MicroRNA-30e-3p reduces coronary microembolism-induced cardiomyocyte pyroptosis and inflammation by sequestering HDAC2 from the SMAD7 promoter.

This study investigates the mechanism by which microRNA (miR)-30e-3p reduces coronary microembolism (CME)-induced cardiomyocyte pyroptosis and inflammation. Cardiac function tests, histological staining, and transmission electron microscopy were performed on CME-model rats injected with adeno-associated viral vectors. Cardiomyocytes were transfected 24 h before a cellular model of pyroptosis was established via treatment with 1 µg/mL lipopolysaccharide (LPS) for 4 h and 5 mM ATP for 30 min. Pyroptosis, inflammation, and Wnt/ß-catenin signaling in cardiomyocytes were detected. Dual-luciferase reporter assays and/or RNA pull-down assays were performed to verify the binding of miR-30e-3p to HDAC2 mRNA or HDAC2 to the SMAD7 promoter. Chromatin immunoprecipitation was used to assess the level of H3K27 acetylation at the SMAD7 promoter. miR-30e-3p and SMAD7 expression levels were downregulated and HDAC2 expression was upregulated with CME. The overexpression of miR-30e-3p restored cardiac functions in CME-model rats and reduced serum cTnI, IL-18, and IL-1ß levels, microinfarcts, inflammatory cell infiltration, apoptosis, collagen content, and GSDMD-N, cleaved caspase-1, and NLRP3 expression in the myocardium, but these effects were reversed by SMAD7 knockdown. The overexpression of miR-30e-3p or knockdown of HDAC2 reduced LDH, IL-18, and IL-1ß secretion, propidium iodide intake, and GSDMD-N, NLRP3, cleaved caspase-1, Wnt3a, Wnt5a, and ß-catenin expression in the cardiomyocyte model. miR-30e-3p inhibited the expression of HDAC2 by binding HDAC2 mRNA. HDAC2 repressed the expression of SMAD7 by catalyzing H3K27 deacetylation at the SMAD7 promoter. miR-30e-3p, by binding HDAC2 to promote SMAD7 expression, reduces CME-induced cardiomyocyte pyroptosis and inflammation.

Recovery of Hypoxic Regions in a Rat Model of Microembolism.

OBJECTIVES: Endovascular treatment (EVT) has become the standard of care for acute ischemic stroke. Despite successful recanalization, a limited subset of patients benefits from the new treatment. Human MRI studies have shown that during removal of the thrombus, a shower of microclots is released from the initial thrombus, possibly causing new ischemic lesions. The aim of the current study is to quantify tissue damage following microembolism. MATERIALS AND METHODS: In a rat model, microembolism was generated by injection of a mixture of polystyrene fluorescent microspheres (15, 25 and 50 µm in diameter). The animals were killed at three time-points: day 1, 3 or 7. AMIRA and IMARIS software was used for 3D reconstruction of brain structure and damage, respectively. CONCLUSIONS: Microembolism induces ischemia, hypoxia and infarction. Infarcted areas persist, but hypoxic regions recover over time suggesting that repair processes in the brain rescue the regions at risk.

Granulocyte colony-stimulating factor attenuates myocardial remodeling and ventricular arrhythmia susceptibility via the JAK2-STAT3 pathway in a rabbit model of coronary microembolization.

BACKGROUND: Coronary microembolization (CME) has a poor prognosis, with ventricular arrhythmia being the most serious consequence. Understanding the underlying mechanisms could improve its management. We investigated the effects of granulocyte colony-stimulating factor (G-CSF) on connexin-43 (Cx43) expression and ventricular arrhythmia susceptibility after CME. METHODS: Forty male rabbits were randomized into four groups (n = 10 each): Sham, CME, G-CSF, and AG490 (a JAK2 selective inhibitor). Rabbits in the CME, G-CSF, and AG490 groups underwent left anterior descending (LAD) artery catheterization and CME. Animals in the G-CSF and AG490 groups received intraperitoneal injection of G-CSF and G-CSF + AG490, respectively. The ventricular structure was assessed by echocardiography. Ventricular electrical properties were analyzed using cardiac electrophysiology. The myocardial interstitial collagen content and morphologic characteristics were evaluated using Masson and hematoxylin-eosin staining, respectively. RESULTS: Western blot and immunohistochemistry were employed to analyze the expressions of Cx43, G-CSF receptor (G-CSFR), JAK2, and STAT3. The ventricular effective refractory period (VERP), VERP dispersion, and inducibility and lethality of ventricular tachycardia/fibrillation were lower in the G-CSF than in the CME group (P < 0.01), indicating less severe myocardial damage and arrhythmias. The G-CSF group showed higher phosphorylated-Cx43 expression (P < 0.01 vs. CME). Those G-CSF-induced changes were reversed by A490, indicating the involvement of JAK2. G-CSFR, phosphorylated-JAK2, and phosphorylated-STAT3 protein levels were higher in the G-CSF group than in the AG490 (P < 0.01) and Sham (P < 0.05) groups. CONCLUSION: G-CSF might attenuate myocardial remodeling via JAK2-STAT3 signaling and thereby reduce ventricular arrhythmia susceptibility after CME.

Transcranial measurement of cerebral microembolic signals during left-sided catheter ablation with the use of different approaches- the potential microembolic risk of a transseptal approach.

Aims: Subclinical brain damage due to microembolization could occur during catheter ablation procedures. We evaluated the microembolic signals (MESs) detected by transcranial Doppler during ablation of supraventricular tachycardias (SVTs) or idiopathic ventricular arrhythmias (VAs) with the use of different approaches. Methods and results: This study included 36 patients (23 men, 49 ± 21 years) who underwent catheter ablation of SVTs (n = 27) or idiopathic VAs (n = 9). Left-sided ablation was performed by either a transaortic (Group 1, n = 11) or transseptal approach (Group 2, n = 9). A sole right-sided ablation was performed in the remaining 16 patients (Group 3). The MESs were counted throughout the procedure, and then analysed offline with a frequency analysis. The mean number of radiofrequency applications, total energy delivery time, total application energy, and total procedure time were 5.8 ± 5.0, 4.3 ± 3.3 min, 6625 ± 4633 J, and 81 ± 40 min, respectively, and there was no significant difference in the parameters between the three groups. The mean total number of MESs was 3.8 ± 3.1 in Group 1, 75 ± 58 in Group 2, and 0.3 ± 0.6 in Group 3 (P = 0.001). Few MESs were detectable during the radiofrequency energy deliveries in all groups. In Group 2, 19 ± 18 MESs were detected during the transseptal puncture period, and subsequently a relatively even distribution of emboli formation was observed. A frequency analysis suggested that 99, 91, and 100% of MESs were gaseous, in Group 1, Group 2, and Group 3, respectively. No neurological impairment was observed in any patients after the procedure. Conclusion: The retrograde aortic approach might potentially have a lower risk of subclinical brain damage than the transseptal approach during left-sided catheter ablation.

Cerebral microembolism in patients with segmental left ventricular wall motion abnormalities.

BACKGROUND AND PURPOSE: The significance of segmental heart wall motion abnormalities for stroke is unknown. The aims of the study included (1) comparison of the frequency and type of embolic signals in the middle cerebral artery in patients with segmental left ventricular wall hypokinesis due to coronary heart disease with and without stroke, and (2) determination of the relationship between inflammatory parameters, fibrinogen level, dyslipidemia and microembolic signals in the middle cerebral artery in patients with segmental heart hypokinesis. MATERIAL AND METHODS: The study included 68 patients with segmental heart hypokinesis (33 without stroke [group I] and 35 with stroke [group II]), as well as 37 healthy volunteers and a reference group of 30 patients. Echocardiography and carotid/transcranial Doppler with detection of microembolic signals were performed. Patients from group I and II had erythrocyte sedimentation rate, leucocyte count, triglycerides, total cholesterol, HDL, and LDL examined. RESULTS: Embolic signals were detected in patients with segmental heart hypokinesis significantly more frequently than in the control and reference groups. The high number of embolic signals, signals of high intensity, hypokinesis of the distal part of the intraventricular septum, increased cholesterol levels, LDL and triglycerides were all found more frequently in patients from group II than in group I. Embolic signals were detected more frequently in patients with high fibrinogen levels and leukocytosis. CONCLUSIONS: Embolic signals in the middle cerebral artery in patients with segmental left ventricular hypokinesis have to be considered as a risk factor of stroke. The following changes are observed in patients with cardiogenic stroke: hypokinetic intraventricular septum, high intensity embolic signals, increased serum fibrinogen levels and leucocyte count. It may indicate the importance of these factors in the aetiology of stroke.

Brain emboli distribution and differentiation during cardiopulmonary bypass.

OBJECTIVE: Cardiopulmonary bypass (CPB) is a lifesaving practice in cardiac surgery, but its use frequently is associated with cerebral injury and neurocognitive dysfunctions. Despite the involvement of numerous factors, microembolism occurring during CPB seems to be one of the main mechanisms leading to such alterations. The aim of the present study was to characterize the occurrence of cerebral microembolism with reference to microembolic amount, nature, and distribution in different combinations of cardiac procedures and CPB on the microembolic load. DESIGN: A retrospective observational clinical study. SETTING: A single-center regional hospital. PARTICIPANTS: Fifty-five patients undergoing elective cardiac surgery with CPB. INTERVENTIONS: Bilateral detection of the patients' middle cerebral arteries using a multifrequency transcranial Doppler. MEASUREMENTS AND MAIN RESULTS: Patients were divided into 3 groups depending on the CPB circuit used (open, open with vacuum, or closed). There was a significant difference between the number of solid and gaseous microemboli (p<0.001), with the solid lower than the gaseous ones. The number of solid microemboli was affected by group (p< 0.05), CPB phase (p<0.001), and laterality (p<0.01). The number of gaseous microemboli was affected only by group (p<0.05) and CPB phase (p<0.001). Generally, the length of CPB phase did not affect the number of microemboli. CONCLUSIONS: Surgical procedures combined with CPB circuits, but not the CPB phase length, affected the occurrence, nature, and laterality of microemboli.

Bone Cement and Its Anesthetic Complications: A Narrative Review.

The concept of bone cement implantation syndrome (BCIS) is not yet fully understood. In patients undergoing cemented hip arthroplasty, it is a significant factor in intraoperative mortality and morbidity. It may also manifest in a milder form postoperatively, resulting in hypoxia and confusion. In the older population, hip replacement surgery is becoming more prevalent. The risks of elderly patients suffering BCIS may be increased due to co-existing conditions. In this article, we present a narrative review of BCIS including its definition, incidence, risk factors, etiology, pathophysiology, clinical features, prevention, and management, all from an anesthetic point of view.

Prevention of cerebral thromboembolism by oral anticoagulation with dabigatran after pulmonary vein isolation for atrial fibrillation: the ODIn-AF trial.

BACKGROUND AND OBJECTIVES: Long-term oral anticoagulation (OAC) following successful catheter ablation of atrial fibrillation (AF) remains controversial. Prospective data are missing. The ODIn-AF study aimed to evaluate the effect of OAC on the incidence of silent cerebral embolic events and clinically relevant cardioembolic events in patients at intermediate to high risk for embolic events, free from AF after pulmonary vein isolation (PVI). METHODS: This prospective, randomized, multicenter, open-label, blinded endpoint interventional trial enrolled patients who were scheduled for PVI to treat paroxysmal or persistent AF. Six months after PVI, AF-free patients were randomized to receive either continued OAC with dabigatran or no OAC. The primary endpoint was the incidence of new silent micro- and macro-embolic lesions detected on brain MRI at 12 months of follow-up compared to baseline. Safety analysis included bleedings, clinically evident cardioembolic, and serious adverse events (SAE). RESULTS: Between 2015 and 2021, 200 patients were randomized into 2 study arms (on OAC: n = 99, off OAC: n = 101). There was no significant difference in the occurrence of new cerebral microlesions between the on OAC and off OAC arm [2 (2%) versus 0 (0%); P = 0.1517] after 12 months. MRI showed no new macro-embolic lesion, no clinical apparent strokes were present in both groups. SAE were more frequent in the OAC arm [on OAC n = 34 (31.8%), off OAC n = 18 (19.4%); P = 0.0460]; bleedings did not differ. CONCLUSION: Discontinuation of OAC after successful PVI was not found to be associated with an elevated risk of cerebral embolic events compared with continued OAC after a follow-up of 12 months.

Different effects of air microembolism through patent foramen ovale in patients with migraine: A quantitative electroencephalogram case series.

Background: Literature suggests an association between patent foramen ovale (PFO) and migraine, mostly migraine with aura (MA). Previous data suggest that air microembolism through PFO can lead to bioelectrical abnormalities detectable at electroencephalogram (EEG) in patients with MA, thus suggesting a pathophysiological mechanism for the MA-PFO association. However, those data lack replication. Methods: Patients with MA or migraine without aura (MO) and large PFO underwent a 19-channel EEG recording before and after injection of air microbubbles. We compared EEG power before and after microbubble injection for each electrode location, for each frequency band (theta: 5-7 Hz; alpha: 8-12 Hz; beta: 13-30 Hz; lower gamma: 31-45 Hz), and for total global power (the average of EEG power at each location and frequency band). Results: We included 10 patients, four with MA and six with MO; six patients had medium-to-high migraine frequency (four or more monthly migraine days), while four had low frequency (one monthly migraine day). EEG power changes after air microembolism varied across patients. Considering the overall group, total global EEG power did not change; however, EEG power in the higher frequency ranges (beta and lower gamma) increased in patients with MA. Conclusions: We did not replicate the effects of air microembolism previously reported in patients with migraine. Aura status, migraine frequency, and medications might influence patients' response to microembolism. More refined EEG measurements are needed to clarify the dynamic role of PFO on migraine occurrence.

A case of accidental local pulmonary 99mTc-MDP uptake on bone SPECT/CT.

We report a case of accidental local 99mTc-MDP uptake in left lung on bone scan without pulmonary parenchymal abnormality on SPECT/CT. The abnormal uptake disappeared on repeated bone scan and SPECT/CT after 3 days. It is speculated that the high radioactivity focus is a microthrombus in pulmonary artery.

COVID-19-Induced Hypercoagulability: A Case Report.

We report a case of atherothrombotic microembolism in a 53-year-old male diagnosed with coronavirus disease 2019 (COVID-19) prior to hospital admission. Upon admission, Day 9 after diagnosis, he presented with COVID-19 pneumonia and mottling of the lower extremities. The patient was treated with anticoagulation therapy. The lower extremity angiogram showed a patent posterior tibial artery and a patent peroneal artery. Despite initial anticoagulation therapy, toe and transmetatarsal amputations were required. However, a below-the-knee amputation was subsequently required due to continued worsening and extension of mottling. Unfortunately, the patient ultimately expired from cardiopulmonary arrest before any other surgical intervention could be done.

Retinal Infarction: A Pilot Study on the Efficacy and Safety of Intravenous Thrombolysis and Underlying Aetiologies.

Background: Treatment of non-arteritic central retinal artery occlusion is still inconsistent. Therefore, the current study aimed to evaluate the efficacy of intravenous thrombolysis (IVT) and describe the prevalence of co-occurring ischemic brain lesions in patients with acute visual loss due to ischemia. Methods: We analysed 38 consecutive patients with acute visual loss between January 2015 and June 2020. Patients presenting within 4.5 h of symptom onset without any contraindication were treated with IVT. Patients underwent neurologic and ophthalmologic examination and diagnostic workup for the underlying aetiology. Follow-up was performed after 3 and 12 months. Results: Patients treated with IVT had a significantly better functional outcome at discharge compared to patients treated conservatively. No additional ischemic brain lesions were detected (0 of 38). Three patients had extracranial carotid artery stenosis ≥50%. Atrial fibrillation was present in four patients, three of whom already received oral anticoagulation. In the remaining 31 patients no embolic source was detected. However, the number of plaques were rated mild to moderate. Within three months, one patient developed transient visual loss while another suffered a contralateral transient ischemic attack. Conclusions: IVT may represent a safe and effective treatment option in patients with isolated visual loss due to ischemia. The aetiology was atherosclerotic burden rather than embolism caused by carotid stenosis or atrial fibrillation, bringing the current diagnostic procedure and therapy into question. Randomized trials are necessary to evaluate the efficacy and safety of IV thrombolysis and clarify the aetiology of isolated visual loss due to ischemia.

68Ga-DOTATOC Embolus Manifestation and Spontaneous Resolution by PET/CT.

68Ga-labeled somatostatin receptor analogs physiologic distribution patterns have become recognizable among nuclear medicine physicians because of the increasing routine clinical use of this modality in the work-up of neuroendocrine tumors. Some pitfalls during 68Ga-labeled somatostatin receptor PET/CT have recently been reported as causes of misdiagnoses. Iatrogenic microembolism as a cause of 18F-FDG embolus is well-established; however, 68Ga-DOTATOC embolus is not well documented in the literature. In the current case, the presence and the spontaneous resolution of the 68Ga-labeled somatostatin receptor analogs embolus during sequential PET/CT are nicely demonstrated. Awareness of this incidental finding would avoid misdiagnosis and unnecessary investigations.

Persistent respiratory failure after SARS-CoV-2 infection: The role of dual energy computed tomography. A case report.

Background: COVID-19 disease is often complicated by respiratory failure, developing through multiple pathophysiological mechanisms, with pulmonary embolism (PE) and microvascular thrombosis as key and frequent components. Newer imaging modalities such as dual-energy computed tomography (DECT) can represent a turning point in the diagnosis and follow-up of suspected PE during COVID-19. Case presentation: A 78-year-old female presented to our internal medicine 3 weeks after initial hospitalization for COVID-19 disease, for recrudescent respiratory failure needing oxygen therapy. A computed tomography (CT) lungs scan showed a typical SARSCoV-2 pneumonia. Over the following 15 days, respiratory function gradually improved. Unexpectedly, after 21 days from symptom onset, the patient started complaining of breath shortening with remarkable desaturation requiring high-flow oxygen ventilation. CT pulmonary angiography and transthoracic echocardiography were negative for signs of PE. Thereby, Dual-energy CT angiography of the lungs (DECT) was performed and detected diffuse peripheral microembolism. After 2 weeks, a second DECT was performed, showing a good response to the anticoagulation regimen, with reduced extent of microembolism and some of the remaining emboli partially recanalized. Discussion: DECT is an emerging diagnostic technique providing both functional and anatomical information. DECT has been reported to produce a much sharper delineation of perfusion defects than pulmonary scintigraphy, using a significantly lower equivalent dose of mSv. We highlight that DECT is particularly useful in SARS-Cov-2 infection, in order to determine the predominant underlying pathophysiology, particularly when respiratory failure prolongs despite improved lung parenchymal radiological findings.

Postmortem diagnosis of pulmonary tumor thrombotic microangiopathy with rapid exacerbation in a patient with gastric cancer: a case report.

BACKGROUND: Pulmonary tumor thrombotic microangiopathy (PTTM) is a condition that involves the development of pulmonary hypertension due to the presence of microscopic tumor emboli of the peripheral pulmonary arteries. Here, we report a case of rapidly exacerbating PTTM associated with gastric cancer that was identified postmortem through pathological autopsy. CASE PRESENTATION: A 52-year-old Asian woman who experienced anterior chest pain while coughing visited the orthopedic department of the Gifu University Hospital. She was diagnosed as having multiple osteolytic bone metastases throughout her body and was subsequently scheduled to undergo combined positron emission tomography and computed tomography (CT) to search for a primary lesion. However, 4 days after her visit to the orthopedic department, she was unable to stand up and thus visited the emergency department. At the time of admission, physical examination results revealed that she had a percutaneous oxygen saturation level of 90% (on room air) and cyanosis and that she was in a state of hemodynamic shock. Laboratory test results revealed elevated levels of fibrin degradation products and D-dimer in her blood. Chest CT results were normal. She was admitted to the hospital's general ward for follow-up but soon entered a gradually worsening state of shock and respiratory failure. Electrocardiography revealed findings associated with right heart strain; however, contrast-enhanced CT did not reveal the presence of pulmonary embolism. She was admitted to the intensive care unit and was treated for pulmonary hypertension; however, 45 h after her arrival at the hospital, she died of respiratory failure. A pathological autopsy revealed the presence of gastric cancer, tumor microemboli, and fibrous intimal thickening of the peripheral arteries of both lungs; thus, a diagnosis of PTTM was made. CONCLUSIONS: In patients with carcinoma of unknown primary site and pulmonary hypertension with pulmonary embolism ruled out by CT, emergency physicians and intensivists must consider the possibility of PTTM, which represents an oncologic emergency, and initiate chemotherapy administration as soon as possible.

Prostaglandin E1 prevents histopathological changes improving renal function in experimental nephropathy induced by renal microembolism.

This study investigated the effect of prostaglandin E1 (PGE-1) treatment on the biochemical and histopathological changes in a model of nephropathy that was induced using renal microembolism in rats. Wistar rats were assigned to three groups: a control group (C, normal), a renal microembolism (RM) group, and a renal microembolism treated with PGE-1 (RM + PGE-1) group. The renal microembolism was induced by an arterial injection of polymethylmethacrylate microbeads into the remaining kidney of nephrectomized rats. Intramuscular treatment with PGE-1 was initiated on the day of the induction of the renal microembolism and continued once weekly for up to 60 days. At the end of the treatment period, blood samples were taken to assess the serum creatinine and urea concentrations, and 24-h urine samples were collected to determine the total protein levels. The rats' kidneys were removed and processed for histopathological analysis using the hematoxylin and eosin, periodic acid-Schiff, Mallory-Azan, and Picro-Sirius techniques. An immunohistochemical assay with vascular endothelial growth factor receptor-2 (anti-VEGFR-2) was also performed. The results showed that the PGE-1 treatment prevented vascular, glomerular, tubular, and interstitial alterations and reduced the biochemical changes, thus improving the renal function in rats that were subjected to renal microembolism. These effects could be partially attributable to an increase in the PGE-1-induced angiogenesis, because we observed an increase in the tissue expression of VEGFR-2, a specific marker of angiogenesis.

Transplantation of Endothelial Progenitor Cells in the Treatment of Coronary Artery Microembolism in Rats.

As the impairment of myocardial microenvironments due to coronary microembolization (CME) compromises the treatment effect of percutaneous coronary intervention and leads to adverse prognosis, we hypothesized that endothelial progenitor cells (EPCs) transplantation could improve cardiac function in the condition of CME. Low- (2 × 105) and high- (2 × 106) dose rat bone marrow-derived EPCs were transplanted in a model of CME. To develop a CME model, rats were injected with autologous micro-blood-clots into the left ventricle. Echocardiograph was examined before and 1, 7, and 28 days after EPC transplantation; serum cardiac troponin I (cTNI), von Willebrand factor (vWF), and cardiac microRNA expression were examined one day after EPCs transplantation. Heart morphology and vascular endothelial growth factor (VEGF), vWF, and basic fibroblast growth factor (bFGF) expression were examined one day after EPC transplantation. After 10 days of culture inductions, BM-EPCs have high purity as confirmed by flow cytometry. Cardiac function reflected by left ventricular ejection fraction significantly decreased after CME treatment and rescued by low-dose EPC. Compared to the sham group, cTNI and vWF serum levels increased significantly after CME treatment and rescued by low-dose EPC and high-dose EPC. Low-dose EPC treatment decreased myocardial necrosis and fibrosis and elevated cardiac expression of VEGF and vWF, while decreasing the cardiac expression of bFGF. Low-dose EPC treatment significantly suppressed cardiac expression of microRNA-19a but significantly enhanced microRNA-21, microRNA-214, and microRNA-486-3p expression. In conclusion, our results indicate that low-dose EPC transplantation may play a proangiogenic, antifibroblast, antifibrosis, and antinecrosis role and enhance cardiac function in a rat model of CME through a microRNA-related pathway.

Cerebral microembolism during atrial fibrillation ablation can result from the technical aspects and mostly does not cause permanent neurological deficit.

INTRODUCTION: Atrial fibrillation ablation can be associated with microembolism detected in the intracranial arteries and risk of neurological incidents. The aims of this study were to evaluate microembolic signals (MES) during pulmonary vein isolation (PVI) and establish the potential significance of MES for damage of the brain in radiological investigation and neurological state. MATERIAL AND METHODS: In the prospective study we included patients with atrial fibrillation undergoing percutaneous pulmonary vein isolation (radiofrequency ablation/balloon cryoablation) with ultrasound monitoring of microembolisms in the middle cerebral artery. Neurological examination and MRI of the head were performed in all participants. RESULTS: The study enrolled 80 patients at a mean age of 58 years. Microembolisms during the monitoring of the flow in the right middle cerebral artery were recorded in 61 (76.3%) patients in the amount of 51-489 (mean: 239). Most often the microembolic signals were registered during the trans-septal puncture and the stage of ablation. In 89%, microembolisms were gaseous. Mean score on the Fazekas scale for the whole group before ablation: 0.87 ±0.7 (0-3, med. 1); after: 0.93 ±0.71. In 3 (4.3%) patients the lesions worsened during the follow-up period. None of the patients revealed a cardiovascular event during the follow-up period and no changes were observed in the neurological status. CONCLUSIONS: The majority of cerebral microembolisms generated during PVI are gaseous in nature. The cerebral microembolisms associated with PVI probably result from the technical aspects of the procedure and do not cause either permanent brain damage in the radiological investigation or neurological deficit.