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PubMed2003

Right-to-left shunting through a patent foramen ovale in right ventricular infarction: improvement of hypoxemia and hemodynamics with inhaled nitric oxide.

Inhaled nitric oxide is a selective pulmonary vasodilator that has been used successfully to treat hemodynamic embarrassment and right-to-left interatrial shunting in acute right heart failure. Previous reports have been in the setting of disorders causing elevated right heart afterload, such as pulmonary embolism, acute respiratory distress syndrome, and chronic obstructive pulmonary disease. Right ventricular infarction is a less common, but important cause of acute right heart failure with which the intensivist should be familiar. We report a patient with right ventricular infarction for whom cardiogenic shock and refractory hypoxemia due to right-to-left interatrial shunting were effectively treated with inhaled nitric oxide. The potential for broader application of inhaled nitric oxide as a therapy for right ventricular infarction is discussed.

Aged↗
PubMed1999

Experience with an adjustable pulmonary artery banding device in two cases: initial success--midterm failure.

Retraining of the left ventricle in congenitally corrected TGA or after Senning or Mustard operation is necessary when right-ventricular failure is developing and an arterial switch operation is indicated. As these hearts have little tolerance of marginal overbanding, a long-term adjustable pulmonary artery banding device would lower stress and risk of training. Although the inserted device (Osypka) allowed convenient intraoperative pressure ratio adjustment, mid-term adjustment failed due to dysfunction of the system.

Cardiac Surgical Procedures↗
PubMed2006

Genetic knowledge and moral responsibility: ambiguity at the interface of genetic research and clinical practice.

Despite a rapidly expanding literature on the issue of duty to warn at-risk relatives in the context of clinical genetic testing, little has been written on parallel issues with regard to the management of genetic research results. Some might view this lack as an indication that there is little to discuss in this regard. That is, standard practice is that data obtained through medical research should not be treated as though they are clinically relevant, and this standard should hold for genetic research as well. This paper challenges this conclusion and its underlying assumptions. We argue that the line between genetic research and clinical practice is often ambiguous. In some cases, research data gathered from a very small number of subjects could have immediate clinical implications. Hence, it is unethical for genetic researchers to absolve themselves of clinical responsibilities for research subjects and/or their families, on the grounds that the data were obtained for research purposes. Indeed, we argue that it could well be unethical to embark on some forms of genetic research unless advance arrangements have been made for genetic counseling and clinical follow-up. Furthermore, in some cases, it might be unethical to enroll subjects in studies if the subjects are unwilling to receive their individual results.

Arrhythmogenic Right Ventricular Dysplasia↗
PubMed2005

Arrhythmogenic right ventricular cardiomyopathy in two cats.

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a disease characterised by infiltration of the myocardium by adipose and fibrous tissue. The disease is an important cause of sudden death in humans, but has rarely been described in animals. This report describes ARVC in two cats with right-sided congestive heart failure. One cat had also experienced previous episodes of syncope. Standard six-lead and 24-hour (Holter) electrocardiogram recording revealed complete atrioventricular block and multiform ventricular ectopics in both cats, with the addition of ventricular tachycardia, ventricular bigeminy and R-on-T phenomenon in one of them. On echocardiography, the right ventricle and atrium were massively dilated and hypokinetic. The survival times of the cats were three days and 16 days following diagnosis. Histopathology in one case revealed fibro-fatty infiltration of the myocardium, predominantly affecting the right ventricular free wall.

Animals↗
PubMed2006

Important role of endogenous erythropoietin system in recruitment of endothelial progenitor cells in hypoxia-induced pulmonary hypertension in mice.

BACKGROUND: Recent studies have suggested that endogenous erythropoietin (Epo) plays an important role in the mobilization of bone marrow-derived endothelial progenitor cells (EPCs). However, it remains to be elucidated whether the Epo system exerts protective effects on pulmonary hypertension (PH), a fatal disorder encountered in cardiovascular medicine. METHODS AND RESULTS: A mouse model of hypoxia-induced PH was used for study. We evaluated right ventricular systolic pressure, right ventricular hypertrophy, and pulmonary vascular remodeling in mice lacking the Epo receptor (EpoR) in nonerythroid lineages (EpoR(-/-) rescued mice) after 3 weeks of exposure to hypoxia. Those mice lack EpoR in the cardiovascular system but not in the hematopoietic system. The development of PH and pulmonary vascular remodeling were accelerated in EpoR(-/-) rescued mice compared with wild-type mice. The mobilization of EPCs and their recruitment to the pulmonary endothelium were significantly impaired in EpoR(-/-) rescued mice. By contrast, reconstitution of the bone marrow with wild-type bone marrow cells ameliorated PH in the EpoR(-/-) rescued mice. Hypoxia enhanced the expression of EpoR on pulmonary endothelial cells in wild-type but not EpoR(-/-) rescued mice. Finally, hypoxia activated endothelial nitric oxide synthase in the lungs in wild-type mice but not in EpoR(-/-) rescued mice. CONCLUSIONS: These results indicate that the endogenous Epo/EpoR system plays an important role in the recruitment of EPCs and prevents the development of PH during chronic hypoxia in mice in vivo, suggesting the therapeutic importance of the system for the treatment of PH.

Animals↗
PubMed2005

Pulmonary hypertension and right heart failure in chronic obstructive pulmonary disease.

Pulmonary hypertension is a common complication of chronic obstructive pulmonary disease (COPD). The increase in pulmonary artery pressures is often mild to moderate. However, 5-10% of patients with advanced COPD may suffer from severe pulmonary hypertension and present with a progressively downhill clinical course because of right heart failure added to ventilatory handicap. The prevalence of clinically significant severe pulmonary hypertension in COPD is roughly estimated to be of 1-2/1,000. The cause of pulmonary hypertension in COPD is generally assumed to be hypoxic pulmonary vasoconstriction leading to permanent medial hypertrophy. However, recent pathologic studies point rather at extensive remodeling of all layers of the pulmonary arterial walls. These aspects account for minimal reversibility with supplemental oxygen. There may be a case for pharmacologic treatment of pulmonary hypertension in selected patients with advanced COPD and right heart failure. However, it will be a challenge for randomized controlled trials to overcome the difficulties of the diagnosis of right ventricular failure and the definition of a relevant primary endpoint in pulmonary hypertensive patients with COPD.

Antihypertensive Agents↗
PubMed1997

Influence of pulmonic position on durability of bioprosthetic heart valves.

BACKGROUND: The insertion of bioprosthetic valves into the pulmonic position is not performed commonly because of uncertainty concerning the necessity and durability of such valves. METHODS: We reviewed the long-term outcome of 10 patients who underwent pulmonary valve replacement with bioprostheses between March 1985 and March 1997. A Carpentier-Edwards supraannular bioprosthesis was used in 7 patients, a Hancock II bioprosthesis was used in 2 patients, and a Carpentier-Edwards pericardial bioprosthesis was used in 1 patient. The mean patient age at the time of pulmonary valve replacement was 38.9 +/- 16.3 years (range, 15 to 63 years). The diagnoses were pulmonary valvular regurgitation after corrective surgery for tetralogy of Fallot in 7 patients, right ventricular outflow tract stenosis and absent right pulmonary artery combined with a double-outlet right ventricle in 1 patient, pulmonary valvular regurgitation with pulmonary artery dilatation in 1 patient, and aortic valve stenosis treated with our modification of the Ross procedure using a pulmonary bioprosthesis in 1 patient. Survivors were followed up for a mean of 5 years and 5 months. RESULTS: One patient underwent reoperation because of infective endocarditis of the bioprosthesis. No bioprosthetic valve dysfunction has been observed on Doppler echocardiography during a maximum follow-up period of 12.2 years, except in the patient who underwent replacement at 15 years of age. CONCLUSIONS: Bioprostheses in the pulmonic position are durable in adult patients because they face a minimal hemodynamic load, but they may undergo early leaflet degeneration in younger patients.

Adolescent↗
PubMed1995

[Electrocardiographic findings in arrhythmogenic right ventricular dysplasia (ARVD) evaluated by body surface mapping].

Electrocardiographic characteristics evaluated by body surface mapping were investigated, comparing with the other clinical findings. Isopotential maps were abnormal at the end of QRS period when the positive area persisted in the anterior middle and lower chest. VAT was also prolonged in these area. Post excitation (Epsilon) waves appeared at that period in accordance with the rapid potential change on upper anterior chest which reflected right ventricular conduction delay. There was no difference in electrophysiologic findings in patients with or without Epsilon waves. Negative potentials were present on the anterior chest in ST-T isopotential, ST-T and QRST isointegral maps in all of the patients. The area of these negative potentials was closely correlated with RV dilatation and dysfunction. It is concluded that Epsilon waves are not the direct counterpart of delayed potentials, but the reflection of the peripheral induction delay, and that primary change seems to play large part of the genesis in negative T waves.

Arrhythmias, Cardiac↗
PubMed2006

Isolated subvalvular pulmonary stenosis: depiction at whole heart magnetic resonance imaging.

Isolated subvalvular pulmonary stenosis is a rare condition and its morphological evaluation is obscure. Whole heart magnetic resonance imaging (MRI) is a new, totally non-invasive technique which allows three-dimensional comprehension of the cardiac structure. We describe a patient with isolated subvalvular pulmonary stenosis, in whom whole heart MRI was useful to detect and evaluate the right ventricular outflow obstruction.

Humans↗
PubMed2002

Effects of vasopressin on right ventricular function in an experimental model of acute pulmonary hypertension.

OBJECTIVE: Arginine vasopressin is a promising systemic vasopressor in settings such as vasodilatory shock and cardiopulmonary resuscitation. The evidence that arginine vasopressin may also have a pulmonary vasodilatory effect makes it an attractive drug for the treatment of circulatory shock secondary to right ventricular failure and pulmonary hypertension. In the present study, we evaluated the effects of arginine vasopressin on right ventricular function and ventriculovascular coupling in the setting of moderate acute pulmonary hypertension and compared these effects with those of phenylephrine. DESIGN: Prospective laboratory investigation using an established model of acute pulmonary hypertension. SETTING: University hospital laboratory. SUBJECTS: Seven adult beagle dogs weighing 8-14 kg. INTERVENTIONS: After acute instrumentation to measure right ventricular pressure and volume with the conductance technique and pulmonary artery flow and pressure with high-fidelity transducers, the stable thromboxane analogue U46619 was infused continuously to obtain stable pulmonary hypertension. Phenylephrine and arginine vasopressin were administered consecutively in continuous infusions at doses titrated to achieve a 25% increase in aortic pressure. MEASUREMENTS AND MAIN RESULTS: Phenylephrine and arginine vasopressin both increased total pulmonary vascular resistance and arterial elastance without influencing characteristic impedance. Both drugs decreased cardiac output and stroke volume. Right ventricular hydraulic power output was reduced by arginine vasopressin but not by phenylephrine. Most importantly, arginine vasopressin caused a 31% decrease in right ventricular contractility measured as the slope of the preload recruitable stroke work relationship, whereas contractility was preserved during phenylephrine infusion. CONCLUSIONS: In the present model, arginine vasopressin causes pulmonary vascular constriction and exerts an important negative inotropic effect on the right ventricle. These findings suggest that one should be cautious in the use of arginine vasopressin when right ventricular function is compromised.

Acute Disease↗
PubMed2001

[Anesthetic management for left ventricular assist device implantation in patients waiting for heart transplantation].

We report the anesthetic management of patients with dilated cardiomyopathy who underwent left ventricular assist device implantation (LVAD). Anesthesia was induced and maintained with midazolam and fentanyl. Transesophageal echocardiography (TEE) and a PA catheter were useful for hemodynamic monitoring and management of the patients. Furthermore, TEE is useful for the early detection of inflow of the air which is absorbed by negative pressure derived from high LVAD support pressure. On starting LVAD support, evaluation of right ventricular function and treatment for right ventricular failure were important and necessary for the patients. Added to conventional therapy using catecholamines, inhaled nitric oxide may provide a favorable effect for right ventricular failure.

Adult↗
PubMed1996

Preload-recruitable stroke work relationships and diastolic dysfunction in the brain-dead organ donor.

BACKGROUND: Acute graft failure is an important cause of morbidity and mortality in cardiac transplantation, and it may be associated with myocardial changes that occur during brain death (BD). This study investigates the changes in biventricular systolic and diastolic function that occur after BD in a validated canine model. METHODS AND RESULTS: The hearts of 20 mongrel canines (23 to 31 kg) were instrumented with micromanometers, flow probes, and dimension transducers to measure minor/major axes as well as left and right ventricular (LV/RV) septum-to-free wall distances. LV/RV volumes were measured according to the shell subtraction method. LV/RV systolic function was analyzed by ventricular stroke work plotted versus end-diastolic volume during a caval occlusion (preload-independent recruitable systolic work, PRSW). The nonlinear relationships between diastatic pressure (stress) and LV/RV septum-to-free wall distances and volumes (strain) from successive diastoles during caval occlusion were used to evaluate LV/RV diastolic mechanics. The Cushing phenomenon, hyperdynamic response, and diabetes insipidus were observed in each animal after BD. Results are expressed as mean +/- SEM (P < .05 versus baseline, ANOVA, paired two-tailed Student's t test). Biventricular systolic function deteriorated significantly from baseline PRSW 6 to 7 hours after BD. The diastatic LV/RV pressure dimension relationships were significantly different after BD, indicating a decrease in ventricular chamber compliance during diastole. CONCLUSIONS: BD causes a significant loss of systolic and diastolic LV/RV function in the brain-dead, heart-beating cadaver, which may contribute to early postoperative cardiac graft failure in the recipient. These findings have significant clinical applications and may help to avoid suboptimal donor/recipient matches.

Animals↗
PubMed2000

A case with Uhl's anomaly presenting with severe right heart failure.

Uhl's anomaly was first reported by Uhl in 1952 and is characterized by congenital partial or complete absence of right ventricular myocardium. It is a very rare anomaly with unknown aetiology. Associations with other congenital heart diseases, familial occurrency, sudden death and arrhythmia with Uhl's anomaly have been reported. Pathologic findings vary with the patient's age and severity of the right ventricular disorder. In infancy, it may occur with severe right-sided heart failure as well as asymptomatic cardiomegaly. Despite its rarity, Uhl's anomaly may be considered in patients with right ventricular failure due to dilated cardiomyopathy of the right ventricle. We report the case of six-year-old boy presenting with striking ascites due to severe right heart failure of Uhl's anomaly.

Cardiotonic Agents↗
PubMed2005

A novel regional right ventricular wall-motion abnormality observed in a case of acute pulmonary embolism (reverse McConnell sign).

Among various echocardiographic parameters for diagnosis of pulmonary embolism, an abnormal regional contraction pattern of the right ventricular free wall consisting of normokinesia of the apical segment and akinesia of the midfree wall with persistence of abnormal wall motion at the base has proved to be fairly specific for pulmonary embolism. This echocardiographic abnormality has been termed "McConnell sign." We describe the case of a patient with acute pulmonary embolism who developed reversible akinesia of the apex and right ventricular midfree wall, a finding we would like to term "reverse McConnell sign."

Acute Disease↗
PubMed1997

Prolonged ECG abnormalities in a subject with high altitude pulmonary edema (HAPE).

High Altitude Pulmonary Edema (HAPE) is an uncommon type of non-cardiogenic pulmonary edema. Few data are available regarding ECG abnormalities in patients with HAPE. They are usually slight and related to acute pulmonary hypertension. This paper describes a case of prolonged ECG abnormalities in a subject with HAPE, with no proven cardiac diseases. The Authors discuss the pathopysiological aspects of this kind of hypoxic-induced right ventricular overload with extensive T-wave negativity in precordial leads.

Adult↗