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IMPORTANCE In a randomized clinical trial, heart failure (HF) hospitalizations were lower in patients managed with guidance from an implantable pulmonary artery pressure sensor compared with usual care. It remains unclear if ambulatory monitoring could also improve long-term clinical outcomes in real-world practice. OBJECTIVE To determine the association between ambulatory hemodynamic monitoring and rates of HF hospitalization at 12 months in clinical practice. DESIGN, SETTING, AND PARTICIPANTS This matched cohort study of Medicare beneficiaries used claims data collected between June 1, 2014, and March 31, 2016. Medicare patients who received implants of a pulmonary artery pressure sensor were identified from the 100% Medicare claims database. Each patient who received an implant was matched to a control patient by demographic features, history of HF hospitalization, and number of all-cause hospitalizations. Propensity scoring based on comorbidities (arrhythmia, hypertension, diabetes, pulmonary disease, and renal disease) was used for additional matching. Data analysis was completed from July 2017 through January 2019. EXPOSURES Implantable pulmonary artery pressure monitoring system. MAIN OUTCOMES AND MEASURES The rates of HF hospitalization were compared using the Andersen-Gill method. Days lost owing to events were compared using a nonparametric bootstrap method. RESULTS The study cohort consisted of 1087 patients who received an implantable pulmonary artery pressure sensors and 1087 matched control patients. The treatment and control cohorts were well matched by age (mean [SD], 72.7 [10.2] years vs 72.9 [10.1] years) and sex (381 of 1087 female patients [35.1%] in each group), medical history, comorbidities, and timing of preimplant HF hospitalization. At 12 months postimplant, 616 HF hospitalizations occurred in the treatment cohort compared with 784 HF hospitalizations in the control cohort. The rate of HF hospitalization was lower in the treatment cohort at 12 months postimplant (hazard ratio [HR], 0.76 [95% CI, 0.65-0.89]; P < .001). The percentage of days lost to HF hospitalizations or death were lower in the treatment group (HR, 0.73 [95% CI, 0.64-0.84]; P < .001) and the percentage of days lost owing to all-cause hospitalization or death were also lower (HR, 0.77 [95% CI, 0.68-0.88]; P < .001). CONCLUSIONS AND RELEVANCE Patients with HF who were implanted with a pulmonary artery pressure sensor had lower rates of HF hospitalization than matched controls and spent more time alive out of hospital. Ambulatory hemodynamic monitoring may improve outcomes in patients with chronic HF.

Acute cardiorenal syndrome, also known as cardiorenal syndrome type 1, is defined as an abrupt worsening of cardiac function that occurs in at least 30 % of patients with acute decompensated heart failure and can lead to the development of acute kidney injury. The changes in renal function that occur in this setting have variable prognostic implications, as both poorer and better outcomes have been reported when renal function worsens during treatment of heart failure decompensation. Furthermore, it remains unclear when worsening renal function is actually a manifestation of true acute kidney injury or simply an indicator of hemoconcentration. Given these gaps in the understanding of the significance of renal function changes in the setting of decompensated heart failure, it is not surprising that studies on the effects of available therapies, including diuretics, vasoactive drugs, and mechanical fluid removal have yielded inconsistent results. The purpose of this review is to analyze critically the current knowledge on the pathophysiology, epidemiology, prognosis, and treatment of acute cardiorenal syndrome.

Heart failure syndromes are often associated with multi-organ dysfunction, and concomitant liver, renal, and neurologic involvement is very common. Neuro-hormonal antagonism plays a key role in the management of this syndrome, and angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are one of the cornerstones of therapy. Cardiorenal physiology is becoming more recognized in these patients with advanced heart failure, and the role of neuro-hormonal blockade in this setting is vaguely defined in the literature. Often, angiotensin-converting enzyme inhibitors are decreased or even withheld in these circumstances. The purpose of this article is to review the role and pathophysiology of ace inhibition and angiotensin receptor blockade in patients with acute and chronic heart failure syndromes and concomitant cardiorenal physiology.