Multicenter registry and test bed for extended outpatient hemodynamic monitoring: the hemodynamic frontiers in heart failure (HF2) initiative.

Background: Hemodynamic Frontiers in Heart Failure (HF2) is a multicenter academic research consortium comprised of 14 US institutions with mature remote monitoring programs for ambulatory patients with heart failure (HF). The consortium developed a retrospective and prospective registry of patients implanted with a wireless pulmonary artery pressure (PAP) sensor. Goals/aims: HF2 registry collects demographic, clinical, laboratory, echocardiographic (ECHO), and hemodynamic data from patients with PAP sensors. The aims of HF2 are to advance understanding of HF and to accelerate development of novel diagnostic and therapeutic innovations. Methods: HF2 includes adult patients implanted with a PAP sensor as per FDA indications (New York Heart Association (NYHA) Class III HF functional class with a prior hospitalization, or patients with NYHA Class II or brain natriuretic peptide (BNP) elevation without hospitalization) at a HF2 member site between 1/1/19 to present. HF2 registry is maintained at University of Kansas Medical Center (KUMC). The registry was approved by the institutional review board (IRB) at all participating institutions with required data use agreements. Institutions report data into the electronic registry database using REDCap, housed at KUMC. Results: This initial data set includes 254 patients implanted from the start of 2019 until May 2023. At time of device implant, the cohort average age is 73 years old, 59.8% are male, 72% have NYHA Class III HF, 40% have left ventricular ejection fraction (LVEF) < 40%, 35% have LVEF > 50%, mean BNP is 560 pg/ml, mean N-Terminal pro-BNP (NTproBNP) is 5,490 pg/ml, mean creatinine is 1.65 mg/dl. Average baseline hemodynamics at device implant are right atrial pressure (RAP) of 11 mmHg, pulmonary artery systolic pressure (PASP) of 47 mmHg, pulmonary artery diastolic pressure (PADP) 21 mmHg, mean pulmonary artery pressure (mPAP) of 20 mmHg, pulmonary capillary wedge pressure (PCWP) of 19 mmHg, cardiac output (CO) of 5.3 L/min, and cardiac index (CI) of 2.5 L/min/m2. Conclusion: A real-world registry of patients implanted with a PAP sensor enables long-term evaluation of hemodynamic and clinic outcomes in highly-phenotyped ambulatory HF patients, and creates a unique opportunity to validate and test novel diagnostic and therapeutic approaches to HF.

The Society of Thoracic Surgeons Intermacs 2022 Annual Report: Focus on the 2018 Heart Transplant Allocation System.

The 13th annual report from The Society of Thoracic Surgeons (STS) Interagency Registry for Mechanically Assisted Circulatory Support (Intermacs) highlights outcomes for 27,314 patients receiving continuous-flow durable left ventricular assist devices (LVAD) during the last decade (2012-2021). In 2021, 2464 primary LVADs were implanted, representing a 23.5% reduction in the annual volume compared with peak implantation in 2019 and an ongoing trend from the prior year. This decline is likely a reflection of the untoward effects of the coronavirus disease 2019 pandemic and the change in the United States heart transplant allocation system in 2018. The last several years have been characterized by a shift in device indication and type, with 81.1% of patients now implanted as destination therapy and 92.7% receiving an LVAD with full magnetic levitation in 2021. However, despite an older, more ill population being increasingly supported preimplant with temporary circulatory devices in the recent (2017-2021) vs prior (2012-2016) eras, the 1- and 5-year survival continues to improve, at 83.0% and 51.9%, respectively. The adverse events profile has also improved, with a significant reduction in stroke, gastrointestinal bleeding, and hospital readmissions. Finally, we examined the impact of the change in the heart transplant allocation system in 2018 on LVAD candidacy, implant strategy, and outcomes. In the competing-outcomes analysis, the proportion of transplant-eligible patients receiving a transplant has declined from 56.5% to 46.0% at 3 years, whereas the proportion remaining alive with ongoing support has improved from 24.1% to 38.1% at 3 years, underscoring the durability of the currently available technology.

Heart and heart-liver transplantation in patients with hemochromatosis.

BACKGROUND: Hemochromatosis predisposes to dilated or restrictive cardiomyopathy which can progress to end-stage heart failure, requiring the use of advanced heart therapies including heart (HT) and heart liver (HLT) transplantation. Little is known about the characteristics and outcomes of these patients. METHODS AND RESULTS: We queried the United Network for Organ Sharing (UNOS) registry for all patients listed for HT or HLT for a diagnosis of 'hemochromatosis' between 1987 and 2014. Waitlist and post-transplantation outcomes were compared between patients with hemochromatosis (HT vs HLT) and other etiologies. Of the 81,356 adults listed for heart transplantation, 23 patients with hemochromatosis were identified (16 listed for HLT; and 7 listed for HT). Compared with other etiologies, HC patients were younger (39 vs 51years, p<0.0001), and more likely to need inotropes (56.5% vs 25.6%, p=0.003) and mechanical ventilation (13% vs 3.4%, p=0.041). Cumulative hazards of waitlist mortality or delisting were higher in hemochromatosis patients than for other etiologies of heart failure (p<0.001). There were 4 HT and 4 HLT during the study period. Post-transplantation, patients with HC had a 1- and 2-year cumulative survival of 88% and 75%, respectively. CONCLUSIONS: Both HT and HLT are viable options for patients with hemochromatosis. Patients with hemochromatosis are younger with increased wait-list mortality compared with other etiologies.

Contemporary clinical trial updates in heart failure.

PURPOSE OF REVIEW: Heart failure is a major source of cardiovascular morbidity and mortality worldwide. The field has benefited from steady progress, and there are now multiple strategies - medical and surgical - to improve cardiovascular outcomes. The quest continues for enhanced pathophysiologic insights and therapies. RECENT FINDINGS: The chosen studies highlight new ways of treating heart failure with reduced ejection fraction (HFrEF) with pharmacotherapy such as sacubitril/valsartan and explore the role of antimicrobial therapy for chronic Chagas' cardiomyopathy. The role of iron supplementation, spinal cord stimulation and gene therapy are evaluated. The treatment of heart failure with preserved ejection fraction (HFpEF) is scrutinized, and the role of nitrates is discussed. The use of left ventricular assist devices in wider populations of HFrEF patients is considered. SUMMARY: These pivotal contemporary trials will impact bedside management. Sacubitril/valsartan's mortality benefit in HFrEF and the negative effect of nitrates in HFpEF provide novel insights. Progress with durable mechanical circulatory support and nonpharmacological approaches to heart failure management expand therapeutic options.

Ventricular hypertrophy and cavity dilatation in relation to body mass index in women with uncomplicated obesity.

OBJECTIVE: The traditionally accepted mechanism for ventricular adaptation to obesity suggests that cavity dilatation in response to increased blood volume and elevated filling pressure results in ventricular hypertrophy as a compensatory mechanism. Our hypothesis was that, instead, initiation of ventricular hypertrophy in obesity may be explained by changes in hormonal milieu and not by cavity dilatation. RESEARCH DESIGN AND METHODS: 88 female subjects without identifiable cardiovascular risk factors, covering a wide range of body mass indices (BMI), from normal (21.2 ± 1.6 kg/m(2)) to severely obese (45.0 ± 4.6 kg/m(2)), underwent cardiovascular MRI to determine left ventricular (LV) and right ventricular (RV) mass and volumes. RESULTS: BMI correlated positively with LV and RV mass and end-diastolic volumes (EDV). However overweight is associated with a significant LV and RV hypertrophy (LV: 78 ± 11 g vs 103 ± 16 g, p<0.01; RV: 26 ± 7 g vs 40 ± 11 g, p<0.01) was observed in the absence of differences in LV and RV volumes (LV: EDV 119 ± 15 vs 121 ± 21 ml, p>0.99, RV: 131 ± 17 vs 130 ± 24 ml; p>0.99). Furthermore, significant increases of serum leptin occurred at this pre-obese stage (15.6 ± 19 vs 36.5 ± 22 ng/ml; p=0.013). CONCLUSION: In a cohort of healthy female subjects with a wide range of BMIs, ventricular hypertrophy occurs without associated cavity dilatation in overweight individuals, while in manifest obesity, both cavity dilatation and ventricular hypertrophy occur. Elevated leptin levels may have a role in this effect on ventricular mass.

The effect of obesity and weight loss on aortic pulse wave velocity as assessed by magnetic resonance imaging.

Obesity is an escalating global health problem associated with both an increased risk of death and an increased risk of cardiovascular events. Our goal was to use magnetic resonance imaging (MRI) to determine the effect of obesity and weight loss, in the absence of the traditional cardiovascular risk factors, on aortic pulse wave velocity (PWV) a reliable, reproducible, and accurate clinical measure of aortic stiffness linked to increased mortality. Fifty obese (BMI 38.3 ± 6.8 kg/m(2)) and eighteen normal-weight controls (BMI 22.0 ± 1.7 kg/m(2)) with no identifiable cardiovascular risk factors underwent vascular MRI to assess PWV between the ascending aorta at the level of the pulmonary artery and the abdominal aorta (AA). Twenty-eight subjects underwent repeat imaging after a 1-year period of weight loss. Both groups were well matched for age, systolic blood pressure, fasting glucose, and total cholesterol. Obesity was associated with a 14% increase in PWV (P = 0.021), and with elevated C-reactive protein (CRP) (P < 0.01) and leptin levels (P < 0.001) factors known to cause increase arterial stiffness. Weight loss (average 50% excess weight) was associated with a 14% improvement in PWV (P = 0.03), and with reductions in serum leptin levels (P < 0.01). Obesity, in the absence of the traditional cardiovascular risk factors, is associated with increased aortic PWV, a noninvasive clinical measure of aortic stiffness independently predictive of cardiovascular mortality. Significant weight loss results in improvements in aortic PWV. This may provide a potential link between both obesity and increased mortality, and the reduction in mortality that occurs with weight loss.

Electrocardiographic body surface mapping: potential tool for the detection of transient myocardial ischemia in the 21st century?

Coronary artery disease (CAD) is one of the leading causes of cardiovascular mortality and morbidity worldwide. CAD presents as a wide spectrum of clinical disease from stable angina to ST segment elevation myocardial infarction. The 12-lead electrocardiogram (ECG) has been the main tool for the diagnosis of these events for almost a century but is limited in its diagnostic ability. For patients with suspected angina, the exercise tolerance test is often used to provoke and detect stress-induced ischemia but does not provide a definitive answer in a substantial proportion of patients. Body surface mapping (BSM) is a technique that samples multiple points around the thorax to provide a more comprehensive electrocardiographic data set than the conventional 12-lead ECG. Moreover, recent preliminary data demonstrate that BSM can detect and display transient regional myocardial ischemia in an intuitive fashion, employing subtraction color mapping, making it potentially valuable for diagnosing CAD causing transient regional ischemia. Research is ongoing to determine the full extent of its utility.

Uncomplicated obesity is associated with abnormal aortic function assessed by cardiovascular magnetic resonance.

AIMS: Obese subjects with insulin resistance and hypertension have abnormal aortic elastic function, which may predispose them to the development of left ventricular dysfunction. We hypothesised that obesity, uncomplicated by other cardiovascular risk factors, is independently associated with aortic function. METHODS AND RESULTS: We used magnetic resonance imaging to measure aortic compliance, distensibility and stiffness index in 27 obese subjects (BMI 33 kg/m2) without insulin resistance and with normal cholesterol and blood pressure, and 12 controls (BMI 23 kg/m2). Obesity was associated with reduced aortic compliance (0.9 +/- 0.1 vs. 1.5 +/- 0.2 mm2/mmHg in controls, p < 0.02) and distensibility (3.3 +/- 0.01 vs. 5.6 +/- 0.01 mmHg-1 x 10-3, p < 0.02), as well as higher stiffness index (3.4 +/- 0.3 vs. 2.1 +/- 0.1, p < 0.02). Body mass index and fat mass were negatively correlated with aortic function. Leptin was higher in obesity (8.9 +/- 0.6 vs. 4.7 +/- 0.6 ng/ml, p < 0.001) and also correlated with aortic measures. In multiple regression models, fat mass, leptin and body mass index were independent predictors of aortic function. CONCLUSION: Aortic elastic function is abnormal in obese subjects without other cardiovascular risk factors. These findings highlight the independent importance of obesity in the development of cardiovascular disease.