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Global and regional diastolic filling dynamics in compensated dilated cardiomyopathy
K Katayama1, M Matsuzaki, M Khono
1Department of Internal Medicine, Yamaguchi University School of Medicine, Japan.
Insights
In compensated dilated cardiomyopathy (DCM), early diastolic filling, particularly in the left ventricle (LV) apex, compensates for impaired relaxation. This regional lengthening helps maintain transmitral flow in DCM patients.
Area of Science:
- Cardiology
- Cardiovascular Physiology
Background:
- Dilated cardiomyopathy (DCM) is characterized by impaired left ventricular (LV) function.
- Understanding diastolic filling dynamics is crucial for managing DCM.
Purpose of the Study:
- To evaluate global and regional LV diastolic filling in compensated DCM.
- To investigate the compensatory mechanisms in DCM patients.
Main Methods:
- Measured LV pressure and volume using angiography in 7 controls and 6 DCM patients.
- Calculated global and regional peak filling rate (PFR), time constant of LV pressure decline (T), and LV chamber stiffness (k).
Main Results:
- DCM patients had larger LV end-diastolic volume but similar stroke index, indicating compensation.
- LV relaxation time constant (T) was prolonged in DCM, but global PFR and stiffness (k) were not significantly different.
- Apical regional PFR was higher in DCM, suggesting regional compensation.
Conclusions:
- Early diastolic filling, especially in the LV apex, plays a key role in maintaining transmitral flow in compensated DCM.
- Accelerated regional lengthening of the LV apical region may be a primary compensatory mechanism in DCM.
Abstract:
To assess the left ventricular (LV) global and regional (anterior, apical, inferior) diastolic filling dynamics in compensated dilated cardiomyopathy (DCM), we measured left ventricular pressure and instantaneous volume from angiography in 7 normal controls (CTL) and 6 DCM patients with sinus rhythm. Global and regional peak filling rate (PER), time constant of LV pressure decline (T; Weiss's method) and LV chamber stiffness (k; Gaasch's method) were calculated. In DCM, left ventricular end-diastolic volume (ml/m2) was larger than in CTL (137 +/- 29 vs. 74 +/- 6, p less than 0.001), and stroke index (ml/m2) was not different from CTL (46 +/- 14 vs. 46 +/- 8, NS), indicating a compensated state of LV. Mitral valve opening pressure (mmHg) tended to increase in DCM compared with CTL (12 +/- 6 vs. 8 +/- 4). Global PFR (ml/sec/m2) (CTL = 216 +/- 47 vs. DCM = 201 +/- 36) and k (CTL = 0.044 +/- 0.023 vs. DCM = 0.029 +/- 0.016) were not different between 2 groups. However, T (msec) was markedly prolonged in DCM compared with CTL (61 +/- 10 vs. 35 +/- 5, p less than 0.001). In CTL, regional PFR (1/sec) showed almost the same values in each region, but in DCM, apical region showed higher PFR than in other regions. Thus, early diastolic filling might play an important role in maintaining the total transmitral flow in DCM despite severe impairment of LV relaxation. This compensation could be related mainly to accelerated regional lengthening of the LV apical region.