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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The literature points out the meaning of risk factors causing stroke as well as their therapy or elimination as an effective prevention of cerebrovascular disease. Hypertension increases the risk of apoplexy by 4-fold, with regard to the diastolic values of blood pressure by the 5-fold up to the 10-fold. Consistent hypertension therapy decreases significantly the incidence of cerebral apoplectic attacks. Manifested diabetes mellitus and even reduced glucose tolerance raise the risk of stroke by the 3-fold, even though factors frequently associated with diabetes are taken into consideration. Hyperlipidemia, hypercholesteremia, and hypertriglyceridemia stipulate an increase of stroke incidence by the 2-fold to the 3-fold. Morbidity rate rises if these abnormalities coincide with further risk factors, up to the 6-fold. Nicotine consumption alone increases the risk of cerebral apoplectic attacks in relation to age, by the 3-fold up to the 5-fold. In combination with the use of hormonal contraceptive drugs, the risk of morbidity rate in women rises to the 7-fold. Overweight of more than 30% aggravates twice the risk of stroke. Heart diseases of different kind increase the risk of apoplectic attacks by the 2-fold, in combination with hypertension by the 5-fold. The intake of oral contraceptives (OCs) causes an increase of cerebral thromboembolic attacks by the 3-fold up to the 5-fold, whereby a relation to estrogen content and to hemorheology disturbances is proven. Blood coagulation disturbances, especially hypercoagulability with increase of blood level of fibrinogen, fibrin, and enhanced adhesiveness of thrombocytes in cerebrovascular disease are proven to be valid. By combination of various risk factors apoplexy risk is additionally increased. The possibility of surgical and neurosurgical prophylactic treatment in all stages of cerebral ischemia, caused by occlusive disease of the cartoid, vertebral, and intracranial arteries, exists in 75% of patients. With regard to the longterm results of patients with extraintracranial bypass surgery, due to stenosis or occlusion of the carotid artery in its high cervical or intracranial course, or of the middle cerebral artery, the operated group clearly was better than the nonoperated group in frequency of cerebral ischemia recurrence. The therapeutic effect of inhibitors of thrombocytic aggregates and of anticoagulants for the chemotherapeutic prevention of cerebral ischemia, is proven for acetylsalicylic acid and derivatives of coumarin. Both diminish significantly the rate of cerebral ischemia when compared with placebo-treated control groups.
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PMID:[Prevention of cerebrovascular circulatory disorders]. 404 14

Forty patients with Parkinsonism and heart disease were studied before and during the administration of levodopa. Patients with increasing angina, myocardial infarction within the previous year, pre-existing severe postural hypotension, or transient cerebral ischaemia were excluded. Thirty-eight patients showed no adverse effects; angina improved in one patient but later worsened; one patient died of myocardial infarction after a severe gastrointestinal haemorrhage. Therapy with levodopa appears to pose little increased hazard to patients with most forms of heart disease. Inpatient monitoring is recommended at the beginning of therapy, and antiarrhythmic agents should be used when required.
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PMID:Levodopa therapy of patients with Parkinsonism and heart disease. 453 97

Prospective longitudinal cerebral blood flow values were serially plotted over a four-year interval against the course of cerebral ischemia before, during, and after onset of clinical symptoms. Of 161 normal subjects (mean age, 62 years), 86 were risk free and 75 had hypertension, heart disease, diabetes mellitus, and/or hyperlipidemia. Twenty-one subjects developed cerebrovascular symptoms during the prospective trial. Mean hemispheric cerebral blood flow values were significantly lower for at risk than for risk-free subjects. Symptomatic subjects showed lower values than those in either of the two asymptomatic groups at every session. Statistical analysis of cerebral blood flow values for symptomatic patients compared one and two years prior to onset of symptoms, at the onset of symptoms, and 1 year later showed reductions compared to asymptomatic risk-factored subjects tested in a similar prospective manner. Measurable declines in cerebral perfusion accompany development and progression of aortocerebral atherosclerosis prior to clinical appearance of signs and symptoms of cerebrovascular disease. If confirmed, these observations should permit the institution of preventive medical and/or surgical interventive measures and an evaluation of their outcome.
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PMID:Progressive cerebral ischemia antedates cerebrovascular symptoms by two years. 648 37

Patients who have undergone a Blalock-Taussig anastomosis for treatment of congenital heart disease may have the vascular anatomy of the subclavian steal syndrome. Cerebral ischemia has been reported in such patients, but not when total surgical correction has eliminated other predisposing factors. We report a patient who developed vertebrobasilar insufficiency 31 years after Blalock-Taussig anastomosis and 4 years after total intracardiac repair of tetralogy of Fallot. He had angiographically proven subclavian steal and no other known predisposing factor for cerebral ischemia. This case suggests that symptomatic subclavian steal may be a late risk of surgical treatment of congenital heart disease that leaves the vascular anatomy of subclavian steal intact. Vascular reconstructive surgery can be effective treatment for these patients and may be indicated prophylactically at the time of intracardiac repair if subclavian steal syndrome becomes a more frequently recognized sequela of prior Blalock-Taussig anastomosis.
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PMID:Vertebrobasilar ischemia after total repair of tetralogy of Fallot: significance of subclavian steal created by Blalock-Taussig anastomosis. Vertebrobasilar ischemia after correction of tetralogy of Fallot. 670 43

The clinical story and the results of radiological and angiocardiographic investigations in 2 patients with proven mitral valve prolapse and cerebral ischemia are reported. Significant risk factors for stroke other than mitral valve prolapse were lacking. Cerebral angiography showed in one case a distal occlusion suggesting embolic brain lesion and was normal in the other case. This report suggests: 1) that mitral valve prolapse is a real risk factor for stroke in young people; 2) that two-dimensional echocardiography or angiocardiography are valuable investigations in young patients with cerebral ischemia, when clinical or electrocardiographical findings of cardiopathy are present.
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PMID:[Mitral valve prolapse and cerebral ischemic strokes]. 687 78

The present study has been devoted to the analysis of 120 patients presenting with reversible focal cerebral ischemia without conventional signs of cardiopathy and/or relevant atherosclerotic disease. In 77% of the patients vascular risk factors, such as hypertension or hyperlipemia, were present. In 23% of the patients, no abnormal finding was discovered at clinical, hematochemical and cardiological examinations. In these patients a further cardiological evaluation was performed with echocardiography. Dynamic electrocardiography was performed in 52 patients. Echocardiography and dynamic electrocardiography revealed the occurrence of 6 cases of mitral valve prolapse (MVP), 2 cases of frequent premature ventricular beats, and 1 proximal atrial arrhythmia. All 6 cases of MVP were detected in the subgroups of patients without vascular risk factors. In our patients younger than 45 years, the relative frequency of MVP attains 21.5%. This study confirms that MVP has to be regarded as a risk factor for focal cerebral ischemia in young patients.
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PMID:Mitral valve prolapse as a risk factor for TIA. A study with echocardiography and dynamic ECG. 688 93

One hundred and one patients below 45 years and showing objective signs of cerebral ischemia were studied retrospectively for pathogenic factors. Twelve were below 15 years; the male to female ratio was 1:1. Factors known as predisposing (heart disease, hypertension, hyperlipemia, diabetes mellitus or infectious diseases) and other possible factors (e.g. trauma, abuse) were found in 41 patients. Among women using contraceptive pills there might be an increased risk of development of cerebral thrombosis, but the material was not large enough to warrant statistical analysis. In 64 patients one or more abnormal coagulation values were found, the most frequent being a deficient vessel wall fibrinolysis, which was noted in 38%. We therefore consider it worthwhile to investigate the fibrinolytic defence mechanism of the vessel wall in patients with cerebral thrombosis, since it is possible to treat this condition with specific fibrinolytic stimulating agents.
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PMID:Coagulation studies in children and young adults with cerebral ischemic episodes. 732 67

Transient ischaemic attacks (TIA) are defined by the focal and sudden loss of a cerebral function or the vision of one eye, resolving without sequelae within 24 hours and related to a vascular cause, thromboembolic much more frequently than haemodynamic. TIA represent between 9% and 25% of all cerebrovascular accident (CVA) with a variable global incidence from one study to another, between 0.2 and 3.3/1,000/year. The natural history of TIA is characterized by an excess mortality and an increased risk of cerebral infarction and myocardial infarction. It is therefore essential to recognize these events in order to prescribe effective preventive treatment. The clinical picture is characterized by a usually brief focal deficit (2 to 30 min, on average) and a normal clinical examination. The diagnosis is therefore exclusively based on the clinical interview. Complementary investigations have a dual objective: 1) to eliminate other diseases likely to cause transient neurological manifestations, and 2) to detect the mechanism and cause of cerebral ischaemia; the commonest causes are atheromatous stenosis and emboligenic heart disease. In addition to the routine laboratory examinations, basic complementary investigations consist of cerebral CT scan, cervical ultrasound and echocardiography. Conventional angiography is performed less and less frequently due to the progress in ultrasound and vascular imaging (helicoidal CT scan and magnetic resonance angiography). The treatment of TIA is designed to prevent cerebral and myocardial infarction, and to decrease the cardiovascular mortality [2]. In the short-term, it is essentially based on heparin, while waiting for the results of the aetiological assessment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Transient cerebral ischemic complications. The neurologist's point of view]. 763 3

Cerebrovascular disease with consecutive stroke is the third leading cause of death, behind only heart disease and cancer. The cost to society, both directly in health care and indirectly in lost income, amounts to 15 billion Dollar in the USA. The leading cause of stroke is focal cerebral ischemia. The general approach to the acute stroke patient remains one of therapeutic nihilism, despite effective interventional neuroradiological methods such as local intraarterial fibrinolysis and percutaneous transluminal angioplasty. These methods can be applied in a narrow timeframe only. One case of successful treatment is presented. The effort should be the development of regionalized systems of early transfer to "stroke units" capable of providing the modern spectrum of acute care to stroke patients.
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PMID:[Neuroradiologic therapy of stroke]. 776 15

The clinical characteristics and neurologic outcome of 15 newborn infants with seizures due to hypocalcemia and hypomagnesemia have been studied with careful exclusion of those patients who had other possible etiologies for seizures. Associated diagnoses included severe congenital heart disease in 7 of 15 (47%) patients. Possible causes for this association with congenital heart disease include a forme fruste of DiGeorge syndrome, hypocalcemia and hypomagnesemia due to critical illness, and subtle embolic cerebral ischemia. In contrast with previous studies, no abnormalities of formula milk feeding were observed. Five patients (36%) died of causes unrelated to seizures. Follow-up in 8 of 9 patients who had no cerebral insults other than neonatal seizures at a mean age of 57.8 +/- 10.5 months found neurologic abnormalities in 2 (22%), both with an endocrine etiology for hypocalcemia. We conclude that infants with severe congenital heart disease should be investigated for hypocalcemia and hypomagnesemia. Previous observations of a universally favorable neurologic outcome in newborns with hypocalcemic or hypomagnesemic seizures may be valid for those who have a nutritional etiology for the metabolic disturbance but are less relevant to the current population in whom hypocalcemia or hypomagnesemia due to errors in formula milk feeding is seldom observed. In this group, neurologic prognosis may be more related to associated medical conditions.
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PMID:Natural history and outcome of neonatal hypocalcemic and hypomagnesemic seizures. 798 88


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