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Correlation between left ventricular contractility and relaxation in patients with idiopathic dilated cardiomyopathy
1First Department of Internal Medicine, Nagoya University School of Medicine, Japan.
Insights
In patients with dilated cardiomyopathy (DCM), diastolic relaxation abnormalities do not directly correlate with systolic dysfunction. However, most DCM patients exhibit both prolonged relaxation and depressed contractility.
Area of Science:
- Cardiology
- Physiology
Background:
- The relationship between left ventricular (LV) relaxation and systolic function in idiopathic dilated cardiomyopathy (DCM) remains unclear.
- Investigating this relationship is crucial for understanding DCM pathophysiology.
Purpose of the Study:
- To investigate the relationship between left ventricular (LV) systole and diastolic relaxation in patients with DCM.
- To determine if diastolic dysfunction precedes or follows systolic dysfunction in DCM.
Main Methods:
- Hemodynamic data were collected from 38 DCM patients.
- Continuous pressure-volume relationships were obtained using a conductance catheter.
- Left ventricular end-systolic elastance (Ees) was measured.
Main Results:
- LV ejection fraction and contractility indices were significantly depressed.
- LV end-diastolic volume and relaxation time constants (TL, TD) were increased.
- Ees was depressed and showed limited correlation with systolic/diastolic indices; 79% of patients had both impaired relaxation and contractility.
Conclusions:
- Diastolic relaxation abnormalities are not directly correlated with systolic dysfunction in DCM patients at rest.
- Most DCM patients present with concurrent relaxation and contractility impairments.
- Some DCM patients may exhibit preserved relaxation despite severe contractility issues, suggesting transient or compensated abnormalities.
Background And Hypothesis:
It is not fully understood whether alterations in left ventricular (LV) relaxation in patients with idiopathic dilated cardiomyopathy (DCM) precede or follow alterations in LV systolic function. Accordingly, we investigated the relationship between LV systole and diastolic relaxation in patients with DCM using LV pressure-volume analysis.
Methods:
Hemodynamic data were collected for 38 consecutive patients with DCM in normal sinus rhythm and in the resting steady state (New York Heart Association functional class II to III). Continuous simultaneous pressure-volume relationships were obtained by conductance catheter. Left ventricular end-systolic elastance (Ees) was determined during transient occlusion of the inferior vena cava.
Results:
Left ventricular ejection fraction, peak negative dP/dt, and peak positive dP/dt were depressed (31 +/- 11%, -1242 +/- 351 mmHg/s, and 1118 +/- 253 mmHg/s, respectively). The LV end-diastolic volume index, the time constants of isovolumic LV pressure decay TL and TD were increased (141 +/- 38 ml/m2, 54 +/- 14 ms, and 69 +/- 17 ms, respectively). Ees was markedly depressed (0.9 +/- 0.5 mmHg/ml) and was not correlated with established systolic or diastolic indices except for peak positive dP/dt. Our results showed that abnormalities of relaxation were not correlated with contractile dysfunction in patients with DCM in the resting steady state; however, most patients (79%) had both prolonged relaxation and extremely depressed contractility. Abnormal relaxation may have been transient or compensated in some patients (21%) with DCM who had preserved relaxation despite severely depressed contractility.