BACKGROUND: In pulmonary arterial hypertension (PAH) a prolonged time interval between pulmonary valve closure and tricuspid valve opening is found. This period is interpreted as prolonged right ventricular (RV) relaxation, and thus a reflection of diastolic dysfunction. This concept recently has been questioned, since it was shown that RV contraction continues after pulmonary valve closure causing a post-systolic contraction period. OBJECTIVES: To investigate in PAH whether the increased RV post-systolic isovolumic period is caused by either an additional post-systolic contraction period, or an increased relaxation period (diastolic dysfunction). METHODS: 23 patients with PAH (mean pulmonary arterial pressure 54 ± 12 mm Hg), and 18 healthy subjects were studied using cardiac MRI. In a RV two-chamber view, times of pulmonary valve closure (T(PVC)) and tricuspid valve opening (T(TVO)) were measured, defining the total post-systolic isovolumic period. Time to peak of RV free wall contraction (T(peak)RV) was determined with myocardial tagging. Post-systolic contraction and relaxation periods were defined as the time intervals between T(PVC) and T(peak)RV and between T(peak)RV and T(TVO), respectively. These periods were normalised to an RR interval. RESULTS: The total post-systolic isovolumic period was longer in patients than in healthy subjects (0.15 ± 0.04 vs 0.04 ± 0.02, p < 0.001), but the relaxation period was not different (0.06 ± 0.02 vs 0.05 ± 0.02, p = 0.09). The post-systolic contraction period in patients was strongly related to the total post-systolic isovolumic period (y = 0.98x-0.05; r = 0.89, p < 0.001), and was associated with disease severity. CONCLUSION: In PAH, the prolonged post-systolic isovolumic period is caused by an additional post-systolic contraction period, rather than by an increased relaxation period.
BACKGROUND: In pulmonary arterial hypertension (PAH) a prolonged time interval between pulmonary valve closure and tricuspid valve opening is found. This period is interpreted as prolonged right ventricular (RV) relaxation, and thus a reflection of diastolic dysfunction. This concept recently has been questioned, since it was shown that RV contraction continues after pulmonary valve closure causing a post-systolic contraction period. OBJECTIVES: To investigate in PAH whether the increased RV post-systolic isovolumic period is caused by either an additional post-systolic contraction period, or an increased relaxation period (diastolic dysfunction). METHODS: 23 patients with PAH (mean pulmonary arterial pressure 54 ± 12 mm Hg), and 18 healthy subjects were studied using cardiac MRI. In a RV two-chamber view, times of pulmonary valve closure (T(PVC)) and tricuspid valve opening (T(TVO)) were measured, defining the total post-systolic isovolumic period. Time to peak of RV free wall contraction (T(peak)RV) was determined with myocardial tagging. Post-systolic contraction and relaxation periods were defined as the time intervals between T(PVC) and T(peak)RV and between T(peak)RV and T(TVO), respectively. These periods were normalised to an RR interval. RESULTS: The total post-systolic isovolumic period was longer in patients than in healthy subjects (0.15 ± 0.04 vs 0.04 ± 0.02, p < 0.001), but the relaxation period was not different (0.06 ± 0.02 vs 0.05 ± 0.02, p = 0.09). The post-systolic contraction period in patients was strongly related to the total post-systolic isovolumic period (y = 0.98x-0.05; r = 0.89, p < 0.001), and was associated with disease severity. CONCLUSION: In PAH, the prolonged post-systolic isovolumic period is caused by an additional post-systolic contraction period, rather than by an increased relaxation period.
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