American journal of cardiovascular disease最新文献

Globally, the incidence of newly diagnosed human immunodeficiency virus (HIV) infections is concerning. Despite enhancing the quality of life for this patient population, antiretroviral therapy (ART) is linked to an increased risk of cardiovascular disease (CVD). In people living with HIV (PLWH) undergoing ART, recent research has demonstrated that the use of statins and aspirin (ASA) can reduce the incidence or progression of CVD. However, research has demonstrated that interactions may occur when these medications are used concurrently in the treatment regimen of PLWH. Therefore, we conclude this systematic review to evaluate the use of ART in HIV individuals with CVD and also the effect of adding ASA and statins to ART for reducing the cardiac adverse events.

Colchicine is one of the established drugs of choice for post-myocardial infarction (MI) induced pericarditis, given its anti-inflammatory properties. Recently, colchicine received FDA approval for secondary prevention of atherosclerotic cardiovascular disease, which leads to concerns regarding its anti-healing effects on myocardial tissue post-infarction. We present a case of a suspected colchicine-induced myocardial rupture in an elderly male, who presented with a syncopal episode while on colchicine three weeks after the late presentation of infero-posterior ST-elevation myocardial infarction.

Objective: Proteasome activation by the cAMP-dependent protein kinase (PKA) was long suggested and recent studies using both cell cultures and genetically engineered mice have established that direct phosphorylation of RPN6/PSMD11 at Serine14 (pS14-RPN6) mediates the activation of 26S proteasomes by PKA. Genetic mimicry of pS14-RPN6 has been shown to be benign at baseline and capable of protecting against cardiac proteinopathy in mice. Here we report the results from a comprehensive baseline characterization of the Rpn6^S14A mice (S14A), the first animal model of genetic blockade of the activation of 26S proteasomes by PKA.

Method: Wild type and homozygous S14A littermate mice were subjected to serial M-mode echocardiography at 1 through 7 months of age, to left ventricular (LV) catheterization via the carotid artery for assessment of LV mechanical performance, and to cardiac gravimetric analyses at 26 weeks of age. Mouse mortality and morbidity were monitored daily for up to one year. Males and females were studied in parallel.

Results: Mice homozygous for S14A were viable and fertile and did not show discernible developmental abnormalities or increased mortality or morbidity compared with their Rpn6 wild type littermates by at least one year of age, the longest cohort observed thus far. Neither serial echocardiography nor hemodynamic assessments detected a remarkable difference in cardiac morphometry and function between S14A and wild type littermate mice. No cardiac gravimetric difference was observed.

Conclusion: The findings of the present study indicate that genetic blockade of the activation of 26S proteasomes by PKA is well tolerated by mice at baseline. Therefore, the S14A mouse provides a desirable genetic tool for further investigating the in vivo pathophysiological and pharmacological significance of pS14-RPN6.

Background: Permanent pacemaker implantation is increasing exponentially to treat atrio-ventricular block and symptomatic bradyarrhythmia. Despite being a minor surgery, immediate complications such as pocket infection, pocket hematoma, pneumothorax, hemopericardium, and lead displacement do occur.

Methods: The Nationwide Inpatient Sample was queried from 2016 to 2018 to identify patients with pacemakers using ICD-10 procedure code. The Chi-square test was used for statistical analysis.

Results: The sample size consisted of 443,460 patients with a pacemaker, 26% were <70 years (male 57%, mean age of (60.6±9.7) yr, Caucasian 70%) and 74% were ≥70 years (male 50%, mean age of (81.4±5.9) yr, Caucasian 79%). Upon comparison of rates in the young vs elderly: mortality (1.6% vs 1.5%; P<0.01), obesity (26% vs 13%; P<0.001), coronary artery disease (40% vs 49%; P<0.001), HTN (74% vs 87%; P<0.01), anemia (4% vs 5%; P<0.01), atrial fibrillation (34% vs 49%; P<0.01), peripheral artery disease (1.7% vs 3%; P<0.01), CHF (31% vs 39%; P<0.001), diabetes (31% vs 27.4%; P<0.01), vascular complications (1.1% vs 1.2%; P<0.01), pocket hematoma (0.5% vs 0.8%; P<0.01), AKI (16% vs 21%; P<0.01), hemopericardium (0.1% vs 0.1%; P = 0.1), hemothorax (0.3% vs 0.2%; P<0.01), cardiac tamponade (0.4% vs 0.5%; P<0.01), pericardiocentesis (0.4% vs 0.4%; P<0.01), cardiogenic shock (4% vs 2.3%; P<0.01), respiratory complications (1.9% vs 0.9%; P<0.01), mechanical ventilation (5.1% vs 2.9%; P<0.01); post-op bleed (0.5% vs 0.3%; P<0.01), need for transfusion (4.8% vs 3.8%; P<0.01), severe sepsis (0.6% vs 0.5%; P<0.01 ), septic shock (2% vs 1%; P<0.01), bacteraemia (0.8% vs 0.4%; P<0.01), lead dislodgement (1.4% vs 1.1%; P<0.01).

Conclusions: Our study revealed that the overall complication rates were lower in the elderly despite higher co-morbidities. This aligns with previous studies which showed lower rates in the elderly. Hence providers should not hesitate to provide guideline driven pacemaker placement in the elderly especially in patients with good life expectancy.

Background: Elevated circulating levels of albumin (ALB) are often associated with improved prognosis in patients with heart failure (HF). However, investigations of its association with hospital death and long-term death in HF patients in the intensive care unit (ICU) are limited.

Aim: We examined whether increased blood ALB levels (first value at admission and maximum and minimum values in the ICU) were related to a greater risk of hospital death and long-term death in ICU patients with HF.

Methods: For the first time, we analyzed 4084 ICU patients with HF admitted to the ICU in The Medical Information Mart for Intensive Care III (MIMIC-III) database.

Results: Among 4084 HF patients, 774 (18.95%), 1056 (25.86%) and 1720 (42.12%) died in the hospital, within 30 days and 1 year, respectively. We conducted a logistic regression analysis and found significant inverse associations between blood ALB concentration and risk of hospital death, 30-day death and 1-year death when the covariates including age, sex, myocardial infarction (MI), hypertension, diabetes, valvular diseases, atrial fibrillation, stroke and chronic kidney disease (CKD) were adjusted. We additionally used a smooth curve for univariate analysis to establish an association between blood ALB concentration and death risk. Surprisingly, we observed U-shaped correlations between blood ALB concentration and hospital mortality, 30-day mortality and 1-year mortality. We found that the "inflection point" for the blood ALB concentration at the lowest risk of death was 3.5 g/dL. We further observed that a higher blood ALB concentration (albumin-max) did not contribute to a reduced risk of death (hospital death, 30-day death and 1-year death) in HF patients with an albumin concentration >3.5 g/dL.

Conclusions: A lower blood ALB concentration contributed to a greater risk of hospital death and long-term death in HF patients admitted to the ICU, further suggesting that nutritional support in the ICU is highly important for improving the short-term and long-term mortality of HF patients. However, in HF patients without hypoproteinaemia (>3.5 g/dL), the impact of increased serum ALB on patient prognosis still needs to be demonstrated.

Background: Data on the impact of chronic thrombocytopenia (CT) on outcomes following chronic total occlusion (CTO) percutaneous coronary interventions (PCI) is limited. Most studies are case reports and focused on postprocedural thrombocytopenia. The purpose of this present study is to assess the impact of CT (> one year) on health resource utilization (HRU), in-hospital outcomes, and cost following CTO PCI.

Methods: We used discharge data from the 2016-2018 National Inpatient Sample and propensity score-weighted approach to examine the association between CT and HRU among patients undergoing CTO PCI. HRU was measured as a binary indicator defined as a length of stay greater than seven days and/or discharge to a non-home setting. The cost was measured as total charges standardized to 2018 dollars. Both outcomes were assessed using generalized linear models adjusted for survey year, and baseline characteristics.

Results: Relative to its absence, the presence of CT following CTO PCI was associated with a 4.8% increased probability of high HRU (Population Average Treatment Effect (PATE) estimate = 0.048; 95% Confidence Interval (CI) = 0.041-0.055; P<0.001) and approximately $18,000 more in total hospital charges (PATE estimate = +$18,297.98; 95% CI = $15,101.33-$21,494.63, P<0.001).

Conclusion: Among chronic total occlusion patients undergoing percutaneous coronary intervention, those with chronic thrombocytopenia had higher resource use, including total hospital charges, and worse in-hospital outcomes when compared with those without chronic thrombocytopenia.

Background: Dilated cardiomyopathy (DCM) caused by Lamin A/C gene (LMNA) mutation is complicated with atrioventricular conduction disturbances, malignant ventricular arrhythmias and progressive severe heart failure.

Objective: We hypothesized that early cardiac resynchronization therapy (CRT) implantation in LMNA mutation carriers with an established indication for pacemaker or implantable cardioverter defibrillator (ICD), may preserve ejection fraction, and delay disease progression to end stage heart failure.

Methods: We compared the primary outcomes: time to heart transplantation, death due to end stage heart failure or ventricular tachycardia (VT) ablation and secondary outcomes: change in left ventricular ejection fraction (EF) and ventricular arrhythmia burden between LMNA DCM patients in the early CRT and non-CRT groups.

Results: Of ten LMNA DCM patients (age 51±10 years, QRS 96±14 msec, EF 55±7%) with indication for pacemaker or ICD implantation, five underwent early CRT-D implantation. After 7.2±4 years, three patients (60%) in the non-CRT group reached the primary outcome, compared to no patients in the CRT group (P=0.046). Four patients in non-CRT group (80%) experienced sustained ventricular tachycardia or received appropriate ICD shock compared to 1 patient (20%) in the CRT group (P=0.058). LMNA patients without early CRT had a higher burden of VPC/24 h in 12-lead holter (median 2352 vs 185, P=0.09). Echocardiography showed statistically lower LVEF in the non-CRT group compared to CRT group [(32±15)% vs (61±4)%, 95% CI: 32.97-61.03, P=0.016].

Conclusion: Early CRT implantation in LMNA cardiomyopathy patients, with an indication for pacemaker or ICD, may reduce heart failure deterioration and life-threatening heart failure complications.

Objective: This study aimed to create a predictive model for hyperuricemia (HUA) in patients diagnosed with hypertension and evaluate its predictive accuracy.

Methods: Employing a retrospective cohort design, this study investigated HUA incidence and clinical data among 228 patients with essential hypertension selected from the Department of Cardiology at a tertiary A-level hospital in Anhui Province, China, between January 2018 and June 2021. The patients were divided randomly into a training group (168 cases) and a validation group (60 cases) at a 7:3 ratio. The training group underwent univariate and multivariate logistic regression analyses to identify risk factors for HUA. Additionally, an R software-generated nomogram model estimated HUA risk in hypertensive patients. The validation group assessed the nomogram model's discriminatory power and calibration using receiver operating characteristic curve analysis and the Hosmer-Lemeshow goodness-of-fit test.

Results: The study found a 29.39% prevalence of HUA among the 228 participants. Logistic regression analyses identified age, body mass index, and concomitant coronary heart disease as independent HUA risk factors (odds ratio [OR] > 1 and P < 0.05). Conversely, high-density lipoprotein cholesterol emerged as an independent protective factor against HUA in hypertensive patients (OR < 1 and P < 0.05). Using these factors, a nomogram model was constructed to assess HUA risk, with an AUC of 0.873 (95% confidence interval [CI]: 0.818-0.928) in the training group and 0.841 (95% CI: 0.735-0.946) in the validation group, indicating a strong discriminatory ability. The Hosmer-Lemeshow goodness-of-fit test showed no significant deviation between predicted and actual HUA frequency in both groups (χ² = 5.980, 9.780, P = 0.649, 0.281), supporting the nomogram's reliability.

Conclusion: The developed nomogram model, utilizing independent risk factors for HUA in hypertensive patients, exhibits strong discrimination and calibration. It holds promise as a valuable tool for cardiovascular professionals in clinical decision-making.

Background: The timing of coronary angiography in patients with non-ST elevation myocardial infarction (NSTEMI) needs to be well defined. In this study, based on the timing of percutaneous coronary intervention (PCI), we evaluated the incidence of major adverse cardiovascular events (MACE) in NSTEMI patients.

Methods: In this longitudinal study, we included 156 NSTEMI patients who underwent a PCI at three time points, including <12 hr. (n = 53), 12-24 hr. (n = 54), and ≥24 hr. (n = 49) and followed them for one, three, and six months to monitor major cardiovascular events. The data analyses were conducted using SPSS version 20.

Result: Four patients (2.56%) were hospitalized during the one-month follow-up, and only one patient (0.06%) had NSTEMI. The incidence of complications, such as readmission, acute coronary syndrome (ACS; 4 patients [2.56%]), and unstable angina (UA; 3 patients [1.92%]) did not differ significantly among the three intervention times. The occurrence of NSTEMI, UA, and recurrent PCI was 2.56%, 3.20%, and 5.12% in four, five, and eight patients, respectively, and no significant differences were observed among the aforementioned times. In the follow-up after six months, the incidence of STEMI, stroke, TLR, and other all-course deaths was observed in one person (0.06%), which all occurred within 12-24 hours. The difference among the three intervention times was non-significant.

Conclusion: Our findings revealed an insignificant difference between the incidence of complications and the three-intervention time.

Objective: To evaluate the impact of varying dosages of Spironolactone on the short-term effectiveness and ventricular remodeling indicators in patients with Heart Failure of Ischemic Cardiomyopathy (HFIC).

Methods: A cohort of 141 HFIC patients, admitted to our hospital between October 2018 and February 2023, were enrolled for this study. Alongside the standard treatment for Chronic Congestive Heart Failure (CHF), these patients were randomly assigned to either a low-dose (20 mg/d, N=70) or a high-dose (60 mg/d, N=71) Spironolactone group. After four weeks, various parameters were assessed and compared within each group before and after the treatment. These parameters included echocardiographic indices (LVEF, LVESD, LVEDD, LVESV, and LVEDV), New York Heart Association (NYHA) cardiac function classification, ventricular remodeling markers (hs-CRP, TNF-α, NT-pro BNP, Gal-3, MMP-9, and TIMP-4), and the Six Minute Walk Distance (6MWD).

Results: Both low-dose and high-dose Spironolactone significantly improved LVEF and 6MWD in HFIC patients (P<0.05), as well as markedly reduced LVESD, LVEDD, LVESV, LVEDV, and NYHA cardiac function grades (P<0.05). The high-dose group exhibited the most pronounced improvements (P<0.05). High-dose Spironolactone was more effective in improving the clinical and total effective rate compared to the low-dose, significantly reducing treatment inefficacy (P<0.05). Both dosages significantly increased serum potassium levels within normal ranges. They also improved the expression of ventricular remodeling markers (hs-CRP, TNF-α, NT-pro BNP, Gal-3, MMP-9, and TIMP-4) in HFIC patients, with the high-dose group showing the most significant results (P<0.05).

Conclusion: High-dose Spironolactone (60 mg/d) demonstrates superior efficacy over the low-dose (20 mg/d) in rapidly diminishing ventricular remodeling damage and enhancing cardiac function and clinical symptoms in HFIC patients over a short duration.