Risultati per: Le cause della polmonite nei bambini

Circulation, Volume 150, Issue Suppl_1, Page A4136480-A4136480, November 12, 2024. Background:Myocarditis is a cause of non-ischemic cardiomyopathy (NICM) and troponin elevation. There are many causes including uncontrolled thyroid disorder (TD). A thorough history, cardiac MRI (cMRI) followed by an endomyocardial biopsy (EMB) is necessary for diagnosis. This case illustrates a classic presentation of NSTEMI with a rare cause of myocarditis due to uncontrolled hypothyroidism.Description of Case:A 39-year-old female with history of congenital hypothyroidism and tobacco use disorder presented to the Emergency Department with sudden onset of unprovoked sub-sternal chest pain. She stated she had stopped taking her levothyroxine years ago due to side effects such as abdominal discomfort. On admission, work up included high sensitivity troponin (Hs-cTn), EKG, urine drug screen (UDS), and thyroid panel. There was no evidence of ischemic changes on EKG, Hs-cTn was 3600 (normal: 3-54) which up-trended to 43,742, and UDS was negative. She was placed on appropriate medical therapy for NSTEMI and taken for urgent coronary angiography wbich showed normal epicardial arteries. A transthoracic echocardiogram (TTE) was unremarkable with a normal ejection fraction (EF). However, she continued to complain of chest discomfort and palpitations. Her vital signs remained stable but her thyroid panel revealed a TSH of 127 (normal: 0.27-4.2), T4 of 0.18 (normal: 0.92 – 1.6) and T3 of 1.0 (normal: 2.3-4.2). Inflammatory markers were also elevated. A cMRI was obtained revealing gadolinium enhancement in the anterior septal wall with extension into the subepicardium of the inferior wall suggestive of possible myocarditis. An EMB was performed to elucidate etiology. Pathology results were only remarkable for edema but newly reduced EF of 30-35% was noted on TTE at time of biopsy. Endocrinology was consulted for untreated hypothyroidism and patient was initiated on levothyroxine leading to improvement of her symptoms.Discussion:Our patient’s history and work up were consistent with myocarditis induced by severe hypothyroidism. TD is a rare cause of reversible NICM and symptoms improve once TD is controlled. While there are several cases reported on hyperthyroidism associated myocarditis, there are only a few cases of myocarditis associated with uncontrolled hypothyroidism. Clinicians should maintain a broad differential to ensure a thorough work up in a patient presenting with NSTEMI, and a thyroid panel should be included especially if myocarditis is suspected.

Circulation, Volume 150, Issue Suppl_1, Page A4144394-A4144394, November 12, 2024. Introduction:Cardiac resynchronization therapy (CRT) reduces mortality in patients with moderate to severe heart failure (HF) and reduced ejection fraction. However, outcomes associated with CRT in CCC patients are still controversial. We conducted a meta-analysis to quantify total mortality in patients with chronic Chagas cardiomyopathy compared to HF of other etiologies (Non-Chagas).Objectives:To perform a meta-analysis of studies to measure all-cause mortality in CCC patients compared to patients of other etiologies (Non-Chagas) when undergoing CRT.Methods:A literature search was conducted in PubMed, Cochrane, Embase, Scielo for English, Portuguese, and Spanish comparing all-cause mortality in patients undergoing CRT in CCC and other etiologies (Non-Chagas). The Non-Chagas group included patients with HF of ischemic, dilated, or idiopathic etiology. Statistical analysis was performed in RevMan 5.18. Heterogeneity was assessed by I2 statistics.Results:577 patients from 3 studies were included, with 170 patients having Chronic Chagas Cardiomyopathy. Follow-up time ranged from 12 to 41 months. Mean age was 61.7 +/- 11.6 years and 61.5% were male. Mean ejection fraction across studies was 25.8% +/- 6.4.All-cause mortality (OR: 2.41; 95% CI: 1.65-3.53; p < 0.00001, I2 = 0%) was significantly higher in patients with Chronic Chagas Cardiomyopathy compared to the Non-Chagas group.Conclusion:Patients with CCC had higher all-cause mortality compared to Non-Chagas patients when undergoing CRT. These results highlight the importance of prospective controlled studies comparing Cardiac Resynchronization Therapy with other treatments to define the optimal therapy for patients with heart failure with reduced ejection fraction due to Chagas disease.

Circulation, Volume 150, Issue Suppl_1, Page A4125729-A4125729, November 12, 2024. Background:Transcatheter edge-to-edge mitral valve repair (TEER) is an established procedure in patients with severe mitral regurgitation (MR) and elevated surgical risk on optimal medical therapy. However, there remains considerable mortality in this patient population. Some studies have shown that serum brain natriuretic peptide (BNP) and N-terminal pro b-type natriuretic peptide (NT-proBNP) predict all-cause mortality after TEER, whereas other studies have shown mortality to be independent of these markers. To address this gap in knowledge, we sought to examine the existing literature to determine whether there is an association between pre-procedural serum natriuretic peptides and mortality after TEER.Hypothesis:Among patients undergoing TEER, elevated pre-procedural BNP and NT-proBNP are associated with increased all-cause mortality.Methods:Databases including MEDLINE, Embase, and Cochrane Library were searched from inception through September 2023 for studies assessing pre-procedural serum natriuretic peptide levels and mortality among patients undergoing TEER. Pooled hazard ratios (HR) and standardized mean differences (SMD) were calculated using a random-effects model estimated by restricted maximum likelihood with the Hartung-Knapp modification.Results:A total of 30 studies comprising 10259 patients undergoing TEER met inclusion criteria. 25 studies measured NT-proBNP and 5 studies measured BNP. Elevated pre-procedural NT-proBNP ( >5000 or >10000 pg/mL) was associated with increased all-cause mortality in both adjusted (HR = 2.94; 95% CI = 1.75 – 4.95; I2 = 46.8%) and unadjusted (HR = 5.16; 95% CI = 1.85 – 14.40; I2 = 0.0%) analyses (Figures 1 and 2). Pre-procedural BNP and NT-proBNP were also significantly lower among survivors at 12 months compared to non-survivors (SMD = 0.82; 95% CI = 0.37 – 1.27; I2 = 78.3%) (Figure 3). This association was demonstrated in patients with primary or secondary MR.Conclusions:Pre-procedural BNP and NT-proBNP levels are significant predictors of all-cause mortality in patients undergoing TEER for primary or secondary MR. This supports the inclusion of BNP or NT-proBNP in pre-procedural assessments to help inform patient discussions and guide post-procedural follow-up and monitoring.

Circulation, Volume 150, Issue Suppl_1, Page A4135239-A4135239, November 12, 2024. A 67-year-old male with a history of hypertension presented to the emergency department with abnormal cardiac monitor results. Prior to this, he was diagnosed with primary open-angle glaucoma by ophthalmology and underwent left-sided aqueous tube shunt placement, which was complicated by hypotony requiring revision and holding of all topical glaucoma medications. Concurrently, he was noted to have an irregular heart rhythm during a routine physical. In office ECG showed normal sinus rhythm, but subsequent 14-day continuous ECG monitor showed sinus bradycardia with nadir heart rate of 21 beats-per-minute and 114 ventricular pauses (longest 4.8 seconds) primarily due to second-degree atrioventricular (AV) block, Mobitz type 1, but also periods of high-grade AV block. He was sent to the emergency department for expedited pacemaker evaluation. On further review, heart block and ventricular pauses occurred exclusively over a 12-hour period that temporally coincided with a hospitalization for acute ocular hypertension following shunt revision. His intraocular pressure peaked at 56 mmHg (normal range 10-21 mmHg), then normalized to 21 mmHg after acetazolamide and anterior chamber paracentesis. Bradycardia resolved following ophthalmic intervention. Bradyarrhythmias were attributed to excess vagal tone from acute ocular hypertension via an atypical but recognized cause of the oculocardiac reflex, and pacemaker placement was avoided.The oculocardiac reflex is a reflex bradycardia involving the trigeminal and vagus nerves. Cardiac effects are consistent with other vagally-mediated bradyarrhythmias, including sinus bradycardia, AV block, and even asystole. This reflex occurs commonly during traction on extraocular muscles during strabismus surgery, but can be seen in other orbital and ocular stimuli. To our knowledge, this is the first documented case of ocular hypertension leading to atrioventricular block through this mechanism. This case illustrates the importance of (1) clinical context of abnormal events during extended cardiac monitoring, (2) understanding the oculocardiac reflex as a cause of bradyarrhythmias, and (3) ruling out reversible medical causes of dysrhythmias prior to permanent device implantation.

Circulation, Volume 150, Issue Suppl_1, Page A4137939-A4137939, November 12, 2024. Introduction:Mosaic loss of Y chromosome (LOY), a common subtype of somatic mosaicism, is characterized as loss of the entire Y chromosome in a mosaic manner and increases with age. Accumulating evidence has manifested the positive link between LOY and shorter life expectations in elderly men as well as common age-associated diseases, such as cancer and cardiovascular diseases. Experimental studies also demonstrated that hematopoietic LOY in mice induced cardiac fibrosis and led to increased mortality. However, little is known about LOY and prognosis of ST-segment elevation myocardial infarction (STEMI).Hypothesis:We hypothesized that LOY may be associated with lower survival rate of patients with STEMI.Aims:Investigating the impact of LOY in peripheral blood cells on prognosis of patients with STEMI.Methods:This study prospectively enrolled 928 males and 272 females undergoing primary percutaneous coronary intervention for STEMI. LOY was measured in 928 males using droplet digital polymerase chain reaction technique.Results:During a median follow-up of 3.99 years, 93 males (10.0%) and 45 females (16.5%) died. After adjusting for traditional cardiovascular risk factors, the risk of all-cause mortality in males with LOY ≥ 18% (the 90th percentile of LOY) increased to 2.45 (95% confidence intervals [CI]: 1.16–5.15,P= 0.018), 2.11 (95% CI: 1.11–4.01,P= 0.024), and 1.88 (95% CI: 1.02–3.45,P= 0.043) times during 1-, 2-, and 3-year follow-up, respectively, compared to males with LOY < 18%. Among males without prior MI, those with LOY ≥ 18% had an increased risk of all-cause mortality compared to those with LOY < 18% (adjusted hazard ratio 1.93, 95% CI: 1.01–3.67;P= 0.045); this was not observed for males with prior MI. Female patients had a 1.71-fold (95%CI: 1.04–2.81;P= 0.035) increased risk of all-cause mortality than males with LOY < 18%, whereas the risk was similar to males with LOY ≥ 18%.Conclusion:LOY was associated with an increased risk of all-cause mortality in male STEMI patients, particularly in those without prior MI. Detecting LOY in STEMI patients could help further refine sex differences in prognosis and assist in identifying male patients with better prognoses.

Circulation, Volume 150, Issue Suppl_1, Page A4120274-A4120274, November 12, 2024. Background:Individual symptoms are predictors of mortality in adults with heart failure (HF). However, symptom clusters may be more predictive of future risks than isolated symptoms, yet research on these symptom clusters in older adults with HF is limited.Aims:To explore the extent to which symptom cluster profiles predict all-cause mortality among community-dwelling older adults with HF, while adjusting for known risk factors.Methods:We conducted a secondary analysis of data of the 2008 to 2016 surveys of the U.S. Health and Retirement Study using latent class analysis to identify baseline cluster profiles, and survival analysis for time to death with Cox proportional hazard (Cox PH) models, and Kaplan Meier survival analyses.Results:We included 684 participants [mean age=74.9, (SD=10) years, 56.6% female, 16.2% Black/African American]. Three baseline symptom cluster profiles were identified: high-burden (pain, shortness of breath, fatigue, swelling, depressive symptoms, dizziness), low-burden, and cardiopulmonary-depressive (shortness of breath, pain, and dizziness). The estimated median time-to-death was 71 (95% CI=64, 79) months. Of the 364 participants in the cardiopulmonary-depressive profile, 240 (65.9%) died (median time= 65 months, 95% CI= 55, 73) compared to those in the low-burden profile, of which 49% died. Approximately 61% in the high burden profile died (median time=67 months, 95% CI= 51, 90). A significant difference in survival times between the 3 cluster profiles was found (Log-rank= 9.13,p= 0.01). In the adjusted Cox PH model, participants in the high symptom burden and respiratory-depressive distress profiles had adjusted HR of 1.48 (95% CI=1.15, 1.94) and 1.44 (95% CI=1.14, 1.80) compared to those in the low burden symptom cluster profile, after controlling for age, gender, smoking, and comorbidities.Conclusions:The identified symptom cluster profiles predict 8-year all-cause mortality in older adults with HF, after controlling for known risk factors. An evaluation of symptom clusters, rather than individual symptoms, may provide additive prognostic information.

Circulation, Volume 150, Issue Suppl_1, Page A4144238-A4144238, November 12, 2024. Background and Aims:High neutrophil counts, an easily accessible inflammation biomarker, has been linked to risk of cardiovascular disease (CVD), and mortality, but with mixed results. We aimed to summarize published associations between neutrophil counts with risk of CVD and all-cause and cause-specific mortality among generally healthy populations.Methods:We searched Medline, Embase, Web of Science, and Cochrane CENTRAL databases until March 2024. Random effect meta-analysis was conducted to calculate pooled risk ratios (RRs) and 95% confidence intervals (95%CIs) for highest versus lowest categories of neutrophil counts in relation to risk of CVD and all-cause and cause-specific mortality among general healthy populations. Linear and non-linear dose-response analyses were also performed.Results:Our systematic review and meta-analysis included 22 prospective cohort studies. During a median/mean follow-up period of 3.8 to 18.3 years, 73,934 CVD events and 80,317 deaths occurred among 1,962,191 participants. Higher neutrophil counts were associated with a higher risk of CVD incidence and all-cause mortality, CVD mortality, and non-CVD mortality. The pooled RRs (95%CIs) of highest versus lowest categories of neutrophil counts were 1.32 (1.20, 1.45) for risk of CVD incidence, 1.61 (1.23, 2.11) for all-cause mortality, 1.71 (1.45, 2.01) for CVD mortality, and 1.68 (1.17, 2.40) for non-CVD mortality. Further, per 1 SD increase of neutrophil counts was associated with a 4%, 12%, 14%, and 24% higher risk for CVD events, all-cause mortality, CVD mortality, and non-CVD mortality, respectively. In addition, a secondary dose-response analysis revealed a non-linear association of neutrophil counts with risk of CVD events (Pnon-linearity= 0.01), but a linear positive association with CVD mortality (Pnon-linearity= 0.87). The pooled associations of neutrophil counts with CVD risk, and all-cause, CVD, and non-CVD mortality did not differ by age, sex, region, and follow-up duration.Conclusions:Higher neutrophil counts were associated with a substantially higher risk of CVD events and all-cause, CVD, and non-CVD mortality.

Circulation, Volume 150, Issue Suppl_1, Page A4143807-A4143807, November 12, 2024. Introduction:Aortic stenosis is the most common valvular heart disease and is managed by aortic valve replacement (AVR) procedures. Comorbid conditions may impact survival after AVR.Methods:We evaluated risk factors for all-cause mortality after AVR in the Veterans Affairs (VA) healthcare system for individuals with an AVR between January 1st2007 and December 31st2017, with National Death Index mortality data through December 31st, 2020. Clinical diagnoses and procedures were established byInternational Classifications of Disease(ICD) andCurrent Procedural Terminology(CPT) codes both in the VA and the Center for Medicare and Medicaid Services. Hazard rates for the primary outcome of all-cause mortality were calculated using a cox proportional hazards model adjusted for age at AVR, sex, and prevalent clinical risk factors (heart failure [HF], obesity, type 2 diabetes [T2D], and myocardial infarction [MI]).Results:There were 7,984,029 individuals seen regularly at the VA between 2007 and 2017. Within this group, there were 783,772 (9.8%) individuals with an established diagnosis of AS without prior valve replacement with a median (interquartile [IQR]) age of 73.5 [67.4-80.3] years, and 98% male. Between 2007-2017, 66,931 individuals had an AVR with median [IQR] age 72.8 [66.6-79.3] years, 98% male. Of the individuals with an AVR, 24,253 (36.2%) died prior to the end of follow up, with a median [IQR] time to death of 3.3 [2.8-5.3] years. At the time of valve replacement, there were 16,301 (24%) diagnoses of CKD, 11,916 (18%) diagnoses of HF, 21,575 (32%) diagnoses of T2D, and 4,211 (6%) diagnoses of prior MI. In a multivariable model, with adjustment for age, sex, and all clinical risk factors, a prevalent HF diagnosis portended the highest risk of all-cause mortality after AVR (HR 1.57 [1.52-1.62], p < 0.001), followed by T2D (HR 1.13 [1.09-1.16], p < 0.001), CKD (HR 1.11 [1.08-1.15], p < 0.001), and MI (1.05 [0.99-1.11], p = 0.06).Conclusions:Common clinical comorbidities including HF, CKD, and T2D, but not MI independently increase the risk of all-cause mortality after AVR.

Circulation, Volume 150, Issue Suppl_1, Page A4143662-A4143662, November 12, 2024. Background:Hypoxia-inducible factor-1 (HIF-1) is a heterodimeric transcription factor composed of a constitutively expressed β subunit (HIF-1β) and an oxygen-dependent α subunit (HIF-1α). HIF-1α has an important protective effect on the pathophysiology underlying coronary artery disease (CAD). However, the association between serum HIF-1α levels and mortality in patients with suspected or known CAD is unknown.Methods and Results:Serum levels of HIF-1α were measured in 2,418 patients with suspected or known CAD using a commercially available enzyme-linked immunosorbent assay kit (sensitivity, 30 pg/mL). The outcomes were all-cause death, cardiovascular (CV) death, and non-CV death. Patients were divided into 5 groups according to HIF-1α levels; below the sensitivity (Q0,

Circulation, Volume 150, Issue Suppl_1, Page A4146070-A4146070, November 12, 2024. Background:Accurate risk prediction of heart failure patients is essential for identifying high risk patients, developing targeted treatment strategies and prognostication. Existing traditional risk scores offer modest discriminative value, and rely on rigid predictor variables. A form of artificial intelligence, machine learning (ML) models provide alternate risk stratification that may improve predictive accuracy. This systematic review and meta-analysis compared machine learning models with traditional risk scores for predicting all-cause mortality and readmission in patients with heart failure.Methods:PubMed, EMBASE, Web of Science and Cochrane databases were searched until 1st May, 2024 for studies comparing ML models with traditional statistical methods for prediction of all-cause mortality and hospital re-admission following an index admission with CHF. The primary outcome was comparative discrimination measured by C-statistics with 95% confidence intervals between ML models and traditional methods in estimating the risk of all-cause mortality and hospital readmission at 30 days.Results:Twenty observational studies were included (558,233 patients). The summary C-statistic of the top-performing ML models for all-cause mortality was 0.76 (95% CI, 0.72-0.80), compared to traditional risk scores 0.71 (95% CI, 0.68-0.74). The difference in C-statistic between ML models and traditional methods was 0.05 (95% CI 0.04-0.06, p

Circulation, Volume 150, Issue Suppl_1, Page A4144083-A4144083, November 12, 2024. Background:The AI-CVD initiative aims to extract all useful opportunistic screening information from coronary artery calcium (CAC) scans and combines them with traditional risk factors to create a stronger predictor of cardiovascular diseases (CVD). These measurements include cardiac chambers volumes (left atrium (LA), left ventricle (LV), right atrium (RA), right ventricle (RV), and left ventricular mass (LVM)), aortic wall and valvular calcification, aorta and pulmonary artery volumes, torso visceral fat, emphysema score, thoracic bone mineral density, and fatty liver score. We have previously reported that the automated cardiac chambers volumetry component of AI-CVD predicts incident atrial fibrillation (AF), heart failure (HF), and stroke in the Multi-Ethnic Study of Atherosclerosis (MESA). In this report, we examine the contribution of other AI-CVD components for all coronary heart disease (CHD), AF, HF, stroke plus transient ischemic attack (TIA), all-CVD, and all-cause mortality.Methods:We applied AI-CVD to CAC scans of 5830 individuals (52.2% women, age 61.7±10.2 years) without known CVD that were previously obtained for CAC scoring at MESA baseline examination. We used 10-year outcomes data and assessed hazard ratios for AI-CVD components plus CAC score and known CVD risk factors (age, sex, diabetes, smoking, LDL-C, HDL-C, systolic and diastolic blood pressure, hypertension medication). AI-CVD predictors were modeled per standard deviation (SD) increase using Cox proportional hazards regression.Results:Over 10 years of follow-up, 1058 CVD (550 AF, 198 HF, 163 stroke, 389 CHD) and 628 all-cause mortality events accrued with some cases having multiple events. Among AI-CVD components, CAC score and chamber volumes were the strongest predictors of different outcomes. Expectedly, age was the strongest predictor for all outcomes except HF where LV volume and LV mass were stronger predictors than age. Figure 1 shows contribution of each predictor for various outcomes.Conclusion:AI-enabled opportunistic screening of useful information in CAC scans contributes substantially to CVD and total mortality prediction independently of CAC score and CVD risk factors. Further studies are warranted to evaluate the clinical utility of AI-CVD.

Circulation, Volume 150, Issue Suppl_1, Page A4143511-A4143511, November 12, 2024. Background:The Triglyceride-glucose (TyG) index , a novel indicator of insulin resistance, has been associated with mortality from non-alcoholic fatty liver disease (NAFLD) and cardiovascular disease (CVD). However, the association between the TyG index and the derived index of TyG (TyG-WHtR) and CVD in NAFLD patients remains unclear.Methods:This study enrolled 6627 adults aged 18 and above diagnosed NAFLD from the National Health and Nutrition Examination Survey (NHANES, 1999-2018). Binary weighted logistic regression analyses, cox proportional hazards model, restricted cubic spline (RCS), and receiver operating characteristic (ROC) were used to analyze the relationship between TyG and TyG-WHtR and all-cause mortality, CVD mortality and CVD related diseases. Mediation analysis explored the mediating role of glycohemoglobin (HbA1c), insulin and hypertension in the above relationships.Results:Except for no significant association between TyG and all-cause mortality and chronic heart failure (CHF), both TyG and TyG-WHtR exhibited significant positive correlations or trends of positive correlation with all-cause mortality, CVD mortality, total-CVD, CHF, coronary heart disease (CHD) and angina pectoris. For all-cause mortality, CVD mortality and CHF, TyG-WHtR was a better predictor than TyG (HR 1.31, 95%CI 1.03-1.66; HR 2.22, 95%CI 1.42-3.47; OR 3.99, 95%CI 1.79-8.93). However, TyG index demonstrated a stronger association with total-CVD, CHD and angina pectoris (OR 2.00, 95%CI 1.26-3.18; OR 1.85, 95%CI 1.19-2.91; OR 2.93, 95%CI 1.23-7.00). Otherwise, the ROC curve illustrated that, for all-cause mortality, CVD mortality, CHD and angina pectoris, TyG had a higher diagnostic efficacy. For CHF, the diagnostic efficacy of TyG-WHtR is higher. For total-CVD, TyG and TyG-WHtR had approximately equal diagnostic efficacy. RCS analysis showed that after adjusting for covariates, most of the above relationships were linearly correlated (P-overall < 0.0001, P-nonlinear > 0.05), while TyG and TyG-WHtR were non-linearly associated with all-cause mortality and CHF (P-overall < 0.0001, P-nonlinear< 0.05) in NAFLD patients.Conclusions:The predictive value of TyG or TyG-WHtR for mortality and cardiovascular risk in NAFLD patients was significant. The TyG index and TyG-WHtR might be a valid predictor of cardiovascular outcomes of patients with NAFLD.

Circulation, Volume 150, Issue Suppl_1, Page A4145632-A4145632, November 12, 2024. Background:High circulating levels of galectin-3 are associated with all-cause and cardiovascular (CV) mortality in patients with coronary artery disease (CAD). However, the impact of anemia on the prediction of galectin-3 with cause-specific mortality in patients with suspected or known CAD is unknown.Methods:Serum levels of galectin-3 were measured in 2,418 patients with suspected or known CAD undergoing elective coronary angiography. The outcomes were all-cause death, CV death, and non-CV death. Patients were divided into 2 groups according to the presence (n=882) or absence (n=1,536) of anemia, and followed up over a 6-year period.Results:During the follow-up, 329 anemic and 207 non-anemic patients died of any cause, 116 anemic and 50 non-anemic patients died of CV diseases, and 187 anemic and 139 non-anemic patients died of non-CV diseases. After adjustment for potential clinical confounders and established CV biomarkers, log-transformed (Ln-) galectin-3 levels were significantly associated with all-cause death (hazard ratio [HR] for 1-SD increase, 1.23; 95% confidence interval [CI], 1.10–1.37) and non-CV death (HR, 1.30; 95% CI, 1.13–1.50), but not with CV death (HR, 1.16; 95% CI, 0.95–1.41) in the entire cohort; significantly associated with all-cause death (HR, 1.20; 95% CI, 1.03–1.41) and non-CV death (HR, 1.49; 95% CI, 1.20–1.85), but not with CV death (HR, 0.95; 95% CI, 0.72–1.24), in anemic patients; and significantly associated with all-cause death (HR, 1.33; 95% CI, 1.13–1.57) and CV death (HR, 1.19; 95% CI, 1.00–1.42), but not with non-CV death (HR, 1.17; 95% CI, 0.95–1.43), in non-anemic patients. We also evaluated the incremental predictive performance of galectin-3 by calculating continuous net reclassification improvement, and integrated discrimination improvement metrics. The addition of Ln-galectin-3 levels to the model with potential clinical confounders and established CV biomarkers further improved the prediction of all-cause death and non-CV death, but not that of CV death, in the entire cohort and in anemic patients, and the prediction of all-cause death and CV death, but not that of non-CV death, in non-anemic patients.Conclusions:In patients with suspected or known CAD, distinct differences were observed between anemic and non-anemic patients, in the prediction for cause-specific mortality by galectin-3 levels, which independently predicted non-CV mortality in anemic patients and CV mortality in non-anemic patients.

Circulation, Volume 150, Issue Suppl_1, Page A4145353-A4145353, November 12, 2024. Background:Myocardial injury complicating percutaneous coronary intervention (PCI) is associated with mortality, but sex differences in outcomes are uncertain. We explored sex differences in the incidence and long-term outcomes of post-PCI myocardial injury (PPMI).Methods:Adults who underwent PCI at NYU between 2011-2020 were included in this retrospective analysis. Patients with ACS as the indication for PCI were excluded. PPMI was defined as a peak CKMB concentration >99% of the upper reference limit. The incidence of PPMI by sex was compared by Chi-square tests. Independent predictors of elevated CKMB post-PCI were evaluated with linear regression models in subgroups by sex. Cox proportional hazard models were generated to evaluate relationships between PPMI and all-cause mortality by sex.Results:Of 10,807 adults undergoing PCI, 24.9% (2,694) were female. Females were older than males at the time of PCI (68.9 vs. 65.8, p

Circulation, Volume 150, Issue Suppl_1, Page A4126304-A4126304, November 12, 2024. Background:About one in five adults at age 40 will develop heart failure (HF) during their lifetime. Risk factors for HF (e.g., hypertension, etc.) alter cardiomyocytes structure and function resulting in HF. At the cellular level, these changes consist of mis/over-expression of genes that regulate cardiac identity (e.g., CamK2d, PKC, etc). The current paradigm for treating HF is pharmacological intervention or surgery; however, with few exceptions, the condition worsens with time. We are proposing a paradigm-shift for treating HF from a drug-centric system to a molecular approach that would reverse hypertrophy and adverse remodeling.Methods:A cardiac targeting peptide (CTP) was generated and linked by disulfide bond to miRNA106a, which was then introduced into a HF mouse model to measure its ability to reverse multiple heart failure parameters. CTP-miRNA106a was also introduced into a human cardiac cell line, followed by multiple analyses including Western Blot, qPCR, FACS, immunofluorescence all used to identify mechanism(s) utilized by CTP-miRNA106a to reverse HF characteristics.Results:Bio-distribution studies showed CTP delivered its miRNA106a cargo specifically to the heart within 30 mins, followed by clearance of CTP from the heart to the kidneys and liver by 3-5hrs post systemic drug injection. MiRNA106a persisted in cardiomyocytes until day 7 (latest tested time-point). CTP-miRNA106a reversed Ang2/Iso induced hypertrophy in 90% of the experimental mice (Fig1). We also identified two potential HF intracellular signaling mechanisms (PLCb1/PKC/IP3 and NfkB) targeted by CTP-miRNA106a that could benefit both types of HF, HFrEF and HFpEF. PLCβ1 is a direct target for miRNA106a while the Nfkb pathway is indirectly targeted by decreased Camk2d (an miRNA106a target) signaling to IκBα. NfkB activity is quelled by miRNA106a.Conclusions:Our approach utilizes the function of miRNA106a to downregulate genes involved in cardiac hypertrophy and inflammation through the PLCb1 and CamKIId/Nfkb pathways. Most importantly, using a CTP-miRNA106a, we show delivery of miRNA106a cargo is specific to cardiomyocytes bothin vitroandin vivoand that once delivered, many HF parameters including hypertrophy are reversed.

Circulation, Volume 150, Issue Suppl_1, Page A4138303-A4138303, November 12, 2024. Background:A higher stress hyperglycemic ratio (SHR) has been reported to be associated with adverse cardiac outcomes. However, the role of SHR in predicting clinical outcomes by comparing patients with and without diabetes mellitus is yet to be explored.Objective:To evaluate the prognostic value of the SHR for predicting major adverse cardiovascular (MACE) and all-cause mortality in ACS patients with and without diabetes mellitus.Methods:Per PRISMA guidelines, we comprehensively reviewed PubMed, Google Scholar, and SCOPUS for eligible studies reporting on SHR and its association with MACE (8 studies) and all-cause mortality (7 studies) in ACS patients. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using a binary random-effects model, with results displayed as forest plots. Heterogeneity was assessed using I2 statistics, and a leave-one-out sensitivity analysis was performed. P