BACKGROUND: Aprotinin is a serine protease inhibitor, which is usually used during cardiac surgery to reduce blood loss. There is evidence that aprotinin has neuroprotective effects during ischemia. We planned this study to evaluate its potential neuroprotective efficacy during hypothermic circulatory arrest (HCA). METHODS: Twenty piglets with a median weight of 25.7 kg (interquartile range, 23.9-26.6) were randomly assigned to receive aprotinin or placebo prior to a 75-minute period of HCA at 18 degrees C. Brain microdialysis parameters and neurological and histological scores were the primary outcome measures. RESULTS: Changes in brain metabolic parameters and histopathological findings were favorable in the aprotinin group. Brain lactate concentrations were significantly lower in the aprotinin group during the experiment (P = .02) along with blood lactate concentrations in the aprotinin group (P = .023). Brain glucose was significantly higher during the experiment (P = 0.02). Intracranial pressure tended to be higher in the control group. Two of 10 animals in the aprotinin group and 4 of 10 in the control group failed to reach full recovery on the seventh postoperative day. Four animals of 10 in the aprotinin group and 6 animals of 10 in the control group had brain infarction (P = .40). CONCLUSIONS: The present data suggest that aprotinin mitigates cerebral damage and improves neurological outcome following a period of HCA.
Approximately 500,000 Canadians live with heart failure (Ross et al., 2006). These numbers continue to rise due to advancing technology and successes in treating cardiac conditions and potentially fatal events such as myocardial infarctions. According to Carrier (2005), individuals with damaged hearts are living longer, and lives are being successfully saved with the surge of cardiovascular assist devices developed in recent years, which are increasingly used as a bridge to transplant. Despite the lifesaving capabilities of ventricular-assist devices, these innovations pose risks and complications that can be debilitating for patients and their families (Carrier, 2005). As this complex trajectory is navigated, nurses provide care and support to the patient and family while playing a unique role in the assessment and monitoring of these devices. A family-centred nursing model provides a framework for practice when nursing patients and families are in crisis. The foundations of the McGill Model of Nursing are focused on a strengths-based approach, revolving around collaboration between patients, family resources, and tailored interventions (Gottlieb & Feeley, 2005). As students placed in a critical care setting, we began to realize the complexity of care required to nurse these patients and their families. In this paper, a case study is used to describe and share our learning experiences of caring for a patient with a biventricular assist device, as well as the principles that guided our interventions.
Due to an increase in age of the patient population in cardiac surgery, cerebral complications are increasing in frequency, also as a cause of death. In order to reveal cerebral pathology associated with a fatal outcome after cardiac surgery, we re-evaluated the cast angiographs and medico-legal autopsy documents of 144 adult cardiac surgery subjects over a 7-year period. Special attention was paid to the ability of post-mortem cast angiography to aid in diagnosing cerebral pathology. The autopsy detected new ischemic cerebral lesions in 29 (20%) cases, of which 22 (15.3%) were recent infarcts, and 7 were cases of anoxic brain damage. Of the recent cerebral infarcts, 12 were associated with cerebral artery thrombosis, 4 showed multiple lesions, and the remaining 6 were small single infarcts. In addition, one subject had an intracerebral hemorrhage and 72 (50%) cerebral edema. By cast angiography, the leakage of contrast medium in the case of intracerebral hemorrhage and stenoses of intracranial and cervical arteries could be well demonstrated and also revealed 17 (77%) of the 22 recent cerebral infarcts. It was found to be suitable for detecting recent brain infarcts associated with main cerebral artery thrombosis, with a sensitivity of 92% (11 out of 12 cases), but was less sensitive in showing small recent infarcts with a sensitivity of 60% (6 out of 10 cases) and inferior for the older ones where none of the 6 cases were detected. Filling defects caused by cerebral edema were difficult to differentiate from technical errors and were encountered in 7 (4.8%) cases. A significant predictor for the 29 recent ischemic brain lesions was perioperative hypotension. The immediate cause of death was most often of cardiac (83%) and cerebral (14%) origin. In 14 cases, cerebral damage was considered to be an additional cause of death. The use of cerebral post-mortem cast angiography should be recommended, especially for its excellent ability to visualize intravascular pathology such as arterial stenoses and thromboses, with a 92% sensitivity in showing new main cerebral artery thromboses, before likely distortion of the vascular anatomy by dissection.
BACKGROUND: Young patients with cerebral infarction may differ from old patients with regard to clinical and prognostic aspects, and this may have implications for clinical management. MATERIAL AND METHODS: The article is based on literature found on PubMed and results from the authors' population-based study of 232 patients (aged 15-49) with cerebral infarction in Hordaland, Norway. RESULTS AND INTERPRETATION: The aetiology of cerebral infarction differs between young and old patients. Prothrombotic states and dissection are more frequent, while atherosclerosis is a relatively rare cause of cerebral infarction among young patients. After 6 years of follow-up in the Hordaland study; 9.9% of the patients had died, 9.9% had recurrence of cerebral infarction, and 10.5% had developed post-stroke seizures. Recurrence of cerebral infarction was strongly associated with the number of traditional risk factors. Even though most studies report that a majority of patients are functionally independent upon discharge from the hospital, many of these patients drop out of their jobs. The aetiology of the disease is unknown in a large proportion of young patients and it is not known why so many drop out of their jobs; future studies should address these issues.
Comment In: Tidsskr Nor Laegeforen. 2007 May 17;127(10):1401; author reply 1401-217520003
The syndrome of mitochondrial encephalomyopathy, lactic acidosis, and strokelike episodes (MELAS) may present with symptoms that resemble a stroke. The strokelike episodes most commonly involve the posterior part of the cerebrum. We identified retrospectively 38 patients with an occipital stroke between ages 18 to 45 years during a 19-year period in a hospital serving as the only neurologic center for a specific population. The common MELAS mutation at the base pair 3243 (A3243G) of the mitochondrial DNA (mtDNA) was analyzed in blood samples. We found four patients (10%) with a clinical or molecular diagnosis of a mitochondrial disorder. Two of the patients carried the A3243G mutation, suggesting frequencies of 6% among patients younger than 45 years of age and 14% among patients younger than 30 years for this mutation. Furthermore, we identified two patients with a clinically definite mitochondrial disorder, and sequencing of the 22 transfer RNA genes revealed the mtDNA mutation A12308G in one patient. Clinical evaluation revealed that occipital stroke was part of a more complex syndrome in these four patients. These population-based findings demonstrate that the A3243G mutation in the mtDNA, and mitochondrial disorders are not uncommon among young patients with occipital stroke.
To assess the risk of incident cardiovascular disease in patients with primary Sjögren's syndrome, overall and stratified by Ro/SSA and La/SSB autoantibody status.
A cohort of patients with primary Sjögren's syndrome in Sweden (n = 960) and matched controls from the general population (n = 9035) were included, and data extracted from the National Patient Register to identify events of myocardial infarction, cerebral infarction and venous thromboembolism. Hazard ratios were estimated using cox proportional hazard regressions.
During a median follow-up of 9.5 years, the overall hazard ratio (HR) was 1.6 (95% CI 1.2-2.1) for myocardial infarction, 1.2 (95% CI 0.9-1.7) for cerebral infarction and 2.1 (95% CI 1.6-2.9) for venous thromboembolism. Patients positive for both Ro/SSA and La/SSB autoantibodies had a substantially higher risk of cerebral infarction (HR 1.7, 95% CI 1.0-2.9) and venous thromboembolism (HR 3.1, 95% CI 1.9-4.8) than the general population. These risks were not significantly increased in Ro/SSA- and La/SSB-negative patients. Among autoantibody-positive patients, the highest HR of cerebral infarction was seen after =10 years disease duration (HR 2.8, 95% CI 1.4-5.4), while the HR for venous thromboembolism was highest 0-5 years after disease diagnosis (HR 4.7, 95% CI 2.3-9.3) and remained high throughout disease duration.
Primary Sjögren's syndrome is associated with a markedly increased risk of cardiovascular disease and the presence of Ro/SSA and La/SSB autoantibodies identify the subgroup of patients carrying the highest risk. These findings suggest that monitoring and prevention of cardiovascular disease in this patient group should be considered.
A high protein intake may reduce the risk of stroke but epidemiologic data on protein intake in relation to stroke risk are limited and inconsistent. Our objective was to test the hypothesis that protein intake would be inversely associated with risk of stroke.
We conducted a population-based prospective cohort study consisting of 34,670 Swedish women who were free of cardiovascular disease and cancer in 1997. Diet was assessed with a food-frequency questionnaire. Incident cases of stroke were ascertained from the Swedish Hospital Discharge Registry. We estimated relative risks (RR) with 95% confidence intervals (CI) using Cox proportional hazard regression model. During 10.4 years of follow-up, 1680 stroke events were identified, including 1310 cerebral infarctions, 154 intracerebral hemorrhages, 79 subarachnoid hemorrhages, and 137 unspecified strokes. Intake of total and animal protein, but not vegetable protein, was statistically significantly inversely associated with risk of total stroke and cerebral infarction after adjustment for other risk factors for stroke. The multivariable RRs of total stroke for the highest versus lowest quintile of intake were 0.74 (95% CI: 0.61, 0.91; P for trend = 0.006) for total protein and 0.71 (95% CI: 0.57, 0.88; P for trend = 0.01) for animal protein. The associations were stronger in women with a history of hypertension (RR of total stroke = 0.56; 95% CI: 0.40, 0.78 for highest versus lowest quintile of total protein).
These findings suggest that dietary protein intake is inversely associated with risk of stroke in women with hypertension.
One hundred consecutive patients (67 men, 33 women) aged from 15-55 with acute ischemic brain infarction verified by computed tomography and/or angiography and/or brain scanning were studied. In 40 cases the onset of symptoms was preceded within 24 hours by ethanol intoxication. Ethanol intoxication preceding brain infarction was 4-7 times as common in men and 6-15 times as common in women as ethanol intoxication in the general Finnish population of the same age and sex. Nineteen of the patients were heavy drinkers. Heavy drinking was twice as common in men and 5 times as common in women as heavy drinking in the general Finnish population of the same age and sex. Both occasional ethanol intoxication and regular heavy drinking seem to carry an increased risk of ischemic brain infarction. The ethanol-induced risk was highest in middle-aged women and young men.
We sought to study the etiology of and risk factors for cerebral infarction in young adults in Hordaland County, Norway. All patients aged 15-49 years living in Hordaland County with a first-ever cerebral infarction during 1988-97 were included. Etiology was analyzed in subgroups defined by sex, age (/=40 years), circulation territory (anterior versus posterior circulation) and short-term functional outcome [modified Rankin score (mRS) 2]. A questionnaire was used to evaluate possible risk factors amongst the patients compared with an age- and sex-matched control group. The distribution of etiology was significantly different in all subgroups. Atherosclerosis was frequent amongst men (22.8% vs. 4.2%) and patients >/= 40 years (20.8% vs. 2.7%). All patients with microangiopathy had favorable short-term outcome. Significant risk factors were smoking more than 15 cigarettes per day (P
A 4-year follow-up study was carried out on the prognosis of 54 patients (36 men and 18 women) who survived their first ischaemic brain infarction which had occurred under the age of 65. Twenty patients (15 men and 5 women) already had documented atherosclerotic vascular disease other than ischaemic brain infarction at the time of the hospital admission (atherosclerotic group). When both sexes were considered together, mortality during the 4-year follow-up was significantly higher in the atherosclerotic group than in the non-atherosclerotic group (6/20 versus 3/34; p less than 0.05) and this was due to an excess of cerebrovascular mortality (4/20 versus 0/34; p less than 0.05). The incidence of recurrent fatal or non-fatal ischaemic brain infarction was significantly higher in the atherosclerotic group than in the non-atherosclerotic group (8/20 versus 3/34; p less than 0.01). Among those patients who survived the 4-year follow-up period the incidence of new non-fatal atherosclerotic vascular events (cerebrovascular accident, myocardial infarction, other heart disease or intermittent claudication) was significantly higher in the atherosclerotic group than in the non-atherosclerotic group (8/14 versus 8/31; p less than 0.05). It is concluded, that the presence of atherosclerotic vascular disease at the time of first ischaemic brain infarction in patients under the age of 65 is associated with a significantly increased risk for recurrent ischaemic brain infarction or other new atherosclerotic vascular events.