Systolic myocardial volume gain in dilated, hypertrophied and normal heart. CMR study.

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.

Stable right ventricular size and function during short-term follow-up in patients with pulmonary regurgitation after tetralogy of Fallot repair.

AIM: To assess changes in ventricular size and function over time in conservatively treated adult patients with repaired tetralogy of Fallot (TOF) and significant pulmonary regurgitation (PR). MATERIALS AND METHODS: Patients with repaired TOF who had undergone more than one cardiac magnetic resonance study were identified. To confine the cause of ventricular size and function deviation to PR, patients with residual ventricular septal defect, more than mild regurgitation at a valve other than the pulmonary valve, and known coronary artery disease were excluded. RESULTS: The final analysis included 27 adults with PR fraction >20%. During a follow-up of mean 2.1 ± 0.8 years, there was no change in right ventricular (RV) end-diastolic volume (EDV; 162.1 ± 27.6 versus 164 ± 29.6 ml/m(2), p = 0.5). Left ventricular (LV) EDV showed a small decrease (85.1 ± 16.2 versus 81.5 ± 14.1 ml/m(2), p = 0.02). The mean PR fraction, PR volume, and peak RV outflow tract gradient did not change. Additionally, both RV ejection fraction (EF) and LVEF remained stable over the follow-up period (48.1 ± 6.5 versus 48.4 ± 6.7%, p = 0.83, and 57.3 ± 5.4 versus 57.2 ± 5.1 %, p = 0.91, respectively). Only two asymptomatic patients (7.4% of the study group) developed symptoms and the remaining did not deteriorate. CONCLUSION: The RVEDV, RVEF, and LVEF remained stable over a mean follow-up of approximately 2 years in the majority of adult patients after TOF repair with significant PR and a wide range of RVEDV.