Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 30 patients with congenital or acquired heart disease the haemodynamic effects of diazepam (Valium) 0.3 mg/kg were investigated during surgical procedures under neuroleptanalgesia. The following parameters were measured or calculated: Heart rate (HR), arterial pressure (-Part, Psyst, Pdiast), pulmonary artery pressure (-PAP), right (-PRA) and left atrial pressure (-PLA), left ventricular pressure (PLV), left ventricular enddiastolic pressure (PLVED), left ventricular peak dp/dt (dp/dtmax), cardiac output (CO), cardiac index (CI), stroke volume (SV), stroke index (SI), total systemic resistance (TSR), total pulmonary resistance (TPR), work index of the right (RVWI) and left ventricle (LVWI). In comparison with a control group (n = 36) diazepam caused a decrease in arterial pressure cardiac index, stroke index, right and left atrial pressure and dp/dtmax. This, however, was mainly attributable to vasodilatation and not to a negative inotropic effect, which is of only minor importance with diazepam. These haemodynamic changes resulted in a reduction in myocardial oxygen consumption. Diazepam is a valuable drug in neuroleptanalgesia, when an increase in blood pressure can not be controlled by fentanyl or droperidol.
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PMID:[Diazepam (valium). Changes in haemodynamics, myocardial oxygen consumption and vascular tone (author's transl)]. 69 81

In 36 patients with acquired heart disease effects of 0.15 mg/kg piritramide on hemodynamics, inotropic state and myocardial oxygen consumption were investigated during and after cardiac surgery (basic neuroleptanalgesia). It could be demonstrated, that piritramide is not inducing any negative inotropic effects compared to a control group (n = 36) and a fentanyl group (0.003 mg/kg, n = 31). There were only small changes in HR, SV, PRA and PLA. A slight decrease in Part, PLV, and arterial perfusion pressure during extracorporeal circulation is interpreted as a peripheral vasodilatation. The resulting decrease in heart work caused a significant decrease in myocardial oxygen consumption (-18%), which is of special advantage in patients with coronary heart disease.
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PMID:[Comparative clinical investigations on the cardiovascular effects of piritramide (dipidolor) and fentanyl (author's transl)]. 724

In 52 patients with acquired heart disease haemodynamic effects of 0,2 mg/kg and 1,0 mg/kg morphine were investigated during surgical procedures under neuroleptanalgesia. The following parameters were measured or calculated: heart rate (HR), arterial pressure (Part, Psyst, Pdiast), pulmonary artery pressure (PAP), right (PRA) and left atrial pressure (PLA), left ventricular pressure (PLV), left ventricular end-diastolic pressure (PLVED), left ventricular peak dp/dt (dp/dtmax), cardiac output (CO), cardiac index (CI), stroke volume (SV), stroke index (SI), total systemic resistance (TSR), total pulmonary resistance (TPR), work index of the right (RVWI) and left ventricle (LVWI). Myocardial oxygen consumption (EG) was calculated according to the method of Bretschneider. There was almost no change in cardiac index and stroke index. In comparison to a control group (n=36) morphine caused a dose-dependent decrease in arterial pressure and in arterial perfusion pressure during extracorporeal circulation. This, however, was mainly attributable to vasodilatation and not to a negative inotropic effect. In accordance with the changes in haemodynamics there was a remarkable decrease in myocardial oxygen consumption (EG: -21.1%; 1,0 mg/kg morphine).
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PMID:[Haemodynamic effects of morphine in man (author's transl)]. 728 4

We measured fibrinogen levels as well as the fibrinolytic parameters tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor 1 (PAI-1) in plasma samples obtained at basal conditions and after stimulating the fibrinolytic system by venous occlusion (VO). Samples were taken from patients with primary pulmonary hypertension (PPH), with secondary thromboembolic pulmonary hypertension (SPHTH), with secondary pulmonary hypertension due to congenital heart disease with Eisenmenger's reaction (SPHCD), and from healthy control individuals (CON). Fibrinogen levels were not significantly different between the groups with PPH and SPHTH or between SPHCD and CON. The latter groups, however, exhibited significantly lower fibrinogen plasma levels compared with PPH or SPHTH (p < 0.01). Basal plasma levels of t-PA antigen, t-PA activity, and PAI-1 activity, respectively, did not differ significantly between the study groups. After VO, mean t-PA activity levels increased to a higher extent in control subjects compared with patients with PPH, or SPHTH, or SPHCD, with significant differences only between CON and SPHTH or CON and PPH (p < 0.03). Patients with PPH and SPHTH exhibit both increased fibrinogen plasma levels and a diminished fibrinolytic response compared with healthy subjects. Moreover, the fibrinogen plasma levels in patients with SPHCD are in normal range, and the fibrinolytic response is similar to CON compared with PPH and SPHTH, thus indicating the existence of a comparable prothrombotic situation in patients with PPH and SPHTH.
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PMID:Fibrinogen, t-PA, and PAI-1 plasma levels in patients with pulmonary hypertension. 792 65

The data gained from clinical studies in the past years have indicated that the thrombolytic therapy (TL) has favourable effect on patients with acute myocardial infarction (AMI). It is aimed at reperfusion in the ischaemic area, a decrease in the extent of infarction site and a decrease in mortality. TL administered within the initial hours after the onset of AMI leads to better results than when administered after several hours. Currently, TL is not limited by age. The patients who were given streptokinase (SK) or anistreplase (APSAC) prior to more than 4 days, if necessary, urokinase or alteplase (rt-PA) should be given. There are differences in the opinions as to the optimal selection of thrombolytic drugs. However, all currently used drugs lead to a significant decrease in mortality due to AMI. The preferential use of accelerated administration of rt-PA in contrast to SK is justified in younger patients with extensive AMI of the anterior wall, in whom the therapy has begun within 4 hours since its onset. The occurence of severe bleeding indicates that TL should be halted and coagulation factors should be replaces by freshly frozen plasma or fibrinogen concentrate, if necessary, transfusion of full blood should take place. If the severe bleeding occurs shortly after the administration of SK, the persisting plasminaemia can be arranged by antifibrinolytic drugs. An improvement in TL results can be achieved by adjuvant antithrombotic therapy. At the same time, in addition to acetylsalicylic acid, the patient treated with rt-PA should be given heparin. Heparin administration is not necessary in patients treated with SK or APSAC. However, heparin is indicated in patients at risk due to systemic embolization in congestive heart disease, extensive infarction or atrial fibrillation. (Tab. 1, Ref. 28).
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PMID:[In Process Citation] 966 37

The data gained from clinical studies in the past years have indicated that the thrombolytic therapy (TL) has favourable effect on patients with acute myocardial infarction (AMI). It is aimed at reperfusion in the ischaemic area, a decrease in the extent of infarction site and a decrease in mortality. TL administered within the initial hours after the onset of AMI leads to better results than when administered after several hours. Currently, TL is not limited by age. The patients who were given streptokinase (SK) or anistreplase (APSAC) prior to more than 4 days, if necessary, urokinase or alteplase (rt-PA) should be given. There are differences in the opinions as to the optimal selection of thrombolytic drugs. However, all currently used drugs lead to a significant decrease in mortality due to AMI. The preferential use of accelerated administration of rt-PA in contrast to SK is justified in younger patients with extensive AMI of the anterior wall, in whom the therapy has begun within 4 hours since its onset. The occurrence of severe bleeding indicates that TL should be halted and coagulation factors should be replaced by freshly frozen plasma or fibrinogen concentrate, if necessary, transfusion of full blood should take place. If the severe bleeding occurs shortly after the administration of SK, the persisting plasminaemia can be arranged by antifibrinolytic drugs. An improvement in TL results can be achieved by adjuvant antithrombotic therapy. At the same time, in addition to acetylsalicylic acid, the patient treated with rt-PA should be given heparin. Heparin administration is not necessary in patients treated with SK or APSAC. However, heparin is indicated in patients at risk due to systemic embolization in congestive heart disease, extensive infarction or atrial fibrillation. (Tab. 1, Ref. 28.)
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PMID:[Thrombolytic therapy in acute myocardial infarct]. 991 45

Stroke remains one of the major causes of death and permanent disability in the United States, ranking as the third leading cause of death behind heart disease and cancer. It affects an estimated 700,000 persons each year; about two-thirds of those with a new or recurrent stroke survive. The aggregate cost of stroke in the United States is more than $40 billion per year, with an average cost per case of approximately $50,000. With the advent of recombinant tissue-type plasminogen activator (t-PA) for acute stroke, clinical pathways have been developed to provide efficient care to acute stroke patients. Efforts must be aimed at educating the public and all members of the healthcare team about proper stroke care. Surprisingly, only 20%-30% of all hospitals have stroke teams in place. To bring stroke care into the 21st century, this deficiency must be addressed and additional treatment agents such as neuroprotective medications need to be approved.
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PMID:Establishment of stroke treatment plans: one hospital's experience. 1115 44

We evaluated the association of hemostatic factors with insulin resistance in relation to reproductive hormones including FSH, estradiol, testosterone, and SHBG. SHBG was used to calculate the free estradiol index and free androgen index. We studied 3,200 women, aged 42-52 yr, in the Study of Women's Health Across the Nation, a prospective multiethnic study of the menopausal transition. We measured the hemostatic factors, fibrinogen, factor VIIc, tissue plasminogen activator (t-PA), and plasminogen activator inhibitor type 1 (PAI-1), as well as glucose and insulin to calculate insulin resistance. After adjustment for body mass index, site, and ethnicity, SHBG was correlated with PAI-1 (partial r = -0.30) and t-PA (partial r = -0.12). Although testosterone was associated with t-PA (partial r = 0.13) and PAI-1 (partial r = 0.07), free androgen index was strongly correlated with t-PA (partial r = 0.18) and PAI-1 (partial r = 0.26). SHBG modified the association of hemostatic factors with insulin resistance. Women with greater insulin resistance had lower SHBG and higher PAI-1. Estrogen measures were not associated with insulin resistance. The influence of sex hormones on hemostatic factors and insulin resistance is poorly understood. SHBG, which influences the amount of bioavailable hormone, significantly modified the association of PAI-1 and t-PA with insulin resistance. The longitudinal Study of Women's Health Across the Nation will help us discern whether this interaction contributes to heart disease and diabetes among postmenopausal women.
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PMID:Insulin resistance, hemostatic factors, and hormone interactions in pre- and perimenopausal women: SWAN. 1455 72

Pulmonary arterial thrombosis (PAT) may complicate the clinical course of pulmonary hypertension associated with congenital heart disease (so-called Eisenmenger syndrome, ES). In this study, variables were sought that could represent risk factors for the occurrence of this complication. Twenty patients aged 11 to 53 (median, 33) years were studied. The presence of PAT (spiral computed tomography angiography) was correlated with age, gender group, PAP, hematocrit, peripheral oxygen saturation (SpO(2)), and plasma levels of endothelial and coagulation dysfunction markers: von Willebrand factor antigen (vWF:Ag), tissue plasminogen activator (t-PA), and D-dimer (enzyme immunoassay). Patients were classified according to the presence (group 1, N=7), or absence (group 2, N=13) of PAT. Group 1 patients were older (42+/-8 vs. 27+/-10 years in group 2, p=0.0051), had lower SpO(2) (82+/-7% vs. 89+/-6% in group 2, p=0.0462) and increased D-dimer levels (637 vs. 149 ng/mL in group 2, median values, p=0.0235). A trend was observed toward an increase in vWF:Ag (125+/-29 vs. 103+/-18 U/dL in group 2, p=0.0789) and t-PA (15.7 vs. 9.4 ng/mL in group 2, median values, p=0.0689). Age was the main variable influencing the occurrence of PAT in multivariate analysis (p=0.0026), with odds ratio of 1.204 per year. The age of 35 years was 86% sensitive and 85% specific for occurrence of PAT. Age correlated positively with t-PA (r=0.57, p=0.0111). Thus, PAT is highly prevalent in ES as an age-dependent event, probably associated with endothelial dysfunction. Prophylactic anticoagulation should be considered before the age of 30 years, in particular in subjects with low SpO(2) and increased D-dimer levels.
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PMID:Age-dependent likelihood of in situ thrombosis in secondary pulmonary hypertension. 1524 78

Diet is one of the environmental factors that influences thrombosis and hemostasis. Macronutrients, micronutrients, and other bioactive food components alter the predisposition to thrombosis. The type and amount of dietary fat has been shown to alter thromboxane A2 production and platelet aggregation, bleeding time, factor VII, fibrinogen, tissue plasminogen activator (t-PA) and plasminogen activator inhibitor 1 (PAI-1). Both epidemiological studies and clinical trials indicate that the very long chain n-3 fatty acids lower thrombotic tendency and risk of heart disease. Other polyunsaturated fats and monounsaturated fat appear to have antithrombotic properties, but further studies are indicated. Hypercaloric diets and those with high glycemic loads are associated with elevations of PAI-1. Moderate consumption of alcohol is associated with decreased platelet aggregation. Low intakes of folate, vitamin B12, and vitamin B6 predispose to hyperhomocysteinemia, and the benefits of supplementation in decreasing vascular disease are under investigation. In a limited number of clinical and laboratory studies, vitamin E has been shown to decrease platelet aggregation and the concentration of PAI-1. Flavonoids and isoflavones appear to inhibit platelet aggregation at pharmacologic concentrations only. Nutritional status frequently declines with aging and may exacerbate the already increased risk for thrombosis. Diet presents an interesting area for research into thrombophilia, but additional work is indicated before specific recommendations are made.
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PMID:Diet and aging: bearing on thrombosis and hemostasis. 1570 83


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