Efficacy of regional renal nerve blockade in patients with chronic refractory heart failure / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Increased renal sympathetic nerve activity can result in diuretic resistance in patients with chronic congestive heart failure. We investigated the effect of regional renal nerve blockade on the patients with chronic refractory heart failure and diuretic resistance.</p><p><b>METHODS</b>Eighteen patients with chronic refractory heart failure were enrolled (mean age (64 ± 11) years). The patients were randomly divided into two groups (renal nerve blockade group and standard therapy group, n = 9 each). Renal nerve blockade was performed by percutaneous injection of local anaesthetic under computed tomographic guidance. Heart rate, mean arterial blood pressure, plasma and urine electrolytes, neurohormones, factional excretion of sodium (FENa), 24-hour urine volume were monitored at baseline and the first 24 hours after therapy. Dyspnea and oedema were also evaluated. The major adverse cardiovascular events (MACE), plasma brain natriuretic peptide (BNP) level and left ventricular ejection fraction (LVEF) were compared between the two groups during the 3 - 12 months follow-up period.</p><p><b>RESULTS</b>No complication was observed during the acute phase of renal nerve blockade. After renal nerve blockade, the 24-hour urine volume and FENa were significantly increased, while the level of plasma rennin, angiotensin II, aldosterone, BNP and atrial natriuretic peptide as well as dyspnea and oedema were significantly reduced in renal nerve blockade group compared with baseline and standard therapy group. During three to 12 months of follow-up, the rate of MACE and plasma BNP level were significantly lower, while LVEF was significantly higher in renal nerve blockade group than those in standard therapy group.</p><p><b>CONCLUSION</b>Regional renal nerve blockade may be a safe and effective treatment for patients with chronic refractory heart failure.</p>

Fluvastatin attenuates myocardial interstitial fibrosis and cardiac dysfunction in diabetic rats by inhibiting over-expression of connective tissue growth factor / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Diabetic myocardiopathy is characterized by myocardial interstitial fibrosis and cardiac dysfunction. Statins were found to exert protective effects on cardiovascular disease by suppressing activation of small G proteins, independently of their lipid-lowering effect. The study investigated the effect of fluvastatin on myocardial interstitial fibrosis, cardiac function and mechanism of its action in diabetic rats.</p><p><b>METHODS</b>Twenty-four male SD rats were randomly assigned to 3 groups: control rats (n = 8), streptozotocin (STZ)-induced diabetic rats (n = 8), and diabetic rats treated with fluvastatin (administered fluvastatin orally, 10 mg/kg body weight per day, n = 8). Twelve weeks later, miniature cardiac catheter was inserted into the left ventricle to conduct hemodynamic examination. Then myocardium tissues were collected, collagen content was detected by picro-sirius red staining, real-time quantitative reverse transcription polymerase chain reaction (RT-PCR) was used to detect the mRNA expression of connective tissue growth factor (CTGF), and Western blotting was used to detect the protein expression of CTGF. Rho activity was determined by pull-down assay.</p><p><b>RESULTS</b>After 12 weeks, the left ventricular systolic pressure (LVSP) and maximum rate of left ventricular (LV) pressure rise and fall (+dP/dt max and -dP/dt max) were significantly lower and left ventricular end diastolic pressure (LVEDP) was higher in the diabetic rats than those in the control rats (P < 0.01). Moreover, in LV myocardial tissue of diabetic rats the collagen content, fibronectin, mRNA and protein expression of CTGF and the activity of RhoA were all significantly increased compared with the control rats (P < 0.01). Administration of fluvastain obviously improved the cardiac function of diabetic rats, attenuated fibronectin expression, mRNA and protein expression of CTGF and the activity of RhoA in LV myocardium of diabetic rats.</p><p><b>CONCLUSIONS</b>Fluvastatin attenuates cardiac dysfunction and myocardial interstitial fibrosis of diabetic rat by inhibiting activity of RhoA to down-regulate the overexpression of CTGF, and Rho/Rho-kinase pathway may be an important target in the treatment of diabetic cardiomyopathy.</p>