Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Controversy exists regarding the relative safety of intravenously administered lidocaine and procainamide to patients with acutely impaired hemodynamics. Accordingly, their effects were studied in 15 such patients, 14 with acute myocardial infarction and one with cardiomyopathy and severe congestive heart failure. All had elevated levels of pulmonary capillary wedge pressure (greater than 15 mm Hg) and/or low cardiac index (less than 2.5 liters/min/m2). Patients were given lidocaine, a 100 mg bolus followed by a 3 mg/min infusion and, after at least a 30 minute recovery period, procainamide, a 100 mg bolus over 2 minutes followed by a 20 mg/min infusion for 20 to 25 minutes. Hemodynamic measurements were compared early and late in the infusion of each drug. Small, clinically insignificant differences were observed in the hemodynamic responses to the drugs, and no clinically significant deterioration occurred with either. Conventional therapeutic doses of intravenous procainamide can be administered by this regimen, to patients with acute myocardial infarction complicated by cardiac failure or low cardiac output, without producing deleterious hemodynamic effects.
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PMID:Comparative effects of lidocaine and procainamide on acutely impaired hemodynamics. 95 94

Two hundred and twelve patients with acute myocardial infarction were treated for 14 days with daily doses of potassium (3 gm orally), glucose (280 gm orally) and regular insulin (16 units subcutaneously), all given in 4 fractional doses. The incidences of arrhythmias, heart failure and systolic blood pressure below 70 mm Hg, as well as the mortality rate, were compared with those for another group of 600 myocardial infarction patients who were not given this treatment. Though there was some reduction in the incidence of cardiac arrhythmias, it was not statistically significant. However, there was a strikingly significant decrease in the incidences of heart failure and blood pressure below 70 mm, as well as in the early mortality rate. Our findings should encourage the continued use of potassium, glucose and insulin therapy in acute myocardial infarction.
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PMID:Potassium, glucose and insulin administration in acute myocardial infarction: a five-year study. 99 44

Pulmonary extravascular volume or lung water (PEV), arterial blood gases, and cardiac hemodynamics were measured in 88 patients with acute myocardial infarction. A progressive increase in PEV and a decrease in arterial oxygen tension (PaO2) were observed from Class I (uncomplicated) patients to Class III (frank pulmonary edema) patients. Heart rate and pulmonary wedge pressure (Pw) rose and cardiac index declined with increasing severity of heart failure by clinical classification. There was a significant correlation between PEV and Pw independent of clinical class (r = 0.47, p less than 0.01). PaO2 had a negative correlation with Pw (r = -0.28, p less than 0.01) as well as PEV (r = -0.26, p less than 0.02). We conclude therefore that increased pulmonary hydrostatic pressure secondary to pulmonary venous hypertension in patients with acute myocardial infarction is a major determinant of interstitial edema. At higher values of PEV, PaO2 was lower. The mechanism of hypoxemia in the presence of excessive lung water may be due to multiple factors, including small airway dysfunction and intrapulmonary shunting.
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PMID:Hypoxemia and lung water in acute myocardial infarction. 99 75

Serial measurements on serum creatine phosphokinase (CPK) and alpha-hydroxybutyrate dehydrogenase (HBD) activity were made in 17 patients with acute myocardial infarction. Activities of both enzymes were measured 4-hourly from less than 12 h after the onset of chest pain until CPK activity had returned to near-normal levels. Blood was then sampled twice daily for a further 4--6 days in order to follow the decline in HBD activity. Degradation rates (KD) were calculated for both enzymes, and individual figures for KD were used in order to estimate the total cumulative release of each enzyme. We found a significant correlation between the duration (r = 0.66, P less than 0.01) and magnitude (r = 0.67, P less than 0.01) of release of the 2 enzymes, comparing different patients with one another. Duration od HBD release was 11 h greater than the duration of CPK release in 9 of the 17 patients who were suffering from cardiac failure (t = 0.01, P less than 0.02). Degradation rate (KD) for HBD was on average about one quarter of that for CPK, but there was no significant correlation between KD for the 2 enzymes. KD did not appear to be reduced in patients with cardiac failure. We conclude that the release patterns of CPK and HBD after myocardial infarction are similar, and this strengthens the case for acceptance of total enzyme release as a valid index of myocardial infarct size.
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PMID:Enzyme release after myocardial infarction: comparison of serial serum alpha-hydroxybutyrate dehydrogenase with creatine phosphokinase levels. 100 39

One hundred patients were treated with arterial counterpulsation over a 52-month period, indications being acute myocardial infarction complicated by cardiogenic shock or refractory cardiac failure, or elective cardiac surgery complicated by continued dependence on cardiopulmonary bypass. Virtually all patients showed initial improvement and 45 were hospital survivors. Serious complications of treatment were relatively infrequent. Long-term results were good, particularly in patients treated early, and in those with infarction who suffered mechanical complications that could be corrected surgically results suggest an important role of arterial counterpulsation in acute coronary artery disease.
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PMID:Arterial counterpulsation: review of the first 100 patients. 100 49

It was established by means of radioimmunoassay that the blood concentration of Digoxin in patients with congestive heart failure depends not only on the dose of the drug given, but also on the stage of cardiac insufficiency. With equal daily doses, higher Digoxin concentrations were observed in patients with more severe cardiac insufficiency. The analysis of the obtained data has demonstrated that in 75% of the patients with signs of digitalis intoxication the concentration of Digoxin in blood exceeded 2.5 ng/ml. In animal experiments it was established that a distinct reduction of the toxic threshold took place in rabbits with acute myocardial infarction, acute pulmonary embolism, congestive cardiac failure, this threshold being determined by the amount of intravenously injected Strophantin that causes persistent ventricular tachycardia.
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PMID:[Digitalis poisoning, risk factors and digitalis intolerance]. 101 87

Digoxin concentrations were studied in the blood serum of 128 patients with cardiac insufficiency of different etiology (acute myocardial infarction, postinfarction cardiosclerosis, mitral valve disease). Radioimmunoassay with standard kits was employed, the kits containing 125 I-labelled Digoxin. Mean concentrations of Digoxin were determined in the blood serum corresponding to different maintenance doses of the drug. It was found that signs of overdosage usually appear with concentrations exceeding 2.5 ng/ml. Disorders in the renal excretory function in patients with severe edematous syndrome help a prompt cumulation of Digoxin and the development of glucoside intoxication. Some patients demonstrated a reduced Digoxin tolerance in the acute period of their myocardial infarction. The advantages of the radioimmunoassay, especially in severely ill patients with cardiac pathology are emphasized.
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PMID:[Radioimmune method of determining the concentration of digoxin in the blood during treatment of patients with cardiac insufficiency]. 101 88

The observation was conducted in 92 patients with rhythm and conductivity disorders induced by cardiac glycosides. Most of the patients had ischaemic heart disease, 60 of them having had acute myocardial infarction. All patients were prescribed cardiac glycosides (usually Strophantin and digitalis preparations) due to the appearance of cardiac insufficiency. The most frequently observed rhythm disorder consisted in ventricular extrasystole (69.5% of the cases), bigeminy, polytopic or group extrasystole being observed in many cases. Often arrhythmias consisted in atrial extrasystole, atrial fibrillation, atrial and ventricular tachycardia, atrioventricular block. "Digitalis" arrhythmias were treated with beta-adrenergic blockers: Inderal, Viskene, Eraldin, Trasicor and Aptin. These drugs proved effective in most cases with atrial arrhythmias and in some--with ventricular arrhythmias. Lidocain was more effective in cases of ventricular arrhythmias. Effective drugs of a broad spectrum are also Aimalin, Pulsenorma and Ritmodan.
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PMID:["Digitalis" arrhythmias and their treatment]. 101 1

Mortality during the hospitalization period was analyzed in a sample of 786 patients with acute myocardial infarction [AMI], admitted to the coronary care unit within a five-year period from a catchment area of 200 000 urban inhabitants. The total mortality during the hospitalization period amounted to 19.2%. The prognostic significance of certain clinically meaningful phenomena was appraised on the basis of their association to the mortality. It was demonstrated that the factors decisive for the prognosis of a patient with AMI are age, previous myocardial infarction, extent and localization of the ischaemic lesion apparent from the ECG tracing, and, in addition, presence of the atrioventricular and intraventricular conduction defects, especially if combined with anterior myocardial infarction. Patients with a high cumulation of these prognostic factors exhibited severe signs of mechanical heart failure, which is the mechanism of death in practically all of the deceased patients under the present possibilities of treatment.
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PMID:Hospital mortality in patients with acute myocardial infarction: five-year experience. 102 1

Serial determinations of CPK enzyme were performed every 4 hours during a 72 hour period in 40 patients with acute myocardial infarction (AMI) admitted to the Coronary Care Unit in the first 6 hours (average 2.6) from the appearance of symptoms. The peak ratio of activity of CPK was 708 mU/ml +/- 48 E.S. as medium value in the whole group was reached in a medium period of 21,1 +/- 0,74 E.S. hours from the attack. Half value of the peak ratio activity was reached after a medium time of 19,1 +/- 1,0 E.S. hours. A significant statistical correlation between the CPK peak ratio and the prognostic index of Selvini et al. was found. The peak ratio resulted in 571 +/- 41 E.S. in patients with uncomplicated AMI, whereas in those with complications such as arrhythmias and heart failure the average value was 901 +/- 136 E.S. No significant correlation between CPK values and ST wave evolution of the ECG peak ratio of 1638 mU/ml was found; however, one patient who died of cardiac rupture showed a low level of 395 mU/ml. The diagnostic and prognostic value of the serial determination of CPK during the first 48 hours of a coronary attack is emphasized.
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PMID:[Prognostic value of serial determination of CPK in acute myocardial infarction (author's transl)]. 102 19


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