Open Heart最新文献

Objectives: Elevations of cardiac troponin T (cTnT) levels are common after strenuous exercise. We assessed whether the composition of cTnT release after marathon race differs from that of acute myocardial infarction (MI).

Methods: Troponin composition was analysed in plasma samples taken from 45 runners after marathon race and from 84 patients with type 1 MI. The concentration of long cTnT (intact and mildly fragmented cTnT) was measured with a novel upconversion luminescence immunoassay, total cTnT with a commercial high-sensitivity cTnT assay, and the ratio of long to total cTnT (troponin ratio) was determined as a measure of troponin fragmentation.

Results: Total cTnT exceeded the upper reference limit (>14 ng/L) in 37 (82%) runners. Troponin ratio was lower in runners ((IQR) 0.17 (0.11-0.24) vs 0.62 (0.29-0.96), p<0.001). With increasing troponin release the troponin ratio decreased (r=-0.497, p<0.001) in marathon runners and the concentration of long cTnT remained in all runners below 8.4 ng/L. In contrast to marathon runners, troponin ratio increased (r=0.565, p<0.001) with the increase of cTnT release in patients with MI. The median total and long cTnT concentrations were lower in marathon runners than in patients with MI (25 ng/L vs 835 ng/L and 4.1 vs 385 ng/L, p<0.001 for both).

Conclusion: In contrast to type 1 MI, only a small fraction of circulating cTnT exists as intact cTnT or long molecular forms after strenuous exercise and the difference in troponin composition is more pronounced in runners with higher troponin release.

Trial registration number: NCT06000930.

Background: Whether, and how, co-occurring HIV-1 infection (HIV) and tuberculosis (TB) impact cardiovascular status, especially in adolescents with perinatally acquired HIV (APHIV), have not been examined. We hypothesised that APHIV with previous TB disease have worse cardiac efficiency than APHIV without TB, which is mediated by increased inflammation and disordered cardiometabolism.

Methods: APHIV in Cape Town, South Africa, completed 3T cardiovascular magnetic resonance examination and high sensitivity C reactive protein (hsCRP), fasting plasma glucose (FPG), low-density lipoprotein (LDL) and triglyceride measurement. Ventriculoarterial coupling (VAC) was estimated as the ratio of arterial elastance (Ea) to ventricular end-systolic elastance (Ees). Regression models were applied to estimate cross-sectional associations between Ea/Ees ratio and TB status, with decomposition of these associations into direct and mediated effects of hsCRP, FPG and dyslipidaemia, if any, attempted.

Results: We enrolled 43 APHIV with prior TB and 23 without TB of mean (SD) age 15.0 (1.5) and 15.4 (1.7) years, respectively. Prior TB was associated with lower Ea/Ees ratio (0.59 (0.56 to 0.64)) than no TB (0.66 (0.62 to 0.70)), which corresponded to an adjusted mean difference -0.06 (-0.12 to 0.01) (p=0.048). However, previous TB was not associated with increased hsCRP, FPG, LDL or triglycerides nor were hsCRP, FPG, LDL and triglycerides associated with Ea/Ees ruling out their mediated effects in the association between TB and cardiac efficiency.

Conclusions: Previous TB in APHIV is associated with comparatively reduced cardiac efficiency, related to altered VAC. The clinical significance of these findings requires further study, including a wider range of biomarkers of specific immune pathways.

Background: Variant transthyretin amyloidosis (ATTRv) is a hereditary multisystem disorder with clinical spectrum ranging from predominant cardiomyopathy to polyneuropathy. In the Irish population, the T60A mutation has been previously recognised as the most common genotype.

Objectives: The aim of this study is to describe the diagnostic and phenotypic spectrum of patients with T60A ATTRv attending an Irish Expert Amyloidosis Network.

Methods: In this observational study design, the medical, laboratory and radiological records of patients enrolled in our amyloidosis registry with a confirmed genotype diagnosis of T60A ATTRv were reviewed.

Results: A cohort of 24 patients (12 female) met criteria for inclusion. The median age at diagnosis was 65 years (IQR 59.5-66.5) and median follow-up 44 months (IQR 31-58). Carpal tunnel syndrome was the initial manifestation in almost half (46%) of patients. Overall, a mixed cardioneuro phenotype was demonstrated including autonomic (75%), small (58%) and large fibre (46%) neuropathy largely predating a cardiac phenotype consisting of heart failure (63%), atrial arrhythmia (42%) and bradycardia (13%).

Conclusion: The contemporary clinical spectrum of T60A ATTRv in Ireland is one of patients typically presenting in the seventh decade with an already manifest neuropathy phenotype, largely predating a cardiac phenotype dominated by heart failure.

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.