Glenfield Hospital

To investigate whether preoperative noninvasive measurement of right ventricle-to-pulmonary artery coupling, assessed by the tricuspid annular plane systolic excursion-to-pulmonary artery systolic pressure (TAPSE:PASP) ratio, is associated with perioperative outcomes following pulmonary endarterectomy (PEA). Retrospective, single-center cohort study. Tertiary university hospital: national center for chronic thromboembolic pulmonary hypertension (CTEPH) treatment. Patients with CTEPH eligible for PEA. Patients underwent transthoracic echocardiography and right heart catheterization before undergoing PEA. The TAPSE:PASP ratio was calculated from preoperative echocardiography and dichotomized at 0.17 mm/mmHg. The primary outcome was intensive care unit (ICU) length of stay (LOS). Secondary outcomes included vasoactive and inotropic therapy, representing perioperative hemodynamic instability. Sixty patients were included. The median TAPSE:PASP ratio was 0.20 mm/mmHg (interquartile range [IQR], 0.15-0.29 mm/mmHg); 38% of patients had ratios below 0.17 mm/mmHg. A lower TAPSE:PASP ratio was associated with higher N-terminal pro-brain natriuretic peptide levels and pulmonary vascular resistance, as well as greater right ventricular dilatation. The median ICU LOS was longer in patients with a TAPSE:PASP ratio below 0.17 mm/mmHg (96 hours [IQR, 60-218 hours] v 63 hours [IQR, 41-93 hours], p = 0.0044), with an odds ratio (OR) of 3.45 (95% confidence interval [CI], 1.16-11.11) for ICU LOS greater than 72 hours. Patients with lower TAPSE:PASP ratios had a higher (OR, 3.33; 95% CI, 1.11-10.00; p = 0.032) and prolonged (OR, 3.70; 95% CI, 1.23-11.11; p = 0.019) need for vasoactive and inotropic therapy. A lower preoperative TAPSE:PASP ratio was associated with prolonged ICU stay and hemodynamic compromise after PEA. The TAPSE:PASP ratio may serve as a valuable, noninvasive tool for preoperative risk stratification in patients with CTEPH undergoing surgical treatment.

The present study aimed to report the early and late clinical outcomes of patients who underwent surgical repair for acute type A aortic dissection requiring concomitant coronary artery bypass grafting (CABG), and to explore potential risk factors associated with the need for this additional procedure. Data were retrieved from the multicenter European Registry of Type A Aortic Dissection (ERTAAD). Bootstrapped least absolute shrinkage and selection operator logistic regression and multilevel multivariate logistic regression were performed for variable selection to identify predictors of hospital death, and logistic regression was used for the prediction of CABG. A total of 292 (8.04%) of 3633 patients required additional CABG. The in-hospital mortality rate was 33% for patients undergoing CABG vs 16% of non-CABG recipients (P < .001; odds ratio [OR], 2.52; 95% CI, 1.93-3.35). Dissection of the aortic root involving the right coronary cusp (P < .001; OR, 7.83; 95% CI, 5.55-11.0), a tear in the aortic root (P = .002; OR, 2.08; 95% CI, 1.29-3.32), mitral valve insufficiency (P = .034; OR, 1.33; 95% CI, 1.01-1.71), and a genetic syndrome (P < .001; OR, 3.23; 95% CI, 1.66-5.99) independently predicted the need for CABG. The need for additional CABG is not a rare occurrence during repair of type A aortic dissection and is associated with an increased mortality risk. Intimal tear localization and right coronary sinus dissection should be carefully examined in the preoperative image evaluation to stratify the risk of revascularization and plan the most appropriate approach.

We investigated symptoms reported before and after heart failure (HF) diagnosis and their associations with 3-month hospitalisation and mortality. To examine associations between symptoms recorded in primary care and short-term hospitalisation and mortality in HF patients. Landmark analysis using Royston-Parmar survival models at baseline (diagnosis), 6 and 12 months post-diagnosis. Primary care database (Clinical Practice Research Datalink) linked to hospital and mortality data (1998-2020). Adults (>40 years) with a first HF diagnosis. Shortness of breath, ankle swelling, oedema, fatigue, chest pain, depression and anxiety in the 3 months before diagnosis and at 6 and 12 months. 3-month all-cause hospitalisation and mortality; secondary outcomes included HF and non-cardiovascular hospitalisation. Among 86 882 HF patients (62 742 and 54 555 surviving to 6 and 12 months, respectively), the magnitude of symptom risk varied by timepoint. Specifically, the symptoms with the strongest associations with adverse outcomes were: depression for all-cause hospitalisation at diagnosis (HR: 1.26; 95% CI 1.15 to 1.39) and 6 months (1.46; 1.25 to 1.70); ankle swelling for mortality (1.49; 1.14 to 1.94) at 6 months and SOB for HF hospitalisation (1.18; 1.12 to 1.26) at diagnosis and 12 months (1.99; 1.68 to 2.35). Symptoms persisted and were more prominent at 6 and 12 months post-diagnosis than at diagnosis.

Acute myocardial infarction is a major cause of mortality in individuals with obstructive airway disease. The impact of inpatient care quality following non-ST elevation myocardial infarction (NSTEMI) on long-term mortality among those with chronic obstructive pulmonary disease (COPD) and asthma remains poorly understood. We analysed 499 318 adults with NSTEMI from the Myocardial Ischaemia National Audit Project registry between 2005 and 2019, linked with Hospital Episode Statistics for airway disease diagnosis and Office for National Statistics data for mortality outcomes. Inpatient care quality was measured using the opportunity-based quality-indicator (OBQI) score. Long-term outcomes were evaluated using multivariable Cox regression and Kaplan-Meier analyses. Individuals with COPD and asthma received lower quality of care (OBQI score: no airways disease: 83.5 vs COPD: 78.1, asthma: 80.8, P < .001). Percutaneous coronary intervention was less frequent in COPD patients (22%) than in those without airway disease (30%) or with asthma (31%), P < .001. COPD was associated with higher 10-year mortality (hazard ratio [HR]: 1.58, 95% CI 1.56-1.60), whereas those with asthma had lower risk (HR: 0.97, 95% CI 0.95-0.98). COPD was associated with increased adjusted cardiovascular mortality (sub-distribution HR: 1.89, 95% CI 1.84-1.95). Individuals with COPD received lower-quality inpatient care and fewer coronary interventions, which was associated with higher long-term mortality.

BackgroundPulsed field ablation (PFA) is an emerging non-thermal ablation modality for atrial fibrillation (AF), characterized by its myocardial selectivity and reduced risk of collateral damage to extracardiac structures such as the oesophagus and phrenic nerve (PN). While transient phrenic nerve injury (PNI) has been reported, persistent diaphragmatic paralysis remains exceedingly rare.Case presentationWe report the case of a 49-year-old man with paroxysmal AF, refractory to medical therapy, who underwent pulmonary vein isolation using the FARAPULSE PFA system. The procedure was uneventful, and the patient was discharged the same day. However, he reported significant breathlessness on minimal exertion starting the day after the procedure. At his 6-week follow-up, physical examination revealed reduced air entry at the right lung base. A contrast-enhanced computed tomography chest confirmed an elevated right hemidiaphragm (9.0 cm posteriorly, 7.5 cm anteriorly), consistent with right PN palsy. The patient remained in sinus rhythm and asymptomatic from an arrhythmic standpoint, but continues to experience persistent dyspnoea.DiscussionTo our knowledge, this represents one of the early cases of persistent PN palsy following PFA with the FARAPULSE system. Although PFA is designed to target cardiomyocytes while sparing adjacent tissues selectively, proximity to the right PN—particularly near the right superior pulmonary vein—may still pose a risk. This case highlights the importance of procedural vigilance, including meticulous catheter positioning and careful consideration of nerve proximity. It highlights that persistent PNI, while rare, remains a potential complication of PFA.

Stage B heart failure (SBHF) increases the risk of symptomatic HF. Current guideline criteria for SBHF lack sex and ethnic thresholding and cardiac magnetic resonance (CMR) imaging cut-offs. We aimed to assess the prevalence of SBHF in a large cohort of people with type 2 diabetes (T2D) and healthy controls and propose a refined CMR definition for SBHF. Sex- and ethnic-specific thresholds for imaging criteria were derived from 373 healthy controls, who underwent CMR cine imaging. The current definition for SBHF and refined criteria was applied to our prospectively recruited and intensively phenotyped cohort of asymptomatic people with T2D and no evidence of cardiovascular disease. The prevalence of SBHF by different definitions was calculated and patient characteristics, including exercise capacity, were compared between those classified as Stage A vs. B HF. Finally, the refined criteria were also applied to the following two historical cohorts with symptomatic cardiovascular disease: severe aortic stenosis (AS n = 70) and HF with preserved ejection fraction (HFpEF n = 136). A total of 423 people with T2D and a subset of 102 healthy controls who underwent echocardiography were prospectively recruited. Current guideline criteria classified 91% of those with T2D and 69% of the healthy controls as SBHF, suggesting a lack of specificity. Applying derived sex- and ethnicity-specific thresholds, combining echo and CMR measures, the prevalence of SBHF was reduced to 30% in those with T2D. Using the refined definition, those with Stage B HF had lower exercise capacity than those with Stage A HF (percentage predicted maximal oxygen consumption 81 ± 16% vs. 91 ± 20%, p < 0.001). Applying the refined definition to symptomatic AS and HFpEF participants classified 89% and 85% with abnormal cardiac remodelling. Current guideline criteria for SBHF are non-specific and likely of limited value in clinical practice. Refining these criteria with sex- and ethnic-specific thresholds may improve identification of those at risk of developing symptomatic disease. Further research is required to validate these criteria.