Pulmonary Artery Pressure-Guided Heart Failure Management Reduces Hospitalizations in Patients With Chronic Kidney Disease.

BACKGROUND: Hemodynamic-guided heart failure management is a superior strategy to prevent decompensation leading to hospitalization compared with traditional clinical methods. It remains unstudied if hemodynamic-guided care is effective across severities of comorbid renal insufficiency or if this strategy impacts renal function over time. METHODS: In the CardioMEMS US PAS (Post-Approval Study), heart failure hospitalizations were compared from 1 year before and after pulmonary artery sensor implantation in 1200 patients with New York Heart Association class III symptoms and a previous hospitalization. Hospitalization rates were evaluated in all patients grouped into baseline estimated glomerular filtration rate (eGFR) quartiles. Chronic kidney disease progression was evaluated in patients with renal function follow-up data (n=911). RESULTS: Patients with stage 2 or greater chronic kidney disease at baseline exceeded 80%. Heart failure hospitalization risk was lower in all eGFR quartiles ranging from a hazard ratio of 0.35 (0.27-0.46; P<0.0001) in patients with eGFR >65 mL/min per 1.73 m2 to 0.53 (0.45-0.62; P<0.0001) in patients with eGFR ≤37 mL/min per 1.73 m2. Renal function was preserved or improved in most patients. Survival was different between quartiles and lower in quartiles with more advanced chronic kidney disease. CONCLUSIONS: Hemodynamic-guided heart failure management using remotely obtained pulmonary artery pressures is associated with lower hospitalization rates and general preservation of renal function in all eGFR quartiles or chronic kidney disease stages.

Reduction in 90 day readmission rates utilizing ambulatory pulmonary pressure monitoring.

AIMS: In the CHAMPION (CardioMEMS Heart Sensor Allows Monitoring of Pressure to Improve Outcomes in New York Heart Association Functional Class III Heart Failure Patients) trial, heart failure hospitalization (HFH) rates were lower in patients with ambulatory pulmonary artery pressure (PAP) monitoring guidance. We investigated the effect of ambulatory haemodynamic monitoring on 90 day readmission rates after HFH. METHODS AND RESULTS: We retrospectively analysed patients across the Advocate Aurora Health hospital network who had undergone PAP sensor implantation between 1 October 2015 and 31 October 2019. Patients with a ventricular assist device (VAD) or transplant prior to implantation were excluded. Rates of total HFH and 30 and 90 day all-cause readmission up to 12 months after implantation were collected, while censoring for an endpoint of heart transplantation, VAD, or death. Event rates were compared using Poisson regression. Of 459 patients included, there were 404 HFHs before and 179 after implantation. Compared with pre-implantation, 30 day all-cause readmission [incidence rate ratio (IRR): 0.55 (0.39-0.77), P = 0.0006] and 90 day all cause readmission rates were lower post-implantation [IRR: 0.45 (0.35-0.58), P < 0.0001]. The effect of PAP sensor implantation on 90 day all-cause readmission incidence rates was consistent across multiple subgroups. CONCLUSIONS: Across a large hospital network, ambulatory haemodynamic monitoring was associated with lower HFH rates, as well as 30 and 90 day all-cause readmission rates. This supports the utility of ambulatory PAP monitoring to improve HF management in the era of value-based medicine.

Association of Ambulatory Hemodynamic Monitoring of Heart Failure With Clinical Outcomes in a Concurrent Matched Cohort Analysis.

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.

Importance of baseline heart rate as a predictor of cardiac functional recovery in newly diagnosed heart failure with reduced ejection fraction.

BACKGROUND: Left ventricular ejection fraction (LVEF) has shown to predict outcomes in patients with heart failure (HF). Left ventricular recovery (LVR) has shown to improve prognosis. HYPOTHESIS: Guideline-directed medical therapy will predict LVR in patients with HF and reduced LVEF. METHODS: We studied 244 patients with newly diagnosed HF and an LVEF ≤35%. LVR was defined as an increase in LVEF ≥40%. Patients who experienced LVR were compared with those who had persistent left ventricular dysfunction. RESULTS: Population characteristics included ischemic etiology, 38.1%; baseline LVEF, 23% ±6%; and mean baseline heart rate (HR), 75 ±13 bpm. Guideline-directed medical therapy was achieved as follows: angiotensin-converting enzyme inhibitors, 74.3%; ß-blockers (BB), 95.4%; target dosing of angiotensin-converting enzyme inhibitors, 33.7%; target dosing of BB, 40.2%. LVR occurred in 154/244 patients (63.1%). By multivariable analysis, baseline HR ≤70 bpm was the only independent predictor of LVR (odds ratio: 3.39, 95% confidence interval: 1.5-7.5, P = 0.003). Target dosing of BB therapy was predictive of LVR only in the univariate analysis (odds ratio: 1.9, 95% confidence interval: 1.1-3.4, P = 0.03). Furthermore, the composite endpoint of HF hospitalization or mortality occurred less frequently in those who did vs those who did not achieve target BB doses (5.4% vs 16.7%, respectively; P = 0.023). CONCLUSIONS: The novel findings of our analysis reveal that the only predictor of LVR in this study was a low baseline HR. Early modulation of HR in newly diagnosed HF patients may increase the rates of LVR.

Sleep-Disordered Breathing During Congestive Heart Failure: To Intervene or Not to Intervene?

Sleep-disordered breathing is common in heart failure patients and is associated with increased morbidity and mortality. Central sleep apnea occurs more commonly in heart failure-reduced ejection fraction, and obstructive sleep apnea occurs more frequently in heart failure with preserved ejection fraction. Although the two types of sleep-disordered breathing have distinct pathophysiologic mechanisms, both contribute to abnormal cardiovascular consequences. Treatment with continuous positive airway pressure for obstructive sleep apnea in heart failure has been well defined, whereas treatment strategies for central sleep apnea in heart failure continue to evolve. Unilateral transvenous neurostimulation has shown promise for the treatment of central sleep apnea. In this paper, we examine the current state of knowledge of treatment options for sleep-disordered breathing in heart failure.

The acute cardiorenal syndrome type I: considerations on physiology, epidemiology, and therapy.

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.

Ace inhibitor therapy for heart failure in patients with impaired renal function: a review of the literature.

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.

Normal coronary arteries are rare in young patients with acute myocardial infarction.

OBJECTIVE: To delineate the angiographic extent of coronary atherosclerosis in young patients (<45 years) with acute myocardial infarction (MI). BACKGROUND: Prior studies suggest 20% of young patients with acute MI have normal coronary arteries. However, most such studies defined "normal" as absence of stenoses >50% luminal diameter, ignoring the presence of nonflow limiting disease that may harbor culprit plaques. METHODS: We retrospectively analyzed 131 patients <45 years old with ST-segment elevation MI undergoing emergency catheterization. Angiograms were analyzed for the presence and extent of disease, including lesion "complexity" indicative of plaque instability. "Normal" vessels were defined as absence of any disease. RESULTS: Mean patient age was 40 +/- 7 years. The infarct related artery and an obvious complex culprit lesion was identified in all (100%) cases (left anterior descending 44%, right coronary 38%, and circumflex 18%). Single vessel disease involving the culprit vessel only was identified in 60% of cases, whereas additional disease was found in 40% of others (two-vessel in 29% and three-vessel disease in 11% of patients). CONCLUSION: These findings demonstrate that young patients with acute MI typically manifest an identifiable complex culprit atherosclerotic coronary lesion. Furthermore, they often have multivessel atherosclerosis.

Possible paradoxical embolism as a rare cause for an acute myocardial infarction.

Paradoxical embolus is a rare entity and it has been incriminated as a cause of both cryptogenic strokes and myocardial infarctions (MI). Herein, we present a case of a patient diagnosed with a pulmonary embolism 1 week prior who now presented with an acute MI. Subsequent evaluation revealed a patent foramen ovale and a large thrombus in the right pulmonary artery. It was presumed that the etiology of her infarct was due to paradoxical embolus. The management of the patient is discussed and the literature is reviewed.

Caught in the act: serial, real time images of a thrombus traversing from the right to left atrium across a patent foramen ovale.

AIMS: To illustrate the association between a patent foramen ovale (PFO) and paradoxical embolization. METHODS AND RESULTS: We report a unique case of a paradoxical embolization across a PFO noted during a transesophageal echocardiographic study. Serial images demonstrate the thrombus migrating from the superior vena cava to the left atrium across the PFO. CONCLUSIONS: This case establishes the association between the PFO and paradoxical embolism unequivocally.

Comparison of transthoracic versus transesophageal echocardiography for detection of right-to-left atrial shunting using agitated saline contrast.

Agitated saline contrast studies (bubble studies) can be performed with either transthoracic or transesophageal echocardiography for the detection of right-to-left atrial shunts. The echocardiograms of 94 consecutive patients who underwent saline contrast studies with transthoracic and transesophageal approaches were reviewed to compare the ability of these modalities to detect right-to-left atrial shunts.