Publications

Coronary luminal dimensions change during the cardiac cycle. However, contemporary volumetric intravascular ultrasound (IVUS) analysis is performed in non-gated images as existing methods to acquire gated or to retrospectively gate IVUS images have failed to dominate in research. We developed a novel deep learning (DL)-methodology for end-diastolic frame detection in IVUS and compared its efficacy against expert analysts and a previously established methodology using electrocardiographic (ECG)-estimations as reference standard. Near-infrared spectroscopy-IVUS (NIRS-IVUS) data were prospectively acquired from 20 coronary arteries and co-registered with the concurrent ECG-signal to identify end-diastolic frames. A DL-methodology which takes advantage of changes in intensity of corresponding pixels in consecutive NIRS-IVUS frames and consists of a network model designed in a bidirectional gated-recurrent-unit (Bi-GRU) structure was trained to detect end-diastolic frames. The efficacy of the DL-methodology in identifying end-diastolic frames was compared with two expert analysts and a conventional image-based (CIB)-methodology that relies on detecting vessel movement to estimate phases of the cardiac cycle. A window of ± 100 ms from the ECG estimations was used to define accurate end-diastolic frames detection. The ECG-signal identified 3,167 end-diastolic frames. The mean difference between DL and ECG estimations was 3 ± 112 ms while the mean differences between the 1st-analyst and ECG, 2nd-analyst and ECG and CIB-methodology and ECG were 86 ± 192 ms, 78 ± 183 ms and 59 ± 207 ms, respectively. The DL-methodology was able to accurately detect 80.4%, while the two analysts and the CIB-methodology detected 39.0%, 43.4% and 42.8% of end-diastolic frames, respectively (P < 0.05). The DL-methodology can identify NIRS-IVUS end-diastolic frames accurately and should be preferred over expert analysts and CIB-methodologies, which have limited efficacy.

From 1972 to 1979 intra aortic balloon pumping (IABP) was attempted in 181 patients; catheter insertion failed in 13 (8%). More complications occurred with prolonged treatment but all three lethal complications (2%) were related to catheter insertion. Seventy-six patients had clinical cardiogenic shock after myocardial infarction (CSMI). Haemodynamically, 23 were classified as preshock: 15 (66%) could be weaned, 12 (53%) survived over 3 months; whereas only 27/51 patients (51%) haemodynamically classified as shock could be weaned and 21 (40%) survived over 3 months. Of forty-two patients with refractory angina at rest, 41 had prompt relief of pain after IABP, and subsequently underwent coronary artery bypasss grafting (CABG). Perioperative infarction rate was 8% (4/41), perioperative mortality was 7% (3/41). Total infarction rate was 11% (5/42), and total mortality 7% (3/41). Pain relief was prompt in 14/17 patients (82%) with refractory angina after infarction. Pain persisted in three patients: all three sustained an infarction, one died. Two patients were excluded from surgery. Twelve patients underwent CABG; none died, none developed MI. In eight patients persistence of pain suggested a slowly evolving MI, IABP abolished pain in seven. Conclusion: IABP has demonstrated its efficacy both in pump failure and in refractory ischaemia. However, its use is not without risks.

Chronic inflammation in asthmatic airways can lead to characteristic airway smooth muscle (ASM) thickening and pathological changes within the airway wall. This study assessed the effect of repeated allergen exposure on ASM and epithelial cell deoxyribonucleic acid (DNA) synthesis, cell recruitment and airway wall pathology. Brown-Norway rats were sensitized and then exposed to ovalbumin or saline aerosol every 3 days on six occasions. After the final exposure, rats were administered twice daily for 7 days with the DNA S-phase marker bromodeoxyuridine (BrdU). Using a triple immunohistochemical staining technique, BrdU incorporation into ASM and epithelium was quantified employing computer-assisted image analysis. There were &gt;3-fold mean increases in BrdU incorporation into ASM from 1.3% of cells (95% confidence interval (CI) 1.0-1.6) in saline controls to 4.7% (95% CI 2.6-6.7) after allergen exposure (p&lt;0.001), and in airway epithelium, from 1.3 (95% CI 0.6-2.0) BrdU-positive cells x mm basement membrane(-1) in saline controls to 4.9 (95% CI 3.0-6.7) after allergen exposure (p&lt;0.001). There was increased subepithelial collagen deposition and mucus secretion along with a significant eosinophil and lymphocyte recruitment to the airways. Increased rates of deoxyribonucleic acid synthesis in both airway smooth muscle and epithelial cells along with changes to the airway wall pathology may precede the establishment of smooth muscle thickening and airway remodelling after repeated allergen exposure in rats. This model seems to be appropriate for studying structural changes within the airways as observed in asthma.

No abstract is provided for this article.

A novel dedicated 3-dimensional quantitative coronary analysis methodology for bifurcation lesions

No abstract is provided for this article.

Background The purpose of this study was to compare the safety, efficacy, and costs of complete versus “culprit” vessel revascularization in multivessel coronary artery disease treated with percutaneous coronary interventions (PCI). Methods Patients with multivessel disease and an identified culprit vessel were randomly assigned to complete revascularization of vessels ≥50% stenoses (n = 108) versus revascularization limited to the culprit vessel (n = 111). The primary end point, major adverse cardiac events (MACE), were defined as cardiac or noncardiac death, myocardial infarction, need for coronary artery bypass graft surgery, and repeat PCI up to 1 year. Results Despite equal MACE at 24 hours (6.3% vs 7.4%), strategy success was higher in the culprit vessel than in the complete revascularization group (93.7% vs 81.5%, P = .007). MACE rates at 1 month (14.4% vs 9.3%), 1 year (32.4% vs 26.9%), and 4.6 ± 1.2 years (40.4% vs 34.6%) were similar in both groups. Repeat PCI was performed more often in the culprit vessel group (31.2% vs 21.2%, P = .06). A lower consumption of medical material was associated with lower procedural costs in the culprit vessel group (5784 vs 7315 Euros; P < .001). However, between 1 year and the end of follow-up, costs had equalized in both groups. Conclusions Complete versus culprit vessel revascularization in multivessel coronary disease treated with PCI was associated with a lower strategy success rate, similar MACE rates, and initially higher costs. However, over the long term, more repeat PCIs were conducted in patients treated by culprit revascularization only, mostly because of the need to treat lesions initially left untreated. As a consequence, incremental costs had equalized within 1 year. The decision of whether to perform culprit vessel or complete revascularization can be made on an individual basis.

The inflammatory environment which protects against viral infections such as SARS-CoV-2 is dynamic. Elucidating the interaction of immune mediators will provide insight into disease pathogenesis and assist the development of therapeutics to treat disease caused by viral insults. Using previously published upper respiratory tract network analysis, we dissected clinical symptom severity (FLU-PRO questionnaire) and self-reported clinical recovery based on immune node clusters from 139 participants in a community-based randomised clinical trial in early onset SARS-CoV-2 (The STOIC study, NCT04416399). Primary outcome events reported included urgent care, emergency department visit or hospitalisation for COVID-19. Nodes at study enrolment were defined as interferon, innate immunity-like, chemokine-dominant, and mucosal immunity-like. Participants were stratified based on viral burden (30-cycle thresholds) and treatment (budesonide or usual care) with node expression also compared to 22 healthy controls. Interferon and chemokine node expression increased dependent on viral burden as compared to health, as expected. Elevated IL-33, CCL26, CCL13, CCL17 and IL-5 expression in the mucosal node (p=0.0163) was associated with a mean 3.7-day quicker clinical recovery with no primary outcome events irrespective of treatment. Symptom severity differences were specific to nasal (p=0.0264) and throat (p=0.0020) symptoms at day 0 only in high mucosal node expressing participants. Overall,&nbsp;these data offer insight into mucosal&nbsp;mediators key to the control and swift symptom resolution of SARS-CoV-2 which can be utilised for future therapeutics.&nbsp;

The safety and efficacy of sirolimus-eluting stenting have been demonstrated, but the outcome of patients treated with this novel technology beyond the first year remains unknown. We sought to evaluate the angiographic, intravascular ultrasound (IVUS), and clinical outcomes of patients treated with sirolimus-eluting stents 2 years after implantation.This study included 30 patients treated with sirolimus-eluting Bx Velocity stenting (slow release [SR], n=15, and fast release [FR], n=15) in São Paulo, Brazil. Twenty-eight patients underwent 2-year angiographic and IVUS follow-up. No deaths occurred during the study period. In-stent late loss was slightly greater in the FR group (0.28+/-0.4 mm) than in the SR group (-0.09+/-0.23 mm, P=0.007). No patient had in-stent restenosis. At 2-year follow-up, only 1 patient (FR group) had a 52% diameter stenosis within the lesion segment, which required repeat revascularization. The target-vessel revascularization rate for the entire cohort was 10% (3/30) at 2 years. All other patients had < or =35% diameter stenosis. Angiographic lumen loss at the stent edges was also minimal (in-lesion late loss was 0.33+/-0.42 mm [FR] and 0.13+/-0.29 mm [SR]). In-stent neointimal hyperplasia volume, as detected by IVUS, remained minimal after 2 years (FR= 9.90+/-9 mm3 and SR=10.35+/-9.3 mm3).This study demonstrates the safety and efficacy of sirolimus-eluting Bx Velocity stents 2 years after implantation in humans. In-stent lumen dimensions remained essentially unchanged at 2-year follow-up in the 2 groups, although angiographic lumen loss was slightly higher in the FR group. Restenosis "catch-up" was not found in our patient population.

The present analysis was performed to evaluate the impact of diabetes mellitus (DM) status on the severity of coronary artery disease (CAD) and current approaches in interventional treatment.Little is known about the effect of DM treated with diet, oral agents, or insulin on lesion characteristics and anatomical pattern of CAD and their interventional treatment.Patients (n = 46,779) of the contemporary Euro Heart Survey PCI registry with known DM status were included in this analysis. Nondiabetics (n = 35,280, 75.4%) were compared with diabetics treated with diet (n = 1,533, 3.3%), oral agents (n = 7,222, 15.4%), and insulin (n = 2,744, 5.8%). Diabetic patients were older, suffered more frequently from comorbidities and presented more often with cardiogenic shock. The number of severely stenosed (≥ 70%) segments incrementally increased from nondiabetics to insulin-requiring diabetics. The location of lesions did not differ between patients with and without DM. The ratio stenosed/treated segments progressively rose among the four patient cohorts. The severity of DM negatively correlated with the extent of complete revascularization. After adjustment for confounding variables no significant differences in hospital mortality could be observed between patients without DM and diabetics treated with diet, but a significantly higher rate of death was seen in diabetic patients with oral medication and insulin therapy.Although CAD was more severe in patients with DM the percentage of treated segments with ≥ 70% stenosis was lower. Adjusted hospital mortality was increased among diabetics treated with oral medication or insulin, but not among those treated with diet.