Ł Mazurkiewicz1, E Orłowska-Baranowska2, J Petryka3, M Śpiewak4, M Gawor5, B Miłosz-Wieczorek4, K Werys4, Ł A Małek6, M Marczak4, J Grzybowski5. 1. Department of Cardiomyopathies, CMR Unit, Institute of Cardiology, Warsaw, Poland. Electronic address: lmazurkiewicz@ikard.pl. 2. Department of Acquired Cardiac Defects, Institute of Cardiology, Warsaw, Poland. 3. Department of Coronary and Structural Heart Diseases, CMR Unit, Institute of Cardiology, Warsaw, Poland. 4. CMR Unit, Institute of Cardiology, Warsaw, Poland. 5. Department of Cardiomyopathies, Institute of Cardiology, Warsaw, Poland. 6. Institute of Cardiology, Warsaw, Poland.
Abstract
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.
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, DCMpatients 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 DCMpatients 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.