Ischemic Episodes Research Articles

(270) LISWT Before Penile Prosthesis Implantation Might Facilitate Dilation of Fibrotic Corpora

Abstract Introduction Severe corporeal fibrosis presents significant challenges in penile implant insertion. LISWT studies in rats and humans have suggested its ability to rejuvenate cavernous bodies through various mechanisms and growth factors. Objective This prompted our evaluation of LISWT's effectiveness in facilitating prosthesis implantation in patients with penile fibrosis, which are typically considered difficult cases. Methods A 34-year-old male smoker with a history of sickle cell disease, bilateral hip replacements, and splenectomy due to sickle cell crisis sought penile prosthesis implantation. He presented with severe erectile dysfunction and corporeal fibrosis following two ischemic priapism episodes caused by sickle cell disease, which were treated with distal shunts 4 and 1 years prior, respectively (Fig. 1). After obtaining consent, the patient underwent four cycles of LISWT, spaced one month apart. Each cycle consisted of four weekly sessions using the PiezoWave2 device from Richard WOLF with settings of 0.16mj/mm2 energy flux density, 6Hz frequency, and 10mm wave focus penetration depth. In each session, the patient received a total of 6000 shocks, distributed between the perineum, dorsum penis, and the lateral aspect of the penis. Results A month post-LISWT, the patient's Erection Hardness Score (EHS) improved from 0 to 1 following an intracavernous injection of 20 mcg of alprostadil (Fig. 2). Subsequently, he underwent a malleable penile implant procedure through the penoscrotal approach. Cavernosal dilation was successful up to 10mm using a Hegar dilator, with bilateral corporal measurements of 8cm proximally and 9cm distally. A Tactra malleable penile prosthesis (9.5mm girth and 17cm length) from Boston Scientific was implanted without complications (Fig. 3.A.B) Conclusions In cases of severe corporeal fibrosis, pre-treatment with LISWT may aid in the dilation of the corpora during penile prosthesis implantation, potentially reducing complications. Randomized studies are warranted to validate this indication Disclosure No.

A Look at the Etiology of Alzheimer's Disease based on the Brain Ischemia Model.

Alzheimer's disease (AD) is the frequent form of dementia in the world. Despite over 100 years of research into the causes of AD, including amyloid and tau protein, the research has stalled and has not led to any conclusions. Moreover, numerous projects aimed at finding a cure for AD have also failed to achieve a breakthrough. Thus, the failure of anti-amyloid and anti-tau protein therapy to treat AD significantly influenced the way we began to think about the etiology of the disease. This situation prompted a group of researchers to focus on ischemic brain episodes, which, like AD, mostly present alterations in the hippocampus. In this context, it has been proposed that cerebral ischemic incidents may play a major role in promoting amyloid and tau protein in neurodegeneration in AD. In this review, we summarized the experimental and clinical research conducted over several years on the role of ischemic brain episodes in the development of AD. Studies have shown changes typical of AD in the course of brain neurodegeneration post-ischemia, i.e., progressive brain and hippocampal atrophy, increased amyloid production, and modification of tau protein. In the post-ischemic brain, the diffuse and senile amyloid plaques and the development of neurofibrillary tangles characteristic of AD were revealed. The above data evidently showed that after brain ischemia, there are modifications in protein folding, leading to massive neuronal death and damage to the neuronal network, which triggers dementia with the AD phenotype.

Incidence and patterns of atrial fibrillation after catheter ablation of typical atrial flutter-the FLUTFIB study.

In patients with atrial flutter (AFL), ablation of the cavotricuspid isthmus (CTI) is a highly effective procedure to prevent AFL recurrence, but atrial fibrillation (AF) may occur during follow-up. The presented FLUTFIB study was designed to identify the exact incidence, duration, timely occurrence, and associated symptoms of AF after CTI ablation using continuous cardiac monitoring via implantable loop recorders. One hundred patients with AFL without prior AF diagnosis were included after CTI ablation (mean age 69.7 ± 9.7 years, 18% female) and received an implantable loop recorder for AF detection. After a median follow-up of 24 months 77 patients (77%) were diagnosed with AF episodes. Median time to first AF occurrence was 180 (43-298) days. Episodes lasted longer than 1 h in most patients (45/77, 58%). Forty patients (52%) had AF-associated symptoms.Patients with and without AF development showed similar baseline characteristics and neither HATCH- nor CHA2DS2-VASc scores were predictive of future AF episodes. Oral anticoagulation (OAC) was stopped during FU in 32 patients (32%) and was re-initiated after AF detection in 15 patients (15%). No strokes or transient ischaemic attack episodes were observed during follow-up. This study represents the largest investigation using implantable loop recorders (ILRs) to detect AF after AFL ablation and shows a high incidence of AF episodes, most of them being asymptomatic and lasting longer than 1 h. In anticipation of trials determining the duration of AF episodes that should trigger OAC initiation, these results will help to guide anticoagulation management after CTI ablation.

RNF213 in moyamoya disease: Genotype-phenotype association and the underlying mechanism.

Moyamoya disease (MMD) is a cerebrovascular disorder characterized by a steno-occlusive internal carotid artery and compensatory vascular network formation. Although the precise pathogenic mechanism remains elusive, genetic association studies have identified RNF213 as the principal susceptibility gene for MMD, with the single nucleotide polymorphism p.R4810K recognized as the founder variant predominantly in the Asian populations. Distinct genotype-phenotype correlations are observable in RNF213-related MMD. The clinical manifestations linked to p.R4810K bear commonalities within Asian cohort, including familial predisposition, earlier age of onset, ischemic episodes, and involvement of the posterior cerebral artery (PCA). However, despite these shared phenotypic characteristics, there is significant heterogeneity in RNF213-related MMD presentations. This diversity manifests as variations across ethnic groups, inconsistent clinical symptoms and prognosis, and occurrence of other vasculopathies involving RNF213. This heterogeneity, in conjunction with the observed low disease penetrance of RNF213 mutations, suggests that the presence of these mutations may not be sufficient to cause MMD, underscoring the potential influence of other genetic or environmental factors. Although the current research might not have fully identified these additional contributors, experimental evidence points toward the involvement of RNF213 in angiogenesis, lipid metabolism, and the immune response. Future research is required to unveil the molecular mechanisms and identify the factors that synergize with RNF213 in the pathogenesis of MMD.

Inhibition of NOX2 or NLRP3 inflammasome prevents cardiac remote ischemic preconditioning.

Introduction: Short episodes of ischemia-reperfusion (IR) in the heart (classical ischemic preconditioning, IPC) or in a limb (remote ischemic preconditioning, RIPC) before a prolonged ischemic episode, reduce the size of the infarct. It is unknown whether IPC and RIPC share common mechanisms of protection. Animals KO for NOX2, a superoxide-producing enzyme, or KO for NLRP3, a protein component of inflammasome, are not protected by IPC. The aim of this study was to investigate if NOX2 or NLRP3 inflammasome are involved in the protection induced by RIPC. Methods: We preconditioned rats using 4 × 5min periods of IR in the limb with or without a NOX2 inhibitor (apocynin) or an NLRP3 inhibitor (Bay117082). In isolated hearts, we measured the infarct size after 30min of ischemia and 60min of reperfusion. In hearts from preconditioned rats we measured the activity of NOX2; the mRNA of Nrf2, gamma-glutamylcysteine ligase, glutathione dehydrogenase, thioredoxin reductase and sulfiredoxin by RT-qPCR; the content of glutathione; the activation of the NLRP3 inflammasome and the content of IL-1β and IL-10 in cardiac tissue. In exosomes isolated from plasma, we quantified NOX2 activity. Results: The infarct size after IR decreased from 40% in controls to 9% of the heart volume after RIPC. This protective effect was lost in the presence of both inhibitors. RIPC increased NOX2 activity in the heart and exosomes, as indicated by the increased association of p47phox to the membrane and by the increased oxidation rate of NADPH. RIPC also increased the mRNA of Nrf2 and antioxidant enzymes. Also, RIPC increased the content of glutathione and the GSH/GSSG ratio. The inflammasome proteins NLRP3, procaspase-1, and caspase-1 were all increased in the hearts of RIPC rats. At the end of RIPC protocol, IL-1β increased in plasma but decreased in cardiac tissue. At the same time, IL-10 did not change in cardiac tissue but increased by 70% during the next 50min of perfusion. Conclusion: RIPC activates NOX2 which upregulates the heart's antioxidant defenses and activates the NLRP3 inflammasome which stimulates a cardiac anti-inflammatory response. These changes may underlie the decrease in the infarct size induced by RIPC.

Evaluation of Ambient Sensor Systems for the Early Detection of Heart Failure Decompensation in Older Patients Living at Home Alone: Protocol for a Prospective Cohort Study.

The results of telemedicine intervention studies in patients with heart failure (HF) to reduce rehospitalization rate and mortality by early detection of HF decompensation are encouraging. However, the benefits are lower than expected. A possible reason for this could be the fact that vital signs, including blood pressure, heart rate, heart rhythm, and weight changes, may not be ideal indicators of the early stages of HF decompensation but are more sensitive for acute events triggered by ischemic episodes or rhythm disturbances. Preliminary results indicate a potential role of ambient sensor-derived digital biomarkers in this setting. The aim of this study is to identify changes in ambient sensor system-derived digital biomarkers with a high potential for early detection of HF decompensation. This is a prospective interventional cohort study. A total of 24 consecutive patients with HF aged 70 years and older, living alone, and hospitalized for HF decompensation will be included. Physical activity in the apartment and toilet visits are quantified using a commercially available, passive, infrared motion sensing system (DomoHealth SA). Heart rate, respiration rate, and toss-and-turns in bed are recorded by using a commercially available Emfit QS device (Emfit Ltd), which is a contact-free piezoelectric sensor placed under the participant's mattress. Sensor data are visualized on a dedicated dashboard for easy monitoring by health professionals. Digital biomarkers are evaluated for predefined signs of HF decompensation, including particularly decreased physical activity; time spent in bed; increasing numbers of toilet visits at night; and increasing heart rate, respiration rate, and motion in bed at night. When predefined changes in digital biomarkers occur, patients will be called in for clinical evaluation, and N-terminal pro b-type natriuretic peptide measurement (an increase of >30% considered as significant) will be performed. The sensitivity and specificity of the different biomarkers and their combinations for the detection of HF decompensation will be calculated. The study is in the data collection phase. Study recruitment started in February 2024. Data analysis is scheduled to start after all data are collected. As of manuscript submission, 5 patients have been recruited. Results are expected to be published by the end of 2025. The results of this study will add to the current knowledge about opportunities for telemedicine to monitor older patients with HF living at home alone by evaluating the potential of ambient sensor systems for this purpose. Timely recognition of HF decompensation could enable proactive management, potentially reducing health care costs associated with preventable emergency presentations or hospitalizations. ClinicalTrials.gov NCT06126848; https://clinicaltrials.gov/study/NCT06126848. PRR1-10.2196/55953.

LRP1 and RAGE Genes Transporting Amyloid and Tau Protein in the Hippocampal CA3 Area in an Ischemic Model of Alzheimer's Disease with 2-Year Survival.

Explaining changes at the gene level that occur during neurodegeneration in the CA3 area is crucial from the point of view of memory impairment and the development of post-ischemic dementia. An ischemic model of Alzheimer's disease was used to evaluate changes in the expression of genes related to amyloid transport in the CA3 region of the hippocampus after 10 min of brain ischemia with survival of 2, 7 and 30 days and 12, 18 and 24 months. The quantitative reverse transcriptase PCR assay revealed that the expression of the LRP1 and RAGE genes involved in amyloid transport was dysregulated from 2 days to 24 months post-ischemia in the CA3 area of the hippocampus. LRP1 gene expression 2 and 7 days after ischemia was below control values. However, its expression from day 30 to 24 months, survival after an ischemic episode was above control values. RAGE gene expression 2 days after ischemia was below control values, reaching a maximum increase 7 and 30 days post-ischemia. Then, after 12, 18 and 24 months, it was again below the control values. The data indicate that in the CA3 area of the hippocampus, an episode of brain ischemia causes the increased expression of the RAGE gene for 7-30 days during the acute phase and that of LRP1 from 1 to 24 months after ischemia during the chronic stage. In other words, in the early post-ischemic stage, the expression of the gene that transport amyloid to the brain increases (7-30 days). Conversely, in the late post-ischemic stage, amyloid scavenging/cleaning gene activity increases, reducing and/or preventing further neuronal damage or facilitating the healing of damaged sites. This is how the new phenomenon of pyramidal neuronal damage in the CA3 area after ischemia is defined. In summary, post-ischemic modification of the LRP1 and RAGE genes is useful in the study of the ischemic pathways and molecular factors involved in the development of Alzheimer's disease.

Neuroprotective-Neurorestorative Effects Induced by Progesterone on Global Cerebral Ischemia: A Narrative Review.

Progesterone (P4) is a neuroactive hormone having pleiotropic effects, supporting its pharmacological potential to treat global (cardiac-arrest-related) cerebral ischemia, a condition associated with an elevated risk of dementia. This review examines the current biochemical, morphological, and functional evidence showing the neuroprotective/neurorestorative effects of P4 against global cerebral ischemia (GCI). Experimental findings show that P4 may counteract pathophysiological mechanisms and/or regulate endogenous mechanisms of plasticity induced by GCI. According to this, P4 treatment consistently improves the performance of cognitive functions, such as learning and memory, impaired by GCI. This functional recovery is related to the significant morphological preservation of brain structures vulnerable to ischemia when the hormone is administered before and/or after a moderate ischemic episode; and with long-term adaptive plastic restoration processes of altered brain morphology when treatment is given after an episode of severe ischemia. The insights presented here may be a guide for future basic research, including the study of P4 administration schemes that focus on promoting its post-ischemia neurorestorative effect. Furthermore, considering that functional recovery is a desired endpoint of pharmacological strategies in the clinic, they could support the study of P4 treatment for decreasing dementia in patients who have suffered an episode of GCI.

Adjunct remote ischemic conditioning to PCI in ST-segment elevation myocardial infraction patients: Systematic review and meta-analysis

Abstract Introduction ST-segment elevation myocardial infarction (STEMI) is the most dangerous presentation of the acute coronary syndrome (ACS). Throughout the last three decades, clinicians have been attempting to reduce the short and long-term major adverse cardiac events (MACE) associated with STEMI. Remote ischemic conditioning (RIC) is one of the new adjunctive modalities to PCI in treating STEMI patients whereby brief reversible episodes of ischemia and reperfusion are applied to the tissue (by alternative cycles of inflation and deflation of a blood pressure cuff on the upper or lower limb) confers global protection and renders remote tissues resistant to ischemia/reperfusion injury. This review aims to provide reliable evidence from published randomized controlled trials (RCTs) regarding whether RIC is beneficial for STEMI patients or not. Methods We followed the PRISMA guidelines during the preparation of this systematic review and meta-analysis. A computer literature search for (PubMed, Web of Science, Scopes, and Google Scholar) was carried out. We included RCT, comparing the remote ischemic conditioning, regardless of its timing of application to PCI, with either placebo or sham procedure, in terms of both short-term and long-term cardio protection. Outcomes of myocardial salvage index, myocardial infarction size, and left ventricular ejection fraction were pooled as the standardized mean difference between the two groups from baseline to endpoint. Results 11 RCTs (7151 patients), were included in this analysis. The overall effect on short-term outcomes, was in favor of PCI only in terms of myocardial salvage index(P value=0.04, 95% CI [0.00-0.08]), and left ventricular ejection fraction(P value=0.05, 95% CI [0.02,2.16]), while the adjunctive application of remote ischemic conditioning was beneficial in terms of: myocardial infarct size ( P value=0.004, 95% CI [-3.22,-0.62]). Regarding the long-term outcomes, the overall effect did not show any benefit in either of the two groups in terms of: major adverse cardiac and cerebrovascular events (MACCE) (P value=0.13, 95% CI [0.48,1.10]), hospitalization for heart failure (P value=1.00, 95% CI [0.83,1.20]), and cardiac death (P value=0.91, 95% CI [0.73,1.32]). Conclusion The adjunctive application of RIC to PCI during treatment of STEMI patients showed a beneficial effect only on short-term reduction of myocardial infarct size, nevertheless, it was not of benefit regarding the other short and long-term metrics of myocardial salvage and left ventricular function.

Abstract 12554: Machine Learning-Based Detection of Intraoperative Ischemia Utilizing the VitalDB Database

Introduction: Myocardial ischemia, characterized by insufficient blood supply to the heart, is a critical condition often associated with adverse cardiac events, including myocardial infarction. Detecting intraoperative ischemia holds substantial clinical significance. This study aims to develop a machine-learning (ML) model to detect intraoperative hypotension as a marker of ischemia using electrocardiogram (ECG) features. Hypothesis: We hypothesize that machine-learning algorithms can detect changes in ECG episodes during ischemic or subischemic events associated with prolonged hypotension. Methods: The study utilized the VitalDB database, a comprehensive repository of intraoperative data of 6,388 patients, including ECG recordings and other vital signs. The ML model was a binary classifier of a hypotensive event (MBP <65 mm Hg) or a non-hypotensive event (MBP >75 mm Hg) by analyzing ECG-II and ECG-V5 waveforms. We extracted relevant ECG features such as ST-deviation (ST-elevation or ST-depression), as clinical indicators of myocardial ischemia. The adaptive boosting (AdaBoost), Gradient boosting (GB), and Extreme gradient boosting (XGB) methods, ML boosting techniques, were employed to develop a hypotension predictive model for detecting ischemic episodes. The primary outcomes were the accuracy and the area under the receiver operating characteristic (AUROC) curve. Additionally, we utilized the Shapley Additive Explanations (SHAP) to determine the contribution of the ECG features to the ML model. Results: The GB machine learning model exhibited the best results (Accuracy: 89%, AUROC: 0.92) in predicting hypotensive events. Furthermore, the model achieved high sensitivity and specificity in identifying ischemic episodes. SHAP analysis revealed that ST-deviation is the most significant contributing ECG feature in predicting intraoperative hypotension. Conclusions: These results demonstrate the potential utility of ML-based identification of ECG features in accurately identifying ischemic episodes. Implementation of an improved diagnostic methodology for intraoperative ischemia detection can have a significant impact on patient care, enhancing patient safety and improving surgical outcomes.

Non-peptide orphanin receptor antagonist activity in rat myocardial ischemia-induced cardiac arrhythmias

One of the causes of sudden cardiac death is arrhythmia after acute myocardial ischemia. After ischemia, endogenous orphanin (N/OFQ) plays a role in the development of arrhythmias. It is discussed in this paper how nonpeptide orphanin receptor (ORL1) antagonists such as J-113397, SB-612111 and compound-24 (C-24) affect arrhythmia in rats following acute myocardial ischemia and what the optimal concentrations for these antagonists are. The electrocardiogram of the rat was recorded as part of the experiment. The concentrations of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in the myocardium were measured following euthanasia. Following the use of three antagonists, we found the lowest inflammatory factor concentrations and the smallest number of ischemic arrhythmia episodes. All of them had a small impact on cardiac function. LF/HF values were significantly reduced in all three antagonist groups, suggesting that they are involved in the regulation of sympathetic nerves. In conclusion, pretreatment with the three antagonist groups can effectively reduce the concentration of TNF-α and IL-1β, and the occurrence of arrhythmias after ischemia can also be significantly reduced. Inflammation and sympathetic activity may be related to the mechanism of action of antagonists.

Syncope and Cannabis: hypervagotonia from chronic abuse? A case report and literature review

BackgroundCannabis is the most consumed drug worldwide and number of users is increasing, particularly among youth. Moreover, cannabis potential therapeutic properties have renewed interest to make it available as a treatment for a variety of conditions. Albeit rarely, cannabis consumption has been associated with cardiovascular diseases such as arrhythmias, myocardial infarction (MI) and potentially sudden death.Case presentationA 24-year-old woman presented to the emergency department sent by her cardiologist because of a recent finding of a 16 seconds asystole on the implantable loop recorder (ILR) she implanted 7 months before for recurrent syncopes. She declared that she is a heavy cannabis user (at least 5 cannabis-cigarette per day, not mixed up with tobacco, for no less than 12 years) and all syncopes occurred shortly after cannabis consumption. After a collective discussion with the heart team, syncope unit, electrophysiologists and toxicologist, we decided to implant a dual chamber pacemaker with a rate response algorithm due to the high risk of trauma of the syncopal episodes. 24 months follow-up period was uneventful.ConclusionsCannabis cardiovascular effects are not well known and, although rare, among these we find ischemic episodes, tachyarrhythmias, symptomatic sinus bradycardia, sinus arrest, ventricular asystole and possibly death. Because of cannabis growing consumption both for medical and recreational purpose, cardiovascular diseases associated with cannabis use may become more and more frequent. In the light of the poor literature, we believe that cannabis may produce opposite adverse effects depending on the duration of the habit. Acute administration increases sympathetic tone and reduces parasympathetic tone; conversely, with chronic intake an opposite effect is observed: repetitive dosing decreases sympathetic activity and increases parasympathetic activity. Clinicians should be aware of the increased risk of cardiovascular complications associated with cannabis use and should investigate its consumption especially in young patients presenting with cardiac dysrhythmias.

Modern strategy of combined antihyperlipidemic therapy in the post-infarction period: focus on phytosteroid saponins

Patients who have suffered a myocardial infarction have a high risk of recurrent cardiovascular events – almost every fifth patient develops new episodes of acute myocardial ischemia during the first year [5]. One of the most important tasks of the therapy of these patients is the most effective and early reduction of atherogenic lipoprotein fractions to target values. The initiating basic therapy is statins, which have proven to be highly effective. However, in a number of patients, the necessary high-dose statin treatment cannot be implemented due to developing side effects or intolerance. The article discusses the issues of combined antihyperlipidemic therapy with a discussion of the role of all available groups of drugs. A possible clinical and pharmacological niche of phyto-steroid saponins is being considered.

A case of moyamoya disease

Moyamoya Disease (MMD) is a rare cause of stroke with progressive stenosis of the end of the internal carotid artery and compensatory capillaries. The symptoms and course of moyamoya disease depend on the age of the patient at the time of symptom onset and the type of first episode (ischemic or hemorrhagic), but vary in severity from transient ischemic episodes to persistent neurological deficits [1].

A synthetic cardiac episode generator for explainable, pathology based action potential using heuristic polynomial signatures

Synthetic generation of biophysical signals caters to diverse applications of test vectors generation, exploration, data augmentation and machine learning training. Arrhythmiator, our contribution is a Python framework to generate synthetically, action potential for explain-ability and explore-ability of pathology (Arrhythmia) influenced cardiac episodes. In this work, we address the problem of large cardiac data-sets need, for deep learning models which are hindered by privacy laws by synthetic generation. We have addressed the problem of explainable computations, multi-scale, by virtue of novel stack sliced polynomial signatures, piece-wise linear and application context driven fitting/filtering in algorithmic framework. To account the problem of lack of standardised pathology specifications we developed PDL (Pathology descriptive language) portal which can be customised. We also addressed the challenge of high turnaround development cycle, inter-operate-ability computation issue by developing a single unified Python framework. To address computational costs, we leverage domain-specific heuristics through sliced state space control algorithms and a constant temporal resolution. We demonstrate the utility of our framework by generating two cases of Tachycardia, one influenced by sodium pump inhibition of spontaneous diastolic depolarisation (SDD) slope and other by ischaemic episode causing maximum diastolic depolarisation (MDP) shift. The concept of the pacemaker hierarchy is encompassed by developing pathology explainable computation as a structure (PECS). We showcase the flexibility and explore-ability of our framework through ease of filter connect profile plug-ins for action potential states upstroke and plateau. We validated the generated waveforms by developing trace and debug algorithms and a reference deviation score which marks the pathology influence. The validator module is a vectored attribute of action potential based on state space control algorithms.

A Non-Linear Role of Hyperlipidemia on Progression of Intracranial Atherosclerotic Plaques and Acute Downstream Ischemic Events.

Intracranial atherosclerotic stenosis (ICAS) is the leading cause of ischemic stroke worldwide. Hyperlipidemia is a major contributor to atherosclerosis. However, the effect of hyperlipidemia on the evolution of intracranial atherosclerotic plaques and downstream ischemic episodes remains unclear. In this study, we aimed to assess the radiological features of ICAS plaques and to explore the relationship between hyperlipidemia and plaque progression. We included people with ICAS (≥50% stenosis) undergoing high-resolution magnetic resonance imaging. The culprit plaque was defined as the sole, or in case of multiple stenosis, the narrowest plaque on the intracranial artery responsible for acute ischemic stroke. Demographic, clinical data, plaque features on MRI, and lipid parameters were compared between culprit and non-culprit plaques. Plaque enhancement was graded as Grade 0, 1 and 2 by comparing to the adjacent normal vessel wall and pituitary funnel after contrast enhancement on T1-weighted sequences. 162 patients were included (mean age 57.7±12.1 years, male 61.6%), 110 of whom were identified as culprit plaque with an ipsilateral acute stroke. High-grade enhancement was the most prominent MRI feature of the culpable plaque (Grade-2: OR 6.539, 95%CI 1.706-23.707, p=0.006). LDL cholesterol was significantly associated with overall acute ischemic stroke caused by culprit plaque. After stratification by enhancement grading LDL was independently associated with ischemic events in Grade-1 enhancement plaques (OR 6.778, 95%CI 2.122-21.649, p=0.001). In patients with Grade-2 enhancement plaques, however, LDL was not associated with ischemic event; in contrast, Neutrophil/Lymphocyte ratio was independently associated with ischemic events caused by Grade-2 enhancement plaques (OR 2.188, 95%CI 1.209-3.961, p=0.010). LDL was related with ischemia events in intermediate stage of intracranial atherosclerotic plaque progression, an excellent period for intensive lipid-lowering treatment. In advanced stage, inflammatory agents maybe the main contributor to ischemic events.

Destabilization of the Organized Structure of Ventricular Fibrillation During Reperfusion

Aim: to study the effect of reperfusion on the organized frequency-amplitude structure of ventricular fibrillation (VF) in the dog heart.Materials and methods. We conducted 4 experiments on 8 dogs. In each experiment, the isolated heart of one dog was perfused with the blood of the second (supporting) dog. In 4 experiments on an isolated artificially perfused heart, 6 episodes of 3 min ischemia and 10 min reperfusion of the heart were performed in VF (1–2 episodes of ischemia-reperfusion in one experiment). Each episode of 3 min ischemia in VF was preceded by a 10 min perfusion of the heart in VF. Ventricular electrogram was recorded during VF episodes. A frequencyamplitude (spectral) analysis of 1 sec segments of the electrogram was performed, and the proportion (in %) of 0.5–15 Hz frequency oscillations in 10 sec segments of the electrogram was determined in 6 episodes of perfusion, ischemia and reperfusion in VF (M±m, N=60). The VF frequency-amplitude structures during ischemia and reperfusion were compared with the stable VF frequency-amplitude structure during perfusion taken as the control. The nonparametric Welch criterion in the «The R Project for Statistical Computing» software environment was used to compare the VF parameters during perfusion, ischemia and reperfusion. Results. 9–10 Hz frequency oscillations dominated in the VF frequency-amplitude structure during heart perfusion, taken as the control. In the first 30 sec of ischemia, the frequency and amplitude of the dominant oscillations did not significantly change vs VF control obtained during cardiac perfusion. A decrease of dominant oscillations frequency up to 6.5–7.5 Hz, and of the proportion of oscillations — up to 26% was documented at the 3rd min of ischemia. At the 1st min of reperfusion, the frequency of dominant oscillations increased to 13.5–14.5 Hz, but the proportion of oscillations remained reduced to 26%, as at the 3rd min of ischemia. At the 2nd min of reperfusion, the frequency of dominant oscillations decreased to 9.5–10.5 Hz, and the proportion of dominant oscillations increased to 33%. The frequency and amplitude of the dominant oscillations stabilized at 3–10 min of reperfusion: oscillations at 9–10 Hz frequency accounted for 32–33% of the spectral power.Conclusion. Reperfusion in VF is characterized by transient destabilization of VF organized structure at the 1st min of the procedure. VF organized structure regains stabilization within 2–10 min of reperfusion. Cardiac perfusion in intentionally induced VF can be used instead of cardioplegia during major cardiac surgery to boost cardiac resistance to ischemia and prevent or reduce reperfusion complications.

КЛИНИЧЕСКИЙ СЛУЧАЙ ВАЗОСПАСТИЧЕСКОЙ СТЕНОКАРДИИ У ПАЦИЕНТА С ГАСТРОЭЗОФАГЕАЛЬНОЙ РЕФЛЮКСНОЙ БОЛЕЗНЬЮ

Introduction. The combination of CAD and GERD is a common clinical situation. In recent years, more and more information has appeared indicating that the coexistence of both diseases is not accidental. Clinical example. A 51-year-old man was admitted to the KGBUZ "AKKD" by transfer from the Central District Hospital with complaints of burning, pressing pains behind the sternum without a clear connection with physical activity, more often in the early morning hours, lasting up to 5 minutes, stopped by sitting, drinking cold water. Upon admission, the state of the average degree. BMI 23.9 kg/m2. Temperature 36.6 0С. NPV 16 per min. SpO2 - 96%. Heart rate 55 beats. in min. AD = 110/60 mm. rt. Art. Vesicular breathing in the lungs, no wheezing. The heart sounds are clear, the rhythm is correct. There are no edema. The abdomen is soft and painless. ECG at admission: sinus rhythm with a heart rate of 55 per minute. Negative T wave II, III, aVF, V7-V9. From the anamnesis: he had not previously controlled blood pressure, he did not take regular medications. Long history of smoking. During the year, he began to notice rare episodes of burning behind the sternum lasting up to 10 minutes without a clear connection with physical activity. He was examined at the place of residence, EGD was performed, where a hernia of the esophageal opening of the diaphragm, chronic atrophic gastritis were diagnosed. During the week before hospitalization, the condition worsened in the form of a decrease in exercise tolerance, an increase in burning sensation, pressing pain behind the sternum. On May 11, 23, due to a long-term pain syndrome behind the sternum, he called an ambulance, was hospitalized at the Central District Hospital, and then transferred to the AKKD. Upon admission to the AKKD, emergency coronary angiography was performed, where subocclusion of the circumflex artery (OA) was diagnosed, stenting of the OA with a drug-eluting stent. Echocardiography revealed hypokinesis along the lateral wall, the ejection fraction of the left ventricle was 59%. Laboratory: troponin I at admission and in dynamics within the reference values; dyslipidemia. After PCI in the department, daily recurrences of burning in the epigastrium and behind the sternum more often at night. Repeated EGD - reflux gastritis with metaplasia, cardiac insufficiency. HMECG recorded episodes of ST segment elevation in II, III, aVF, V5-V6, duration up to 70 minutes; frequent polymorphic ventricular extrasystole. Taking into account recurrent pains, the results of HMECG, a control coronary angiography was performed - the coronary arteries were without pathology, the OA stent was passable. Treatment was corrected, antianginal therapy was increased with beta-blockers, dihydropyridine calcium antagonists and long-acting nitrates, as well as therapy with proton pump inhibitors. During therapy, the condition improved, anginal pain did not recur. According to HMECG in dynamics - no ischemic changes. Discharged from the hospital in a satisfactory condition with recommendations. Conclusion. To date, a number of pathophysiological mechanisms have been established, both causing the pathogenetic relationship between IHD and GERD, and contributing to their mutual aggravation. The basis of the occurrence of associated angina pectoris is the esophagocardial reflex, caused by irritation of the esophagus and the development of coronary spasm as a result. In patients with variant angina pectoris, a time relationship was found between periods of esophageal spasm and episodes of ECG-registered ischemia. At the same time, it was found that with impaired esophageal motility in patients with coronary artery disease, a vicious circle may form: esophagospasm provokes myocardial ischemia, which, in turn, contributes to new episodes of esophageal spasm.

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.