Congestive Heart Failure and Pulmonary Edema Publications (3539)
Congestive Heart Failure and Pulmonary Edema Publications
GLOMMS-II is a large population cohort from one health authority in Scotland, combining hospital episode data and complete serial biochemistry results through data-linkage. 16453 people (2623 with AKI and 13830 without AKI) from GLOMMS-II who survived an index hospital admission in 2003 were used to identify the causes of and predict readmissions. The main outcome was "unplanned readmission or death" within 90 days of discharge. In a secondary analysis, the outcome was limited to readmissions with acute pulmonary oedema. 26 candidate predictors during the index admission included AKI (defined and staged 1-3 using an automated e-alert algorithm), prior AKI episodes, baseline kidney function, index admission circumstances and comorbidities. Prediction models were developed and assessed using multivariable logistic regression (stepwise variable selection), C statistics, bootstrap validation and decision curve analysis.
Three thousand sixty-five (18.6%) patients had the main outcome (2702 readmitted, 363 died without readmission). The outcome was strongly predicted by AKI. Multivariable odds ratios for AKI stage 3; 2 and 1 (vs no AKI) were 2.80 (2.22-3.53); 2.23 (1.85-2.68) and 1.50 (1.33-1.70). Acute pulmonary oedema was the reason for readmission in 26.6% with AKI and eGFR < 60; and 4.0% with no AKI and eGFR ≥ 60. The best stepwise model from all candidate predictors had a C statistic of 0.698 for the main outcome. In a secondary analysis, a model for readmission with acute pulmonary oedema had a C statistic of 0.853. In decision curve analysis, AKI improved clinical utility when added to any model, although the incremental benefit was small when predicting the main outcome.
AKI is a strong, consistent and independent risk factor for unplanned readmissions - particularly readmissions with acute pulmonary oedema. Pre-emptive planning at discharge should be considered to minimise avoidable readmissions in this high risk group.
3 ± 12.1 months. Univariate analysis revealed that dyspnea, pulmonary edema, and vertebral heart score were significantly associated with the survival times (P < 0.05). Additionally, age, left atrial-to-aortic root ratio, ejection fraction, and left ventricular end diastolic volume were associated with increased risk of death (P < 0.1), while body weight, body condition score, systolic blood pressure, arrhythmia, syncope, fractional shortening, and end systolic volume were not associated with the risk of death. These results suggest that, among the variables, dyspnea, pulmonary edema, and vertebral heart score could be useful prognostic factors when giving information about patients to owners.
These clinical and paraclinical aspects were: stasis hepatomegaly with hepatojugular reflux, pulmonary congestion with stasis rales, peripheral edema, transudative polyserositis - pericarditis, hydrothorax, ascites, dilatation of inferior vena cava and suprahepatic veins, decrease of arterial blood pressure, tissue and cutaneous vasoconstriction. Anatomical and clinical aspects, with major alterations (Vth degree hepatomegaly, polyserositis, peripheral edema, tachyarrhythmic heart contractions, hypotension, pallor accentuated by vasoconstriction) acutely installed in a previously healthy young person, require a rapid lesions diagnosis and emergency treatment due to vital risk, control of acute heart failure manifestations remission and proper monitoring. Differential diagnosis was focused on determining possible aspects like: acute heart failure (of various etiology), internal post-traumatic lesions or hemorrhages, tuberculosis polyserositis, collagenosis, nephrotic syndrome, protein deficiencies, neoplasia with hepatic determinations, hematological diseases (lymphomas, leukemias), considered in young patients. Severe visceral, vascular and tissular pathological alterations were reactively induced in a young person, by stasis and hypoperfusion due to hypodiastolic heart failure caused by persistent supraventricular tachyarrhythmia triggered post-traumatic, on a proarrhythmic structural heart.
Moreover, the surgical site is one of the most important risk factors associated with PPC, and aortic surgery carries the highest risk. The aim of this systematic review was to obtain an additional understanding of the real incidence of PPC after open abdominal aortic surgery and the impact of PPC on survival.
Systematic review and meta-analysis.
Hospitals PARTICIPANTS: Patients who underwent open abdominal aortic surgery.
A literature search was performed on BioMedCentral, PubMed, Embase, and the Cochrane Register of clinical trials. All prospective or retrospective studies reporting data on PPC after open abdominal aortic surgery were included. Co-primary endpoints were the PPC rate and the correlation between PPC and perioperative mortality. The secondary endpoint was the difference in the PPC rate and mortality between elective and urgent surgery. Data on 269,637 patients from 213 studies were analyzed. The overall median incidence of PPC was 10.3% (interquartile range 5.55%-19.1%). Pneumonia, respiratory insufficiency, prolonged mechanical ventilation, need for unplanned mechanical ventilation, atelectasis, acute respiratory distress syndrome, pulmonary edema, and pleural effusions were the most common PPC reported in the literature. Occurrence of PPC was associated with postoperative mortality (r = 0.65, p<0.01) and was significantly higher in urgent procedures (p<0.001).
Incidence of PPC after open abdominal aortic surgery is high and is associated with increased postoperative morbidity and mortality.
Early complications after the procedures were defined as newly respiratory failure, arrhythmia requiring treatment, severe hemoptysis, pneumothorax, pneumomediastinum, pulmonary edema, tracheoesophageal fistulae, bronchopleural fistulae, acute coronary syndrome, acute cerebrovascular accident, and death. Patient-related clinical risk factors were defined as coronary atherosclerotic heart disease, cerebral infarction, diabetes mellitus, cirrhosis, chronic kidney disease, arrhythmia, asthma, chronic obstructive pulmonary disease, hypertension, and previous interventional pulmonology treatment. The patient-related independent clinical risk factors which had close relations to the occurrence of early complications were analyzed by multivariate statistical analysis with Logistic regression.
There were 56.4% male and 43.6% female subjects in this study. There were 10.6% current smokers, 26.6% former smokers, and 62.8% non-smokers. The overall early complication rate was 8.3%. In all the subjects groups, the patient-related independent clinical risk factors for the early complication rate were coronary atherosclerotic heart disease (B=1.545, P=0.006, OR=4.686, 95% CI 1.568-14.006), chronic obstructive pulmonary disease (B=1.037, P=0.049, OR=2.820, 95% CI 1.675-11.790), and current smoking status (B=1.412, P=0.032, OR=4.139, 95% CI 1.134-15.109); for the newly respiratory failure rates were coronary atherosclerotic heart disease (B=2.207, P=0.004, OR=9.087, 95% CI 2.028-40.714), chronic obstructive pulmonary disease (B=1.646, P=0.048, OR=5.188, 95% CI 1.783-34.375), and lesions involving three central airways (B=1.899, P=0.032, OR=6.680, 95% CI 1.182-37.740). In the malignant group, the patient-related independent clinical risk factor for the early complication rate was current smoking status (B=2.953, P=0.006, OR=19.161, 95% CI 2.360-155.572). In the benign group, the patient-related independent clinical risk factor for the early complication rate was only coronary atherosclerotic heart disease (B=1.976, P=0.022, OR=7.214, 95% CI 1.324-39.298).
Closer monitoring of patients with identified clinical risk factors is advisable prior and immediately after interventional pulmonology procedures. In order to avoid or minimize early complications, special attention should be directed toward patients who are current smokers, or patients with lesions involving three central airways, or with coronary atherosclerotic heart disease or chronic obstructive pulmonary disease.
However, acute increases in left atrial volume index, pulmonary artery systolic pressure, and hyperdynamic left ventricular function (as evidenced by increased left ventricular ejection fraction to 74% with cardiac index of 5.1 L/min/m(2) ) occurred preceding fetal death at GW 21(+4) in the presence of increased inferior vena cava diameter (23 mm) and relatively low systemic vascular resistance of 752 dyn·s/cm(5) . These findings suggested life-threatening heart failure and required cesarean delivery at GW 21(+5) resulting in complete recovery. The placenta suggested cytomegalovirus infection.
Data collected included baseline co-morbid conditions, annualized prescribed medications and laboratory data (serum creatinine [υmol/L], proteinuria [g/24 h]). Multivariable Cox regression analysis was used to explore association with these end-points: death, end-stage kidney disease (ESKD), cardiovascular event (CVE) and the first of any of these events.
A total of 872 patients were recruited into this study. However, 42 patients were excluded due to missing baseline data and hence case records for 830 patients were reviewed. Over median follow-up of 57.1 months (interquartile range: 21.7-96.9), incidence per 100 patient years of death, ESKD, CVE and any event was 13.5, 4.2, 8.9 and 21.0 respectively. Macrovascular disease (MVD), congestive heart failure (CHF), flash pulmonary oedema (FPE) and greater proteinuria at baseline were individually associated with increased risk for all end-points in multivariable analysis (Death: MVD -HR 1.24 [95% CI 1.02-1.50]; CHF -HR 1.33 [95% CI 1.08-1.64]; FPE - HR 2.10 [95% CI 1.50-2.92]; proteinuria - HR 1.14 [95% CI 1.08-1.20]). Higher estimated glomerular filtration rate at time of diagnosis was significantly associated with reduced risk of all end-points (Death: HR 0.92 [95% CI 0.89-0.94])., Administration of statins and renin angiotensin blockade (RAB) at baseline were also associated with reduced adverse events, especially death (RAB: HR 0.83 [95% CI 0.70-0.98]; statins: HR 0.79 [95% CI 0.66-.94]) and ESKD (RAB: HR 0.84 [95% CI 0.71-1.00]; statins: HR 0.79 [95% CI 0.66-0.93]). Revascularization was associated with reduced risk of death (HR 0.65 [95% CI 0.51-0.83]) and ESKD (HR 0.59 [95% CI 0.46-0.76]).
All patients with ARVD require intensive vascular protection therapy to help mitigate systemic atherosclerosis, optimize cardiovascular risk and improve clinical outcomes. More effort is required to identify the minority of patients who may benefit from revascularization.
Blood samples for PSA, NT-proBNP, and TnT were obtained at baseline and after 1, 3, and 6 months.
Five patients (29.4%) experienced G3 to 4 cardiac SAEs after a median of 13 weeks (range, 9-32), including pulmonary edema, heart failure, acute coronary syndrome, sinus bradycardia with syncope, and pulmonary edema. At baseline, 4 weeks, and 3 months, median NT-proBNP and TnT levels were higher in patients with subsequent cardiac SAEs (P= .03 and P= .04 for NT-proBNP and TnT at 3 months, respectively). After switching to dexametasone and introducing canrenone, no additional cardiac SAEs were noted. Overall response rate was 67%.
Our study suggests a higher than expected risk of cardiac SAEs during abiraterone treatment which may well be due to the small sample size and the unrestricted entry criteria. However, baseline and frequent NT-proBNP and TnT monitoring predicted a higher risk for cardiac SAE. Larger studies should confirm our findings.
The in vivo performance of optimum formulation was assessed by pharmacokinetic evaluation of drug after orally administration of free and loaded in microspheres to rats (4 mg/Kg). For this reason, the concentration of drug in plasma was measured by a new developed and sensitive method of HPLC. Acceptable drug loading and encapsulation efficiency of microspheres were obtained to be 70.43 and 85.21 %, respectively. Microspheres provided improved pharmacokinetic parameters (Cmax = 147.94 ng/ml, Tmax = 1.92 hr) in rats as compared with pure drug (Cmax = 75.69 ng/ml, Tmax = 1.5 hr). The obtained AUC of drug in microsphere was 10 fold higher than of the free drug.
The results showed that the prepared microspheres successfully improved BA of the poorly water-soluble drug effectively.
EVLW was derived as Vtis - Vc.
Before administration of albuterol, Vtis and EVLW were higher in HFrEF vs control (998 ± 200 vs 884 ± 123 ml, p = 0.041; and 943 ± 202 vs 802 ± 133 ml, p = 0.015, respectively). Albuterol decreased Vtis and EVLW in HFrEF patients (-4.6 ± 7.8%, p = 0.010; -4.6 ± 8.8%, p = 0.018) and control subjects (-2.8 ± 4.9%, p = 0.029; -3.0 ± 5.7%, p = 0.045). There was an inverse relationship between pre-albuterol values and pre- to post-albuterol change for EVLW (r(2) = -0.264, p = 0.015) and DmCO (r(2) = -0.343, p = 0.004) in HFrEF only.
Lung fluid is elevated in stable HFrEF patients relative to healthy subjects. Stimulation of β2ARs may cause fluid removal in HFrEF, especially in patients with greater evidence of increased lung water at baseline.