digoxin and Hypertension--Pulmonary

Pulmonary arterial hypertension (PAH) is a disease characterized by an elevation in pulmonary artery pressure that can lead to right ventricular failure and death. The pulmonary circulation has to accommodate the entire cardiac output in each cardiac cycle and evolution has adapted to this by making it a low-pressure high-flow system. However, pathology can affect both the arterial and venous components of this system. Pulmonary venous hypertension mainly refers to diseases that result in elevated venous pressure and occurs mainly from mitral valve and left-sided heart disease. Standard treatment options include oral anticoagulation, diuretics, oxygen supplementation, and for a small percentage of patients, calcium channel blockers. Newer treatments include prostacyclin analogues, endothelin receptor antagonists, and phosphodiesterase type 5 inhibitors. This article reviews the current treatments strategies for PAH and provides guidelines for its management.

Topics: Atrial Septum; Calcium Channel Blockers; Digoxin; Diuretics; Drug Therapy, Combination; Endothelin Receptor Antagonists; Humans; Hypertension, Pulmonary; Oxygen Inhalation Therapy; Phosphodiesterase 5 Inhibitors; Phosphodiesterase Inhibitors; Prostaglandins

Recent advances in pulmonary arterial hypertension (PAH) research have created a new era of PAH-specific therapies. Although these therapeutics have revolutionized PAH therapy, their innovation was predated by supportive but nonspecific medical therapies adapted from their use in more common cardiopulmonary diseases. These therapies include oxygen therapy, diuretics, digoxin, anticoagulation, and high-dose calcium channel blockers. Expert opinion continues to support the use of adjunct therapies based on current pathologic understandings of PAH combined with some evidence extrapolated from small studies. This article discusses why these therapies continue to play an important role in the treatment of patients with PAH.

Topics: Calcium Channel Blockers; Digoxin; Diuretics; Familial Primary Pulmonary Hypertension; Humans; Hypertension, Pulmonary; Oxygen Inhalation Therapy

Heart failure (HF) is a leading cause of morbidity and mortality. Appropriate medical therapy using angiotensin converting enzyme inhibitors and beta-blockers improves outcomes in HF, whereas the role of digoxin is still not clearly defined. Digoxin is currently recommended for patients with HF who are symptomatic despite standard therapy and for controlling the ventricular rate in atrial fibrillation. Digoxin is a time-tested drug that accounts for 20 million drug prescriptions annually in the United States. It has favorable hemodynamic effects for patients with HF and atrial tachyarrhythmias. We conducted a systematic literature search for the current indications for digoxin. Despite extensive research and safety data, the literature suggests that digoxin is underused in clinical settings. Citing the literature where available, our review highlights the various clinical settings where digoxin is indicated. Despite difficulties with designing prospective studies in acute HF settings and lack of outcomes data, we believe that digoxin will continue to serve an important role in optimizing care in certain acute and chronic cardiac conditions.

Topics: Cardiotonic Agents; Digoxin; Heart; Heart Diseases; Humans; Hypertension, Pulmonary; Vascular Diseases

Pulmonary veno-occlusive disease (PVOD) is a rare and usually survival poor disorder. We report a patient with a long history of progressive dyspnea of over 8 years, who with a diagnosis of chronic cor pulmonale confirmed elsewhere, was ultimately diagnosed as PVOD via histological analysis of a lung biopsy. After treatment with combined bosentan, diuretics and digoxin, his symptoms and function improved. This case highlights that PVOD is an under-recognised and often misdiagnosed disease, especially in its chronic form. Understanding its pathogenesis, its poor response to medical therapy and its dismal prognosis remain challenges for the treatment of PVOD.

Topics: Adult; Antihypertensive Agents; Biopsy; Bosentan; Cardiotonic Agents; Diagnosis, Differential; Digoxin; Diuretics; Drug Therapy, Combination; Dyspnea; Humans; Hypertension, Pulmonary; Male; Pulmonary Heart Disease; Pulmonary Veno-Occlusive Disease; Sulfonamides; Time Factors; Tomography, X-Ray Computed

Treatment of pulmonary arterial hypertension (group 1 of clinical classification) has been recently characterized by important progresses, particularly in pharmacological therapy. Only until few years ago, patients with pulmonary arterial hypertension were treated with non-specific drugs, such as diuretics and digoxin for right heart failure and calcium-channel blockers in the minority of cases, responders to the acute vasoreactivity test. In addition, use of oral anticoagulant treatment was supported by uncontrolled studies. In the last 15 years (in particular in the last 8 years) different randomized controlled trials assessing the functional, clinical and hemodynamic efficacy of three classes of targeted drugs (prostanoids, endothelin receptor antagonists and phosphodiesterase type 5 inhibitors) with pulmonary vascular dilating and antiproliferative effects have been performed. This information has allowed the proposal of an evidence-based treatment algorithm. Treatment starts with general measures (physical activity, fertility control, respiratory tract infection, etc.) and supportive therapy (anticoagulant therapy, diuretics, oxygen, digoxin). Patients who respond to the acute vasoreactivity test (10% of idiopathic form) are treated with high doses of calcium-channel blockers, non-responders with targeted therapies either on monotherapy or combination. Usually an oral active drug is initiated and a second compound of a different class is combined in case of non-satisfactory response to the first treatment. Combination therapy should be performed only in specialized centers with large experience on use of targeted therapies and their relevant side effects. In case of failure of medical therapy, possible options are balloon atrial septostomy and/or listing for lung or heart-lung transplantation. As available treatments do not constitute a cure for pulmonary arterial hypertension, further progresses are expected in the near future.

Topics: Algorithms; Angioplasty, Balloon; Anticoagulants; Calcium Channel Blockers; Cardiotonic Agents; Digoxin; Diuretics; Drug Therapy, Combination; Endothelin Receptor Antagonists; Evidence-Based Medicine; Heart-Lung Transplantation; Humans; Hypertension, Pulmonary; Oxygen; Phosphodiesterase 5 Inhibitors; Phosphodiesterase Inhibitors; Prostaglandins; Randomized Controlled Trials as Topic; Treatment Outcome

In a series of articles the authors discuss literature data concerning epidemiology of pulmonary hypertension (PH), its modern classification; peculiarities of its pathogenesis and treatment in various diseases and conditions. In the nine communication they describe presentations of PH and methods of its instrumental diagnostics. This part also contains discussion of problems of differential diagnosis of diseases which can be complicated by PH, contemplation of natural course of primary (idiopathic) PH and factors determining its prognosis.

Topics: Antihypertensive Agents; Calcium Channel Blockers; Cardiotonic Agents; Diagnosis, Differential; Digoxin; Diuretics; Humans; Hypertension, Pulmonary; Oxygen; Vasodilator Agents; Ventricular Dysfunction, Right

Topics: Acute Disease; Cardiac Catheterization; Cardiomegaly; Child; Child, Preschool; Chronic Disease; Cystic Fibrosis; Digoxin; Electrocardiography; Female; Humans; Hypertension, Pulmonary; Infant; Infant, Newborn; Lung; Male; Pulmonary Heart Disease; Radiography; Vectorcardiography

This study assessed the relationship between dose and plasma concentration following administration of treprostinil sodium infusion therapy in pulmonary arterial hypertension patients. This was a multicenter, open-label, multiple-cohort, steady-state, pharmacokinetic study in subjects with pulmonary arterial hypertension receiving treprostinil by continuous intravenous or subcutaneous infusion at doses between 10 and 125 ng/kg/min. A blood sample was obtained from each patient at steady state and analyzed via a liquid chromatography/tandem mass spectrometry method. Forty-nine subjects receiving treprostinil were enrolled. Treprostinil doses ranged from 12.1 to 125 ng/kg/min; treprostinil plasma concentrations ranged from 14.9 to 18 248 pg/mL. Linear regression analysis revealed a correlation between treprostinil dose and treprostinil plasma concentration with an R2 value of 0.561. Using a power model to assess dose proportionality, the estimated nonproportionality parameter was 0.641 (95% confidence interval: 0.083-1.199), reflecting consistency with dose proportionality. Subset linear regression analysis, which excluded 2 subjects with anomalous treprostinil plasma concentrations, increased the R2 value to 0.796. Using a power model to assess dose proportionality of this subset, the estimated nonproportionality parameter was 0.941 (95% confidence interval: 0.809-1.073). This study supports previous findings of linearity at lower doses up to 15 ng/kg/min and demonstrates linearity at treprostinil doses up to 125 ng/kg/min.

Topics: Adult; Aged; Aged, 80 and over; Anticoagulants; Antihypertensive Agents; Calcium Channel Blockers; Chromatography, Liquid; Digoxin; Diuretics; Dose-Response Relationship, Drug; Drug Therapy, Combination; Epoprostenol; Female; Humans; Hypertension, Pulmonary; Infusions, Intravenous; Injections, Subcutaneous; Male; Mass Spectrometry; Middle Aged; Oxygen; Phosphodiesterase 5 Inhibitors; Regression Analysis

Background Digoxin acutely increases cardiac output in patients with pulmonary arterial hypertension (PAH) and right ventricular failure; however, the effects of chronic digoxin use in PAH are unclear. Methods and Results Data from the Minnesota Pulmonary Hypertension Repository were used. The primary analysis used likelihood of digoxin prescription. The primary end point was a composite of all-cause mortality or heart failure (HF) hospitalization. Secondary end points included all-cause mortality, HF hospitalization, and transplant-free survival. Multivariable Cox proportional hazards analyses determined the hazard ratios (HR) and 95% CIs for the primary and secondary end points. Among 205 patients with PAH in the repository, 32.7% (n=67) were on digoxin. Digoxin was more often prescribed to patients with severe PAH and right ventricular failure. After propensity score-matching, 49 patients were digoxin users, and 70 patients were nonusers; of these 31 (63.3%) in the digoxin group and 41 (58.6%) in nondigoxin group met the primary end point during a median follow-up time of 2.1 (0.6-5.0) years. Digoxin users had a higher combined all-cause mortality or HF hospitalization (HR, 1.82 [95% CI, 1.11-2.99]), all-cause mortality (HR, 1.92 [95% CI, 1.06-3.49]), HF hospitalization (HR, 1.89 [95% CI, 1.07-3.35]), and worse transplant-free survival (HR, 2.00 [95% CI, 1.12-3.58]) even after adjusting for patient characteristics and severity of PAH and right ventricular failure. Conclusions In this retrospective, nonrandomized cohort, digoxin treatment was associated with greater all-cause mortality and HF hospitalization, even after multivariate correction. Future randomized controlled trials should assess the safety and efficacy of chronic digoxin use in PAH.

Topics: Digoxin; Familial Primary Pulmonary Hypertension; Heart Failure; Hospitalization; Humans; Hypertension, Pulmonary; Pulmonary Arterial Hypertension; Retrospective Studies; Treatment Outcome

Topics: Aged; Anti-Arrhythmia Agents; Anti-Bacterial Agents; Cheek; Diagnosis, Differential; Digoxin; Diuretics; Exanthema; Female; Humans; Hypertension, Pulmonary; Nose; Oxygen; Pulmonary Disease, Chronic Obstructive

Topics: Causality; Cerebrospinal Fluid Pressure; Digoxin; Diuretics; Emergencies; Female; Humans; Hypertension, Pulmonary; Middle Aged; Papilledema; Pseudotumor Cerebri; Vision Disorders

To explore the effects of digoxin on hypoxia-induced pulmonary artery hypertension (PAH) and the possible mechanisms.. A total of 48 Sprague-Dawley rats were randomly divided into 4 groups: normoxia control, normoxia+digoxin, hypoxia control and hypoxia+digoxin. The animals were exposed to chronic intermittent hypoxia (PO₂: (10.5 ± 0.5) %, 8:00-16:00) or room air for 21 days.Each rat received a daily intraperitoneal injection of either digoxin (1.0 mg × kg⁻¹ × d⁻¹) or an equal volume of vehicle, starting at the first day of hypoxia or normoxia. At Day 21, mean pulmonary arterial pressure (mPAP), right ventricular hypertrophy (RV/(LV+S)) and index of wall thickness of small pulmonary artery (WT% and WA%) among groups were compared. And in vitro the changes of pulmonary artery smooth muscle cells (PASMCs) proliferation were determined by methyl thiazolyl tetrazolium (MTT) assay. Migration assay was performed with a Transwell chamber.Real-time quantitative polymerase chain reaction (PCR) was performed to quantify the mRNA levels of smooth muscle cell phenotype markers such as smooth muscle-α-actin, calponin and smooth muscle 22α under normoxic or hypoxic conditions in the absence or presence of digoxin. And the protein expressions of matrix metalloproteinase (MMPs) were determined by Western blot.. Digoxin treatment significantly lowered mPAP, reduced WT% and WA% and right ventricular hypertrophy compared with those of the hypoxic group (mPAP: (27.3 ± 2.7) vs (38.5 ± 2.3) mmHg (1 mmHg = 0.133 kPa); RV/(LV+S): (30.9 ± 3.3)% vs (42.8 ± 2.6)%, WT%: (21.7 ± 3.6)% vs (39.3 ± 2.0)%; WA%: (56.3 ± 4.7)% vs (79.5 ± 5.7)%, all P < 0.05). And in vitro, digoxin restored the hypoxia-induced inhibition of the expression of smooth muscle cell phenotype markers and prevented the hypoxia-induced activation of MMPs in PASMCs.. Early digoxin therapy reduces pulmonary artery remodeling in hypoxia-induced PAH rat model and this effect is probably correlated with the inhibitions of proliferation, migration, phenotype switching and expression of MMPs induced by hypoxia in PASMCs.

Topics: Animals; Cell Proliferation; Digoxin; Hypertension, Pulmonary; Hypoxia; Matrix Metalloproteinases; Muscle Cells; Muscle, Smooth, Vascular; Pulmonary Artery; Rats; Rats, Sprague-Dawley

A massive lethal overdose with beta-metildigoxin in a 36-week-old infant is presented. Determination of beta-metildigoxin and its metabolites digoxin, digoxigenin and digoxigenin-monodigitoxosid is achieved by a liquid chromatographic mass spectrometric (LC-MS/MS) method. Measured concentrations for beta-metildigoxin and digoxin in peripheral blood were 40.2 ng/ml and 25.6 ng/ml, respectively. Tissue distribution showed highest concentrations in kidney tissue and gastric content. The metabolite digoxigenin-monodigitoxosid could be detected in heart blood, duodenal content, gastric content and fat tissue while the metabolite digoxigenin could only be detected in gastric content since the drug was given by a stomach tube.

Topics: Cardiotonic Agents; Chromatography, Liquid; Digoxigenin; Digoxin; Drug Overdose; Forensic Toxicology; Humans; Hypertension, Pulmonary; Infant; Male; Medication Errors; Medigoxin; Tandem Mass Spectrometry; Tissue Distribution

Chronic hypoxia is an inciting factor for the development of pulmonary arterial hypertension. The mechanisms involved in the development of hypoxic pulmonary hypertension (HPH) include hypoxia-inducible factor 1 (HIF-1)-dependent transactivation of genes controlling pulmonary arterial smooth muscle cell (PASMC) intracellular calcium concentration ([Ca(2+)](i)) and pH. Recently, digoxin was shown to inhibit HIF-1 transcriptional activity. In this study, we tested the hypothesis that digoxin could prevent and reverse the development of HPH. Mice were injected daily with saline or digoxin and exposed to room air or ambient hypoxia for 3 wk. Treatment with digoxin attenuated the development of right ventricle (RV) hypertrophy and prevented the pulmonary vascular remodeling and increases in PASMC [Ca(2+)](i), pH, and RV pressure that occur in mice exposed to chronic hypoxia. When started after pulmonary hypertension was established, digoxin attenuated the hypoxia-induced increases in RV pressure and PASMC pH and [Ca(2+)](i). These preclinical data support a role for HIF-1 inhibitors in the treatment of HPH.

Topics: Analysis of Variance; Animals; Blood Pressure; Calcium; Digoxin; Hypertension, Pulmonary; Hypertrophy, Right Ventricular; Hypoxia; Hypoxia-Inducible Factor 1; Mice; Microscopy, Confocal; Myocytes, Smooth Muscle; Pulmonary Artery; Real-Time Polymerase Chain Reaction; Reverse Transcriptase Polymerase Chain Reaction; Transcriptional Activation

We describe the case of an 83-year-old man with a family history of pulmonary hypertension (PH) who presented with severe pulmonary arterial hypertension (PAH) and later tested positive for a novel bone morphogenetic protein receptor 2 (BMPR2) gene mutation. To our knowledge, this may be the oldest reported patient with PAH in whom a BMPR2 mutation was initially identified.

Topics: Aged, 80 and over; Amlodipine; Bone Morphogenetic Protein Receptors, Type II; Bosentan; Digoxin; Dyspnea; Humans; Hypertension, Pulmonary; Male; Pulmonary Artery; Sulfonamides; Warfarin

The 2009 European Guidelines on Diagnosis and Treatment of Pulmonary Hypertension have been adopted for Germany. The guidelines contain detailed recommendations for the treatment of pulmonary arterial hypertension (PAH). However, the practical implementation of the European Guidelines in Germany requires the consideration of several country-specific issues and already existing novel data. This requires a detailed commentary to the guidelines, and in some aspects an update already appears necessary. In June 2010, a Consensus Conference organized by the PH working groups of the German Society of Cardiology (DGK), the German Society of Respiratory Medicine (DGP) and the German Society of Pediatric Cardiology (DGPK) was held in Cologne, Germany. This conference aimed to solve practical and controversial issues surrounding the implementation of the European Guidelines in Germany. To this end, a number of working groups was initiated, one of which was specifically dedicated to the treatment of PAH. This commentary summarizes the results and recommendations of the working group on treatment of PAH.

Topics: Algorithms; Anti-Arrhythmia Agents; Anticoagulants; Calcium Channel Blockers; Combined Modality Therapy; Cooperative Behavior; Digoxin; Drug Therapy, Combination; Endothelin Receptor Antagonists; Evidence-Based Medicine; Exercise Therapy; Female; Germany; Humans; Hypertension, Pulmonary; Interdisciplinary Communication; Oxygen Inhalation Therapy; Patient Care Team; Phosphodiesterase 5 Inhibitors; Phosphodiesterase Inhibitors; Pregnancy; Prostaglandins; Vasodilator Agents

This report describes the diagnosis and treatment of pulmonary arterial hypertension (PAH) in an adult male captive chimpanzee. Although cardiovascular disease in general is common in human and great apes, diagnosis and treatment of PAH in nonhuman primates are uncommon. In the case we present, the adult chimpanzee was diagnosed with an arrhythmia during an annual physical examination and later with PAH during a scheduled cardiovascular evaluation. PAH can either be primary or secondary and can lead to right ventricular overload and heart failure. This description is the first case study of pulmonary arterial hypertension in a great ape species.

Topics: Animals; Antihypertensive Agents; Aspirin; Atrial Fibrillation; Cardiotonic Agents; Digoxin; Diuretics; Enalapril; Furosemide; Hypertension, Pulmonary; Liver; Lung; Male; Myocardium; Pan troglodytes; Platelet Aggregation Inhibitors; Primate Diseases

Topics: Aged; Amlodipine; Atrial Fibrillation; Digoxin; Female; Graves Disease; Humans; Hypertension, Pulmonary; Methimazole; Recurrence; Syncope; Treatment Outcome; Vertigo

Pulmonary arterial hypertension (PAH) is characterized by elevated pulmonary vascular resistance which leads to right ventricular failure. Serotonin and the serotonin transporter play an important role in animal and human studies of PAH. We therefore hypothesized that PAH patients treated with high-affinity selective serotonin reuptake inhibitors (SSRIs) would have a reduced risk of death compared to PAH patients not treated with SSRIs.. We performed a retrospective cohort study of 84 consecutive adult PAH patients who underwent initial evaluation from January 1994 to June 2002 at the Pulmonary Hypertension Center of the New York Presbyterian Hospital. Patient-time while receiving high-affinity SSRIs (K(d)<1nmol) (paroxetine, sertraline, or fluoxetine) was considered "exposed". Patient-time while receiving tricyclic, atypical, or no antidepressants was considered "unexposed".. Thirteen of the 84 patients (15%) used high-affinity SSRIs during the study period. Five patients were taking high-affinity SSRIs at baseline and 8 initiated high-affinity SSRIs during the follow-up period. The median time from baseline evaluation until initiation of high-affinity SSRIs was 125 (0-1227) days. The median duration of high-affinity SSRI use was 482 (110-1624) days and the total at-risk time on high-affinity SSRIs was 18.1 person-years. Seventy-nine (94%) patients were treated with warfarin; 38 (45%) received continuous intravenous epoprostenol; 12 (14%) received continuous subcutaneous treprostinil, and 23 (27%) were treated with oral bosentan. The median follow-up was 764 days. Twenty-four patients died and one underwent lung transplantation during the study period. There were no differences in age, gender, diagnosis, hemodynamics, or incidence of acute vasoreactivity between SSRI users and non-users. The risk of death for high-affinity SSRI users was lower but not statistically significantly different from that of non-users (hazard ratio=0.53, 95% CI 0.07 to 3.9, p=0.53). Adjustment for demographics, diagnosis, hemodynamics, or other therapies did not significantly change this result.. SSRI use was associated with a 50% reduction in the risk of death in a cohort of PAH patients which was not statistically significant. Larger cohort studies may better define this relationship; an adequately powered trial of high-affinity SSRIs in PAH patients may be warranted.

Topics: Adult; Bosentan; Cardiac Catheterization; Cohort Studies; Digoxin; Drug Administration Routes; Epoprostenol; Female; Follow-Up Studies; Hemodynamics; Humans; Hypertension, Pulmonary; Lung Transplantation; Male; Pulmonary Circulation; Retrospective Studies; Selective Serotonin Reuptake Inhibitors; Sulfonamides; Survival Analysis; Treatment Outcome; Vasodilation; Warfarin

Topics: Activities of Daily Living; Azathioprine; Blood Pressure; Digoxin; Dilatation, Pathologic; Drug Therapy, Combination; Female; Furosemide; Humans; Hypertension, Pulmonary; Mixed Connective Tissue Disease; Pulmonary Artery; Radiography; Treatment Outcome

We report a case of a 33 yr old woman with pulmonary hypertension secondary to uncorrected right coronary artery to pulmonary artery fistula who underwent two successful operative deliveries under general anesthesia.. This woman underwent an emergency Caesarean section at 32 wk gestation because she presented in NYHA Class IV, heart failure and premature labour. She did not have antenatal follow-up. For her second pregnancy, she was managed from the first trimester of pregnancy by the cardiologist, obstetrician and anesthesiologist. She received oral furosemide and digoxin from eight weeks gestation. Pregnancy was managed to term before she progressed to NYHA Class IV and cardiac failure at 37 wk gestation. She had a Caesarean section under general anesthesia. She received rapid sequence induction of anesthesia and tracheal intubation with 0.1 mg x kg(-1) etomidate, 2 mg x kg(-1) succinylcholine and maintenance with nitrous oxide 50% in oxygen, isoflurane 1% and 0.1 mg x kg(-1) vecuronium. Fentanyl, 2 microg x kg(-1) helped to obtund the hypertensive response to intubation. Analgesia was provided with 1 mg x kg(-1) morphine. Glyceryl trinitrate infusion, 10-30 microg x min(-1) was used in addition to the anti-heart failure therapy. End-tidal capnography, electrocardiogram, pulse oximetry, continuous arterial blood pressure and pulmonary arterial catheter provided hemodynamic monitoring. The lungs were mechanically ventilated for 24 hr postoperatively. She received anti-heart failure therapy which she continued after discharge. She was NYHA class II upon discharge. She defaulted from further follow-up.. Although the literature advocates, in this situation, controlled vaginal delivery utilising epidural analgesia, we describe the successful outcome for operative delivery under general anesthesia in a patient with secondary pulmonary hypertension and heart failure.

Topics: Adult; Analgesics, Opioid; Anesthesia, Inhalation; Anesthesia, Intravenous; Anesthesia, Obstetrical; Arterio-Arterial Fistula; Blood Pressure; Cardiac Output, Low; Cardiotonic Agents; Cesarean Section; Coronary Vessel Anomalies; Digoxin; Diuretics; Female; Furosemide; Humans; Hypertension, Pulmonary; Intubation, Intratracheal; Morphine; Neuromuscular Blockade; Nitroglycerin; Pregnancy; Pregnancy Complications, Cardiovascular; Pulmonary Artery; Respiration, Artificial; Vasodilator Agents

Studies on the effects of digoxin in patients with right ventricular failure and normal left ventricular function have not been performed. We evaluated the short-term effects of digoxin administration in patients with primary pulmonary hypertension on hemodynamics, neurohormones, and baroreceptor responsiveness.. This was a prospective study with patients serving as their own controls.. University Hospital Intensive Care Unit with central monitoring.. Seventeen patients with primary pulmonary hypertension and symptomatic heart failure were enrolled.. Following baseline hemodynamics, neurohormonal samples were drawn and the heart rate response to change in blood pressure following a challenge of phenylephrine and nitroprusside were recorded. One mg of intravenous digoxin was given and the measurements repeated after 2 hours.. Following digoxin there was a significant increase in cardiac output (3.49+/-1.2 to 3.81+/-1.2 L/min., p=0.028), a significant fall in norepinephrine (680+/-89 to 580+/-85 pg/ml, p=.013), and a significant increase in atrial natriuretic peptide (311+/-44 to 421+/-9 pg/ml, p=0.01). All of the patients had changes in heart rate and blood pressure following phenylephrine and nitroprusside challenge, but there was no significant difference in the change in heart rate response to change in blood pressure when rechallenged after digoxin treatment.. Digoxin produces a modest increase in cardiac output in patients with pulmonary hypertension and right ventricular failure, as well as a significant reduction in circulating norepinephrine. No detectable effects of digoxin on baroreceptor responsiveness were apparent. The use of digoxin in pulmonary hypertension is warranted.

Topics: Adult; Atrial Natriuretic Factor; Blood Pressure; Cardiac Output; Cardiotonic Agents; Digoxin; Female; Heart Rate; Humans; Hypertension, Pulmonary; Male; Middle Aged; Norepinephrine; Pressoreceptors; Prospective Studies; Pulmonary Heart Disease; Renin; Ventricular Dysfunction, Right

In addition to positive inotropic and atrioventricular conduction-blocking properties, digoxin is capable of producing systemic and pulmonary vasoconstriction. However, whether chronic digoxin treatment exacerbates the pulmonary hypertension that results from left atrial (LA) outflow obstruction has not been specifically examined. This study assessed the vascular and inotropic responses to 5 days of digoxin treatment in six conscious dogs before and after filling a permanently implanted LA balloon. Dogs were also instrumented to measure left ventricular (LV) pressure, LV dP/dt, mean systemic arterial (MAP), right atrial (RAP), pulmonary arterial, and pulmonary capillary wedge pressures, as well as cardiac output (CO). Under normal conditions with the balloon empty, digoxin treatment (40 micrograms/kg loading dose and 12 micrograms/kg/d for 5 days) reduced CO (-17%) and increased systemic (SVR) and pulmonary (PVR) vascular resistances 27% and 37%, respectively; heart rate (HR) and LV dP/dt were not changed. Filling the balloon with enough saline to double PVR also increased SVR (52%), HR (42%), and RAP (92%), and reduced CO (-24%). During LA outflow obstruction, 5 days of digoxin reduced HR (-17%), SVR (-29%), and RAP (-23%), but did not alter PVR, CO, or LV dP/dt. This study demonstrates that although systemic and pulmonary vasoconstriction result from chronic digoxin treatment under normal conditions, the drug produces systemic vasodilation and no change in PVR during LA outflow obstruction.

Topics: Animals; Atrial Function, Left; Blood Pressure; Cardiac Output; Catheterization; Consciousness; Digoxin; Dogs; Heart Rate; Hypertension, Pulmonary; Pulmonary Artery; Pulmonary Wedge Pressure; Vascular Resistance; Ventricular Outflow Obstruction

A critically ill 21-month-old girl with congenital absence of the right pulmonary artery and severe pulmonary hypertension and congestive heart failure underwent conduit restoration of flow to the right lung. This patient had marked clinical improvement and reduction in pulmonary hypertension and represents the second reported surgically-treated case for absent right pulmonary artery. Reestablishment of pulmonary artery continuity is therefore recommended when cardiac failure and pulmonary hypertension occurs.

Topics: Blood Vessel Prosthesis; Cardiac Catheterization; Digoxin; Diuretics; Female; Heart Failure; Heart Septal Defects, Atrial; Humans; Hypertension, Pulmonary; Infant; Pulmonary Artery

Topics: Adult; Digoxin; Dopamine; Female; Humans; Hypertension, Pulmonary; Isoproterenol; Respiratory Distress Syndrome; Stroke Volume

The successful simultaneous closure of a persistent ductus arteriosus and mitral valve replacement in a 65-year-old woman with pulmonary hypertension is reported. The approach through a left thoracotomy gave good exposure and momentary cessation of cardiopulmonary bypass made ligation of the calcified ductus possible. Although this seems to be a rare association, when mitral valve disease is significant the simultaneous closure of the duct and mitral valve surgery is the treatment of choice.

Topics: Aged; Blood Pressure; Cardiac Catheterization; Cardiopulmonary Bypass; Cineangiography; Digoxin; Ductus Arteriosus, Patent; Female; Heart Rate; Humans; Hypertension, Pulmonary; Ligation; Methods; Mitral Valve; Mitral Valve Insufficiency; Practolol

Topics: Arrhythmias, Cardiac; Carbon Dioxide; Cardiac Complexes, Premature; Cardiomegaly; Coronary Disease; Digoxin; Heart Failure; Heart Rate; Humans; Hypertension, Pulmonary; Male; Oxygen; Potassium; Pulmonary Heart Disease

Topics: Angiocardiography; Cardiac Catheterization; Cardiomegaly; Digoxin; Electrocardiography; Extracorporeal Circulation; Female; Furosemide; Heart Auscultation; Heart Defects, Congenital; Heart Septal Defects, Ventricular; Heart Ventricles; Humans; Hypertension, Pulmonary; Infant; Infant, Newborn; Male; Oxygen Inhalation Therapy; Pulmonary Valve Stenosis; Pulmonary Veins; Respiratory Insufficiency

Topics: Aortic Coarctation; Aortic Valve Stenosis; Child, Preschool; Digoxin; Diuretics; Heart Defects, Congenital; Heart Failure; Heart Septal Defects, Ventricular; Humans; Hypertension, Pulmonary; Infant; Infant, Newborn; Pulmonary Valve Stenosis; Transposition of Great Vessels

Topics: Blood Gas Analysis; Blood Pressure; Cardiac Catheterization; Chronic Disease; Diagnosis, Differential; Digoxin; Electrocardiography; Female; Heart Failure; Heparin; Humans; Hypertension, Pulmonary; Middle Aged; Pulmonary Circulation; Pulmonary Embolism; Radiography; Radionuclide Imaging; Recurrence; Tetracycline; Thrombosis

Topics: Animals; Aorta; Aortography; Arteriovenous Fistula; Blood Pressure; Cardiomegaly; Catheterization; Digoxin; Dogs; Female; Femoral Artery; Heart Diseases; Heart Ventricles; Hypertension, Pulmonary; Male; Oxygen; Pulmonary Artery; Pulmonary Circulation; Regional Blood Flow

Topics: Adolescent; Adult; Arrhythmias, Cardiac; Atrial Fibrillation; Atrial Flutter; Child; Child, Preschool; Digoxin; Electric Countershock; Electrocardiography; Female; Heart Block; Heart Septal Defects, Atrial; Humans; Hypertension, Pulmonary; Hypothermia, Induced; Male; Postoperative Complications; Quinidine

Topics: Angiocardiography; Bradycardia; Cardiomegaly; Digoxin; Electrocardiography; Female; Heart Block; Heart Septal Defects, Ventricular; Hepatomegaly; Humans; Hypertension, Pulmonary; Infant; Pacemaker, Artificial

Topics: Adrenal Cortex Hormones; Altitude; Altitude Sickness; Anti-Bacterial Agents; Diagnosis; Digoxin; Diuretics; Drug Therapy; Humans; Hypertension, Pulmonary; Morphine; Oxygen Inhalation Therapy; Pulmonary Edema

Topics: Acetylcholine; Blood Pressure; Blood Vessels; Cardiac Catheterization; Cardiomegaly; Digoxin; Familial Primary Pulmonary Hypertension; Humans; Hypertension; Hypertension, Pulmonary; Infusions, Parenteral; Lung; Lupus Erythematosus, Systemic; Metabolism; Prednisone; Pulmonary Heart Disease; Tolazoline

Topics: Chronic Disease; Digoxin; Humans; Hypertension, Pulmonary; Pulmonary Heart Disease; Tuberculosis; Tuberculosis, Pulmonary

Topics: Blood; Digitalis; Digitalis Glycosides; Digoxin; Heart; Humans; Hypertension, Pulmonary; Pulmonary Heart Disease