Aortic distensibility and aortic stiffness index were measured at the ascending aorta (3 cm above the aortic valve) and the mid-portion of the abdominal aorta from the changes in echocardiographic diameters and pulse pressure in 14 patients with the Marfan syndrome and 15 age- and gender-matched normal control subjects. The following formulas were used: 1) Aortic distensibility = 2(Changes in aortic diameter)/(Diastolic aortic diameter) (Pulse pressure); and 2) Aortic stiffness index = ln(Systolic blood pressure)/(Diastolic blood pressure)(Changes in aortic diameter)/Diastolic aortic diameter. Pulse wave velocity was also measured. Compared with normal subjects, patients with the Marfan syndrome had decreased aortic distensibility in the ascending and the abdominal aorta (2.9 +/- 1.3 vs. 5.6 +/- 1.4 cm2 dynes-1, p less than 0.001 and 4.5 +/- 2.1, vs. 7.7 +/- 2.5, cm2 dynes-1, p less than 0.001, respectively) and had an increased aortic stiffness index in the ascending and the abdominal aorta (10.9 +/- 5.6 vs. 5.9 +/- 2.2, p less than 0.005 and 7.1 +/- 3.1 vs. 3.9 +/- 1.2, p less than 0.005, respectively). Aortic diameters in the ascending aorta were larger in these patients than in normal subjects, but those in the abdominal aorta were similar in the two groups. Linear correlations for both aortic distensibility and stiffness index were found between the ascending and the abdominal aorta (r = 0.85 and 0.71, respectively). Pulse wave velocity was more rapid in the patients than in the normal subjects (11.6 +/- 2.5 vs. 9.5 +/- 1.4 m/s, respectively, p less than 0.01). Thus, aortic elastic properties are abnormal in patients with the Marfan syndrome irrespective of the aortic diameter, which suggests an intrinsic abnormality of the aortic arterial wall.

on behalf of J-MINUET InvestigatorsBackground: According to troponin-based criteria of myocardial infarction (MI), patients without elevation of creatine kinase (CK), formerly classified as unstable angina (UA), are now diagnosed as non-ST-elevation MI (NSTEMI), but little is known about their outcomes.

High levels of blood urea nitrogen (BUN) have been demonstrated to significantly predict poor prognosis in patients with acute decompensated heart failure. However, this relationship has not been fully investigated in patients with acute myocardial infarction (AMI). We investigated whether a high level of BUN is a significant predictor for in-hospital mortality and other clinical outcomes in patients with AMI. The Japanese registry of acute Myocardial INfarction diagnosed by Universal dEfiniTion (J-MINUET) is a prospective, observational, multicenter study conducted in 28 institutions, in which 3,283 consecutive AMI patients were enrolled. We excluded 98 patients in whom BUN levels were not recorded at admission and 190 patients who were undergoing hemodialysis. A total of 2,995 patients were retrospectively analyzed. BUN tertiles were 1.5-14.4 mg/dL (tertile 1), 14.5-19.4 mg/dL (tertile 2), and 19.5-240 mg/dL (tertile 3). Increasing tertiles of BUN were associated with stepwise increased risk of in-hospital mortality (2.5, 5.1, and 11%, respectively; P < 0.001). These relationships were also observed after adjusting for reduced estimated glomerular filtration rate (estimated GFR < 60 mL/minute/1.73 m) or Killip classifications. In multivariable analysis, high levels of BUN significantly predicted in-hospital mortality, after adjusting for creatinine and other known predictors (BUN tertile 3 versus 1, adjusted odds ratio [OR]: 2.59, 95% confidence interval [95% CI]: 1.57-4.25, P < 0.001; BUN tertile 2 versus 1, adjusted OR: 1.60, 95% CI: 0.94-2.73, P = 0.081). A high level of BUN could be a useful predictor of in-hospital mortality in AMI patients.

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