Objective: Our aim was to study the effect of primary hyperparathyroidism (PHPT) and parathyroidectomy (PTX) on left ventricular (LV) wall thicknesses and systolic and diastolic function. Methods: Fifteen patients with untreated PHPT were evaluated by applying Doppler and digitized M-mode echocardiography before and 2–3 months after PTX. Fifteen age- and sex-matched healthy controls were also examined echocardiographically. Results: Prior to PTX, interventricular septal thickness (IVST), LV mass (LVM), aortic root dimension and left atrium dimension were greater and LV fractional shortening was slightly decreased in patients as compared to controls. Significantly increased LV peak late diastolic velocity (Amax) and isovolumic relaxation time, and a slightly decreased ratio of peak early to peak late diastolic velocities (E/Amax) in the patients indicated impairment of LV diastolic function in hyperparathyroidism. PTX reduced serum total Ca from 2.79 ± 0.13 to 2.39 ± 0.09 mmol/l (p < 0.001) and tended to reduce IVST [10.6 ± 2.1 vs. 10.4 ± 2.0 mm; not significant (n.s.)], LV posterior wall thickness (9.6 ± 2.0 vs. 9.2 ± 1.0 mm, n.s.) and LVM (250 ± 102 vs. 213 ± 42 g; n.s.). Before PTX, there was a significant correlation between serum total Ca and LVM (r = 0.63, p < 0.05), and the PTX-induced change in serum total calcium correlated with the change in LVM (r = 0.59, p < 0.05). PTX induced no significant changes in LV systolic or diastolic function during the follow-up of 2–3 months. Conclusions: The present findings indicate that PHPT induces LV hypertrophy, slight impairment of LV systolic function and significant impairment of LV diastolic function, which are not substantially improved after TX and 2–3 months of normocalcemia.
We investigated the effect of mannan-binding lectin (MBL) deficiency on the susceptibility to bypass graft occlusion in 62 patients with coronary heart disease. MBL deficiency appeared to be associated with occlusion (p = 0.0099). A high level of anti-cardiolipin IgG as well as the number of venous bypass grafts were also involved (p = 0.0018 and p = 0.0104, respectively). Since early occlusion (<5 years after surgery) of a venous bypass graft is considered to be caused by thrombosis or fibro-intimal hyperplasia superimposed by thrombosis, our finding also implies an association of MBL deficiency with thrombotic events. It remains unclear whether the previously confirmed effect of MBL deficiency in coronary disease is mediated through this possible thrombotic mechanism, or whether plaque formation is also involved in the process. Further studies are clearly warranted.
Common chronic infections including those caused by cytomegalovirus (CMV), herpes simplex viruses (HSV), Helicobacter pylori and Chlamydia pneumoniae have previously been related to increased risk of coronary heart disease (CHD). We investigated the association between serology of these chronic infections and coronary bypass graft occlusions in 61 patients. As a result, IgG seropositivity rate against H. pylori was higher among patients without occlusion (82%) than in those with occlusion (45%) or apparently healthy controls (57%) (p = 0.004 and p = 0.008, respectively). In conclusion, H. pylori infection, as judged by IgG seropositivity, is associated with lower occurrence of venous bypass graft occlusion in patients with CHD and may thus be connected with better outcome and prognosis of CHD patients after bypass graft surgery.
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