Correlation between Morphological and Hemodynamic Parameters of Carotid Arteries and Cerebral Vasomotor Reactivity.

The function of cerebral small vessels can be assessed using cerebral vasomotor reactivity (VMR). Our aim in this retrospective cross-sectional study was to investigate a correlation between carotid artery stenosis measured through ultrasonographic morphological and hemodynamic parameters and cerebral VMR. A total of 285 patients (125 males; mean age 54) were included. The breath-holding index (BHI) was used to evaluate cerebral VMR. Ultrasonographic carotid artery parameters were collected: the presence and characteristics of carotid plaques, the degree of carotid diameter stenosis, intima-media thickness (IMT), peak systolic velocity (PSV), and end diastolic velocity (EDV). Additionally, hemodynamic parameters of the middle cerebral artery (MCA) were evaluated, including the mean flow velocity (MFV) and pulsatility index (PI). The following was collected from patients' medical histories: age, gender, and vascular risk factors. A negative correlation between the BHI and age (r = -0.242, p < 0.01), BHI and the presence of carotid plaques, BHI and IMT (r = -0.203, p < 0.01), and BHI and the PI of MCA on both sides (r = -0.268, p < 0.01) was found. We found a positive correlation between the BHI in the left MCA and EDV in the left internal carotid artery (r = 0.121, p < 0.05). This study shows the correlation between cerebral VMR and carotid stenosis but indicates a higher influence of morphological parameters on VMR values.

Ligamentum flavum analysis in patients with lumbar discus hernia and lumbar spinal stenosis.

The normal ligamentum flavum (LF) is a well-defined elastic structure with specific innervation. Several studies investigated LF in patients with lumbar spinal stenosis (LSS) and used lumbar discus hernia (LDH) patients as control group, only on the presumed thesis that LF in this patients have normal morphology. In patients with LSS thickening of the LF is the main cause of stenosis, which is most often presented with neurogenic claudication, whose pathophysiological mechanism is not completely understood. We conducted observational cohort study of 60 operated patients divided into two groups. The first group of 30 patients underwent micro-discectomy (LSH group), and second group with 30 patients underwent decompression, after which analysis of harvested LF was performed. Patients from the LDH group and LSS group differed significantly in the frequencies of chief complaints, duration of symptoms, physical examination, and specific morphological/radiological parameters. The LF analysis showed that the groups differed significantly in the amount of collagen and elastic fibers, as well as in the histological appearance/architectonics of elastic fibers. Also, groups differ in the presence of LF nerve fibers. Our findings speak in favor of the recently postulated inflammatory theory in the origin of spinal neurogenic claudication's.

Can MDCT Enhancement Patterns Be Helpful in Differentiating Secretory from Non-Functional Adrenal Adenoma?

Background and Objectives: Primary adrenal tumors (AT) are a heterogeneous group of neoplasms due to their functional heterogeneity, which results in the diverse clinical presentation of these tumors. The purpose of this study was to examine cross-sectional imaging characteristics using multi-detector computed tomography (MDCT) to provide insight into the lesion characterization and functional status of these tumors. The radionuclide imaging using Technetium-99m radiolabeled hydrazinonicotinylacid-d-phenylalanyl1-tyrosine3-octreotide (99mTc-HYNIC-TOC), was also used in the diagnostic evaluation of these tumors. Materials and Methods: This cross-sectional study included 50 patients with confirmed diagnoses of AT (21 hormone-secreting and 29 non-functional) at the University Clinical Center, Kragujevac, Serbia, during the 2019-2022 year period. The morphological and dynamic characteristics using MDCT were performed, using qualitative, semi-quantitative, and quantitative analysis. Absolute washout (APW) and relative washout (RPW) values were also calculated. A semi-quantitative analysis of all visual findings with 99mTc-HYNIC-TOC was performed to compare the tumor to non-tumor tracer uptake. Results: A statistically significant difference was found in the MDCT values in the native phase (p < 0.05), the venous phase (p < 0.05), and the delayed phase (p < 0.001) to detect the existence of adrenal tumors. Most of these functional adrenocortical lesions (n = 44) can be differentiated using the delayed phase (p < 0.05), absolute percentage washout (APW) (p < 0.05), and relative percentage washout (RPW) (p < 0.001). Furthermore, 99mTc-HYNIC-TOC could have a high diagnostic yield to detect adrenal tumor existence (p < 0.001). There is a positive correlation between radionuclide imaging scan and APW to detect all AT (p < 0.01) and adrenocortical adenomas as well (p < 0.01). Conclusions: The results can be very helpful in a diagnostic algorithm to quickly and precisely diagnose the expansive processes of the adrenal glands, as well as to learn about the advantages and limitations of the mentioned imaging modalities.

Dural metastasis of prostate carcinoma misdiagnosed as a bilateral subdural hematoma: A case report.

Dural metastases originating from prostate cancer are exceedingly uncommon and may clinically imitate a subdural hematoma. Additionally, head computed tomography scan findings can be mistaken for meningioma or subdural hematoma. We present a 75-year-old male patient with dural metastasis as a first presenting sign of prostate cancer, misdiagnosed as a bilateral subdural hematoma on initial non-contrast brain CT scan. Also, a review of literature is presented. We found 12 cases of dural metastasis of prostate cancer mimicking subdural hematoma described in the literature, and unlike in our case, prostate cancer was already diagnosed.

Relationship between bone disorders and stroke.

Bone disorders are among the most uncommon causes of stroke, but they should be considered as stroke cause in particular clinical scenarios. On the other hand, osteoporosis/osteopenia and increased fracture risk are well documented post stroke complications. The relationship between stroke and bone health is complex. The current facts suggest that these two conditions share same risk factors, but also are risk factors for each other. However, the evidence shows more clear effect of stroke on the bone health, than in the opposite direction. This extensive review is aiming to fill the huge gap of evidence about this topic, and since bone pathology is extremely rare cause of cerebrovascular accident, although a complex connection between these two conditions definitely exists.

Hyperbaric oxygen therapy in acute stroke: is it time for Justitia to open her eyes?

Hypoxia is a critical component of neuronal death in patients with stroke. Therefore increasing oxygenation of brain tissue seems to be a logical therapy against cerebral ischemia. Oxygen therapy exists in two modalities: normobaric hyperoxia therapy and hyperbaric oxygen therapy (HBO). HBO is a therapeutic procedure in which pure (100%) oxygen is administered at greater than atmospheric pressure in HBO therapy chambers. In this review article, we aimed to summarize the current knowledge regarding the therapeutic use of HBO in acute stroke patients. Literature review and electronic search were performed using PubMed, Medscape, and UpToDate with the keywords stroke, acute stroke, hyperbaric oxygen therapy, and hyperoxia. According to the reviewed literature, the use of HBO as routine stroke therapy cannot be justified in acute stage of stroke. More randomized, controlled studies are needed regarding safety and especially effectives of HBO in stroke patients. Also, standardized definitionof HBO should be proposed and used in all future studies.

Full-endoscopic interlaminar operations in lumbar compressive lesions surgery: prospective study of 350 patients - "ENDOS" Study.

BACKGROUND: Full-endoscopic operations of lumbar spine are truly minimally invasive surgical procedures. Endoscopic techniques have become the standard in many areas because of the advantages they offer intraoperatively and after surgery. With the interlaminar and transforaminal approach, two full-endoscopic procedures are available for lumbar compressive lesion operations. Our aim was to present and explain all aspects of the full-endoscopic operative technique, and presentation of results of lumbar discectomies and monosegmental decompression in full-endoscopic interlaminar technique performed during 3-year period in comparison with conventional microsurgical operations reported in literature. METHODS: A series of 350 patients underwent full-endoscopic interlaminar lumbar discectomy, and spinal canal decompression, during a 3-year period, is analyzed. In addition to general and specific parameters, VAS and ODI scale are used as measuring instruments. RESULTS: In our clinical series of full-endoscopic operations 88% of the patients no longer had leg pain postoperatively, and 7% had only occasional pain. In 7 (2%) patients minor nerve damage resulted in transient paresthesias, and in 2 patients resulted in neurological deficit. Dural tear occurred in 8 (2.3%) patients, and only 1 had reoperation for direct dural repair. The recurrence rate was 5.7% (3.7% had reoperation). Resection of the herniated disc and sufficient decompression was technically possible in all cases. CONCLUSIONS: The clinical results of the full-endoscopic technique are at least equal to those of the conventional microsurgical discectomy with advantages such as reduced tissue trauma, improved patient mobility, and lower overall complication rate. With the possibility of selecting the most adequate approach, lumbar disc herniations inside and outside the spinal canal, can be sufficiently removed using the full-endoscopic technique, when taking the appropriate indication criteria into account.

Role of prediabetes in stroke.

Stroke is one of the leading causes of death and probably the greatest cause of adult disability worldwide. Diabetes mellitus (DM) is a state of accelerated aging of blood vessels. Patients with diabetes have increased risk of stroke. Hyperglycemia represents a risk factor for poor outcome following stroke, and probably is just a marker of poor outcome rather than a cause. Lowering of blood glucose levels has not been shown to improve prognosis. Also, prevention of stroke risk among patients with DM is not improved with therapy for reduction of glucose levels. On the other hand, prediabetes, a metabolic state between normal glucose metabolism and diabetes, is a risk factor for the development of DM type 2 and subsequently for stroke. Several methods are known to identify prediabetes patients, including fasting plasma glucose levels, 2-hour post load glucose levels, and glycosylated hemoglobin levels. In this text, we tried to summarize known data about diagnosis, epidemiology, risk factors, pathophysiology, and prevention of prediabetes in relation to DM and stroke.

Post-stroke dementia - a comprehensive review.

Post-stroke dementia (PSD) or post-stroke cognitive impairment (PSCI) may affect up to one third of stroke survivors. Various definitions of PSCI and PSD have been described. We propose PSD as a label for any dementia following stroke in temporal relation. Various tools are available to screen and assess cognition, with few PSD-specific instruments. Choice will depend on purpose of assessment, with differing instruments needed for brief screening (e.g., Montreal Cognitive Assessment) or diagnostic formulation (e.g., NINDS VCI battery). A comprehensive evaluation should include assessment of pre-stroke cognition (e.g., using Informant Questionnaire for Cognitive Decline in the Elderly), mood (e.g., using Hospital Anxiety and Depression Scale), and functional consequences of cognitive impairments (e.g., using modified Rankin Scale). A large number of biomarkers for PSD, including indicators for genetic polymorphisms, biomarkers in the cerebrospinal fluid and in the serum, inflammatory mediators, and peripheral microRNA profiles have been proposed. Currently, no specific biomarkers have been proven to robustly discriminate vulnerable patients ('at risk brains') from those with better prognosis or to discriminate Alzheimer's disease dementia from PSD. Further, neuroimaging is an important diagnostic tool in PSD. The role of computerized tomography is limited to demonstrating type and location of the underlying primary lesion and indicating atrophy and severe white matter changes. Magnetic resonance imaging is the key neuroimaging modality and has high sensitivity and specificity for detecting pathological changes, including small vessel disease. Advanced multi-modal imaging includes diffusion tensor imaging for fiber tracking, by which changes in networks can be detected. Quantitative imaging of cerebral blood flow and metabolism by positron emission tomography can differentiate between vascular dementia and degenerative dementia and show the interaction between vascular and metabolic changes. Additionally, inflammatory changes after ischemia in the brain can be detected, which may play a role together with amyloid deposition in the development of PSD. Prevention of PSD can be achieved by prevention of stroke. As treatment strategies to inhibit the development and mitigate the course of PSD, lowering of blood pressure, statins, neuroprotective drugs, and anti-inflammatory agents have all been studied without convincing evidence of efficacy. Lifestyle interventions, physical activity, and cognitive training have been recently tested, but large controlled trials are still missing.

Giant Vertebrobasilar Fusiform Aneurysm as a Cerebellopontine Angle Mass.

INTRODUCTION: According to the literature, a fusiform aneurysm located in the cerebellopontine angle (CPA) is an extremely rare condition. CASE OUTLINE: We report a case of a 59-year-old patient with initial dizziness and left-sided sensorineural hearing loss that had gradually developed over six months. Vertebrobasilar fusiform aneurysm, with intraluminal thrombus, which was displaced to the right cerebellopontine angle, creating mass effect, was diagnosed using brain magnetic resonance imaging and magnetic resonance angiography. CONCLUSION: Atherosclerosis may be the essential factor in the pathogenesis of a fusiform aneurysm of the basilar artery, especially in elderly patients. The best treatment option is yet to be determined, but in soite of numerous previous large studies, personalized approach is probably the best.

Cluster headache as a first manifestation of multiple sclerosis: case report and literature review.

Cluster headache (CH) is estimated to be the most common primary trigeminal autonomic headache, although it is a rare disabling medical condition. Dominant symptoms of CH include severe unilateral orbital, supraorbital, and/or temporal pain, lasting from 15 to 180 minutes if untreated, associated with at least one of various autonomic symptoms during the headache, such as conjunctival injection, lacrimation, nasal congestion and rhinorrhea, facial sweating, miosis, ptosis, and eyelid edema. Headache is not frequently a symptom of multiple sclerosis (MS). The most commonly reported primary headaches are migraine without aura and a tension-type headache. Several described cases involved complicated migraine, ophthalmoplegic migraine-like headache, and finally cluster-like headache. We present a case of a 45-year-old male patient who had typical CH attacks as the initial and only clinical manifestation of MS, which was diagnosed after cerebrospinal fluid (CSF) isoelectric focusing and brain magnetic resonance imaging (MRI) investigation. He presented as a typical cluster-like headache patient since in the background of the CH symptoms and signs, were MS demyelinating lesions. In a patient with CH symptoms one should always think about the possibility of cluster-like-headache, which presents the CH patient with different underlying diseases, so we proposed a protocol to evaluate such patients and exclude diseases that could be in the background of CH symptoms.

Time-dependent changes and association between liver free fatty acids, serum lipid profile and histological features in mice model of nonalcoholic fatty liver disease.

BACKGROUND AND AIMS: Methionine-choline deficient (MCD) diet duration necessary for development of non-alcoholic fatty liver disease (NAFLD) and the dynamic of lipid profile and fatty acids are not completely established. The study examined dynamics and association between liver free fatty acids (FFA), serum lipid profile and liver morphological changes on MCD diet-induced NAFLD in mice. METHODS: Male C57BL/6 mice (n = 28) were divided into four groups (n = 7 per group): control: fed with standard chow, MCD diet-fed groups: 2, 4 or 6 weeks. After treatment, liver and blood samples were taken for histopathology, serum lipid profile, and liver FFA composition. RESULTS: Hepatic FFA profile showed a decrease in saturated acids, arachidonic and docosahexaenoic acid, whereas proportions of docosapentaenoic, oleic and linoleic acid were increased. Total cholesterol, HDL and triglycerides progressively decreased, whereas LDL level progressively increased. Focal fatty change in the liver appeared after 2 weeks, whereas diffuse fatty change with severe inflammation and ballooned hepatocytes were evident after 6 weeks. CONCLUSIONS: Six-week diet model may be appropriate for investigation of the role of lipotoxicity in the progression of NAFLD. Therefore, supplementation with n-3 polyunsaturated acid like DHA, rather than DPA, especially in the initial stage of fatty liver disease, may potentially have preventive effects and alleviate development of NAFLD/NASH and may also potentially reduce cardiovascular risk by moderating dyslipidemia.

Neurosarcoidosis: two case reports with multiple cranial nerve involvement and review of the literature.

BACKGROUND: Involvement of the central nervous system is registered in a relatively small number of patients with sarcoidosis. In this article we present two cases with various neurological symptoms that fulfill criteria for neurosarcoidosis (NS). In addition, we review the literature on NS with special attention to isolated cranial nerve involvement. METHODS AND RESULTS: First patient: Neurological examination identified multiple cranial neuropathy, moderate right-sided hemiparesis, polyradiculoneuritis of the lower limbs and positive meningeal signs. Laboratory tests showed serum and cerebrospinal fluid (CSF) inflammatory abnormalities, with increased values of the angiotensin-converting enzyme (ACE). CSF analysis also showed presence of 9 oligoclonal IgG bands. Brain and spine magnetic resonance imaging (MRI) revealed diffuse meningopathy, and focal granulomatous lesion in the body of the L5 vertebra. Lung sarcoidosis was confirmed by additional diagnostic procedures. The patient was treated with Methylprednisolone and a tapering course of oral Prednisone, which reduced the pain in the back and legs and improved the strength of the right leg. However, the other neurological deficiencies remained. After confirming lung sarcoidosis, the patient received Methotrexate in addition to Prednisone but during the following 2 years the patient's condition progressively worsened and ended in death. Second patient: Neurological findings showed weakness of the right n. oculomotorius and the right n. trochlearis, as well as the right-side face weakness. We found raised level of the ACE in serum and CSF. Thorax high-definition computed tomography (HDCTT) showed ribbon-like domains of discrete changes in the pulmonary parenchyma. MRI of the brain showed multiple white matter lesions. This patient also received Methylprednisolone followed by Prednisone, and after two months, ocular motility normalized. CONCLUSION: The diagnosis of NS is always a challenge. For this rerason definitive diagnosis requires the exclusion of other causes of neuropathy. Multiple cranial neuropathies should always arouse suspicion of NS.

The effects of caloric restriction against ethanol-induced oxidative and nitrosative cardiotoxicity and plasma lipids in rats.

Caloric restriction (CR) prevents or delays a wide range of aging-related diseases possibly through alleviation of oxidative stress. The aim of our study was to examine the effect of CR on oxidative and nitrosative cardiac damage in rats, induced by acute ethanol intoxication. Male Wistar rats were divided into following groups: control; calorie-restricted groups with intake of 60-70% (CR60-70) and 40-50% of daily energy needs (CR40-50); ethanol-treated group (E); calorie-restricted, ethanol-treated groups (CR60-70 + E, CR40-50 + E). Ethanol was administered in five doses of 2 g/kg every 12 h, while the duration of CR was five weeks before ethanol treatment. Malondialdehyde level was significantly lower in CR60-70 + E and significantly higher in CR40-50 + E vs. control. Nitrite and nitrate level was significantly higher in CR40-50 + E compared to control group. Activity of total superoxide dismutase (SOD) and its isoenzyme, copper/zinc-SOD (Cu/ZnSOD), was significantly higher in CR60-70 + E and lower in CR40-50 + E vs. control. Activity of manganese-SOD (MnSOD), that is also SOD isoenzyme, was significantly lower in CR40-50 + E compared to control group. Plasma content of sulfhydryl (SH) groups was significantly higher in CR60-70 group vs. control. Plasma concentration of total cholesterol, triacylglycerol, low-density lipoproteins and high-density lipoproteins was significantly lower in CR60-70 group compared to control values. Food restriction to 60-70% of daily energy needs has a protective effect on acute ethanol-induced oxidative and nitrosative cardiac damage, at least partly due to alleviation of ethanol-induced decrease in SOD activity, while restriction to 40-50% of energy needs aggravates lipid peroxidation and nitrosative stress.

[Vascular dementia: facts and controversies].

Vascular dementia (VaD) is the second most frequent dementia after Alzheimer's disease, and is diagnosed during lifetime in 20% of demented patients. Five-year survival rate in VaD is 39%, while it is estimated to be 75% in healthy persons of the same age. It is therefore important to make correct diagnosis of VaD early in the course of the disease. Risk factors forVaD are identical to stroke risk factors, and there are significant possibilities for the prevention of vascular cognitive decline. Cognitive decline develops acutely or step-by-step within three months after stroke, but more gradual progression of intellectual decline is also possible. Neurological examination can reveal pyramidal and extrapyramidal signs, pseudobulbar palsy, gait disturbance and urinary incontinence. Neuropsychological profile comprises the loss of cognitive set shifting, decline in word fluency, verbal learning difficulties, perseverations, difficulties in complex figure copying, and in patients with cortically located lesions also problems with speech and praxia. The basis of the diagnosis is, besides history, neurological examination and neuropsychological assessment, computed tomography and/ or magnetic resonance brain imaging. Vascular risk factors control is the most important measure in VaD prevention. Modern guidelines for the treatment of cognitive decline in VaD emphasize that donepezil can be useful in the improvement of cognitive status at the level of Class Ila recommendation at the level of evidence A, while memantine may be useful in patients with mixed VaD and Alzheimer's disease dementia.

The effect of calorie restriction on acute ethanol-induced oxidative and nitrosative liver injury in rats.

The aim of our study was to examine the effect of calorie restriction (CR) on oxidative and nitrosative liver injury in rats, induced by acute ethanol intoxication. Male Wistar rats were divided into groups: (1) control; (2) calorie-restricted groups with intake of 60-70% (CR60-70) and 40-50% of daily energy needs (CR40-50); (3) ethanol-treated group (E); (4) calorie-restricted, ethanol-treated groups (E+CR60-70 and E+CR40-50). Ethanol was administered in 5 doses of 2g/kg every 12h, and duration of CR was 5 weeks before ethanol treatment. Malondialdehyde and nitrite and nitrate level were significantly lower in E+CR60-70 and higher in E+CR40-50 vs. E group. Liver reduced glutathione content and activity of both superoxide dismutase izoenzymes were significantly higher in E+CR60-70 and lower in E+CR40-50 vs. E group. Oxidative stress may be a potential mechanism of hormetic effects of CR on acute ethanol-induced liver injury.

Alcoholic liver disease/nonalcoholic fatty liver disease index: distinguishing alcoholic from nonalcoholic fatty liver disease.

OBJECTIVE: The alcoholic liver disease (ALD)/nonalcoholic fatty liver disease (NAFLD) (ANI) scoring system was constructed as a response to a clinical need for avoiding the risks of liver biopsy in diagnosing the etiology of fatty liver disease. The aim of this study was to test the reliability of ANI as a noninvasive method to distinguish ALD from NAFLD. MATERIALS AND METHODS: One hundred and thirty-five patients were classified into two groups, ALD and NAFLD, according to the pathohistological results. Parameters for ANI are aspartate aminotransferase, alanine aminotransferase, mean corpuscular volume, BMI, and sex. ANI was calculated using an online calculator, official site of Mayo Clinic. RESULTS: ANI was significantly higher in patients with ALD than NAFLD (P<0.01). The cutoff point of ANI is -0.66. ANI greater than -0.66 indicates ALD, whereas ANI less than -0.66 yields a higher probability of NAFLD with high specificity (96.7%) and sensitivity (84.1%). The mean corpuscular volume and aspartate aminotransferase/alanine aminotransferase ratio were higher, whereas BMI was lower in patients with ALD than in NAFLD (P<0.01). CONCLUSION: The ANI scoring system may be used for the estimation of alcoholic origin of steatosis/steatohepatitis and may help in triaging patients for liver biopsy. ANI less than -0.66 indicates NAFLD, whereas ANI greater than -0.66 confirms the alcoholic etiology, but does not exclude the contribution of associated factors toward the development of fatty liver in a Serbian population.

Forensic aspects of water intoxication: four case reports and review of relevant literature.

Water intoxication (WI) is a rare condition that originates from over-consumption of water, with a potentially fatal outcome. Increased water intake (polydipsia) is followed by urination of high amount of diluted urine (polyuria) which are the main initial symptoms of WI. We present four case reports of WI. Two of them are unusual pediatric clinical cases using medical documentation and police case files, one of which is related to child abuse, and the other to a psychiatric disorder. The other two cases are fatal adult cases submitted to autopsy from a psychiatric hospital. Also, we present a diagnostic algorithm for polydipsia and polyuria before death. WI is usually seen in patients with psychiatric disorders, victims of child abuse or torture, drug abusers or it can be iatrogenically induced.

Unusual case of right atrial reinfarction.

It is well known that atrial infarctions are rare comparing to the ventricular. They cannot easily be verified on ECG and the standard autopsy technique does not include a detailed review of the atrial wall, so the atrial infarction often remains undiagnosed. A 63-year-old male was treated and died in an intensive care unit due to decompensated liver insufficiency and cardiac disease following long-lasting alcohol abuse. At autopsy, the extreme cardiomegaly was found, severe atherosclerosis of the anterior descending branch of left coronary artery. The posterior wall of the right atrium was thickened (cca 9 mm) in diameter of cca 3 × 3 cm, and this area was yellowish in the luminal part, while the central part was filled with dark red blood. A detailed dissection of the coronary arteries showed the complete occlusion of the atrial branch of the right coronary artery wreath as far as the place of sinoatrial artery branching, which corresponded anatomically to the described area of infarction on the posterior wall of the right atrium. Histopathological examination of the previously described area of the posterior wall of the right atrium, showed four zones of heart muscle changes: 1. zone of partially preserved structure of the heart muscle, 2. zone of cellular (immature) connective tissue, 3. areas of bleeding in cellular connective tissue, and 4. zone of acellular (old) connective tissue. These histopathological changes indicated that the posterior wall of the right atrium was affected by myocardial necrosis in at least two and possibly more times. It is reasonable to think that bleeding in the third zone of the posterior wall of the right atrium contributed greatly to the death due to the anatomical proximity to the sinoatrial node. It was confirmed by the existence of bradycardia with a prolonged PR interval, PR segment elevation in D1 and aVL lead and PR depression in the D3 lead on the ECG. These ECG changes appeared immediately before asystolia and the death of the patient, but not ventricular fibrillation or electromechanical dissociation due to ventricular infarction. The presented case shows that detailed autopsy examination of atrial wall and blood vessels can sometimes be crucial in disclosing the cause and mode of death if the ischemia and necrosis attack only the atrial wall, especially in the region of the heart conduction system.

Renal cancer and Wegener's granulomatosis: a case report.

Wegener's granulomatosis (WG) is a systemic disorder characterized by necrotizing vasculitis involving the respiratory tract, and in most cases, the kidneys. The most common manifestation of WG in the kidneys is segmental necrotizing glomerulonephritis. The presence of a renal mass as a manifestation of WG is rare. We report a patient with WG in whom a CT scan revealed an infiltrating mass in the lower portion of the left kidney. After surgical exploration, we performed an open radical nephrectomy. Histopathology showed clear cell type renal cell carcinoma (RCC). RCC associated with WG has been reported in only a few cases, and in most of them, the diseases started simultaneously, suggesting common pathogenetic pathways. Long-term immunosuppressive treatment is a known risk factor in the development of malignancies, so occurrence of RCC in WG has been proposed as a side effect of cyclophosphamide treatment. Furthermore, it is important to make a differential diagnosis between RCC and pseudotumors in WG as they cannot be distinguished solely on basis of imaging findings. Due to the higher risk of urologic malignancies, more frequent checkups and screening of WG patients should be considered.