Non-invasive detection of coronary artery stenosis: a comparison among power-Doppler contrast echo, 99Tc-Sestamibi SPECT and echo wall-motion analysis.
A retrospective case series was undertaken of 1126 patients with a LV ejection fraction <36% on transthoracic echocardiograms performed between 1 October 1997 and 31 March 2011 in Nelson Marlborough District Health Board. All-cause mortality and hospitalisation data were analysed for all participants. Substudies were undertaken regarding pharmacotherapy, demographics, implantable cardioverter-defibrillator implantation rates and quality of life based on the EQ-5D questionnaire and New York Heart Association class.
Low renin hypertension comprises a spectrum of disorders ranging from primary aldosteronism to obvious disorders of other mineralocorticoids, as well as a variety of miscellaneous disorders. The largest group of patients with low renin hypertension have no clear abnormality in mineralocorticoid production. However, many lines of evidence suggest the critical role of volume excess in the pathogenesis of hypertension in these patients. More detailed physiological studies must be performed in order to totally understand the spectrum of pathophysiology in low renin hypertension. However, while such studies are in progress the evidence from the literature suggests that these patients must be treated and that in most of these patients diuretic administration, either spironolactone or the thiazide group of diuretics, is usually effective in achieving a reduction of blood pressure to normal.
These results indicate that the elevated plasma TNF-alpha is partly derived from the failing heart in patients with DCM and that TNF-alpha plays a potential role in structural LV remodeling in patients with DCM.
Spironolactone with propranolol results in a better response with a greater reduction in hepatic venous pressure gradient in the secondary prophylaxis of variceal bleeding. A greater number of patients may be protected by this combination therapy than by propranolol alone. Hence, this combination may be recommended for secondary prophylaxis in patients with variceal bleeding.
Because the renin-angiotensin-aldosterone system has been implicated in the development of insulin resistance and promotion of fibrosis in some tissues, such as the vasculature, we examined the effect of eplerenone, a selective mineralocorticoid receptor (MR) antagonist, on nonalcoholic steatohepatitis (NASH) and metabolic phenotypes in a mouse model reflecting metabolic syndrome in humans. We adopted liver-specific transgenic (Tg) mice overexpressing the active form of sterol response element binding protein-1c (SREBP-1c) fed a high-fat and fructose diet (HFFD) as the animal model in the present study. When wild-type (WT) C57BL/6 and liver-specific SREBP-1c Tg mice grew while being fed HFFD for 12 wk, body weight and epididymal fat weight increased in both groups with an elevation in blood pressure and dyslipidemia. Glucose intolerance and insulin resistance were also observed. Adipose tissue hypertrophy and macrophage infiltration with crown-like structure formation were also noted in mice fed HFFD. Interestingly, the changes noted in both genotypes fed HFFD were significantly ameliorated with eplerenone. HFFD-fed Tg mice exhibited the histological features of NASH in the liver, including macrovesicular steatosis and fibrosis, whereas HFFD-fed WT mice had hepatic steatosis without apparent fibrotic changes. Eplerenone effectively ameliorated these histological abnormalities. Moreover, the direct suppressive effects of eplerenone on lipopolysaccharide-induced TNFα production in the presence and absence of aldosterone were observed in primary-cultured Kupffer cells and bone marrow-derived macrophages. These results indicated that eplerenone prevented the development of NASH and metabolic abnormalities in mice by inhibiting inflammatory responses in both Kupffer cells and macrophages.
This study demonstrates that SPL exerts a protective effect on hypertension and dyslipidemia. This protective effect may depend, at least in part, on MAPK and PI3-K pathways.
We have previously reported that cognitive deficits are cross-sectionally associated with elevated cortisol in depressed patients. Here, we longitudinally examined if changes in cortisol secretion during treatment are associated with improvement of cognition.
These data show that although participation of other neurohormones cannot be ruled out, aldosterone blockade (eplerenon) ameliorates myocardial dysfunction persisting after ventricular tachycardia by preventing coronary endothelial dysfunction.
A case of AME due to a novel mutation in HSD11B2 showed the usual features of AME but exhibited an inadequate response to spironolactone. A small dose of dexamethasone resulted in an excellent response.
Two morphological expressions of myocardial fibrosis are evident, a perivascular and interstitial fibrosis, not related to cardiac myocyte necrosis, and microscopic scarring that replaces lost myocytes. The former, a reactive fibrosis, is related to elevations in circulating mineralocorticoids (aldosterone or deoxycorticosterone) with increased dietary sodium, and not to arterial hypertension or ventricular loading. Scarring follows the cytotoxicity associated with elevated plasma angiotensin II levels and the increased K+ excretion that accompanies chronic mineralocorticoid excess.