Total Calcification Score Research Articles

Efficacy of hyperphosphatemia control in the progression of chronic renal failure and the prevalence of cardiovascular calcification

Chronic kidney disease mineral- and bone disorder (CKD-MBD) has been studied more often in dialysis than in predialysis CKD patients. The association between efficacy of hyperphosphatemia control and chronic renal failure (CRF) progression, prevalence of bone disease and cardiovascular calcification was the objective of the present investigation. 42 patients with CKD in Stage 5, regularly monitored for 5 years, were divided into Group 1 of 20 patients with normal serum phosphate (sPO4) levels and Group 2 of 22 patients with hyperphosphatemia registered at the majority of checks. Serum urea, creatinine, calcium (sCa) and sPO4 levels were regularly determined in the retrospective 5-year period. At the end of this period iPTH, bone alkaline phosphatase-BAP and inflammation markers (CRP, fetuin-A) were measured, valvular and arterial calcifications were detected by B mode echocardiogram and soft-tissue native radiograms of the pelvis and the wrist. Progression of CRF (1/sCr over time) was faster in Group 2 than in Group 1 (b = -0.0577 vs. -0.0288, p = 0.003) during the study period. Average BAP and iPTH values were similar in both groups and 23/42 patients had PTH > 300 pg/ml. Arterial and valvular calcifications were found in 5/23 patients from Group 1 and 14/22 patients from Group 2 (p = 0.011). Linear regression analysis revealed sPO4 as a predictor for total calcification number, inflammatory diseases as a predictor for valvular calcifications, while sPO4 and iPTH were predictors for arterial calcifications. More than half the patients with Stage 5 CKD not yet on dialysis exhibited elevated PTH. Faster CRF progression and frequent arterial and valvular calcifications were seen in patients with poor phosphate control and sPO4 was selected as an independent predictor of total calcification score.

Reduction in emergency department visits by patients attending an anticoagulation clinic

Introduction Recent studies suggest that warfarin therapy may be linked to cardiac valve calcification. We aimed to establish whether calcification (C) of valves or other tissue occurs with warfarin and to examine if such C was influenced by treatment duration, age, or gender. Methods We performed a retrospective review of 50 long-term warfarin recipients and 50 untreated controls, matched for age, gender, and comorbidity. For inclusion, patients required a recent echocardiogram (within 18 months) and at least one CT-scan and X-ray. We determined a calcification score (CS) for each patient; one point per site was given for C reported in the aortic, mitral, or tricuspid valve, aorta, coronary and carotid arteries, peripheral vessels, kidney, lung, or other locations. Results The groups were matched for hypertension, diabetes, and coronary disease (P = NS); however, males were younger (64 ± 3 vs. 73 ± 2 years; P = 0.03). Most patients received warfarin for valve replacement (42%) or atrial fibrillation (36%); mean treatment duration, 99 ± 3 months. Analysis revealed five main results; (1) Warfarin-associated CS was increased in cardiac valves (P = 0.01 vs. control) and at each assessed site except the coronary arteries. (2) Total CS was higher with warfarin (2.7 ± 0.3) than controls (1.8 ± 0.2; P = 0.02). (3) CS correlated with warfarin treatment duration (P = 0.03). (4) When all patients were assessed, CS correlated with age for both groups, but was always higher with warfarin (P = 0.02 vs. control). (5) However, this effect was due to warfarin-induced C in males. Total CS was higher for warfarin-treated males (2.4 ± 0.4) versus controls (1.2 ± 0.2; P \ 0.01), irrespective of age (P \ 0.01). In contrast, we found no differences between warfarin-treated and control females. Conclusions Long-term warfarin therapy was associated with tissue calcification not only in valves, but also at other sites. For our entire warfarintreated group, calcification correlated with treatment duration and age; however, the most pronounced increases occurred in males.

Tracking coronary calcification by using dual-section spiral CT: a 3-year follow-up.

To investigate the accuracy of dual-section spiral computed tomography (CT) in tracking the progression of coronary calcification, as measured during a 3-year follow-up. Two hundred forty-six patients with hypertension (mean age, 66 years +/- 6 [SD]) were preselected in accordance with the International Nifedipine Study Intervention as a Goal for Hypertension Therapy protocol. Subjects had no clinical coronary arterial disease prior to the study and no cardiovascular events during follow-up. All participants underwent baseline CT (3.2-mm section thickness; reconstruction increment, 1.5 mm) and follow-up CT after 3 years. Calcification progression was defined as any increase in total calcification score (TCS) and analyzed in accordance with five baseline TCS categories: 1-9, 10-35, 36-100, 101-250, and greater than 250. At baseline CT, 152 patients had a TCS greater than 0, and 106 (70%) showed progression after 3 years, while 94 had a baseline TCS of 0; of these, 26 (28%) showed progression (P: <.01 between groups). The mean TCS was significantly higher in each baseline TCS category after 3 years. The percentage increase was negatively correlated with baseline TCS (P: <.01) and ranged from 466% in the lowest category to 38% in the highest. Dual-section spiral CT depicts significant change in TCS over time and is useful in tracking calcified coronary atherosclerosis.

Does the pilocarpine phenylephrine provocative test help in the management of acute and subacute angle closure glaucoma?

The pilocarpine phenylephrine provocative test (PPPT) has been described as a highly sensitive method to identify eyes suffering from or at risk of angle closure glaucoma (ACG). This paper reports on average 10 years follow-up of the outcome of cases of primary acute ACG and subacute ACG in which the management was determined by the result of the PPPT--a positive result indicating the need for a peripheral iridectomy, a negative result conservative treatment. In spite of a negative PPPT the fellow eyes of cases of acute ACG treated conservatively had a high rate (40%) of development of ACG. Similarly, in eyes with a history of subacute ACG with a negative PPPT, ACG developed at some stage during the follow-up in 60%. Peripheral iridectomy alone resulted in normal intraocular pressure in 63% of eyes that had suffered an attack of acute ACG. In hypertensive eyes that presented with subacute ACG, however, only one eye became normotensive following peripheral iridectomy alone. In the subacute ACG group a positive PPPT was closely related to the presence of glaucomatous optic disc damage. These results indicate that the PPPT lacks sensitivity in detecting eyes at risk of angle closure glaucoma, and a positive result is likely in eyes with damaged outflow that will not respond to peripheral iridectomy.