVEDV, and LVESD. Additionally, acupuncture alleviated TCM chest pain symptoms, shortened ICU stays, lowered MACE incidence, and improved 6MWT and SAQ indicators. No adverse reactions were reported. Conclusion: Acupuncture attenuates myocardial injury, inflammation, and oxidative stress while activating anti-inflammatory and immune responses, enhancing cardiac function, and mitigating ventricular remodeling. Furthermore, it alleviates chest pain, shortens ICU stays, reduces adverse cardiovascular events, and improves 6MWT and SAQ indicators.