LETTER TO THE EDITOR
Quantitative relationship between severity of pulmonary hypertension and LV diastolic function has been established
Eddy Barasch, MD*
* St. Francis Hospital,The Heart Center,Department of Research and Education,100 Port Washington Boulevard, Roslyn, New York 11576, USA
Ali Moustapha, MD ,
Vinod Kaushik, MD,
Susana Diaz, BS and
Seung-Ho Kang, PhD
The University of Texas–Houston Medical School and, Memorial–Hermann Hospital,Houston, Texas, USA
Eddy.Barasch{at}chsli.org
We read with interest the article entitled "Correlation of Left Ventricular Filling Characteristics With Right Ventricular Overload and Pulmonary Artery Pressure in Chronic Thromboembolic Pulmonary Hypertension" published in the July 17, 2002, issue of the Journal (1). Dr. Mahmud and his colleagues identified an impaired relaxation pattern of left ventricular (LV) filling in 39 patients with chronic thromboembolic pulmonary hypertension (CTPH), with a mean pulmonary artery pressure >30 mm Hg, which normalized after successful pulmonary thromboendarterectomy. The objective (e.g., finding a quantitative relationship between the right ventricular [RV] pressure overload and the type of LV diastolic dysfunction) and some of the results of this study (only patients with severe pulmonary hypertension have an altered LV filling) resemble those published by our group in 2001 (2). We were disappointed by the investigators’ claim in the Objectives section of their Abstract that "a quantitative relationship between RV pressure overload and LV diastolic function has not been established."
We examined by Doppler-echocardiography 120 patients with chronic pulmonary hypertension (of whom 12 patients had CTPH), and we found that only in patients with a systolic pulmonary artery pressure (SPAP)  60 mm Hg is LV diastolic filling altered in the form of impaired relaxation pattern. In addition, we also found that the late systolic and early diastolic interventricular septum flatting occurs in 70% of patients with SPAP 60 mm Hg and only in 6% of those with SPAP <60 mm Hg. Therefore, a quantitative relationship between the severity of pulmonary hypertension and LV diastolic function was already established.
We would like to add that, in addition to abnormal geometrical configuration and motion of interventricular septum mentioned by Dr. Mahmud, other possible mechanisms of LV diastolic dysfunction in patients with severe pulmonary hypertension might be related to the presence of some degree of LV interstitial edema, which increases the LV wall stiffness and alters its normal diastolic filling (3) and the diastolic asynchrony found in the apical and lateral walls (4).
Finally, we believe that the findings of both reports complement each other and enlarge our understanding of the mechanisms of dyspnea in patients with severe pulmonary hypertension.
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References
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1. Mahmud E, Raisinghani A, Hassankhani A, et al. Correlation of left ventricular filling characteristics with right ventricular overload and pulmonary artery pressure in chronic thromboembolic pulmonary hypertension. J Am Coll Cardiol. 2002;40:318–324[Abstract/Free Full Text]
2. Moustapha A, Kaushik V, Diaz S, Kang S-H, Barasch E. Echocardiographic evaluation of left-ventricular diastolic function in patients with chronic pulmonary hypertension. Cardiology. 2001;95:96–100[CrossRef][Medline]
3. Davis KL, Mehlhorn U, Laine GA, Allen SJ. Myocardial edema, left ventricular function and pulmonary hypertension. J Appl Physiol. 1995;78:132–137[Abstract/Free Full Text]
4. Bhargava V, Sunnerhagen KS. Left ventricular asynchrony in patients with pulmonary hypertension. J Appl Physiol. 1990;69:517–522[Abstract/Free Full Text]
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