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)

A 62-year-old male patient, suffering from a hypertensive cardiopathy, an arteriopathy of the lower extremities and a type II insulin independent diabetes had a prothrombin time ratio R of 2.15 (therapeutic range: 2.1-1.45) during a daily treatment of 4-6 mg acenocoumarin. On admission to the psychiatric hospital for depression, a mianserin treatment was commenced, leading to a sharp modification in the PT ratio R, in effect that the acenocoumarin treatment had to be increased to keep R within the therapeutic range. The possible mechanism of this interaction between mianserin and acenocoumarin is discussed, taking into account the possible role of the comedicated amiodarone.
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PMID:Interaction between mianserin and acenocoumarin: a single case study. 803 74

An increase in factor VII was found to be a risk factor for ischemic heart disease. The present study was designed to test the hypothesis that this increase in factor VII is part of a general increase in vitamin K-dependent clotting factors. Initially, a prospective analysis of factor VII antigen and prothrombin activity was performed in two groups of young subjects without symptoms who differed in their risk of ischemic heart disease based on a history (or lack thereof) of premature heart disease in a first-degree relative. A statistically significant increase in prothrombin activity and factor VII antigen was found in the high-risk group of subjects when compared with the low-risk group. In a second series of subjects, factor IX and X activity assays were also performed, and all four of the vitamin K-dependent clotting factors were found to be significantly higher in high-risk subjects when compared with low-risk subjects. A second goal of the study was to explore whether correlations between factor VII and cholesterol and triglycerides might be due to binding of factor VII with apolipoprotein B. Although a significant correlation of factor VII antigen with apolipoprotein B (rho = 0.523, p < 0.025) was found in our high-risk group of subjects, the correlation between factor VII and triglycerides (rho = 0.641, p < 0.005) was even stronger statistically, suggesting a probable interaction of factor VII with very-low-density lipoproteins in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vitamin K-dependent clotting factors are elevated in young adults who have close relatives with ischemic heart disease. 824 91

The time period after implantation of a ventricular assist device in patients with end-stage heart disease is complicated by hemorrhage in the early postoperative period and by thromboembolism in the later course. To investigate the pathophysiologic role of contact activation in 12 bridging patients (10 patients with a paracorporeal Berlin Heart [Berlin Heart GmbH, Berlin, Germany], 2 patients with an intracorporeal Novacor system [Novacor N100; Baxter, Oakland, CA]), hemostatic parameters were determined until heart transplantation or at least up to the 51st postoperative day. The following were observed: 1) In the early postoperative period, until day 15, levels of contact factors XI, XII, and prekallikrein were below normal, whereas levels of plasmin-a2-antiplasmin (PAP) complexes were elevated. Thrombin-antithrombin III (TAT) complexes, as well as platelet factor 4 and beta-thromboglobulin, significantly increased immediately after surgery. 2) In the later postoperative period, starting with the third postoperative week, an increase of factors XI, XII, and prekallikrein was observed. PAP and TAT complexes, as well as platelet factor 4 and beta-thromboglobulin, remained elevated. It is concluded that, in the early postoperative period, hemostasis is influenced mainly by an activation of the intrinsic contact system dependent fibrinolytic system with consumption of contact factors and increased levels of PAP complexes, whereas later system dependent fibrinolysis becomes less important, leading to a shift of the balance toward coagulation, with sustained prothrombin and platelet activation. This is in accord with the observed clinical complications (e.g., early postoperative bleeding, and thromboembolic events later on).
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PMID:Pathophysiologic role of contact activation in bleeding followed by thromboembolic complications after implantation of a ventricular assist device. 857 16

Prolonged Q-T interval predicts severe arrhythmias and sudden death, and has been shown to occur in alcoholic liver disease and cirrhotic patients who are candidates for liver transplantation. This study first evaluated the prevalence of prolonged Q-T interval in a large population of unselected patients with cirrhosis, and assessed the relationship between abnormal Q-T, etiology, and severity of liver disease and mortality of patients. Possible causes of Q-T abnormality were also explored. Ninety-four patients with cirrhosis without overt heart disease and 37 control subjects with mild chronic active hepatitis were enrolled. Rate-corrected Q-T interval (Q-Tc) was assessed along with routine liver tests, Child-Pugh score, serum bile salts, electrolytes and creatinine, plasma renin activity, aldosterone, norepinephrine, atrial natriuretic factor and, gonadal hormones. Q-Tc was longer in patients with cirrhosis than in controls (440.3 +/- 3.2 vs. 393.6 +/- 3.7 ms; P < .001) and prolonged (> 440 ms) in 44 patients (46.8%) and 2 controls (5.4%; P < .001). Q-Tc length was not influenced by the etiology of cirrhosis and correlated with Child-Pugh score (r = .53; P < .001), liver tests such as prothrombin activity, and serum concentrations of albumin and bilirubin, plasma bile salts, and plasma norepinephrine. Multivariate analysis showed that only Child-Pugh score and plasma norepinephrine were independently correlated with Q-Tc duration. Over a median follow-up period of 19 months (range, 2-33 months), patients with Q-Tc longer than 440 ms had a significantly lower survival rate than those with normal Q-Tc. Q-T interval is frequently prolonged in patients with cirrhosis, regardless the etiology of the disease, worsens in parallel with the severity of the disease, and may have an important prognostic meaning. In addition to other undefined factors related to the severity of cirrhosis, sympathoadrenergic hyperactivity may play a pathogenetic role.
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PMID:Q-T interval prolongation in cirrhosis: prevalence, relationship with severity, and etiology of the disease and possible pathogenetic factors. 942 13

Severe coagulation defects often develop in neonates undergoing cardiac surgery, both as a result of the surgical intervention, and as pre-existing defects in the hemostatic mechanisms. The following case report describes a newborn patient with complex congenital heart disease and respiratory failure whose pre-operative coagulopathy was aggressively managed prior to surgical correction. A 5-day-old, 2.5 kg child presented with interrupted aortic arch, ventricular septal defect, atrial septal defect, and patent ductus arteriosus. On admission, he was in respiratory arrest suffering from profound acidemia. In addition, the child was hypothermic (30.1 degrees C), septic (Streptococcus viridans), and coagulopathic (disseminated intravascular coagulation-DIC). The patient was immediately intubated and initial coagulation assessment revealed the following: prothrombin time (PT) 48.9 s (international normalized ratio (INR) 15.7), activated partial thromboplastin time (aPTT) >106 s, platelet count 30,000 mm(3), fibrinogen 15 mg dL(-1) and antithrombin III (AT-III) 10%. Before cardiac surgery could be performed, the patient's DIC was corrected with the administration of cryoprecipitate (15 ml), fresh frozen plasma (300 ml), and platelets (195 ml). In spite of the large transfusion of fresh frozen plasma, the AT-III activity, measured as a percentage, remained depressed at 33. Initial thromboelastographic (TEG) determination revealed an index of +2.02, and following 100 IU administration of an AT-III concentrate, declined to -2.32. Sequential TEG profiles were performed over several days, with the results used to guide both transfusion and medical therapy. The congenital heart defect correction was subsequently performed with satisfactory initial results, but the patient developed a fungal infection and expired on the 16th post-operative day. The present case describes techniques of coagulation management for a newborn with both a severe hemostatic defect and congenital heart disease.
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PMID:Pre-operative coagulopathy management of a neonate with complex congenital heart disease: a case study. 1078 72

Mechanisms of bleeding common to virtually all patients after heart surgery are platelet dysfunction, enhanced fibrinolysis, dilution of all components of the coagulation system, and the presence of heparin and protamine. The use of warfarin is increasing in patients with heart disease requiring surgery. The replenishment of vitamin K-dependent factors beyond a normal prothrombin time is not assessable, and the dilution associated with cardiopulmonary bypass can reach coagulopathic levels. Optimal preoperative preparation is required and intraoperative therapy initiated when indicated. Individualized heparin and protamine dosing, antifibrinolytic drug administration, minimization of blood loss and dilution, and minimal time on cardiopulmonary bypass are basic adjuncts to meticulous surgical hemostasis. When bleeding is observed in the postoperative period, a sequential assessment of the probable cause leads to initial therapy while laboratory test results are obtained. Ongoing assessment for hemodynamic instability caused by accumulated mediastinal blood is needed while managing the bleeding patient. A chest radiograph and transesophageal echocardiogram can be useful in diagnosing cardiac tamponade.
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PMID:Management of bleeding and coagulopathy after heart surgery. 1115 28

This study was undertaken to screen children with congenital heart disease for coagulation abnormalities and to compare the groups of cyanotic and acyanotic children with congenital heart disease with respect to abnormalities of the coagulation system. Following investigations were done in all the patients: complete blood count, erythrocyte sedimentation rate, peripheral smear examination, bleeding time, prothrombin time, activated partial thromboplastin time, assay of fibrinogen, D-dimer, factors VII and VIII and antithrombin III. Red cell indices were determined in 12 control, 12 acyanotic and 20 cyanotic children. Twenty-five patients each, with echocardiographically proven cyanotic and acyanotic congenital heart disease under 12 years of age constituted the study group; as many children of the same age group were included as the control group. The results showed isolated abnormalities of laboratory tests with equal frequency (28%) in acyanotic and cyanotic groups but coexisting abnormalities of more than one test were seen in significantly larger number of cyanotic children (5/25 and 16/25, respectively). A significant association was noted between thrombocytopenia and a high haematocrit in cyanotic patients. It is concluded that laboratory abnormalities of tests of haemostasis are more common in cyanotic congenital heart disease patients. The patterns of laboratory abnormalities suggest a chronic compensated disseminated intravascular coagulation at a subclinical level, reduced synthesis of clotting factors and/or deranged platelet aggregation in different subgroups of patients.
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PMID:Haemostatic changes in children with cyanotic and acyanotic congenital heart disease. 1125 79

Fortuitously discovered after an episode of bovine hemorrhagic disease, the oral antivitamin K anticoagulants inhibit a posttranslational modification of coagulation factors II, VII, IX, and X that is essential for bioactivity. They also influence formation of regulatory proteins C and S. Although their influence on the extrinsic pathway may be measured using the prothrombin time, a modification thereof produces the International Normalized Ratio (INR) which should allow for less interlaboratory variation. Finding utility in both prophylaxis and treatment of thromboembolic disease, these agents have rendered themselves important pharmacologic tools in the management of deep venous thrombosic, nonvalvular atrial fibrillation, structural heart disease, myocardial infarction, and following major surgical procedures.
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PMID:Warfarin and Other "Anti"-Vitamin K Anticoagulants: Pharmacodynamics and Clinical Use. 1186 37

This study analyzed 28 thrombotic children with various cardiac disorders. They comprise 17% of a total of 168 patients with thrombosis from a single center. Among the 28 patients, 21 had congenital heart disease and 7 were diagnosed with cardiomyopathy. The patients with thrombosis were evaluated for congenital and acquired thrombotic risk factors. In addition to cardiac disorders, two, three, or more risk factors were present in 61% of the children with thrombosis. Two common mutations, namely factor V Leiden and prothrombin G20210A mutations, were found in 6 patients (22%). Nine patients (32%) died of infection, congenital heart disease, cardiomyopathy, thrombosis, operation, or a combination of these; two patients required surgical intervention. Following cardiac angiography, due to necrosis, amputation of the right index finger and right lower extremity was performed on 1 patient. The second patient's index fingers had to be amputated and resection of the bowel was performed following the operation on coarctation of the aorta. This study indicates that congenital heart disease and cardiomyopathy are two common cardiac disorders that may lead to the development of thrombosis. The majority of thrombosis develops within the heart and/or its great vessels. The second predominant site for thromboembolic symptoms is in the brain, including sinovenous thrombosis.
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PMID:Thrombosis in children with cardiac pathology: frequency of factor V Leiden and prothrombin G20210A mutations. 1252 59

OBJECTIVE: The objective of this study was to analyze the incidence and significance of hepatic dysfunction after cardiac surgery in children. DESIGN: Prospective, observational study. SETTING: Pediatric intensive care unit of a university hospital. PATIENTS: The study consisted of 232 children ranging in age from newborn to 17 years with no history of liver disease. MEASUREMENTS AND MAIN RESULTS: Aspartate aminotransferase (AST), alanine aminotransferase (ALT), gammaglutamyltranspeptidase (GGT), alkaline phosphatase, total and conjugated bilirubin, blood glucose, urea, creatinine, and coagulation studies were determined at admission, at 24 and 48 hrs, and at 7 days. Hepatic dysfunction was taken as an ALT of > 100 IU/L or a moderate or high hepatic score. The statistical study included bivariate analysis and multivariate logistic regression to study the risk factors for hepatic dysfunction. Twenty-one patients (9%) showed an ALT > 100 IU/L, and 29.3% had a moderate or high hepatic score. A relationship was found between hepatic dysfunction and the type of cardiopathy (D-transposition of the great arteries and coarctation of the aorta), shock, the administration of dopamine or epinephrine, renal insufficiency, the presence of pulmonary changes (pulmonary edema, atelectasis, pulmonary hypertension, hypoxemia), hematologic disturbances (prothrombin time, kaolin-cephalin time, fibrinogen, and platelets), and the need for a greater number of transfusions of packed cells, plasma, and platelets. Compared with 7.6% of the rest of the patients (p <.001), 38% of patients with an ALT > 100 IU/L died. The hepatic score of those patients who died was 4.2 (2.3)-higher than that of the survivors at 1.5 (1.8), (p <.001). Shock and renal insufficiency were the factors most significantly related to the development of hepatic dysfunction. CONCLUSIONS: Hepatic dysfunction is an uncommon complication in children after cardiac surgery. This complication is related mainly to hemodynamic disturbances and renal insufficiency and is an indicator of poor prognosis.
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PMID:Hepatic dysfunction after cardiac surgery in children. 1279 88


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