Cardiology and cardiovascular medicine最新文献

Background: Patients with PR intervals >240ms have atrio-ventricular (AV) dyssynchrony, which can increase risk of atrial fibrillation and all-cause mortality. When requiring pacing, long AV delays (AVDs) have been programmed to avoid ventricular dyssychrony. His bundle pacing (HBP) may provide improved AV synchrony in patients with prolonged PR.

Methods: 10 patients with sinus node dysfunction and prolonged PR who received HBP were studied. Real-time echocardiographic was performed with 3 pacemaker modes (RV septal, non-selective HBP, and selective HBP) using the following pacemaker settings: control (no ventricular pacing), pacing with AVD of 180ms, 150ms, 120ms, 100ms, and 70ms. Echocardiographic Doppler measurements: EA/RR, >40% = AV synchrony; E/e', <8 = normal left atrial pressure; pulmonic-to-aortic pre-ejection time difference, <40ms = interventricular synchrony; septal-to-lateral wall activation time difference, <56ms = intraventricular synchrony; and LVOT VTI. Unpaired T test was used to evaluate for significance. Exclusion criteria: persistent atrial fibrillation, second-degree AV block.

Results: Compared to control programming, HBP showed a 31.5% increase in EA/RR time, a decrease in E/e' of 26.9%, and an increase in the LVOT VTI of 21.3%. Compared to RV septal pacing, there was a similar increase in LVOT VTI. These findings met statistical significance and were considered optimal based on Doppler echocardiography findings primarily at AVDs of 150ms and 120ms. Comparisons between selective and non-selective pacing were not significantly different.

Conclusion: Compared to controls and RV septal pacing, physiologic His bundle pacing was shown to increase markers of AV synchrony and LV stroke volume while maintaining ventricular synchrony.

Background: Transcatheter Aortic Valve Implantation (TAVI) has emerged over time, reflected in appropriate adjustments in the European Society of Cardiology (ESC) guidelines in 2007, 2012 and 2017.

Objective: The aim of this study was to analyze in-hospital outcomes after TAVI in the development within a single heart center over a period of 10 years depending on adjustments in the guidelines, infrastructural and procedural determinants.

Methods: 489 consecutive patients who underwent TAVI from 2010 and 2019 at our center were analyzed retrospectively. Patients were divided into 3 groups of different treatment circumstances depending on guidelines adjustments and local infrastructural progress (group 1: 2010-2015 (n = 132), group 2: 2016-2017 (n = 155), group 3: 2018-2019 (n = 202). The primary endpoint was defined as all-cause in-hospital mortality. Secondary endpoints were selected according to the Valve Academic Research Consortium (VARC)-2 definitions. Multivariate logistic regression analysis was performed to determine predictors of in-hospital mortality. Statistical significance was assumed for p < 0.05.

Results: 489 patients (346 (70.8 %) transfemoral and 143 (29.2 %) transapical) underwent TAVI. Comparing periods (group 1 vs. 2 vs. 3) age (82.1 ± 6.2 vs. 82.5 ± 4.8 vs. 81.1 ± 5.1 years, p = 0.012) and EuroSCORE II (8.4 ± 6.0 vs. 5.8 ± 4.9 vs. 5.5 ± 5.0 %, p < 0.001) declined over time. Rates of in-hospital mortality decreased significantly (9.1 % vs. 5.8 % vs. 2.5 %, p = 0.029), especially with observed-to-expected mortality ratios indicating a disproportionate decline of in-hospital mortality (1.08 vs. 1.00 vs. 0.45). Furthermore, post-procedural complications, such as acute kidney injury stage 3 (10.6 % vs. 3.2 % vs. 4.5 %, p = 0.016) and bleeding complications (14.4 % vs. 11.6 % vs 7.9 %, p = 0.165) decreased from group 1 to 3. However, rates of permanent pacemaker implantations (7.6 % vs. 11.0 % vs. 22.8 %, p < 0.001) increased, associated with a switch towards self-expanding valves (0.0 % vs. 61.3 % vs. 76.7 %, p < 0.001). Length of hospitalization as well as stay at intensive care and intermediate care unit could be reduced significantly during the observation period. In multivariate analysis age (OR: 1.103; 95 % CI: 1.013 - 1.202; p = 0.025), creatinine level before TAVI (OR: 1.497; 95 % CI: 1.013 - 2.212; p = 0.043), atrial fibrillation (OR: 2.956; 95 % CI: 1.127 - 7.749; p = 0.028) and procedure duration (OR: 1.017; 95 % CI: 1.009 - 1.025; p < 0.001) could be identified as independent predictors of in-hospital mortality.

Conclusion: This study identified age, creatinine level before TAVI, the presence of atrial fibrillation and procedure duration as independent predictors for in-hospital mortality. Although these predictors decreased during the observation period, the decline in hospital-mortality was disproportionate, w

SARS-CoV-2 is a +ssRNA helical coronavirus responsible for the global pandemic caused by coronavirus disease 19 (COVID-19). Classical clinical symptoms from primary COVID-19 when symptomatic include cough, fever, pneumonia or even ARDS; however, they are limited primarily to the respiratory system. Long-COVID-19 sequalae is responsible for many pathologies in almost every organ system and may be present in up to 30% of patients who have developed COVID-19. Our review focuses on how long-COVID-19 (3 -24 weeks after primary symptoms) may lead to an increased risk for stroke and thromboembolism. Patients who were found to be primarily at risk for thrombotic events included critically ill and immunocompromised patients. Additional risk factors for thromboembolism and stroke included diabetes, hypertension, respiratory and cardiovascular disease, and obesity. The etiology of how long-COVID-19 leads to a hypercoagulable state are yet to be definitively elucidated. However, anti-phospholipid antibodies and elevated D-dimer are present in many patients who develop thromboembolism. In addition, chronic upregulation and exhaustion of the immune system may lead to a pro-inflammatory and hypercoagulable state, increasing the likelihood for induction of thromboembolism or stroke. This article provides an up-to-date review on the proposed etiologies for thromboembolism and stroke in patients with long-COVID-19 and to assist health care providers in examining patients who may be at a higher risk for developing these pathologies.

Wrist-based wearables have been FDA approved for AF detection. However, the health behavior impact of false AF alerts from wearables on older patients at high risk for AF are not known. In this work, we analyzed data from the Pulsewatch (NCT03761394) study, which randomized patients (≥50 years) with history of stroke or transient ischemic attack to wear a patch monitor and a smartwatch linked to a smartphone running the Pulsewatch application vs to only the cardiac patch monitor over 14 days. At baseline and 14 days, participants completed validated instruments to assess for anxiety, patient activation, perceived mental and physical health, chronic symptom management self-efficacy, and medicine adherence. We employed linear regression to examine associations between false AF alerts with change in patient-reported outcomes. Receipt of false AF alerts was related to a dose-dependent decline in self-perceived physical health and levels of disease self-management. We developed a novel convolutional denoising autoencoder (CDA) to remove motion and noise artifacts in photoplethysmography (PPG) segments to optimize AF detection, which substantially reduced the number of false alerts. A promising approach to avoid negative impact of false alerts is to employ artificial intelligence driven algorithms to improve accuracy.

Atherosclerosis is a chronic inflammatory disease and hypercholesterolemia is a risk factor. This study aims to compare the potency of lipopolysaccharide (LPS) and oxidized low-density lipoproteins (oxLDL) to induce plaque formation and increase plaque vulnerability in the carotid artery of hypercholesterolemic Yucatan microswine. Atherosclerotic lesions at the common carotid artery junction and ascending pharyngeal artery were induced in hypercholesterolemic Yucatan microswine at 5-6 months of age with balloon angioplasty. LPS or oxLDL were administered intraluminally at the site of injury after occluding the arterial flow temporarily. Pre-intervention ultrasound (US), angiography, and optical coherence tomography (OCT) were done at baseline and just before euthanasia to assess post-op parameters. The images from the US, OCT, and angiography in the LPS and the oxLDL-treated group showed increased plaque formation with features suggestive of unstable plaque, including necrotic core, thin fibrous caps, and a signal poor region more with oxLDL compared to LPS. Histomorphology of the carotid artery tissue near the injury corroborated the presence of severe lesions in both LPS and oxLDL-treated pigs but more in the oxLDL group. Vascular smooth muscle and endothelial cells treated with LPS and oxLDL showed increased folds changes in mRNA transcripts of the biomarkers of inflammation and plaque vulnerability compared to untreated cells. Collectively, the results suggest that angioplasty-mediated intimal injury of the carotid arteries in atherosclerotic swine with local administration of LPS or ox-LDL induces vulnerable plaques compared to angioplasty alone and oxLDL is relatively more potent than LPS in inducing vulnerable plaque.