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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In treating heart failure, the physician must remain cognizant of pathophysiology as he prescribes and monitors therapy. In addition to seeking underlying and precipitating causes of the patient's heart failure, he must treat the congestive state by enhancing myocardial contractility, controlling excessive fluid retention, and reducing afterload. Figure 7 summarizes the theoretical shifts on a patient's left ventricular function curves that might occur with therapy. Left ventricular function might move from point A to point B with diuretic therapy, but overdiuresis could aggravate symptoms of low cardiac output, including postural hypotension. Digitalis would effect a shift from A to C. Isosorbide dinitrate would produce a shift from A to D in a patient not on digitalis and from C to D in a patient already receiving digitalis. Isosorbide dinitrate, in conjunction with more usual therapeutic measures, has proved clinically beneficial in the treatment of heart failure.
Compr Ther 1976 Dec
PMID:Treatment of congestive heart failure. 82 68

The acute hemodynamic effects of dobutamine and nitroprusside were compared in 19 patients with low output cardiac failure. At dosage levels yielding similar increases in cardiac index (12 patients), nitroprusside resulted in significantly lower arterial systolic and wedge pressures and did not increase heart rate suggesting advantages over dobutamine when reduction in myocardial oxygen requirement or pulmonary congestion is a major goal. Systemic arterial mean and diastolic pressures were minimally changed with dobutamine, but fell significantly with nitroprusside suggesting advantages of dobutamine over nitroprusside in patients where hypotension could limit coronary blood flow or perfusion of other vital organs. Reduction in pulmonary arteriolar resistance occurred only with nitroprusside. Arterial hypoxemia developed in three patients during nitroprusside infusion suggesting the possibility of increased right-to-left intrapulmonary shunting resulting from a direct vasodilating effect of nitroprusside on pulmonary arteriole smooth muscle. Although both inotropic and vasodilator drugs can result in hemodynamic improvement when administered to patients with chronic low output cardiac failure, significant differences of potential clinical importance exist between these two modes of therapy.
Circulation 1977 Dec
PMID:Comparative responses to dobutamine and nitroprusside in patients with chronic low output cardiac failure. 92 60

Sodium nitroprusside is an excellent agent for lowering blood pressure in hypertensive emergencies, for producing controlled hypotension during anesthesia, and for treating acute myocardial infarction and chronic heart failure. Toxic effects of this drug have been reported and above-normal cyanide and thiocyanate concentrations have been observed in the blood of a small proportion of subjects receiving nitroprusside. Nitrite, syanide, and thiocyanate are major decomposition products of nitroprusside, resulting from an in vitro reaction with human blood. On the basis of the conversion mechanism, we suggest that, in the cyanide/thiocyanate cycle, only cyanide is directly responsible for any acute toxicity attributed to sodium nitroprusside. In this work, the extent of cyanide production by erythrocytes in vitro was studied. The rate of detoxification of cyanide by human liver in vitro was experimentally determined and data from a search for a possible inhibitor of the nitroprusside/hemoglobin reaction are presented. Also, the possible mechanism of the nitroprusside/hemoglobin reaction is discussed.
Clin Chem 1977 Dec
PMID:Some aspects of sodium nitroprusside reaction with human erythrocytes. 92 83

The Valsalva maneuver was evaluated by echocardiography in three groups: A) 10 normal volunteers, B) 10 patients with no history of heart failure and normal ejection fractions, and C) 10 patients with heart failure and depressed ejection fractions. Groups A and B had a significant fall in left ventricular internal dimensions and calculated stroke volume by end strain which returned rapidly to baseline in recovery without significant overshoot. Arterial pressure showed a signoidal strain pattern with a normal overshoot in early recovery in all group B patients. In group C ventricular dimensions did not diminish during strain; arterial pressures showed a "square wave" pressure elevation during strain without an overshoot in recovery. Echocardiography allows a new approach to evaluate further the left ventricular response to the Valsalva maneuver. Patients with severely depressed ejection fractions, unlike those with normal ventricular function, are unable to alter stroke output in response to acutely increased intrathoracic pressure. A square wave pressure response is a likely consequence of a fixed stroke output during the strain maneuver.
Circulation 1976 Dec
PMID:Echocardiographic evaluation of the Valsalva Maneuver in healthy subjects and patients with and without heart failure. 99 7

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.
J Am Geriatr Soc 1976 Dec
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.
Am Heart J 1976 Dec
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.
Eur J Cardiol 1976 Dec
PMID:Enzyme release after myocardial infarction: comparison of serial serum alpha-hydroxybutyrate dehydrogenase with creatine phosphokinase levels. 100 39

Left ventricular function was studied in 14 patients with end-stage chronic renal failure using non-invasive methods (echocardiography and systolic time intervals). Patients were divided into 3 groups. Group 1 consisted of 5 patients who were normotensive at the time of study and group 2 of 7 patients who were hypertensive when studied. Group 3 consisted of 2 patients: one was receiving propranolol and the other, studied 302 days after renal transplantation, was receiving digitalis for recurrent episodes of cardiac failure. All except the patient receiving propranolol had normal left ventricular function in systole with normal measurements of fractional fibre shortening (% delta S, EF) and normal measurements relating to the velocity of ventricular contraction (mean Vcf, mean velocity of posterior wall motion). Stroke volume and cardiac output were normal in some patients but were increased in patients with fluid overload. Early diastolic compliance of the left ventricle seemed to be normal except in the patient with recurrent cardiac failure. The study provided no evidence for the existence of a specific uraemic cardiomyopathy.
Br Heart J 1976 Dec
PMID:Left ventricular function in chronic renal failure. 100 67

During the 10 years from 1964 to 1973, fifteen patients with severe syphilitic aortic regurgitation were treated surgically at the National Heart Hospital. In thirteen the valve was replaced and in two it was repaired. In addition four had replacement of an aneurysmal ascending aorta with a Dacron graft and seven some form of plastic repair to the coronary ostia. Three patients died within 1 month of surgery and a further six during the follow-up period which varied from 1 to 55 months (mean 25-5). The six survivors have been followed-up for an average of 33 months. Factors contributing to this high mortality were analysed and it was found that the mean duration of effort dyspnoea was 22 months in the survivors compared with 48 months in those who had died. Similarly the average duration of nocturnal dyspnoea was 4 months in the survivors compared with a mean of 8 months in those who had died. Only six out of the fifteen patients had angina; this was present in two of the survivors and in four of the fatalities. The pulse pressure, heart size, and haemodynamic findings were similar in the two groups. The prognostic value of an elevated erythocyte sedimentation rate was also examined. It was concluded that preoperative investigations should include aortography, coronary arteriography, an assessment of left ventricular function, and whenever possible myocardial biopsy. These data were interpreted as suggesting that patients should be referred for surgery at an earlier stage in the disease--certainly before the onset of cardiac failure and--and that if this more aggresive attitude was adopted, as it has been in non-syphilitic cases of aortic valve disease, the present high mortality in this group would be reduced.
Br J Vener Dis 1976 Dec
PMID:Syphilitic aortic regurgitation. An appraisal of surgical treatment. 100 17

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.
Kardiologiia 1976 Dec
PMID:[Digitalis poisoning, risk factors and digitalis intolerance]. 101 87


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