Systolic myocardial volume gain in dilated, hypertrophied and normal heart. CMR study
Ł Mazurkiewicz1, E Orłowska-Baranowska2, J Petryka3
1Department of Cardiomyopathies, CMR Unit, Institute of Cardiology, Warsaw, Poland.
Insights
Myocardial tissue volume increases during the cardiac cycle in healthy individuals and patients with heart conditions like hypertrophic cardiomyopathy (HCM) and aortic stenosis (AS), challenging the non-compressibility hypothesis.
Area of Science:
- Cardiology
- Cardiac Physiology
- Biomedical Imaging
Background:
- The myocardium's non-compressibility is a long-standing hypothesis in cardiac physiology.
- Understanding myocardial volume changes is crucial for diagnosing and managing various heart conditions.
Purpose of the Study:
- To investigate myocardial tissue volume changes during the cardiac cycle.
- To test the hypothesis of myocardial non-compressibility in healthy individuals (HI) and patients with hypertrophic cardiomyopathy (HCM), dilated cardiomyopathy (DCM), and aortic stenosis (AS).
Main Methods:
- Cardiac magnetic resonance imaging (CMR) was used to assess left ventricular (LV) function.
- End-diastolic and end-systolic volumes were calculated for 30 HI and 110 HCM, 89 DCM, and 78 AS patients.
Main Results:
- End-systolic myocardial volume was significantly higher than end-diastolic volume across all groups (p<0.001).
- Systolic volume gain was significantly greater in HCM and AS patients compared to HI (p<0.01).
- DCM patients showed smaller increases in systolic volume gain compared to HCM and AS patients (p<0.02).
Conclusions:
- The myocardium is not incompressible, as evidenced by increased systolic volume gain during the cardiac cycle.
- Hypertrophic conditions (HCM, AS) exhibit greater systolic volume gain than non-hypertrophic conditions (DCM, HI).
Aim:
To investigate changes in myocardial tissue volume during the cardiac cycle to verify the hypothesis of non-compressibility of the myocardium in healthy individuals (HI) as well as in patients with hypertrophic cardiomyopathy (HCM), dilated cardiomyopathy (DCM), and aortic stenosis (AS).
Materials And Methods:
The study group included 30 HI, and patients with HCM (n=110), DCM (n=89), and AS (n=78). Left ventricular (LV) function, end-diastolic, and end-systolic volumes were calculated based on cardiac magnetic resonance imaging (CMR) for all participants.
Results:
End-systolic myocardial volumes were higher than end-diastolic in both controls (91.2±26.6 versus 85.1±24.3 ml, p<0.001) and in all patient groups: HCM (214.3±81.6 versus 176±64.2 ml, p<0.01), DCM (128.4±43.1 versus 115.4±42.9 ml, p<0.001) and AS (155.1±37.1 versus 129.4±34.6 ml, p<0.001). HCM and AS patients had significantly higher systolic volume gain than HI (21.5±8.3 versus 10.6±6.3%, p<0.01 and 18.3±5.7 versus 10.6±6.3% p=0.013, respectively). Conversely, DCM patients had lesser increases in myocardial systolic volume than HCM patients (11.2±4.8% versus 21.5±8.3, p=0.01) and AS patients (11.2±4.8% versus 18.3±5.7, p=0.02). No differences were found in systolic volume gain between AS and HCM patients (p=ns) or between DCM patients and HI (p=ns).
Conclusion:
End-systolic myocardial volume was significantly higher than end-diastolic volume in all subsets of patients. The systolic volume gain was greater in individuals with hypertrophy than in those without.
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