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Updated: Aug 7, 2026

Echocardiographic Assessment of Cardiac Anatomy and Function in Adult Rats
Published on: December 13, 2019
Insights
Left ventricular relaxation is impaired in various heart conditions, including hypertrophic cardiomyopathy and mitral stenosis. This abnormality may be an early sign of left ventricular mechanical dysfunction.
Area of Science:
- Cardiology
- Cardiovascular Physiology
Background:
- Left ventricular (LV) relaxation is crucial for diastolic function.
- Abnormalities in LV relaxation are observed in numerous cardiac diseases.
Purpose of the Study:
- To investigate and quantify left ventricular (LV) relaxation using time constant T and peak negative dP/dt in patients with various cardiomyopathies and valvular heart diseases.
- To determine if LV relaxation abnormalities are an early indicator of mechanical dysfunction.
Main Methods:
- Studied LV relaxation in patients with hypertrophic cardiomyopathy (HCM), congestive cardiomyopathy (CCM), hypertensive heart disease (HHD), coronary artery disease (CAD) with/without asynergy, mitral stenosis (MS), and mitral regurgitation (MR).
- Utilized time constant T and peak negative dP/dt as primary indices of LV relaxation.
- Included 18 normal subjects as controls.
Main Results:
- The time constant T was significantly prolonged in HCM, CCM, CAD (with and without asynergy), and MS compared to normal controls.
- Peak negative dP/dt was significantly reduced in HCM, CCM, CAD with asynergy, MS, and MR.
- Prolongation of the time constant T was also observed in elderly normal subjects, suggesting aging contributes to impaired relaxation.
Conclusions:
- LV relaxation abnormalities are prevalent across a spectrum of cardiac conditions, including cardiomyopathies and valvular diseases.
- The exact causes of LV relaxation impairment appear multifactorial.
- LV relaxation abnormality may represent one of the earliest signs of mechanical dysfunction in the human left ventricle.
Abstract:
Left ventricular (LV) relaxation was studied in patients with hypertrophic cardiomyopathy (HCM, n =18), congestive cardiomyopathy (CCM, n = 11), hypertensive heart disease (HHD, n = 8), coronary artery disease (CAD) without left ventricular (LV) asynergy (n = 9) and with LV asynergy (n =17), mitral stenosis (MS, n = 16), and mitral regurgitation (MR, n = 8). The time constant T and peak negative dP/dt were used as indexes of LV relaxation, and 18 normal subjects served as controls. The time constant T was higher in elderly patients among normal contros (r = 0.652, p < 0.01), which suggests that prolongation of relaxation is a phenomenon of aging. The normal value of the time constant T was 33 +/- 8 msec (mean +/- SD), and that of peak negative dp/dt was 1864 +/- 390 mm Hg/sec. The time constant T was significantly higher in HCM (64 +/- 20 msec), CCM (56 +/- 14 msec), CAD without asynergy (53 +/- 16 msec), CAD with asynergy (57 +/- 13 msec) and MS (47 +/- 12 msec). Peak negative dP/dt was significantly lower in HCM (998 +/- 303 mm Hg/sec), CCM (1060 +/- 334 mm Hg/sec), CAD with asynergy (1370 +/- 299 mm Hg/sec), MS (1367 +/- 313 mm Hg/sec) and MR (1139 +/- 305 mm Hg/sec). Although the genesis of LV relaxation abnormality is not clear from this investigation, it seems to have multiple causes. Relaxation abnormality seems to be one of the earliest manifestations of mechanical dysfunction of the human left ventricle.
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