Association between coronary artery calcium and all-cause mortality: A large single-center retrospective cohort study.

OBJECTIVE: Previous studies have revealed that coronary artery calcium is related to cardiovascular diseases and mortality. However, most studies have been conducted in Western countries and have excluded patients with pre-existing heart disease. We investigated the association between coronary artery calcium (CAC) and all-cause mortality in an Asian cohort and in subgroups stratified by age, sex, smoking, obesity, diabetes, cardiovascular disease, blood pressure, and biochemical parameters. METHODS: We conducted a retrospective cohort study on 4529 health examinees who underwent multidetector computed tomography in a tertiary medical center in Taiwan between 2011 and 2016. The mean follow-up was 3.5 years. Cox regression was used to estimate the relative hazards of death. Stratified analyses were performed. RESULTS: The all-cause mortality rates were 2.94, 4.88, 17.6, and 33.1 per 1000 person-years for CAC scores of 0, 1-100, 101-400, and >400, respectively. The multivariable adjusted hazard ratios (95% confidence intervals [CIs]) for all-cause mortality were 0.95 (0.53, 1.72), 1.87 (0.89, 3.90), and 3.05 (1.46, 6.39) for CAC scores of 1-100, 101-400, and >400, respectively, relative to a CAC score of 0. Compared with CAC ≤ 400, the HRs (95% CIs) for CAC > 400 were 6.46 (2.44, 17.15) and 1.94 (1.00, 3.76) in younger and older adults, respectively, indicating that age was a moderating variable (p = 0.02). CONCLUSION: High CAC scores were associated with increased all-cause mortality. Although older adult patients had higher risks of death, the relative risk of death for patients with CAC > 400 was more prominent in people younger than 65 years.

Association of poorly controlled HbA1c with increased risk of progression to end-stage kidney disease and all-cause mortality in patients with diabetes and chronic kidney disease.

Glycosylated hemoglobin (HbA1c) targets for patients with chronic kidney disease (CKD) and type 2 diabetes remain controversial. To evaluate whether baseline HbA1c and HbA1c trajectories are associated with the risk of end-stage kidney disease (ESKD) and all-cause mortality, we recruited adult patients with CKD and type 2 diabetes from a "Pre-ESKD Program" at a medical center in Taiwan from 2003 to 2017. Group-based trajectory modeling was performed to identify distinct patient groups that contained patients with similar longitudinal HbA1c patterns. Cox proportional hazard models were used to estimate hazard ratios (HRs) of ESKD and mortality associated with baseline HbA1c levels and HbA1c trajectories. In the analysis related to baseline HbA1c (n = 4543), the adjusted HRs [95% confidence interval (CI)] of all-cause mortality were 1.06 (0.95-1.18) and 1.25 (95% CI, 1.07-1.46) in patients with an HbA1c level of 7%-9% (53-75 mmol/mol) and >9% (>75 mmol/mol), respectively, as compared with those with an HbA1c level < 7% (<53 mmol/mol). In the trajectory analysis (n = 2692), three distinct longitudinal HbA1c trajectories were identified: nearly optimal (55.9%), moderate to stable (34.2%), and poor control (9.9%). Compared with the "nearly optimal" HbA1c trajectory group, the "moderate-to-stable" group did not have significantly higher mortality, but the "poorly controlled" group had 35% higher risk of mortality (adjusted HR = 1.35, 95% CI = 1.06-1.71). Neither baseline levels of HbA1c nor trajectories were associated with ESKD risk. In conclusion, in patients with CKD and type 2 diabetes, poor glycemic control was associated with an elevated risk of mortality but not associated with a risk of progression to ESKD.

Pharmacological blood pressure control and outcomes in patients with hypertensive crisis discharged from the emergency department.

Pharmacological blood pressure (BP) intervention for high blood pressure is controversial for a wide spectrum of hypertensive crisis in the emergency department (ED). We evaluated whether medical control of BP altered the short- and long-term outcomes among patients with hypertensive crisis who were discharged from the ED under universal health care. This retrospective cohort comprised 22 906 adults discharged from the ED of a tertiary hospital with initial systolic BP ≥ 180 mmHg or diastolic BP ≥ 120 mmHg between 2010 and 2016. The main exposure was the use of antihypertensive medication during the ED stay. Clinical endpoints were revisits to the ED or inpatient admission (at 7, 30, and 60 days), cardiovascular mortality (at 1, 3, and 5 years), and incident stroke (at 1, 3, and 5 years). The associations between pharmacological intervention for BP and outcomes were evaluated using multivariable Cox proportional-hazards models. Of the patient data analyzed, 72.2% were not treated pharmacologically and 68.4% underwent evaluation of end-organ damage. Pharmacological intervention for BP was significantly associated with a 11% and 11% reduced risk of hospital revisits within 30 or 60 days of discharge from ED, respectively, particularly among patients with polypharmacy. No association between pharmacological intervention for BP and incident stroke and cardiovascular mortality was observed. A revision of diagnostic criteria for hypertensive crisis is essential. Although pharmacological intervention for BP may not alter the long-term risk of cardiovascular mortality, it significantly reduces short-term health care utilization.

The ratio and difference of urine protein-to-creatinine ratio and albumin-to-creatinine ratio facilitate risk prediction of all-cause mortality.

The role of the difference and ratio of albuminuria (urine albumin-to-creatinine ratio, uACR) and proteinuria (urine protein-to-creatinine ratio, uPCR) has not been systematically evaluated with all-cause mortality. We retrospectively analyzed 2904 patients with concurrently measured uACR and uPCR from the same urine specimen in a tertiary hospital in Taiwan. The urinary albumin-to-protein ratio (uAPR) was derived by dividing uACR by uPCR, whereas urinary non-albumin protein (uNAP) was calculated by subtracting uACR from uPCR. Conventional severity categories of uACR and uPCR were also used to establish a concordance matrix and develop a corresponding risk matrix. The median age at enrollment was 58.6 years (interquartile range 45.4-70.8). During the 12,391 person-years of follow-up, 657 deaths occurred. For each doubling increase in uPCR, uACR, and uNAP, the adjusted hazard ratios (aHRs) of all-cause mortality were 1.29 (95% confidence interval [CI] 1.24-1.35), 1.12 (1.09-1.16), and 1.41 (1.34-1.49), respectively. For each 10% increase in uAPR, it was 1.02 (95% CI 0.98-1.06). The linear dose-response association with all-cause mortality was only observed with uPCR and uNAP. The 3 × 3 risk matrices revealed that patients with severe proteinuria and normal albuminuria had the highest risk of all-cause mortality (aHR 5.25, 95% CI 1.88, 14.63). uNAP significantly improved the discriminative performance compared to that of uPCR (c statistics: 0.834 vs. 0.828, p-value = 0.032). Our study findings advocate for simultaneous measurements of uPCR and uACR in daily practice to derive uAPR and uNAP, which can provide a better mortality prognostic assessment.

Elevated plasma stromal cell-derived factor 1 protein and its gene polymorphism in patients with pelvic inflammatory disease.

The objective was to compare the expression of plasma stromal cell-derived factor 1 and the gene polymorphism in patients with pelvic inflammatory disease and healthy controls. The enzyme-linked immunosorbent assay and polymerase chain reaction-restriction fragment length polymorphism were, respectively, used to measure the plasma stromal cell-derived factor 1alpha level and stromal cell-derived factor 1 polymorphism in 50 healthy controls and in 44 patients with pelvic inflammatory disease before and after they received routine treatment protocols. The level of plasma stromal cell-derived factor 1alpha was elevated in patients with pelvic inflammatory disease compared to normal controls and decreased significantly after treatment. There were significant correlations between plasma stromal cell-derived factor 1alpha level and neutrophil count as well as between stromal cell-derived factor 1alpha level and white blood cell count in patients with pelvic inflammatory disease. There was no significantly different distribution of stromal cell-derived factor 1 genotypes between patients with pelvic inflammatory disease and normal controls. Patients with pelvic inflammatory disease having stromal cell-derived factor 1-3'A allele were associated with significantly elevated plasma stromal cell-derived factor 1alpha concentration compared to patients with pelvic inflammatory disease having G/G homozygous alleles (P < .02). In normal controls, there was no significant difference in the plasma stromal cell-derived factor 1 level between individuals with and without stromal cell-derived factor 1-3'A allele. When the cutoff level of plasma stromal cell-derived factor 1alpha level was determined to be 2192 pg/mL based on receiver-operating characteristic curve, the sensitivity, specificity, positive predictive value, and negative predictive value as well as accuracy were 77.3%, 88.0%, 85.0%, 81.5%, and 83.0%. In conclusion, when the cutoff level was determined to be 2192 pg/mL, plasma stromal cell-derived factor 1alpha level can be used to predict pelvic inflammatory disease.