Cerebrovascular complications after orthotopic heart transplantation (OHT) are more common in comparison with neurological sequelae subsequent to routine cardiac surgery. Ischemic stroke and transient ischemic attack (TIA) are more common (with an incidence of up to 13%) than intracranial hemorrhage (2.5%). Clinically, ischemic stroke is manifested by the appearance of focal neurologic deficits, although sometimes a stroke may be silent or manifests itself by the appearance of encephalopathy, reflecting a diffuse brain disorder. Ischemic stroke subtypes distribution in perioperative and postoperative period after OHT is very different from classical distribution, with different pathogenic mechanisms. Infact, ischemic stroke may be caused by less common and unusual mechanisms, linked to surgical procedures and to postoperative inflammation, peculiar to this group of patients. However, many strokes (40%) occur without a well-defined etiology (cryptogenic strokes). A silent atrial fibrillation (AF) may play a role in pathogenesis of these strokes and P wave dispersion may represent a predictor of AF. In OHT patients, P wave dispersion correlates with homocysteine plasma levels and hyperhomocysteinemia could play a role in the pathogenesis of these strokes with multiple mechanisms increasing the risk of AF. In conclusion, stroke after heart transplantation represents a complication with considerable impact not only on mortality but also on subsequent poor functional outcome.
Atrial Fibrillation ; Brain Diseases ; Heart Transplantation* ; Heart* ; Homocysteine ; Humans ; Hyperhomocysteinemia ; Incidence ; Inflammation ; Intracranial Hemorrhages ; Ischemic Attack, Transient ; Mortality ; Neurologic Manifestations ; Plasma ; Postoperative Period ; Stroke* ; Thoracic Surgery

No abstract available.
Antihypertensive Agents* ; Cerebral Hemorrhage* ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors* ; Vascular Stiffness*

BACKGROUND AND PURPOSE: Intracerebral hemorrhage (ICH) accounts for approximately 10% of stroke cases. Hypertension may play a role in the pathogenesis of ICH that occurs in the basal ganglia, thalamus, pons, and cerebellum, but not in that of lobar ICH. Hypertension contributes to decreased elasticity of arteries, thereby increasing the likelihood of rupture in response to acute elevation in intravascular pressure. This study aimed to evaluate arterial stiffness (using the arterial stiffness index [ASI]) in patients with deep (putaminal and thalamic) ICH in comparison with patients with lobar ICH. METHODS: We enrolled 64 patients (mean+/-SD age: 69.3+/-10.7 years; 47 men and 17 women) among 73 who referred consecutively to our department for intraparenchymal hemorrhage and underwent brain computed tomography (CT) and cerebral angio-CT. In all the subjects, 24-hour heart rates and blood pressures were monitored. The linear regression slope of diastolic on systolic blood pressure was assumed as a global measure of arterial compliance, and its complement (1 minus the slope), ASI, has been considered as a measure of arterial stiffness. RESULTS: In the patients with deep ICH, ASI was significantly higher than in the patients with lobar ICH (0.64+/-0.19 vs. 0.53+/-0.17, P=0.04). CONCLUSIONS: Our results suggest that in deep ICH, arterial stiffening represents a possible pathogenetic factor that modifies arterial wall properties and contributes to vascular rupture in response to intravascular pressure acute elevation. Therapeutic strategies that reduce arterial stiffness may potentially lower the incidence of deep hemorrhagic stroke.
Arteries ; Basal Ganglia ; Blood Pressure ; Brain ; Cerebellum ; Cerebral Hemorrhage* ; Complement System Proteins ; Compliance ; Elasticity ; Heart Rate ; Hemorrhage ; Humans ; Hypertension ; Incidence ; Linear Models ; Male ; Pons ; Rupture ; Stroke ; Thalamus ; Vascular Stiffness*

BACKGROUND AND PURPOSE: Intracerebral hemorrhage (ICH) accounts for approximately 10% of stroke cases. Hypertension may play a role in the pathogenesis of ICH that occurs in the basal ganglia, thalamus, pons, and cerebellum, but not in that of lobar ICH. Hypertension contributes to decreased elasticity of arteries, thereby increasing the likelihood of rupture in response to acute elevation in intravascular pressure. This study aimed to evaluate arterial stiffness (using the arterial stiffness index [ASI]) in patients with deep (putaminal and thalamic) ICH in comparison with patients with lobar ICH. METHODS: We enrolled 64 patients (mean+/-SD age: 69.3+/-10.7 years; 47 men and 17 women) among 73 who referred consecutively to our department for intraparenchymal hemorrhage and underwent brain computed tomography (CT) and cerebral angio-CT. In all the subjects, 24-hour heart rates and blood pressures were monitored. The linear regression slope of diastolic on systolic blood pressure was assumed as a global measure of arterial compliance, and its complement (1 minus the slope), ASI, has been considered as a measure of arterial stiffness. RESULTS: In the patients with deep ICH, ASI was significantly higher than in the patients with lobar ICH (0.64+/-0.19 vs. 0.53+/-0.17, P=0.04). CONCLUSIONS: Our results suggest that in deep ICH, arterial stiffening represents a possible pathogenetic factor that modifies arterial wall properties and contributes to vascular rupture in response to intravascular pressure acute elevation. Therapeutic strategies that reduce arterial stiffness may potentially lower the incidence of deep hemorrhagic stroke.
Arteries ; Basal Ganglia ; Blood Pressure ; Brain ; Cerebellum ; Cerebral Hemorrhage* ; Complement System Proteins ; Compliance ; Elasticity ; Heart Rate ; Hemorrhage ; Humans ; Hypertension ; Incidence ; Linear Models ; Male ; Pons ; Rupture ; Stroke ; Thalamus ; Vascular Stiffness*