Abstract-We have shown previously that patients with resistant hypertension and hyperaldosteronism have increased brain natriuretic peptide suggestive of increased intravascular volume. In the present study, we tested the hypothesis that hyperaldosteronism contributes to cardiac volume overload. Thirty-seven resistant hypertensive patients with hyperaldosteronism (urinary aldosterone Ն12 g/24 hours and plasma renin activity Յ1.0 ng/mL per hour) and 71 patients with normal aldosterone status were studied. Both groups had similar blood pressure and left ventricular mass, whereas left and right ventricular end-diastolic volumes measured by cardiac MRI were greater in high versus normal aldosterone subjects (PϽ0.05). Spironolactone treatment (19 patients in the high aldosterone group and 15 patients from the normal aldosterone group participated in the follow-up) resulted in a significant decrease in clinic systolic blood pressure, right and left ventricular end diastolic volumes, left atrial volume, left ventricular mass, and brain natriuretic peptide at 3 and 6 months of follow-up in patients with high aldosterone, whereas in those with normal aldosterone status, spironolactone decreased blood pressure and left ventricular mass without changes in ventricular or atrial volumes or plasma brain natriuretic peptide. Hyperaldosteronism causes intracardiac volume overload in patients with resistant hypertension in spite of conventional thiazide diuretic use. Mineralocorticoid receptor blockade induces rapid regression of left ventricular hypertrophy irrespective of aldosterone status. In subjects with high aldosterone, mineralocorticoid receptor blockade induces a prominent diuretic effect compared with a greater vasodilatory effect in subjects with normal aldosterone status. (Hypertension. 2010;55:1137-1142.)Key Words: resistant hypertension Ⅲ hyperaldosteronism Ⅲ cardiac volume Ⅲ cardiac hypertrophy A ldosterone excess is increasingly recognized as a common cause of hypertension. [1][2][3][4][5][6][7][8][9][10][11] Compared with patients with similar levels of hypertension, patients with hyperaldosteronism have greater left ventricular (LV) hypertrophy, worse diastolic function, and an increased rate of cardiovascular complications including myocardial infarction, stroke, and atrial fibrillation. [12][13][14][15] In such patients, echocardiographic/Doppler studies provide support for aldosterone-induced myocardial fibrosis and hypertrophy separate from changes in blood pressure (BP). 16 -19 A large body of experimental literature, including landmark studies by Brilla and Weber, 20 clearly demonstrates that aldosterone excess in the presence of high dietary salt intake induces LV hypertrophy and fibrosis. [21][22][23] These effects are attributable, at least in part, to aldosterone-induced urinary and fecal loss of Ca 2ϩ and Mg 2ϩ , with consequent hypocalcemia, hypomagnesia, and secondary hyperparathyroidism. This secondary increase in parathyroid hormone promotes intracellular Ca 2ϩ overloading in various tissues, ...

The incidence of PP after implantation of new generation tubular stents in patients with diabetes remains high. Drug-eluting stent implantation was not associated with increased risk of PP. Plaque prolapse was not associated with stent thrombosis or increased neointimal proliferation.

OBJECTIVE-The aim of this study was to determine the natural history of vascular remodeling of atherosclerotic plaques in patients with type 2 diabetes and the predictors of vessel shrinkage.RESEARCH DESIGN AND METHODS-In this serial intracoronary ultrasound (IVUS) study, 237 coronary segments from 45 patients enrolled in the DIABETES I, II, and III trials were included. Quantitative volumetric IVUS analyses (motorized pullbacks at 0.5 mm/s) were performed in the same coronary segment after the index procedure and at the 9-month follow-up. Nontreated mild lesions (angiographic stenosis Ͻ25%) with Ն0.5 mm plaque thickening and length of Ն5 mm assessed by IVUS were included. Vessel shrinkage was defined as a ⌬external elastic membrane area/⌬plaque area Ͻ 0. Statistical adjustment by multiple segments and multiple lesions per patient was performed.RESULTS-Vessel shrinkage was identified in 37.1% of segments and was associated with a significant decrease in lumen area at 9 months (vessel shrinkage, 10 Ϯ 4 mm 2 vs. non-vessel shrinkage, 11 Ϯ 4 mm 2 ; P ϭ 0.04). Independent predictors of vessel shrinkage were insulin requirements (odds ratio 4.6 [95% CI 1.40 -15.10]; P ϭ 0.01), glycated hemoglobin (1.5 [1.05-2.10]; P ϭ 0.02), apolipoprotein B (0.96 [0.94 -0.98]; P Ͻ 0.001), hypertension (3.7 [1.40 -10.30]; P ϭ 0.009), number of diseased vessels (5.6 [2.50 -12.50]; P Ͻ 0.001), and prior revascularization (17.5 [6.50 -46.90]; P Ͻ 0.001).CONCLUSIONS-This serial IVUS study suggests that progression of coronary artery disease in patients with type 2 diabetes may be mainly attributed to vessel shrinkage. Besides, vessel shrinkage is influenced by insulin requirements and metabolic control and is associated with more advanced coronary atherosclerosis. Diabetes 58:209-214, 2009 C oronary artery remodeling is a phenomenon by which vessel dimension changes in response to atherosclerotic plaque accumulation. This concept was initially described by Glagov et al. (1) in a postmortem, histopathological study and confirmed by in vivo studies using intracoronary ultrasound (IVUS) analysis (2-7). Two different patterns of coronary remodeling have been described: a compensatory enlargement of the vessel in response to an increase of atherosclerotic plaque (positive remodeling) and a failure to enlarge or even vessel shrinkage (negative remodeling). The latter is a common finding in coronary stenosis of diabetic patients (8,9). In cross-sectional studies, negative remodeling has been associated with coronary risk factors, such as hypertension (5) and smoking (4), with the type of plaque (2,7) (calcified, hard plaques), and with metabolic control in diabetic patients (10 -12). In most studies, remodeling has been evaluated only at a single time point. Therefore, the natural history of this process has not been properly addressed. In addition, remodeling index has been assessed by comparing vessel dimension at target site and that at the most normal-looking cross-section within 10 mm from the lesion taken as reference segment (2-7). Howev...