PATIENTS AND METHODS: Materials and methods: Based on autopsy materials, we conducted a morphological study of patients (n = 20) aged 45 to 55 years who were observed in cardiac and neurological hospitals for 5-7 years. We removed kidney, heart and aorta samples from patients. For the study, a histological and immunohistochemical methods were used.
RESULTS: Results and conclusions: Morphological study of vessels endothelium of kidneys, heart and aorta demonstrated that in the majority of observations intima underwentprofound pathological changes, manifested by different degrees of disorganization of endothelial lining and violations of structural and functional organization of the endotheliocytes, subendothelial layer, basal membrane. These pathological processes in all cases had similar features with the development of immune inflammation. Inflammatory infiltration was represented by macrophages, mast cells, plasma cells. Biological mediators of the presented cells can aggravate the damage to endothelial cells. Indirect signs of low ability to restore the structure of the vessel wall and endothelial lining may be a weak expression of the VEGF and bcl-2 vascular endothelial growth factor.
METHODS/RESULTS: 32 cases of which 12 females and 20 male and 18 out of 32 cases were aged below 40. All of the cases were examined macroscopically and microscopically. 30 out of 32 cases (93%) died due to rupture associated with the AD. Two unusual complications were proximal extension of AD into left coronary artery (CA) with intramural haematoma blocking the vessel and AD involving the ostium of the right CA resulting in avulsion of the right CA from the aorta. Mode of death in both these cases were myocardial ischemia. Sections of the aorta in all cases confirmed extensive cystic medial degeneration with disorganisation, fragmentation and disappearance of the elastin fibres with increased collagen and smooth muscle nuclear degeneration.
CONCLUSION: Pathologists should be thorough when examining the aorta, the aortic valve and root in AD. When a rupture site cannot be found it is important to look for unusual complications involving the CAs. Histology plays an important role to corroborate the cause of death.
Methods: By means of propensity score (PS) matching 234 individuals with de novo CAD were identified with similar demographic characteristics. This patient population was stratified in a 1:1 fashion according to a reference vessel diameter cut-off of 2.75 mm in small and large vessel disease. The primary endpoint was the rate of clinically driven target lesion revascularization (TLR) at 9 months.
Results: Patients with small vessel disease had an average reference diameter of 2.45 ± 0.23 mm, while the large vessel group averaged 3.16 ± 0.27 mm. Regarding 9-month major adverse cardiac event (MACE), 5.7% of the patients with small and 6.1% of the patients with large vessels had MACE (p=0.903). Analysis of the individual MACE components revealed a TLR rate of 3.8% in small and 1.0% in large vessels (p=0.200). Of note, no thrombotic events in the DCB treated coronary segments occurred in either group during the 9-month follow-up.
Conclusions: Our data demonstrate for the first time that DCB-only PCI of de novo lesions in large coronary arteries (>2.75 mm) is safe and as effective. Interventional treatment for CAD without permanent or temporary scaffolding, demonstrated a similar efficacy for large and small vessels.