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Role of electrocardiography in identifying right ventricular dysfunction in acute pulmonary embolism.

The role of electrocardiography in identifying right ventricular (RV) dysfunction in acute pulmonary embolism (APE) was evaluated in 81 patients with APE. The electrocardiographic markers studied were T-wave inversion in leads V1 to V3, the S1Q3T3 pattern, right bundle branch block, and sinus tachycardia. T-wave inversion in leads V1 to V3 had the greatest sensitivity and diagnostic accuracy for identifying RV dysfunction in patients with APE. The S1Q3T3 pattern and right bundle branch block had good specificity but moderate accuracy.

Acute Disease↗

Carcinoid crisis and reversible right ventricular dysfunction after embolization in untreated carcinoid syndrome.

A 59-year-old white male with carcinoid tumor and hepatic metastases underwent hepatic artery embolization. The patient developed carcinoid crisis and a subsequent transthoracic echocardiogram showed classic findings of carcinoid heart disease along with a dilated hypertrophied right ventricle and severely depressed right ventricular ejection fraction. After treatment with octreotide the patient's clinical condition improved and a repeat transthoracic echocardiogram showed a significant improvement and normalization of right ventricular systolic function. Serotonin levels showed a progressive decline that correlated well with the patient's improved clinical condition. These findings suggest that the acute right ventricular dysfunction was secondary to acute carcinoid crisis and resolution resulted in a significant improvement of both right ventricular systolic function and clinical condition.

Acute Disease↗

Echocardiography Doppler in pulmonary embolism: right ventricular dysfunction as a predictor of mortality rate.

To test the hypothesis that right ventricular (RV) systolic dysfunction at the time of diagnosis of pulmonary embolism (PE) is a predictor of mortality rate, 126 consecutive patients with PE were examined with echocardiography Doppler (ED) on the day of diagnosis. RV function was assessed by evaluation of wall motion on a four-point scale. The material was divided into two groups: group A (n = 56) with normal or slightly reduced RV function and group B (n = 70) with moderately or severely reduced RV function. The overall mortality rate was 7.9% in the hospital and 15.1% within 1 year. Four deaths occurred in group A and 15 in group B (p = 0.04). All in-hospital deaths (n = 10) occurred in group B (p = 0.002). The variables associated with mortality rate were RV dysfunction and cancer (in-hospital, p = 0.002 and 0.004; 1 year, p = 0.04 and < 0.001, respectively). Nine (7.1%) deaths (all in-hospital) were caused by PE. Five of these patients had advanced-stage cancer. The in-hospital mortality rate in patients without cancer was 4%, all from PE and all in group B. In conclusion, RV dysfunction when diagnosis of PE is established is associated with mortality rate. A strategy for risk stratification of patients with PE with ED may be of clinical usefulness.

Aged↗

Regional right ventricular dysfunction detected by echocardiography in acute pulmonary embolism.

This study analyzed the regional pattern of right ventricular (RV) dysfunction on transthoracic echocardiograms in patients with and without acute pulmonary embolism. Quantitative (centerline) and qualitative (wall motion score) analyses of segmental RV free wall motion were performed on a "training" cohort of 41 patients (group 1), including 14 patients with acute pulmonary embolism, 9 patients with primary pulmonary hypertension, and 18 normal subjects. Patients with acute pulmonary embolism had a distinct regional pattern of RV dysfunction, with akinesia of the mid-free wall (centerline excursion: -0.2 +/- 0.8 mm, p = 0.0001 vs normal) but normal motion at the apex (centerline excursion: 5.7 +/- 0.8 mm, p = NS vs normal). In contrast, patients with primary pulmonary hypertension had abnormal wall motion in all regions (p <0.03 vs normal). This echocardiographic finding of normal wall motion at the apex and abnormal wall motion in the mid-free wall in acute pulmonary embolism was then tested in a "validation" cohort of 85 patients (group 2), consisting of hospitalized patients with RV dysfunction from any cause, including 13 patients with acute pulmonary embolism. The finding had a 77% sensitivity and a 94% specificity for the diagnosis of acute pulmonary embolism, with a positive predictive value of 71% and a negative predictive value of 96%. Thus, a distinct echocardiographic pattern of regional RV dysfunction, in which the apex is spared occurs in acute pulmonary embolism. This finding should raise the level of clinical suspicion for the diagnosis of acute pulmonary embolism.

Acute Disease↗

Role of helical CT in detecting right ventricular dysfunction secondary to acute pulmonary embolism.

OBJECTIVE: The purpose of this study was to evaluate the role of helical CT in detecting right ventricular dysfunction (RVD) after acute pulmonary embolism (PE). METHODS: This was a retrospective study consisting of 25 patients with CT scans positive for acute pulmonary embolism who had either follow-up echocardiography (23 patients) or pulmonary angiography (2 patients). CT scans were reviewed for findings suggestive of RVD. Scans were considered positive for RVD if the right ventricle (RV) was dilated or if the interventricular septum was deviated towards the left ventricle. Results were then correlated with the results of echocardiography or pulmonary angiography to estimate the sensitivity and specificity of CT in detecting RVD associated with PE. RESULTS: Within this group of 25 patients with PE, CT demonstrated sensitivity of 78% (7/9), specificity of 100% (16/16), and positive predictive value of 100% (7/7) in detection of RVD. CONCLUSION: CT may be useful in detecting RVD in patients with acute PE.

Acute Disease↗

[Biohumoral markers and right ventricular dysfunction in acute pulmonary embolism: the answer to thrombolytic therapy].

BACKGROUND: Recent data suggest that brain natriuretic peptide (BNP) and troponin I (TnII) are useful markers of right ventricular dysfunction (RVD) and initial myocardial injury in acute pulmonary embolism. The aim of this study was to evaluate biohumoral activation and right ventricular function in patients with acute pulmonary embolism diagnosed at pulmonary scintigraphy. METHODS: We observed 12 patients with massive pulmonary embolism (MPE), 8 with non-massive pulmonary embolism (NMPE) and RVD, 6 with NMPE without RVD. All the patients with MPE and 5 patients with NMPE-RVD received thrombolytic therapy (urokinase or recombinant tissue-type plasminogen activator), the others were treated with heparin. At the beginning and after pharmacological treatment all the 26 patients underwent standard echocardiography and blood test analysis. RESULTS: BNP and Tn1 were significantly high in MPE (BNP p < 0.001 and Tn1I p < 0.005 vs NMPE) and in NMPE-RVD (BNP p < 0.03 and Tnl p < 0.02 vs NMPE). MPE and NMPE-RVD had similar RVD (p = NS), thrombolysis significantly reduced BNP, TnI, systolic pulmonary pressure, both in MPE (p < 0.001) and in NMNPE-RVD (BNP and Tnl p < 0.05, systolic pulmonary pressure p < 0.001). COULSION: Our data sustain the utility of BNP and Tnl as markers of RVD in acute pulmonary embolism; they focus on patients with NMPE-RVD and high levels of BNP and Tnl in whom an aggressive therapy as the thrombolytic one is necessary; they suggest the importance of biohumoral markers as indicators of the efficacy of pharmacological treatment in patients with acute pulmonary embolism.

Acute Disease↗

Right ventricular dysfunction in chronic dilated cardiomyopathy and heart failure.

In patients with advanced heart failure, the main focus has traditionally been placed on the functional assessment of the left ventricle. Therefore, the current body of literature examining the right ventricle and its influence on the pathophysiological processes in heart failure has been limited. Methods currently employed to assess the size and function of the right ventricle include: high frequency thermodilution, contrast ventriculography, radionuclide ventriculography, echocardiography, and magnetic resonance imaging; however, none of these techniques has proven to be a 'gold standard' for the assessment of right ventricular function. Nevertheless, when these methods are employed, right ventricular dysfunction has been shown to be a powerful predictor of reduced exercise capacity and survival. This relationship holds true for patients with heart failure secondary to either ischemic or non-ischemic dilated cardiomyopathy.

Cardiomyopathy, Dilated↗

Troponin I as a marker of right ventricular dysfunction and severity of pulmonary embolism.

BACKGROUND: Cardiac troponin I (cTnI) is a specific marker which allows detection of minor myocardial cell damage. In patients with severe pulmonary embolism (PE), the rise in pulmonary artery pressure can lead to progressive right ventricular dysfunction (RVD), and clinical studies have demonstrated the presence of ischemia and even right ventricular infarction. Our aims were to determine the prevalence and diagnostic utility of cTnI in identifying patients with RVD and to ascertain whether it correlates with severity of PE. METHODS: We studied 77 patients with PE diagnosed by pulmonary angiography, ventilation-perfusion lung scan, spiral computed tomography scan or a combination of abnormal echocardiogram with clinical presentation suggestive of PE or with positive subsidiary exams (d-dimers, venous Doppler of the lower limbs, ECG, blood gas analysis). We further classified the PE according to the European Society of Cardiology severity levels, the PE being: 1) massive, if there was shock and/or hypotension; 2) submassive, if we found right ventricular hypokinesis on the echocardiogram; and 3) non-massive, in the remaining cases. We considered the highest cTnI serum value from the admission to 24 hours and a normal value of < 0.10 ng/ml. RESULTS: Among the 60 patients with cTnI measurements, 42 had elevated values. Among those with RVD, 26 (81.3%) had increased cTnI levels and only 14 (35%) with elevated cTnI values did not have RVD, indicating that positive cTnI tests were significantly associated with RVD (p = 0.038). Patients with positive cTnI tests had earlier onset of symptoms (24.0 vs. 144.0 hours, p=0.02), higher prevalence of emboli in proximal vessels (pulmonary trunk and right or left main pulmonary arteries) (OR = 12, CI= 1.6-88.7), and received more thrombolytic therapy (OR = 5.4, CI = 1.1-26.8) than those with normal cTnI tests. cTnI levels were higher among patients with submassive PE (median: 0.77 ng/ml) and lower in those with non-massive PE (0.08 mg/ml, p < 0.05). CONCLUSIONS: Around 70% of patients with PE have elevated cTnI values and this test is significantly associated with RVD. cTnI measurements provide additional information in the evaluation of patients with PE by identifying more severe cases and those at increased risk of hemodynamic deterioration, who can benefit from more aggressive therapeutic strategies.

Biomarkers↗

Severe right ventricular dysfunction following pericardiocentesis for cardiac tamponade.

The accumulation of fluid in the pericardium in an amount sufficient to cause severe obstruction to blood inflow to the ventricles results in cardiac tamponade. In this condition, relief of intrapericardial pressure by pericardiocentesis usually dramatically improves cardiac output, and can be lifesaving. We report a case of a patient with malignant cardiac tamponade in which cardiogenic shock developed after pericardiocentesis due to severe right ventricular dysfunction.

Adenocarcinoma↗

Treatment of right ventricular dysfunction in acute respiratory failure.

The pathophysiology and managements of right ventricular (RV) dysfunction in acute respiratory failure (ARF) is complicated. Results presented in this paper indicate that volume expansion may not be appropriate therapy to maintain or increase cardiac output (CO) when flow is reduced because of increased RV afterload. Volume will increase RV wall stress and O2 requirements so that despite increased preload, CO may fall. If RV afterload is significantly increased, such changes can occur despite a relatively normal RV end-diastolic pressure (RVEDP). Further, increased RV afterload and/or volume expansion can result in increased RV volumes and secondary alteration in left ventricular (LV) diastolic mechanics. Such changes, especially if wedge pressure increases, would tend to increase pulmonary edema. Also, because of potential changes in viscosity and pulmonary vascular resistance (PVR), packed red blood cells may not be indicated to increase CO, arterial O2 content and tissue O2 delivery in the setting of ARF. Therapy designed to reduce PVR may be appropriate to increase flow in the setting of increased RV afterload. However, such therapy may also reduce systemic vascular resistance, blood pressure (BP) and RV perfusion pressure. Such changes could lead to RV ischemia and reduced CO. Alternatively, agents which increased RV perfusion and/or contractility will increase CO by reducing RV end-diastolic and end-systolic volumes and may be the treatment of choice to increase flow when RV afterload is elevated.

Aged↗

Right ventricular dysfunction in septic patients.

OBJECTIVE: To compare right ventricular ejection fraction in trauma and septic patients during the hyperdynamic circulatory phase of these states. DESIGN: Prospective, consecutive study. SETTING: University hospital ICU. PATIENTS: Eleven trauma patients (group 1) and ten septic patients (group 2) were studied. Patients with circulatory shock were excluded from the study. INTERVENTIONS: Right ventricular ejection fraction was measured with a modified pulmonary artery catheter using the thermodilution method. Patients requiring catecholamines to maintain a systolic BP greater than 90 mm Hg were excluded from the study. MEASUREMENTS AND MAIN RESULTS: Both groups 1 and 2 had high mean cardiac output values (cardiac indices 4.7 +/- 0.9 [SD] and 4.6 +/- 1.4 L/min/m2, respectively). Right ventricular ejection fraction was significantly (p less than .005) reduced in septic patients (47 +/- 7.0% vs. 36 +/- 9.7%; group 1 vs. group 2) and end-diastolic volume index was significantly (p less than .01) increased (101 +/- 34 vs. 122 +/- 40 mL/m2; group 1 vs. group 2) in comparison with the trauma patients. However, there were no significant differences in afterload between the two groups. CONCLUSIONS: Hemodynamic measurements comparing septic and trauma patients showed increased cardiac output in both groups and no differences in the pulmonary resistance. Right ventricular ejection fraction in the septic patients was significantly reduced compared with the trauma patients. Therefore, we concluded that right ventricular contractility may be decreased in septic patients.

Adult↗

Right ventricular dysfunction and pulmonary obstruction index at helical CT: prediction of clinical outcome during 3-month follow-up in patients with acute pulmonary embolism.

PURPOSE: To retrospectively quantify right ventricular dysfunction (RVD) and the pulmonary artery obstruction index at helical computed tomography (CT) on the basis of various criteria proposed in the literature and to assess the predictive value of these CT parameters for mortality within 3 months after the initial diagnosis of pulmonary embolism (PE). MATERIALS AND METHODS: Institutional review board approval was obtained, and informed consent was not required for retrospective study. In 120 consecutive patients (55 men, 65 women; mean age +/- standard deviation, 59 years +/- 18) with proved PE, two readers assessed the extent of RVD by quantifying the ratio of the right ventricle to left ventricle short-axis diameters (RV/LV) and the pulmonary artery to ascending aorta diameters, the shape of the interventricular septum, and the extent of obstruction to the pulmonary artery circulation on helical CT images, which were blinded for clinical outcome in consensus reading. Regression analysis was used to correlate these parameters with patient outcome. RESULTS: CT signs of RVD (RV/LV ratio, >1.0) were seen in 69 patients (57.5%). During follow-up, seven patients died of PE. Both the RV/LV ratio and the obstruction index were shown to be significant risk factors for mortality within 3 months (P = .04 and .01, respectively). No such relationship was found for the ratio of the pulmonary artery to ascending aorta diameters (P = .66) or for the shape of the interventricular septum (P = .20). The positive predictive value for PE-related mortality with an RV/LV ratio greater than 1.0 was 10.1% (95% confidence interval [CI]: 2.9%, 17.4%). The negative predictive value for an uneventful outcome with an RV/LV ratio of 1.0 or less was 100% (95% CI: 94.3%, 100%). There was a 11.2-fold increased risk of dying of PE for patients with an obstruction index of 40% or higher (95% CI: 1.3, 93.6). CONCLUSION: Markers of RVD and pulmonary vascular obstruction, assessed with helical CT at baseline, help predict mortality during follow-up.

Acute Disease↗

Prevalence and extent of right ventricular dysfunction after myocardial infarction--relation to location and extent of infarction and left ventricular function.

In view of today's efforts to preserve myocardial function in acute myocardial infarction, the prevalence and extent of persistent right ventricular dysfunction was analysed in a prospective study of 127 patients admitted with a first myocardial infarction without thrombolysis. Right ventricular ejection fraction measured at hospital discharge by radionuclide angiocardiography was related to the location of infarction as judged electrocardiographically, its size as estimated enzymatically, and by the simultaneously measured left ventricular ejection fraction. Two opposite patterns of right and left ventricular function were observed in relation to the location of infarction: the right ventricular ejection fraction was significantly depressed in inferior, but not in anterior, infarction and the reverse was true for left ventricular ejection fraction (P less than 0.001 between infarct locations for both right ventricular ejection fraction and left ventricular ejection fraction). There were significant correlations between peak levels of creatine kinase and left ventricular ejection fraction for anterior (r = 0.76, P less than 0.001) and inferior (r = 0.57, P less than 0.001) infarction, while peak levels of creatine kinase and right ventricular ejection fraction correlated only in inferior infarction (r = 0.45, P less than 0.01). There was no overall correlation for left ventricular ejection fraction and right ventricular ejection fraction (r = 0.28, P NS), despite the fact that right ventricular ejection fraction was lower in patients with severely reduced left ventricular ejection fraction than in those with normal left ventricular function (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Cardiac troponin I elevation in acute pulmonary embolism is associated with right ventricular dysfunction.

OBJECTIVES: The purpose of this study was to evaluate the prevalence and diagnostic utility of cardiac troponin I to identify patients with right ventricular (RV) dysfunction in pulmonary embolism. BACKGROUND: Right ventricular overload resulting from elevated pulmonary resistance is a common finding in major pulmonary embolism. However, biochemical markers to assess the degree of RV dysfunction have not been evaluated so far. METHODS: In this prospective, double-blind study we included 36 study patients diagnosed as having acute pulmonary embolism. RESULTS: Among the whole study population, 14 patients (39%) had positive troponin I tests. Ten of 16 patients (62.5%) with RV dilatation had increased serum troponin I levels, while only 4 of 14 patients (28.6%) with elevated troponin I values had a normal RV diameter as assessed by echocardiography, indicating that positive troponin I tests were significantly associated with RV dilatation (p = 0.009). Patients with positive troponin I tests had significantly more segmental defects in ventilation/perfusion lung scans than patients with normal serum troponin I (p = 0.0002). CONCLUSIONS: Our data demonstrate that more than one-third of patients clinically diagnosed as having pulmonary embolism presented with elevated serum troponin I concentrations. Troponin I tests helped to identify patients with RV dilatation who had significantly more segmental defects in lung scans. Thus, troponin I assays are useful to detect minor myocardial damage in pulmonary embolism.

Acute Disease↗

Right ventricular dysfunction and pulmonary valve replacement after correction of tetralogy of Fallot.

BACKGROUND: Correction of tetralogy of Fallot often leads to pulmonary regurgitation, sometimes warranting pulmonary valve replacement, for which indications and timing to achieve optimal results are not yet clear. This retrospective study describes follow-up and reinterventions in our tetralogy of Fallot population. METHODS: Review of all consecutive patients operated on for tetralogy of Fallot between 1977 and 2000 was conducted. Included are date and type of repair, Doppler echocardiography (two-dimensional echocardiography), electrocardiographs, reoperations, and physical condition. RESULTS: Total repair was performed in 171 patients at a mean age 1.9 +/- 2.5 years, follow-up time counted 9.6 +/- 7.0 years. Right ventriculotomy was used in 92%, and transatrial ventricular septal defect closure was used in 8%; 74% received a transannular outflow patch. Twenty-year survival was 91%. Last follow-up electrocardiographs showed right bundle branch block in 67% and serious arrhythmias in 11%. Two-dimensional echocardiography demonstrated severe pulmonary insufficiency and dilated right ventricle in 31% and 38%, respectively, increasing with postrepair age (p < 0.001). Poor clinical condition (New York Heart Association class II+) and echocardiographic proof of right atrial dilatation (p = 0.012) and arrhythmias (p = 0.03) were significantly associated. Furthermore, the influence of residual hemodynamic lesions, such as a remaining ventricular septal defect or pulmonary stenosis, or right ventricular dilatation was important (p = 0.04). Reintervention was necessary in 32 patients (19%; 10-year freedom, 83%), including angioplasty for residual stenosis and pulmonary valve replacement. At a mean age of 9.2 years after correction, 14 patients received a homograft, and 2 patients received a heterograft. In 7 patients the right ventricle returned to normal dimensions and symptoms disappeared. The incidence of right ventricular dilatation was considerably higher (p = 0.020) in patients with a transannular patch; the transatrial approach showed the opposite (p = 0.03), and patients presented with lower QRS duration (p = 0.007), although no difference could be found between survival after both surgical techniques. Effects of early timing (correction < 6 months) on right ventricular dysfunction could not be established. CONCLUSIONS: Severe right ventricular dilatation and pulmonary regurgitation secondary to outflow tract repair in tetralogy of Fallot are frequently occurring sequelae developing slowly over time. Indications for pulmonary valve replacement remain controversial because echocardiographic findings or arrhythmias are not always accompanied by deterioration of clinical condition. However, right atrial dilatation and additional hemodynamic lesions demand increased vigilance. Transatrial repair is associated with a favorable outcome.

Adolescent↗

Right ventricular dysfunction in chronic heart failure patients.

AIM: To evaluate any differences in haemodynamic and echocardiographic parameters in patients with both left (LV) and right ventricular (RV) systolic dysfunction and in patients with isolated LV systolic dysfunction. STUDY GROUP: One hundred patients with RV systolic dysfunction defined as peak velocity of tricuspid annular motion in systole (Sa)<11.5 cm/s, and 55 patients without RV systolic dysfunction Sa>11.5 cm/s. All patients had LV systolic dysfunction, LV ejection fraction (EF) below 40%, NYHA II-IV. METHODS: LV diameters, volumes and EF were measured by echocardiography. Patients underwent tissue Doppler imaging (TDI) of tricuspid annular motion with measurement of peak systolic velocity (Sa), peak early (Ea) and peak late (Aa) diastolic velocities. Right heart catheterization was also performed. RESULTS: Patients with RV systolic dysfunction did not differ from those without RV systolic dysfunction in terms of LV function. Patients with RV systolic dysfunction had larger RV dimension 30.6+/-5.8 vs. 33.9+/-6.7 mm, p<0.002. The patients with RV systolic dysfunction had higher values on right heart catheterization: MPAP 29.6+/-12.1 vs. 24.9+/-11.4 mm Hg, p<0.02, PCWP 20.8+/-10.0 vs. 17.3+/-9.3 mm Hg, p<0.03, PVR 189.9+/-123.3 vs. 137.7+/-94.9 dyn s cm(-5), p<0.008, CVP 7.7+/-5.6 vs. 5.1+/-3.9 mm Hg, p<0.002. The patients with RV systolic dysfunction had more pronounced diastolic dysfunction measured by TDI: Ea 9.9+/-2.3 vs. 11.4+/-2.5 cm/s, p<0.0001 and Aa 13.1+/-4.0 vs. 16.5+/-4.7 cm/s, p<0.000007. CONCLUSION: Patients with heart failure and both left and right ventricular systolic dysfunction showed more serious findings on central haemodynamics as well as more pronounced right ventricular diastolic dysfunction than those with isolated left ventricular systolic dysfunction.

Female↗

Scintigraphically detected predominant right ventricular dysfunction in acute myocardial infarction: clinical and hemodynamic correlates and implications for therapy and prognosis.

To determine the clinical and hemodynamic correlates as well as therapeutic and prognostic implications of predominant right ventricular dysfunction complicating acute myocardial infarction, 43 consecutive patients with scintigraphic evidence of right ventricular dyssynergy and a depressed right ventricular ejection fraction (less than 0.39) in association with normal or near normal left ventricular ejection fraction (greater than or equal to 0.45) were prospectively evaluated. All 43 patients had acute inferior infarction, forming 40% of patients with acute inferior infarction, and only eight (24%) had elevated jugular venous pressure on admission. On hemodynamic monitoring, 74% of patients had a depressed cardiac index (less than or equal to 2.5 liters/min per m2), averaging 2.0 +/- 0.05 for the group. Of these, 30% did not demonstrate previously described hemodynamic criteria of predominant right ventricular infarction (right atrial pressure greater than or equal to 10 mm Hg or right atrial to pulmonary capillary wedge pressure ratio greater than or equal to 0.8, or both). The left ventricular end-diastolic volume was reduced to 49 +/- 11 ml/m2 (n = 22) and correlated significantly with the stroke volume index (r = 0.82; p less than 0.0001) and cardiac index (r = 0.57; p = 0.005). The follow-up right ventricular ejection fraction, determined in 33 patients, showed an increase of 10% or greater in 26 (79%), increasing from a mean value of 0.30 +/- 0.06 to 0.40 +/- 0.09 (p less than 0.0001) without a significant overall change in the mean left ventricular ejection fraction (0.56 +/- 0.10 to 0.56 +/- 0.11, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

Right ventricular dysfunction in advanced heart failure.

For many years cardiologists were not interested in studying right ventricular function and the role of the right ventricle in heart failure and in other disease states has therefore been largely underestimated. More recently a consensus has grown on the critical role of right ventricular function in patients with advanced congestive heart failure. The estimation of right ventricular function is nowadays warranted in the standard evaluation of patients with heart failure either due to ischemic heart disease or to primary dilated cardiomyopathy, since it is helpful in the clinical assessment and in the prognostic stratification of such patients. Most information may be obtained non-invasively using sound but simple and reproducible echocardiographic indicators of right ventricular function.

Disease Progression↗