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M Metra

Publications and source records attributed to M Metra.

At least 55 records · Page 3Linked to original sources
PubMed1992

Combined invasive and noninvasive study of left ventricular systolic and diastolic function following acute administration of cicloprolol to subjects with normal cardiac function.

Cicloprolol is a new beta-blocking agent with high selectivity for beta 1 receptors and high intrinsic sympathomimetic activity. We studied the acute hemodynamic effects of cicloprolol in nine subjects with no evidence of left ventricular dysfunction who underwent cardiac catheterization for the evaluation of chest pain. All patients had normal coronary angiography and left ventriculography. Left ventricular pressure was determined throughout the cardiac cycle using a Millar 8Fr Minotip catheter; an echocardiogram, phonocardiogram, and ECG were simultaneously recorded to obtain left ventricular pressure-diameter loops. All the measurements were repeated before and after the intravenous administration of cicloprolol. Cicloprolol was administered at increasing doses of 0.05, 0.10, and 0.25 mg/kg until a cardiac output increase of at least 15% over basal values was achieved. A decrease of mean arterial pressure or cardiac output after cicloprolol was not observed in any patient. Cicloprolol administration significantly increased cardiac output (24%), stroke volume (22%), and peak positive dP/dt (25%); no significant changes in heart rate, systemic blood pressure, right atrial pressure, or pulmonary artery pressures were observed. No significant change in the echocardiographic parameters occurred. Among the indices of left ventricular diastolic function, the time constant of isovolumetric relaxation was significantly decreased (-43%) after cicloprolol; moreover, the left ventricular pressure-diameter loop in the protodiastolic phase was shifted to the left following cicloprolol infusion. This study confirms that in subjects with normal left ventricular function cicloprolol can improve resting left ventricular systolic function, and it shows that this action can also be attended by a more rapid isovolumetric relaxation, similar to what has been observed with other sympathomimetic amines.

Adrenergic beta-Agonists↗
PubMed1992

Assessment of myocardial perfusion with thallium-201 scintigraphy in exercise-induced left bundle branch block: diagnostic value and clinical significance.

Myocardial perfusion scintigraphy with thallium-201 was performed in 33 subjects (mean age 45 years, range 28-61) with exercise-induced, rate-dependent left bundle branch block (LBBB) in order to assess both the value of Thallium-201 myocardial imaging for the diagnosis of coronary artery disease (CAD) and the pathogenesis (ischaemic or not) of the conduction defect. Of the 33 patients evaluated, 16 had chest pain suggestive of CAD and 17 were asymptomatic. None had a history of prior myocardial infarction or clinical and echocardiographic signs of heart disease. LBBB appeared at a heart rate ranging from 70 to 160 b.min-1. Eighteen patients showed repolarization abnormalities (ST segment depression with deep inverted T waves) compatible with ischaemia, after QRS normalization. Thallium-201 myocardial uptake was normal in 12 subjects; in the remaining 21, reversible Thallium-201 defects were demonstrated in the septum (18 patients), septum and apex (2), and septum and infero-apical wall (1). No patient had irreversible defects and all had normal coronary angiography, with negative ergonovine tests for coronary artery spasm. The patients were followed up for a mean of 43 months (range 16-80). One patient died from sudden death, but no cardiac event occurred in the other patients. In conclusion, exercise Thallium-201 myocardial scintigraphy showed a high prevalence (64%) of reversible perfusion defects in a group of patients with exercise-induced LBBB without any evidence of CAD at angiography or coronary spasm at ergonovine test. Moreover, follow-up showed a relatively low rate of major cardiac events.

Adult↗
PubMed1992

[The antianginal effects of a new delayed-release formulation of diltiazem in patients with stable angina pectoris: its evaluation by the ergometry test and dynamic electrocardiogram].

The antianginal efficacy and duration of action of slow-release (SR) diltiazem were evaluated in 12 patients with stable angina. Patients underwent maximal symptom limited bicycle exercise testing and 24-hour Holter monitoring at the end of 1-week placebo run-in phase and after 1-month therapy with either placebo or SR-diltiazem (120 mgs bid) using a placebo controlled, double-blind, randomized cross-over trial. No concomitant antianginal therapy, except sublingual nitroglycerin, was allowed during the trial. Exercise testing was performed 3 and 12 hours after drug administration. Blood samples were obtained for the determination of diltiazem plasma concentrations. After diltiazem administration, peak exercise duration increased significantly in comparison both with placebo and the run-in phase: from 292 +/- 48 to 378 +/- 113 s at 3 hours and from 286 +/- 59 to 366 +/- 109 s 12 hours after drug administration. Similarly, ST depression time increased from 240 +/- 59 to 374 +/- 123 s at 3 hours and from 231 +/- 57 to 332 +/- 123 s 12 hours after diltiazem. No significant changes of heart rate, blood pressure and double product were detected. Diltiazem plasma concentrations averaged, respectively, 175 +/- 86 pg/ml and 109 +/- 43 pg/ml 3 and 12 hours after its administration. No correlation was found between plasma concentrations and antianginal effects of diltiazem. At 24 hours Holter monitoring, SR-diltiazem induced a significant decrease of mean heart rate with a reduction in the number and duration of ischemic episodes.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1991

Improvement in exercise capacity after correction of anemia in patients with end-stage renal failure.

Changes in exercise tolerance occurring after correction of anemia with recombinant human erythropoietin in a group of patients with end-stage renal failure were evaluated. Ten patients, aged 29 +/- 11 years, on chronic hemodialysis treatment, with no associated diseases, were evaluated by cardiopulmonary bicycle exercise testing and M-mode, 2-dimensional and pulsed doppler echocardiography before and after anemia correction. After 1 and 3 months of therapy, hemoglobin plasma levels increased from 5.9 +/- 1.2 to 7.7 +/- 1.3 and 9.9 +/- 1.4 g/dl, with a concomitant increase in peak oxygen consumption (VO2) from 21.4 +/- 4.3 to 24.4 +/- 4.3 and 26.6 +/- 4.6 ml/kg/min and of VO2 at the ventilatory threshold from 15.0 +/- 3.7 to 17.3 +/- 3.7 and 16.8 +/- 3.4 ml/kg/min. After 3 months of therapy, systolic blood pressure significantly decreased both at peak exercise (159 +/- 35 to 134 +/- 22 mm Hg) and ventilatory threshold (140 +/- 27 to 123 +/- 19 mm Hg), whereas cardiac index at rest decreased from 3.3 +/- 0.7 to 2.8 +/- 0.5 liters/min/m2 and heart rate from 77 +/- 12 to 70 +/- 10 beats/min. However, no significant relation was found between hemoglobin plasma levels and peak VO2, whereas a significant relation was found between hemoglobin concentration and cardiac index at rest.

Adult↗
PubMed1991

[Effects of amrinone on isolated heart preparations: comparative study with other inotropic agents].

We compared the effects of the phosphodiesterase inhibitor amrinone, the beta-adrenergic partial agonist xamoterol and the digitalis glycoside, ouabain, on isolated rabbit hearts perfused with the Langendorff technique. Heart rate, left ventricular pressure, as an index of myocardial contractility and coronary perfusion pressure, as an index of coronary resistances, were assessed before and after each drug. Perfusion with concentrations of each agent varying from 10(-9) to 10(-4) M induced a dose-dependent increase of left ventricular systolic pressure averaging 32.5 +/- 1.5% after amrinone (10(-5) M), 46.2 +/- 0.5% after xamoterol (10(-5) M) and 19.0 +/- 2.1% after ouabain (10(-4) M). Among the 3 agents, only amrinone was able to reduce basal coronary perfusion pressure (18.4 +/- 1.2% at the dose of 10(-5) M) and inhibit vasopressin-induced coronary spasm (86.8 +/- 2.5% inhibition at 10(-5) M); no significant change of coronary perfusion pressure was noted with either xamoterol or ouabain. Heart rate was not significantly modified by amrinone whereas, at the doses of 10(-5)-10(-4) M, xamoterol increased it by 21.6 +/- 0.7% and ouabain reduced it by 12.3 +/- 1.1%. Our results show that amrinone, in comparison with digitalis glycosides and beta-adrenergic agonists, presents the unique property to increase myocardial contractility with concomitant coronary vasodilation without significant changes of heart rate. Ouabain has a less potent positive inotropic activity and a slight negative chronotropic action, whereas xamoterol inotropic effect is accompanied by an increase of heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗
PubMed1991

[Hemodynamic and clinical effects and treatment tolerance with low-dose iv amrinone in patients with refractory heart failure: a multicenter study. The Group for Research on Amrinone in the Treatment of Refractory Heart Failure].

We report the results of a multicenter study performed on 70 patients with severe congestive heart failure of different etiology (ischemic, idiopathic, alcoholic, valvular and secondary to antiblastic drugs) to evaluate the clinical and hemodynamic effects and tolerability of low dose amrinone iv (0.75 mg bolus followed by a continuous 48-hour infusion at the dose of 5-10 mcg/kg/min). Forty-one patients underwent invasive hemodynamic monitoring with right heart Swan-Ganz catheterization. Heart rate (HR), systolic (SBP) and diastolic blood pressure (DBP), mean arterial pressure (MAP), cardiac index (CI), stroke volume index (SVI), stroke work index (SWI), right atrial pressure (RAP), pulmonary wedge pressure (PWP), mean arterial pulmonary pressure (PAP), systemic vascular resistance (SVR), pulmonary vascular resistance (PVR) and total pulmonary resistance (TPR) were evaluated before and after 1, 4, 6, 24 and 48 hours of amrinone infusion and 2 and 4 hours after amrinone withdrawal. Clinical parameters (dyspnea, orthopnea, pulmonary congestion) were quantitated using a score; diuresis was assessed hourly; hematochemical parameters were evaluated before and 48 hours after amrinone infusion. HR and MAP were not significantly changed; CI, SVI and SWI presented, respectively, a significant 31.6, 55.1 and 72% increment, which peaked 48 hours after amrinone infusion. Concomitantly RAP, PAP, PWP, SVR, PVR and TPR were significantly reduced to 36.6, 22, 23.6, 9.4, 39.2 and 37.7% of the basal values, respectively. Two and 4 hours after amrinone withdrawal, hemodynamic changes similar to those observed acutely, were still present. Diuresis increased from 58.25 ml/hr to 113.18 ml/hr after 24 hours (+95%) and to 88.9 ml/hr (+53%) after 48 hours.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

[The acute, chronic continuous after treatment and chronic intermittent with a variable therapeutic window (4 and 6 hours) hemodynamic effects induced with transdermal nitroglycerin in patients with congestive heart failure].

The aim of this study was to assess the minimum time interval necessary to avoid the development of tolerance during nitroglycerin patch application. We studied 24 patients, aged 23 to 73 years, with ischemic or idiopathic dilated cardiomyopathy (LV EF less than 0.40) and stable clinical conditions during 30 days before the study. All patients had significant reduction of systemic and pulmonary arterial pressure after sublingual nitroglycerin. After the hemodynamic assessment of the response to the first dose of the nitroglycerin patch, the patients were randomized to 1 of 3 chronic treatment groups: continuous patch application (Group A), intermittent application with 4 hours intervals (Group B), intermittent application with 6 hours intervals (Group C). All patients were studied by right heart Swan-Ganz catheterization; the hemodynamic response to a 10 mg multilayer matrix nitroglycerin patch was assessed before and every hour, in the next 4 hours, after both the first application of the patch and after 1 month of therapy; after chronic intermittent therapy, hemodynamic parameters were also measured 24 hours after drug withdrawal. Hemodynamic parameters were significantly changed after the first nitroglycerin patch application: particularly, mean systemic arterial (MAP), right atrial (RAP) and pulmonary wedge pressures (PWP) declined from 96 +/- 10, 8.9 +/- 1.8 and 20.1 +/- 5 to 81 +/- 6, 4.7 +/- 1.5 and 12.2 +/- 3 mmHg (-15.6, -47.2 and -59.3%, respectively); systemic vascular resistance (SVR) and heart rate (HR) were reduced from 1645 +/- 121 to 1288 +/- 89 dyne.s.cm-5 and from 85 +/- 7 to 81 +/- 7 b/min; lastly, cardiac index (CI), stroke volume (SVI) and stroke work index (SWI) increased from 2.3 +/- 0.3, 28.2 +/- 5 and 28.7 +/- 9 to 2.7 +/- 0.3 l/min/m2, 33.3 +/- 5 ml/min/m2 and 31.5 +/- 8 g.m/m2 (+17.4, 18.1 and 9.7%). After 1 month of either continuous or intermittent patch application with 4 hours intervals, hemodynamic parameters returned to control values with no significant change after patch application. In contrast, after intermittent patch application with 6 hours intervals, a persistent hemodynamic response to nitroglycerin patches was still present.(ABSTRACT TRUNCATED AT 400 WORDS)

Administration, Cutaneous↗
PubMed1990

Assessment of peak oxygen consumption, lactate and ventilatory thresholds and correlation with resting and exercise hemodynamic data in chronic congestive heart failure.

To determine the clinical value of respiratory gas analysis during exercise, oxygen consumption (VO2) at peak exercise and at lactate and ventilatory threshold was assessed in 34 patients with chronic heart failure who underwent maximal exercise testing with expiratory gas monitoring and serial determinations of mixed venous lactate and hemodynamics by Swan-Ganz catheterization. A lactate threshold, defined as the point of abrupt increment of blood lactate, could be identified in every patient; the ventilatory threshold, detected on the basis of the respiratory changes, was found in 26 patients (77%). Lactate and ventilatory thresholds were significantly related to each other (r = 0.94; p less than 0.001) and to peak VO2 (r = 0.89; p less than 0.001 in both). Among the resting hemodynamic measurements, peak VO2 was significantly related only to total pulmonary resistances (r = -0.35). Among the parameters at maximal exercise, it was positively related to cardiac index, stroke work, stroke volume index and mean arterial pressure (r = 0.89, 0.74, 0.74 and 0.56, respectively) and inversely related to systemic vascular and total pulmonary resistances (r = -0.74 and -0.63). Using multivariate stepwise regression analysis only maximal cardiac index and, to a lesser degree, total pulmonary resistance were related to peak VO2. Similar correlations were found between the hemodynamics and the lactate and ventilatory threshold. Thus, peak VO2, lactate and ventilatory thresholds can be detected in most patients with chronic heart failure. These parameters are highly correlated to each other and bear similar relations to the hemodynamic response to exercise. The cardiac index is the main central hemodynamic determinant of exercise capacity.

Adult↗
PubMed1990

[Comparative effects of atrial and ventricular stimulation on morbidity and mortality in patients with sinus node disease].

In patients with sinus node disease (SND) the VVI pacing seems an inappropriate mode of cardiac stimulation because of its potential hemodynamic and arrhythmic adverse effects. The AAI-DDD pacing, preferred because of a lower morbidity, might also determine higher survival. We examined retrospectively 2 groups of patients with SND respectively stimulated with VVI pacing (Group I:57 patients) and AAI (Group II:53 patients). The mean follow-up was 43 months for Group I and 50 for Group II: 10 (17.5%) patients in VVI group and 5 (9.4%) in AAI group died. During the follow-up in the VVI group 3 patients developed congestive heart failure and 10 chronic atrial fibrillation whereas 1 case of heart failure and 2 of atrial fibrillation have been recorded in AAI group. Moreover, 4 patients had embolic complications in Group I; 5 (9.4%) patients with VVI pacing were converted into sequential pacing owing to occurrence of II degree heart block. The statistical analysis was performed by chi 2 test for the comparison among the proportions of events (atrial fibrillation, congestive heart failure, embolic accidents) in the 2 groups: a significative higher morbidity (p less than 0.01) was recorded in VVI group. Survival also is higher in AAI patients but the survival rate difference, calculated with Mantel-Cox method, is not statistically significant. The findings of this study show that in SND the superiority of AAI pacing over VVI is statistically significant as regards morbidity and we have also noticed an evident but not statistically significant superiority as regards mortality.

Aged↗
PubMed1990

[Thrombolytic therapy in the treatment of thromboembolism of the right cardiac cavity during pulmonary embolism: our experience with rt-PA and review of the literature].

In 4 consecutive patients admitted for multiple pulmonary embolism 2-dimensional echocardiography showed large right atrial migrant thromboemboli in transit, floating and prolapsing into the right ventricle in diastole. This pattern was always associated with the echocardiographic signs of pulmonary hypertension. All the patients were treated with intravenous infusion of 100 mg of rt-PA in 3 hours. rt-PA determined the dissolution and disappearance of the right atrial thromboemboli (it took 4 hours in 2 patients and 5 hours in the remaining 2), and the concomitant disappearance of the echocardiographic signs of pulmonary hypertension. During and after the rt-PA therapy there was no evidence of further pulmonary embolism. The fibrinolytic treatment for right atrial thromboemboli during multiple pulmonary embolism is a promising alternative to right atrial thrombectomy: our results indicate that rt-PA acts rapidly and is effective and safe; if these results will be confirmed in a larger group of patients, rt-PA could become the first-choice therapy of right atrial thromboembolus.

Aged↗
PubMed1989

Dopamine receptors in the stellate ganglion of the dog.

Effects of fenoldopam, a selective DA1 dopamine receptor agonist, and dipropyl dopamine and propylphenethyl dopamine, preferential DA2 dopamine receptor agonists, on ganglion transmission were studied in pentobarbital-anesthetized, open-chest dogs. Tachycardia induced by electrical stimulation (supramaximal voltage, 0.5 ms duration, 1-2 Hz) of the preganglionic cardio-accelerator nerves was monitored as a measure of ganglionic transmission. Drugs were injected into the costocervical artery (i.a.) close to the arterial supply of the ganglion. Doses required to produce 30-40% inhibition of ganglionic transmission by the i.a. route were 2-8 micrograms for dipropyl dopamine, 4-16 micrograms for propylphenethyl dopamine, and 100 micrograms for fenoldopam. At these doses none of the agonists affected tachycardia induced by electrical stimulation of the postganglionic nerve. Domperidone (5 micrograms/kg i.v.), a selective DA2 dopamine receptor antagonist, markedly antagonized the effects of dipropyl dopamine and propylphenethyl dopamine, but had only minor (and statistically insignificant) effects on the inhibitory effect of fenoldopam. SCH 23390 (5 micrograms/kg i.v.), a selective and potent DA1 antagonist, failed to modify the effects of any of the agonists. In a separate series, infusion of fenoldopam, 20 micrograms/kg per min i.v. for 5-7 min, facilitated postganglionic nerve stimulation and blocked the inhibitory effect of UK 14,304, an alpha 2-adrenoceptor agonist, on the postganglionic nerve. These results confirm and support the presence of DA2 but do not support the presence of the prototypal DA1 dopamine receptor in the mammalian ganglia. Furthermore, the alpha 2-adrenoceptor blocking property of fenoldopam points to the complication of using i.v. administration for studying its ganglionic actions while monitoring the target tissue effects in response to preganglionic nerve stimulation.

Animals↗
PubMed1989

Diagnosis of acute myocardial infarction by indium-111 antimyosin antibodies and correlation with the traditional techniques for the evaluation of extent and localization.

This clinical study evaluated the accuracy of planar myocardial scintigraphy with antimyosin monoclonal antibodies radiolabeled with indium-111 (AMA-Fab) in the detection and localization of acute myocardial infarction (AMI). Fifty-seven patients admitted for suspected AMI were studied; 17 patients underwent thrombolytic therapy with intravenous streptokinase and 11 had clinical signs of reperfusion; 9 had had a previous myocardial infarction. Fifty of 57 patients were discharged from the coronary care unit with a confirmed diagnosis of AMI. The AMA-Fab study results were positive for AMI in 49 patients (98%) and negative in 1 (2%). Among the 7 patients without AMI, 5 had unstable angina, 1 had Prinzmetal's variant angina and 1 had acute pancreatitis. AMA-Fab results were negative in 6 of 7 patients (85%) and positive in 1 (15%). Therefore, the sensitivity and specificity of AMA-Fab scintigraphy were 0.98 and 0.85, respectively. To assess accuracy in defining the extent and location of AMI, AMA-Fab results were compared with those of the electrocardiogram, echocardiogram, technetium-99m pyrophosphate myocardial scintigraphy and coronary angiography and left ventriculography. AMA-Fab scintigraphy showed a good concordance with the traditional techniques in the topographic definition of the infarcted regions. No uptake of AMA-Fab was seen in the regions of previous old infarcts. Ten healthy volunteers also underwent AMA-Fab scintigraphy. No evidence of myocardial tracer uptake was noted in them. No adverse reactions or side effects were noted after injection of AMA-Fab in any patient. It is concluded that planar myocardial scintigraphy with AMA-Fab is a reliable method for AMI detection and location.

Adult↗
PubMed1989

Survival rates after pacemaker implantation: a study of patients paced for sick sinus syndrome and atrioventricular block.

It is still a matter of controversy as to whether the patients paced for atrioventricular block (AVB) have different prognosis and survival rates than those paced for Sick Sinus Syndrome (SSS). We have compared the survival rates of 962 AVB patients (group A) with that of 283 SSS patients (group B) who underwent pacemaker implantation during the period January 1968 to December 1986. The survival rate graphs of the examined groups were calculated using the actuarial method and the differences in the survival rates between the groups were evaluated using the Logrank test. Our results show that SSS patients have a higher survival rate than AV block with a difference on the rate of survival between the two groups reaching the borderline of statistical significance. Multivariate discriminant analysis was then used to assess that of the parameters (i.e., age at the time of implantation, sex, electrophysiological indication to pacing, etiology or pacing mode) could have had the main influence upon mortality and the different pattern of the survival rate graph within the two groups of patients. Our data show that survival is mostly related to age, pacing mode and, although more slightly, to underlying heart disease; the electrophysiological indication to pacing, instead, does not significantly influence it.

Age Factors↗
PubMed1989

Efficacy of ibopamine treatment in patients with advanced heart failure: purpose of a new therapeutic scheme with multiple daily administrations.

Eighteen patients with severe unstable heart failure who presented with hemodynamic deterioration after withdrawal of i.v. dopamine were treated with high doses of ibopamine (100 mg eight times a day, orally) in association with digitalis, diuretic, and vasodilator therapy. Ibopamine, used at these dosages, could effectively substitute for the i.v. infusion of dopamine in 15 of the 18 studied patients. Each patient was studied by right heart Swan-Ganz catheterization and two-dimensional echocardiography before and during ibopamine infusion, after dopamine withdrawal, and after acute ibopamine administration; measurements were then made after 3 months of chronic ibopamine treatment (100 mg eight times a day). Blood samples for plasma dopamine and epinine concentrations were obtained at the time of the hemodynamic measurements. Both drugs did not induce any significant change in arterial pressure whereas heart rate was slightly reduced after dopamine and chronic ibopamine. Cardiac index and stroke volume index were significantly increased by dopamine (from 1.81 to 2.24 L/min/m2 and from 20.3 +/- 6.5 to 27.7 +/- 8.1 ml/beat/m2) and acute and chronic ibopamine (from 1.80 to 2.15 and 2.23 L/min/m2 and from 22.4 +/- 6.8 to 28.2 +/- 7.5 and 30.3 +/- 7.0 ml/beat/m2, respectively); these changes were attended by a decrease in systemic vascular resistance; pulmonary pressures were not significantly modified. No significant change of the echocardiographic parameters was noted. During dopamine infusion, mean dopamine plasma concentrations were 211.8 +/- 32.4 pmol/ml; after acute and repeated administration of ibopamine, free epinine plasma concentrations averaged 45.1 +/- 14.5 and 62.2 +/- 12.7 pmol/ml, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1989

Clinical pharmacology of inodilators.

Recent advances in our knowledge of heart failure have shown that both a central and a peripheral factor are involved in this syndrome. Therefore, the ideal drug should combine the properties of a positive inotropic agent with those of a peripheral vasodilator; many drugs recently introduced into clinical practice have been shown to present both of these features, and the term "inodilators" has been used to characterize them. Inodilators can be further classified on the basis of their mechanism of action, i.e., phosphodiesterase inhibitors, and sympathomimetic and dopaminergic drugs. Phosphodiesterase inhibitors include bipyridine, imidazolone, and benzimidazole derivatives, which present potent inotropic and vasodilatatory actions. Despite their favorable acute effects, long-term studies have often yielded controversial, and sometimes disappointing, results as their chronic administration seems often to be associated with untoward effects and, above all, a poor prognosis. Sympathomimetic agonists act by stimulation of beta-receptors, with a consequent increase of myocardial contractility and peripheral vasodilation. Differently from the parenteral drugs (e.g., dobutamine), the oral agents present many important shortcomings including central nervous system effects, increased myocardial oxygen consumption, tachyarrhythmias, and, above all, development of tolerance during chronic administration. Dopaminergic drugs possess a unique pharmacologic profile since they add to the adrenergic stimulation their selective action on dopaminergic receptors. Dopamine is still one of the most useful drugs for the treatment of acute heart failure; the two oral drugs that more closely resemble its actions are levodopa and ibopamine. The administration of levodopa to patients with heart failure can induce a significant hemodynamic improvement that is maintained during chronic therapy. Ibopamine has been widely shown to cause a significant hemodynamic improvement in patients with heart failure. Its effects can be ascribed to a moderate increase of myocardial contractility accompanied by peripheral and renal vasodilatatory actions. This drug can also counteract some of the neurohumoral mechanisms (e.g., sympathetic stimulation and aldosterone secretion) that are activated in heart failure. These features can explain the favorable results that have also been recently obtained after the chronic administration of ibopamine.

Cardiotonic Agents↗
PubMed1989

Inhibition of aldosterone secretion by dopamine, ibopamine, and dihydroergotoxine in patients with congestive heart failure.

There is now evidence for the presence of a dopaminergic inhibitory modulation of aldosterone production that is mediated by D-2 receptors in the adrenal cortex. In this study we evaluated the effects of dopamine and the dopaminergic agonists ibopamine and dihydroergotoxine on aldosterone secretion and plasma renin activity in 13 patients with chronic heart failure. Two groups of patients were noted: one responding to dopaminergic drugs with a decrease in plasma aldosterone and the other without dopamine agonist-related aldosterone suppression. No effect on plasma renin activity was found after each drug administration. A correlation was found between the response to dopamine agonists and basal plasma aldosterone levels. These data are of therapeutic value in showing the detrimental effect of the activation of the renin-angiotensin-aldosterone system occurring in heart failure: a drug reducing this activation appears promising for both its acute and long-term effects.

Aged↗