Artificial Intelligence–Enabled Analysis of Thermography to Diagnose Acute Decompensated Heart Failure

Rafael Correo, de izquierdas, y Alvaro Noboa, magnate conservador, vencieron con un discurso clientelista en el pais mas inestable de America Latina.

Increased left ventricular filling pressure is a hallmark of heart failure (HF) caused by left ventricular dysfunction (LVD). Within the closed hemodynamic system, increased LV filling pressure results in elevated pressures in the left atrium and pulmonary venous vasculature. When pulmonary hypertension (PH, defined by mean pulmonary artery pressure [mPAP] >25 mm Hg) is associated with an abnormally elevated pulmonary capillary wedge pressure (PCWP >15 mm Hg) or left ventricular end-diastolic pressure (LVEDP >18 mm Hg),1 it has been variably termed World Health Organization (WHO) Group 2 PH,1 pulmonary venous hypertension,2 “postcapillary PH,”3 or “passive PH.”4 Article see p 644 Patients with LVD also have a propensity to develop a precapillary pulmonary arterial contribution to PH, reflected by an increased transpulmonary gradient (TPG, defined as mPAP-PCWP that exceeds 12 to 15 mm Hg) or an elevated pulmonary vascular resistance (PVR, defined as TPG/cardiac output that exceeds 2.5 to 3 Wood units [WU]).5,6 This type of PH, which is “out of proportion” to underlying left-sided disease in the setting of normalized volume status, has been termed “mixed PH,” given both precapillary and postcapillary contributions to elevated PAP.7 PH in HF can be simplistically organized along 2 sequential dyads: (1) the presence or absence of a significant precapillary contribution to elevated PAP (ie, mixed PH as opposed to purely passive PH) and (2) if present, the relative fixed (ie, nonreversible with lowering left-sided filling pressures) or reactive (ie, reversible with reduction of left-sided filling pressures) character of the precapillary contribution to PH (Figure). Figure. Diagnostic framework for pulmonary hypertension in heart failure (HF). mPAP indicates mean pulmonary artery pressure; PCWP, pulmonary capillary wedge pressure; PVR, pulmonary vascular resistance; and PH, pulmonary hypertension. There are no widely established cut-points to define PVR and transpulmonary …

IN THIS ISSUE OF JAMA, 2 ARTICLES REPORT FINDINGS FROM the Efficacy of Vasopressin Antagonism in Heart Failure Outcome Study With Tolvaptan (EVEREST) clinical trials program. Konstam et al report the overall longterm effects of tolvaptan in terms of safety and clinical outcomes for patients with worsening heart failure (HF) requiring hospitalization. Gheorghiade et al report shortterm effects of tolvaptan for acute symptom relief in these same patients, but presented as 2 trials that were based on study center assignment following completion of patient enrollment and randomization in the long-term trial. The aggregate findings demonstrate that tolvaptan relieves some symptoms associated with acute decompensated heart failure (ADHF) and has no demonstrable evidence of harm such as worsening of renal failure, but importantly, does not reduce mortality or HF-related morbidity at 1 year. In the context of ADHF, these are noteworthy findings. To date, no other therapeutic intervention has been demonstrated in large-scale randomized, placebo-controlled studies to positively influence symptoms in ADHF without generating a question of harm. Inotropes have been associated with increased mortality risk, and calcium sensitizers have been associated with increased cardiovascular mortality. Nesiritide was shown to relieve dyspnea and to reduce pulmonary congestion over the short term, but also was associated with increased intermediate-term mortality risks. Traditional vasodilator therapy relieves HF symptoms, but neither nitroglycerin nor nitroprusside has been subjected to prospective randomized controlled study, and effects on mortality are unknown. Even diuretics, which clearly relieve congestion, have uncertain effects on outcomes. Addressing the challenge of ADHF has been daunting. Acute decompensated HF accounts for more than 1 million acute hospitalizations per year in the United States at an annual cost of more than $30 billion and is associated with significant mortality. The risk of inpatient death is approximately 4% (but ranges from 2%-22%), and the risk of death/rehospitalization at 60 to 90 days after an episode of ADHF is 36%. At the core of this challenge, however, is the limited understanding of the pathophysiology of ADHF. While hemodynamic disturbances are clearly responsible for the observed signs and symptoms, plausible causative mechanisms that trigger acute decompensation, eg, ventricular injury and augmented neurohormonal activation, remain uncertain. Thus, therapy for ADHF is relegated to correcting perturbed hemodynamics. Comparison is made with the evolution of therapy for chronic HF—targeting hemodynamic abnormalities did not yield meaningful clinical benefits, but elucidation of relevant pathophysiological mechanisms followed by appropriately focused interventions in largescale trials resulted in salutary improvements. A similar approach is needed for ADHF. Another challenge of ADHF involves clinical trial design and construct. The studies to date have been small to moderate short-term hemodynamic or symptom-focused designs, constructed primarily to meet regulatory requirements. Important questions, including mechanistic hypotheses and the effect of interventions on rehospitalizations/mortality, have been inadequately studied. Trials in ADHF have also been confounded by considerable heterogeneity of the patient phenotype. Patients with ADHF are older, represent a mix of new-onset HF and decompensated chronic HF, have both reduced and preserved ejection fraction HF, have equal gender representation, and frequently have a number of important comorbidities, especially renal insufficiency. Moreover, “standard therapy” does not truly exist, as there are no evidence-based interventions proven to reduce morbidity and mortality associated with ADHF. Guidelines for ADHF have recently been put forward, but the treatment algorithms are sparse and focus on hemodynamic targets. The strategy is to relieve symptoms preferentially with diuretic use, including high-dose loop diuretics and continuous diuretic infusions (the safety of which is not known in HF), and to add vasodilator therapy (nitroglycerin or nitroprusside) if adjunctive approaches are needed. Inotropes are reserved for impending or frank shock but are otherwise dissuaded. Ultrafiltration represents at best an emerging technology with intriguing preliminary data but limited applications.

Introduction: There has been little focus on hospitalized acute decompensated heart failure (ADHF) that develops after admission, which may occur because of comorbid conditions, over-administration of fluid or post-surgical complications. Aims: To compare patient characteristics, case fatality, and hospital length of stay (LOS) associated with ADHF that develops after hospital admission as compared to those with ADHF at admission. Methods: Hospitalizations with possible ADHF were sampled, based on HF ICD codes, among those aged > 55 years from the four communities of the Atherosclerosis Risk in Communities Study (2005-2010). Medical records were abstracted with events classified by physician panel or computer classified. Case fatality was obtained through the National Death Index. We identified 4,503 (unweighted) events with definite/probable ADHF, after excluding those with unknown time of decompensation (n=81), hospital transfers (n=102), and race other than black or white (n=118). Demographic and clinical characteristics were compared by ADHF onset (at/after admission). Logistic regression was used to evaluate the association of ADHF onset with in-hospital mortality, and 28-days and one-year mortality, adjusted for demographics and comorbidity. Linear regression was used to evaluate the association of ADHF onset with log-transformed hospital LOS, adjusted for demographics. All analyses were weighted to account for the stratified sampling design. Results: Of 21,052 (weighted) ADHF events, 7.4% (n=1561) developed ADHF after admission. Patients with ADHF occurring after admission were older (mean: 79 vs. 75 years), and more likely white and female. Those with ADHF at admission were more likely to have a positive smoking history, COPD, and to be on dialysis. Presence of diabetes, hypertension and coronary artery disease were not significantly different between groups. In hospital mortality (16.5% vs. 6.3%; OR= 2.7, 95% CI=1.9-3.8) and 28-day mortality (23.9% vs. 10.1%; OR= 2.4, 95% CI=1.7-3.4) was higher among those who developed ADHF after admission. One-year case fatality was similar (39.4% vs. 33.6%; OR= 1.2, 95% CI=0.9-1.6). Unadjusted mean LOS was longer for those with ADHF occurring after admission (12.8 days, 95% CI=11.8-13.8) than those with ADHF at admission (7.2 days, 95% CI=6.8-7.6). The adjusted and geometric mean LOS was 1.3 days (95% CI=1.2-1.4) longer for those who developed ADHF after admission. Conclusion: Although patients with ADHF onset after admission were slightly older, differences in comorbidity do not indicate an easily identifiable subgroup for closer in-hospital monitoring. Development of ADHF after admission was associated with an alarmingly high early case fatality and longer hospital LOS compared to those with ADHF at hospital admission.

Background and Aims Impaired renal function is a common finding in patients with cardiac diseases and confers an adverse prognosis in this population. To evaluate the incidence, phenotypes and prognostic value of cardiorenal interrelations in patients with acute decompensated heart failure (ADHF) and non-ST-elevation acute coronary syndrome (NSTE-ACS). Method we examined 278 patients with ADHF (85.3% had anamnesis of symptomatic HF with frequent hospitalizations, 20.1% had ejection fraction <35%) and 288 with NSTE-ACS (64.9% developed myocardial infarction (MI)). In ADHF group in comparison with NSTE-ACS the patients were younger (69.7±10.2 vs 72±12.1 years, p<0.01), there were more males (55.4 vs 36.5%, p<0.001), smokers and alcohol abusers (47.8 and 30.6% vs 8 and 5.6%, p<0.001). The comorbidities were more typical for ADHF group: atrial fibrillation 46 vs 24% (p<0.001), obesity 55.8 vs 30.9% (p<0.001), anemia 40.6 vs 25.3% (p<0.001), diabetes mellitus 33.1 vs 23.3% (p<0.01). Chronic kidney disease (CKD) and acute kidney injury (AKI) were diagnosed according to KDIGO 2012 Guidelines. AKI phenotypes were identified depending on time of development (community- or hospital-acquired), persistency (transient or persistent), history of CKD (AKI de novo or AKI on CKD). Results Incidence of CKD in patients with ADHF and NSTE-ACS was 45 and 46.5%, CKD was first diagnosed on admission in 57.6 and 64.2% of patients respectively. In 7.6% cases of ADHF and 14.2% of NSTE-ACS groups the duration of impaired kidney function was unknown. No associations of existing CKD and in-hospital mortality were detected. Incidence of AKI in ADHF and NSTE-ACS groups was 43.5 and 37.2%. The hospital-acquired AKI, AKI on CKD and persistent AKI were found in 52.9, 47.9 and 46.3% of ADHF patients, and in 57.9, 58.9 and 50.5% in NSTE-ACS group respectively. In-hospital mortality was higher in patients with AKI in ADHF and NSTE-ACS groups (12.4 vs 5%, p<0.01 and 17.8 vs 3.3%, p<0.001). Mortality in patients with ADHF and hospital-acquired persistent AKI de novo and community-acquired persistent AKI on CKD was 41 and 29%, and in community-acquired transient AKI on CKD in the NSTE-ACS group – 29%. Conclusion Different cardiorenal interrelations were revealed in 75.2% of patients with ADHF and in 61.8% with NSTE-ACS. In patients with acute cardiac diseases high in-hospital mortality is tightly associated with phenotypes of hospital-acquired persistent AKI de novo and community-acquired persistent AKI on CKD in ADHF, and in community-acquired transient AKI on CKD in the NSTE-ACS.

Acute decompensated heart failure (ADHF) is the most common cause of hospital admission in persons aged >65 years, accounting for 1 000 000 admissions and >6 million hospital days.1 The total cost of HF care in the United States is currently estimated at $21 billion and is projected to increase to $53 billion in 2030 with the majority of costs (80%) related to ADHF hospitalizations.2 The prognosis of patients admitted with ADHF is dismal, with a 20% to 30% readmission rate and a 20% to 30% mortality rate within 6 months after admission.3 Studies have established the prognostic importance of renal function in patients with HF. Analysis from the second prospective randomized study of Ibopamine on mortality and efficacy4 was one of the first to demonstrate that estimated glomerular filtration rate (GFR) was the strongest predictor of mortality in ADHF. In the ADHF national registry (ADHERE), 63% of patients with ADHF had moderate renal dysfunction (GFR<60 mL/min m2) on admission and in-hospital mortality was strongly associated with the severity of renal dysfunction.5 A meta-analysis of 16 studies characterizing the association between renal impairment and mortality in patients with HF indicated that 1-year mortality increased incrementally across the range of renal function with a 7% increase in risk for every 10 mL/min decrease in GFR.6 As recently reviewed,7 numerous more recent studies have confirmed the association of renal dysfunction with adverse short- and long-term outcomes in ADHF, an association which seems equally robust in patients with ADHF with reduced or preserved ejection fraction. In patients hospitalized with ADHF, several studies demonstrated that acute kidney injury (AKI) during treatment of ADHF is common, with increases in creatinine ≥0.3 mg/dL occurring in 25% to 30% of patients. Regardless of baseline renal function, AKI is associated …

Improving renal function during diuresis: usefulinformation or just noise?

BackgroundLow rates of heart failure (HF) hospitalizations were observed during the 2020 peak of the COVID-19 pandemic. Additionally, posthospitalization follow-up transitioned to a predominantly telemedicine model. It is unknown whether the shift to telemedicine impacted disparities in posthospitalization follow-up or HF readmissions.ObjectiveThe aim of this paper is to determine whether the shift to telemedicine impacted racial and ethnic as well as socioeconomic disparities in acute decompensated heart failure (ADHF) follow-up and HF readmissions. We additionally sought to investigate the impact of the COVID-19 pandemic on the severity of ADHF hospitalizations.MethodsThis was a retrospective cohort study of HF admissions across 8 participating hospitals during the initial peak of the COVID-19 pandemic (March 15 to June 1, 2020), compared to the same time frame in 2019. Patients were stratified by race, ethnicity, and median neighborhood income. Hospital and intensive care unit (ICU) admission rates, inpatient mortality, 7-day follow-up, and 30-day readmissions were assessed.ResultsFrom March 15, 2019, to June 1, 2020, there were 1162 hospitalizations for ADHF included in the study. There were significantly fewer admissions for ADHF in 2020, compared with 2019 (442 vs 720; P<.001). Patients in 2020 had higher rates of ICU admission, compared with 2019 (15.8% vs 11.1%; P=.02). This trend was seen across all subgroups and was significant for patients from the highest income quartile (17.89% vs 10.99%; P=.02). While there was a trend toward higher inpatient mortality in 2020 versus 2019 (4.3% vs 2.8%; P=.17), no difference was seen among different racial and socioeconomic groups. Telemedicine comprised 81.6% of 7-day follow-up in 2020, with improvement in 7-day follow-up rates (40.5% vs 29.6%; P<.001). Inequities in 7-day follow-up for patients from non-Hispanic Black racial backgrounds compared to those from non-Hispanic White backgrounds decreased during the pandemic. Additionally, those with telemedicine follow-up were less likely to be readmitted in 30 days when compared to no follow-up (13.8% vs 22.4%; P=.03).ConclusionsThere were no major differences in HF ICU admissions or inpatient mortality for different racial and socioeconomic groups during the COVID-19 pandemic. Inequalities in 7-day follow-up were reduced with the advent of telemedicine and decreased 30-day readmission rates for those who had telemedicine follow-up.

See Article on Page 300-305 Heart failure is a systemic disease based on its chronic inflammation status and because it affects other organs, including the kidneys, lungs, and liver. Acute decompensated heart failure (ADHF) is a more severe form of heart failure that causes an acute change in hemodynamics. ADHF negatively affects renal, hepatic, and pulmonary function and causes peripheral soft tissue edema. Repeated hospital admissions for ADHF is one indicator of a poor clinical outcome in chronic heart failure patients [1,2]. The predictors of readmission and death have been investigated, and major risk factors are a low left ventricular ejection function (LVEF), low initial serum sodium level, increased serum creatinine, anemia, and low admission blood pressure [1,2]. These are markers of hemodynamic change, fluid and electrolyte imbalance, and reduced organ perfusion and function caused by depressed left and right ventricular function. The predictors that indirectly reflect low cardiac function include hepatic congestion, which can be detected with liver function tests (LFTs), including serum bilirubin, alkaline phosphatase, and aminotransferases. These have been suggested as risk factors for future death, cardiovascular events, and readmission [3-6]. Furthermore, recent publications have reported that the type of death from heart failure can be discriminated using the level: increased total was associated with death from pump failure and not with sudden death [5]. Chronic hepatic congestion due to right ventricular dysfunction might increase the possibility of liver cirrhosis, so-called cardiac cirrhosis. In a recent post hoc analysis, the prevalence of LFT abnormalities in ADHF was as much as 46% [2]. The liver and heart are connected intimately, similar to the relationship between the heart and kidney, usually called cardiorenal syndrome, in patients with chronic and acute heart failure. In this issue of Korean Journal of Internal Medicine, Chintanaboina et al. [7] reported an association between serum total and readmission due to ADHF. They demonstrated that patients with a high serum on admission had a high risk of readmission owing to decompensation, and that patients with a >1.3 mg/dL or LVEF <35% were at higher risk. This study once again confirmed the old story that hepatic congestion, which implies advanced heart failure, indicates a poor prognosis in acute and chronic heart failure patients [1-6,8]. Surprisingly, alleged poor risk predictors such as LVEF, serum creatinine, low serum sodium, and B-natriuretic peptide were not independent risk factors for readmission in a multiple regression analysis, as presented in Table 3. Nevertheless, I feel that this small retrospective study had many confounding factors that could not be controlled. Therefore, a refined statistical method should have been applied, and this process should be described in more detail in this article. Although it has substantial limitations, this study has value in that it confirms the correlation between total and hospitalization in ADHF patients, who comprise a small portion of patients compared with those with chronic heart failure in terms of bilirubin and heart failure prognosis. Serum is a potential indicator of risk stratification for rehospitalization, along with other prognostic markers such as low sodium and low initial blood pressure in ADHF. Moreover, it might help to guide the therapeutic options for ADHF. Future studies should aim at improving the prognosis of ADHF patients with the guidance of liver function.

Introduction: An essential link between the kidney and heart in heart failure (HF) has long been known as has the importance of the renin-angiotensin system (RAS). Recent studies in renal disease and in experimental animal models points to existence of renal-specific RAS that may be independent of the circulating RAS and which may be a primary mechanism for renal dysfunction in cardiorenal disease states. Angiotensinogen (AGT) is the precursor peptide which is released by the liver but recent studies have reported its renal production. Due to its large size (453 amino acids) circulating AGT cannot be filtered by the glomerulus and thus urinary AGT (uAGT) is thought to be of renal origin. Angiotensin II (ANGII) (8 amino acids), is the effector peptide and exerts most of its pathological effects through the AT1receptor. The current study was focused on patients hospitalized for acute decompensated HF (ADHF). Hypothesis: The renal RAS and not the circulating RAS is activated based upon the measurement of plasma and urinary AGT and ANGII. Methods: Normal subjects (n = 45) with no history of heart disease, kidney disease or hypertension were recruited from the Mayo Clinic Biobank. ADHF subjects (n = 58) were recruited within 1–2 days of their admission. NTproBNP and urinary creatinine were measured using standard assays. Plasma and urinary AGT were measured using Elisa (IBL, Japan). Plasma and urinary ANGII were measured using RIA (Phoenix Pharmaceuticals, USA). Urinary values were indexed to urinary creatinine values. P < .05 was considered significant Results: Urinary AGT (uAGT) and Ang II (uANGII) were significantly elevated (P < .03) in HF subjects compared to normals after adjusting for age and gender. In contrast, plasma ANGII was not increased in ADHF and plasma AGT decreased. There was little to no correlation between uAGT or uANGII with urine volume(r = 0.11 and 0.06) and GFR (r=-0.19 and -0.23) in ADHF patients. Conclusions: In the setting of ADHF, urinary AGT and ANGII are elevated compared to normal subjects. The levels of uAGT and uANGII in ADHF subjects did not correlate with urinary creatinine, GFR, urine volume, suggesting that this increase is independent of kidney function and effect of diuresis in ADHF subjects. These findings collectively point to an activated intrarenal RAS, which may have a pathophysiological role in progression of ADHF and provides a potential renal therapeutic target for the treatment of ADHF.

The time course of cardiac arrhythmia occurrences and heart failure decompensation (HFD) events has not been well understood. To determine whether high heart rate (HHR) episodes occur more frequently prior to HFD events, the temporal relationship between HHR episodes and HFD events was analyzed from the COMPASS-HF study. The COMPASS-HF study included 274 NYHA class III-IV patients with an implantable hemodynamic monitor (IHM). In addition to monitoring hemodynamic status, the IHMs were set up to detect and store HHR episodes defined as a sensed ventricular HR &gt; 150 bpm for at least 12 of 16 consecutive cardiac cycles. The number of IHM detected HHR episodes during the first 6-months of enrollment in the study was compared to HFD events by two methods: within patients, by comparing HHR episode rate before and after a HFD event in patients with a single HFD event and between patients, by comparing HHR episode rate in patients with HFD events (prior to the first HFD event) to HHR episode rate in patients without HFD events. For those patients with one HFD event (n = 53 patients), HHR episode rates (# of HHR episodes/day) were 0.36 ± 0.82 and 0.05 ± 0.11 (p &lt; 0.01) before and after the HFD event, respectively. Monitoring durations were 94 ± 4 days for before the HFD event and 91 ± 50 days for after the event. HHR episode rates were 0.30 ± 0.77 and 0.19 ± 0. 61 (p &lt; 0.01) for patients with HFD events (n = 104 patients) and without HFD events (n = 170 patients), respectively. Monitoring durations prior to the first HFD event, and in patients without HFD events were 77 ± 46 days and 178 ± 41 days. IHM detected HHR episodes occurred seven times more frequently prior to HFD events than after HFD events. While the IHM could not differentiate the types of HHR rhythms, these data demonstrate a clear association between the rate of HHR episodes and HFD events. The cause and effect relation remains to be more clearly defined.

Development of Acute Decompensated Heart Failure Among Hospital Inpatients: Incidence, Causes and Outcomes

Background: Patients with acute decompensated heart failure (ADHF) often require admission to the Cardiac Care Unit (CCU). Clinical examination alone may be inadequate for management, leading to suboptimal diuretic regimens and prolonged hospital stays. The use of Point-of-care ultrasound (POCUS) to evaluate the lungs for pulmonary edema and inferior vena cava (IVC) for size and collapsibility can enhance volume status evaluation. Aim: Reduce the average duration of IV diuresis by 20% among patients admitted to the CCU for ADHF in 1 year Methods: An algorithm for POCUS guided diuretic regimen escalation was implemented across three Plan-Do-Study-Act (PDSA) cycles. Patients who were intubated, on dialysis, or with isolated RV failure were excluded. PDSA-1 introduced the algorithm and provided training to a team of 5 residents. PDSA-2 included weekly reminders and recruitment of 14 residents to increase buy-in. PDSA-3 focused on incorporating POCUS assessments into nighttime care to facilitate early morning decision-making. Results: Process Measure: Quarterly compliance rates using the number of POCUS orders that were completed- Baseline (0%, n=23), PDSA-1 (0%, n=35), PDSA-2 (19%, n=15), PDSA-3 (31%, n=46). Outcome Measure: The average duration of IV diuresis progressively decreased through the year: Baseline (5 days), PDSA-1 (5.3 days), PDSA-2 (4.4 days), PDSA-3 (3.5 days). There was an increase of 6% in PDSA-1 compared to baseline, but PDSA-2 and 3 showed a progressive reduction of 12% and 30% respectively. Balancing Measure: The mean potassium supplementation showed variation throughout the year: Baseline (63.3 mg), PDSA-1 (141 mg), PDSA-2 (151.7 mg), PDSA-3 (75.7 mg), reflecting no significant negative impact from the intervention. Equity Lens: The duration of IV diuresis, which at baseline ranged from 3 to 8 days across different races, standardized to approximately 5 days for all races by PDSA-3. Conclusion: We progressively reduced the duration of IV diuresis using POCUS-guided lung and IVC assessments with a structured diuretic regimen. This demonstrated improved patient care from early decongestion and symptomatic relief. Additionally, we demonstrate that POCUS plays a crucial role in promoting health equity by providing an objective assessment of volume status across diverse racial groups. This integration promises optimized heart failure management and potential cost reductions from reduced length of stay, highlighting the value of POCUS in clinical practice.

The role of stress hyperglycemia in acute decompensated of heart failure

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