Open Heart最新文献

Objective: To evaluate the impact of intraoperative neuromonitoring (IONM) on stroke and operative mortality after coronary and/or valvular operations.

Methods: This was an observational study of coronary and/or valvular heart operations from 2010 to 2021. Baseline characteristics and postoperative outcomes were compared by the use or non-use of IONM, which included both electroencephalography and somatosensory-evoked potentials. Propensity-score matching was employed to assess the association of IONM usage with operative mortality and stroke.

Results: A total of 19 299 patients underwent a cardiac operation, of which 589 (3.1%) had IONM. Patients with IONM were more likely to have had baseline cerebrovascular disease (60% vs 22%). Patients with IONM had increased operative mortality (5.3% vs 2.5%) and stroke (4.9% vs 1.9%). Moreover, stroke and mortality were highly correlated, with 14% of strokes resulting in death, while only 2% of non-strokes resulted in death (p<0.001). The unadjusted Kaplan-Meier survival estimate was significantly lower among the group with IONM (p<0.001, log-rank). After propensity matching, however, there was no difference in operative mortality or stroke across each group: 3.6% vs 5.3% for mortality and 3.7% vs 5.4% for stroke. In the propensity-matched cohort, the Kaplan-Meier survival estimates were not significantly different across each group (p=0.419, log-rank).

Conclusions: Adjusting for baseline risk, there was no significant difference in adverse outcomes across each group. IONM may serve as a biomarker of cerebral ischaemia, and empirical adjustments based on changes may provide benefits for neurologic outcomes in high-risk patients. The efficacy of IONM during cardiac surgery should be prospectively validated.

Background: Previous research has suggested a heightened risk of acute myocarditis after COVID-19 infection. However, it is not clear from existing work whether this risk is higher than would be expected after comparable viral respiratory infections. This information is important to guide risk assessments and clinical practice.

Methods: A retrospective cohort study of US administrative health claims was conducted to compare the rates of myocarditis after COVID-19 with that after influenza infection and describe the clinical use of diagnostic assessments.Patients with either incident COVID-19 diagnosis (between 1 January 2020 and 31 December 2021) or incident influenza diagnosis (between 1 January 2016 and 31 December 2018), with at least 12 months of continuous enrolment prior to index date and without a previous diagnosis of myocarditis were included.The primary outcome was clinically diagnosed acute myocarditis recorded after COVID-19 or influenza infection. Results are reported as covariate-adjusted subdistribution HRs from competing risk regression with COVID-19 considered as the exposure of interest and influenza as the reference group. Death was considered a competing risk.

Results: 1 120 760 adult COVID-19 patients and 439 278 adult influenza patients were identified, of which 669 (0.06%) adult COVID-19 patients and 91 (0.02%) adult influenza patients received a diagnosis of myocarditis. The myocarditis rate per 1000 person-years was 0.73 (95% CI 0.67 to 0.78) for adult COVID-19 patients and 0.24 (95% CI 0.19 to 0.28) for adult influenza populations. In models comprehensively adjusted for demographic and clinical risk factors, COVID-19 diagnosis (compared with influenza diagnosis), cardiac comorbidities, being male and under the age of 30 were independently associated with an increased risk of myocarditis in the year after diagnosis.

Conclusions: These findings support a distinct link between COVID-19 and myocarditis, which appears greater than after a similar viral respiratory infection. As such, a greater degree of clinical suspicion and investigation according to existing diagnostic pathways is recommended.

Background: Knowledge about how patients with symptomatic aortic stenosis (AS) perform on cardiopulmonary exercise testing (CPET) is sparse. Since exercise testing in patients with symptomatic AS is not advised, submaximal parameters could be of special interest. We aimed to investigate maximal and submaximal physical capacity by CPET before and 1 year after surgical aortic valve replacement (sAVR) in patients with severe AS.

Methods: In this prospective longitudinal study, 30 adult patients (age 66±10 years) with severe AS referred for sAVR underwent maximal CPET (respiratory exchange ratio ≥1.05) on a bicycle ergometer before (PRE) and 1 year after (POST) sAVR. Normally distributed data are presented as mean (±SD) and non-normally distributed data are presented as median (IQR).

Results: Median peak workload increased by 8% from 133 (55) watts at PRE to 144 (67) watts at POST (p<0.001). Median ventilatory threshold (VO₂@VT) increased from 1216 (391) to 1328 (309) mL/min (p=0.001, n=28). Mean peak oxygen uptake (peakVO₂) was not significantly different between PRE and POST; 1871±441 vs 1937±404 mL/min (p=0.08). The oxygen uptake efficacy slope (OUES) was significantly correlated to PeakVO2 at both PRE (r=0.889, p<0.05) and POST (r=0.888, p<0.05) CONCLUSION: Physical work capacity was improved 1 year following sAVR, in terms of higher median peak workload and VO₂@VT. The strong correlation between the submaximal variable OUES and peakVO₂ suggests that OUES might be a useful surrogate of peakVO₂ in this group of patients where maximal exercise testing is not always recommended.

Background: Heart failure (HF) is a leading cause of morbidity and mortality worldwide. Serum uric acid (SUA), a product of purine metabolism, has been implicated in HF progression. However, the association between hyperuricaemia and the short-term readmission and mortality in patients with HF remains controversial.

Methods: In this retrospective cohort study, we analysed data from a HF database specific to the Chinese population. The primary endpoint was short-term readmission or all-cause mortality within 90 days. Participants with HF were categorised into normouricaemia group (NUA) and hyperuricaemia group (HUA) based on a SUA threshold of 420 µmol/L. The association between SUA and primary endpoint was evaluated using Kaplan-Meier survival curves and Cox regression analysis.

Results: Baseline characteristics revealed significant differences between NUA and HUA groups, with the latter exhibiting a higher prevalence of males, chronic kidney disease (CKD) and elevated levels of various biomarkers. During a 90-day follow-up, 493 (26.6%) participants reached the primary endpoint, with a higher incidence observed in the HUA group at 31.2%, compared with 20.1% in the NUA group. When a threshold effect was identified at 420 µmol/L, a non-linear association was observed between SUA and the primary endpoint. After adjusting for gender, age, New York Heart Association class, CKD, systolic blood pressure (SBP) and potassium, the HUA group exhibited a higher risk for the primary endpoint compared with the NUA group (HR: 1.40, 95% CI: 1.14 to 1.72, p=0.001). Additionally, the risk increased across quartiles of SUA (P for trend=0.002). Furthermore, stratified analyses indicated a stronger association in patients without CKD (P interaction=0.033).

Conclusion: Hyperuricaemia is independently associated with an increased risk of short-term readmission and mortality in patients with HF. Our findings suggest that monitoring and managing SUA could be crucial in improving patient with HF outcomes.

Background: Obstructive sleep apnoea (OSA) can cause left atrial (LA) and left ventricular (LV) remodelling, which is linked to atrial fibrillation (AF). Whether continuous positive airway pressure (CPAP) can reverse LA and LV remodelling in patients with OSA and paroxysmal AF (PAF) has yet to be studied. We assessed the impact of CPAP treatment on LA and LV size and function in patients with OSA and PAF before and after catheter ablation.

Methods: In a randomised controlled trial, we screened patients with PAF for OSA. We enrolled patients with an Apnoea-Hypopnoea Index ≥15/hour. The burden of AF was monitored by an implantable loop recorder in all patients. Patients were then randomised to CPAP treatment or standard care. Transthoracic echocardiography was performed at baseline and after 6 and 12 months to assess LV and LA function and remodelling with advanced echocardiographic imaging techniques.

Results: We enrolled 109 patients (63±7 years, body mass index 29.6±4.3, 76% men). 83 patients were scheduled for pulmonary vein isolation (PVI) and 26 for clinical follow-up only. 55 patients were randomised to CPAP and 54 to standard care. The burden of AF decreased significantly in patients who underwent PVI irrespective of treatment with CPAP (p for difference ≤0.001). Patients in the study group had LV ejection fraction (LVEF) and LV global longitudinal strain (GLS) within the normal range, increased LA Volume Index (LAVI), LA volume (by speckle tracking) and decreased LA reservoir strain at baseline. We did not observe any improvement in LVEF, GLS, LAVI, LA volume or LA reservoir strain in either group during the 12 months of follow-up.

Conclusions: In patients with PAF and OSA, treatment with CPAP was not associated with reverse LA remodelling within 12 months of follow-up.

Background: Elevated troponin levels are a sensitive biomarker for cardiac injury. The quick and reliable prediction of troponin elevation for patients with chest pain from readily available ECGs may pose a valuable time-saving diagnostic tool during decision-making concerning this patient population.

Methods and results: The data used included 15 856 ECGs from patients presenting to the emergency rooms with chest pain or dyspnoea at two centres in Sweden from 2015 to June 2023. All patients had high-sensitivity troponin test results within 6 hours after 12-lead ECG. Both troponin I (TnI) and TnT were used, with biomarker-specific cut-offs and sex-specific cut-offs for TnI. On this dataset, a residual convolutional neural network (ResNet) was trained 10 times, each on a unique split of the data. The final model achieved an average area under the curve for the receiver operating characteristic curve of 0.7717 (95% CI±0.0052), calibration curve analysis revealed a mean slope of 1.243 (95% CI±0.075) and intercept of -0.073 (95% CI±0.034), indicating a good correlation between prediction and ground truth. Post-classification, tuned for F1 score, accuracy was 71.43% (95% CI±1.28), with an F1 score of 0.5642 (95% CI±0.0052) and a negative predictive value of 0.8660 (95% CI±0.0048), respectively. The ResNet displayed comparable or surpassing metrics to prior presented models.

Conclusion: The model exhibited clinically meaningful performance, notably its high negative predictive accuracy. Therefore, clinical use of comparable neural networks in first-line, quick-response triage of patients with chest pain or dyspnoea appears as a valuable option in future medical practice.

Background: Echocardiography, cardiac magnetic resonance and cardiac ¹⁸fluorodeoxyglucose positron emission tomography (FDG-PET) imaging play key roles in the diagnosis and management of cardiac sarcoidosis (CS), but the relative value of each modality in predicting outcomes has yet to be determined. This study sought to determine the prognostic importance of multimodality imaging data over and above demographic characteristics and left ventricular ejection fraction (LVEF).

Methods: Consecutive patients newly diagnosed with CS were included. Parameters evaluated included echocardiographic regional wall motion abnormality (RWMA), myocardial strain, LVEF, right ventricular ejection fraction (RVEF), late gadolinium enhancement (LGE) extent, SUVmax and RV FDG uptake. The primary endpoint was a composite of all-cause mortality and serious ventricular arrhythmia.

Results: The study population consisted of 208 patients with mean age of 55±13 years and LVEF of 55±12%. During a median follow-up period of 46 (IQR: 18-55) months, 14 patients died and 28 suffered serious ventricular arrhythmias. On multivariable analysis, RWMA (HR for RWMA presence 2.55, 95% CI 1.27 to 5.28, p=0.008), LGE extent (HR per 1% increase 1.02, 95% CI 1.00 to 1.04, p=0.018), RVEF (HR per 1% decrease 0.97, 95% CI 0.94 to 0.99, p=0.008) and RV FDG uptake (HR for RV FDG presence 2.48, 95% CI 1.15 to 5.33, p=0.020) were independent predictors of the primary endpoint, while LVEF was not predictive. The risk of adverse events was significantly greater in those with LGE extent ≥15% (HR for ≥15% presence 3.96, 95% CI 2.17 to 7.23, p<0.001).

Conclusion: In our CS population, RWMA, LGE extent, RVEF and RV FDG uptake were strong independent predictors of an adverse outcome. These findings offer an important insight into the key multimodality imaging parameters that may be used in a future risk stratification model of patients with CS.

Aims: We set out to explore associations between a 'mitral-specific' cardiac damage score (m-CDS) and survival outcomes in mitral regurgitation (MR) and compare the performance of the m-CDS and an 'aortic-specific' CDS (a-CDS) in patients with MR within the large National Echo Database of Australia.

Methods: Among 620 831 unique adults investigated with echocardiography, there were 17 658 individuals (3.1%) with moderate or greater functional MR (aged 76±13 years, 51% female) who met inclusion criteria. A randomly selected cohort of 5000 of these patients was used to test seven different CDS models for prediction of subsequent all-cause mortality during an average 3.8-year follow-up. The best-performing CDS model in the derivation cohort was then applied to a validation cohort of the remaining 12 658 individuals (aged 76±13 years, 51% female).

Results: The best-performing m-CDS model stratified the full cohort into Stage 0: control (1046 patients, 8%); Stage 1: left atrial damage (3416 patients, 27%); Stage 2: left ventricular damage (3352 patients, 26%); Stage 3: right ventricular damage (1551 patients, 12%) and Stage 4: pulmonary hypertension (3293 patients, 26%). Increasing m-CDS stage was consistently and incrementally associated with both all-cause and cardiovascular mortality at 1 year, 5 years and all-time and remained so after adjustment for increasing age and severity of MR, with a ~35% increase in mortality for each increase in CDS stage (p<0.001).

Conclusion: A m-CDS was robustly and incrementally associated with short-, medium- and long-term risk of all-cause and cardiovascular mortality in patients with functional MR in this large registry study.

Background: Since 2000, the definition of myocardial infarction (MI) has evolved with reliance on cardiac troponin (cTn) tests. The implications of this change on trends of acute coronary syndrome (ACS) subtypes obtained from routinely collected hospital morbidity data are unclear. Using person-linked hospitalisation data, we compared International Classification of Diseases (ICD)-coded data with biomarker-classified admission rates for ST-segment elevation MI (STEMI), non-STEMI (NSTEMI) and unstable angina (UA) in Western Australia (WA).

Methods: We used linked hospitalisation data from all WA tertiary hospitals to identify patients with a principal diagnosis of STEMI, NSTEMI or UA between 2002 and 2016. Linked biomarker results were classified as 'diagnostic' for MI according to established criteria. We calculated age-standardised and sex-standardised rates (ASSRs) for ICD-coded versus biomarker-classified admissions by ACS subtypes and estimated annual change in admissions using Poisson regression adjusting for age and sex.

Results: There were 37 272 ACS admissions in 30 683 patients (64.2% male), and 96% of cases had linked biomarker data, predominantly conventional cTn at the start and high-sensitive cTn from late 2013. Despite lower ASSRs, trends in MI classified with a diagnostic biomarker were concordant with ICD-coded admissions rates for both STEMI and NSTEMI. Between 2002 and 2010, STEMI rates declined by 4.1% (95% CI 5.0%, 3.1%) and 3.4% (95% CI 4.6%, 2.3%) in ICD-coded and biomarker-classified admissions, respectively, and both plateaued thereafter. For NSTEMI between 2002 and 2010, the ICD-coded and biomarker-classified rates increased 8.0% per year (95% CI 7.2%, 8.9%) and 8.0% (95% CI 7.0%, 9.0%), respectively, and both subsequently declined. For UA, both ICD-coded and biomarker-classified UA admission rates declined in a steady and concordant manner between 2002 and 2016.

Conclusions: The present study supports the validity of using administrative data to monitor population trends in ACS subtypes as they appear to generally reflect the redefinition of MI in the troponin era.

Background: Patients with heart failure exhibiting low systolic blood pressure (SBP) have a poor prognosis. Sacubitril/valsartan reduces cardiovascular events; however, its use in patients with low SBP has not been fully examined. Therefore, in this study, we aimed to investigate the association between baseline SBP and adverse events (AEs) in patients starting sacubitril/valsartan therapy using data from a real-world registry in Japan.

Methods: We analysed data from a multicentre retrospective study, including patients who initiated sacubitril/valsartan between August 2020 and August 2021. The patients were categorised into five groups based on their baseline SBP (<100, 100-109, 110-119, 120-129 and ≥130 mm Hg). The composite of AEs occurring within 3 months according to baseline SBP and the patient characteristics associated with AEs in a baseline SBP <110 mm Hg were analysed.

Results: Among the 964 patients newly prescribed sacubitril/valsartan, the median (IQR) age was 73 (61-80) years, and 388 (40.2%) patients had a baseline SBP <110 mm Hg. AEs occurred in 24% (n=232) of patients. The adjusted ORs for all AEs were 1.91 (95% CI (CI) 1.13-3.23; p=0.02) for the SBP <100 mm Hg group and 3.33 (95% CI 1.98 to 5.59; p<0.001) for the SBP 100-109 mm Hg group, compared with the SBP 110-119 mm Hg group. In patients with a baseline SBP <110 mm Hg, factors associated with an increased risk of AEs included a higher New York Heart Association class (II, III or IV) and a lower estimated glomerular filtration rate <30 mL/min/1.73 m².

Conclusions: Caution is needed when initiating sacubitril/valsartan in patients with lower baseline SBP. The severity of heart failure and kidney function may be useful for risk stratification in these high-risk patients.