Findings illuminate role of right ventricular failure in LV free wall mass in patients with CTEPH
Hardziyenka M. J Am Coll Cardiol. 2011;57:921-928.
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Right ventricular failure in patients with chronic thromboembolic pulmonary hypertension was linked with a reversible reduction in left ventricular free wall mass, study data suggest.
“Right ventricular failure secondary to chronic pressure overload determines survival in patients with chronic thromboembolic pulmonary hypertension (CTEPH) and other forms of pulmonary arterial hypertension,” the researchers wrote, adding that it was “associated with reduction in LV free wall mass. This reduction is reversible and can be restored after pulmonary endarterectomy (PEA).”
The researchers retrospectively analyzed LV mass in consecutive patients (n=36) with right ventricular failure secondary to CTEPH using MRI, as well as healthy participants whom they selected to match age and sex characteristics of the patients. They also examined whether LV atrophy was present in rats with right ventricular failure injected with monocrotaline and compared them with controls.
Data from the clinical study indicated that the LV free wall mass indexes were lower in patients with right ventricular failure secondary to CTEPH (35 ± 6 g/m2) when compared with patients without right ventricular failure (44 ± 7 g/m2; P=.007) or healthy participants (42 ± 6 g/m2; P=.006). After PEA, researchers reported an increase in LV free wall mass index (from 38 ± 6 g/m2 to 44 ± 9 g/m2; P=.001) as right ventricular ejection fraction improved (from 31 ± 8% to 56 ± 12%; P<.001).
In the experimental study, rats with right ventricular failure had reduced LV free wall mass and smaller LV free wall myocytes compared with controls. According to the researchers, “Expression of atrial natriuretic peptide was higher, whereas that of alpha-myosin heavy chain and sarcoplasmic reticulum calcium ATPase-2 were lower in [right ventricular failure] than in controls, both in right ventricle and left ventricle.”
Among the study limitations noted by researchers were the limited number of patients studied at baseline and at postoperative follow-up, the different time points after PEA cardiac MRI was performed, and the lack of myocardial biopsies to assess the morphology and confirm atrophic remodeling.
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