CJC Open最新文献

Background

Although ventricular tachycardia (VT) occurring during hospitalization for an acute myocardial infarction (AMI) increases mortality risk, its relationship with 30-day postdischarge rehospitalization has not been examined.

Methods

Using data from the Worcester Heart Attack Study, we examined the association between early (during the first 48 hours of admission) and late (after 48 hours from admission) VT with 30-day postdischarge all-cause and cardiovascular disease (CVD)-related rehospitalization while analytically controlling for several demographic and clinical factors.

Results

The study population consisted of 3534 patients who were hospitalized with an AMI between 2005 and 2015 (average age, 67.2 years; 40.7% women); VT occurred in 452 patients (13.7%), with the majority of instances (81.2%) occurring within 48 hours of admission. The 30-day all-cause rehospitalization rate was 17.3%, with 70.9% of the hospitalizations related to CVD. The odds of rehospitalization were 1.63 times (95% confidence interval [CI] = 0.99-2.69) and 1.12 times (95% CI = 0.83-1.51) higher for patients with AMI who developed late VT and early VT, respectively, compared to patients who did not develop VT. The risk of rehospitalization among patients with late VT was higher (odds ratio = 2.22 (95% CI = 0.79-6.26) in those with ST-segment-elevation AMI, compared to those with non-ST-segment-elevation AMI (odds ratio = 1.45 (95% CI = 0.81-2.57); early VT was not associated with rehospitalization in patients with either AMI subtype. No significant association was present between the occurrence of VT and CVD-related rehospitalization.

Conclusions

Patients who develop late VT may experience a higher risk of 30-day rehospitalization following hospital discharge for AMI, especially among those with ST-segment-elevation AMI. Larger studies are needed to confirm our findings.

Background

Rilonacept inhibits the interleukin-1 pathway, and extended treatment in patients with recurrent pericarditis (RP) reduced recurrence risk by 98% in the phase 3 trial, RHAPSODY long-term extension (LTE). Severe acute respiratory syndrome (SARS)-CoV-2 vaccination and/or infection may trigger pericarditis recurrence, and in clinical practice, it is unknown whether to continue rilonacept during SARS-CoV-2 infection. This post-hoc analysis of the RHAPSODY LTE aimed to inform rilonacept management in RP patients vaccinated against SARS-CoV-2 or who contract COVID-19.

Methods

Analysis was conducted from May 2020 to June 2022. The LTE portion of RHAPSODY LTE enabled up to 24 months of additional open-label rilonacept treatment beyond the pivotal study. Rilonacept efficacy data in preventing pericarditis recurrence were assessed, and concomitant SARS-CoV-2 vaccination and COVID-19 adverse event data were evaluated.

Results

No pericarditis recurrences were temporally associated with vaccination. Sixteen COVID-19 cases were reported; 10 in 30 unvaccinated or partially vaccinated patients (33%) vs 6 of 44 fully vaccinated patients (14%; P = 0.04). Twelve of 16 patients (75%) were receiving rilonacept at the time of infection, and none experienced pericarditis recurrence. One pericarditis recurrence occurred in the peri-COVID-19 period in 1 of 4 patients who had stopped rilonacept treatment > 4.5 months prior. COVID-19 severity was mild in 13 patients, moderate in 2, and severe in 1.

Conclusions

Full vaccination effectively reduced COVID-19 events in patients treated with rilonacept. Vaccination or COVID-19 during rilonacept treatment did not increase pericarditis recurrence. Continued rilonacept treatment in patients contracting COVID-19 did not worsen disease severity, whereas rilonacept interruption increased pericarditis recurrence, supporting a recommendation for continued rilonacept treatment for RP during vaccination or COVID-19.

ClinicalTrials.gov identifier

NCT03737110

Background

Inaccurate blood pressure (BP) classification results in inappropriate treatment. We tested whether machine learning (ML), using routine clinical data, can serve as a reliable alternative to ambulatory BP monitoring (ABPM) in classifying BP status.

Methods

This study employed a multicentre approach involving 3 derivation cohorts from Glasgow, Gdańsk, and Birmingham, and a fourth independent evaluation cohort. ML models were trained using office BP, ABPM, and clinical, laboratory, and demographic data, collected from patients referred for hypertension assessment. Seven ML algorithms were trained to classify patients into 5 groups, named as follows: Normal/Target; Hypertension-Masked; Normal/Target-White-Coat (WC); Hypertension-WC; and Hypertension. The 10-year cardiovascular outcomes and 27-year all-cause mortality risks were calculated for the ML-derived groups using the Cox proportional hazards model.

Results

Overall, extreme gradient boosting (using XGBoost open source software) showed the highest area under the receiver operating characteristic curve of 0.85-0.88 across derivation cohorts, Glasgow (n = 923; 43% female; age 50.7 ± 16.3 years), Gdańsk (n = 709; 46% female; age 54.4 ± 13 years), and Birmingham (n = 1222; 56% female; age 55.7 ± 14 years). But accuracy (0.57-0.72) and F1 (harmonic mean of precision and recall) scores (0.57-0.69) were low across the 3 patient cohorts. The evaluation cohort (n = 6213; 51% female; age 51.2 ± 10.8 years) indicated elevated 10-year risks of composite cardiovascular events in the Normal/Target-WC and the Hypertension-WC groups, with heightened 27-year all-cause mortality observed in all groups, except the Hypertension-Masked group, compared to the Normal/Target group.

Conclusions

ML has limited potential in accurate BP classification when ABPM is unavailable. Larger studies including diverse patient groups and different resource settings are warranted.

Background

Respiratory conditions are major physical triggers of takotsubo syndrome (TTS) and portend worse outcomes. However, data on TTS in patients with coronavirus disease-2019 infection (COVID-19) are limited.

Methods

We searched PubMed, Embase, and Cochrane Library databases for case reports for the period 2019-2022 describing TTS in patients with COVID-19 pneumonia (TTS-COVID). We summarized the clinical data and outcomes and compared them to those in patients with TTS with an acute respiratory disease other than COVID-19 as a trigger (TTS-acute respiratory disease) and those with TTS with no respiratory disease (TTS-no respiratory disease).

Results

The mortality rate was higher in those with TTS-COVID (26.0%) than those with TTS-acute respiratory disease (5.7%) or TTS-no respiratory disease (4.2%; P < 0.001 for both). The proportion of men was higher in TTS-COVID (33.3%) than it was in TTS-no respiratory disease (9.1%; P < 0.001). The manifestations of TTS in COVID patients were atypical (dyspnea [70.3%] and cough [40.6%]); few had chest pain (23.4%). Cardiovascular risk factors were common in the TTS-COVID cohort, but fewer patients were on cardioprotective medications in this group than in the other 2 groups. Level of catecholamine use was higher in the TTS-COVID group (37.7%) than it was in the TTS-no respiratory disease (10.9%; P < 0.001) group. Apical ballooning (72.6%) was the most common TTS subtype, and basal segment type was seen in 11.0% of TTS-COVID patients.

Conclusions

COVID-19 patients who developed TTS had high mortality rates and unique features, compared with those in the TTS-acute respiratory disease group or the TTS-no respiratory disease group. Understanding the pathophysiology of TTS in COVID-19 may help prevent TTS and direct therapy in this setting.

Hypertrophic cardiomyopathy (HCM) is a relatively common inherited cardiac disorder associated with a left ventricular hypertrophy that cannot be explained by another cardiac or systemic disorder. One of the core pathophysiology features is left ventricular outflow tract obstruction (obstructive HCM [oHCM]), and this pathology could lead to complications, including sudden cardiac death and heart failure. Current treatment strategies for symptomatic oHCM consist of historical pharmacologic agents that are often based on nonrandomized, limited data or expert opinion. This article presents a critical appraisal of disopyramide, one of the pharmacologic options available in Canada for managing oHCM. The author concludes that robust clinical evidence supporting the use of disopyramide in treating oHCM is lacking, and that disopyramide should be reserved as a last resort for nonresponders to pharmacologic treatment and for those in whom invasive therapies are not indicated.

The safety of continuing human epidermal growth factor receptor 2 (HER2)–targeted therapy in women with mild cardiotoxicity remains unclear. We performed a retrospective matched cohort study of 14 patients with human epidermal growth factor receptor 2–positive breast cancer receiving sequential anthracycline and trastuzumab therapy, nested within the Evaluation of Myocardial Changes During Breast Adenocarcinoma Therapy to Detect Cardiotoxicity Earlier With MRI (EMBRACE-MRI) trial. Among patients who developed cardiotoxicity and were treated with heart failure therapy, we compared those who had trastuzumab therapy interrupted to a matched cohort who continued trastuzumab therapy. By a median of 2.5 years of follow-up, no significant differences were present between the groups in the proportion with magnetic resonance imaging–measured left ventricular ejection fraction < 40%, magnetic resonance imaging–measured left ventricular volumes, left ventricular ejection fraction, edema, fibrotic markers, cardiopulmonary fitness, or quality of life.

Anthracycline therapy (ANT) is associated with cancer therapy-related cardiac dysfunction. Coronary flow velocity reserve (CFVR) has shown prognostic utility in non-cancer cohorts, but no data have been obtained in a cardio-oncology setting. We investigated the acute effect of ANT on CFVR in breast cancer patients. A total of 12 female breast cancer patients undergoing ANT had pre- and post-ANT CFVR assessment. A significant decline in CFVR occurred (baseline: 2.66 ± 0.41 vs post-ANT: 2.47 ± 0.37, P = 0.016). This prospective study is the first to identify ANT-related coronary physiology changes in humans. Further studies are required to determine their clinical significance.