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

Sixty million Americans have hypertension, a major cardiovascular risk factor. Its presence accelerates the atherosclerotic process, producing strokes, heart attacks, heart failure, renal failure, and peripheral vascular disease. This article highlights the historical landmarks in the study of this disease from the first documented measurement of blood pressure in 1733, through the most recent pharmacologic approaches to treatment. In addition, the roles of the kidney and the renin-angiotensin-aldosterone system are examined.
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PMID:Historical reflections on hypertension. 194 83

Increased sympatho-adrenergic activity is a compensatory mechanism in cardiac failure. Accordingly, beta-receptor blockers are generally regarded as contraindicated for use in heart failure. In 1975, Waagstein reported the first successful use of beta-receptor blockers in patients with idiopathic dilated cardiomyopathy. It was shown that the prognosis of patients with dilated cardiomyopathy could be improved by beta-receptor blockade. In this regard, most experience is associated with metoprolol. It should be stressed that the initial, and long-term dosage, as well, was maintained at a very low level (beginning, for example, with 6.25 mg metoprolol daily). An on-going, international, multicenter study is intended to clarify which patients with dilated cardiomyopathy may benefit from treatment with beta-receptor blockers. Additionally, further information is anticipated with respect to the complex mechanism of action. Beside the direct cardiac action with blockade of the cardiotoxic effect of the extremely high levels of plasma catecholamines, induction of an upregulation of the down-regulated beta-1-receptors there is attenuation of the activity of the renin-angiotensin-aldosterone system. Overall, this leads to interruption of the vicious cycle of maladaption associated with chronic heart failure and its attendant unfavorable vasoconstriction and sodium and water retention. This positive aspect of beta-1-receptor blockade in dilated cardiomyopathy carries with its initially and unavoidable negative inotropic effect and thus, in the individual patient, the net effect is difficult to predict. Consequently, the indication must be established on an individual basis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Sympathetic activity in patients with heart failure due to idiopathic dilated cardiomyopathy: modification by beta receptor blockers--a therapeutic approach?]. 197 15

To study the haemodynamic and neurohumoral effects of nisoldipine (2 X 10 mg) vs captopril (3 X 25 mg), 24 patients with heart failure (New York Heart Association class II and III) due to coronary artery disease were treated in a randomized double-blind trial over 3 months. Both drugs were well tolerated. Clinical status was similarly improved in both groups, nisoldipine exerted an additional antiischaemic effect. Nisoldipine lowered the mean arterial pressure and capillary wedge pressure acutely and also after long-term treatment. The increase in cardiac index and stroke volume index, however, which was pronounced after acute administration, was no longer present after 3 months of therapy at rest and was abolished during exercise. Norepinephrine plasma concentration increased after the first dose, plasma renin activity did not change, and aldosterone plasma concentration showed a small insignificant decrease. Urine concentrations of norepinephrine and vasopressin were slightly elevated after the 3-month therapy. After captopril, mean arterial pressure and pulmonary capillary wedge pressure decreased acutely and at follow up. Cardiac index and stroke volume index increased significantly only during exercise at follow-up. Plasma renin activity was significantly elevated and aldosterone plasma concentration only slightly lowered. In contrast to what was seen with nisoldipine, plasma norepinephrine concentration and urine catecholamine and vasopressin concentrations remained unchanged. In conclusion, the pronounced haemodynamic effects seen after the first dose of nisoldipine are mostly abolished after long-term treatment, probably due to neurohumoral counterregulation. The haemodynamic response to captopril is complete only after long-term treatment, without evidence of activation of the neurohumoral systems.
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PMID:Acute and long-term haemodynamic and neurohumoral response to nisoldipine vs captopril in patients with heart failure: a randomized double-blind study. 168 8

Loss of myocardial contractility, reflexly enhanced vasoconstriction, and neuroendocrine excitation are the pathophysiologic hallmarks of low-output heart failure. Drugs that counter both consequences afford considerable therapeutic potential in retarding and perhaps even in staying the consequences of the syndrome. Ibopamine possesses such potential through its unique ability to stimulate both dopaminergic- and beta-adrenoreceptors in the heart and circulatory system. Stimulation of dopaminergic- receptors and beta 2-adrenoreceptors results in vasodilatation in all regional vascular territories. beta 2-Adrenoreceptor agonist activity also affords mild positive inotropic activity in the heart, whereas stimulation of presynaptic dopaminergic- receptors (DA2) attenuates the increased sympathetic neural outflow. The drug also suppresses the renin-angiotensin-aldosterone system in addition to having a direct natriuretic activity. The pharmacodynamic effects of ibopamine, exerted through its metabolite epinine, are translated into measurable therapeutic benefits in patients with chronic heart failure. The increase in peripheral blood flow induced in all regional vascular territories, including the kidneys, is associated with increased cardiac output and stroke volume and reduction in left ventricular pressure work, wall stress, and myocardial oxygen consumption. Plasma norepinephrine, angiotensin, and aldosterone are also reduced, and renal sodium excretion is enhanced. These hemodynamic and neuroendocrine activities, which are not subject to tolerance during sustained administration of the drug, are accompanied by clinically significant improvement in symptoms, exercise tolerance, and the New York Heart Association classification of disability. More important, no proarrhythmic effects have been observed during sustained treatment, and the minimal side effects observed during long-term treatment enhance the safety profile of the drug.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Efficacy of ibopamine in the treatment of heart failure. 197 82

A group of 30 patients with II-III NYHA class cardiac insufficiency was treated with ibopamine in association with other drugs for a 6-month period. The patients were submitted to a 24-h ambulatory ECG Holter monitoring, chest X-ray, Doppler echocardiography in order to calculate total peripheral vascular resistance. Blood levels of aldosterone and renin-angiotensin activity in plasma were also measured, together with norepinephrine excretion. The measurements and recordings were performed in basal conditions before the trial, and were repeated after the first, second, third and sixth month. Laboratory tests were performed at the baseline and after 6 months. The results showed a significant decline in the number of ventricular and supraventricular ectopic beats after treatment. Heart rate did not change. Cardio-thoracic ratio decreased significantly along with peripheral vascular resistance. A very noticeable decline in all three neurohormonal parameters, i.e. norepinephrine excretion, blood level of aldosterone and renin activity in plasma was observed after 1 month's treatment, and this reduction was still present without any attenuation after 6 months. No significant changes were observed in routine laboratory tests.
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PMID:Long-term treatment of congestive heart failure with oral ibopamine. Effects of rhythm disorders and neurohormonal alterations. 198 Jun 33

Ibopamine is a new, orally active dopamine-like drug with inotropic and vasoactive properties. With a predominant action on dopaminergic (DA) and beta-receptors, ibopamine increases cardiac output, reduces peripheral vascular resistances and increases renal blood flow, exerting a lesser effect on preload parameters. This hemodynamic improvement is manifested in subjects with normal myocardium as well as in patients with heart failure in different stages of the syndrome including refractory heart failure, and it is also present after relatively long-term treatment without evidence of pharmacological tolerance. Probably in relation with DA2 activation, ibopamine also modulates the neurohumoral consequences of heart failure with a decrease in plasma renin activity and norepinephrine and aldosterone plasma levels, both acutely and after chronic administration, an effect that can be beneficial in the long-term treatment of patients with chronic congestive heart failure.
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PMID:Hemodynamic and neurohumoral effects of ibopamine in patients with chronic congestive heart failure. 198 Jun 34

The effects of infusing human alpha-calcitonin gene-related peptide were studied in eight patients with congestive heart failure, five normal rabbits and five rabbits with adriamycin-induced cardiomyopathy. In patients with heart failure, calcitonin gene-related peptide caused a dose-dependent increase in cardiac output and decrease in pulmonary and systemic vascular resistance and pulmonary artery pressure. The systemic blood pressure and right atrial and pulmonary wedge pressures decreased only at the highest infusion rate (16 ng/kg per min). Heart rate remained unchanged. Plasma epinephrine increased (p less than 0.05), whereas aldosterone, atrial natriuretic peptide and prolactin concentrations decreased (p less than 0.05). Plasma norepinephrine, renin activity, cortisol and growth hormone concentrations remained unchanged. In both groups of rabbits, the drug decreased blood pressure and increased cardiac output and heart rate. There was a significant increase in renal blood flow (p less than 0.05). The peptide did not affect the contraction amplitude of human and rabbit ventricular myocytes. These findings suggest that calcitonin gene-related peptide is a vasodilator in the rabbit and humans with little direct effect on ventricular myocardium. This peptide may be useful in some forms of heart failure.
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PMID:Cardiovascular and hormonal effects of calcitonin gene-related peptide in congestive heart failure. 198 28

Changes in vasomotor tone in cardiac failure are related to the severity of the cardiac failure. The causative factors include dysfunction of the baroreceptor reflex, abnormal stimulation of the normal physiological regulators of cardio-circulatory function such as the sympathetic nervous and the renin-angiotensin-aldosterone system, and certain local factors characteristic of cardiac failure such as salt and water retention at vascular wall and interstitial level or changes in the metabolism of certain tissues. These changes are variable according to the region perfused and their interaction results in preferential redistribution of blood flow to the coronary and cerebral circulations at the expense of other regions such as the splanchnic and cutaneous vessels. In addition, they play a key role in the adaptive peripheral mechanisms to left ventricular failure and to the modulation of the vascular effects of drug therapy. An improvement in our understanding of these mechanisms and their consequences is important from the physiopathological, prognostic and therapeutic points of view.
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PMID:[Mechanisms and consequences of changes of the vasomotor activity in cardiac insufficiency]. 205 35

We studied, by 48-hour Holter monitoring, 33 patients with chronic stable heart failure (radionuclide ejection fraction less than 35%), complex ventricular arrhythmias and no electrolyte abnormalities, after a period during which they were treated with digoxin and diuretics. Before Holter monitoring blood samples were analyzed for serum concentration of sodium, potassium, magnesium, urea, creatinine, digoxin, aldosterone and for plasmatic renin activity in addition to urinary aldosterone and catecholamines determination. After these investigations in 23 patients, 5-20 mg of enalapril were progressively added to the conventional therapy, while 10 patients continued the previous therapy. After 8 weeks 30 patients were subjected to a second 48-hour Holter monitoring and to the same biochemical and hormonal tests. One patient died and 2 were lost to follow up. Only the enalapril group showed a significant decrease in the number of premature ventricular complexes (PVC) (p less than 0.01), and the frequency of couplets and episodes of ventricular tachycardia (VT) declined significantly (P less than 0.01). In the two groups there were no significant changes in digoxin, sodium, or magnesium, while potassium concentration increased in both groups (p less than 0.01). In the enalapril group heart rate and systolic and diastolic pressure declined significantly (p less than 0.01), and New York Heart Association class (NYHA) improved (p less than 0.001). In the other group there were no significant changes in these parameters. Enalapril caused a significant increase in the plasmatic renin activity (p less than 0.01) and a significant fall of plasma and urinary aldosterone (p less than 0.01; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reduction of complex ventricular arrhythmias after enalapril treatment in patients with advanced stable heart failure. 205 78

The renin-angiotensin aldosterone system does appear to have a central role in the haemodynamic and metabolic response to declining ventricular function. Human heart failure usually occurs in the setting of preceding disease, which may itself influence the underlying activity of the system. Studies of the renin-angiotensin system after myocardial infarction are in agreement with animal models, that transient activation of the renin-angiotensin system occurs. This may be sustained if the cardiac insult is severe and especially if diuretic therapy is initiated. In those patients in whom the insult is less severe, activity of the renin-angiotensin system wanes. The finding that patients with stable untreated heart failure do not have markedly activated renin-angiotensin systems is not surprising, but correction of the plasma and extracellular volume (for instance with a diuretic) will result in reappearance of activation of these systems. Since the introduction of angiotensin-converting enzyme inhibitors, several new peptides have been discovered (atrial natriuretic peptide, endothelin etc.) that have important effects on cardiovascular function. New potential therapeutic agents with actions on neuroendocrine systems, such as the atrial peptidase inhibitors, angiotensin-II receptor antagonists and renin inhibitors, are on the horizon. Such exciting new discoveries will give as much insight into the pathophysiology of heart failure as the angiotensin-converting enzyme inhibitors have done.
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PMID:The renin-angiotensin system in heart failure. 206 55


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