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PubMed2002

Right ventricular performance during left ventricular unloading conditions: the contribution of the right ventricular free wall.

AIM: Right ventricular (RV) dysfunction is a significant complication following implantation of left ventricular assist device (LVAD). However, RV performance after LVAD implantation remains unclear. We have studied the effects of preload and afterload on RV performance under left ventricular (LV) unloading. METHODS: Six adult mongrel dogs were subjected to cardiopulmonary bypass. RV preload and afterload were independently regulated. Dynamic pressure-length analysis of RV free walls was performed using micromanometer catheter and sonomicrometric dimension transducers. Global RV systolic function was evaluated by the relationship between stroke volume vs. end-diastolic length (EDL) or end-diastolic pressure (EDP). We also examined the afterload dependency of RV performance at constant stroke volume. RESULTS: Stroke volume vs. EDP and stroke volume vs. EDL demonstrated a linear relationship (r(2) = 0.849 +/- 0.147 and 0.776 +/- 0.121, respectively). At constant stroke volume, RV systolic peak pressure vs. EDL or EDP were shown to have a linear relationship (r(2) = 0.906 +/- 0.050 vs. 0.909 +/- 0.047, respectively). CONCLUSION: The Frank-Starling relationship for RV performance was shown in this animal model. Without interventricular interaction, RV preload is dependent on RV afterload.

Animals↗

PubMed2006

New strategies for the treatment of acute venous thromboembolism.

In recent years, new opportunities have emerged that have the potential to change rapidly the therapeutic scenario of patients with acute venous thromboembolism (VTE). Selected patients with deep vein thrombosis (DVT) can be treated effectively and safely at home with fixed doses of low molecular weight heparins. The prompt administration of compression elastic stockings in addition to anticoagulant drugs in patients with acute DVT has the potential to halve the rate of late postthrombotic sequelae. The long-term use of low molecular weight heparins is likely to be more effective than oral anticoagulants for the secondary prevention of VTE in patients with advanced malignancy. Patients with pulmonary embolism and right ventricular dysfunction might benefit from the early administration of thrombolytic drugs in combination with heparin to a greater extent than from heparin alone. Despite an impressive amount of clinical information on the proper duration of oral anticoagulants in patients with unprovoked VTE, the optimal long-term treatment of these patients remains undefined. Finally, new categories of drugs are emerging that have the potential to replace conventional anticoagulants in the near future. They include compounds that inhibit factor Xa or thrombin.

Anticoagulants↗

PubMed2002

Heparin plus alteplase compared with heparin alone in patients with submassive pulmonary embolism.

BACKGROUND: The use of thrombolytic agents in the treatment of hemodynamically stable patients with acute submassive pulmonary embolism remains controversial. METHODS: We conducted a study of patients with acute pulmonary embolism and pulmonary hypertension or right ventricular dysfunction but without arterial hypotension or shock. The patients were randomly assigned in double-blind fashion to receive heparin plus 100 mg of alteplase or heparin plus placebo over a period of two hours. The primary end point was in-hospital death or clinical deterioration requiring an escalation of treatment, which was defined as catecholamine infusion, secondary thrombolysis, endotracheal intubation, cardiopulmonary resuscitation, or emergency surgical embolectomy or thrombus fragmentation by catheter. RESULTS: Of 256 patients enrolled, 118 were randomly assigned to receive heparin plus alteplase and 138 to receive heparin plus placebo. The incidence of the primary end point was significantly higher in the heparin-plus-placebo group than in the heparin-plus-alteplase group (P=0.006), and the probability of 30-day event-free survival (according to Kaplan-Meier analysis) was higher in the heparin-plus-alteplase group (P=0.005). This difference was due to the higher incidence of treatment escalation in the heparin-plus-placebo group (24.6 percent vs. 10.2 percent, P=0.004), since mortality was low in both groups (3.4 percent in the heparin-plus-alteplase group and 2.2 percent in the heparin-plus-placebo group, P=0.71). Treatment with heparin plus placebo was associated with almost three times the risk of death or treatment escalation that was associated with heparin plus alteplase (P=0.006). No fatal bleeding or cerebral bleeding occurred in patients receiving heparin plus alteplase. CONCLUSIONS: When given in conjunction with heparin, alteplase can improve the clinical course of stable patients who have acute submassive pulmonary embolism and can prevent clinical deterioration requiring the escalation of treatment during the hospital stay.

Aged↗

PubMed1982

Pulmonary vascular responses to nitrous oxide in patients with normal and high pulmonary vascular resistance.

The pulmonary vascular responses to 50 per cent nitrous oxide were studied in 32 anesthetized patients ventilated to maintain normal PaCO2. One group consisted of sixteen patients with coronary artery disease (CAD) and normal pulmonary vascular resistance (PVR) about to undergo coronary artery bypass surgery. A second group consisted of 16 patients with markedly elevated PVR values due to chronic mitral valve stenosis (MVS). CAD patients showed a significant increase in PVR irrespective of whether halothane or fentanyl was used as background anesthetic. Individual changes, however, did not exceed the upper limit of normal and therefore are not considered to be of clinical importance in these patients. In patients with MVS subjected to fentanyl anesthesia, N2O caused a marked increase in PVR from 357 to 530 dyn . s. cm-5. Halothane anesthesia did not significantly attenuate the effect of nitrous oxide on the pulmonary vasculature as mean PVR increased from 351 to 451 dyn . s. cm-5. These results suggest that the preexisting PVR value is of more importance for the pulmonary vascular response to N2O than the influence of background anesthesia. We conclude that nitrous oxide should be used with caution in patients with elevated pulmonary vascular resistance, particularly in the presence of right ventricular dysfunction and/or right coronary artery disease.

Coronary Disease↗

PubMed1997

Effects of increasing airway pressure and PEEP on the assessment of cardiac preload.

BACKGROUND: Cardiac preload is most commonly assessed by pulmonary artery wedge pressure. It was postulated that the right ventricular end-diastolic volume index (RVEDVI) derived by thermodilution would be a better predictor of preload in trauma patients with high airway pressures associated with positive pressure ventilation and positive end-expiratory pressure. METHODS: Volumetric thermodilution catheters were placed in 52 mechanically ventilated trauma patients. Regression analysis was performed on 986 sets of hemodynamic data comparing pulmonary artery wedge pressure and RVEDVI to cardiac index (CI) at various airway pressures. RESULTS: There was much better correlation between RVEDVI and CI (r = 0.41) than with pulmonary artery wedge pressure and CI (r = -0.06). This was true of all levels of airway pressure tested. When analyzed by the degree of right ventricular dysfunction, as indexed by right ventricular ejection fraction, the strongest correlation between RVEDVI and CI was noted when right ventricular ejection fraction was > 30%. CONCLUSIONS: Unlike the pulmonary artery wedge pressure, RVEDVI is as reliable indicator of preload in the mechanically ventilated trauma patient. This is especially true when the right ventricular ejection fraction is not severely depressed.

Adult↗

PubMed2001

Concomitant traumatic coronary artery and tricuspid valve injury: a heterogeneous presentation.

Blunt thoracic trauma resulting in both tricuspid valve rupture and coronary artery injury is uncommon, encompasses a large spectrum of presentations and, therefore, can be difficult to diagnose. This report illustrates the heterogeneous presentation and clinical course of two patients with such a combination of cardiac injuries. The patient with associated right coronary artery dissection developed progressive right ventricular failure over a 12-year period before successful surgical repair, whereas another patient with left anterior descending coronary artery thrombosis required urgent operation for acute right ventricular dysfunction and hemodynamic decompensation.

Accidents, Traffic↗

PubMed2001

Inhaled nitric oxide for pulmonary hypertension after heart transplantation.

BACKGROUND: Recipient pulmonary hypertension due to chronic congestive heart failure is a major cause of right ventricular (RV) dysfunction after heart transplantation. We hypothesized that inhaled nitric oxide (NO), in the postoperative period, would a) selectively reduce pulmonary vascular resistance and improve RV hemodynamics and b) reduce the incidence of RV dysfunction compared with a matched historical group. METHODS: Sixteen consecutive adult heart transplant recipients with lowest mean pulmonary artery (PA) pressures >25 mmHg were prospectively enrolled. Inhaled NO at 20 parts per million (ppm) was initiated before termination of cardiopulmonary bypass (CPB). At 6 and 12 hours after CPB, NO was stopped for 15 minutes and systemic and pulmonary hemodynamics were measured. RV dysfunction was defined as central venous pressure >15 mmHg and consistent echocardiographic findings. The incidence of RV dysfunction and 30-day survival in this group was compared with a historical cohort of 16 patients matched for pulmonary hypertension. RESULTS: Discontinuation of NO for 15 minutes at 6 hours after transplantation resulted in a significant rise in mean PA pressure, pulmonary vascular resistance (PVR), and RV stroke work index. Systemic hemodynamics were not affected by NO therapy. One patient in the NO-treated group, compared with 6 patients in the historical cohort group, developed RV dysfunction (P< .05). The 30-day survival in the NO-treated group and the historical cohort group were 100% and 81%, respectively (P> .05). CONCLUSION: In heart transplant recipients with pulmonary hypertension, inhaled NO in the postoperative period selectively reduces PVR and enhances RV stroke work. Furthermore, NO reduces the incidence of RV dysfunction in this group of patients when compared with a historical cohort matched for pulmonary hypertension. Inhaled NO is a useful adjunct to the postoperative treatment protocol of heart transplant patients with pulmonary hypertension.

Administration, Inhalation↗

PubMed2005

Lack of alteration of endogenous nitric oxide pathway during prolonged nitric oxide inhalation in intensive care unit patients.

OBJECTIVE: To compare hemodynamic and gasometric variables and the plasma concentrations of nitric oxide metabolites (cyclic guanosine monophosphate and nitrate and nitrite), endothelin-1, and renin-angiotensin metabolites before and after the start of nitric oxide inhalation, after prolonged nitric oxide inhalation, and before and after nitric oxide withdrawal. DESIGN: Prospective study. SETTING: Surgical intensive care unit, university hospital. SUBJECTS: Patients with acute lung injury and right ventricular failure. INTERVENTIONS: Nitric oxide inhalation (10-12 ppm) during a median of 2.9 days (12 hrs to 6.5 days). MEASUREMENTS AND MAIN RESULTS: The pulmonary vasodilator effects of inhaled nitric oxide improved arterial oxygenation in patients with acute lung injury (p < .05) and reduced right atrial pressure in patients with right ventricular dysfunction (p < .01). These beneficial effects lasted the whole period of prolonged inhaled nitric oxide therapy up to 6.5 days. However, when inhaled nitric oxide was withdrawn, pulmonary vasodilator effects rapidly disappeared, and Pao2/Fio2 ratio markedly deteriorated in all studied patients to return to pre-inhaled nitric oxide levels. Changes in plasma cyclic guanosine monophosphate and nitrate and nitrite paralleled those of pulmonary vasodilatory effects. An immediate increase in plasma cyclic guanosine monophosphate with a slightly delayed increase in plasma nitrate and nitrite was observed at inhaled nitric oxide start with no attenuation during the prolonged inhaled nitric oxide therapy. A marked decrease toward pre-inhaled nitric oxide levels was seen within hours of inhaled nitric oxide withdrawal. In addition, no alteration of plasma endothelin-1 or renin-angiotensin mediators was observed during or after inhaled nitric oxide therapy. CONCLUSIONS: Our study showed a lack of attenuation in the beneficial effects of inhaled nitric oxide and a lack of alteration of endogenous nitric oxide, endothelin-1, and renin-angiotensin pathways during prolonged nitric oxide inhalation.

Administration, Inhalation↗

PubMed1995

Haemodynamic changes in children with portal hypertension during the postoperative period.

The cardiovascular changes following portosystemic shunt surgery (PSSS) in 33 children with extrahepatic portal hypertension (EPH) were studied to determine if portosystemic shunt surgery had any influence on the cardiovascular state. Haemodynamic data were obtained using two-dimensional and M-mode echocardiography, pulsed-wave Doppler and direct invasive techniques. Postoperatively all patients developed a hyperdynamic state, associated with an increase in cardiac index (CI), heart rate (HR) and a decrease in systemic vascular resistance index (SVRI). In 16 patients (group I), who preoperatively exhibited a hyperdynamic state accompanied by pulmonary hypertension, postoperative studies found an increase in acceleration time to ejection time ratio (AT/ET) in the pulmonary artery from 0.32 +/- 0.05 (mean +/- SEM) to 0.43 +/- 0.01; P < 0.01. Nine patients (group II) who were normodynamic preoperatively developed pulmonary hypertension and right ventricular (RV) dysfunction postoperatively: decrease in AT/ET from 0.42 +/- 0.02 (mean +/- SEM) to 0.32 +/- 0.01; P < 0.01 and an increase in maximal peak pulmonary artery velocity to acceleration time ratio (Vmax/AT) from 702.56 +/- 69.10 (mean +/- SEM) to 1127 +/- 105.30 cm.sec-2; P < 0.01. In eight patients (group III) who were normodynamic preoperatively and were treated with dobutamine infusions at a rate of 5 micrograms.kg-1.min-1 postoperatively, the CI was found to increase from 5.28 +/- 1.1 (mean +/- SEM) to 7.97 +/- 1.64 L.min-1.m-2; P < 0.01, left ventricular ejection fraction (LVEF) from 69.0 +/- 4.1 (mean +/- SEM) to 81.0 +/- 2.9%; P < 0.01 and AT/ET from 0.37 +/- 0.04 (mean +/- SEM) to 0.44 +/- 0.03; P < 0.01.(ABSTRACT TRUNCATED AT 250 WORDS)

Acceleration↗

PubMed2005

Brain natriuretic peptide in hemodynamically stable acute pulmonary embolism.

BACKGROUND: Controversy exists about the indication of thrombolytic therapy in the subgroup of hemodynamically stable patients with acute pulmonary embolism (PE) and right ventricular dysfunction. Brain natriuretic peptide (BNP) is excreted from the cardiac ventricles in response to cardiomyocyte stretch and can be measured with an easy-to-perform blood test. OBJECTIVE: The objective of this study was to determine the predictive value of elevated BNP levels for early recurrent venous thromboembolism with or without fatal outcome in hemodynamically stable patients with acute PE. In addition, we assessed the potential clinical consequences of initiating thrombolytic therapy based on the BNP levels alone. METHODS: A nested case-control study was performed within the framework of a large randomized-controlled trial totalling 2213 hemodynamically stable patients with confirmed acute, symptomatic PE. Ninety patients experienced a fatal or non-fatal recurrent venous thromboembolism during the first 3 months of follow-up (cases); Two hundred and ninety-seven patients with uneventful follow-up served as controls. Blood for BNP levels was obtained at referral and assayed in a central laboratory. RESULTS: Cases had significantly higher mean baseline BNP levels (P = 0.0002). The odds ratio (OR) for every logarithmic (log) unit increase in BNP concentration was 2.4 (95% CI: 1.5-3.7). A BNP cut-off level of 1.25 pmol L(-1) [the optimal point on the receiver-operating characteristic (ROC) curve] was associated with a sensitivity and specificity of 60% and 62%, respectively. In theory, for every patient correctly receiving thrombolytic therapy at this cut-off, 16 patients will receive this therapy unnecessarily. CONCLUSIONS: Brain natriuretic peptide level at presentation is significantly associated with early (fatal) recurrent venous thromboembolism in hemodynamically stable patients with acute PE. However, this relationship appears clinically insufficient to guide the initiation of thrombolytic therapy.

Acute Disease↗

PubMed2003

Impaired myocardial blood flow and coronary flow reserve of the anatomical right systemic ventricle in patients with congenitally corrected transposition of the great arteries.

OBJECTIVES: To investigate myocardial blood flow of the morphological right systemic ventricle in unoperated patients with congenitally corrected transposition of the great arteries (CCTGA) by positron emission tomography (PET). DESIGN: Prospective cross sectional clinical study. SETTING: Tertiary referral centre for paediatric cardiology. PATIENTS: 15 patients with CCTGA were investigated by PET with nitrogen-13 ammonia at rest and during adenosine vasodilatation. A subgroup of seven patients had isolated CCTGA (group A, mean (SD) age 30.3 (11.9) years) and the remaining eight patients had complex CCTGA associated with subpulmonary stenosis; four of this second group also had ventricular septal defect (group B, mean (SD) age 30.6 (16.4) years). Eleven healthy adults (mean (SD) age 26.2 (5.1) years) served as the control group. RESULTS: Resting myocardial blood flow was not different between both groups of patients with CCTGA and the controls. Hyperaemic blood flows were significantly lower in both groups of CCTGA than in the control group (mean (SD) 195 (21) ml/100g/min in group A, 201 (27) ml/100g/min in group B, 309 (74) ml/100g/min in the control group; p < 0.001). Thus, coronary flow reserve was significantly lower in both groups of CCTGA than in the control group (mean (SD) 2.5 (0.28) in group A, 2.6 (0.48) in group B, and 4.0 (0.73) in the control group; p < 0.001). CONCLUSION: Blood flow measurements suggest that coronary reserve is decreased in the absence of ischaemic symptoms in patients with CCTGA. The global impairment of stress flow dynamics may indicate altered global vasoreactivity, and quantitative changes in microcirculation suggest that their role in the pathogenesis of systemic right ventricular dysfunction is important.

Adenosine↗

PubMed2006

Pulmonary arterial hypertension in adults born with a heart septal defect: the Euro Heart Survey on adult congenital heart disease.

AIM: To investigate the role of pulmonary arterial hypertension (PAH) in adult patients born with a cardiac septal defect, by assessing its prevalence and its relation with patient characteristics and outcome. METHODS AND RESULTS: From the database of the Euro Heart Survey on adult congenital heart disease (a retrospective cohort study with a 5-year follow-up), the relevant data on all 1877 patients with an atrial septal defect (ASD), a ventricular septal defect (VSD), or a cyanotic defect were analysed. Most patients (83%) attended a specialised centre. There were 896 patients with an ASD (377 closed, 504 open without and 15 with Eisenmenger's syndrome), 710 with a VSD (275, 352 and 83, respectively), 133 with Eisenmenger's syndrome owing to another defect and 138 remaining patients with cyanosis. PAH was present in 531 (28%) patients, or in 34% of patients with an open ASD and 28% of patients with an open VSD, and 12% and 13% of patients with a closed defect, respectively. Mortality was highest in patients with Eisenmenger's syndrome (20.6%). In case of an open defect, PAH entailed an eightfold increased probability of functional limitations (New York Heart Association class >1), with a further sixfold increase when Eisenmenger's syndrome was present. Also, in patients with persisting PAH despite defect closure, functional limitations were more common. In patients with ASD, the prevalence of right ventricular dysfunction increased with systolic pulmonary artery pressure (OR = 1.073 per mm Hg; p<0.001). Major bleeding events were more prevalent in patients with cyanosis with than without Eisenmenger's syndrome (17% vs 3%; p<0.001). CONCLUSION: In this selected population of adults with congenital heart disease, PAH was common and predisposed to more symptoms and further clinical deterioration, even among patients with previous defect closure and patients who had not developed Eisenmenger's physiology.

Adult↗

PubMed2026

Red Flags for Differentiating Desmosomal "Hot-Phase" Cardiomyopathy From Acute Myocarditis.

BACKGROUND: Desmosomal "hot-phase" cardiomyopathy (HPC), characterized by bursts of myocardial inflammation mimicking acute myocarditis (AM), carries relevant risks of adverse outcomes. This study aimed to identify diagnostic "red flags" favoring HPC over AM. METHODS: Patients (n=134) receiving a first diagnosis of AM, proven by endomyocardial biopsy or cardiac magnetic resonance plus troponin elevation, were retrospectively identified at a referral center. HPC was defined by presence of pathogenic desmosomal gene variants (DGVs). Clinical, imaging, and electrical features were compared between HPC cases and controls with gene-negative AM to identify red flags. Diagnostic algorithms were derived and tested in an external multicenter cohort of DGV carriers (n=30). RESULTS: Patients with HPC (n=22; 91% DSP+) were more frequently female (73% versus 24%, P<0.001) and younger than unmatched controls with AM (32±14 versus 41±14 years, P=0.007). When matched 1:1 by age, sex, and presentation, DGV carriers showed distinctive red flags: family history of cardiomyopathy/AM/sudden death; recurrent troponin peaks; persistent left ventricular systolic dysfunction; right ventricular involvement; ring-like late gadolinium enhancement; late gadolinium enhancement persistence or extension; low QRS voltages; life-threatening ventricular arrhythmias at <45 years; persistent >1000/24 hours ventricular ectopy; and recurrent nonsustained ventricular tachycardia. A "first-contact" algorithm based on female sex and age <30 years achieved 77% accuracy, identifying 63% of DGV carriers in the external cohort. An alternative algorithm incorporating ring-like late gadolinium enhancement, right ventricular involvement, and family history showed higher accuracy (93%) and yield (93%). CONCLUSIONS: Myocarditis in DGV carriers predominantly affects young women. A red flag-based approach improves recognition of desmosomal HPC over classic AM.

Humans↗

PubMed1999

Response to inhaled nitric oxide in patients with acute right heart syndrome.

Inhaled nitric oxide (iNO), a selective pulmonary vasodilator, has been shown to decrease pulmonary artery pressures but not increase cardiac output in hemodynamically stable patients with a variety of causes of pulmonary hypertension. The response to iNO in hemodynamically unstable patients with acute right heart syndrome has not been previously described. We determined the response to iNO in 26 critically ill adult patients with acute right heart failure defined by echocardiographic criteria. Patients received iNO through the inspiratory limb of the ventilator in increments of 10 ppm with hemodynamic and gas-exchange measurements made before and after each level. When maximal effect was seen, iNO was discontinued to compare parameters with baseline. iNO significantly increased cardiac output (5.5 +/- 3 to 6.4 +/- 4 L/min), stroke volume (54 +/- 27 to 65 +/- 38 ml), and mixed-venous oxygen saturation (69 +/- 8 to 73 +/- 10%), all p < 0.01. With discontinuation of iNO, all parameters returned immediately to baseline. These parameters of improved perfusion were related to a decrease in pulmonary vascular pressures and resistance. In a subset of approximately 50% of patients, these changes were substantial (> 20%) and in approximately 25% of all patients, the improvement in hemodynamic measures permitted a decrease in other vasoactive drug administration. The mean concentration of iNO required to achieve these effects was 35 ppm, and 85% of patients exhibiting a substantial improvement in hemodynamics did so at a concentration of iNO of less than or equal to 40 ppm. Underlying causes of right heart failure and baseline hemodynamics did not predict response to iNO, but the use of alpha-agonist catecholamines did. We conclude iNO improves hemodynamics in patients with respiratory failure, shock, and right ventricular dysfunction. Although mortality was not a key end point in this pilot study, it was high for both responders and nonresponders to this therapy. Further evaluation of the role of iNO in this patient population is supported by these data.

Acute Disease↗

PubMed2006

Assessment of right ventricular function by strain rate imaging in chronic obstructive pulmonary disease.

The purpose of the current study was to compare right ventricular (RV) myocardial wall velocities (tissue Doppler imaging) and strain rate imaging (SRI) parameters with conventional echocardiographic indices evaluating RV function in chronic obstructive pulmonary disease (COPD) patients. In total, 39 patients with COPD and 22 healthy subjects were included in the current study. Seventeen patients had pulmonary artery pressure <35 mmHg (group I) and 22 patients had pulmonary artery pressure >35 mmHg (group II). Tissue Doppler imaging, strain and strain rate (SR) values were obtained from RV free wall (FW) and interventricular septum. Respiratory function tests were performed (forced expiratory volume in one second/vital capacity (FEV(1)/VC) and carbon monoxide diffusion lung capacity per unit of alveolar volume (D(L,CO)/V(A))). Strain/SR values were reduced in all segments of group II patients compared with group I patients and controls with lowest values at basal FW site. A significant relationship was shown between peak systolic SR at basal FW site and radionuclide RV ejection fraction. A significant relationship was shown between peak systolic SR at basal FW site and D(L,CO)/V(A) and FEV(1)/VC. In conclusion, in chronic obstructive pulmonary disease patients, strain rate imaging parameters can determine right ventricular dysfunction that is complementary to conventional echocardiographic indices and is correlated with pulmonary hypertension and respiratory function tests.

Case-Control Studies↗

PubMed1999

Right ventricular involvement in acute myocardial infarction.

The presence of right ventricular dysfunction in patients with acute myocardial infarction has important implications. It is a marker for in-hospital mortality and failure to recognize it may lead to inappropriate treatment with serious consequences for the patient. Patients surviving the acute event do, however, have a relatively good long-term prognosis.

Echocardiography↗

PubMed1995

Right-to-left flow through a patent foramen ovale in acute right ventricular infarction. Two case reports and a proposal for management.

Right-to-left shunting through a foramen ovale complicating acute right ventricular infarction and resulting in severe arterial hypoxemia has been described eight times before. Treatment strategies have often aimed at reducing the shunt. Four patients died. Less attention has been paid to attempts at revascularization and, despite a high incidence of atrioventricular conduction disturbances, to temporary dual-chamber pacing. We describe herein two patients with postcardiac surgical right ventricular infarction complicated by severe right-to-left interatrial shunting. Treatment strategy was aimed at improving right ventricular function, and right-to-left shunting ceased. All efforts should be directed at treating right ventricular dysfunction, which is the cause of the clinical picture, and not at reducing the shunt, which is a secondary phenomenon.

Adult↗

PubMed2004

Natriuretic peptides, respiratory disease, and the right heart.

It is well-recognized that atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) are raised in conditions with ventricular volume and pressure overload. In addition to this established role in left ventricular congestive cardiac failure, there is good evidence that BNP has a diagnostic role in right ventricular (RV) dysfunction and pulmonary arterial hypertension (PAH). For example, BNP levels can be used to differentiate between dyspneic patients with pure respiratory defects and those with RV dysfunction. Studies in patients with PAH have demonstrated significant correlations between BNP levels and mean pulmonary arterial pressure as well as pulmonary vascular resistance. Additionally, BNP has a prognostic role in patients with RV pressure overload and pulmonary hypertension, and it offers a noninvasive test that can be used to guide therapy in patients with PAH. However, although measured plasma proBNP levels are raised in conditions with RV overload, its biological significance is still not well-understood. In this article, we review the general physiologic and potential therapeutic role of natriuretic peptides in respiratory disease, RV dysfunction, and PAH. Furthermore, we assess the various clues toward natriuretic peptide action coming from laboratory studies. ANP and BNP knockout mice develop cardiac fibrosis and hypertrophy. Potentiation of the natriuretic pathway has been shown to reduce cardiac hypertrophy and PAH. This is likely to take place as a result of increased intracellular cyclic guanosine monophosphate levels and subsequent pulmonary vasorelaxant activity. In view of this evidence, there may be a rationale for the therapeutic use of recombinant BNP or neutral endopeptidase inhibitors under conditions of RV dysfunction and PAH.

Animals↗