Cor pulmonale

The effects of acute right ventricular (RV) pressure and volume overloads on left ventricular (LV) filling are well known, while the significance of chronic RV pressure overload on LV function has been less studied. To evaluate the LV impairment, 30 patients with chronic cor pulmonale and pulmonary arterial hypertension secondary to chronic obstructive lung diseases (COLDs) were studied. All patients underwent respiratory tests and arterial blood gas assessment. An echo-Doppler examination was made to measure LV ejection fraction (EF), RV and LV end-diastolic and end-systolic diameters and areas, RV/LV area indexes, LV diastolic and systolic eccentricity indexes, mitral and tricuspid flow patterns, and mitral flow velocity in late and early diastole (A/E) indexes. A right heart catheterization was carried out to determine the resting mean pulmonary arterial pressure (mPAP). The data showed a marked enlargement of RV, compressing the left through a leftward shift of interventricular septum. A linear regression analysis detected a significant correlation between mPAP and the following parameters: RV/LV diastolic and systolic area indexes (r=0.75, p[less than]0.0001; r=0.84, p[less than]0.000, respectively), mitral A/E index (r=0.61, p[less than]0.0005), and LV diastolic and systolic eccentricity indexes (r=0.93, p[less than]0.0001; and r=0.83, p[less than]0.0001). No correlations were found between echo-Doppler data and functional respiratory parameters. From these results, we conclude that chronic RV pressure overload induces LV filling impairment despite a normal systolic phase, due to septal leftward shift. In fact, chronic RV pressure overload distorts early diastolic LV geometry delaying LV filling phase, and the functional diastolic impairment of the LV is closely correlated to pulmonary hypertension levels.

Key words: chronic cor pulmonale; echo-Doppler evaluation; left ventricular filling

Abbreviations: COLD=chronic obstructive lung disease; LV=left ventricle; mPAP=mean pulmonary arterial pressure; RV=right ventricle

Hypertrophy and functional abnormalities of the right ventricle (RV) resulting from long-standing pulmonary disease have been well documented.(1),(2),(3),(4),(5) Derangement of the left ventricular (LV) function in such patients, in the absence of other disorders affecting the LV, has not been clearly established.(6) Clinical studies have suggested that LV hypertrophy may occur in patients with chronic cor pulmonale by means of biochemical and anatomic changes, including a decreased concentration of norepinephrine, an abnormal histochemical appearance of the adrenergic nerve fibers, a depressed myofibrillar adenosine triphosphatase activity, and an increased amount of collagen fibers.

When compared with values in normal subjects, RV pressure overload in pulmonary hypertension results in substantial leftward ventricular septal shift(7) that is most marked at end-systole and early diastole with a distortion of LV geometry, resulting in prolongation of isovolumetric relaxation time of LV and reduction in early diastolic filling.(8),(9)

The aim of the present study was to investigate the effects of pulmonary hypertension on LV diastolic function and to relate the findings to possible mechanisms of interdependence between the right and left sides of the heart in patients with chronic cor pulmonale and pulmonary hypertension secondary to chronic obstructive lung diseases (COLDs).

MATERIALS AND METHODS

Patients

Thirty patients, 24 men and 6 women (mean age, 62.04[+ or -]9 years; range, 50 to 75 years) with clinical and instrumental evidence of respiratory failure, chronic cor pulmonale, and pulmonary arterial hypertension secondary to COLDs defined by American Thoracic Society classification,(10) were studied.

Statistical Analysis

All values are given as mean and SDs. A linear regression analysis was employed to investigate the correlation between mPAP and each echo-Doppler parameter studied and between echo-Doppler indexes and each functional respiratory test. A p value [less than]0.05 was considered significant.

RESULTS

The demographics of the patients are listed in Table 1.

Several mechanisms have been proposed to explain how right side abnormalities can disturb LV diastolic function in the absence of LV diastolic diseases: compression of LV and alternate wall stiffness by RV distention or hypertrophy or septal shift by raised diastolic pressure. The RV hypertrophy and the reduction in RV output in pulmonary hypertensive patients could result in decreased LV preload and reduced LV atrial filling patterns,(6),(26) but the substantial contribution to this impaired function is due to the septum delaying the opening mitral valve and the start of filling. In fact, the acute normalization of LV filling patterns after relief of RV pressure overload by pulmonary thromboarteriectomy suggests that restoration of LV geometry, and not regression of RV hypertrophy, is responsible for the normalization of early LV filling.(27),(28)

Limitations of the Study

Our study presents some intrinsic limits due to the methods and the fact that a Swan-Ganz catheter was not adapted to measure the wedge pressure. This evaluation would be preferable to ensure that the abnormalities of diastolic function represent a filling problem with the LV rather than an adaptation to inadequate preload. Moreover, the same measurements would be efficient in assessing LV diastolic function from the pressure-volume loop of the LV. Nevertheless, noninvasive assessment of impaired LV filling would be of some value.(6),(8)

Another limit due to the missed recording of the wedge pressure and the direct measure of the preload is that we did not assess the importance and the contribution of the pericardium in the interaction between RV pressure overload and the left diastolic filling.

In conclusion, our results show that a complete evaluation of LV functional impairment in patients with pulmonary hypertension secondary to COLD can also be obtained by the estimation of RV and LV end-diastolic and end-systolic areas in addition to a careful measurement of LV filling flow patterns. The findings suggest the prevalence of RV with septal shift, pathogenetic fulcrum of changes, and anatomic compression of LV, altering diastolic function despite a satisfactory systolic phase (indicated by a normal LV ejection fraction at echocardiographic examination). Distortion of early diastolic LV geometry, prolongation of LV isovolumetric relaxation, and impediment to the rapid filling represent a novel mode of ventricular interaction. Therefore, diastolic ventricular interdependence by means of geometric interaction through the common ventricular septum (as assessed noninvasively) appears to be one of the determinants of these alterations in LV filling pattern.

REFERENCES

(1) Paditz E. Echocardiographic diagnosis of pulmonary hypertension in chronic lung diseases. Pneumologie 1992; 46:131-40

(2) Steiniger L. Current aspects in diagnosis of chronic cor pulmonale. Z Gesamte Inn Med 1993; 48:532-37

(3) Weissman NJ, Fuster V. Diagnosis of pulmonary artery hypertension. Heart Dis Stroke 1992; 1:196-201

(4) Vandiviere HM. Pulmonary hypertension and cor pulmonale. South Med J 1993; 86:2S7-10

(5) Seibold H, Roth U, Lippert R, et al. Left heart function in chronic obstructive lung diseases. Klin Wochenschr 1986; 64:433-36

(6) Louie EK, Rich S, Brundage BH. Doppler echocardiographic assessment of impaired left ventricular filling in patients with right ventricular pressure overload due to primary pulmonary hypertension. J Am Coll Cardiol 1986; 6:1298-1306

(7) Brinker JA, Weiss JL, Lappe DL. Leftward septal displacement during right ventricular loading in man. Circulation 1980; 61:626-33

(8) Stojnic BB, Brecker SJD, Xiao HB, et al. Left ventricular filling characteristics in pulmonary hypertension: a new mode of ventricular interaction. Br Heart J 1992; 68:16-20

(9) Iwase M, Nagata K, Izawa H, et al. Age-related changes in left and right ventricular filling velocity profiles and their relationship in normal subjects. Am Heart J 1993; 126:419-26

(10) American Thoracic Society. Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease (COPD) and asthma. Am Rev Respir Dis 1987; 136:224-44

(11) Schiller NB, Shah PM, Crawford M, et al. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography: American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-Dimensional Echocardiograms. J Am Soc Echocardiogr 1989; 2:358-67

(12) Ryan T, Petrovic O, Dillon JC, et al. An echocardiographic index for separation of right ventricular volume and pressure overload. J Am Coll Cardiol 1985; 5:918-27

(13) Ascah KJ, King ME, Gillam LD, et al. The effects of right ventricular hemodynamics on left ventricular configuration. Can J Cardiol 1990; 6:99-106

(14) Steen T, Steine K, Smiseth OA, et al. Repeatability of colour M-mode Doppler measurements of left ventricular filling. Int J Cardiol 1994; 43:79-85

(15) Machraoui A, Von Dryander S, Himichsen M, et al. Two-dimensional echocardiographic assessment of right cardiac pressure overload in patients with chronic obstructive airway disease. Respiration 1993; 60:65

(16) Hatle L, Anglesen BAJ, Tramsdal A. Non-invasive estimation of pulmonary artery systolic pressure with Doppler ultrasound. Br Heart J 1981; 45:157-65

(17) Janicki JS. Influence of the pericardium and ventricular inter-dependence on left ventricular diastolic and systolic function in patients with heart failure. Circulation 1990; 81 (suppl III):III-15

(18) Lima JAC, Guzman PA, Yin FCP. Septal geometry in the unloaded living human heart. Circulation 1986; 74:463-68

(19) Kaul S. The interventricular septum in health and disease. Am Heart J 1986; 112:568-81

(20) Ascah KJ, King ME, Gillam LD, et al. The effects of right ventricular hemodynamics on left ventricular configuration. Can J Cardiol 1990; 6:99-106

(21) Louie EK, Rich S, Levitsky S, et al. Doppler echocardiographic demonstration of the differential effects of right ventricular pressure and volume overload on left ventricular geometry and filling. J Am Coll Cardiol 1992; 19:84-90

(22) Brecker SJD, Xiao HB, Stojnic BB, et al. Assessment of the peak tricuspid regurgitant velocity from the dynamics of retrograde flow. Int J Cardiol 1992; 34:267-71

(23) Tanaka H, Tei C, Nako S, et al. Diastolic bulging of the interventricular septum toward the left ventricle: an echocardiographic manifestation of negative interventricular pressure gradient between left and right ventricles during diastole. Circulation 1980; 62:558-63

(24) Jessup M, St John Sutton M, Weber KT, et al. The effect of chronic pulmonary hypertension on left ventricular size, function and interventricular septal motion. Am Heart J 1987; 113:1114-22

(25) Reisner SA, Azzan Z, Halmann M, et al. Septal/free wall curvature ratio: a non-invasive index of pulmonary arterial pressure. J Am Soc Echocardiogr 1994; 7:27-35

(26) Louie EK, Bieniarz T, Moore AM, et al. Reduced atrial contribution to left ventricular filling in patients with severe tricuspid regurgitation after tricuspid valvulectomy: a Doppler echocardiographic study. J Am Coll Cardiol 1990; 16:1617-24

(27) Dittrich HC, Nicod PH, Chow LC, et al. Early changes of right heart geometry after pulmonary thromboendarteriectomy. J Am Coll Cardiol 1988; 11:937-43

(28) Dittrich HC, Nicod PH, Thomas TC, et al. Acute intraoperative changes in cardiac geometry and left ventricular diastolic filling during surgical reduction of severe right ventricular pressure overload in man [abstract]. J Am Coll Cardiol 1990; 15:244A

COPYRIGHT 1996 American College of Chest Physicians
COPYRIGHT 2004 Gale Group