digoxin and Angina--Unstable

This prospective hospital-based, case-control study compares the outcome of unstable angina in non-insulin dependent diabetic patients and non-diabetic control subjects. One hundred and sixty-two diabetic patients and 162 non-diabetic control patients with unstable angina were entered into the study. The 3-month mortality was 8.6% (95% confidence interval, CI = 4.4-12.9%) in diabetic patients and 2.5% (CI = 0.1-4.9%) in control patients (p = 0.014). The 1-year mortality was 16.7% (CI = 10.9%-22.4%) in diabetic patients and 8.6% (CI = 4.4%-12.9%) in non-diabetic patients (p = 0.029). Diabetic patients received beta-blockade and underwent coronary angiography and angioplasty less frequently than controls; the frequency of unstable angina, of acute myocardial infarction, and coronary artery bypass grafting was similar in both groups at 1 year of follow-up. It is concluded that diabetic patients with unstable angina have a higher mortality than non-diabetic patients and that this difference is largely accounted for by early (first 3 months) mortality.

Topics: Adrenergic beta-Antagonists; Aged; Angina, Unstable; Angioplasty; Aspirin; Calcium Channel Blockers; Case-Control Studies; Confidence Intervals; Coronary Angiography; Coronary Artery Bypass; Coronary Disease; Diabetic Angiopathies; Digoxin; Female; Follow-Up Studies; Humans; Incidence; Male; Middle Aged; Myocardial Infarction; Nitrates; Prospective Studies; Risk Factors; Time Factors

This case report describes a 69-year-old woman with diabetes mellitus and heart failure who repeatedly had unusual subtherapeutic levels of plasma digoxin. When the drug therapeutic regimen was checked it was found that a new drug, acarbose, had been added to the therapeutic regimen before the unexpected laboratory reported results. Because other drugs included in her therapeutic menu were rejected as being responsible for decreased levels of digoxin, it was recommended to discontinue acarbose to evaluate its role. In the absence of acarbose, the plasma concentration of digoxin increased to the therapeutic range. We concluded that acarbose may be responsible for a pharmacokinetic interaction with digoxin by a still unknown mechanism. Although discontinuation of acarbose was recommended, the attending physician discontinued administration of digoxin because the clinical condition of the patient did not get worse during subtherapeutic levels of digoxin.

Topics: Acarbose; Angina, Unstable; Cardiotonic Agents; Diabetes Mellitus, Type 1; Digoxin; Drug Interactions; Drug Therapy, Combination; Female; Heart Failure; Humans; Hypertension; Hypoglycemic Agents; Middle Aged; Trisaccharides

The main aim of the study was to test the hypotheses that (a) concentrations of endogenous digoxin-like factor (EDLF) are increased in the initial period after acute myocardial infarction (AMI) and (b) may contribute to the onset of ventricular arrhythmias. 54 patients of both sexes with a first transmural AMI were included in a retrospective study. Plasma concentrations of EDLF were measured repeatedly during days 1-14 after AMI using DELFIA digoxin fluoroimmunoassay. 16 male patients with unstable angina pectoris and suspected AMI as well as 8 healthy subjects of both sexes served as controls. Plasma concentrations of EDLF in patients during the first day of AMI were increased (1.25 + (-)0.26 ng/ml, digoxin equivalents, p < 0.05) as compared with both healthy controls (0.34 + (-)0.08 ng/ml) and patients with unstable angina pectoris (0.4 + (-)0.06 ng/ml). First day after AMI plasma levels of EDLF in 7 patients with primary ventricular fibrillation were higher (2.54 + (-)0.67 ng/ml, p < 0.03) than in 47 patients without ventricular fibrillation (1.05 + (-)0.27 ng/ml). In 14 patients with AMI and congestive heart failure (class III, Killip) plasma concentrations of EDLF were significantly lower (0.32 + (-)0.09 ng/ml, p < 0.03) than in 40 patients with AMI without congestive heart failure (1.51 + (-)0.32 ng/ml). Starting from the second day of AMI plasma EDLF decreased to the level of control and did not change during two weeks of observation. These results, being in agreement with our previous experimental data, show an increase of plasma EDLF after AMI and suggest that EDLF may be involved in myocardial ischemia-induced arrhythmogenesis and participate in pathogenesis of congestive heart failure after AMI.

Topics: Adult; Aged; Angina, Unstable; Biomarkers; Cardenolides; Digoxin; Enzyme Inhibitors; Female; Fluoroimmunoassay; Heart Failure; Humans; Male; Middle Aged; Myocardial Infarction; Prognosis; Retrospective Studies; Saponins; Sodium-Potassium-Exchanging ATPase; Tachycardia, Ventricular

The aim was to look for the presence of circulating factor(s) with Na,K-ATPase inhibitory properties and digoxin like immunoreactivity in patients after acute myocardial infarction.. Venous blood samples were obtained when the patients were admitted and different methods were used to monitor the plasma concentrations of factor(s) with properties of digitalis. SUBJECTS - These were 26 patients of both sexes (mean age 57.7 years, range 40-72) during the first 24 h of a first transmural acute myocardial infarct, 11 male patients with unstable angina pectoris (52.5 years, 45-67), and 18 healthy male controls (25 to 50 years).. There was significant inhibition of ouabain sensitive Na,K-ATPase in intact erythrocytes in patients with myocardial infarction [1.4(SEM 0.15)mumol Pi.mg-1.h-1] compared with patients with unstable angina pectoris [3.1(0.4), p less than 0.01] and healthy controls [3.4(0.25), p less than 0.01]. In myocardial infarction complicated by ventricular fibrillation (n = 5) Na,K-ATPase activity was significantly lower than in the other 21 patients [0.95(0.2) and 1.55(0.11) mumol Pi.mg-1.h-1 respectively, p less than 0.05]. There was no change in erythrocyte Na,K-ATPase activity in myocardial infarction complicated by acute pulmonary oedema, nor was there any difference in activity in erythrocyte ghosts obtained from the patients with myocardial infarction v healthy controls, at 0.47(0.13) v 0.50(0.02) mumol Pi.mg-1.h-1. Boiled plasma supernatants obtained from the patients with myocardial infarction inhibited Na,K-ATPase in erythrocytes from healthy subjects. This inhibitory effect was antagonised by antidigoxin antibody. Plasma inhibitory potency was correlated with erythrocyte Na,K-ATPase activity in the patients with myocardial infarction (r = -0.65, p less than 0.001, n = 23). There was a 2.5-fold increase in plasma digoxin like immunoreactivity in the patients with myocardial infarction [1.65(0.5) ng.ml-1] using DELFIA fluoroimmunoassay as compared with five healthy controls [0.04(0.12), p less than 0.05] and nine patients with unstable angina [0.48(0.11), p less than 0.05]. There was no difference in plasma digoxin like immunoreactivity in myocardial infarction complicated or not by ventricular fibrillation, but there was very low digoxin like immunoreactivity in patients with myocardial infarction complicated by acute pulmonary oedema [0.26(0.08) ng.ml-1, n = 7]. There was no correlation between plasma digoxin like immunoreactivity and either plasma Na,K-ATPase inhibitory potency or erythrocyte Na,K-ATPase activity.. The results show that plasma factor(s) with some of the properties of digitalis are increased in acute myocardial infarction.

Topics: Adult; Aged; Angina, Unstable; Blood Proteins; Cardenolides; Digoxin; Erythrocytes; Female; Fluoroimmunoassay; Humans; Male; Middle Aged; Myocardial Infarction; Ouabain; Saponins; Sodium-Potassium-Exchanging ATPase