Related Experiment Videos
Evaluation of left ventricular contractility in hypertrophic cardiomyopathy from end-systolic pressure-volume
Insights
Myocardial contractility in hypertrophic cardiomyopathy (HC) is normal, not supernormal, at both chamber and muscle levels. Increased muscle mass in HC does not enhance overall chamber contractility despite more contractile units.
Area of Science:
- Cardiology
- Cardiovascular Physiology
Background:
- Hypertrophic cardiomyopathy (HC) is characterized by increased left ventricular (LV) muscle mass.
- Assessing myocardial contractility in HC is crucial for understanding disease pathophysiology.
Purpose of the Study:
- To evaluate myocardial contractility in patients with HC.
- To determine if HC exhibits supernormal contractility due to increased muscle mass.
Main Methods:
- Obtained end-systolic pressure-volume relation (ESPVR) and end-systolic stress-volume relation (ESSVR) by altering loading conditions with Angiotensin II.
- Analyzed LV stress-shortening relation to assess myocardial contractility.
- Measured LV end-systolic pressure, volume, stress, and ejection fraction at rest and during Angiotensin II infusion in 9 HC patients and 9 normal subjects.
Main Results:
- No significant difference in ESPVR slopes (Emax) between HC and normal subjects (3.1 +/- 2.3 vs 2.6 +/- 1.4 mmHg/ml).
- Statistically similar ESSVR slopes between HC and normal subjects (5.2 +/- 2.1 vs 6.0 +/- 2.8 g/cm2 ml).
- Similar end-systolic stress-ejection fraction relation slopes between groups (-0.09 +/- 0.05 vs -0.10 +/- 0.05).
Conclusions:
- Myocardial contractility is normal in hypertrophic cardiomyopathy at both chamber and muscle levels.
- Increased muscle mass in HC does not lead to enhanced overall chamber contractility.
- HC does not exhibit supernormal myocardial contractility.
Abstract:
To evaluate myocardial contractility in hypertrophic cardiomyopathy (HC), we obtained the end-systolic pressure-volume relation (ESPVR) and the end-systolic stress-volume relation (ESSVR) by changing loading conditions with Angiotensin II. The left ventricular (LV) stress-shortening relation was also analyzed in order to assess myocardial contractility. LV end-systolic pressure, end-systolic volume, end-systolic stress, and ejection fraction were obtained at rest and during Angiotensin II infusion with simultaneous recordings of pressure and volume in 9 patients with hypertrophic cardiomyopathy and 9 normal subjects (N). The slopes of ESPVR, Emax, showed no significant difference (HC: 3.1 +/- 2.3 vs N: 2.6 +/- 1.4 mmHg/ml, ns). The slopes of ESSVR were statistically similar (HC: 5.2 +/- 2.1 vs N: 6.0 +/- 2.8 g/cm2 ml, ns). The slopes of end-systolic stress-ejection fraction relation were also in the same range in both groups (HC: -0.09 +/- 0.05 vs N: -0.10 +/- 0.05, ns). From these two different analyses of LV contractility, we conclude that myocardial contractility is normal in hypertrophic cardiomyopathy and not supernormal, at both chamber and muscle levels. Considering the increased muscle mass in hypertrophic cardiomyopathy (HC: 134 +/- 46 vs N: 74 +/- 19 g/m2, p less than 0.01), the presence of increased numbers of contractile units does not result in enhanced overall chamber contractility.