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Cardiac physiologic pacing (CPP), encompassing cardiac resynchronization therapy (CRT) and conduction system pacing (CSP), has emerged as a pacing therapy strategy that may mitigate or prevent the development of heart failure (HF) in patients with ventricular dyssynchrony or pacing-induced cardiomyopathy. This clinical practice guideline is intended to provide guidance on indications for CRT for HF therapy and CPP in patients with pacemaker indications or HF, patient selection, pre-procedure evaluation and preparation, implant procedure management, follow-up evaluation and optimization of CPP response, and use in pediatric populations. Gaps in knowledge, pointing to new directions for future research, are also identified.

Background Amyloidosis is a systemic disorder characterized by the deposition of misfolded proteins in various organs. While cardiac transthyretin amyloidosis (ATTR) is well-recognized, pulmonary involvement is rare and often overlooked in clinical practice. Case summary We present a case of severe, and ultimately fatal, cardiac and pulmonary ATTR amyloidosis in a 67-year-old male. The patient's initial complaints included dyspnoea and exercise intolerance. Echocardiography revealed isolated concentric left ventricular hypertrophy, and subsequent cardiac MRI suggested cardiac amyloidosis. Additional diagnostic steps, including bone scan and endomyocardial tissue biopsy, confirmed the diagnosis of ATTR amyloidosis. Intriguingly, this case also unveiled concurrent pulmonary involvement, characterized by ground-glass opacities, lymphadenopathy, and impaired lung function. Despite treatment with tafamidis, the patient's condition deteriorated swiftly. He was admitted to the hospital four months after his initial presentation, and ultimately succumbed to therapy-resistant respiratory distress and heart failure. Post-mortem examination revealed extensive cardiac and pulmonary interstitial ATTR amyloidosis, with the lung exhibiting a fibrotic stage of diffuse alveolar damage. Discussion This case highlights pulmonary involvement as a potential contributor to the clinical picture of ATTR amyloidosis. It also emphasizes the necessity for a multidisciplinary approach, heightened awareness, and further research to enhance the detection and management of pulmonary involvement in ATTR amyloidosis. [ABSTRACT FROM AUTHOR]

Aims: Early evaluation of the natriuretic response is recommended to guide diuretic therapy in acute decompensated heart failure (ADHF). However, its implementation in daily practice is hampered by implementation barriers and increased time constraints. The Readily Available Urinary Sodium Analysis in Patients with Acute Decompensated Heart Failure (EASY‐HF) study assessed the feasibility, efficacy and safety of a nurse‐led urinary sodium‐based diuretic titration protocol with the use of a point‐of‐care urinary sodium sensor. Methods and results: The EASY‐HF study was a single‐centre, randomized, open‐label study comparing diuretic management at the treating physician's discretion as standard of care (SOC) with a nurse‐led natriuresis‐guided protocol in patients with ADHF. The LAQUAtwin Sodium Meter (HORIBA) was used as point‐of‐care sensor to measure urine sodium concentration. The primary endpoint was natriuresis after 48 h. Secondary endpoints included safety profile and user‐friendliness of both the protocol and the point‐of‐care sensor. Sixty patients were randomized towards SOC (n = 30) versus protocolized care (n = 30). The mean age was 80 ± 8 years, 25% were women and median N‐terminal pro‐B‐type natriuretic peptide was 4667 (2667–7709) ng/L. Natriuresis after 48 h was significantly higher in the protocolized versus SOC group (820 ± 279 vs. 657 ± 273 mmol; p = 0.027). Pre‐defined safety endpoints were similar among both groups. The sensor‐based protocol was evaluated as easy to use by the nursing staff, and preferred over urinary collections. Conclusion: A nurse‐led diuretic titration protocol via a point‐of‐care urinary sodium sensor was feasible, safe and resulted in an increased natriuresis in ADHF compared to SOC. [ABSTRACT FROM AUTHOR]

Aim: Among patients discharged after hospitalization for heart failure (HF), a strategy of torsemide versus furosemide showed no difference in all‐cause mortality or hospitalization. Clinicians have traditionally favoured torsemide in the setting of kidney dysfunction due to better oral bioavailability and longer half‐life, but direct supportive evidence is lacking. Methods and results: The TRANSFORM‐HF trial randomized patients hospitalized for HF to a long‐term strategy of torsemide versus furosemide, and enrolled patients across the spectrum of renal function (without dialysis). In this post‐hoc analysis, baseline renal function during the index hospitalization was assessed as categories of estimated glomerular filtration rate (eGFR; <30, 30–<60, ≥60 ml/min/1.73 m2). The interaction between baseline renal function and treatment effect of torsemide versus furosemide was assessed with respect to mortality and hospitalization outcomes, and the change in Kansas City Cardiomyopathy Questionnaire clinical summary score (KCCQ‐CSS). Of 2859 patients randomized, 336 (11.8%) had eGFR <30 ml/min/1.73 m2, 1138 (39.8%) had eGFR 30–<60 ml/min/1.73 m2, and 1385 (48.4%) had eGFR ≥60 ml/min/1.73 m2. Baseline eGFR did not modify treatment effects of torsemide versus furosemide on all adverse clinical outcomes including individual components or composites of all‐cause mortality and all‐cause (re)‐hospitalizations, both when assessing eGFR categorically or continuously (p‐value for interaction all >0.108). Similarly, no treatment effect modification by eGFR was found for the change in KCCQ‐CSS (p‐value for interaction all >0.052) when assessing eGFR categorically or continuously. Conclusion: Among patients discharged after hospitalization for HF, there was no significant difference in clinical and patient‐reported outcomes between torsemide and furosemide, irrespective of renal function. [ABSTRACT FROM AUTHOR]

Aims: In the SIRONA 2 trial, the safety and efficacy of pulmonary artery (PA) pressure (PAP)‐guided heart failure (HF) management using a novel PAP sensor were assessed at 30 and 90 days, respectively, and both endpoints were met. The current study examines the prespecified secondary endpoints of safety and accuracy of the PA sensor along with HF hospitalizations and mortality, HF symptoms, functional capacity, quality of life, and patient compliance through 12 months. Methods and results: SIRONA 2 is a prospective, multi‐centre, open‐label, single‐arm trial evaluating the Cordella™ PA Sensor System in 70 patients with New York Heart Association (NYHA) functional class III HF with a prior HF hospitalization and/or increase of N‐terminal pro‐brain natriuretic peptide within 12 months of enrolment. Sensor accuracy was assessed and compared with measurements obtained by standard right heart catheterization (RHC). Safety was defined as freedom from prespecified adverse events associated with use of the Cordella PA Sensor System and was assessed in all patients who entered the cath lab for PA sensor implant. HF hospitalizations and mortality, HF symptoms, functional capacity, quality of life, and patient compliance were also assessed. At 12 months, there was good agreement between the Cordella PA Sensor System and RHC, with the average difference for mean PAP being 2.9 ± 7.3 mmHg. The device safety profile was excellent with 98.4% freedom from device/system‐related complications. There were no pressure sensor failures. HF hospitalizations and mortality were low with a rate of 0.33 event per patient year. Symptoms as assessed by NYHA (P < 0.0001) and functional capacity as measured by 6 min walk test (P = 0.02) were significantly improved. Patients' adherence to daily transmissions of PAP and vital signs measurements was 95%. Conclusions: Long‐term follow‐up of the SIRONA 2 trial supports the safety and accuracy of the Cordella PA Sensor System in enabling comprehensive HF management in NYHA class III HF patients. [ABSTRACT FROM AUTHOR]

Aim: Cardiac resynchronization therapy (CRT) is a cornerstone in the management of chronic heart failure in patients with a broad or paced QRS. However, data on long‐term outcome after upgrade to CRT are scarce. Methods and results: This international, multicentre retrospective registry included 2275 patients who underwent a de novo or upgrade CRT implantation with a mean follow‐up of 3.6 ± 2.7 years. The primary composite endpoint included all‐cause mortality, heart transplantation, or ventricular assist device implantation. The secondary endpoint was first heart failure admission. Multivariable Cox regression and propensity score matching (PSM) analyses were performed. Patients who underwent CRT upgrade (n = 605, 26.6%) were less likely female (19.7% vs. 28.8%, p < 0.001), more often had ischeemic cardiomyopathy (49.8% vs. 40.2%, p < 0.001), and had worse renal function (median estimated glomerular filtration rate 50.3 ml/min/1.73 m2 [35.8–69.5] vs. 59.9 ml/min/1.73 m2 [43.0–76.5], p < 0.001). The incidence rate of the composite endpoint was 10.8%/year after CRT upgrade versus 7.1%/year for de novo implantations (p < 0.001). PSM for the primary endpoint resulted in 488 pairs. After propensity score matching, upgrade to CRT was associated with a higher chance to reach the composite endpoint (multivariable hazard ratio [HR] 1.35, 95% confidence interval [CI] 1.08–1.70), for both upgrade from pacemaker (multivariable HR 1.33, 95% CI 1.03–1.70) and implantable cardioverter‐defibrillator (ICD) (multivariable HR 1.40, 95% CI 1.01–1.95). PSM for the secondary endpoint resulted in 277 pairs. After PSM, upgrade to CRT was associated with a higher chance for heart failure admission (HR 1.74, 95% CI 1.26–2.41). Conclusion: In this retrospective analysis, the outcome of patients who underwent upgrades to CRT differed significantly from patients who underwent de novo CRT implantation, particularly for upgrades from ICD. Importantly, this difference in outcome does not imply a causal relation between therapy and outcome but rather a difference between two different patient populations. [ABSTRACT FROM AUTHOR]