Incidence Of Cerebral Lesions Research Articles

P472Cerebral thromboembolic risk in atrial fibrillation ablation: a direct comparison of vitamin K antagonists versus non-vitamin K-dependent oral anticoagulants

Abstract Aims Cerebral thromboembolic events are well-known complications of pulmonary vein isolation (PVI) and can manifest as stroke or silent cerebral embolic lesions. Over the last years, the preferred oral anticoagulation in atrial fibrillation (AF) shifted from vitamin K antagonists (VKA) to non-vitamin K-dependent oral anticoagulants (NOAC). The aim of this study was to compare the incidence of cerebral embolic lesions after AF ablation in patients on VKA versus patients on NOAC, and to identify corresponding clinical and procedural risk factors. Methods A total of 421 patients undergoing PVI (by radiofrequency catheter or cryoballoon) were prospectively included into the study. Of these, 43.7% were on VKA and 56.3% on NOAC treatment. In the NOAC group 38% of patients had an interruption of anticoagulation for 24-36 hours. All patients underwent pre- and postprocedural cerebral magnetic resonance imaging. Results Periprocedural cerebral lesions occurred in 13.1% overall. Of these, three (0.7%) resulted in symptomatic cerebrovascular accidents. Incidence of cerebral lesions was significantly higher in patients on NOAC compared to VKA (16% vs. 9.2% respectively, p = 0.04), as well as in patients that had intraprocedural cardioversions compared to no cardivoersions (19.5% vs. 10.4% respectively, p = 0.03). In multivariate analysis both parameters were found to be independent risk factors for cerebral embolism. No significant difference between interrupted and uninterrupted NOAC administration could be detected. Conclusions In patients undergoing AF ablation, we identified the use of NOAC and intraprocedural cardioversion as independent risk factors for the occurrence of periprocedural cerebral embolic lesions. Abstract Figure. Incidence of cerebral embolic lesions

Cerebral thromboembolic risk in atrial fibrillation ablation: a direct comparison of vitamin K antagonists versus non-vitamin K-dependent oral anticoagulants.

Cerebral thromboembolic events are well-known complications of pulmonary vein isolation (PVI) and can manifest as stroke or silent cerebral embolic lesions. The aim of this study was to compare the incidence of cerebral embolic lesions (including silent cerebral embolism and stroke) after AF ablation in patients on vitamin K antagonists versus patients on non-vitamin K-dependent oral anticoagulants, and to identify corresponding clinical and procedural risk factors. A total of 421 patients undergoing PVI were prospectively included into the study. Of these, 43.7% were on VKA and 56.3% on NOAC treatment (dabigatran, rivaroxaban, apixaban, and edoxaban). In the NOAC group, 38% of patients had an interruption of anticoagulation for 24-36h. All patients underwent pre- and postprocedural cerebral magnetic resonance imaging. Periprocedural cerebral lesions occurred in 13.1% overall. Of these, three (0.7%) resulted in symptomatic cerebrovascular accidents and 52 (12.4%) in silent cerebral embolic lesions. Incidence of cerebral lesions was significantly higher in patients on NOAC compared with VKA (16% vs. 9.2%, respectively, p = 0.04), and in patients who had intraprocedural cardioversions compared with no cardivoersions (19.5% vs. 10.4%, respectively, p = 0.03). In multivariate analysis, both parameters were found to be independent risk factors for cerebral embolism. No significant difference between interrupted and uninterrupted NOAC administration could be detected. In patients undergoing AF ablation, we identified the use of NOAC and intraprocedural cardioversion as independent risk factors for the occurrence of periprocedural cerebral embolic lesions.

Management of active infective endocarditis

The pathology of infective endocarditis varies but is classifi ed into infection, cardiac, cerebrovascular, and embolism symptoms. Fever as a symptom of infection is the typical remittent fever observed in bacteremia; however, fever is often mild in patients who have already received antibiotics. Once treatment is initiated, the fever abates and the sense of serious illness disappears; therefore, endocardial lesions may not be examined for some weeks. In such a situation, endocardial or cerebrovascular infection lesions have not always been controlled despite the mild fever. When poor results of treatment for infection lead to a terminal condition of bacteremia, septic shock develops. In septic shock, the peripheral blood vessels are abnormally dilated; the heart develops a high-output hyperdynamic state as if a large arteriovenous shunt had formed while blood fl ow in major organs decreases, and renal and respiratory failure rapidly progresses. Cerebrovascular as well as cardiac lesions observed in infective endocarditis are serious and often fatal. A study involving 2523 patients who underwent surgery for valvular disease of the heart associated with infective endocarditis showed an incidence of cerebral lesions of 9.7%. Such cerebral lesions are caused by infective cerebral vasculitis (including infective cerebral aneurysms) and bacteria-associated embolism. As a result, cerebral hemorrhage (subarachnoid, intracranial), cerebral infarction, and hemorrhagic infarction occur. Cerebral abscess or meningitis also sometimes develops. The statistics cited above revealed the following make-up of cerebral lesions: cerebral infarction, 65%; cerebral hemorrhage, 32%; cerebral abscess, 3%; and meningitis, 1%. Bacteria-associated cerebral aneurysms develop in 4%– 15% of cases of infective endocarditis. However, the cause of intracranial hemorrhage is hemorrhagic infarction in 75% of cases and bacteria-associated cerebral aneurysms in only 19%. Some studies have also suggested that pyrogenic arteritis that does not induce arterial wall dilation is the source of hemorrhage. As a result of infective embolism of small vessels, infl ammation develops fi rst in the adventitia. The presence of cerebral lesions markedly limits the indications for cardiac surgery by cardiopulmonary bypass.

CHLORIDE ION INGESTED WITH SODIUM AFFECTS THE DEVELOPMENT OF CEREBRAL LESIONS IN STROKE-PRONE SPONTANEOUSLY HYPERTENSIVE RATS

1. To determine the effect of chloride ion on the development of hypertension and the incidence of cerebral lesions in stroke-prone spontaneously hypertensive rats (SHRSP), groups of 10 rats were administered chronically with either 171 mmol/L sodium chloride or equimolar sodium provided as sodium citrate in the drinking water from the age of 12 weeks. 2. The life span was significantly extended in SHRSP given sodium citrate (336 +/- 28 vs 246 +/- 26 days, mean +/- s.e.m., P less than 0.05) but their development of hypertension was not different from SHRSP given sodium chloride. 3. In order to determine the role of calcium homeostasis, calcium in urine was collected. Urinary calcium in SHRSP given sodium citrate was significantly decreased (1.0 +/- 0.12 vs 1.8 +/- 0.18 mg/24 h urine, P less than 0.05). 4. If the normal life span is 320 +/- 35 days, this suggests that chloride ion ingested with sodium accelerates the development of cerebrovascular diseases, and that increased urinary calcium excretion may be related to this adverse chloride effect on the development of hypertension in SHRSP.

Myocardial Infarction in the Differential Diagnosis of Dementias in the Elderly

The incidence of cerebral lesions in relation to myocardial infarction (MI) was evaluated on the basis of data obtained from medical records and autopsy reports on 269 psychogeriatric patients, in a 13-year retrospective study. Among 84 demented patients with MI, brain infarcts and hemorrhages were found in 42 percent, and Alzheimer's disease in 17 percent; (combination in 8 percent). In contrast, among 70 demented patients without MI, brain infarcts and hemorrhages were found in 11 percent, and Alzheimer's disease in 43 percent; (combination in 6 percent). Therefore, when it is difficult to differentiate senile dementia (Alzheimer's disease) from dementia due to cerebrovascular impairment, data on the presence or absence of myocardial infarction may prove useful.

Incidence of cerebral and spinal vascular lesions in stroke-prone SHR (SHRSP)--pathohistological and electromyographical confirmation [proceedings

From these results, it is confirmed that generalized and focal signs, such as paraparesis or hemiparesis which are observed at the symptomatological grades 2, 3 and 4 SHRSP do scarcely result from the spinal cord lesions, and therefore, neurological signs and symptoms of SHRSP are manifestations due to cerebral lesions in most cases. In SHRSP, the incidence of cerebral lesions is much higher than that of spinal lesions, among all vascular lesions in the central nervous system as in humans

What makes the renin-angiotensin system a pathogenic factor?

Three types of renal hypertension in the rat have been compared with respect to blood pressure increase, activity of the RAS, and secretion of aldosterone and corticosterone: type I - unilateral stenosis of the renal artery in the presence of an intact contralateral kidney; type II - unilateral stenosis of the renal artery after contralateral nephrectomy; type III - bilateral stenosis of the renal arteries. Blood pressure rose more rapidly and reached higher values in type II and type III hypertension than in type I hypertension. In the latter group, the activity of the RAS was more stimulated than in types II and III. The marked stimulation of the RAS in type I hypertension is ascribed to the negative fluid and sodium balance, which is the consequence of a pressure-induced diuresis of the unclamped contralateral kidney. Suppression of the activity of the RAS by a 4-week pretreatment with DOC-TMA and saline or by the administration of DOCA and saline as from the induction of renal artery stenosis did not prevent the development of hypertension caused by the clamping of one renal artery (type I). In spontaneously hypertensive rats of the stroke-prone substrain, high dietary salt intake caused higher blood pressure values and a higher incidence of cerebral lesions than normal dietary salt intake. Low salt intake was followed by a marked stimulation of the RAS, but blood pressure rose only slightly and no symptoms of cerebrovascular lesions were observed. It is concluded that neither in hypertension induced by renal artery stenosis nor in spontaneously hypertensive rats, the RAS contributes significantly to the increase in blood pressure nor does it play a major part in the pathogenesis of vascular lesions. These seem to be related to the retention of sodium, which may be obtained by renal artery stenosis, by excessive salt intake, or by the administration of a mineralocorticoid and salt.