Coronary heart disease extension as a predictor of atherosclerotic renal artery stenosis.

BACKGROUND: Although the association of renal artery stenosis with coronary artery disease is well established, the best cutoff of diseased coronary vessels predicting atherosclerotic narrowing of renal artery remains still undefined. METHODS: In 109 consecutive patients (78/31 M/F) submitted to elective coronary angiography because of effort angina, renal angiography was also performed in the same session. We considered only renal artery stenosis > or =60% to be of clinical relevance. RESULTS: Coronary artery stenosis was present in 87 patients (80%), while significant narrowing of renal arteries was found in 42 patients (39%). On univariate analysis, the odds ratio (OR) of renal artery stenosis associated with 1 stenotic coronary vessel was 1.76 (95% confidence interval [95% CI], 1.34-2.33, p<0.001). This estimate was confirmed in a multiple logistic regression model adjusting for a series of potential confounders (OR=1.83, 95% CI, 1.34-2.48, p<0.001). On receiver operating characteristic curve analysis (area under the curve: 0.74 +/- 0.05, p<0.001), the presence of 3 diseased coronary vessels provided the best cutoff for the diagnosis of concomitant renal artery stenosis (positive predictive value: 63%; negative predictive value: 76%). CONCLUSIONS: There is a strong parallelism between the number of diseased coronary vessels and the occurrence of renal vascular disease. The presence of 3 diseased coronary vessels may corroborate the decision of performing renal angiography in patients with ischemic heart disease.

Lack of activation of molecular forms of the BNP system in human grade 1 hypertension and relationship to cardiac hypertrophy.

We evaluated relationships among two circulating molecular forms of brain natriuretic peptide (BNP32 and NT-proBNP), severity of hypertension (HTN), and cardiac hypertrophy in subjects with mild, moderate, and severe HTN. We prospectively studied 78 patients (43 males; mean age 51.4 +/- 11 yr) with essential HTN and 28 age- and sex-matched controls. BNP32 and NT-proBNP were measured by radioimmunoassay. In grade 1 HTN, BNP32 was not elevated and NT-proBNP was reduced (P = 0.030) compared with controls. However, log-transformed values of BNP32 and NT-proBNP were both increased with severity of HTN from grade 1 to 3 (P <0.0001 and P = 0.003, respectively). By multivariate analysis, log BNP32 was independently predicted by age (beta = 0.210, P = 0.026) and HTN grade (beta = 0.274, P = 0.004), whereas log NT-proBNP was independently predicted by sex (beta = 0.235, P = 0.012) and HTN grade (beta = 0.218, P = 0.0023). Two forms of BNP were measured in normal subjects and patients with essential HTN. In grade 1 HTN, BNP32 was unchanged and NT-proBNP was significantly reduced compared with controls. As severity increased in humans with grade 1 to 3 HTN, both BNP32 and NT-proBNP levels were increased while not being affected by the presence of left ventricular hypertrophy. The lack of activation of BNP32 together with the reduction of NT-proBNP in grade 1 HTN may represent an impaired response of the BNP system in the early phase of HTN. The later activation of both forms of BNP may be a late compensatory effect, because it correlates with severity of HTN rather than cardiac hypertrophy/remodeling.