Copyright © 2005, The European Society of Cardiology
Echocardiographic diagnosis of pulmonary embolism: a rise and fall of McConnell sign?
Department of Internal Medicine, National Institute for Lung Diseases, Ul Plocka 26, 01-138 Warsaw, Poland
* Tel.: +48 22 691 2114; fax: +48 22 691 2414. torbi{at}pol.pl
Please see page 11 for the article by Casazza et al. (doi: 10.1016/j.euje.2004.06.002) to which this editorial pertains.
Formally, the place of echocardiography in diagnostic assessment of patients with suspected pulmonary embolism is neither strong nor definitely established. In recent guidelines of British Thoracic Society transthoracic echocardiography is hardly mentioned.1 However, there is a universal agreement, that in an acutely unstable patient echocardiography may be highly suggestive of PE. In such an emergency case thrombolysis may be justified if other diagnostic test would result in additional risk or in delay of treatment. This approach had been formally accepted by a multidisciplinary ESC Task Force and published in the ESC Guidelines in 2000.2
Admittedly, in the majority of cases echocardiography provides only indirect signs of PE, predominantly consisting of signs of RV pressure overload. Such signs have been reported to be reasonably specific for PE in patients without prior cardio-respiratory diseases. In the largest study published so far Nazeyrollas et al. used the RV/LVEDD>0.5 (parasternal M-mode echo) and tricuspid insufficiency (TI) with a jet velocity>2.5m/s as diagnostic criteria. They reported a sensitivity of 93% with a specificity of 81% in 137 patients free from known cardio-respiratory disease.3 Unfortunately, in real life we often deal with patients known or suspected of having previous cardio-respiratory problems.
There were a few attempts to validate diagnostic signs which could be specific in an unselected population of patients with suspected acute PE.
Among those, "McConnell sign" defined as right ventricular (RV) free wall hypokinesis in the presence of normal RV apical contractility has been studied. It was originally suggested as a useful criteria for the diagnosis of acute PE mostly because it was observed in the setting of acute but not chronic pulmonary hypertension.4 In this issue of the European Journal of Echocardiography, Casazza et al. reassessed the McConnell sign in a different clinical setting. A retrospective blinded study and comparison of two-dimensional echo recordings of patients with acute PE and acute RV infarction were performed. The data show that the previously described abnormal pattern of regional RV contractility does not allow to differentiate between those two conditions. In fact RV wall motion abnormalities in acute PE are virtually identical to those observed in acute RV infarction. As in the original report on McConnell's sign, Casazza and colleagues were also unable to give a clear explanation of the cause of preserved RV apical contractility in acute pulmonary embolism and RV infarction.
Should this mean that the diagnostic value of McConnell's sign in acute PE should be questioned or abandoned? Not necessarily: the simplest solution would be to accept that to be of diagnostic value McConnell's sign should be associated with signs of RV pressure overload such as increased tricuspid jet velocity as assessed by Doppler echocardiography. While not explicitly stated in the original McConnell's report such definition seems logical and would be helpful in the differential diagnosis between acute PE and RV infarction.
Admittedly, in clinical practice the regurgitant tricuspid jet waveform is not always clearly seen, and this may create a problem especially because the jet velocity in sub-massive and massive PE is often only mildly to moderately increased. Therefore, it maybe useful to look at a somewhat forgotten sign of right ventricular afterload based on the flow velocity pattern of RV ejection into main pulmonary artery. Early echo-Doppler reports include many data and excellent correlations between time from onset to peak flow velocity (acceleration time, AcT) and pulmonary arterial pressure. These non-invasive estimations of mean pulmonary arterial pressure based on AcT did not withstand the test of time, however. Yet, flow velocity pattern during RV ejection contains potentially useful information about its true afterload under conditions of pulsatile flow hemodynamics.5 The short acceleration time and mid-systolic deceleration of flow velocity in the RV outflow tract are predominantly caused by increased pulmonary arterial input impedance and the premature return of reflected pressure waves.6 This is why the flow velocity curve is disturbed not only in severe chronic pulmonary hypertension but also in acute pulmonary embolism. In the latter situation forward pressure waves are probably reflected by intraluminar emboli lodged in pulmonary arteries and therefore return very early despite only mild to moderate elevation of pulmonary arterial pressure. In fact an echocardiographic sign ("60/60 sign") based on those mechanisms and tested in a prospective trial enrolling unselected population was found to be highly specific for the diagnosis of acute PE.7
When comparing both, McConnell's and "60/60 sign" (acceleration time below 60ms in the presence of TIPG above 30 but below 60mmHg) they both showed a low sensitivity and high specificity in diagnosing acute PE. However, rather than confronting those two signs it would be more useful to combine both signs in clinical practice. Common sense as well as data provided by Casazza et al. tells us that, without accounting for RV afterload McConnell's sign is of little practical value. Therefore, in doubtful cases, the flow velocity curve in the right ventricular outflow tract can give useful information regarding RV afterload regardless the presence and cause of RV dysfunction.
It should be remembered that even more sophisticated methods of evaluation of the right heart with Doppler echocardiography provide indirect signs of acute PE. All efforts should be made to directly visualize intraluminar thrombi and/or emboli. This can be made more effective by integrating transthoracic, venous and transesophageal imaging in the echocardiographic examination.8,9 Such integrated examination is especially rewarding when performed at the bedside of more compromised patients10 and the decision regarding thrombolysis or embolectomy becomes much easier.
 |
References |
|---|
 Top References |
|---|
- British Thoracic Society guidelines for the management of suspected acute pulmonary embolism. Thorax (2003) 58(6):470–483.
[Free Full Text] - Guidelines on diagnosis and management of acute pulmonary embolism. Task force on pulmonary embolism, European society of cardiology [see comments]. Eur Heart J (2000) 21(16):1301–1336.
[Free Full Text] - Nazeyrollas P., Metz D., Jolly D., Maillier B., Jennesseaux C., Maes D., et al. Use of transthoracic Doppler echocardiography combined with clinical and electrocardiographic data to predict acute pulmonary embolism. Eur Heart J (1996) 17(5):779–786.
[Abstract/Free Full Text] - McConnell M.V., Solomon S.D., Rayan M.E., Come P.C., Goldhaber S.Z., Lee R.T. Regional right ventricular dysfunction detected by echocardiography in acute pulmonary embolism. Am J Cardiol (1996) 78(4):469–473.[CrossRef][Web of Science][Medline]
- Naeije R., Torbicki A. More on the noninvasive diagnosis of pulmonary hypertension: Doppler echocardiography revisited. Eur Respir J (1995) 8(9):1445–1449.[Web of Science][Medline]
- Torbicki A., Kurzyna M., Ciurzynski M., Pruszczyk P., Pacho R., Kuch-Wocial A., et al. Proximal pulmonary emboli modify right ventricular ejection pattern. Eur Respir J (1999) 13(3):616–621.[Abstract]
- Kurzyna M., Torbicki A., Pruszczyk P., Burakowska B., Fijalkowska A., Kober J., et al. Disturbed right ventricular ejection pattern as a new Doppler echocardiographic sign of acute pulmonary embolism. Am J Cardiol (2002) 90(5):507–511.[CrossRef][Web of Science][Medline]
- Grifoni S., Olivotto I., Cecchini P., Pieralli F., Camaiti A., Santoro G., et al. Utility of an integrated clinical, echocardiographic, and venous ultrasonographic approach for triage of patients with suspected pulmonary embolism. Am J Cardiol (1998) 82(10):1230–1235.[CrossRef][Web of Science][Medline]
- Pruszczyk P., Torbicki A., Kuch-Wocial A., Chlebus M., Miskiewicz Z.C., Jedrusik P. Transoesophageal echocardiography for definitive diagnosis of haemodynamically significant pulmonary embolism. Eur Heart J (1995) 16(4):534–538.
[Abstract/Free Full Text] - Torbicki A. Imaging venous thromboembolism with emphasis on ultrasound, chest CT, angiography and echocardiography. Thromb Haemost (1999) 82(2):907–912.[Web of Science][Medline]
CiteULike 
Connotea 
Del.icio.us What's this?
Related articles in Eur J Echocardiogr:
- Regional right ventricular dysfunction in acute pulmonary embolism and right ventricular infarction
- Franco Casazza, Amedeo Bongarzoni, Angela Capozi, and Ornella Agostoni
Eur J Echocardiogr 2005 6: 11-14.[Abstract] [FREE Full Text]
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||