POSSIBLE CAUSES OF DISSOCIATION BETWEEN PULMONARY EMBOLISM VOLUME AND RIGHT VENTRICULAR DYSFUNCTION DEGREE
Abstract
Aim. To study possible causes of the dissociation between pulmonary embolism volume and right ventricular (RV) dysfunction degree. Material and methods. The main group included 37 patients with pulmonary embolism (PE); the comparison group consisted of 15 patients with coronary heart disease (CHD) and NYHA functional class (FC) I–II heart failure (HF). All participants underwent ventilation-perfusion lung scintigraphy, gated blood pool single photon emission computed tomography (GBPS), and the measurement of plasma levels of stable NO metabolites, endotelin‑1, and 6‑keto-prostaglandin (Pg) F1α. Results. In PE patients, RV contractility parameters were significantly lower than those in the comparison group. Among patients with moderate PE volume (3–7 bronchopulmonary segments), no correlation was observed between the number of hypoperfused segments and RV dysfunction degree. In PE patients, compared to the comparison group, plasma levels of endotelin‑1, stable NO metabolites, and stable prostacyclin metabolite 6‑keto-Pg F1α were significantly higher. Conclusion. In PE patients, the most important GBPS parameters of RV dysfunction included reduced ejection fraction, stroke volume, peak ejection rate, and mean filling rate. The dissociation between PE volume and RV dysfunction degree could be caused by disturbed humoral regulation of pulmonary vascular tone.
About the Authors
Yu. B. Lishmanov
Research Institute of Cardiology, Siberian Branch, Russian Academy of Medical Sciences, Tomsk
Russian Federation
Russian Federation
A. N. Pankova
Research Institute of Cardiology, Siberian Branch, Russian Academy of Medical Sciences, Tomsk
Russian Federation
Russian Federation
K. V. Zavadovskyi
Research Institute of Cardiology, Siberian Branch, Russian Academy of Medical Sciences, Tomsk
Russian Federation
Russian Federation
References
1. Torbicki A., Perrier A., Konstantinides S., et al. ESC Committee for Practice Guidelines (CPG). 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 (18):2276–2315.
2. Anderson F.A.Jr., Spencer F.A. Risk factors for venous thromboembolism. Circulation 2003; 107:9–16.
3. Meer van der R.W., Pattynama P.M., van Strijen M.J., et al. 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. Radiology. 2005; 235 (3):798–803.
4. Daou D., Coaguila C., Helal B.O., et al. Repeatability of left and right ventricular function measured with ECG-gated blood-pool SPECT versus planar radionuclide cardiac angiography.J. Nucl. Med. 2001; 42:137–141.
5. Said S.I. Mediators and modulators of pulmonary arterial hypertension. Am J Physiol Lung Cell Mol Physiol. 2006; 291 (4):547–558.
6. Stratmann G., Gregory GA. Neurogenic and humoral vasoconstriction in acute pulmonary thromboembolism. Anesth Analg. 2003; 97 (2):341–54.
7. Gomazkov O.A. Endothelin in Cardiology: molecular, physiological and pathological aspects. Kardiologija 2001; 2:50–56.Russian (Гомазков О.А. Эндотелин в кардиологии: молекулярные, физиологические и патологические аспекты. Кардиология 2001; 2:50–56).
8. Lee J., Chun Y., Lee I., et al. Pathogenic Role of Endothelin 1 in Hemodynamic Dysfunction in Experimental Acute Pulmonary Thromboembolism. Am J Respir Crit Care Med. 2001; 164:1282–1287.
9. Gutte H. Neuroendocrine activation and diagnostics in pulmonary embolism: Translational studies. Dan Med Bull. 2011; 58 (3): B4258.
10. Ignarro L.J., Cirino G., Casini A. et al. Nitric oxide as a signaling molecule in the vascular system: an overview.J. Cardiovasc Pharmacol. 1999; 34 (6):879–886.
11. Kjaer A, Hesse B. Heart failure and neuroendocrine activation: diagnostic, prognostic and therapeutic perspectives. Clin Phys Funct Imag. 2001; 21:661–672.
12. Berger R.M., Geiger R., Hess J., et al. Altered arterial expression patterns of inducible and endothelial nitric oxide synthase in pulmonary plexogenic arteriopathy caused by congenital heart disease. Am.J. Respir. Crit. Care Med. 2001; 163 (6):1493–1499.
13. Fagan K.A., Morrissey B., Fouty B.W., et al. Upregulation of nitric oxide synthase in mice with severe hypoxia-induced pulmonary hypertension. Respir. Res. 2001; 2 (5):306–313.
Review
For citations:
Lishmanov Yu.B., Pankova A.N., Zavadovskyi K.V. POSSIBLE CAUSES OF DISSOCIATION BETWEEN PULMONARY EMBOLISM VOLUME AND RIGHT VENTRICULAR DYSFUNCTION DEGREE. Russian Journal of Cardiology. 2012;(3):28-32. (In Russ.)
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