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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A rare case of extracranial internal carotid occlusion with a coexisting ipsilateral internal carotid aneurysm is reported. A 50-year-old male had a sudden onset of severe headache, vomiting and right motor weakness on May 14, 1984. Two days later the patient was transferred to our hospital. On admission he was alert but presented with nuchal rigidity and right moderate hemiparesis. He had an episode of a blunt head injury 12 years previously, but no history of hypertension, diabetes mellitus or cerebral stroke. A computed tomography revealed mild subarachnoid hemorrhage and mild ventricular dilatation. A cerebral angiography did not demonstrate any aneurysms but it revealed occlusion of the right internal carotid artery at the cervical bifurcation. The repeated angiography on May 31 disclosed a saccular aneurysm arising anteromedially at the level of the junction of the right posterior communicating artery and the internal carotid artery. The cervical internal carotid artery remained occluded at the same site. The middle cerebral artery was supplied through the well-developed posterior communicating artery, and the right anterior cerebral artery was supplied through the anterior communicating artery. Clipping of the aneurysm was attempted but it was forcibly trapped because of premature bleeding on June 5. The right V-P shunt was performed for the progressive ventricular dilatation on June 12. The patient was discharged with no paresis on June 20. It has been well known that the uni- or bilateral carotid occlusion, whatever the origins are, are often associated with cerebral aneurysms.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Extracranial internal carotid occlusion and coexisting ipsilateral intracranial internal carotid aneurysm]. 361 34

Recent studies in human and animal subjects have suggested a relationship between intracranial pressure (ICP) and ventricular dilatation and multimodality evoked responses which, if substantiated, would be of value to clinical practice as a noninvasive way of assessing the need for shunting in selected patients in whom computed tomography (CT) is not definitive. In an attempt to better define these changes, auditory evoked response (BAER) and somatosensory evoked response (SER) were performed on 16 cats as a base line, after which they were made hydrocephalic by the cisternal injection of kaolin. Nine cats survived, and CT or magnetic resonance scans were performed on them 4 to 6 weeks later. In those animals in which ventricular dilatation was noted, repeat evoked responses were recorded. In the 6 hydrocephalic cats, the ventricle was punctured to measure ICP, which in all cases was less then 5 mm Hg. The lumbar spinal dural sac was then ligated, which resulted in periodic plateau waves up to 75 to 100 mm Hg after 4 to 6 hours, lasting up to 10 minutes. In neither group of cats was any change in either BAER or SER observed until preterminally, when ICP was in the range of 75 to 100 mm HG and cerebral perfusion pressure was compromised. This suggests that the BAER and SER are not sensitive to either ventricular dilatation or intracranial hypertension.
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PMID:Effects of hydrocephalus and increased intracranial pressure on auditory and somatosensory evoked responses. 373 4

We reviewed the computed tomographic findings after 1055 intracranial operations to determine the incidence of postoperative extradural hematomas. There were 11 medium and 5 large hematomas after 1055 operations (1.0%). Ten of the 16 hematomas were operated upon (10/1055, 0.9%). Four of the 10 hematomas were seen after 278 brain tumor removals (1.4%), another four after 190 aneurysmal operations (2.1%), one after 14 intracerebral hematoma removals (7.1%), and the last one after 251 ventricular shunting or drainage procedures (0.4%). In 4 of the 10 operated hematomas, sites were regional, in five sites were adjacent, and in one the site was distant. All of the five adjacent hematomas extended downward from a lower rim of the operative locus. Causes were analyzed in the three types of the hematomas. In case of the regional hematomas, the causes were incomplete hemostasis of the dura mater or the bone in all four patients, nonperformance of central stay sutures in three, systemic hypertension in one, and hypofibrinogenemia in one. In the adjacent hematomas, we could find dural separation at an edge of craniotomy in all five patients, abrupt collapse of the brain in all, ventricular dilatation in two, and systemic hypertension during immediate postoperative period in two. In one distant hematoma, ventricular dilatation and ventricular shunting procedure were themselves thought to be the causal factors.
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PMID:Postoperative extradural hematomas: computed tomographic survey of 1105 intracranial operations. 378 96

In two children with the haemolytic uraemic syndrome dilated cardiomyopathy occurred in the absence of hypertension, or fluid or electrolyte disturbance. These cases presented with acute left ventricular failure. Echocardiography showed left ventricular dilatation and reduced contractility. There was also ventricular wall thickening, which persisted. Twelve other children with haemolytic uraemic syndrome had prospective echocardiography. Eleven of them showed no evidence of cardiomyopathy and in one transient dilatation and reduced contractility developed without clinical signs. Dilated cardiomyopathy is a rare but important extrarenal manifestation of the haemolytic uraemic syndrome and is best demonstrated by echocardiography.
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PMID:Dilated cardiomyopathy associated with haemolytic uraemic syndrome. 381 52

In the past few years patients having severe head trauma have survived in growing numbers, and it is likely that they will be more frequently seen on rehabilitation units. They display, in addition to direct structural damage, medical and neurologic problems which may be encountered during their rehabilitative phase. The purpose of this study will be to identify those medical and neurologic problems of consequence and describe their frequency of occurrence within a population of head injured patients. A consecutive series of 180 patients with head trauma undergoing rehabilitation were therefore reviewed, and the type and frequency of medical problems were noted. Neurologic, gastrointestinal, genitourinary, respiratory, cardiovascular, skin, musculoskeletal, and endocrinologic problems were encountered most frequently. Of these, ventricular dilatation, posttraumatic seizures, abnormal liver function tests, hypertension, thrombophlebitis, respiratory infections, periarticular heterotopic ossification, and pituitary-hypothalamic dysfunction are discussed in terms of their morbidity, clinical significance, and therapeutic approach. In many instances, these problems were not identified in the acute care hospital. Awareness of these potential conditions during the rehabilitation period can result in early detection and treatment.
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PMID:Medical problems encountered during rehabilitation of patients with head injury. 391 61

To assess the prevalence and significance of left ventricular dilatation in patients with severe left ventricular dysfunction secondary to coronary artery disease (or coronary artery cardiomyopathy), we studied 70 patients with an ejection fraction of 35 percent or less and one-vessel coronary artery disease (n = 14) or with multivessel coronary artery disease (n = 56). None had had a recent myocardial infarction or valvular heart disease. Patients who underwent myocardial revascularization during follow-up were excluded. The left ventricular end-diastolic volume (measured by contrast ventriculography) was less than 110 ml/sq m in 14 patients (20 percent) (group 1), and was 110 ml/sq m or more in 56 patients (80 percent) (group 2). There were no differences between the two groups in age, sex, diabetes mellitus, hypertension, extent of coronary artery disease, or left ventricular asynergy. Patients in group 1 had lower pulmonary arterial wedge pressure (13 +/- 6 vs 22 +/- 10 mm Hg; p = 0.0008), lower left ventricular end-diastolic pressure (21 +/- 6 vs 27 +/- 9 mm Hg; p = 0.007), and higher left ventricular ejection fraction (31 +/- 2 vs 25 +/- 7 percent; p = 0.001) than patients in group 2. At a mean follow-up of 27 months, 24 patients had died of cardiac causes, all of whom were in group 2. Survival was significantly better in group 1 than in group 2 (Mantel-Cox, p = 0.009). Survival analysis (Cox models) of 20 clinical, hemodynamic, and angiographic variables showed that ejection fraction (chi2 = 13.6; p less than 0.001) and end-diastolic volume chi2 = 4.7; p = 0.03) were the most significant predictors of death. Thus, minimally dilated coronary artery cardiomyopathy is a distinct entity with favorable hemodynamics. Prognostically, the end-diastolic volume adds significant predictive information to the ejection fraction among conservatively treated patients.
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PMID:Coronary artery cardiomyopathy. Hemodynamic and prognostic implications. 394 48

Radiographic chest findings from 57 men, aged 17 to 64, with untreated systemic arterial hypertension of varying severity were related to systemic haemodynamics, both at rest and during standardized exercise in the sitting position. The haemodynamic findings were compared with corresponding data from 59 normotensive male volunteers. In classifying the radiographic findings into four different groups, not only the heart size but also the appearance of the aorta and left ventricle were taken into account. While there was only a poor correlation between calculated heart volume and resting mean brachial artery pressure or systemic vascular resistance, the classification system used resulted in a good separation for haemodynamic functions of patients with normal chest films, those with elongated and widened aorta, and those with signs of left ventricular hypertrophy. On the other hand, there was no definite difference in the functions studied for hypertensive patients with left ventricular hypertrophy and those with, in addition, signs of left ventricular dilatation. Hypertensive men with normal chest radiographs stood out as characterized by increased heart rate and cardiac output at rest, while the systemic vascular resistance was not different from that of the controls. Already the presence of an elongated and widened aorta changed this haemodynamic pattern to that characteristic of established arterial hypertension with normal resting heart rate and cardiac output, and increased systemic vascular resistance. Considerably better information on the haemodynamic events in systemic arterial hypertension is possible to achieve with a thorough evaluation of the radiological appearance of the aorta and left ventricle, rather than with estimation of the heart size only.
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PMID:Correlation between radiological chest findings and systemic haemodynamics in human arterial hypertension. 424 18

Semantic difficulties arise when hypertrophic obstructive cardiomyopathy is seen without obstruction and with congestive failure, and also when congestive cardiomyopathy is seen with gross hypertrophy but without heart failure. Retention of a small left ventricular cavity and a normal ejection fraction characterizes hypertrophic cardiomyopathy at all stages of the disorder. Congestive cardiomyopathy is recognized by the presence of a dilated left ventricular cavity and reduced ejection fraction regardless of the amount of hypertrophy and the presence or not of heart failure. Longevity in congestive cardiomyopathy seems to be promoted when hypertrophy is great relative to the amount of pump failure as measured by increase in cavity size. Conversely, death in hypertrophic cardiomyopathy is most likely when hypertrophy is greatest at a time when outflow tract obstruction has been replaced by inflow restriction caused by diminishing ventricular distensibility. Hypertrophy is thus beneficial and compensatory in congestive cardiomyopathy, whereas it may be the primary disorder and eventual cause of death in hypertrophic cardiomyopathy. Reasons are given for believing that hypertension may have been the original cause of left ventricular dilatation in some case of congestive cardiomyopathy in which loss of stroke output thenceforward is followed by normotension. Development of severe hypertension in these patients after recovery from a prolonged period of left ventricular failure with normotension lends weight to this hypothesis. No fault has been found in the large or small coronary arteries in either hypertrophic cardiomyopathy or congestive cardiomyopathy when they have been examined in life by selective coronary angiography, or by histological methods in biopsy or post-mortem material. Coronary blood supply may be a limiting factor in the compensatory hypertrophy of congestive cardiomyopathy, and the ability to hypertrophy may explain the better prognosis of some patients. In hypertrophic cardiomyopathy excessive metabolic demand may not be met, and inadequacy of blood flow may contribute both to sudden death and to progressive replacement fibrosis in this disease. Histochemical and ultrastructural methods have failed to show any fundamental differences between hypertrophic cardiomyopathy and congestive cardiomyopathy, whereas conventional histology permits recognition of hypertrophic cardiomyopathy and distinction both from congestive cardiomyopathy and from ;normal' secondary hypertrophy in organic aortic stenosis.
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PMID:Ventricular hypertrophy in cardiomyopathy. 425 44

A case of aortitis syndrome associated with hypertensive intracranial hemorrhage is reported. A 38-year-old female was admitted in 1980 suffering from hypertension and blood pressure difference between the left and right arms which had existed for 10 years. Two weeks prior to admission, she noticed weakness and numbness of the right arm and leg. She was orientated and alert at the time of admission. Her right upper and lower extremities could not function with full strength against resistance. Also, right hemihypesthesia and hemiparesthesia were present. Left arm systolic blood pressure was 195 mmHg. Her pulse was palpable in both radial arteries. CT scans revealed a small high density area in the posterior crus of the internal capsule with a slight mass effect. There was no ventricular dilatation. She was given conservative treatment, such as with antihemorrhagic and antihypertensive drugs, and was discharged with good recovery after three months. Various studies were performed during her hospital stay. Based on angiographic findings, the most probable diagnosis was an extensive type of aortitis syndrome. Hypertension resulted from narrowing of the abdominal aorta and the right renal artery. Pulmonary scintiscanning using 99mTc-macroaggregated albumin revealed that her pulmonary arteries were also involved. Aortitis syndrome is not infrequent, but intracranial hemorrhage following after aortitis syndrome is rare. This may be because the carotid artery is involved in a high incidence of such cases, and therefore the intracranial blood flow is disturbed in most cases. Although the left common carotid artery was involved in the subject case, hypertensive intracranial hemorrhage occurred in the left posterior crus of the internal capsule. In a case of aortitis syndrome, therapy resulting in recirculation to the carotid artery involved is generally carried out in order to improve poor intracranial blood flow. However, it is suggested that control of blood pressure is necessary to prevent intracranial hemorrhage in aortitis syndrome.
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PMID:[A case of aortitis syndrome associated with hypertensive intracranial hemorrhage (author's transl)]. 612 63

The spontaneously hypertensive rat (SHR) exhibits both a compensated phase of cardiac hypertrophy in which forward output is maintained despite persistently elevated systemic arterial pressures and a decompensated phase in which cardiac performance has deteriorated in spite of further hypertrophic growth. To determine whether chronic antihypertensive therapy prevents the development of heart failure and the progression of cardiac hypertrophy in SHR with advanced hypertension, captopril (2 g/l of drinking water), a converting enzyme inhibitor, was administered to 14 month old female SHR and normotensive American Wistar rats (NWR) for 10 months. The severe left ventricular hypertrophy of the 24 month old untreated SHR (4.37 +/- 0.2 mg/g v. 2.50 +/- 0.06 mg/g, untreated NWR) was markedly reduced (P less than 0.02) by captopril (3.01 +/- 0.1 mg/g). Chronic therapy prevented the reduction of both baseline and maximal cardiac indices in SHR, but did not alter blood flow in NWR. Left ventricular dilatation was present in 24 month old SHR and, as peak stroke volume index was diminished, the ejection fraction index of the SHR was reduced. Captopril restored this index in SHR to normal. The relation of ejection fraction index and afterload (peak systolic wall stress) was depressed in untreated SHR, but was normal in treated SHR. Thus, chronic therapy with captopril prevented the development of severe cardiac dysfunction and produced a marked regression of cardiac hypertrophy in SHR with advanced hypertensive heart disease.
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PMID:Prevention of the development of heart failure and the regression of cardiac hypertrophy by captopril in the spontaneously hypertensive rat. 622 Aug 93


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