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A patient with bacterial endocarditis had headaches, cerebrospinal fluid pleocytosis and normal cerebral angiograms. Fifteen days later, while on appropriate antibiotic therapy, he developed an intracerebral hematoma due to a mycotic aneurysm. Mycotic aneurysm is an infrequent but serious complication of bacterial endocarditis. An aneurysm should be considered whenever a patient with bacterial endocarditis has neurologic symptoms even when the patient is receiving antibiotics.
Stroke
PMID:Cerebral hemorrhage from a mycotic aneurysm developing during appropriate antibiotic therapy. 58 May 12

(1) Neurologic complications remain a significant problem in bacterial endocarditis. Of 218 patients with endocarditis, 84 (39%) had a neurologic complication and 58% of these 84 patients died. In contrast, the mortality rate was only 20% among those endocarditis patients without neurologic complications. (2) Of the neurologic complications, cerebral embolism is the most frequent and important. An embolic stroke occurred in 37 (17%) of our patients, with 30 of these patients dying. Emboli are important not only in terms of the direct morbidity and mortality they cause via cerebral infarction, but also because of their role in the causation of mycotic aneurysms, brain abscesses, and abnormal CSF formulae. (3) Cerebral emboli are particularly common in patients with mitral valve infection, and in patients with infection due to virulent organisms, particularly S. aureus and enteric gram-negative bacilli. (4) Mycotic aneurysms occur more frequently in the course of acute endocarditis rather than late in the course of subacute disease. Management of angiographically demonstrated mycotic aneurysms is dependent upon the presence or absence of hemorrhage, the anatomic location of the aneurysm, and the clinical course of the patient. Healing of mycotic aneurysms can occur during the course of effective antimicrobial therapy, thus obviating the need for neurosurgical intervention in all such patients. (5) Macroscopic brain abscess is a rare complication of bacterial endocarditis. Miliary microscopic abscesses are more common than larger abscesses, particularly in patients with acute disease and miliary infection in other organs of the body. (6) Focal seizures occur most commonly in endocarditis patients with acute embolic disease; generalized seizures are of diverse etiologies, with metabolic factors being most important. Penicillin neurotoxicity should be considered in patients with impaired renal function who are receiving high dose penicillin. (7) With the exception of hemorrhagic complications, lumbar puncture results tend to reflect the nature of the infecting organism rather than the nature of the neurologic complication. Endocarditis due to virulent organisms such as S. aureus is usually associated with a purulent CSF formula while nonvirulent organisms, such as viridans streptococci, susually have aseptic or normal CSF formulae.
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PMID:Neurologic complications of bacterial endocarditis. 58 Jul 94

We reviewed 538 charts of patients hospitalized with acute ischemic strokes between 1983 and 1991. The inclusion criteria for cardioembolism were: 1) sudden onset and maximal neurological focal deficit from the beginning, 2) brain CT showing an ischemic infarct, hemorrhagic infarct, or multiple infarcts, 3) cardioembolic sources demonstrated by echocardiography or heart catheterization, and 4) absence of stenotic-occlusive cerebrovascular disease. Sixty-nine patients (12.8%) filled the criteria for cardiogenic brain embolism. Cardiac sources were: 1) nonvalvular atrial fibrillation in 20 patients (29.0%), 2) rheumatic heart disease in 14 (20.3%), 3) nonischemic dilated cardiomyopathy in 13 (18.8%). Nine of these (69%) had cardiac involvement due to Chagas' disease, 4) ischemic heart disease in 11 (15.9%), and 5) other less common conditions such as bacterial endocarditis, mitral valve, and congenital heart malformation in 11 (15.9). Transient ischemic attacks preceding stroke occurred in 11 patients (15.9%), six patients had previous strokes, and 14 patients (20.3%) had silent infarcts. Early recurrence of embolism (three initial weeks) occurred in 5 patients (7.2%), and 28.6% of the patients had hemorrhagic transformation within this period. Taken together, our figures show that, although they are well in line with the current literature, nonischemic dilated cardiomyopathy is one of the main causes of cerebral embolism in our community. This reflects the presence of a regional factor, namely Chagas' disease.
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PMID:[Cerebral embolism of cardiac origin]. 134 85

Mitral valve prolapse is found in 2-5% of the whole population and is thus the most common valvular anomaly. The vast majority of patients are asymptomatic and remain free of complications during the follow-up. The most important complications are severe mitral regurgitation, bacterial endocarditis, cerebral ischemic stroke and arrhythmias. The risk of these complications is increased in patients with a holosystolic murmur, enlarged left atrium and/or ventricle, and redundant, thickened mitral leaflets. The complication rate increases with age and is generally higher in males. The risk of complications is very low in patients with an isolated systolic click or silent prolapse. Prophylactic treatment for endocarditis is recommended for patients with a systolic murmur. For patients surviving ischemic stroke, aspirin is recommended. Where the left atrium is enlarged and rhythm disturbances are present, anticoagulation treatment is preferable. Rhythm disturbances should be treated only when symptomatic. In cases of severe mitral regurgitation surgery should be considered early, since reconstruction of the valve can be achieved in the majority of patients.
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PMID:[Mitral valve prolapse--clinical significance of a frequent diagnosis]. 204 27

The timing for valve replacement in patients with aortic regurgitation remains a complex clinical problem. Rest radionuclide angiography measurement of ejection fraction is a simple informative study to help evaluate the appropriate timing for valve replacement in the asymptomatic patients or those with mild symptoms. In patients with normal ejection fractions the disease probably has not yet evolved to the phase in which valve replacement is essential. If the ejection fraction is mildly depressed (0.40 to 0.49) the time is right for intervention. By the time the ejection fraction falls to less than 0.40 the left ventricle is likely damaged and unlikely to regain normal function. If the patient has severe symptoms with maximal medical therapy, surgery is indicated no matter what the ejection fraction. The latter situation can arise especially when aortic regurgitation evolves over a short period, as might be the case in patients with bacterial endocarditis. A single ejection fraction measurement is not as reliable as serial studies. If, for example, the ejection fraction (under similar circumstances) falls from the greater than or equal to 0.50 range to the 0.40 to 0.49 range, the physician should be altered to the possibility that the left ventricle is deteriorating, and surgery should be considered. It should be understood that multiple hemodynamic factors in aortic regurgitation can alter the ejection fraction and could limit its use as the sole measure of left ventricular performance. Other systolic or diastolic parameters cannot be relied on in isolation as an indication or contraindication for aortic valve replacement. The exercise ejection fraction response reflects the total stroke volume and does not distinguish between regurgitant flow and forward flow. It is therefore possible to observe a decrease in ejection fraction in association with an increase in forward stroke volume during exercise as a result of an increase in heart rate and a decrease in peripheral resistance. Accordingly, it is not appropriate to compare the ejection fraction during exercise in aortic insufficiency with the expected response of the normal ventricle. Exercise position (sitting vs. supine) affects loading conditions and ejection fraction response. Because of the complexity of the exercise ejection fraction response, it is not clear that there is a role for exercise ejection fraction measurements in determining the appropriate time for aortic valve replacement. Criteria based on supine exercise may not be applicable to studies in the upright position.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Radionuclide evaluation of aortic regurgitation. 217 74

Calcific emboli from a calcific aortic stenosis is an uncommon event, usually following local trauma, as from cardiac surgery or left heart catheterization or as a sequel to bacterial endocarditis. We report what we believe to be the first case of a spontaneous calcareous emboli demonstrated by cranial computed tomography. In this patient, systemic hypertension and mild aortic insufficiency may have caused increasing mechanical forces acting on the aortic cusps and may have precipitated embolism.
Stroke 1989 May
PMID:Spontaneous calcific cerebral embolus from a calcific aortic stenosis in a middle cerebral artery infarct. 265 88

We have reviewed 108 cases of bacterial endocarditis treated surgically since 1968. The mean age of the patients was 47.7 +/- 15.6 years (+/- SD) (range, 14-79 yr). Seventy-seven percent were male. The most common causative organisms were staphylococci (46%), streptococci viridans group (5%), and other streptococci (20%). Forty-five percent, 25%, and 13% of patients had native aortic valve, native mitral valve, or native double valve (AV/MV) involvement, respectively. Eighteen patients had prosthetic valve endocarditis. No patient underwent surgery for tricuspid valve endocarditis. Seventy-three patients were considered to have active endocarditis (AE) (positive blood or tissue cultures and/or annular abscess). The 35 remaining patients had healed endocarditis (HE). Preoperative complications in patients with either AE or HE were stroke (11%, 11%), renal failure (33%, 3%; p less than 0.001), pulmonary edema (83%, 34%; p less than 0.001), anemia (36%, 8%; p less than 0.01), and inotrope dependence (22%, 6%; p less than 0.05). Hospital mortality for native valve AE was 19.5% (11/56), and for healed endocarditis, 5.7% (2/35). Independent predictors of hospital mortality were inotrope dependence (p less than 0.001), annular abscess (p less than 0.01), pulmonary edema (p less than 0.01), and staphylococcal infection (p less than 0.05). The 5-year actuarial survival for operative survivors was 68.4 +/- 7.5% (AE) and 78.3 +/- 9.2% (HE). We conclude that the operative mortality for patients with continuing sepsis is high and that surgery should be undertaken early in staphylococcal endocarditis. If surgery is successful, then the long-term prognosis is good.
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PMID:The surgical treatment of infective endocarditis. 272 63

Eighteen patients with occipital hematomas are analyzed. Six patients with medial occipital hematomas presented with headache and visual blurring and examination showed homonymous hemianopsia. Three of these six patients were normotensive; three others were hypertensive with chronic vascular changes. Three patients with lateral occipital hematomas presented with headache but had no neurological deficit. All were hypertensive and had evidence of chronic hypertensive vascular changes. Nine patients with larger occipital hematomas which extended into the temporal and parietal region with intraventricular and tentorial extension had an underlying etiology defined by laboratory studies (excessive anticoagulation, coagulation disorder, systemic lupus erythematosus, bacterial endocarditis). None of these patients were hypertensive. The clinical outcome was good in patients with medial and occipital hematomas; however with the larger and more extensive occipital hematomas, clinical outcome was dependent upon the underlying etiology. None of these 18 patients had recurrent stroke.
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PMID:Occipital lobe hemorrhages; clinical-computed tomographic correlations. 320 38

In spite of two decades of research, the precise relationship of anatomic mitral valve prolapse (floppy valve) to the neuroendocrine disorder (MVP syndrome) remains unclear. In all likelihood they are two separate genetic disorders which travel together in some fashion. Mitral valve prolapse is a common disorder but progressive mitral regurgitation usually occurs late in life and in only a few patients. Other complications such as bacterial endocarditis, stroke, and sudden death are far less common but can occur at younger ages. The neuroendocrine syndrome in civilian life is mainly seen in young females (interestingly the peak incidence years correspond to peak female sex hormone output) but can be seen in males when subjected to unusual stress such as military service. More recent echocardiographic studies have questioned whether all prolapsing valves are truly abnormal. It has been shown that echographic prolapse can be produced in normal subjects by reducing venous return and impaired venous return may be present in some patients with the MVP syndrome. However, clicks and murmurs are apparently not heard when normal valves prolapse. It is our opinion that the presence of a click or typical murmur requires some anatomic abnormality of the mitral valve. One wonders if minimal valve abnormality (noted and dismissed by Davies) is the valve abnormality present in many young females with MVP syndrome, and that it may remain a mild abnormality throughout life. Recent psychiatric studies suggest that MVP is present in 30% of patients with Panic Disorder. It is not clear that this psychiatric syndrome is the same thing as the MVP syndrome. In Devereux's study, anxiety proneness was no different in the MVP cohort than in relatives without MVP. It is possible that diagnostic mixing of two similar but separate disorders has occurred, as has been the case since World War I. Perhaps the most important question is whether young patients with MVP syndrome and no echocardiographic criteria for "floppiness" will develop progressive mitral regurgitation or other complications in later life. In other words, how often is MVP syndrome in a young individual without echocardiographic evidence of a floppy valve a precourser to eventual progressive mitral regurgitation? Are there two different populations? Because of the long course of the disorder, several more years of observation (and, it is hoped, prospective longitudinal study) will be required to answer this question.
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PMID:The mitral valve prolapse epidemic: fact or fiction. 330 18

The clinical and pathologic findings in 42 autopsy proved cases of cerebral infarction from cancer-associated non-bacterial thrombotic endocarditis were reviewed. Carcinoma of the lung was the most common malignancy. Most patients had disseminated cancer, but in six patients, the condition was stable or in remission, and six patients had localized cancer; two patients were not known to have cancer until neurologic symptoms developed. Neurologic symptoms were focal, suggesting stroke in 18; diffuse, suggesting metabolic encephalopathy in nine; and mixed in five. Neurologic signs were often the only evidence of thromboembolism. The definitive diagnostic test was cerebral angiography showing multiple arterial occlusions. Anticoagulation with heparin appeared to help some patients and did not promote brain hemorrhage. Early diagnosis and vigorous treatment of non-bacterial endocarditis may prevent severe neurologic disability.
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PMID:Cerebral infarction from non-bacterial thrombotic endocarditis. Clinical and pathological study including the effects of anticoagulation. 367 60


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