Serum beta2-microglobulin concentration as a novel marker to distinguish levels of risk in acute heart failure patients.

BACKGROUND: Recently, serum beta2-microglobulin, an endogenous marker for renal function, has been shown to be an independent predictor of mortality in older adults. However, the prognostic role of beta2-microglobulin in heart failure has not been elucidated. METHODS: We prospectively evaluated serum beta2-microglobulin and creatinine concentrations, creatinine-based renal parameters (estimated glomerular filtration rate and creatinine clearance), and echocardiographic data in 131 patients with acute heart failure and creatinine concentrations < or =3.0mg/dL admitted to our hospitals. RESULTS: During 2.3+/-1.3 years, 42 patients died of cardiovascular causes and 12 died of noncardiac causes. Cardiovascular events were observed in 63 patients: 53 were readmitted due to worsening heart failure, 5 readmitted for cerebral embolism, and 5 died from sudden cardiac death. According to multivariate stepwise Cox proportional hazard analysis, higher baseline serum beta2-microglobulin concentrations (X(2)=16, p<0.0001), previous congestive heart failure (X(2)=11, p<0.001), presence of chronic obstructive pulmonary disease (X(2)=8, p<0.01), and lower diastolic blood pressure (X(2)=6, p<0.05) were independent predictors of increased cardiovascular events. Also, higher baseline serum beta2-microglobulin (X(2)=20, p<0.0001), lower systolic blood pressure (X(2)=11, p<0.001), higher relative left ventricular wall thickness (X(2)=6, p<0.05), and lower body mass index (X(2)=5, p<0.05) were independent predictors of increased cardiac mortality. The adjusted hazard ratio for cardiovascular events increased with baseline serum beta2-microglobulin above 2.1 mg/L: 2.9 with beta2-microglobulin of 2.2-2.6 mg/L (95%CI 1.2-6.9, p<0.05), 2.9 with beta2-microglobulin of 2.7-3.9 mg/L (95%CI 1.2-7.2, p<0.05), and 4.7 with beta2-microglobulin of > or =4.0 mg/L (95%CI 2.0-11, p<0.001). CONCLUSIONS: Higher baseline serum beta2-microglobulin concentration could be a promising risk marker in acute heart failure patients with creatinine < or =3.0 mg/dL.

Visualization of coronary arterial wall based on maximum intensity fusion of whole-heart MR angiograms and water suppression SPIR 3D T(1) TFE images.

PURPOSE: We estimated the coronary artery wall using maximum intensity fusion (MIF) of whole-heart magnetic resonance (MR) angiography (WHCA) and water suppression-spectral presaturation with inversion recovery (WS-SPIR) 3D T(1)-weighted turbo field echo (3DT(1) TFE). METHODS: We created a phantom using a wall of plastic bottles varied with plastic tapes measuring 0.4 to 3.0 mm thick (0-14 sheets) by vernier caliper and compared widths with those on profile curves. In 3 patients, to clarify the capacity to visualize the coronary wall in vulnerable plaque, we acquired WS-SPIR 3D T(1) TFE and WS-spectral attenuation with inversion recovery (SPAIR) (inversion time [TI] 400 ms) 3D T(1) TFE images of carotid vulnerable plaque; also termed "lipid-rich plaque," vulnerable plaque is considered to be visualized in high intensity. We utilized the same geometric parameters and rest period on WHCA as for WS-SPIR 3D T(1) TFE. We obtained MIF of WHCA and WS-SPIR 3D T(1) TFE and measured thickness of the right coronary artery (RCA) wall on the profile curve in 18 cases. RESULTS: The widths of the dip of the lower third of the bottom to head on the profile curve were consistent with actual measurement at 1-2 mm, the usual coronary artery wall thickness. Carotid plaques of high intensity by T(1)-weighted black-blood (T(1)BB) and T(2)-weighted BB (T(2)BB) methods showed high intensity on WS-SPAIR (TI 400 ms) 3D T(1) TFE and low intensity on WS-SPIR 3D T(1) TFE. With or without vulnerable plaque in the coronary artery wall, MIF of WHCA and WS-SPIR 3D T(1) TFE reflected the coronary artery wall. We obtained bands of low intensity in MIF between epicardial fat of WS-SPIR 3D T(1) TFE and coronary artery lumen of WHCA all but mid RCA in all 18 cases. We were unable to detect mid RCA in 5 cases. The outline of the obstructed mid RCA in 1 case was clear in WS-SPIR 3D T(1) TFE. The higher velocity of RCA movement caused blurring in another 4 cases in both WHCA and WS-SPIR 3D T(1) TFE. Those wall thickness of proximal or mid RCA averaged 1.3+/-0.2 mm. CONCLUSION: Bands of low intensity between epicardial fat and coronary artery lumen on MIF of WHCA and WS-SPIR 3D T(1) TFE can reflect the coronary artery wall.