Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirteen patients with chronic congestive cardiac failure and refractory oedema were treated by haemodialysis. All patients had severe cardiac failure (Class IV NYHA) due to primary myocardial disease (5 cases), ischaemic heart disease (4 cases) or valvular heart disease (4 cases). Haemodialysis was performed via a Shaldon Y-shaped catheter in the internal jugular vein, with input and output through the same catheter using an alternating clamp. Filtration was carried out through a highly permeable membrane by a simple hydrostatic pressure gradient without a dialysis bath. The sessions were monitored haemodynamically by measuring the pulmonary artery pressures. The mean weight loss was 4.9 +/- 0.4 kg obtained after 3 three hour dialysis sessions with 24 hour intervals between each session (mean filtration flow = 12 ml/min). Hypotension was observed in one patient with low initial pulmonary artery pressures; two patients with severe valvular stenosis (1 mitral stenosis; 1 aortic stenosis) failed to lose weight. In the 10 remaining cases, there was a clearcut symptomatic improvement (5 patients Class III; 5 patients Class II NYHA) with total regression of oedema. There was a significant fall in pulmonary artery (mean PAP 40.5 +/- 6.5 mmHg to 34.6 +/- 6.5 mmHg; p less than 0.001) and pulmonary capillary pressure (27.6 +/- 6.9 mmHg to 22.5 +/- 5.8 mmHg; p less than 0.05) in these 10 cases. Cardiac output did not change significantly (cardiac index 2.2 +/- 0.5 l/m2/min compared to 2.3 +/- 0.4 l/m2/min after dialysis).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Treatment of cardiac failure with refractory edema using extracorporeal ultrafiltration]. 643 80

The aim of the present study was to find out whether plasminogen activator inhibitor type-1 (PAI-1) controls the formation of plasmin in patients with ischaemic heart disease. We examined PAI activity, PAI-1 antigen, tissue type plasminogen activator (t-PA) activity, t-PA antigen, plasmin-alpha2-antiplasmin complex (PAP-complex) and fibrin degradation products D-dimer in 62 patients before (unstimulated) and after infusion of 1-desamino-8-D-arginine vasopressin (DDAVP; stimulated). DDAVP was used in a standardized dose to trigger the release of t-PA from the vascular endothelium. We observed that under basal conditions (unstimulated) median plasma t-PA activity for the whole group of patients was 86.5 mIU/ml (0-900), and after stimulation 2550 mIU/ml (0-6800), P < 0.0001; median plasma concentration of t-PA antigen was 14.7 ng/ml (7.0-115.5) under basal conditions, and after stimulation 34.1 ng/ml (15.8-58.6), P < 0.0001; median plasma PAI activity was 16.9 IU/ml (1.5-144.8) under basal conditions, and after stimulation 3.1 IU/ml (0-118.5), P < 0.0001; median plasma concentration of PAI-1 antigen was 21.5 ng/ml (8.1-132.2) under basal conditions, and after stimulation 14.9 ng/ml (4.8-149.0), P < 0.0001; the median plasma concentration of PAP-complex was 469.5 ng/ml (185.0-1802.0) under basal conditions, and after stimulation 695.5 (243.0-2292.0), P < 0.0001; median plasma concentration of D-dimer was 298.0 ng/ml (103.0-948.0) under basal conditions, and after stimulation 296.5 ng/ml (97.0-917.0), P < 0.0008.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasminogen activator inhibitor type-1 determines plasmin formation in patients with ischaemic heart disease. 748 12

Increasing concern over complications related to blood transfusions has prompted a reevaluation of what constitutes an "adequate" perioperative hemoglobin concentration, particularly in patients undergoing coronary artery bypass graft (CABG) surgery. Data from 224 patients with preserved ventricular function (ejection fraction > 50%), undergoing CABG surgery, previously studied under a variety of anesthetic protocols, were reexamined to determine the effect of hemoglobin (HGB) concentration on myocardial lactate flux (MLF) (as an index of ischemia). The interaction of MLF and HGB concentration, anesthetic technique (ANES), and hemodynamic variables (including systemic and pulmonary arterial pressures (SAP and PAP), cardiac output (CO), and myocardial oxygen consumption (MVO2) was determined from a pool of 1598 data sets obtained from 224 patients. Data were collected from just prior to induction of anesthesia until 24 h postoperatively. Univariate analysis revealed a statistically significant relationship between MLF and HGB concentration (P < 0.001) but the correlation coefficient was only 0.09. Multiple regression analysis did not determine HGB concentration to be a significant independent term affecting MLF in either the overall group or in a subgroup of 22 patients having an adverse outcome (myocardial infarction, stroke, or death). For patients undergoing CABG surgery, HGB concentrations within the range of 58-172 g/L were not a significant variable in production of global myocardial ischemia as evidenced by MLF. This suggests that HGB concentrations as low as 60-70 g/L in the perioperative period are well tolerated and are not associated with an increased incidence of myocardial ischemia.
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PMID:Does hemoglobin concentration affect perioperative myocardial lactate flux in patients undergoing coronary artery bypass surgery? 772 33

The authors describe a rare case of pulmonary thromboembolism with unusual clinical findings and emphasized the large difficulty encountered in formuling a correct diagnosis in a reasonable time. A man, 60 years old, was admitted to a Medical Division of our hospital for the appearance of chest pain and epigastric pain during effort in the last year. He smoked 20 cigarettes a day and drank wine (1 or 2 litres a day). He was affected by hypercholesterolemia and in the past reported relapsed thrombophlebitis in the left leg. Four years before admission to our hospital he underwent large and small left saphenectomy. He had no cardiac events in the past. After a non significant exercise stress test the patient was treated with nitrates and asa and was discharged from the hospital. At home the symptoms increased and after 8 months the patient was admitted again to the Cardiologic Division of the hospital. At admission he reported dyspnea and chest pain at rest, not only during effort and the ECG showed negative T waves in anterior and inferior leads. Intravenous heparine, nitrates and calcium antagonists stabilized the clinical picture. The following examinations revealed: reduction of the T wave negativity at the ECG registered during chest pain; mild enlargement of the heart at the chest roentgenogram; normal value of the left ventricle and apical and midseptal by ipokinesia at the transthoracic echocardiogram; normal coronary artery at the coronary arteriography. "Vasospastic angina" was diagnosed and the patient was discharged after 20 days, asymptomatic. After 15 days he returned to the hospital again for chest pain, dyspnea, hypotension and syncope despite therapy. At physical examination he showed a painful left tibio-tarsal tumefaction, an increased and splitting second heart sound in the pulmonary area and a systolic murmur in the third and fourth left interspace. The ECG showed a severe anterior ischemia, while a new transthoracic echocardiogram revealed a considerable dilatation of the right atrium, right ventricle and the main pulmonary artery with severe tricuspid regurgitation and pulmonary hypertension (mean PAP about 50 mmHg). The following pulmonary perfusion scintigraphy confirmed the diagnosis of pulmonary embolism and the selective right and left pulmonary arteriography exhibited multiple thrombi and large intravascular filling defects. The right heart catheterization confirmed a chronic precapillary pulmonary hypertension (mean PAP = 55 mmHg). About 24 hours after these examinations the patient died because of a cardiac arrest with electromechanical dissociation. Pulmonary thromboembolism is a potentially fatal disease characterized by a largely variable clinical presentation. Frequently pulmonary embolism diagnosis is difficult especially when clinical findings are unusual. In the case observed the "typical" chest and epigastric pains associated with the electrocardiographic findings directed diagnosis towards myocardial ischemia. Also after the coronary arteriography that showed normal coronary artery, the erroneous diagnosis persisted. Pulmonary embolism was correctly diagnosed too late to begin an effective therapy. These unusual clinical findings and diagnostic mistakes are stressed and critically reviewed in the article.
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PMID:[Pulmonary thromboembolism. A clinical case with unusual presentation]. 871 Jan 39