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Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

22 cases of aortic valvular insufficiency treated by prosthesis and in which the acinetic areas of the left ventricle were eliminated at the same time are reported. Only one postoperative death (ventricular fibrillation) was encountered; one after 1 year (emboly as a result of endocarditis) and one as a result of an unknown cause. Emphasis is laid upon the frequency of this associated complication, its seriously negative incidence on ventricular haemodynamics, the need for surgical treatment, and its favourable immediate and long-term results.
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PMID:[Akinetic zones of the left ventricle in aortic insufficiency. Treatment]. 12 52

A 61-year-old man with Trichosporon cutaneum (T. cutaneum) prosthetic valve endocarditis is reported. He had had an aortic valve replacement for rheumatic heart disease 3 years earlier. Onset of the valve infection was subacute. A systolic murmur was noted on admission. Subsequently, he developed conjunctival hemorrhages, hematuria and transient episodes of confusion, aphasia and cranial nerve palsies. Three of 17 blood cultures taken over 3 weeks were positive for T. cutaneum. He was given amphotericin B (AmB) and 5-fluorocytosine (5FC); T. cutaneum infection of prosthetic aortic valve was identified. The aortic valve was replaced. Postoperatively he developed refractory ventricular fibrillation and died. Striking synergy to AmB-5FC and AmB-rifampin combinations was demonstrated in vitro.
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PMID:Trichosporon cutaneum endocarditis. 71 85

A 65 year-old-man was admitted to our hospital complaining of orthopnea and precordial oppressive feeling. Chest roentgenogram revealed congestive heart failure. Electrocardiogram revealed acute myocardial infarction-like pattern. Serum enzymes (CPK, GOT, LDH) were slightly elevated, but serum antiviral antibodies were not elevated. Echocardiogram showed severe symmetrical left ventricular (LV) hypertrophy, but there was no abnormality of LV wall motion. He died of progressive heart failure and ventricular fibrillation on the second hospital day. A necropsy was performed within one hour of death. The heart was enlarged (690 g) with both left and right ventricular hypertrophy. The myocardium disclosed a diffuse infiltration predominantly of eosinophilic leucocytes. Histopathological study revealed giant cell formation and granulomatous lesions in the myocardium. There was no overt endocarditis or pericarditis. We concluded that the severe LV hypertrophy was due to myocardial inflammatory swelling. From these findings, we diagnosed this case as acute isolated (Fielder's) myocarditis.
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PMID:[A case of acute isolated (Fiedler's) myocarditis diagnosed by histopathological study with rapid unfortunate course]. 158 53

We report on two patients with actinomycosis. The first case was a 45-year-old cachectic man with extensive bilateral pulmonary infiltrates. The lesions remained unclear for 18 months and only open lung biopsy with microscopic and cultural evaluation led to the diagnosis of actinomycosis. In the second case, classic cervico-facial actinomycosis in a 69-year-old farmer is described. Diagnosis was established on the basis of microscopic findings of "sulphur granules" eroding the mandible. Furthermore, the clinical presentation, with an indurated swelling of the jaw and intraoral fistula formation, was typical. The patient had a severe combined aortic valve lesion and died after ventricular fibrillation during hospitalization. Diagnosis could not be confirmed by culture, probably due to antibiotic prophylaxis against endocarditis during tooth extraction on the first day of admission. Diagnostic difficulties and microbiologic aspects are discussed, with special focus on the rare species of Actinomyces meyeri which was cultured from biopsy specimens from the lung of the first patient. So far this species has been described in only 13 patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Actinomycosis--clinical and therapeutic considerations based on 2 personal case reports]. 192 61

Twenty one patients (15 males and 6 females, mean age, 35.0 +/- 1.6 years) with myocarditis combined with symptoms of Stages II-III circulatory failure were examined. This group of patients was identified as a high-risk group as to an unfavourable outcome of myocarditis. Within the follow-up from 3 to 36 months, all the patients died: the case of death was arrhythmia in 17 and circulatory failure in 4. The unfavourable prognosis of the disease was evidenced by high pulmonary capillary pressure and pulmonary end-diastolic pressure that exceeded 20 mm Hg the cardiac index that was less than 31/min.m-2. The ratio of left ventricular end-systolic and end-diastolic volumes to the left ventricular cross-shortening were important signs of the unfavourable prognosis, i.e. death of congestive circulatory failure. In addition to complications of myocarditis such as sudden ventricular fibrillation, progressive congestive circulatory failure and thromboembolism, there were more rare complications such as development of left ventricular aneurysms and damage to the endocardium as abacterial endocarditis.
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PMID:[Characteristics of the course of complicated myocarditis]. 216 81

Tined transvenous pacing leads were inserted into nine healthy large-breed dogs as part of an experimental study evaluating an implantable defibrillator. The pacing leads were used to induce ventricular fibrillation on the day of insertion, two and four weeks after insertion and then monthly. Despite daily running exercise on and off a leash, the tined leads remained firmly anchored to the right ventricular apex for the full experimental period of up to 12 months. Apart from mechanical endocarditis of the tricuspid valve, and partial penetration of the ventricular wall in one dog, problems associated with the pacing leads were not encountered. The use of tined leads and careful technique may minimise the likelihood of transvenous lead displacement.
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PMID:Transvenous pacemaker leads in the dog: an experimental study. 223 19

Thirty one (78%) of 40 consecutive patients (aged 13-79, mean 44 years) with infective endocarditis had congestive heart failure at presentation. Twenty six (65%) had had rheumatic heart disease and 17 (43%) patients had prosthetic valves. Eight (20%) patients had undergone dental procedures within three months of presentation. Blood cultures were positive in only 22 (55%) of the patients. In nine (41%) of them streptococci of the viridans group were isolated and in seven (32%) patients endocarditis was due to Staphylococcus aureus. Eight patients had Q fever endocarditis. Sixteen patients required operation because of haemodynamic deterioration while they were in hospital; 11 patients had native valves and five had prosthetic valves. Seven had emergency operations and were pyrexial at that time. Four of the seven died in hospital. Of the 12 who were alive and well after surgery only two required further surgery two and three years after the initial operation. Twelve (30%) of the 40 patients died in hospital; in 10 death was mainly due to left ventricular failure or congestive heart failure. All patients died who had renal failure (four cases), myocardial infarction (two cases), complete heart block (one case), or ventricular fibrillation (two cases) before operation. Six (33%) of the 18 patients with culture negative endocarditis died. Two of the four patients seen and treated more than 12 weeks after the onset of symptoms died, as did three of the five patients with prosthetic valves who required surgery while in hospital. Three patients with neurological complications survived and only two (29%) of the seven patients with blood cultures that were positive for Staphylococcus aureus died. Of these 40 high risk patients optimal antibiotic treatment and early surgery for haemodynamic difficulty ensured that 28 (70%) were discharged from hospital alive and well.
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PMID:Heart failure associated with infective endocarditis. A review of 40 cases. 394 52

Whether total surgical correction of tetralogy of Fallot in adults aged 40 years old or older has acceptable operative risk and gratifying long-term results is unknown. The Mayo Clinic experience (June 1960 to May 1982) with 30 patients 40 to 60 years old (mean 47) who had total surgical correction of tetralogy of Fallot was reviewed. Preoperatively, 4 patients (13%) were in functional class I, 9 (30%) in class II and 17 (57%) in classes III and IV. Eight patients (27%) had had preoperative complications: five had a cerebrovascular accident and three had infective endocarditis. Only 11 patients (37%) had had palliative surgery 16 to 34 years (mean 22) before total surgical correction. Total surgical correction was successful in all patients. Right ventricular to left ventricular (RV/LV) pressure ratio of 0.65 or less was achieved in 28 (93%) of the 30 patients. One patient died of ventricular fibrillation (RV/LV ratio = 0.8) 2 days postoperatively, one had complete heart block and one had a cerebrovascular accident 7 days after operation. At follow-up of 5 to 266 months (mean 110), there were seven late deaths: two sudden at 5 and 21 years, respectively, after operation, one from myocardial infarction at 11 years, one from cerebrovascular accident at 11 years, one from congestive heart failure (RV/LV ratio = 1.0) at 8 years and two from noncardiac causes. Of the 22 patients who survived, 16 are in class I, 5 are in class II and 1 is in class III.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Total correction of tetralogy of Fallot at age 40 years and older: long-term follow-up. 396 7

For the determination of the risk factors associated with the development of and death caused by prosthetic valve endocarditis, data were reviewed from 66 patients who were prospectively entered into the Veterans Affairs Cooperative Study on Valvular Heart Disease and in whom prosthetic valve endocarditis subsequently developed. Data were recorded at 13 medical centers between October 1977 and September 1982 in patients randomized to receive a mechanical valve (Bjork-Shiley spherical disc, n = 510 patients) or a bioprosthetic valve (Hancock porcine heterograft, n = 522 patients). The average rate of prosthetic valve endocarditis development was 0.8% per year over an average follow-up period of 7.7 years. Of the 66 patients in whom prosthetic valve endocarditis developed (5.8%), 15 cases occurred within 2 months of operation (early) and 51 occurred after operation (late). The most significant preoperative predictor of prosthetic valve endocarditis was active endocarditis at the time of operation (7.4% versus 0.9%) (p = 0.001). Early prosthetic valve endocarditis occurred more frequently in patients who underwent operation for multivalvular disease (p = 0.023). Significantly related perioperative variables were coma, prolonged mechanical ventilation, deep postoperative wound infection, postoperative jaundice, ventricular tachycardia, ventricular fibrillation, and replacement of more than one valve (p < 0.05). Multivariate predictors were hypoxia (p = 0.001), preoperative endocarditis (p = 0.003), preoperative valve lesion (p = 0.020), and resident surgeon (p = 0.05). Significant preoperative variables predictive of late prosthetic valve endocarditis were mitral stenosis and mixed mitral stenosis-regurgitation. The only multivariate predictor of late prosthetic valve endocarditis was superficial wound infection (p = 0.004). Of deaths attributable to prosthetic valve endocarditis, 41% occurred in patients treated with antibiotics alone, 48% occurred in patients treated with surgical intervention and antibiotics, and death resulted in both patients who received no treatment. No difference was found in the risk of early or late postoperative prosthetic valve endocarditis developing in patients receiving the mechanical valve versus those receiving the bioprosthetic valve.
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PMID:Determinants of the occurrence of and survival from prosthetic valve endocarditis. Experience of the Veterans Affairs Cooperative Study on Valvular Heart Disease. 804 Nov 68

We report a 75-year-old man with parkinsonism who died suddenly. The patient was well until 64 years of the age when he had an onset of tremor in his left hand. He was treated with a medicine in another hospital, and his tremor subsided. Five years after the onset, he started to note difficulty in fine finger movements and gait disturbance. He tended to lean backward with frequent falls. He was treated with bromocriptine, trihexyphenydil, and L-dops without apparent improvement. He visited our out patient clinic on November 11, 1993 when he was 75 years of the age. Neurologic examination at that time revealed an alert and well oriented man in no acute distress. Higher cerebral functions were intact. In the cranial nerves, he showed restriction in the upward as well as down ward gaze (40% of normal). He showed masking of the face and spoke in small voice. He walked in a stooped posture with small steps; retropulsion was present. Muscle rigidity was moderately positive in the neck, however, no rigidity was noted in the limbs. No abnormal involuntary movements were seen. He showed moderate bradykinesia and difficulty in finger tapping. Muscle stretch reflexes were normally elicited and the plantar response was flexor bilaterally. Sensation was intact. The autonomic nervous system appeared intact. He was treated with 300 mg/day of Sinemet with marginal improvement in his balance. In February 4, 1994, he had a common cold. On the next day, his parkinsonism worsened and he became unable to walk by himself. He was found unconscious in the bathroom on the same day. He was brought to our hospital by an ambulance. Upon arrival, he was unresponsive and was not breathing. Blood pressure could not be measured. Pupils were dilated without reaction to light. Cardiac resuscitation was attempted, however, ventricular fibrillation appeared on an EEG monitor, and he was pronounced dead at eleven o'clock in the morning. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had progressive supranuclear palsy because of vertical gaze palsy, axial rigidity, and poor response to levodopa. Regarding the cause of his sudden death, the chief discussant thought that he developed pulmonary embolism. Postmortem examination revealed non-bacterial thrombotic endocarditis in the heart, but this did not appeared to be related to his sudden death. Multiple disseminated small emboli were found occluding small arteries of the left lung; this was consistent with acute pulmonary embolism, and this was thought to be the cause of his sudden death. In the central nervous system, marked atrophy of the globus pallidus was noted; both internal as well as external segments showed marked atrophy; no myelinated fibers were seen in the globus pallidus. Neuronal cell loss was marked in the globus pallidus, the subthalamic nucleus, and the substantia nigra. No Lewy bodies or tangles were seen. The histologic diagnosis was consistent with pallido-nigro-luysian atrophy. Brownish pigments such as seen in Hallervorden-Spatz disease were seen in the globus pallidus. In addition, formy spheroids were seen in the substantia nigra. However, iron deposits were not so strong as to suggest Hallervorden-Spatz disease. Pallido-nigro-luysian atrophy is a rare neurodegenerative disorder. It is interesting to note that this condition may mimic progressive supranuclear palsy or pure akinesia clinically.
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PMID:[A 75-year-old man with parkinsonism and sudden death]. 853 59


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