Risultati per: Incontinenza urinaria da stress o mista

Circulation, Volume 146, Issue Suppl_1, Page A14807-A14807, November 8, 2022. Introduction:Stress-induced cardiomyopathy (SIC) is a form of transient non-ischemic cardiomyopathy that is precipitated in the setting of acute emotional or physical stress. Postulated hypothesis implicated catecholaminergic excess and a role of the brain-heart axis behind its pathogenesis. The impact of different psychiatric illnesses on the outcomes of SIC is not clear.Method:We conducted a retrospective study using National Readmission Database (NRD) from 2011 to 2019 using ICD-10-CM (International Classification of Diseases, 10th Edition, Clinical Modification) and ICD-9-CM codes to identify the admissions with the discharge diagnosis of SIC and stratified them based on the presence of psychiatric illnesses. The primary outcome was six-month readmission and predictors of readmission.Result:We included a total of 98,721 admissions with a diagnosis of SIC. Among them, 12.9% had major depression, 1.8% had bipolar disorder, 17.6% had an anxiety disorder, and 0.6% had schizophrenia. Overall, patients with psychiatric illnesses were younger. Patients with psychiatric illnesses had a higher burden of comorbidities. Patients with schizophrenia had higher in-hospital mortality. Patients with psychiatric illnesses had a higher likelihood of getting readmitted within six months (p

Circulation, Volume 146, Issue Suppl_1, Page A13156-A13156, November 8, 2022. Introduction:The presence of multiple high-risk prognostic features enhances risk-stratification of plaques prone to destabilization and major adverse cardiac events (MACE). Spatial superimposition of high-risk features (concordance) likely amplifies local risk. Local endothelial shear stress (ESS) and plaque structural stress (PSS) metrics predict MACE, but their spatial concordance and their location relative to the minimal lumen area (MLA) is unknown. If the highest-risk plaque area is distant from the MLA, then PCI of the MLA alone will leave high-risk plaque areas untreated.Purpose:To identify the site of high-risk features of low ESS and high PSS heterogeneity (HI) along the course of a plaque in patients who develop MACE, and the site of their spatial concordance relative to the MLA.Methods:We examined ESS, PSS, and PSS HI in 22 non-culprit lesions (NCL) leading to MACE, and 64 randomly selected control NCLs without MACE from the PROSPECT study. ESS was calculated by computational fluid dynamics and PSS by finite element analysis on co-registered lesions. We examined high-risk plaques with empirically-derived (ROC curve) ESS < 1.3 Pa and PSS HI > 0.29 in 16 lesions leading to future MACE, and 11 control lesions without MACE.Results:MACE outcomes were significantly more frequent in plaques with combined low ESS+high PSS HI vs plaques with low ESS alone (72.7% vs 27.3%, p

Circulation, Volume 146, Issue Suppl_1, Page A13208-A13208, November 8, 2022. Introduction:Posttraumatic stress disorder (PTSD) is associated with increased risk of ischemic heart disease (IHD). It is unclear if this excess risk is entirely mediated through traditional IHD risk factors (hyperlipidemia, hypertension, diabetes, and smoking). We examined 13 potential mediators of the PTSD-IHD association in a large cohort of women veterans: traditional risk factors, other conditions (obesity, chronic kidney disease, neuroendocrine disorders), women-specific risk factors (e.g., gestational diabetes and hypertension, pre-eclampsia), and psychiatric disorders (depression, anxiety, psychotic disorders, alcohol dependence, and drug dependence).Methods:The study cohort included women veterans ≥18 years of age who were enrolled in Veterans Health Administration care between 1/1/2000 to12/31/2017. Diagnosis of each risk factor and disorder was based on administrative billing codes (International Classification of Disease versions 9 and 10). The final study cohorts included 1:2 propensity-score matched group of patients with and without PTSD respectively. The cohorts were matched for age, number of prior visits, and presence of the above risk factors. Cox regression examined associations of PTSD with time to development of the above 13 risk factors. Cox regression with time-varying covariates was used to model time to development of IHD as a function of PTSD and each of above 13 risk factors as time-varying predictors in separate models.Results:The cohorts included 132,293 patients with, and 265,846 patients without PTSD. PTSD was positively associated with each of the 13 risk factors. Results are tabulated in the table below.Conclusion: Traditional risk factors cumulatively accounted for just one third of the risk of IHD posed by PTSD, and all examined risk factors accounted for less than half of the increased risk associated with PTSD. More research is needed to identify pathways by which PTSD accelerates cardiovascular risk.

Circulation, Volume 146, Issue Suppl_1, Page A10351-A10351, November 8, 2022. Introduction:The cumulative burden of chronic stress and life events can be measured by Allostatic load (AL), whose high values are related to poorer health outcomes and increased risk of cardiovascular disease (CVD). The primary objective of this study is to analyze the impact of androgen deprivation therapy (ADT) on AL variation in patients upon diagnosis of prostate cancer (PC).Hypothesis:ADT may increase AL variation in prostate cancer patients.Methods:Data were obtained from a Cleveland area integrated health care systems informatics platform. The initial cohort included males ≥18 years diagnosed with PC between 2005 and 2022. AL was calculated using multiple markers representing the cardiovascular, metabolic, and immune systems (Table 1) before diagnosis and monthly during the first year. ADT use was captured based on prescribed medications. A linear-mixed-effects model, adjusted for patient demographics, CVD risk factors, and cancer characteristics, and treatment, was used to study AL monthly variation. The analysis was stratified by Non-Hispanic White (NHW) and Non-Hispanic Black (NHB) race.Results:We analyzed a total of 7,168 PC adenocarcinoma patients (31.7% NHB vs 68.3% NHW), of which 20.9% received ADT. NHBs had higher AL pre-PC diagnosis than NHWs (p=0.001). AL monthly variation was 0.15 (±0.02) higher in all PC patients on ADT (p

Circulation, Volume 146, Issue Suppl_1, Page A9608-A9608, November 8, 2022. Background:Recent evidence highlights oxidative stress as an important mechanism to cardiac dysfunction in type 2 diabetes (T2D) and altered β3-adrenergic receptor (AR)-activated nitric oxide synthase (NOS) pathway contributing to this process. However, the NOS isoforms involved are controversial. The mechanism of how β3-AR stimulation impacts ROS, SERCA2a, and cardiac function in T2D is unclear. We tested the hypothesis that oxidant stress from upregulation of LV β3-AR-activated iNOS uncoupling promotes T2D cardiomyopathy.Methods:We compared myocyte β1- and β3-AR, NOS, peroxynitrite (NT), NADPH and SERCA2a expressions and myocyte functional responses to β- and β3-AR stimulation with isoproterenol (ISO,10-8M) and BRL-37344 (BRL,10-8M), respectively, in the absence and presence of iNOS inhibitor, 1400W (10-5M) of female mice over 14 weeks (W): 7 normal and 7 with T2D induced by 14 W high-fat diet (HFD) intake, but after HFD for 4 W receiving streptozotocin (STZ, 40 mg/kg/day, i.p. 5 days).Results:Versus normal myocytes, T2D myocytes had significantly increased protein levels of β3-AR (0.25 vs 0.14) and iNOS (0.25 vs 0.15) accompanied with increased oxidative stress indicated by significantly-elevated NT formation, NADPH (P67-phox, 33% and p22-phox, 29%) and decreased GTPCH expression (0.43 vs 0.85) and activity. T2D myocytes had significantly decreased β1-AR (0.35 vs 0.49) and SERCA2a (0.19 vs 0.29). These changes were associated with reduced cell contraction (dL/dtmax, 75.4 vs 133.7 μm/s), relaxation (dR/dtmax, 59.6 vs 113.8 μ m/s), and [Ca2+]iT(0.16 vs 0.21) accompanied by diminished β-AR-stimulated positive inotropic response, but enhanced β3-AR-induced negative inotropic response. Only in T2D myocytes, pretreatment with 1400W improved basal cell function and augmented ISO-increased dL/dtmax(64.5%) and [Ca2+]iT(29.2%), but significantly limited BRL-induced decrease in dL/dtmax(12.7%) and [Ca2+]iT(9.8%).Conclusions:T2D is associated with contrasting changes on myocyte β1- and β3-AR expression with decreased SERCA2a and increased iNOS. Upregulation of β3-AR triggers iNOS uncoupling, leading to oxidative stress, thus promoting intrinsic myocyte dysfunction with impaired [Ca2+]iregulation and reduced β-AR reserve.

Circulation, Volume 146, Issue Suppl_1, Page A14497-A14497, November 8, 2022. Introduction:Hypertensive response during stress echocardiography has been predominately studied in a healthy population without many comorbidities, unlike the patients for which these tests are indicated. We performed a retrospective study identifying clinical predictors of hypertensive response to both exercise (EXE) and dobutamine (DSE) stress echo.Methods:Retrospective analysis was performed on all patients who underwent stress echo from January 1, 2015 to February 28, 2017 in a tertiary care academic center. Patient demographics, comorbidities, medications and stress echo parameters were evaluated. Patients were characterized based on stress echo completed as EXE or DSE. The primary outcome was hypertensive response.Results:4670 patients were enrolled: 1238 in the DSE group and 3432 in the EXE group. On multivariable analysis, only resting SBP remained a significant predictor of hypertensive response during DSE (odds ratio (OR) per 20mmHg 3.21, CI 1.57-6.59,p=.001) with an AUC of 0.76. On multivariable analysis, obesity (OR 2.27, CI 1.08-4.8,p=.03), diabetes (OR 3.24, CI 1.22-8.6,p=.02), resting SBP (OR 4.44, CI 2.35-8.38,p

Circulation, Volume 146, Issue Suppl_1, Page A15056-A15056, November 8, 2022. Ischemic heart disease (IHD), a major cause of heart failure, is characterized by metabolic dysfunction and myocardial cell death. Cellular hypoxia activates hypoxia inducible factor 1α (HIF1α) to initiate metabolic, angiogenic, and growth-factor related responses. Under normoxia, HIF1α is degraded by prolyl hydroxylase (PHD) domain-containing proteins via the proteasome. Due to the short half-life of HIF1α (

Circulation, Volume 146, Issue Suppl_1, Page A9376-A9376, November 8, 2022. Introduction:Our previous study has shown that 6-week low-Mg diet-induced hypomagnesemia results in mitochondrial dysfunction, cardiac diastolic dysfunction, and seizure-related death. Transient receptor potential cation channel subfamily M 7 (TRPM7) is a Mg transporter with both channel and kinase function located in the plasma membrane. We investigated the role of TRPM7 in hypomagnesemia-associated changes.Methods:For cardiac-specific knockdown of TRPM7, pAAV[miR30]-cTnT >EGFP:Scramble-shRNA as control (Con) and pAAV[miR30]-cTnT >EGFP:TRPM7 shRNA as TRPM7 knockdown (T7KD) were injected into mice through the jugular vein at 10 weeks old. One week later, mice were fed with a normal diet (nlMg, 2000 mg/kg Mg) or a low-Mg diet (HypoMg, 15-30 mg/kg Mg) for 4 weeks.Results:TRPM7 was increased significantly in wild type mouse hearts under the low-Mg diet (1.45±0.18-fold of mice with normal diet, P

Circulation, Volume 146, Issue Suppl_1, Page A13332-A13332, November 8, 2022. Introduction:Stress Cardiomyopathy (SCM), is an acute reversible myocardial injury associated with transient left ventricular dysfunction. Risk factors include female sex, post-menopause, anxiety, depression, schizophrenia, asthma and chronic obstructive pulmonary disease, diabetes, and substance use. Obesity has an increased sympathetic tone and state of chronic metabolic stress, both of which are similar in etiology to SCM. We postulate that obesity may have high prevalence in patients with SCM.Methods:We queried the Nationwide Inpatient Sample database (2016-2019) to identify adult patients with SCM with and without obesity, along with other common co-morbidities using ICD-10 codes. We compared the categorical and continuous variables by Pearson χ2 and Student t test.Results:There were 31,725 patients with SCM. The mean age was 67.15+14 years and the population was predominately female, n=26409 (83.2%). Racial distribution consisted of White (n=24713 77.9%), Black (n=24713, 8%), and Hispanic (n=1918, 6%). There were 3816 (12%) who were diagnosed with obesity. When comparing both groups, obese patients were found to be younger than non-obese, 63.3+14 years vs. 67.68+13 years, p

Circulation, Volume 146, Issue Suppl_1, Page A11394-A11394, November 8, 2022. Introduction:Chest pain is a common presentation in the emergency department and physician office visits. Identifying coronary artery disease (CAD) as the cause of chest pain is essential for improving prognosis. The 2021 AHA/ACC guidelines do not advocate for testing in patients with low pretest probability (PTP

Circulation, Volume 146, Issue Suppl_1, Page A10038-A10038, November 8, 2022. Introduction:Low endothelial shear stress (ESS) is a pro-atherogenic stimulus associated with coronary plaque development, while high plaque structural stress (PSS) and its heterogeneity is associated with plaque destabilization. Previous studies showed that combining ESS and PSS additively predicts plaque progression, but no studies have determined their ability to predict major adverse cardiovascular events (MACE). We examined whether combining ESS and PSS improves MACE prediction in patients with acute coronary syndrome.Methods:We examined baseline ESS, ESS gradient, PSS, and PSS heterogeneity index (HI) in 22 non-culprit lesions (NCL) leading to future MACE, and 64 randomly selected control NCLs without MACE from the PROSPECT (Providing Regional Observations to Study Predictors of Events in the Coronary Tree) study. ESS was calculated by computational fluid dynamics and PSS by finite element analysis on co-registered lesions.Results:86 lesions (55 thin-cap and 31 thick-cap fibroatheromas) were analyzed from 67 patients. Lesions that caused future MACE showed baseline higher PSS HI (0.32 vs. 0.24, p

Circulation, Volume 146, Issue Suppl_1, Page A11502-A11502, November 8, 2022. Background -Mitral valve prolapse (MVP) is a common valvular abnormality found in approximately 2.4% of the population. Whereas the majority of cases are benign, an increasingly recognized sequela of MVP is sudden cardiac death (SCD), but triggers and risk factors for SCD are not well-defined. It is theorized that increased stretch on the papillary muscles due to MVP leads to papillary muscle fibrosis and cellular changes of local conduction properties, increasing the risk of ventricular arrhythmias and SCD.Hypothesis- We hypothesized that patients with MVP and SCD would have increased ventricular arrhythmias and ECG changes compared to MVP controls during exercise stress testing.Methods -The study population was generated from the Duke Epic. Patients were included if they had guideline-based diagnosis of MVP on echocardiogram or cardiac magnetic resonance imaging. Increase in ventricular arrhythmias during exercise was defined as >/= 10 PVCs per minute, multifocal PVCs, or >/= 2 PVCs in a row.Results-A total 2,513 patients with MVP were screened. 18 patients with SCD. Patients with SCD were younger [(47.22 +/- 12.2 ) vs. (58.0 +/- 18.7), p=0.02], more likely to be female (89.9% vs 64%, p=0.04) and had increased rate of bileaflet prolapse (72% vs. 40%, p=0.01) compared to controls. Patients with sudden cardiac death had either dynamic T wave changes or increased ventricular arrhythmias with stress testing versus controls [12/18 (66.7%) vs 17/75 (22.6%), p

Circulation, Volume 146, Issue Suppl_1, Page A12919-A12919, November 8, 2022. Introduction:The SARS-CoV-2 virus has potential to cause acute and long-term cardiac effects. The vaccines were developed to prevent severe illness, but there are concerns about vaccine related side effects. Specific to the heart there have been case reports of mRNA vaccine related cardiomyopathies, particularly myocarditis. We present a case of a patient with presumptive stress induced cardiomyopathy in the setting of recent Covid-19 mRNA vaccination.Case Presentation:A 93-year-old female with a past medical history of hypertension presented with worsening shortness of breath and bilateral lower extremity edema. She received her second dose of the Covid-19 mRNA vaccine five days prior to presentation. She had no history of heart disease, was a nonsmoker, and denied alcohol or drug use. In the ED she was noted to be fluid-overloaded, and her CT chest showed minimal coronary calcification and bilateral pleural effusions. She was admitted for heart failure exacerbation and started on IV furosemide. Her transthoracic echocardiogram showed an ejection fraction of 40-45%. The pattern of left ventricular dysfunction was consistent with stress induced cardiomyopathy with apical akinesis and basal sparing of the left ventricular wall segments. Cardiology was consulted and recommended management with diuretics and beta blocker. She had a diuresis of 5 liters during her hospitalization. At clinic follow-up, dyspnea had improved, and her peripheral edema had resolved. Repeat echocardiogram showed recovery of left ventricular ejection fraction to 61% by Simpsons biplane technique with no regional wall motion abnormalities. Further cardiac assessment to evaluate for obstructive coronary artery disease and myocarditis was discussed and offered to the patient but was declined due to her positive response to conservative management.Discussion:The precise etiology of stress induced cardiomyopathy is unknown, but it is thought to be secondary to the sudden release of stress hormones. There are isolated reports of stress induced cardiomyopathy associated with Covid-19 vaccination, but the potential mechanism is unclear. An improved understanding of the potential effects of mRNA vaccines may help guide decisions regarding future booster vaccinations.

Circulation, Volume 146, Issue Suppl_1, Page A15165-A15165, November 8, 2022. Introduction:Guidelines recommend the use of Dobutamine stress echocardiography (DSE) in case of low flow low gradient aortic stenosis (LFLG AS) when left ventricular ejection fraction (LVEF)

Circulation, Volume 146, Issue Suppl_1, Page A12676-A12676, November 8, 2022. Backgrounds:Psychological stress increases leukocyte accumulation within atherosclerotic lesions and exacerbates plaque vulnerability. However, the stress-induced real-time behavior of immune cells in the atheroma has been poorly definedin vivo. Here, we aim to investigate whether stress stimulates the inflammatory leukocyte dynamics in the atherosclerotic plaques and destabilizes the lesions using customizedin vivocell tracking strategies.Methods and Results:We developed a system and motion reconstruction algorithm that can probe and compensate for respiratory and pulsatile movements. Individual leukocytes near the atherosclerotic plaques were imaged in real-time by adapting a custom-built high-speed intravital microscopy system with multiple fluorescence channels. Stress was achieved by immobilization procedures and/or stereotaxic application of stress stimulus onto the brain amygdala. The high spatial and temporal resolution of our real-time cell tracking system allowed clear identification of rhodamine 6G-positive leukocytesin vivo. In the common femoral artery bifurcation of apolipoprotein E knockout mice, white blood cells firmly adhered to the inner layer of the vessel walls while some slowly flowed along the endothelium (Figure). We further demonstrate that the stress increased the rolling and adhesion of inflammatory leukocyte subsets near the atherosclerotic lesions, and enhanced the plaque macrophage activity as assessed byin vivoimaging. Confocal laser scanning microscopy and immunostaining analyses corroborated thein vivofindings that the stress induced the destabilization of the atherosclerotic plaques.Conclusion:Our data show that stress stimulated the dynamics of inflammatory leukocyte subsets in atherosclerotic environments and increased the plaque vulnerability as assessed by the customized high-resolution motion-compensatedin vivoimaging strategy.

Circulation, Volume 146, Issue Suppl_1, Page A14532-A14532, November 8, 2022. Introduction:Severe COVID-19 infection is known to alter myocardial perfusion through its effects on the endothelium and microvasculature. However, a significant proportion of the world population suffered from only mild COVID-19 symptoms, and it is unknown if their myocardial perfusion is altered following their recovery.Hypothesis:In this study, we aimed to determine if there are detectable abnormalities to myocardial perfusion using cardiac magnetic resonance (CMR) in individuals who have recovered from mild COVID-19 infection.Methods:We conducted a prospective, comparative study of individuals who have recovered from COVID-19 infection (n=33) and risk-factor matched controls (n=27) using regadenoson stress CMR by a 1.5T MR scanner (GE Signa Artist) (figure). Quantitative stress perfusion images were acquired using the dual sequence technique. MBF was measured during rest (rMBF) and stress (sMBF) using Cvi42 software(figure). Myocardial perfusion reserve (MPR) was calculated as sMBF/rMBF. Unpairedttest or the Mann-Whitney U test was used to test differences between the two groups.Results:The median time interval between COVID-19 infection and CMR was 6 (4, 9) months. 31/33 (94%) patients in COVID-19 infection were not hospitalized. Symptoms including chest pain, shortness of breath, syncope, and palpitations were greater in COVID-19 group than in the matched controls (19/33 (58%) vs 2/27 (7%), p