Ischemic Episodes Research Articles

Cerebellar Infarction: Physiotherapeutic Approach an Overview of Existing Studies

Objectives: Cerebellar infarction is an ischemic or hemorrhagic type episode involving the three main cerebellar arteries. An infarction in each of these arteries causes different but common symptoms, requiring a particularly important contribution of physiotherapy to its treatment. This overview aimed to investigate the effectiveness of physiotherapy programs on the symptoms of patients with cerebellar infarction. Methods: A literature search was performed using eight databases and the keywords, including physiotherapy, physical therapy, rehabilitation, therapeutic exercise, exercise, cerebellar infarct, cerebellar infarction, and cerebellar blockage. The selection process of the final studies was carried out after setting inclusion and exclusion criteria and separately by two reviewers. Results: Out of 1477 initial records, six studies met the inclusion criteria for this overview. Interventions focused on a balance training program and walking training, as opposed to a treadmill training program, seem to improve symptoms in these patients. Also, task-oriented approach was a promising method of rehabilitation. Discussion: Physiotherapy has a beneficial effect on the symptoms of patients with cerebellar infarction and should be considered for the overall recovery of the patient. However, future research is needed due to the small number of studies and to find therapeutically proven forms of intervention.

CHRONIC CEREBRAL ISCHEMIA. MODERN VIEW OF THE PROBLEM

Introduction. Chronic cerebral ischemia (CCI) is considered a syndrome that develops as a result of a slowly progressive reduction in cerebral blood flow. This reduction occurs due to the gradual accumulation of ischemic and secondary degenerative changes in the brain, which are caused by repeated ischemic episodes resulting from the development of atherosclerosis and arterial hypertension. These changes lead to impairment of brain functions, manifested by progressive neurological, neuropsychological, and mental disorders.
 The aim. To analyze the problems of pathogenesis, diagnosis, and treatment of CCI from the sources of modern literature in order to optimize the treatment of this group of patients.
 Materials and methods. Bibliosemantic, comparative and method of system analysis.
 Results. The pathogenetic mechanisms underlying CCI remain controversial due to the heterogeneity of causes and the complexity of the neuropathology associated with the disease. However, one common reason that can be named is dysregulation of cerebral blood flow, that results in chronic cerebral hypoperfusion, which can lead to the development of vascular cognitive impairment and dementia. Detection of biological markers in the patients' blood in combination with neuropsychological testing, neurophysiological (CEP P300, EEG) and neuroimaging (CT, MRI, Doppler Ultrasound of the head and neck) methods, which confirms the morphological substrate of vascular disease (leukoareosis, focal changes, multi-infarct condition, cerebral atrophy) and provides the possibility of choosing an effective pathogenetically-justified treatment.
 Conclusions. The rating of effectiveness of treatment in CCI is complicated considering difficulties in the selection of the efficiency criteria due to the significant differences in the methodology and research formats, as well as problem of a significant medication-related burden in the case of comorbidities. In this regard, the main direction in therapy is combined neuroprotection, which allows to optimize the possibilities of this strategy and to increase its clinical significance in angioneurology.

Heart rate reduction after genetic ablation of L-type Cav1.3 channels induces cardioprotection against ischemia-reperfusion injury.

Acute myocardial infarction (AMI) is the major cause of cardiovascular mortality worldwide. Most ischemic episodes are triggered by an increase in heart rate, which induces an imbalance between myocardial oxygen delivery and consumption. Developing drugs that selectively reduce heart rate by inhibiting ion channels involved in heart rate control could provide more clinical benefits. The Cav1.3-mediated L-type Ca2+ current (ICav1.3) play important roles in the generation of heart rate. Therefore, they can constitute relevant targets for selective control of heart rate and cardioprotection during AMI. We aimed to investigate the relationship between heart rate and infarct size using mouse strains knockout for Cav1.3 (Cav1.3-/-) L-type calcium channel and of the cardiac G protein gated potassium channel (Girk4-/-) in association with the funny (f)-channel inhibitor ivabradine. Wild-type (WT), Cav1.3+/-, Cav1.3-/- and Girk4-/- mice were used as models of respectively normal heart rate, moderate heart rate reduction, bradycardia, and mild tachycardia, respectively. Mice underwent a surgical protocol of myocardial IR (40 min ischemia and 60 min reperfusion). Heart rate was recorded by one-lead surface ECG recording, and infarct size measured by triphenyl tetrazolium chloride staining. In addition, Cav1.3-/- and WT hearts perfused on a Langendorff system were subjected to the same ischemia-reperfusion protocol ex vivo, without or with atrial pacing, and the coronary flow was recorded. Cav1.3-/- mice presented reduced infarct size (-29%), while Girk4-/- displayed increased infarct size (+30%) compared to WT mice. Consistently, heart rate reduction in Cav1.3+/- or by the f-channel blocker ivabradine was associated with significant decrease in infarct size (-27% and -32%, respectively) in comparison to WT mice. Our results show that decreasing heart rate allows to protect the myocardium against IR injury in vivo and reveal a close relationship between basal heart rate and IR injury. In addition, this study suggests that targeting Cav1.3 channels could constitute a relevant target for reducing infarct size, since maximal heart rate dependent cardioprotective effect is already observed in Cav1.3+/- mice.

Indocyanin Green Fluorescence Evaluation of Colonic Perfusion During Elective Open Abdominal Aortic Aneurysm Repair.

Colonic ischaemia is a rare but devastating complication of open aortic aneurysm repair and is associated with high morbidity and a mortality of up to 50%. The aim of this study was to determine the safety and effectiveness of using indocyanin green florescence (ICG) to interrogate colonic perfusion intra-operatively. Prospective observational study. All elective open abdominal aneurysm repairs over a 6month period underwent colonic perfusion interrogation with ICG according to a pre-defined protocol. Patient demographics and imaging findings were recorded prior to surgery. ICG was given just prior to laparotomy closure. Time to florescence was measured from the start of IV administration to surgeon defined maximal florescence of the sigmoid colon. Ten patients fulfilled the inclusion criteria. All patients were male with an average age of 69.7years. Inferior mesenteric artery reimplantation was performed in 5 patients. Median colonic fluorescence time was 58s. No complications related to ICG were identified. A single patient had clinical concern of colonic ischaemia and delayed perfusion (>3min) on ICG; colorectal opinion advised not for immediate resection. At relook laparotomy, ischaemic colon at the area of demarcation was noted and a Hartmann's procedure was performed. No other patients had delayed perfusion and no further episodes of colonic ischaemia were noted. IMA reimplantation did not show statistical difference in colonic ICG time (P = .81, 95% CI -1.98 to 2.45). There was no statistical difference between operating times between the cohort and all repairs performed 6 months before the data collection (P = .59, 95% CI -.73 to 1.24). In this pilot study ICG appears to be a safe and useful adjunct in objective assessment of colonic perfusion during open AAA repair. Further research is required to fully determine its role in this cohort of patients.

A Model of Ischaemia-Induced Renal Interstitial Fibrosis in Mice with Established Diabetes

ABSTRACT Background: Diabetes is a well-established clinical risk factor for the development of acute kidney injury (AKI) following an episode of renal ischaemia. However, we lack a robust animal model to investigate the pathological mechanisms underpinning the increased susceptibility of the diabetic kidney to ischaemia-induced AKI and the transition to chronic kidney disease. The aim of this study was to develop a mouse model in which renal ischaemia induces renal interstitial fibrosis in diabetic mice, but not in control mice. Methods: C57BL6/J mice were made diabetic via 5 low dose streptozotocin injections. 8 weeks later, diabetic mice underwent 12 min of bilateral renal ischaemia and were killed on days 1, 7 or 28 after reperfusion. For comparison, groups of age-matched non-diabetic mice underwent the same renal ischaemia/reperfusion injury (IRI) protocol. Results: Non-diabetic mice developed AKI on day 1 which showed a virtually complete recovery of structure and function by day 7. By contrast, diabetic mice exhibited a state of chronic renal inflammation and developed a much more severe AKI on day 1 after IRI. Diabetic mice showed a marked delay in the repair response on day 7, and exhibited chronic tubular damage, inflammation and robust interstitial fibrosis on day 28. Conclusion: We have developed a mouse model suitable for the dissection of the mechanisms by which diabetes makes the kidney highly susceptible to an ischaemic insult and the transition to chronic kidney disease.

Features of the course of stable exertional angina against the background of iron deficiency anemia in outpatient practice

Introduction. Iron-deficiency accompanies many diseases, including cardiovascular pathology, so timely diagnosis and correction of this condition is necessary. Aim. To study the features of the course of stable exertional angina against the background of iron deficiency anemia before and after correction with iron (III) polymaltose hydroxide in patients in primary health care using a computerized patient register. Materials and methods. 1210 patients with stable exertional angina aged 50–85 years (309 men, 901 women) were included. A special computer program was created for data analysis. In 500 out of 1210 patients, IDA was detected (385 women, 115 men). Mild anemia – 410 patients, moderate – 75, severe – 15. The main group – patients with stable exertional angina and Irondeficiency anemia (the first subgroup – patients treated with iron (III) polymaltose hydroxide and the second subgroup – patients who did not receive the drug iron (III) polymaltose hydroxide due to refusal of treatment or contraindications) and the control group – patients with stable exertional angina without Iron-deficiency anemia. All patients received standard therapy recommended for the treatment of stable exertional angina (the main group additionally received iron (III) polymaltose hydroxide). Results. In the first subgroup of the main group, after treatment with iron (III) hydroxide polymaltose, there was a statistically significant increase in hemoglobin levels by 11,7%, hematocrit by 5%, erythrocytes by 4%, serum iron by 112,8%, and an improvement in exercise tolerance by 48,7%, episodes of ST segment depression by 30,2%. In the second subgroup and the control group, there were no significant changes in the above parameters. Conclusion. Iron-deficiency anemia contributes to the severe course of stable exertional angina, which is confirmed by the high frequency of III-IV functional class exertional angina, a decrease in tolerance to exercise stress. Correction of Iron-deficiency anemia reduces the frequency of episodes of transient myocardial ischemia in the main group.

SILENT MYOCARDIAL ISCHEMIA IN PATIENTS WITH ACUTE CORONARY SYNDROME AND DIABETES MELLITUS

ST-segment elevation myocardial infarction, stenting of the infarct-related coronary artery, silent (painless) myocardial ischemia, diabetes mellitus, 24-hour electrocardiographic monitoring.
 Introduction. Currently, approximately 422 million people in the world have diabetes mellitus, and over 1.3 million individuals in Ukraine are diagnosed with diabetes mellitus. Diabetic neuropathy is known to contribute to the development of atypical and painless variants of ischemic heart disease in individuals with diabetes. This poses a challenge for timely diagnosis and obscures the course of ischemic heart disease, as the prevalence of silent myocardial ischemia is significantly high in these patients. Therefore, the aim of this study is to investigate the occurrence of myocardial ischemia episodes in patients with ST-elevation myocardial infarction within the first day following stenting of the infarct-related coronary artery. Furthermore, we aimed to demonstrate the painless nature of these episodes in the presence of type 2 diabetes mellitus through a clinical case presentation.
 Materials and methods. 30 patients with ST-segment elevation myocardial infarction were examined, and 24-hour electrocardiographic monitoring was performed during the first day after the infarct-related coronary artery stenting. Results. Episodes of transient myocardial ischemia were registered in 50% of people. We found that the majority of episodes (80%) were painless. In the presence of diabetes mellitus, only episodes of painless myocardial ischemia were noted that is supported by the example of a clinical case. The study highlighted the informativeness of 24-hour electrocardiographic monitoring in identifying episodes of myocardial ischemia, particularly in its painless variant. The results demonstrate that patients with ST-elevation myocardial infarction (STEMI) experience episodes of transient myocardial ischemia within the first day after coronary artery stenting, with a majority of these episodes being painless. Furthermore, in the presence of diabetes mellitus, ischemic episodes tend to be painless. Therefore, 24-hour electrocardiographic monitoring serves as a valuable method for the detection of myocardial ischemia.

C41 CAROTID OCCLUSION AT THE CAROTID SIPHON LEVEL IN A CHILD WITH PROGERIA

Abstract Introduction Hutchinson–Gilford Progeria syndrome (HGPS) is a rare disease affecting 1 in 4–8 million children, caused by a sporadic mutation of the LMNA gene and expression of a mutant product called progerin. Patients develop a progressive and severe premature aging disease characterized by failure to thrive, alopecia, bone and joint abnormalities, loss of subcutaneous fat, and severe atherosclerosis. Patients live an average of 14.6 years, and most die in their early teens from myocardial infarction or stroke due to rapidly progressive atherosclerosis. Clinical case The 8–year–old patient, affected by progeria, arrived for relapsing strokes. The clinical history began with a picture of severe acro–mandibular hypoplasia with obstruction of the upper airways, treated with early tracheostomy and subsequent percutaneous gastrostomy. Further progeroid phenotypic characters developed were: poor body growth, sui generis facies with prominent eyes and beaked nose, alopecia, micrognathia, discolored, thin, hypoelastic skin; poorly represented panniculus adiposus; scoliosis. Genetic tests have highlighted two pathogenic heterozygous mutations, of the LMNA gene (C.168 C>A) probably deriving from the mother (mosaicism), and the other of the ZMPSTF24 gene, (c.846 C>T) paternally inherited. The major complications are secondary to severe atherosclerosis of the cerebral district, resulting in repeated strokes. Brain MRA (Fig.1 and 2) documented the absence of signal at the level of the right carotid siphon and of the whole intracranial tract of the right carotid artery and poor signal in correspondence with the intracranial tract of the left carotid artery distal to the carotid siphon in a picture of diffuse atherosclerosis. The marked predisposition and the recurrence of ischemic episodes required the patient to have thrombophilic screening, positive for a heterozygous mutation for the prothrombin gene (G20210A), known for thrombophilic predisposition. Conclusions Progeria is a rare syndrome that requires an adequate multidisciplinary approach and clinical care management aimed at improving the quality of life of our patients.

Distal perfusion cannula on VA-ECMO: do not blindly trust! A case report

Distal perfusion cannulas, DPCs, are increasingly used to prevent limb ischemia, frequent and potentially serious complication on peripheral veno-arterial extracorporeal membrane oxygenation (V-A ECMO) support. We report the case of a patient treated with femoro-femoral V-A ECMO who developed a sudden, significant asymmetric decrease in cannulated limb regional oxygen saturation, rSO2, signal, despite the presence of a DPC. This finding, noticed within 6 hours after the implementation of extracorporeal cardiopulmonary resuscitation (ECPR) in a patient experiencing refractory intra-hospital cardiac arrest (IHCA), suggested ongoing limb ischemia. After careful monitoring, a clot was detected in the line supplying DPC, which appeared completely kinked at dressing removal. Line patency and reperfusion were promptly re-established. No additional ischemic episodes occurred, and the patient was successfully weaned from extracorporeal support, and experienced full functional recovery, with no sensory or motor deficit. This case highlights the strict need for a careful, continuous monitoring of limb perfusion during V-A ECMO, even if limb perfusion through DPC is implemented, in order to prevent severe limb complications, negatively impacting on outcome.

Transcriptome analysis reveals ADAMTS15 is a potential inflammation-related gene in remote ischemic postconditioning.

Remote ischemic postconditioning (RIPostC) induced by brief episodes of the limb ischemia is a potential therapeutic strategy for myocardial ischemia/reperfusion injury, achieved by reducing cardiomyocyte death, inflammation and so on. The actual mechanisms underlying cardioprotection conferred by RIPostC remain unclear. Exploring gene expression profiles in myocardium at transcriptional level is helpful to deepen the understanding on the cardioprotective mechanisms of RIPostC. This study aims to investigate the effect of RIPostC on gene expressions in rat myocardium using transcriptome sequencing. Rat myocardium samples from the RIPostC group, the control group (myocardial ischemia/reperfusion group) and the sham group were performed transcriptome analysis using RNA sequencing. The levels of cardiac IL-1β, IL-6, IL-10 and TNFα were analyzed by Elisa. The expression levels of candidate genes were verified by qRT-PCR technique. Infarct size was measured by Evans blue and TTC staining. Apoptosis was assessed by TUNEL assays and caspase-3 levels were detected using western blotting. RIPostC can markedly decrease infarct size and reduce the levels of cardiac IL-1β, IL-6 and increase the level of cardiac IL-10. This transcriptome analysis showed that 2 genes were up-regulated (Prodh1 and ADAMTS15) and 5 genes (Caspase-6, Claudin-5, Sccpdh, Robo4 and AABR07011951.1) were down-regulated in the RIPostC group. Go annotation analysis showed that Go terms mainly included cellular process, metabolic process, cell part, organelle, catalytic activity and binding. The KEGG annotation analysis of DEGs found only one pathway, amino acid metabolism, was up-regulated. The relative mRNA expression levels of ADAMTS15, Caspase-6, Claudin-5 and Prodh1 were verified by qRT-PCR, which were consistent with the RNA-seq results. In addition, the relative expression of ADAMTS15 was negatively correlated with the level of cardiac IL-1β (r = -0.748, P = 0.005) and positively correlated with the level of cardiac IL-10 (r = 0.698, P = 0.012). A negative correlation statistical trend was found between the relative expression of ADAMTS15 and the level of cardiac IL-6 (r = -0.545, P = 0.067). ADAMTS15 may be a potential inflammation-related gene in regulation of cardioprotection conferred by remote ischemic postconditioning and a possible therapeutic target for myocardial ischemia reperfusion injury in the future.

Study of the Efficacy of Ischemia Reversal Program along with Restricted Diet in an Elderly Myocardial Ischemic Patient with a Known History of Hypertension - A Case Study

The biggest global cause of morbidity and mortality, according to the World Health Organization, are cardiovascular diseases (CVDs). Consequently, there is a need for new therapeutic modalities that will complement current CVD care tools. To evaluate the effectiveness of the Ischemia Reversal Program along with a restricted diet in an elderly myocardial ischemic patient with other comorbidities like Hypertension (HTN) and Hypokinesia. 60-year-old male had a myocardial ischemia episode in April 2020 and received standard allopathic medical care. The patient had a history of HTN. This patient opted for Ischemia Reversal Program (IRP) and dietary modification with Ayurveda-based medicines as an add-on complementary treatment to accelerate the healing process. The patient had elevated HTN (SBP/DBP: 123/74) according to the ambulatory blood pressure monitoring (ABMP) report which was reduced post-intervention (SBP/DBP: 109/66). The patient also showed hypokinetic anterior wall LV according to the 2D ECHO report while the post-intervention 2D ECHO report showed no regional wall motion abnormality. Findings of our study suggest that IRP which includes Ayurveda-based Panchakarma therapy along with dietary modifications can serve as treatment for patients with myocardial ischemia and other comorbidities like HTN, and hypokinesia.

Detection of brief atrial fibrillation in continuous 12-lead ECG recordings using an algorithm for computerized resting ECG interpretation combined with convolutional neural network for reducing false detections

Existing criteria recommended by ACC/ESC for identifying patients with ST elevation myocardial infarction (STEMI) from the 12-lead ECG perform with high specificity (SP), but low sensitivity (SE). In our previous studies, we found that the SE of ischemia detection can be markedly improved without any loss of SP by calculating, from the 12-lead ECG, ST deviation in 3 “optimal” vessel-specific leads (VSLs). Our original VSLs, based on ΔST body-surface potential maps (BSPMs), have been modified by using the more appropriate J-point BSPMs at peak ischemia (without subtraction of pre-occlusion distributions). The aim of the present study was to compare the performance of these new VSLs with that achieved by the STEMI criteria used in current practice.Two independent datasets of 12-lead ECGs were used: the STAFF III dataset acquired during ischemic episodes caused by balloon inflation in LAD (n = 35), RCA (n = 47), and LCx (n = 17) coronary arteries, and the Glasgow dataset comprising admission 12-lead ECGs of 116 patients who were hospitalized for chest pain and underwent contrast-enhanced cardiac MRI that confirmed AMI in 58 patients (50%).We found that, in the STAFF III dataset, the detection of ischemic state by the STEMI criteria attained SE/SP of 60/97%, whereas SE/SP values of VSLs were 72/98%. In the Glasgow dataset, STEMI criteria yielded SE/SP of 43/98%, whereas the VSLs improved SE/SP to 60/98%. The most significant increase in diagnostic performance appeared in patients with LCx coronary artery occlusion: in STAFF III data (n = 17) SE achieved by STEMI criteria was improved by the VSLs from 35% to 71%; in Glasgow data (n = 12) SE of 31% achieved by STEMI criteria was improved by the VSLs to 69%.In our study population, existing ACC/ESC STEMI criteria complemented by the new VSLs yielded much improved sensitivity of ischemia detection without any detrimental effect on specificity. This finding needs to be corroborated on a larger chest-pain patient population with typical prevalence of acute ischemia presented to the emergency rooms.

ESTIMATION OF ACUTE KIDNEY INJURY AND DYSELECTROLYTEMIA IN ASPHYXIATED NEWBORNS - A SINGLE CENTRE STUDY

Background: In babies with perinatal asphyxia, hypoxia and ischemia can cause damage to almost every tissue and organ of the body and kidneys are one of the most commonly affected organs. Renal insufciency may occur within 24 hours of a hypoxic ischemic episode leading to variable degree of kidney injury. Serum electrolyte levels are also found to be signicantly affected in perinatal asphyxia.Aims & Objective: Estimation of acute kidney injury and its correlation with severity of perinatal asphyxia and assess electrolyte imbalance in term neonates with perinatal asphyxia. Materials and Methods: It is a prospective observational study conducted at a tertiary care centre during the study period. Renal parameters and serum electrolytes of asphyxiated newborns were evaluated and kidney injury was classied on the basis of AKIN criteria. Results: Among 175 newborns with perinatal asphyxia, 29.7% had HIE1, 14.3% of them developed HIE 3 while maximum of them (56%) had HIE stage 2. It was observed that 38.3% of the enrolled babies developed acute kidney injury. 14.9 % of cases had stage 1 AKI, stage 2 acute kidney injury was found in 16.6 % of cases and stage 3 acute kidney injury developed in 6.8 % of cases. Among total babies, 77.1% of the babies had hyponatremia while 9.7% of the babies had hyperkalemia. Out of 160 babies who were followed till outcome, 90% discharged while 10% of them died. Conclusion: Perinatal asphyxia is an important cause of renal dysfunction which plays an important role in mortality and morbidity of the asphyxiated newborn. Early diagnosis and management of AKI in babies with perinatal asphyxia can improve their outcome. Electrolyte disturbance in the form of hyponatremia and hyperkalemia is also an important derangement in babies with birth asphyxia which needs accurate and careful management for better outcome.

Asymptomatic Moyamoya Disease: An experience from Eastern India (P14-5.011)

<h3>Objective:</h3> <i>This study was undertaken to clarify the clinic-radiological characteristics and prospective follow-up of apparently “asymptomatic” MMA, if it is truly asymptomatic or not.</i> <h3>Background:</h3> <i>“Asymptomatic” Moyamoya Angiopathy (MMA) has been defined as absence of ischemic or hemorrhagic episodes in MMA patients. An ambiguous definition has led to its variable adaptation in the limited studies in the past.</i> <h3>Design/Methods:</h3> <i>Of the 122 angiographically proven MMA in our center over last 6 years, 6 patients had an initial diagnosis of “asymptomatic” MMA following evaluation by atleast one post-graduate doctor. These 6 cases were then further scrutinized by 3 different neurologists for epidemiological, clinical, radiological characteristics and subsequent follow-up. Data were analyzed using descriptive statistics.</i> <h3>Results:</h3> <i>The mean age at diagnosis was 23.7±13.14 years. 3 of the 6 patients had undergone brain imaging for evaluation of non-migraine-like headache, 1 for dizziness, 2 as a part of familial screening for MMA. 4 of the 6 patients had specific triggers for aggravation of symptoms. Brain imaging revealed old vascular insults and ivy sign in 5 of 6 patients(83.3%), cerebral microbleeds in 1 of 6 patients(16.7%), and mean suzuki staging3.6±0.82. 4 of the 6 patients who underwent cerebral perfusion study, all having hypoperfusion. Revascularization surgery was done in 2 of the 6 patients, rest were managed conservatively. None of the patients had any new onset neurological deficit or radiological progression over a mean follow-up period of 22.3±20.22 months.</i> <h3>Conclusions:</h3> <i>Subtle “paroxysmal events” often precipitated by specific triggers might be indicative of transient cerebral hypoperfusion in an apparently “asymptomatic” MMA and are likely indicative of ischemic symptoms, and warrants for a more precise definition to avoid misclassification of “asymptomatic” MMA.</i> <b>Disclosure:</b> Dr. Das has nothing to disclose. Souvik Dubey has nothing to disclose. Dr. Ray has nothing to disclose.

Chronic troponin elevation assessed by myocardial T1 mapping in patients with stable coronary artery disease.

Cardiac troponin detected with sensitive assays can be chronically elevated, in the absence of unstable coronary syndromes. In patients with chronic coronary artery disease, clinically silent ischemic episodes may cause chronic troponin release. T1 mapping is a cardiovascular magnetic resonance technique useful in quantitative cardiac tissue characterization. We selected patients with anatomically and functionally normal hearts to investigate associations between chronic troponin release and myocardial tissue characteristics assessed by T1 mapping. We investigated the relationship between cardiac troponin I concentrations and cardiovascular magnetic resonance T1 mapping parameters in patients with stable coronary artery disease enrolled in MASS V study before elective revascularization. Participants had no previous myocardial infarction, negative late gadolinium enhancement, normal left ventricular function, chamber dimensions and wall thickness. A total of 56 patients were analyzed in troponin tertiles: nativeT1 and extracellular volume (ECV) values (expressed as means ± standard deviations) increased across tertiles: nativeT1 (1006 ± 27 ms vs 1016 ± 27 ms vs 1034 ± 37 ms, ptrend = 0.006) and ECV (22 ± 3% vs 23 ± 1.9% vs 25 ± 3%, ptrend = 0.007). Cardiac troponin I concentrations correlated with native T1(R = 0.33, P = .012) and ECV (R = 0.3, P = .025), and were independently associated with nativeT1 (P = .049) and ventricular mass index (P = .041) in multivariable analysis. In patients with chronic coronary artery disease and structurally normal hearts, troponin I concentrations correlated with T1 mapping parameters, suggesting that diffuse edema or fibrosis scattered in normal myocardium might be associated with chronic troponin release.

ГЕМОРЕОЛОГИЯ И ГЕЛИОГЕОФИЗИЧЕСКАЯ ВОЗМУЩЕННОСТЬ: СОВРЕМЕННОЕ СОСТОЯНИЕ ВОПРОСА (ОБЗОР)

There are quite a lot of scientific works that reveal some aspects of the heliogeophysical factors’s influence on the state of the rheological properties of human blood. Nevertheless, the study of the mechanisms of such influence remains open, which is associated with the difficulty of reproducing laboratory experiments, the heterogeneity and short duration of the analyzed time series of medical and biological data, as well as the interdisciplinarity of this area. The aim of this review is to analyze current research results and new original approaches to studying this issue. The results of studies published in the PubMed, Cyberleninka and eLibrary databases for the period from 1990-2021 were devoted to the study of the influence of heliogeophysical disturbances on the state of human hemorheology, and also this data was analyzed. The analysis of the literature showed a connection between heliogeophysical disturbance and the development of hemocoagulation disorders of humans, a tendency to an increase in the degree of platelet aggregation and an acceleration of the onset of thrombosis, a deterioration in the state of the microvasculature, which is most pronounced among people with diseases of the cardiovascular system. In patients with coronary artery disease, the same type of reactions was revealed, expressed by an increase in coagulation, there were heart rhythm disorders and the appearance of episodes of myocardial ischemia.

Efficacy, Safety, and Role of Antiplatelet Drugs in the Management of Acute Coronary Syndrome: A Comprehensive Review of Literature.

Acute coronary syndrome (ACS) is a complex condition characterized by myocardial ischemia or infarctionwhich can lead to significant morbidity and death. Antiplatelet drugs play a crucial role in the management of ACS and have been shown to minimize the incidence of significant adverse cardiovascular events and recurrent myocardial infarction (MI). This comprehensive literature review is intended to summarize current information on the effectiveness, safety, and function of frequently used antiplatelet medications in treating ACS. Aspirin, clopidogrel, prasugrel, ticagrelor, abciximab, tirofiban, dipyridamole, cilostazol, and novel antiplatelets are included in the review. Aspirin's effectiveness as a first-line antiplatelet medication in ACS is well established. It has significantly lowered the risk of serious adverse cardiovascular events. Clopidogrel, prasugrel, and ticagrelor are P2Y12 receptor inhibitors found to lower the incidence of recurrent ischemia episodes in ACS patients. Using glycoprotein IIb/IIIa inhibitors such as abciximab, tirofiban, and eptifibatide is effective in managing ACS, especially in high-risk patients. Dipyridamole effectively reduces the risk of recurrent ischemic events in patients with ACS, particularly when used with aspirin. Cilostazol, a phosphodiesterase III inhibitor, has also been shown to reduce the risk of major adverse cardiovascular events (MACE) in patients with ACS. Antiplatelet drugs' safety in managing ACS has also been well established. Aspirin is generally well-tolerated with a low risk of adverse effects, although the risk of bleeding events, particularly gastrointestinal bleeding, cannot be eliminated. The P2Y12 receptor inhibitors have been associated with a small increase in the risk of bleeding events, particularly in patients with a high risk of bleeding. The glycoprotein IIb/IIIa inhibitors are associated with a higher risk of bleeding than other antiplatelet drugs, especially in high-risk patients. To summarize, antiplatelet drugs play a crucial role in the management of ACS, and the efficacy and safety of these drugs have been well-established in the literature. The choice of antiplatelet drugs will depend on the patient's risk factors, including age, comorbidities, and bleeding risk. The novel antiplatelets may offer new therapeutic options for managing ACS, and further studies are needed to determine their role in managing this complex condition.

Post-stroke periodic estrogen receptor-beta agonist improves cognition in aged female rats

Women have a higher risk of having an ischemic stroke and increased cognitive decline after stroke as compared to men. The female sex hormone 17β-estradiol (E2) is a potent neuro- and cognitive-protective agent. Periodic E2 or estrogen receptor subtype-beta (ER-β) agonist pre-treatments every 48 h before an ischemic episode ameliorated ischemic brain damage in young ovariectomized or reproductively senescent (RS) aged female rats. The current study aims to investigate the efficacy of post-stroke ER-β agonist treatments in reducing ischemic brain damage and cognitive deficits in RS female rats. Retired breeder (9–10 months) Sprague–Dawley female rats were considered RS after remaining in constant diestrus phase for more than a month. The RS rats were exposed to transient middle cerebral artery occlusion (tMCAO) for 90 min and treated with either ER-β agonist (beta 2, 3-bis(4-hydroxyphenyl) propionitrile; DPN; 1 mg/kg; s.c.) or DMSO vehicle at 4.5 h after induction of tMCAO. Subsequently, rats were treated with either ER-β agonist or DMSO vehicle every 48 h for ten injections. Forty-eight hours after the last treatment, animals were tested for contextual fear conditioning to measure post-stroke cognitive outcome. Neurobehavioral testing, infarct volume quantification, and hippocampal neuronal survival were employed to determine severity of stroke. Periodic post-stroke ER-β agonist treatment reduced infarct volume, improved recovery of cognitive capacity by increasing freezing in contextual fear conditioning, and decreased hippocampal neuronal death in RS female rats. These data suggest that periodic post-stroke ER-β agonist treatment to reduce stroke severity and improve post-stroke cognitive outcome in menopausal women has potential for future clinical investigation.

The accumulated oxygen deficit as an indicator of the ischemic retinal insult

We here attempt to improve quantification of the ischemic retinal insult, that is, what is imposed on the retinal tissue by ischemia, especially in experimental models of ischemia. The ischemic retinal insult initiates the ischemic retinal injury (or outcome). Accordingly, it is reasonable to assume that the better the quantification of the insult, the better the correlation with, and thereby estimation of, the injury. The insult seldom has been quantified in terms of the relevant physiological factors, especially in connection with the rate of oxygen delivery (DO2). We here propose the accumulated oxygen deficit (AO2D) as an indicator of the ischemic retinal insult. We hypothesized that AO2D is correlated with the rate of oxygen metabolism measured 1 h after reperfusion following an episode of ischemia (MO2_1_Hr). Previously, we showed that MO2_1_Hr is related to the electroretinogram amplitude and the retinal thickness when they are measured seven days after reperfusion. We studied 27 rats, as well as 26 rats from our published data on retinal ischemia in which we had measurements of DO2 and duration of ischemia (T) of various levels and durations. We also measured DO2 in 29 rats treated with sham surgery. Ischemia was induced by either ipsilateral or bilateral common carotid artery occlusion or by ophthalmic artery occlusion, which gave a wide range of DO2. DO2 and MO2_1_Hr were evaluated based on three types of images: 1) red-free images to measure vessel diameters, 2) fluorescence images to estimate blood velocities by the displacement of intravascular fluorescent microspheres over time, and 3) phosphorescence images to quantify vascular oxygen tension from the phosphorescence lifetime of an intravascular oxygen sensitive phosphor. Loss of oxygen delivery (DO2L) was calculated as the difference between DO2 under normal/sham condition and DO2 during ischemia. AO2D, a volume of oxygen, was calculated as the product DO2L and T. Including all data, the linear relationship between AO2D and MO2_1_Hr was significant (R2 = 0.261, P = 0.0003). Limiting data to that in which T or DO2L was maximal also yielded significant relationships, and revealed that DO2L at a long duration of ischemia contributed disproportionately more than T to MO2_1_Hr. We discuss the potential of AO2D for quantifying the ischemic retinal insult, predicting the ischemic retinal injury and evaluating the likelihood of infarction.

A clinical case of anosognosia in a CADASIL disease.

IntroductionCADASIL (Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy) is a cerebrovascular disease, tht appears in 1.98/100,000. It´s caused by a mutation of the Notch3 gene and is characterized by accumulation of granular osmiophilic material in the middle layer of the small and median sized cerebral arteries.Sypmtoms are migraine, recurrent cerebral ischemic episodes, dementia, neuropsychiatric disorders (anosognosia, character disorders, apathy and cognitive impairment). It usually appears between 30-60 years, although there is an important variability. There is no curative treatment, only palliative.ObjectivesClinical review of anosognosia and its presence in CADASIL disease.MethodsClinical case and literatura review.ResultsWe presented the clinical case of a 68-year-old man, who was diagnosed with CADASIL after a stroke 3 years earlier. In his family, his brother was diagnosed also with CADASIL. The patient had previously presented disturbances in impulse control (hyperorality) and important executive failures. He currently presented anosognosia, deficits in verbal memory, spatial perception and executive functions, in addition to behavioral alterations and apathy. Due to these deficits he was prohibited from certain activities (driving, hunting).The patient was not aware of these deficits and becouse of his “no knowledge of his illness”, he disagreed with these prohibitions, so he showed rage and anger at the impotence of not understanding why certain actions are prohibited.In the consultation, mnesic errors and in naming objects were also objectified, for which it was recommended to carry out cognitive stimulation on a daily basis. In addition, he presented failures of sphincter incontinence, especially of urine and occasionally also of the anal sphincter. He had previously had episodes of myoclonus or fasciculations.A genetic study by massive sequencing confirmed the heterozygous presence of the pathogenic variant c.1819C&gt;T p.(Arg607Cys) in the NOTCH3 gene, a CADASIL disease.ConclusionsThe anosognosia that many patients with CADASIL disease present constitutes a problem because it contributes to the delay in consultation and, therefore, the delay in the adequate diagnostic approach, therapeutic possibilities and family genetic counseling. Due in part to anosognosia, CADASIL is considered an underdiagnosed entity. Due to the lack of awareness and the consequent lack of recognition of the deficit, these people are often seen as stubborn and difficult to deal with by people in their immediate environment.In addition, there is general difficulty in the rehabilitation process, since patients do not think the neccesity to be treated. This can generate frustration and despair both in their relatives and in the health personnel.For all these reasons, both in anosognosia and in CADASIL disease, adequate psychological support is needed for both those affected and their families.Disclosure of InterestNone Declared