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

Using non-invasive radionuclide techniques, we studied the arterial and venous effects of 0.1 mg/kg oral felodipine in 12 men with heart failure due to ischaemic heart disease aged 37-72 y. All were in New York Heart Association Class II or III, required frusemide 40-120 mg daily and were clinically stable. Felodipine produced significant falls in blood pressure (-19%) and systemic vascular resistance (-39%) with increases in cardiac index (+34%), heart rate (+12%) and left ventricular ejection fraction (from 0.25 to 0.32). Peripheral venous volume fell by 10.6% after felodipine indicating venoconstriction rather than venodilatation and may be caused by an acute sympathetic reflex associated with the increase in heart rate. Our results confirm that felodipine is an arterial vasodilator. The previously observed changes in cardiac filling pressures may simply represent improved ventricular function as a consequence of reduced afterload, not venodilatation.
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PMID:Central and peripheral haemodynamic responses to felodipine in congestive heart failure. 174 53

Felodipine is a potent arteriolar vasodilator. Its possible myocardial effects were studied by placing dogs anaesthetized with chloralose on cardiopulmonary bypass. A balloon was then inserted into the left ventricular cavity with a vent alongside it. Isovolumic contractions (developed pressure or maximal rate of rise of pressure) were studied as the intraventricular balloon was inflated to various levels. Total coronary venous return was collected to measure coronary blood flow and felodipine concentrations. In seven vagotomized and beta-blocked preparations, a small positive inotropic effect was found [32 +/- 11 (SEM)%, p less than 0.05]; the maximum effect was reached at arterial plasma felodipine concentrations of between 7 and 20 nM and was accompanied by appreciable coronary vasodilatation. In five dogs, infusion of the solvent vehicle (5% polyethylene glycol) alone had no effect. In three more dogs, an infusion of nitroprusside caused coronary vasodilatation, but no positive inotropic effect. The results show that at low concentrations, felodipine has a positive inotropic effect in vivo. These findings suggest that the properties of myocardial calcium agonist and vascular smooth muscle antagonist properties may coexist in the same dihydropyridine molecule. The favorable effects of this drug in the treatment of heart failure can be explained not only by reduction of peripheral resistance, but also by a moderate positive inotropic effect.
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PMID:The positive inotropic effect of felodipine in isovolumically beating dog heart. 244 2

The efficacy of felodipine, a vasodilating calcium antagonist, was analysed in 23 patients with congestive heart failure, New York Heart Association class III, during an 8-week, double-blind, randomized, placebo-controlled, parallel study. After felodipine, exercise duration increased significantly without changes in oxygen consumption. Heart rate, arterial pressures and rate pressure product decreased at similar submaximal exercise levels. Invasive haemodynamics before and after 8 weeks of therapy revealed arterial vasodilation without reflex tachycardia and no significant reduction in right atrial, pulmonary and capillary wedge pressures. Subjective symptom scores improved and side-effects were minor. Fluid retention, as assessed by body weight and ankle circumference did not occur. Felodipine has a beneficial effect in patients with moderately severe heart failure. Further research is necessary to demonstrate its long-term efficacy and safety.
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PMID:Efficacy of felodipine in congestive heart failure. 265 66

The hemodynamic effects of increasing dosages of felodipine, a new calcium antagonist with selective vasodilator properties, were studied in 13 patients with chronic cardiac failure. A Swan-Ganz thermodilution catheter was positioned in the pulmonary artery and hemodynamic parameters were monitored from 9 am to 6 pm for five days. On the first and the fifth day patients received placebo (P) and on the second, third, and fourth day patients received felodipine 5, 10, and 20 mg, respectively. Symptom-limited exercise tests with a bicycle ergometer were performed on both days of P and on the fourth day. A marked reduction of systemic vascular resistance (SVR) and a significant increase of cardiac index without increments of heart rate (HR) were observed after felodipine at rest. A dose response effect could be demonstrated. During exercise a significant increment of cardiac index and decrease of pulmonary wedge pressure was observed after felodipine. Felodipine showed a potent vasodilator action on systemic circulation with significant changes on both stroke volume and filling pressures at rest and during exercise without side effects.
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PMID:Hemodynamic effects of felodipine in congestive heart failure. 315 19

1. The efficacy of felodipine a new calcium channel blocker with selective vasodilator activity in the management of severe low output cardiac failure, secondary to coronary heart disease, was determined in 10 patients. 2. Haemodynamic measurements were made at rest and during dynamic exercise and left ventricular function was assessed by radionuclide ventriculography. 3. Significant increases in cardiac index, stroke volume index and ejection fraction were found particularly during exercise, both acutely and following 4 weeks administration of felodipine therapy. 4. Felodipine could well have a significant role in the long term management of the patient with chronic cardiac failure.
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PMID:Sustained haemodynamic effects of felodipine in patients with chronic cardiac failure. 320 40

Previous open studies have suggested that felodipine, a selective calcium antagonist and vasodilator, may be useful in the treatment of heart failure. A double blind placebo controlled crossover trial was therefore conducted to investigate the clinical and haemodynamic effects of felodipine in 15 patients with chronic ischaemic heart failure in New York Heart Association symptom class III. Felodipine significantly increased resting and exercise (25W bicycle ergometry) cardiac output without producing concomitant changes in resting or exercise heart rate or right and left ventricular filling pressures. Felodipine did not significantly improve symptom scores or exercise capacity in the group as a whole. It also resulted in significant fluid retention as shown by a rise in ankle circumference, body weight, and a fall in haematocrit. Further research is required to elucidate the mechanism that is responsible for the discrepancy between the haemodynamic and clinical effects of felodipine in patients with moderately severe heart failure.
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PMID:Felodipine in patients with chronic heart failure: discrepant haemodynamic and clinical effects. 330 72

The systemic and coronary haemodynamic effects of felodipine were evaluated at rest and during stress induced atrial pacing in fourteen patients with chronic cardiac failure, secondary to coronary heart disease. Felodipine was an effective arteriolar vasodilator producing increases in cardiac index from 2.6 +/- 0.1 to 3.5 +/- 0.2 l min-1 m-2 (P less than 0.001) and stroke volume 35.3 +/- 2.7 to 41.4 +/- 2.4 ml beat-1 m-2 (P less than 0.002). Coronary venous flow also increased significantly (126 +/- 8 to 168 +/- 13 ml min-1) (P less than 0.005) and this did not appear to be accompanied by an increase in myocardial oxygen usage, as myocardial oxygen consumption was essentially unchanged. When the myocardium was stressed by atrial pacing the increase in cardiac output and stroke volume was maintained--25% and 23%, respectively (P less than 0.01). These results suggest that felodipine may well have a significant role in the management of patients with congestive cardiac failure.
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PMID:Felodipine in ventricular dysfunction. 395 23

Felodipine is a new calcium antagonist with a high degree of vascular selectivity. Its potential role in the treatment of congestive heart failure was examined in short and long term oral studies. Short term felodipine 5 to 15 mg in 11 patients increased (p less than 0.001) cardiac index (from 2.1 +/- 0.1 to 3.3 +/- 0.2 L/min/m2), and reduced systemic resistance (from 26 +/- 2 to 12 +/- 2 units) and left ventricular end-diastolic pressure (from 26 +/- 2 to 13 +/- 2mm Hg) without affecting heart rate. Left ventricular max dp/dt did not change, but max dp/dt/p increased from 19 +/- 1 to 24 +/- 1 sec-1 (p less than 0.001). Left ventricular unloading was reflected by a shift in the end-systolic pressure-dimension relationship downwards and to the left. Myocardial oxygen supply to demand ratio improved significantly; coronary flow increased from 141 +/- 11 to 176 +/- 15 ml/min and myocardial oxygen consumption fell from 18 +/- 2 to 14 +/- 1 ml/min (p less than 0.05). Long term therapy with felodipine 30 mg daily in 10 patients improved treadmill exercise tolerance after 4 weeks by 24% (p less than 0.001). Stroke index at submaximal exercise increased from 37 +/- 3 to 47 +/- 2 ml/beat/m2 (p less than 0.001). Pulmonary capillary wedge pressure fell significantly (22 +/- 5 to 10 +/- 3mm Hg), as did arteriovenous oxygen difference (12.7 +/- 0.9 to 9.7 +/- 0.6 vols/100ml). Importantly, these beneficial effects with felodipine were sustained during 4 weeks' therapy without evidence of tachyphylaxis. These data indicate that the selective vasodilator properties of felodipine may extend the clinical application of calcium antagonists to include the management of heart failure.
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PMID:Studies with felodipine in congestive heart failure. 398 53

The mechanisms underlying the abnormal responses to orthostatic stress in congestive heart failure are ill defined and little is known about the effects of specific therapy. In the present study intravascular pressures and plasma noradrenaline levels were measured in nine patients with heart failure subjected to 45 degrees and 90 degrees upright tilt. Studies were repeated during 4 weeks of vasodilator therapy with felodipine and again after felodipine withdrawal. Before the introduction of vasodilator therapy, tilt did not activate orthostatic reflexes despite significant reductions in left ventricular filling pressure and cardiac output. Thus, plasma noradrenaline, heart rate and systemic vascular resistance were unaffected and blood pressure fell. Felodipine resulted in a rapid and sustained improvement in left ventricular function but restoration of orthostatic reflexes was delayed and could be detected only after 48 h therapy. At this time, and during the subsequent 4 weeks, tilt-induced reductions in ventricular filling and cardiac output produced a normal rise in plasma noradrenaline and heart rate. A postural drop in blood pressure, however, was not averted because the direct action of felodipine on vascular smooth muscle prevented adrenergically-mediated increments in systemic vascular resistance. Felodipine withdrawal led to a prompt deterioration in left ventricular function. Orthostatic reflexes, however, were still intact 48 h later when tilt elicited a completely normal pattern of responses. These observations confirm that the abnormal responses to orthostatic stress in congestive heart failure are due principally to impairment of autonomic control mechanisms and are not related to the absence of venous pooling. Importantly the autonomic dysfunction is reversible with felodipine therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Restoration of normal reflex responses to orthostatic stress during felodipine therapy in congestive heart failure. 648 31

Calcium channel blockers are used extensively in the treatment of the three major anginal syndromes. In the treatment of Prinzmetal's angina, their antivasospastic properties account for their therapeutic effectiveness. Calcium channel blockers are drugs of first choice in this syndrome. In chronic stable angina, calcium channel blockers may be used as monotherapy or in combination with beta-blockers and/or nitrates. In patients with unstable angina, reduction in the incidence of ischemic episodes produced by calcium channel blockers is well documented. Recent data suggest that calcium channel blockers should generally be used in combination with beta-blockers, nitrates and antithrombotic agents. Patients with ischemic heart disease often exhibit reduced ventricular function. All of the first generation calcium channel blockers exacerbate symptoms in patients with established heart failure and may precipitate heart failure, particularly when combined with beta-blockers. Second generation vascular-selective dihydropyridines have been introduced recently. Vascular selectivity determines the drug's degree of negative inotropic effect. Felodipine is one of the most vascular selective of the available dihydropyridines and has no negative inotropic effects at clinically administered doses. In a long term study, felodipine, 20 mg/day, abolished symptoms and chronic ischemic episodes in 81% of treated subjects with Prinzmetal's angina. In patients with stable angina, felodipine has been found to be effective either as monotherapy or in combination with beta-blockers. In patients with known or suspected ventricular dysfunction, vascular-selective dihydropyridines such as felodipine offer advantages over the nonselective calcium channel blockers, particularly in patients receiving beta-blockers.
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PMID:The evolving role of calcium channel blockers in the treatment of angina pectoris: focus on felodipine. 772 49


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