Ventricular Free Wall Motion Research Articles

Right ventricular free wall motion abnormalities as a simple method of assessment in patients with pulmonary hypertension (RCD code: II 1A.O)

Background : Pulmonary hypertension (PH) is a cardiovascular pathology leading to right-sided heart failure. A qualitative assessment of right ventricular (RV) function in echocardiography provides valuable information on a patient’s condition. The standard echocar- diographic parameter, assessed in PH patients, is RV free wall motion. Aim : To verify the utility of RV free wall motion assessment via echocardiography in PH patients. Methods : Data from 30 PH patients, regardless of aetiology (except for left heart disease), was retrospectively analyzed. Based on the RV free wall motion visual echocardiographic assessment the population was divided into: group 1- normokinetic; group 2- hypokinetic RV. All patients underwent a medical interview, physical examination, basic laboratory work-up, echocardiography, and right heart catheterization (RHC). Twenty-one patients underwent a cardiopulmonary exercise test (CPET). Results : The analysis revealed, that patients with RV free wall hypokinesis were characterized by impaired gas exchange parameters (higher values of ventilatory equivalents for oxygen and carbon dioxide, higher end-tidal oxygen pressures, lower end-tidal carbon dioxide pres- sures and higher minute ventilation – carbon dioxide production relation slope) and cardiovascular response to exercise (lower increase in O2 pulse during exercise) obtained in the CPET. RHC showed that patients with hypokinetic RV had higher diastolic and mean pul- monary artery pressures (dPAP, mPAP), lower cardiac index, and higher pulmonary vascular resistance. Conclusions : RV free wall motion abnormalities, assessed using echocardiography in PH patients, are found in those with more advanced disease. They are characterized by impaired ventilation in the CPET and more advanced haemodynamic abnormalities in RHC. The association between this parameter and prognosis requires validation in a larger population of patients. JRCD 2017; 3 (5): 161–167

Left ventricular systolic dysfunction is associated with adverse outcomes in acute right ventricular infarction.

In patients with acute right ventricular infarction (RVI), global right ventricular (RV) performance is dependent on compensatory left ventricular (LV)-septal contractile contributions. This study was designed to assess the influence of depressed left ventricular ejection fraction (LVEF) on hemodynamics and clinical outcomes in patients with RVI. We retrospectively identified 338 patients with acute inferior ST elevation myocardial infarction (STEMI) undergoing a primary percutaneous coronary intervention. RVI was determined echocardiographically by right ventricular free wall motion abnormalities and depressed global RV performance (fractional area change); LV function was similarly calculated. RVI was documented in 185 (55%) cases. Compared with those with inferior myocardial infarction alone, patients with RVI suffered more hemodynamic compromise (need for inotropes or vasopressors 39 vs. 15%, P<0.0001, and intra-aortic balloon pump 32 vs. 13%, P<0.0001) and higher in-hospital mortality (14 vs. 3%, P=0.0006). In cases without RVI, the status of LV function did not influence in-hospital mortality (ejection fraction≤40%=7.3% vs. ejection fraction>40%=1.8, P=0.12). In contrast, in patients with RVI, LVEF was an important determinant of outcome: those with LVEF ≤ 40% suffered more hemodynamic compromise (need for inotropes or vasopressors 63 vs. 30%, P<0.0001, and intra-aortic balloon pump 59 vs. 22%, P<0.0001) and had markedly higher in-hospital mortality (33 vs. 7%, P<0.0001). In patients with acute inferior myocardial infarction complicated by RVI, depressed LVEF is associated with greater hemodynamic compromise and higher in-hospital mortality. These findings may have clinical implications for supportive efforts in such cases.

Characteristics of right ventricular free wall motion in young patients with ventricular arrhythmia, a cardiac MRI study

Background Right ventricular (RV) regional wall characteristics are important in CMR evaluation for arrhythmogenic RV dysplasia (ARVD). While some features are well defined, others are of uncertain clinical significance, due in part, to the high prevalence of RV wall motion variants found in normal subjects. In this study we performed a retrospective review of RV free wall characteristics in a large cohort of young patients referred for ventricular arrhythmia evaluation and compared the findings with an age-matched normal cohort. Methods The study consisted of 159 consecutive patients aged 18 to 49 years referred for CMR due to ventricular arrhythmias and 51 age-matched normal controls. All subjects underwent CMR. Cine images of the 4-chamber view were reviewed to characterize the RV wall motion as having bulge or outpouching at end systole or at end diastole. The bulges were further classified by location, size and relationship to the moderator band. The size of bulges were graded as small (≤0.5 cm 2 ), moderate (0.5 1c m 2 ) and large (> 1 cm 2 ). Results Mean age was 38 years. Of the 159 patients, 62 (39%) presented with premature ventricular contractions (PVCs) and 97 (61%) with ventricular tachycardia (VT). There was no significant difference in RV size and function between patients and controls. Diastolic bulges were most common in the VT group (10 cases, 10%), rare in PVC and control group (1 case each, 2%). Large diastolic bulges were present only in 6 VT group cases. Systolic bulges were more common, with 11/51 (22%) in normal control, 5/62 (8%) in PVC group and 20/97 (21%) in VT group. All systolic bulges in the control group were small while bulge size was mainly moderate in the PVC group (4/5) and large bulges were only present in the VT group (4/20). All systolic bulges were in close proximity to a moderator band in the control group but 6/34 (18%) were not in the arrhythmic groups. Basal location is uncommon but 5 of 6 cases were found in the VT group, 1 in the PVC group and none in the control group. Conclusions RV characteristics that are predominantly associated with VT include bulges or outpouchings present in diastole, basal location, large size and in the absence of a relation to the moderator band. Our findings suggest that risk stratification of ventricular arrhythmia should consider those RV features particularly in cases where the diagnostic criteria of ARVD are unmet. Funding None.

Ultrasound and magnetic resonance imaging in the assessment of a fetal intracardiac mass

We report on a 29-year-old Caucasian woman who had a routine anomaly scan performed at 20 weeks' gestation. Fetal echocardiography demonstrated an enlarged, echogenic and homogeneous interventricular septum measuring 10 × 10 mm in diameter (Figure 1). There was a reduction in the size of each ventricular cavity, the left ventricle was slit-like and the right ventricle was apically truncated. The arterial relationship was normal and there was no evidence of outflow tract obstruction. There was good ventricular function in systole and diastole. The fetus was not hydropic and Doppler ultrasound examination showed no abnormalities in the ductus venosus. Ultrasound examination showing transverse section of the fetal thorax with an enlarged ventricular septum at 20 weeks' gestation. The diagnosis was that of a cardiac tumor. Other much less likely diagnoses included hypertrophic cardiomyopathy and hypertrophy secondary to a distal obstructive lesion. History and clinical examination were negative for tuberous sclerosis. Invasive testing for metabolic disorders such as Pompe's disease was declined by the patient. At 28 weeks' gestation, magnetic resonance imaging (MRI) was performed. MRI demonstrated a hyperintense well circumscribed mass measuring 30 × 24 × 20 mm (Figure 2). Its signal was much higher than that of the surrounding myocardium, supporting the diagnosis of a tumor rather than hypertrophy. Magnetic resonance images of (a) transverse and (b) sagittal sections of the fetal thorax, showing the interventricular tumor at 28 weeks' gestation. Ultrasound examination at 30 weeks' gestation demonstrated a severe reduction in biventricular cavity size with a narrow and distorted left ventricular outflow tract. There was reduced left ventricular free wall motion. There was no evidence of hydrops. It was felt that elective delivery should be delayed until after 34 weeks' gestation. Thereafter, surgical resection of the fetal tumor could be considered. However, at 32 weeks' gestation intrauterine fetal death was confirmed. Labor was induced and a stillborn 2165-g female fetus was delivered vaginally. At postmortem examination, fetal biometry was consistent with gestational age and the fetus was non-dysmorphic. The body weight to heart weight ratio indicated that the heart was three times the normal weight. The interventricular septum contained a 3 × 2-cm non-encapsulated tumor (Figure 3). Histologically, the tumor had a heterogeneous structure: a vascularized mesodermal tumor with central calcification and necrosis. These findings were consistent with a fibroma. The site of the tumor made it probable that the cause of fetal death was cardiac arrhythmia rather than obstruction of the outflow tract. Gross pathological specimen at postmortem examination showing the ventricular tumor. Fetal cardiac tumors are rare. The most common type is rhabdomyoma1. Its typical appearance on ultrasound examination is of multiple hyperechogenic, well circumscribed, homogeneous masses in the ventricular wall or interventricular septum2. Fibromas are the second most common tumor. These are usually found as solitary masses and are seen on ultrasound examination as hyperechoic lesions often associated with calcification and cystic degeneration3. Fibromas often involve the interventricular septum and cause death by ventricular arrhythmia owing to local compression of the conduction system4. In general, the management of fetal cardiac tumors is conservative. The approach is to optimize neonatal outcome while avoiding iatrogenic premature delivery. Certain lesions may be amenable to surgical resection following delivery. In cases where the tumor is intracardiac, therapeutic options are limited and the prognosis is poor5. Fetal MRI has been used increasingly to confirm equivocal ultrasound findings. It is seldom employed to assess the heart6-8 and some authors believe that MRI is not useful9. In the case described here, fetal MRI was of value as it demonstrated a single, well circumscribed lesion in the interventricular septum. This appearance was consistent with the diagnosis of a tumor and helped exclude cardiomyopathy or hypertrophy secondary to a distal obstructing lesion. Although making the correct antenatal diagnosis did not alter the outcome, this case does demonstrate the evolving role of MRI. However, real-time ultrasound examination will remain invaluable in assessing cardiac function. It is likely that in future both MRI and ultrasound modalities will be used in combination to make a diagnosis and delineate prognosis. S. Ong*, M. Usher-Somers*, S. Philip , P. Miller?, K. Foster?, T. Marton , W. Martin*, M. Kilby*, * Fetal Medicine Department, Birmingham Women's Hospital, B15 2TG, UK, Department of Pathology, Birmingham Women's Hospital, B15 2TG, UK, Department of Obstetrics, City Hospital, Birmingham, UK, ? Department of Cardiology, Birmingham Children's Hospital, Birmingham, UK, ? Department of Radiology, Birmingham Children's Hospital, Birmingham, UK

Midterm Clinical and Echocardiographic Results With Patch Glue Repair of Left Ventricular Free Wall Rupture

Left ventricular free wall rupture (LVFWR) is a dramatic complication after myocardial infarction. We present our mid-term clinical and echocardiographic results of LVFWR with an epicardial patch without cardiopulmonary bypass. From February 1993 to May 2001, 17 patients underwent surgery for LVFWR. The mean age+/-SD of 12 males and 5 females was 68+/-10 years. All patients presented for emergency surgery with cardiac tamponade confirmed on echocardiography. After opening the chest and identification of the site of rupture, a Goretex patch was fashioned and applied with enbucrilate surgical glue. Effective control of bleeding was achieved in all cases. There were no on-table deaths. The operative (30 day) mortality was 23.5% (4/17). One death occurred because of patch failure, two because of cardiogenic shock, and one from pneumonia. On follow-up at a median of 2.2 years (interquartile range, 1.1 to 4.3 years), two further deaths occurred, one from myocardial infarction and another of undetermined etiology. Echocardiography did not reveal any evidence of restriction to left ventricular free wall motion. Patch glue repair is expedient, simple and effective; with no adverse effects on mid-term ventricular dynamics. In view of superior published results to infarctectomy and repair with extra corporeal circulation, it should be considered to be the initial procedure of choice for the surgical repair of LVFWR.

Complete reversal of ischemic wall motion abnormalities by combined use of gene therapy with transmyocardial laser revascularization

Introduction:Transmyocardial laser revascularization is believed to induce an angiogenic response within ischemic myocardium. We evaluated transgene expression in the setting of transmyocardial laser revascularization and hypothesized that intramyocardial injection of plasmid DNA encoding the gene for vascular endothelial growth factor could enhance the revascularization achieved by transmyocardial laser revascularization, resulting in improved cardiac function. Methods: Ten Yorkshire pigs had carbon dioxide–transmyocardial laser revascularization or acupuncture sites with injections of an expression plasmid encoding the gene for β-galactosidase with or without HVJ-liposomes. Three days after transduction, transgene expression was determined by enzyme-linked immunosorbent assay. Six weeks after placement of a constrictor on the left circumflex artery, 29 pigs were randomized to ischemic controls (n = 5), transmyocardial laser revascularization (n = 4), transmyocardial laser revascularization with expression plasmid β-galactosidase injections (n = 5), expression plasmid-vascular endothelial growth factor injections (n = 4), or transmyocardial laser revascularization with expression plasmid-vascular endothelial growth factor (n = 5) and harvested 6 weeks after therapy. Six transmyocardial laser revascularization pigs had either expression plasmid β-galactosidase or expression plasmid-vascular endothelial growth factor injections and were harvested at 2 weeks. Normal pigs (n = 5) were included for comparison. Left ventricular free wall motion was assessed by a cardiologist in a blinded manner. Results: Transgene expression did not vary significantly with or without HVJ-liposomes in transfected transmyocardial laser revascularization myocardium. However, expression was detected in 56 of 60 (93%) transmyocardial laser revascularization–transfected sites, but in only 10 of 20 (50%) non-transmyocardial laser revascularization sites ( P < .001). All (5 of 5 hearts) of the transmyocardial laser revascularization–vascular endothelial growth factor treated hearts displayed no evidence of wall motion abnormalities. Only these hearts had a statistically significantly different rate of wall motion abnormality compared with ischemic controls ( P = .004). Conclusion: Transfection efficiency was improved with the use of transmyocardial laser revascularization. Wall motion abnormalities were completely reversed within 6 weeks after transmyocardial laser revascularization with the direct injection of an expression plasmid encoding vascular endothelial growth factor. (J Thorac Cardiovasc Surg 1998;116:763-9)

Nature of ventricular activation in patients with dilated cardiomyopathy: evidence for bilateral bundle branch block.

To investigate the nature of ventricular activation and its relation with mechanical events in patients with dilated cardiomyopathy. Retrospective and prospective study with 12 lead electrocardiograms, signal averaged electrocardiograms, and M mode and Doppler echocardiograms. Tertiary cardiac referral centre. 77 patients (mean (SD) age 59(13)) with dilated cardiomyopathy, four after aortic valve replacement and three after coronary bypass surgery, and six patients with a normal sized left ventricle and complete right bundle branch block were studied. 15 normal subjects (age 45(20)) were used as controls. In patients with dilated cardiomyopathy, QRS duration was longer (127(25) ms v 90(10), P < 0.05) than normal and was normally distributed (r = 0.991, P < 0.01) on a normal probability plot. 20 had classic left bundle branch block, 29 intraventricular conduction delay, four right bundle branch block, and one bifascicular block. The PR interval was prolonged (185(30) ms v 150(15), P < 0.05). Electromechanical delay, Q to the onset of thickening of the interventricular septum as seen on the transverse M mode echocardiogram, was 75(15) ms in controls, but reduced to 43(15) ms in the patients (P < 0.01). Q to the onset of mitral regurgitation was also short (50(15)) ms, and correlated inversely with PR interval (r = -0.67, n = 73, P < 0.01). Early potentials (< 40 microV) were recorded on the signal averaged electrocardiogram in 33 representative patients and in all controls. Their overall duration was 30(12) ms in the patients, much longer than normal (12(7), P < 0.01)). Early potential time correlated positively with PR interval (r = 0.75, P < 0.01) and QRS duration (r = 0.60, P < 0.01) on a 12 lead electrocardiogram, and negatively with apparent electromechanical delay (r = -0.71, P < 0.01, n = 33), but not with true electromechanical delay (73(15)ms) or true PR interval (163(30)ms), calculated by correcting apparent values for early potential. The onset of left ventricular free wall motion was delayed with respect to the septum beyond 95% of the upper normal limit in all the patients with classic left bundle branch block and intraventricular conduction defect. Motion in the right ventricular free wall was delayed in 13 of 20 patients with left bundle branch block and 24 of 29 with intraventricular conduction defect by 65(20) ms, similar to that (75(10) ms) in patients with right bundle branch block. In most patients with dilated cardiomyopathy and an electrocardiographic pattern of left bundle branch block or intraventricular block, the onset of mechanical systole is strikingly and symmetrically delayed in both ventricles, compatible with bilateral bundle branch block. Complete atrioventricular block does not occur. The ventricle is activated through the upper septum and this activation is detectable only by signal averaged electrocardiography. The anatomical substrates for this abnormal activation could be the high connections described by Mahaim and Winston.

Re-evaluation of normal splitting of the second heart sound in patients with classical left bundle branch block

To study the mechanism of normal splitting of the second heart sound in patients with classical left bundle branch block, we investigated 43 such patients and 15 normal controls, using electro-, phono- and echo-cardiography and comparing the relative timing of mechanical activity in the two ventricles. The splitting of the second heart sound is reversed in only two-thirds of the patients and normal in remaining one-third. Comparing patients with and without reversed splitting, there are no significant differences in left ventricular cavity size, heart rate, pre-ejection period and the distribution of age, gender, or aetiology. QRS duration is longer ( P < 0.01) in patients with reversed splitting. Diastolic events of the left ventricle do not differ between groups. The onset of the left ventricular free wall motion is delayed compared with normal by a similar extent in the two groups. In patients with normal splitting, the onset of the right ventricular wall motion is also delayed, both with respect to normal and to those with reversed splitting to an extent similar to that seen in classical right bundle branch block. Normal splitting of the second heart sound associated with an electrocardiographic pattern of left bundle branch block therefore suggests bilateral block. This combination can be documented from the precise timing of the movement of the two ventricles by M-mode echocardiography and identified by simple auscultation.

Determinants of the recovery of right ventricular performance following experimental chronic right coronary artery occlusion.

Patients with acute ischemic right ventricular dysfunction often develop hemodynamic compromise, yet most manifest spontaneous early clinical improvement and later recovery of global right ventricular performance. This study was designed to delineate the determinants of right ventricular performance following chronic right coronary artery occlusion. Thrombotic right coronary artery occlusion was induced in 16 closed-chest dogs. Acute occlusion depressed right ventricular free wall motion (motion score, 1.0 +/- 0.0 to 3.4 +/- 0.1*) and global performance (right ventricular fractional area change, 29.2 +/- 1.8% to 2.3 +/- 1.9%*). There was right ventricular dilatation and reversed septal curvature, with elevated and equalized diastolic filling pressures. At 5 days, despite persistent severe right ventricular free wall dysfunction (motion score, 3.4 +/- 0.1 to 2.7 +/- 0.1*), global right ventricular performance improved (fractional area change, 2.3 +/- 1.9% to 17.0 +/- 3.8%*), in part due to reduced right ventricular free wall dyskinesis associated with increased right ventricular free wall end-diastolic thickness. At 7 weeks, collateral flow had restored right ventricular free wall perfusion to baseline values. The increased right ventricular free wall thickness had resolved, right ventricular free wall motion was improved (2.7 +/- 0.1 to 1.6 +/- 0.1*), and global right ventricular performance had recovered further (17.0 +/- 3.8 to 20.9 +/- 0.9). Right ventricular dilatation was reduced, septal curvature normalized, and there was resolution of equalized filling pressures. Histopathological analysis demonstrated minimal right ventricular infarction. Acute right coronary artery occlusion results in right ventricular free wall dyskinesis and depressed global right ventricular performance. Global right ventricular function improves early, in part due to reduced right ventricular free wall dyskinesis associated with increased right ventricular free wall diastolic thickness. Collateral restoration of perfusion facilitates late recovery of right ventricular free wall function (*P < .05).

Right Ventricular Infarction: Recognition and Assessment of its Hemodynamic Significance by Two-dimensional Echocardiography

To evaluate the ability of two-dimensional echocardiographic indexes to determine the hemodynamic significance of the right ventricular infarction, 24 patients with electrocardiographic evidence of right ventricular infarction were studied. Hemodynamic significance was defined as a jugular venous pressure greater than 17 cm H2O or a right atrial pressure greater than 13 mm Hg. Patients with hemodynamically significant right ventricular infarctions (group I, n = 9) had a 56% incidence of hypotension (blood pressure less than 90 mm Hg) with a mean systolic blood pressure of 93 +/- 23 mm Hg, whereas patients with nonhemodynamically significant right ventricular infarctions (group II, n = 15) had no hypotension and a mean systolic blood pressure of 121 +/- 18 mm Hg (p less than 0.01). The ratio of right atrial to pulmonary capillary wedge pressure was 1.1 +/- 0.6 in group I and 0.6 +/- 0.2 in group II (p less than 0.05). Echocardiography demonstrated right ventricular free wall motion abnormalities in seven patients in group I and in 10 patients in group II. The descent of the right ventricular base was 0.7 +/- 0.2 cm in group I, 1.3 +/- 0.4 cm in group II, and 2.0 +/- 0.2 cm in a group of 20 normal control patients (p less than 0.001 for all comparisons). The respiratory caval index (percentage of collapse of the inferior vena cava with inspiration) was 22% +/- 11% in group I, 45% +/- 15% in group II, and 64% +/- 17% in the control subjects (p less than 0.05 for all comparisons).(ABSTRACT TRUNCATED AT 250 WORDS)

Chronic effects of myocardial infarction on right ventricular function: A noninvasive assessment

To assess the chronic effects of myocardial infarction on right ventricular function, 48 subjects were studied utilizing radionuclide angiography and two-dimensional echocardiography. Ten were normal subjects (group I), 11 had previous inferior wall myocardial infarction (group II), 10 had previous anteroseptal infarction (group III), 11 had combined anteroseptal and inferior infarction (group IV) and 6 had extensive anterolateral infarction (group V). The mean (+/- standard deviation) left ventricular ejection fraction was 0.66 +/- 0.03 in group I, 0.58 +/- 0.02 in group II, 0.52 +/- 0.02 in group III, 0.33 +/- 0.03 in group IV and 0.33 +/- 0.01 in group V. No systematic correlation between left and right ventricular ejection fraction was observed among the groups. The mean right ventricular ejection fraction was significantly reduced in the presence of inferior myocardial infarction (0.30 +/- 0.03 in group II and 0.29 +/- 0.03 in group IV compared with 0.43 +/- 0.02 in group I [p less than 0.001]). The group II and IV patients also had increased (p less than 0.001) right ventricular end-diastolic area and decreased (p less than 0.001) right ventricular free wall motion by two-dimensional echocardiography. In the presence of anteroseptal infarction (group III), right ventricular free wall motion was increased (p less than 0.05) compared with normal subjects (group I). Thus, the effects of prior myocardial infarction on right ventricular function depend more on the location of infarction than on the extent of left ventricular dysfunction. Inferior infarction was commonly associated with reduced right ventricular ejection fraction and increased right ventricular end-diastolic area. The right ventricular free wall excursion was increased in the presence of anteroseptal infarction, suggested loss of contribution of interventricular septal contraction to right ventricular ejection.

Diastolic collapse of the right ventricle with cardiac tamponade: an echocardiographic study.

The value of a newly described echocardiographic sign for the detection of cardiac tamponade was retrospectively evaluated in 91 patients. M-mode echocardiograms were reviewed in 86 patients, 36 of whom had concurrent two-dimensional echocardiographic examinations; in five patients, only two-dimensional echocardiography was performed. Cardiac tamponade was clinically present in 17 patients, 14 of whom had abnormal posterior motion of the right ventricular free wall in early diastole. Two of the 17 patients with tamponade had equivocally abnormal motion and one had normal wall motion. The patient with normal wall motion was later proved to have predominantly constrictive pericardial disease. In all cases, the abnormal wall motion reverted to normal after a definitive drainage procedure. Two-dimensional echocardiography confirmed that the abnormal right ventricular wall motion represented a true collapse of the right ventricular cavity in early diastole. Of the 69 patients without clinical cardiac tamponade, only seven had abnormal right ventricular wall motion. Detection of abnormal diastolic right ventricular free wall motion may be a sensitive indicator or a hemodynamically significant pericardial effusion. Conversely, the presence of normal motion of the right ventricular free wall appears to be a reliable indicator that the pericardial effusion is exerting little effect on overall cardiac function.

Angiocardiographic differentiation of constrictive pericarditis and restrictive cardiomyopathy due to amyloidosis

The cineangiocardiograms and coronary angiograms of two cases of amyloidosis of the heart were compared to six cases of constrictive pericarditis. Three angiographic differentiating points were seen: (1) right ventricular free wall motion showed diastolic restriction in both disorders, whereas the crista supraventricularis, which moved normally in constrictive pericarditis, demonstrated restriction in amyloidosis; (2) ventricles in cases of constrictive pericarditis showed subtle further expansion during atrial systole after initial rapid filling (atrial kick), while in both cases of amyloidosis there was no motion during atrial systole; (3) pericardial thickening in constrictive pericarditis was demonstrated by failure of the distal coronary arteries to reach the surface of the cardiac image. In amyloidosis, the distal coronary arteries normally reached the periphery of the image. All three signs may be useful in differentiation, but the first is the easiest to evaluate. The right anterior oblique or posteroanterior view is the recommended projection.