Coronary morphologic findings after stent implantation

Clinical studies demonstrated a reduction of acute complications by high-pressure stenting. This study was performed to correlate the histomorphologic changes of the vessel wall after coronary stenting with stent expansion pressure. We studied the effects of intravital and postmortem stenting on coronary morphology in human hearts. Artifact-free analysis and morphometry of the artery segments' cross section was performed after plastic resin embedding and cutting and grinding sectioning. By comparing intra- and postmortem findings we demonstrated that postmortem stent implantation can serve as an adequate model to study the mechanical effects of coronary stenting. A consistent histologic feature was eccentric stent expansion. Larger calcified areas of the vessel wall were not deformed by implanted stents. The highest degree of vessel injury and deformation was apparent in anatomically "nondiseased" or only slightly fibrotic parts of the arterial wall. Dissections were predominantly located directly adjacent to calcified plaques and appeared as "half-moon"-like tears reaching into the arterial media. A statistically significant stent lumen gain was found when the implantation pressure was increased up to 15 atm. Stent symmetry was not influenced by the applied implantation pressure but depended mostly on local coronary morphology. Thus, increasing implantation pressures during coronary stenting seemed to improve the stenting result up to 15 atm. When applying histomorphologic criteria, the higher pressures (>15 atm) did not cause further optimization of stent expansion. Morphometric analysis of stents implanted postmortemly and intravitally revealed comparable results. Postmortem stenting seems to be an appropriate model for studying stent expansion and stenting results in human coronary arteries.     

Thirty-Day Post-Discharge Outcomes Following COVID-19 Infection

BackgroundThe clinical course of COVID-19 includes multiple disease phases. Data describing post-hospital discharge outcomes may provide insight into disease course. Studies describing post-hospitalization outcomes of adults following COVID-19 infection are limited to electronic medical record review, which may underestimate the incidence of outcomes.ObjectiveTo determine 30-day post-hospitalization outcomes following COVID-19 infection.DesignRetrospective cohort studySettingQuaternary referral hospital and community hospital in New York City.ParticipantsCOVID-19 infected patients discharged alive from the emergency department (ED) or hospital between March 3 and May 15, 2020.MeasurementOutcomes included return to an ED, re-hospitalization, and mortality within 30 days of hospital discharge.ResultsThirty-day follow-up data were successfully collected on 94.6% of eligible patients. Among 1344 patients, 16.5% returned to an ED, 9.8% were re-hospitalized, and 2.4% died. Among patients who returned to the ED, 50.0% (108/216) went to a different hospital from the hospital of the index presentation, and 61.1% (132/216) of those who returned were re-hospitalized. In Cox models adjusted for variables selected using the lasso method, age (HR 1.01 per year [95% CI 1.00–1.02]), diabetes (1.54 [1.06–2.23]), and the need for inpatient dialysis (3.78 [2.23–6.43]) during the index presentation were independently associated with a higher re-hospitalization rate. Older age (HR 1.08 [1.05–1.11]) and Asian race (2.89 [1.27–6.61]) were significantly associated with mortality.ConclusionsAmong patients discharged alive following their index presentation for COVID-19, risk for returning to a hospital within 30 days of discharge was substantial. These patients merit close post-discharge follow-up to optimize outcomes.Supplementary InformationThe online version contains supplementary material available at 10.1007/s11606-021-06924-0.KEY WORDS: COVID-19, mortality, re-admission, discharge     

Efficacy and safety of ticlopidine monotherapy versus ticlopidine and aspirin after coronary artery stenting: follow-up results of a randomized study

A combined antiplatelet treatment with ticlopidine and aspirin has been accepted as standard pharmacological regimen after coronary artery stenting. No data of a randomized trial are available on ticlopidine monotherapy. This prospective, randomized monocenter trial investigates the role of ticlopidine monotherapy versus combined antiplatelet therapy with ticlopidine and aspirin in unselected patients undergoing coronary artery stenting. After successful placement of 378 coronary artery stents, two hundred and forty-three consecutive patients were randomly assigned to receive antiplatelet therapy with 2 x 250 mg ticlopidine (121 patients) or a combination of 2 x 250 mg ticlopidine plus 100 mg aspirin (122 patients) daily. The primary endpoint included the absence of death, cardiac events and vascular access-site complications during the in-hospital phase. Angiographic and clinical assessment was repeated at the 3-month follow-up exam. Two hundred and thirty-seven patients (97.5%) were free from cardiac and non-cardiac events. Stent thromboses were seen in 2 patients of the combined treatment group, while none were observed in the monotherapy group. No statistically significant differences were found between the 2 groups regarding the primary endpoint. Angiography performed in 210 patients (86.4%) at follow-up revealed a restenosis rate of 29.4% in the combined treatment group and 27.8% in the monotherapy group. Monotherapy with ticlopidine is as safe and effective as a combined regimen of ticlopidine plus aspirin after coronary artery stenting in an unselected patient population. These results need to be confirmed in a larger multicenter trial.     

Atherosclerotic carotid arteries - calcification and radio-morphological findings

Summary Objectives: Are there any predictable factors influencing the process of calcification in carotid arteries? Background: The carotid arteries and especially the carotid bifurcation are one of the predisposed regions of atherosclerotic disease. Whether topography of the carotid sinus, flow patterns or different patient characteristics (e.g., diabetes mellitus, age, sex) are a factor determining calcification of atherosclerotic lesion is still hardly understood. Methods: Morphological and morphometrical analysis including radiographic classification of different degrees of calcification on postmortal carotid arteries (90 men and 19 women) and 306 surgical samples after intramural desobliterations of carotid arteries 202 patients with diabetes, 104 patients without diabetes). Results. Most common localization of radiographically identified calcified deposits are the carotid bulb (76%) especially on the lateral wall opposite the flow divider and the internal carotid artery (55%) especially the proximal 1 cm section. No difference in degree of calcification was found when comparing patients with and without diabetes (intermediate calcification in 59% of patients with diabetes and 50% without diabetes). More female patients with diabetes show calcification when compared to the group of patients without diabetes. Females produce calcification in atherosclerotic carotid lesions at an older age compared to male patients. Conclusions: Calcification is a frequent finding in advanced atherosclerotic carotid lesions. There is no difference in regard to degree, pattern of calcification or age distribution when comparing patients with and without diabetes mellitus. Atherosclerotic lesions more frequently found in female patients with diabetes may be due to less vasoprotection by estrogenes.     

Gamma (immune) interferon production by leukocytes from a patient with a TG cell proliferative disease

We report a patient with a disease characterized by proliferation of T cells with Fc receptors for IgG (TG). However, unlike lymphoid cells from normal individuals or from patients with other lymphoid malignancies, the patient's lymphocytes spontaneously produced gamma interferon (IFN-gamma) in vitro. The peripheral lymphocytes consisted of 95% TG cells, which exhibited the morphological characteristics of T- cell chronic lymphocytic leukemia (CLL) and were normal on cytochemical and chromosome analysis. The majority of TG cells were OKT3+, OKT8+, and OKT4-, 3A1-. These cells failed to express suppressor cell activity and displayed depressed levels of natural killer activity, but mediated antibody-dependent cell-mediated cytotoxicity. The spontaneous production of IFN-gamma by human peripheral lymphoid cells as demonstrated in this study may serve as a probe for studying the relationship between IFN-gamma and the proliferation of human T-cell subsets.     

Biochemical and physiological studies of the beta-adrenoceptor and the D-2 dopamine receptor in the intermediate lobe of the rat pituitary gland: a review

The intermediate lobe (IL) of the rat pituitary gland responds to catecholamines. Catecholamines interacting with the beta-adrenoceptor stimulate adenylate cyclase activity, enhance cyclic AMP formation and thereby trigger the release of alpha-melanocyte-stimulating hormone (alpha-MSH). Catecholamines interacting with a D-2 dopamine receptor (in the classification schema of Kebabian and Calne) diminish adenylate cyclase activity and thereby decrease the capacity of IL cells to synthesize cyclic AMP. Dopaminergic agonists also inhibit the release of alpha-MSH from IL cells. The homogeneity of the IL facilitates biochemical investigations of this tissue.     

Essential myosin light chain as a target for caspase-3 in failing myocardium

Programmed cell death involves the activation of caspase proteases that can mediate the cleavage of vital cytoskeletal proteins. We have recently reported that, in failing cardiac myocytes, caspase-3 activation is associated with a reduction in contractile performance. In this study we used a modified yeast two-hybrid system to screen for caspase-3 interacting proteins of the cardiac cytoskeleton. We identified ventricular essential myosin light chain (vMLC1) as a target for caspase-3. By sequencing and site-directed mutagenesis, a noncanonical cleavage site for caspase-3 was mapped to the C-terminal DFVE(135)G motif. We demonstrated that vMLC1 cleavage in failing myocardium in vivo is associated with a morphological disruption of the organized vMLC1 staining of sarcomeres, and with a reduction in myocyte contractile performance. Adenoviral gene transfer of the caspase inhibitor p35 in vivo prevented caspase-3 activation and vMLC1 cleavage, with positive impact on contractility. These data suggest that direct cleavage of vMLC1 by activated caspase-3 may contribute to depression of myocyte function by altering cross-bridge interaction between myosin and actin molecules. Therefore, activation of apoptotic pathways in the heart may lead to contractile dysfunction before cell death.     

Charakteristische Elektrolytveränderungen bei der erblichen Myopathie mit Kardiomyopathie des Syrischen Goldhamsters (Stamm BIO 8262)

Zusammenfassung Bei der erblichen Myopathie und Kardiomyopathie des Syrischen Goldhamsters (Stamm BIO 8262) wurden während verschiedener Lebensabschnitte die Elektrolyte Natrium, Kalium, Kalzium und Magnesium im Serum und mehreren Geweben mit entsprechenden Kontrollen verglichen. Die Elektrolytmessung erfolgte mittels Atomabsorptions-Spektrophotometrie. Als hervorstechendstes Merkmal erwies sich eine hochgradige Kalziumakkumulation in der nekrotisierenden Herz- und Skeletmuskulatur, daneben eine ausgeprägte Natriumerhöhung in der myopathischen Skeletmuskulatur. Die muskuläre Natriumerhöhung wird hauptsächlich auf ein interstitielles Ödem, also eine Folge der Myopathie, bezogen. Dagegen wird die myokardiale sowie muskuläre Kalziumakkumulation als wesentliches Glied im Ablauf der, pathogenetischen Prozesse der Erbkrankheit betrachtet. Sie scheint entscheidend für die Nekrotisierung verantwortlich zu sein.

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Characteristic electrolyte changes in the hereditary myopathy and cardiomyopathy of the Syrian golden hamster (strain BIO 8262)

Summary In hamsters of differing ages suffering from a hereditary myopathy and cardiomyopathy (strain BIO 8262), the electrolytes sodium, potassium, calcium, and magnesium in serum, and several tissues were compared with appropriate controls. The determinations of the electrolytes were performed by atomic absorption spectrophotometry. An enormous accumulation of calcium in the necrotizing heart and skeletal muscle was the noticeable feature besides pronounced elevation of the sodium content in the myopathic skeletal muscle. While the latter refers mainly to an interstitial edema which is a consequence of the myopathy, the calcium accumulation is assumed to be an essential part in the cycle of pathologic events occurring in the hereditary disease: it seems to induce the necrotization.

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Mit 4 Tabellen

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Mit Unterstützung der Deutschen Forschungsgemeinschaft