Yuangang Qiu

Differential effects of morning or evening dosing of amlodipine on circadian blood pressure and heart rate.

AbstractObjectives: To compare the effects of morning and evening dosing of amlodipine on both circadian blood pressure (BP) and heart rate (HR) in mild-to-moderate essential hypertension. Design: A perspective, double-blind, randomized, crossover design with dose titration. Patients and methods: Sixty-two patients recruited in the study were aged 21–77 years and had mild-to-moderate essential hypertension. At the end of a 2-week single-blind, placebo run-in period, eligible patients were randomly assigned to morning (7 AM) and evening (9 PM) amlodipine treatment. The initial dose was 5 mg. After 2 weeks of double-blind therapy, patients with a seated diastolic blood pressure ≥90 mm Hg had their doses titrated upward to 10 mg, while the other patients remained on their original 5 mg doses for another 4 weeks period, than crossover to the alternate dosing regimen for 6 additional weeks. The 24-h ambulatory monitoring was performed at baseline and at 6 and 12 weeks after randomization. Results: 24-h diastolic BP load (11.0 ± 17.5% vs. 6.5 ± 9.1%, P < 0.05) and night-time BP load (28.5 ± 31.4%/17.7 ± 28.2% vs. 20.0 ± 27.9%/9.2 ± 17.8%, P < 0.05/0.05) were significantly greater with evening dosing compared with morning dosing. Nocturnal fall of BP was greater with morning dosing than with evening dosing (9.8 ± 6.7/7.4 ± 5.3 vs. 6.7 ± 6.6/5.4 ± 5.4 mm Hg, P < 0.01/0.05). Percentage of nocturnal BP fall was greater with morning dosing versus with evening dosing (7.9 ± 5.3%/9.6 ± 6.8% vs. 5.4 ± 7.0%/7.0 ± 6.9%, P < 0.01/0.05). Conclusions: Morning administered amlodipine had a better effect on the circadian BP compared with evening administrated amlodipine in mild-to-moderate essential hypertension.

Low dose cyclophosphamide rescues myocardial function from ischemia-reperfusion in rats.

OBJECTIVES The effect of low dose of cyclophosphamide (CP) protecting cardiac function from ischemia-reperfusion injury was studied on rats. The premise is that CP inhibits immune and inflammatory process, thereby limits I/R injury and improves myocardial function. METHODS Open chest rats were submitted to 30 min of ischemia followed by 3h, 12h or 24h of reperfusion. Rats were divided into sham group, I/R group and CP group, and each group included 3 time-point subgroups (3h, 12h and 24h; n=8 for each subgroup). A total of 750 mg/m(2) cyclophosphamide was intraperitoneally administrated in CP group and saline was given to I/R group. A polyethylene tube was inserted into the left ventricular cavity to detect left ventricular systolic pressure (LVSP) and +/-dp/dt(max). At the end of the experiment, hearts were harvested for histopathological assessment and infarct size determination. RESULTS Compared with I/R group, rats treated with low dose CP showed a significant recovery in myocardial function with improved LVSP (88+/-11 vs 69+/-11 mmHg of 3h; 92+/-11 vs 64+/-14 mmHg of 12h; 90+/-11 vs 64+/-14 mmHg of 24h; p<0.01 respectively). The +/-dp/dt(max) also had the similar trends. The myocardial infarct size was reduced in CP group compared to that in I/R group; the infiltration of polymorph nuclear leukocytes (PMNs) in myocardium was decreased in CP group. The histopathological damage score was also attenuated. CONCLUSIONS These findings suggest that low dose CP rescues cardiac function from ischemia-reperfusion injury by alleviating histopathological damage in rat myocardium.

Captopril administered at night restores the diurnal blood pessure rhythm in adequately controlled, nondipping hypertensives

The aim of our study was to evaluate whether captopril administered at night, can shift the circadian blood pressure (BP) from a nondipper to a dipper pattern in adequately controlled hypertensive patients, who continued their antihypertensive therapy. In a prospective, randomized, double blind, placebo-controlled designed study, we enrolled 121 treated, adequately controlled nondipping hypertensive patients. All patients were randomly assigned to 12.5 mg captopril or placebo treatment administered at night. In case of nondippers, the dosage of captopril or placebo was doubled after two weeks of treatment, while for dippers antihypertensive regimens were not changed. After another two weeks, all patients underwent ambulatory BP monitoring. Our results show that at the end of the active treatment period, the prevalence of a dipping diurnal BP pattern in the captopril group (70%) was significantly higher than that in the placebo group (9.8%, P < 0.001). Nighttime BP, night/day BP ratio, nighttime BP load and 24-h systolic BP were significantly lower after 4 weeks nighttime captopril treatment compared to baseline. In conclusion, the present study demonstrates for the first time that captopril administered at night can restore the diurnal BP rhythm and decrease the elevated night/day BP ratio in appropriately controlled, nondipper hypertensive patients. These results were mainly due to the decrease of nighttime BP.

Study of the correlation between blood lipid levels and the severity of coronary atherosclerosis in a Chinese population sample.

Objective — To investigate the relationship between blood lipid levels with severity of coronary artery atherosclerosis in a Chinese population sample. Methods and results — According to coronary angiography results, 363patients (287men and 76women) with coronary artery atherosclerosis were divided into four groups: the single-vessel group (I, n=125), the double-vessel group (II, n=113), the triple-vessel group (III, n=107) and the multivessel group (IV, n=18).The severity of coronary artery atherosclerosis was quantified with a modified Gensini score on the basis of angiographic imaging. Serum triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), non-high density lipoprotein cholesterol (non-HDL-C) were measured before angiography in all groups. Levels of serum TC, LDL-C and non-HDL-C of the II, III and IV group were significantly higher than those of the I group (4.78 ± 0.82mmol/L and 4.87 ± 1.50mmol/L and 4.73 ± 0.99mmol/L vs. 4.38 ± 0.93mmol/L, 2.91 ± 0.68mmol/L and 2.74 ± 1.23mmol/L and 2.64 ± 0.84mmol/L vs. 2.30 ± 0.77mmol/L, 3.58 ± 0.75mmol/L and 3.59 ± 1.41mmol/L and 3.43 ± 0.94mmol/L vs. 3.17 ± 0.91mmol/L; p < 0.05); the mean levels of TC, LDL-C and non-HDL-C associated positively with the Gensini score. Conclusion — Serum lipid levels correlate positively with the severity of coronary artery atherosclerosis in a Chinese population sample. Patients with higher levels of serum TC, LDL-C and non-HDL-C have more severe coronary atherosclerosis, compared with those with low levels of serum TC, LDL-C and non-HDL-C.

Effects of diltiazem on platelet activation and cytosolic calcium during percutaneous transluminal coronary angioplasty

Aims: To evaluate effects of diltiazem on platelet hyper-reactivity in situations associated with endothelial injury and their possible relationship to cytosolic calcium concentration. Methods: Blood samples were collected at seven time points from 35 patients undergoing percutaneous transluminal coronary angioplasty (PTCA) who received combined diltiazem and aspirin/ticlopidine therapy or aspirin/ticlopidine therapy alone. Platelet expression of glycoprotein IIb/IIIa and P-selectin, production of thromboxane B2, and cytosolic calcium concentration were measured, respectively, by whole blood flow cytometry, radioimmunoassay, and fluorospectrophotometry. The effects of diltiazem of different concentrations on expression of glycoprotein IIb/IIIa and P-selectin were also studied in vitro in blood samples from patients with chronic stable angina. Results: Of the two treatments, aspirin/ticlopidine therapy did not prevent an acute increase of expression of glycoprotein IIb/IIIa and P-selectin and plasma thromboxane B2 five minutes and 10 minutes after first inflation and 10 minutes after PTCA, whereas combined diltiazem and aspirin/ticlopidine therapy had a significant inhibitory effect. In the group receiving aspirin/ticlopidine therapy, there was a short term increase of platelet [Ca2+]i immediately after PTCA which was significantly reduced by diltiazem treatment. Expression of glycoprotein IIb/IIIa and P-selectin was significantly inhibited in vitro by diltiazem in the concentration of 200 ng/ml or higher, but not 50 ng/ml. Conclusions: Combined diltiazem and aspirin/ticlopidine therapy significantly inhibited platelet activation that continued in the presence of conventional aspirin/ticlopidine treatment. Antiplatelet effects of diltiazem were probably a consequence of reduction of platelet [Ca2+]i and may only be achieved in higher than therapeutic concentrations.

The influence of influenza A (H1N1) virus on creatinine and cystatin C.

BACKGROUND In March 2009, the novel 2009 influenza A (H1N1) virus was first reported in the southwestern USA and Mexico. It rapidly spread to China and worldwide. We investigated possible kidney injury in patients with the 2009 influenza A (H1N1) virus in China. METHODS This study was a retrospective cohort investigation of the potential renal injury in patients of influenza. One hundred and seventy-two patients confirmed to have the 2009 influenza A (H1N1) virus but who had different levels of severity (non-severe, severe, and critically severe) and 21 cases who were influenza A (H1N1)-negative but who had an influenza-like illness were investigated. Blood samples were obtained for the measurement of creatinine (Cr) and cystatin C (Cy-C). RESULTS The influenza A (H1N1) virus caused more illness in middle-aged people in all groups. The patients in the non-severe group were younger than those in the severe group (p<0.05) and the non-influenza A (H1N1) group (p<0.01). Four subjects in the critically severe group died (3 due to respiratory failure, 1 heart injury). A significant difference in the levels of Cr and Cy-C between the groups was not observed (p>0.05). CONCLUSION The 2009 influenza A (H1N1) virus did not cause severe kidney injury in the acute phase in adult patients.

Cyclophosphamide protects against myocardial ischemia/reperfusion injury in rats: one of the therapeutic targets is high sensitivity C-reactive protein.

OBJECTIVE Cyclophosphamide has a role of decreasing high-sensitivity C-reactive protein in the treatment of autoimmune disorders. The effect of cyclophosphasmide on high-sensitivity C-reactive protein was investigated in myocardial ischemia/reperfusion rat. METHODS Open-chest rats were submitted to 30 minutes of ischemia and followed for 3, 12, or 24 hours of reperfusion. All 72 rats survived and were divided into sham, ischemia/reperfusion (I/R) and cyclophosphamide groups, and each group included 3 time-point subgroups (3, 12, and 24 hours; n = 8 for each subgroup). Cyclophosphamide (0.75 g/m(2)) or saline was intraperitoneally administrated in the cyclophosphamide or I/R group. A polyethylene tube was inserted into the left ventricular cavity to detect left ventricular systolic pressure, left ventricular end-diastolic pressure, and maximum rate of rise or fall of left ventricular pressure. In the end, blood was collected for detection of high-sensitivity C-reactive protein, and hearts were harvested for histopathologic assessment and infarct size determination. RESULTS Compared with the I/R group, rats treated with cyclophosphamide showed a significant recovery in myocardial function with improved left ventricular systolic pressure (88.27 +/- 3.78 vs 68.62 +/- 3.78 mm Hg at 3 hours, 92.04 +/- 3.77 vs 63.74 +/- 4.87 mm Hg at 12 hours, and 90.41 +/- 3.98 vs 64.21 +/- 4.88 mm Hg at 24 hours; P < .05, respectively). Left ventricular end-diastolic pressure and maximum rate of rise or fall of left ventricular pressure also had similar trends. Infarct size was reduced (26.1% +/- 0.4% vs 40.4% +/- 0.4% at 3 hours, 21.6% +/- 0.4% vs 49.9% +/- 0.4% at 12 hours, and 21.6% +/- 0.4% vs 40.0% +/- 0.4% at 24 hours; P < .01, respectively). Histopathologic damage score was attenuated (1.83 +/- 0.14 vs 2.17 +/- 0.14 at 3 hours, 2.33 +/- 0.14 vs 3.17 +/- 0.14 at 12 hours, and 2.83 +/- 0.14 vs 3.83 +/- 0.14 at 24 hours; P < .01, respectively). Plasma high-sensitivity C-reactive protein concentration was significantly reduced (29.28 +/- 0.51 vs 32.26 +/- 0.51 ng/mL at 3 hours, 29.06 +/- 0.50 vs 31.8 +/- 0.51 ng/mL at 12 hours, and 28.61 +/- 0.51 vs 31.86 +/- 0.51 ng/mL at 24 h; P < .01, respectively). CONCLUSION Cyclophosphamide protects myocardial ischemia/reperfusion injury in the rat with a decrease in plasma concentration of high-sensitivity C-reactive protein.

Investigation of cystatin C and cystatin C based estimated glomerular filtration rate in pregnant patients with heart failure

Abstract Background: Impaired cardiac function leads to impaired renal function. We assessed renal function in pregnant patients with heart failure. Methods: This was a retrospective study. From 1999 to 2010, 42 pregnant patients with heart failure were classified into the single-pregnancy group and the twin or multifetation group. Clinical manifestations were assessed. Serum concentrations of creatinine and cystatin C were assessed. Estimated glomerular filtration rate (eGFR) based on serum concentrations of creatinine or cystatin C was completed. Results: There were 29 single pregnancies, 12 twin pregnancies, and one multifetation. Ten patients in the twin pregnancy or multifetation group had in-vitro fertilization. The concentration of creatinine was 84.6±33.8 μmol/L and the creatinine-based eGFR was 87.2±34.9 mL/min per 1.73 m2. The percentage of patients with a creatinine based eGFR<60 mL/min per 1.73 m2was 23.8%. The concentration of cystatin C was 1.5±0.7 mg/L and the cystatin C-based eGFR was 65.2±45.8 mL/min per 1.73 m2. The percentage of patients with a cystatin C-based eGFR<60 mL/min per 1.73 m2was 52.4%. Conclusions: Serum concentrations of cystatin C and cystatin C-based eGFR are important indicators of renal impairment in pregnant patients with heart failure.