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

Patients with acute heart failure or cardiogenic shock following myocardial infarction have a high mortality. The first priority is to salvage any remaining viable myocardium, either by thrombolytic agents or, if necessary, by coronary angioplasty. A mechanical cause for the heart failure or shock needs to be excluded. Thereafter, the optimal therapeutic regimen needs to be chosen on the basis of each patient's hemodynamic profile. Patients can be broadly classified into three groups: (1) patients with a high left ventricular filling pressure (> 18 mm Hg) and a cardiac index < 2.2 L/min/m2 but systolic arterial pressure > 100 mm Hg; (2) patients with a systolic arterial pressure < 90 mm Hg, left ventricular filling pressure > 18 mm Hg, and cardiac index < 2.2 L/min/m2; and (3) patients with an elevated right ventricular filling pressure (> 10 mm Hg) and cardiac index < 2.2 L/min/m2 and a systolic arterial pressure < 100 mm Hg. Patients in the first subset usually require the use of vasodilator therapy and/or dobutamine. The choice of inotropic agent in patients in the second hemodynamic subset depends on the degree of systemic hypotension; dopamine is usually preferred initially because it increases arterial pressure in addition to improving cardiac output. Once the systemic blood pressure has been stabilized, dobutamine can be substituted for superior augmentation of cardiac output and its additional beneficial effects on the left ventricular filling pressure. Norepinephrine may be indicated in cases of severe systemic hypotension. Patients in hemodynamic subset 3, ie, right ventricular infarction, are treated with volume expansion and dobutamine. Use of nonpharmacologic means of circulatory support, eg, intra-aortic balloon pump or left ventricular assist device may also be required in any of these subsets.
 ...
PMID:Pathogenesis and management of acute heart failure and cardiogenic shock: role of inotropic therapy. 142 38

The purpose of this study was to investigate circadian changes in noradrenaline (norepinephrine) levels in patients presenting with congestive heart failure. Eighteen patients were investigated with a group mean age of 66 years, 12 in NYHA class III and 6 in class IV. The cause of the heart failure was ischemia in 7 cases, valvular in 1 case and idiopathic in the other 10 cases. The mean follow-up time of the disease was 3.9 years. Six healthy volunteers were investigated following the same protocol. Blood samples were taken while the patient was lying down over a period of 24 hours, after installing a peripheral venous catheter. The assay was carried out by means of high performance liquid chromatography with electrochemical detection. In the controls, the mean noradrenaline level (norepinephrine) was 220 +/- 62 pg/ml, with daytime peaks. The heart failure patients showed a high mean level (230 +/- 404 pg/ml), with less daytime variability than the controls (92% vs 127%; p < 0.05). The 8 a.m. value was reproducible, and there was close correlation between this value and the mean value for the 24 hours (p < 0.001). Thus, the morning sample provides a good estimation of the levels over the 24 hours.
 ...
PMID:[Nocturnal-diurnal changes of norepinephrine blood levels in patients with chronic cardiac insufficiency. Practical values]. 144 57

Reduced left ventricular function and other factors, such as vascular resistances, redistribution of cardiac output and impaired muscular metabolism, limit exercise performance in chronic heart failure. Thyroid hormones have a positive cardiac inotropic effect, stimulate protein synthesis (particularly at muscular level) and reduce peripheral vascular resistances with consequent increase of cardiac output. Therefore, it is possible that thyroid hormones can improve exercise performance in chronic heart failure. We have administered L-thyroxin (100 mcg/die) for 1 week to 9 patients affected by primary dilated cardiomyopathy. All the patients were euthyroid (T3 = 1.06 +/- 0.1 mcg/ml, T4 = 8.5 +/- 1.9 mcg/dl, TSH = 1.32 +/- 0.7 mU/ml) and in II-III NYHA functional class. Before starting the treatment and at the end of it, we performed the cardiopulmonary exercise test and the echocardiogram. We also evaluated the resting hemodynamic parameters through catheterization and the plasmatic values of thyroid hormones and noradrenaline. At the end of the treatment all patients were euthyroid, despite a significant (p less than 0.05) increase of T4 (10.5 +/- 3.2 mcg/dl) and a decrease of TSH (1.1 +/- 0.1 mU/ml). Mean values of effort parameters changed as follows: peak oxygen consumption from 19.6 +/- 1.6 to 20.6 +/- 1.3 ml/min/kg, tolerance time from 460 +/- 61 to 481 +/- 60 s. These variations were not associated with changes in resting hemodynamic parameters and noradrenaline. Left ventricular ejection fraction, calculated by echocardiography, increased from 26 +/- 6 to 28.9 +/- 8% (p less than 0.05). We conclude that in dilated cardiomyopathy short term treatment with L-thyroxin significantly improves patient's response to cardiopulmonary exercise test.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[The improvement in physical exercise capacity in dilated cardiomyopathy during short-term treatment with L-thyroxine]. 158 20

To evaluate the blood flow distribution during exercise, 51 patients with chronic heart failure underwent ergometer exercise testing measuring cardiac output and leg blood flow. At the given workrate (10 watts and 25 watts) cardiac index (L/min/m2) was significantly lower in NYHA class III patients than class I patients (at 10 watts, 4.08 +/- 1.05 in class I, 4.01 +/- 1.29 in class II and 3.00 +/- 0.89 in class III, p less than 0.05; I vs III), while leg blood flow (L/min/m2) was similar among 3 groups (at 10 watts, 1.19 +/- 0.32, 1.29 +/- 0.25 and 1.16 +/- 0.29, ns). Consequently, residual blood flow (L/min/m2) was significantly lower in class III than class I (at 10 watts, 2.89 +/- .92 and 2.78 +/- 1.27 and 1.84 +/- 0.71, p less than 0.05: I vs III). The results at 25 watts were similar. Serum noradrenaline was significantly higher in class III patients than class I patients at both 10 and 25 watts. We concluded that in severe heart failure, agreater blood flow is distributed to the working leg muscle as compared with less severe heart failure. And such an increased distribution of blood flow to working leg plays a role to compensate an insufficient cardiac output response in patients with severe heart failure.
 ...
PMID:The distribution of the blood flow during exercise in chronic heart failure--compensatory mechanism to the decreased cardiac output. 160 98

Adrenaline, noradrenaline and dopamine excretion was investigated in essential hypertension (n = 20), atherosclerotic heart failure (n = 20, NYHA class II and III), chronic angina (n = 10) and in healthy controls, in four time intervals: between 600-1200, 1200-1800, 1800-2400, 2400-600. Fluorimetric method of Anton and Sayre was employed. In patients with essential hypertension the circadian rhythm of adrenaline, noradrenaline and dopamine excretion was maintained but in all time intervals excretion of dopamine was decreased. In individuals with congestive heart failure due to atherosclerosis and in patients with ischemic heart disease, physiological circadian rhythm of adrenaline and noradrenaline excretion was found to be abolished. This was not the case with dopamine excretion which was undisturbed.
 ...
PMID:[Hypertension, heart failure and angina pectoris. Diurnal rhythm of urinary excretion of catecholamines]. 164 Jun 65

1. Resting energy expenditure has previously been shown to be elevated in the acute phase of heart failure, but the situation in the compensated state of chronic cardiac failure is unclear. Resting energy expenditure was assessed in 14 patients with stable chronic cardiac failure and 14 matched control subjects by using indirect calorimetry. 2. Resting energy expenditure was significantly elevated in the patients with chronic cardiac failure (112.6 +/- 18.1 versus 87.1 +/- 12.2 kJ day-1 kg-1 total body weight, P less than 0.0002; mean +/- SD) as were resting O2 consumption (3.88 +/- 0.64 versus 3.00 +/- 0.43 ml min-1 kg-1, P less than 0.0002), ventilation (164 +/- 40.3 versus 104 +/- 16.2 ml min-1 kg-1, P less than 0.0001) and heart rate (85.8 +/- 16.9 versus 66.6 +/- 6.9 beats/min, P less than 0.001). Both the resting plasma concentration of noradrenaline (4.48 +/- 1.52 versus 2.28 +/- 0.96 nmol/l, P less than 0.0001) and the serum concentration of free fatty acids (0.78 +/- 0.21 versus 0.57 +/- 0.27 mmol/l, P less than 0.03) were greater in the patients with chronic cardiac failure. Analysis of covariance indicated that most of the difference in resting energy expenditure could be accounted for by the elevated ventilation in the patients with chronic cardiac failure. Arm muscle area, an index of wasting, was lower in the patients with chronic cardiac failure (39.1 +/- 13.1 versus 50.5 +/- 9.4 cm2, P less than 0.02) and resting energy expenditure was found to account for some of this difference. 3. We conclude that an elevated basal metabolism occurs in chronic cardiac failure.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Resting energy expenditure in chronic cardiac failure. 164 28

The aim of this prospective study was to investigate both vasoconstricting and vasodilating plasma hormones and plasma factors regulating the circulatory homeostasis in patients with endstage congestive heart failure before and early after orthotopic heart transplantation and to evaluate factors which may influence their regulation. 19 patients with endstage congestive heart failure were analyzed serially before and 3-4 weeks after orthotopic heart transplantation. A significant decrease in plasma concentrations of noradrenaline (457 +/- 202 vs. 204 +/- 88 pg/ml; p less than 0.001), adrenaline (43 +/- 32 vs. 26 +/- 11 pg/ml), atrial natriuretic peptide (341 +/- 218 vs. 139 +/- 64 pg/ml; p less than 0.005), cyclic guanosine monophosphate (13.8 +/- 7.8 vs. 6.6 +/- 2.2 pmol/ml, p less than 0.05) and in plasma renin activity (16.6 +/- 13.0 vs. 2.0 +/- 2.4 ng AI/ml/h; p less than 0.01) was found after transplantation. The data indicate that the marked increase in plasma catecholamine concentrations and renin activity in endstage congestive heart failure is reversible as early as 3-4 weeks after heart transplantation. This is most likely the consequence of normalization of cardiac function. While elevation of atrial natriuretic peptide and cyclic guanosine monophosphate as well as increased vasoconstrictor activity in heart failure appear to be related to impaired ventricular function, the persistent moderate elevation of both vasodilating agents after transplantation may be compensatory to counteract cyclosporin-induced arterial hypertension after heart transplantation.
 ...
PMID:Plasma hormones in patients with chronic heart failure before and early after orthotopic heart transplantation. 166 Oct 55

We investigated serial changes in myocardial norepinephrine content and myocardial adrenergic receptors during the development of cardiomyopathy in Syrian hamsters (Bio 14.6) and their age-matched healthy controls. We also examined phosphatidylinositide hydrolysis after alpha 1-adrenergic stimulation and the effects of alpha 1-blockade. We found that in the prehypertrophic stage, myocardial norepinephrine content and densities of alpha 1- and beta-adrenergic receptors were significantly higher in the cardiomyopathic hamsters than in the controls. However, in the early heart failure stage, beta-receptor density was 28% lower than that of the age-matched controls, although alpha 1-receptor density remained 55% higher. Norepinephrine-stimulated phosphatidylinositide hydrolysis in the cardiomyopathic hamster in the hypertrophic stage was twice that in the controls, indicating that the increase in alpha 1-adrenergic receptors is coupled with the intracellular signal transduction. Furthermore, selective alpha 1-adrenoceptor blockade by bunazosin in the cardiomyopathic hamsters from 70 to 170 days of age reduced myocardial hypertrophy and focal myocardial necrosis. Thus we conclude that increased alpha 1-adrenergic activity plays an important role in progression of cardiac hypertrophy is cardiomyopathic Syrian hamsters.
 ...
PMID:Role of increased alpha 1-adrenergic activity in cardiomyopathic Syrian hamster. 167 40

A case is reported of a 50-year-old man who took a massive overdose of diltiazem (5,400 mg), together with 1,350 mg potassium clorazepate and 390 mg nordazepate, five months after having experienced a myocardial infarction (MI). On admission, systolic blood pressure was 80 mmHg, with an irregular heart rate of 60 b.min-1. There was superficial polypnea (40 c.min-1) with hypoxia (PaO2: 63.5 mmHg). The ECG revealed, besides the MI scar, complete sinus arrest. Endotracheal intubation and mechanical ventilation were rapidly required. The patient then had gastric lavage, and was given activated charcoal. Treatment with 1.5 mg atropine and 2 g intravenous calcium chloride were unable to amend the cardiac dysrhythmia. A continuous isoproterenol infusion restored a sinus rhythm, but this was not maintained because of the risk of side-effects. Cardiovascular collapse was treated with dobutamine (10 micrograms.kg-1.min-1). As the peripheral and pulmonary vascular resistances were greatly diminished (464 dyn.s.cm-5 and 86 dyn.s.cm-5 respectively), alpha and beta mimetics were used: 1 microgram.kg-1.min-1 noradrenaline and 15 micrograms.kg-1.min-1 dobutamine. After 7 h of this treatment, spontaneous sinus rhythm returned abruptly. Noradrenaline and dobutamine were replaced thereafter with adrenaline (0.25 microgram.kg-1.min-1), which was stopped 24 h later. There was a marked respiratory and haemodynamic improvement, the patient leaving the intensive care unit on the fourth day and returning home one week after the overdose. The relationships between cellular calcium movements and the adrenergic system are discussed, as well as the possible mechanism of cardiac failure.
 ...
PMID:[Diltiazem poisoning: hemodynamic aspects]. 167 48

Catecholamines mediate their effects in the heart through beta 1- and beta 2-receptors. Beta 1-receptors mediate the effects of sympathetic nerve stimulation. Alpha-receptors may have a role but, unlike the beta-receptor mediated responses, act without producing any increase in cyclic AMP. Prolonged receptor stimulation results in a reduction in beta-receptor sensitivity. In contrast blockade with a non-agonist agent is associated with an increase in catecholamine sensitivity which may be responsible for the withdrawal reactions that can occur when beta-blocking drugs are rapidly withdrawn in patients with ischaemic heart disease. Experimentally, prolonged noradrenaline infusions result in ventricular hypertrophy. Catecholamines have been implicated in several pathologies. High and rising catecholamine levels are associated with worsening of prognosis in patients with heart failure. These patients show a decreased beta-receptor number and cellular concentration of catecholamines. On the other hand cardiomyopathy is associated with an increased sensitivity to catecholamines. Catecholamines aggravate cardiac damage in ischaemia. Excessively high catecholamine loads cause myocardial damage in otherwise normal hearts, for example in patients with a phaeochromocytoma and those with various forms of cerebral damage such as subarachnoid haemorrhage, cerebrovascular accidents, and head injury.
 ...
PMID:Heart and catecholamines. 168 38


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>