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Abstract

  1. Top of page
  2. Abstract
  3. Disclosure of Conflict of Interests
  4. References

See also Baglin T. Fifty per cent of patients with pulmonary embolism can be treated as outpatients. J Thromb Haemost 2010; 8: 2404–5; Baglin T. Hemodynamic consequences of pulmonary embolism: reply to a rebuttal. This issue, pp 413–4.

In his otherwise sound and interesting editorial comment about outpatient treatment for pulmonary embolism (PE), Dr Baglin states that ‘in patients without pre-existing heart or lung disease, (…) with only 5–15% obstruction hypoxemia occurs. When obstruction reaches 25% pulmonary hypertension (pulmonary artery pressure greater than 20 mmHg) occurs and right ventricular dysfunction becomes evident. When 40% obstruction occurs pulmonary hypertension is critical and with more than 50% obstruction the pulmonary artery pressure begins to fall’ [1].

These statements are surprising, unsubstantiated and, I believe, misleading. A mere counterexample could suffice: provided that there is no pre-existing heart or lung disease, pneumonectomy, a sudden complete obstruction of 50% of the pulmonary vascular bed and a routine procedure in lung cancer surgery, does not result in significant changes in cardiac output or mean pulmonary artery pressure at rest (with no hypoxemia at all), and patients can even survive PE on a single lung [2]. Detailed reliable hemodynamic data (obtained through right heart catheterization) in PE patients and their relationship with the degree of pulmonary vascular obstruction can be found in the UPET study, still a gold mine of data for clinicians interested in the diagnosis, treatment and hemodynamic consequences of acute PE [3], as well as in other papers on thrombolytic therapy for acute PE from the ‘pre-echocardiographic’ era [4,5]. Overall, clinicians consider that, in patients with acute PE and without associated cardiac or respiratory disease, clinically detectable hemodynamic compromise (i.e. shock) only occurs when the pulmonary arterial obstruction is comprised between approximately 60 and 80%: virtually no compromise below 60%, virtually no survival beyond 80%.

I would also point out that pulmonary hypertension has a strict definition (mean pulmonary artery pressure greater than 25 mmHg at rest, not ‘pulmonary artery pressure greater than 20 mmHg’, which is well within the normal range if it refers to the systolic pressure provided by echocardiography) [6], and that the words massive, submassive and non-massive PE also should be used rigorously, or even replaced with the terms high-, intermediate and low-risk PE, as suggested by the recent guidelines of the European Society of Cardiology [7]. Interestingly, the level of pulmonary vascular obstruction has no place in the definition of these categories, as it is much less important than the clinical consequences of this obstruction, large or small, in each individual patient.

Although these remarks do not invalidate Dr Baglin’s comments that focused on patients with non-massive/low-risk PE, I just wish he was more prudent in his statements on the hemodynamic consequences of PE.

Disclosure of Conflict of Interests

  1. Top of page
  2. Abstract
  3. Disclosure of Conflict of Interests
  4. References

The author states that there is no conflict of interest.

References

  1. Top of page
  2. Abstract
  3. Disclosure of Conflict of Interests
  4. References
  • 1
    Baglin T. Fifty per cent of patients with pulmonary embolism can be treated as outpatients. J Thromb Haemost 2010; 8: 24045.
  • 2
    Girard P, Baldeyrou P, Le Guillou J-L, Lamer C, Grunenwald D. Thrombolysis for life-threatening pulmonary embolism 2 days after lung resection. Am Rev Respir Dis 1993; 147: 15957.
  • 3
    The urokinase pulmonary embolism trial. A national cooperative study. Circulation 1973; 47 (Suppl): 1100.
  • 4
    Petitpretz P, Simonneau G, Cerrina J, Musset D, Dreyfus M, Vandenbroek M-D, Duroux P. Effects of a single bolus of urokinase in patients with life-threatening pulmonary emboli: a descriptive trial. Circulation 1984; 70: 8616.
  • 5
    Sors H, Pacouret G, Azarian R, Meyer G, Charbonnier B, Simonneau G. Hemodynamic effects of bolus vs 2-h infusion of alteplase in acute massive pulmonary embolism. A randomized controlled multicenter trial. Chest 1994; 106: 71217.
  • 6
    Badesch DB, Champion HC, Sanchez MA, Hoeper MM, Loyd JE, Manes A, McGoon M, Naeije R, Olschewski H, Oudiz RJ, Torbicki A. Diagnosis and assessment of pulmonary arterial hypertension. J Am Coll Cardiol 2009; 54: S5566.
  • 7
    Torbicki A, Perrier A, Konstantinides S, Agnelli G, Galie N, Pruszczyk P, Bengel F, Brady AJ, Ferreira D, Janssens U, Klepetko W, Mayer E, Remy-Jardin M, Bassand JP. Guidelines on the diagnosis and management of acute pulmonary embolism: the task force for the diagnosis and management of acute pulmonary embolism of the European Society of Cardiology (ESC). Eur Heart J 2008; 29: 2276315.