Abdominal contributions to cardiorenal dysfunction in congestive heart failure.

Heart failure with preserved ejection fraction (HFpEF), which currently represents approximately 50 % of heart failure (HF) cases, is common and associated with high morbidity and mortality. Understanding the epidemiology of HFpEF has been difficult due to the challenges in HFpEF diagnosis and the heterogeneous etiologies and pathophysiologies that underlie HFpEF. Nevertheless, several high-quality epidemiology and observational registry studies of HFpEF demonstrate that an increasing prevalence of HFpEF in both the outpatient and inpatient settings, coupled with a lack of evidence-based effective treatments for HFpEF, is resulting in an emerging epidemic of HFpEF. In this review, we discuss the emerging HFpEF epidemic, focusing on: (1) reasons for the rising prevalence of HFpEF; (2) the abnormalities in cardiac structure and function that dictate the transition from risk factors to HFpEF; (3) novel HFpEF mechanisms that may underlie the increase in HFpEF prevalence; (4) prognosis of HFpEF; and (5) risk prediction in HFpEF. We conclude with 10 unanswered questions on HFpEF epidemiology that will be important areas for future investigation.

The Emerging Epidemic of Heart Failure with Preserved Ejection Fraction

Heparin has been recognized as a valuable anticoagulant and antithrombotic for several decades and is still widely used in clinical practice for a variety of indications. The anticoagulant activity of heparin is mainly attributable to the action of a specific pentasaccharide sequence that acts in concert with antithrombin, a plasma coagulation factor inhibitor. This observation has led to the development of synthetic heparin mimetics for clinical use. However, it is increasingly recognized that heparin has many other pharmacological properties, including but not limited to antiviral, anti-inflammatory, and antimetastatic actions. Many of these activities are independent of its anticoagulant activity, although the mechanisms of these other activities are currently less well defined. Nonetheless, heparin is being exploited for clinical uses beyond anticoagulation and developed for a wide range of clinical disorders. This article provides a "state of the art" review of our current understanding of the pharmacology of heparin and related drugs and an overview of the status of development of such drugs.

https://pharmrev.aspetjournals.org/content/pharmrev/68/1/76.full.pdf

Pharmacology of Heparin and Related Drugs

In this article we review recent advances made in the pathophysiology, diagnosis, and treatment of inhalation injury. Historically, the diagnosis of inhalation injury has relied on nonspecific clinical exam findings and bronchoscopic evidence. The development of a grading system and the use of modalities such as chest computed tomography may allow for a more nuanced evaluation of inhalation injury and enhanced ability to prognosticate. Supportive respiratory care remains essential in managing inhalation injury. Adjuncts still lacking definitive evidence of efficacy include bronchodilators, mucolytic agents, inhaled anticoagulants, nonconventional ventilator modes, prone positioning, and extracorporeal membrane oxygenation. Recent research focusing on molecular mechanisms involved in inhalation injury has increased the number of potential therapies.

/pdf/diagnosis-and-management-of-inhalation-injury-an-updated-50t3hvormt.pdf

Diagnosis and management of inhalation injury: an updated review

Acute respiratory distress syndrome (ARDS) is defined as a syndrome of acute onset, with bilateral opacities on chest imaging and respiratory failure not caused by cardiac failure, leading to mild, moderate, or severe oxygenation impairment. The syndrome is most commonly a manifestation of sepsis-induced organ dysfunction, characterized by disruption of endothelial barrier integrity and diffuse lung damage. Imbalance between coagulation and inflammation is a predominant characteristic of ARDS, leading to extreme inflammatory response and diffuse fibrin deposition in vascular capillary bed and alveoli. Activated platelets, neutrophils, endothelial cells, neutrophil extracellular traps, microparticles, and coagulation proteases, participate in the complex process of immunothrombosis, which is a key event in ARDS pathophysiology. The present review is focused on the elucidation of immunothrombosis in ARDS and the potential therapeutic implications.

/pdf/immunothrombosis-in-acute-respiratory-distress-syndrome-3ofvg3pld1.pdf

Immunothrombosis in Acute Respiratory Distress Syndrome: Cross Talks between Inflammation and Coagulation

Background

Renal dysfunction in heart failure is thought to be due to poor perfusion of the kidney.



Hypothesis

We tested the hypothesis that passive congestion is more important than poor perfusion.



Methods

We retrospectively studied the data on 178 patients who underwent right heart catheterization for evaluation of heart failure and had serum creatinine (Cr) measured on the same day.



Results

Serum Cr and glomerular filtration rate (GFR) correlated with central venous pressure (r = 0.22, P = 0.001 and r = −0.55, P < 0.0001, respectively) and renal perfusion pressure (r = 0.21, P = 0.001 and r = 0.27, P = 0.015, respectively). Neither correlated with cardiac index or left ventricular ejection fraction. Serum Cr was significantly higher and GFR was significantly lower in the upper tertile of central venous pressure, pulmonary capillary wedge pressure as well as in the lower tertile of renal perfusion pressure.



Conclusions

Renal dysfunction in heart failure is determined more by passive congestion than by low perfusion. Copyright © 2011 Wiley Periodicals, Inc.



The authors have no funding, financial relationships, or conflicts of interest to disclose.

/pdf/renal-dysfunction-in-heart-failure-is-due-to-congestion-but-1hmkbon28a.pdf

Renal dysfunction in heart failure is due to congestion but not low output.

High levels of B-type natriuretic peptide in cancer patients are poorly studied. Previously published data suggest that they are not related to fluid overload and are encountered mostly in solid cancers. The authors investigated the distribution of amino terminal pro-brain natriuretic peptide (NT-proBNP) between hematologic and solid organ malignancies and the relationship of NT-proBNP with volume status in oncologic patients. A total of 145 consecutive patients with at least one occurrence of NT-proBNP exceeding the upper normal range 10-fold were identified. The authors retrospectively reviewed their records including clinical, laboratory, and radiological data and echocardiograms. More than 70% of patients had hematologic malignancies. Patients with NT-proBNP >50,000 pg/mL had only hematologic malignancies, primarily multiple myeloma. There was no association between M-spike proteins and NT-proBNP. About 80% of patients had signs of fluid overload. The magnitude of NT-proBNP elevation was similar between those with and without heart failure or volume overload, as well as with solid cancers vs hematologic malignancies. Contrary to prior reports, it was found that very high NT-proBNP in cancer patients is usually encountered in the context of fluid overload and most often in hematologic malignancies.

https://www.onlinelibrary.wiley.com/doi/pdf/10.1111/chf.12018

What Is Causing Extremely Elevated Amino Terminal Brain Natriuretic Peptide in Cancer Patients

Purpose of reviewThe aim of this review is to provide a summary of the principal sex-related differences in the presentation, clinical course, and treatment of cardiac arrhythmias as well as the current understanding of the mechanisms underlying these differences.Recent findingsThe mechanisms behind

Sex differences in arrhythmias.

To determine whether the combination of aerosolized unfractionated heparin and N-acetylcystine reduces 28-days mortality and lung injury scores (LISs) in adult patients with smoke inhalation injury requiring mechanical ventilation. The study was a single-center retrospective study with historical control. The authors included 30 mechanically ventilated adult subjects who were admitted within 48 hours of their bronchoscopy confirmed smoke inhalation injury over a 5-year period. The experimental group was treated with nebulized heparin sulfate, N-acetylcystine, and albuterol sulfate. Controls received ventilation support and albuterol sulfate. The authors calculated acute physiology and chronic health evaluation (APACHE)-III scores on admission in addition to daily LIS for 7 days. The experimental group was divided into five APACHE-III subgroups and matched with inhalation lung injury patients in the historical control group. There was no significant difference in initial APACHE-III scores or LISs between groups (alpha = 0.05) upon entry to the study. The experimental group showed significant improvement in LISs, respiratory resistance and compliance measurements, and hypoxia scores as compared with controls throughout the duration of the study. There was a statistically significant survival benefit in the experimental group that was most pronounced in patients with APACHE-III scores >35. Survival for the control vs experimental group was 0.5714 +/- 0.1497 vs 0.9375 +/- 0.0605, respectively, (risk ratio -0.0055; 95% confidence interval -0.0314-0.0204; hazard ratio 1.003; number needed to treat 2.7). The use of aerosolized unfractionated heparin and N-acetylcystine attenuates lung injury and the progression of acute respiratory distress syndrome in ventilated adult patients with acute lung injury following smoke inhalation.

Influence of nebulized unfractionated heparin and N-acetylcysteine in acute lung injury after smoke inhalation injury.

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Renal dysfunction in heart failure is due to congestion but not low output.

What Is Causing Extremely Elevated Amino Terminal Brain Natriuretic Peptide in Cancer Patients

Sex differences in arrhythmias.

Influence of nebulized unfractionated heparin and N-acetylcysteine in acute lung injury after smoke inhalation injury.