稳心颗粒联合β受体阻断剂治疗冠心病心律失常的临床疗效研究

目的：探讨稳心颗粒联合β受体阻断剂治疗冠心病心律失常的临床疗效。方法选取武义县白洋街道社区卫生服务中心心血管内科2012年收治的冠心病心律失常患者150例,以随机抽样方法分为对照组和观察组,每组75例。对照组给予β受体阻断剂酒石酸美托洛尔单用治疗,观察组在对照组基础上加用稳心颗粒治疗;比较两组患者临床疗效、治疗前后心律失常改善情况及12导联心电图ST段压低程度。结果观察组患者临床疗效优于对照组,差异有统计学意义（ P<0.05）。治疗后观察组患者室性期前收缩和房性期前收缩发生频率低于对照组,两组患者治疗后室性期前收缩和房性期前收缩发生频率均低于治疗前,差异有统计学意义（ P<0.05）。观察组患者治疗后12导联心电图ST段压低程度低于对照组,两组患者治疗后12导联心电图ST段压低程度低于治疗前,差异有统计学意义（P<0.05）。两组患者治疗期间不良反应发生率比较,差异无统计学意义（P>0.05）。结论稳心颗粒联合β受体阻断剂治疗冠心病心律失常可有效缓解临床症状,改善夜间睡眠,改善心律失常发生频率及程度。     

Exercise and adrenergic regulation of immunity

Exercise training has a profound impact on immunity, exerting a multitude of positive effects in indications such as immunosenescence, cancer, viral infections and inflammatory diseases. The immune, endocrine and central nervous systems work in a highly synergistic manner and it has become apparent that catecholamine signaling through leukocyte β-adrenergic receptors (β-ARs) is a key mechanism by which exercise mediates improvements in immune function to help mitigate numerous disease conditions. Central to this is the preferential mobilization and redistribution of effector lymphocytes with potent anti-viral and anti-tumor activity, their interaction with muscle-derived cytokines, and the effects of catecholamine signaling on mitochondrial biogenesis, immunometabolism and the resulting inflammatory response. Here, we review the impact of acute and chronic exercise on adrenergic regulation of immunity in the context of aging, cancer, viral infections and inflammatory disease. We also put forth our contention that exercise interventions designed to improve immunity, prevent disease and reduce inflammation should consider the catecholamine-AR signaling axis as a therapeutic target and ask whether or not the adrenergic signaling machinery can be ‘trained’ to improve immune responses to stress, disease or during the normal physiological process of aging. Finally, we discuss potential strategies to augment leukocyte catecholamine signaling to boost the effects of exercise on immunity in individuals with desensitized β-ARs or limited exercise tolerance.     

Cardiac medication during pregnancy,data from the ROPAC

Background

Data on pharmacological management during pregnancy are scarce. The aim of this study was to describe the type and frequency of cardiac medication used in pregnancy in patients with cardiovascular disease and to assess the relationship between medication use and fetal outcome.

Methods and results

Between 2007 and 2011 sixty hospitals in 28 countries enrolled 1321 pregnant women. All patients had structural heart disease (congenital 66%, valvular 25% or cardiomyopathy 7% or ischemic 2%). Medication was used by 424 patients (32%) at some time during pregnancy: 22% used beta-blockers, 8% antiplatelet agents, 7% diuretics, 2.8% ACE inhibitors and 0.5% statins. Compared to those who did not take medication, patients taking medication were older, more likely to be parous, have valvular heart disease and were less often in sinus rhythm. The odds ratio of fetal adverse events in users versus non-users of medication was 2.6 (95% CI 2.0–3.4) and after adjustment for cardiac and obstetric parameter was 2.0 (95% CI 1.4–2.7). Babies of patients treated with beta-blockers had a significantly lower adjusted birth weight (3140 versus 3240 g, p = 0.002). The highest rate of fetal malformation was found in patients taking ACE inhibitors (8%).

Conclusion

One third of pregnant women with heart disease used cardiac medication during their pregnancy, which was associated with an increased rate of adverse fetal events. Birth weight was significantly lower in children of patients taking beta-blockers. A randomized trial is needed to distinguish the effects of the medication from the effects of the underlying maternal cardiac condition.     

Atenolol oral en el manejo del hemangioma infantil: serie de casos de 46 pacientes

Propranolol, a non-selective beta-blocker, remains the first line of treatment for problematic infantile hemangioma. However, although rarely, a subset of patients experience undesirable side effects, raising interest in other selective beta-blockers. We present a large case series of 46 infants treated successfully with oral atenolol, a selective beta-1 blocker.     

Elevated Heart Rate in Cardiovascular Diseases: A Target for Treatment?

Heart rate is a major determinant of myocardial oxygen consumption and of cardiac work, and thus reduction of heart rate may represent an important strategy for the treatment of patients with a wide range of cardiac disorders. In addition, several experimental lines of research point to high heart rate as an important risk factor for atherosclerosis and, thus, pharmacologic heart rate reduction could prevent or retard the development of atherosclerotic plaques and increase survival. Today, in patients with acute or chronic coronary syndromes or with congestive heart failure, reducing heart rate is a generally accepted treatment modality. Up to now, no human study has been performed to demonstrate the efficacy and the risk-benefit ratio of cardiac slowing in patients without cardiac disorders. However, recent retrospective analyses of the INternational VErapamil-SR/trandolapril STudy and the Paris Prospective Study 1 provided promising results. Treatment of high heart rate in healthy subjects appears to be premature, but in clinical conditions such as hypertension or diabetes, the reduction of elevated heart rate appears a desirable additional goal of therapy.     

Effects of AT1 receptor antagonist therapy in patients with severe heart failure pretreated with angiotensin-converting enzyme inhibitors

BACKGROUND:

The efficacy of angiotensin-converting enzyme (ACE) inhibitors is well documented in the treatment of chronic severe heart failure. Because pharmacological mechanisms of angiotensin II type 1 (AT1) receptor antagonists differ from the effects of ACE inhibitors, an additional positive effect can be expected by combining these drugs.

METHODS:

Sixty patients (mean age 68.3±10.0 years) with severe chronic heart failure receiving long term medication with digitalis, diuretics, ACE inhibitors and in part beta-blockers (68.3%) were randomly assigned after clinical recompensation to three groups: additional therapy with eprosartan (477.5±143.7 mg/day), telmisartan (65.9±17.7 mg/day) and control group according to a prospective study design. Hemodynamic measurements by impedance cardiography were performed before and during the observation period (9.6±3.4 days).

RESULTS:

Additional sartan treatment resulted in an improvement in cardiac output from 2.32±0.69 L/min to 3.12±1.24 L/min (P=0.003) in the eprosartan group and from 2.24±0.59 L/min to 2.76±0.91 L/min (P=0.001) in the telmisartan group; cardiac output in the control group did not increase. Furthermore, a significant decrease in total peripheral resistance was observed during treatment with eprosartan (23%, P=0.002) and telmisartan (18%, P=0.002). In the subgroup receiving combined therapy with beta-blockers, ACE inhibitors and AT1 antagonists, a significant increase in cardiac output was also observed.

CONCLUSIONS:

The additional treatment with AT1 receptor antagonists resulted in an increase in the cardiac output and a decrease in the peripheral resistance. This beneficial effect may be due to the additional property of sartans to block the interaction of locally and non-ACE-generated angiotensin II with their respective vascular and myocardial AT1 receptors.     

Ten-year outcome of patients with very small abdominal aortic aneurysm

BACKGROUND: The long-term fate of very small abdominal aortic aneurysms (AAA) is not well known. METHODS: Forty-one patients with asymptomatic small AAA (range 25 to 40 mm) underwent ultrasonographic surveillance. RESULTS: The median follow-up period was 7.3 years. The median linear aneurysm expansion rate was 2.0 mm/year (range 0 to 8.4). Three patients experienced aneurysm rupture (7.3%) which resulted in 1 patient'death. Thirteen patients underwent aneurysm repair (31.7%) and 1 patient died postoperatively (7.7%). The survival rate at 10-year follow-up was 59.0%. The survival rate free from aneurysm rupture and repair at 10-year follow-up was 69.9%. The median time for occurrence of aneurysm rupture was 4.9 years (range 1.8 to 10.5) and the need for aneurysm repair was 4.5 years (range 1.4 to 10.4). CONCLUSIONS: The fate of very small AAA is to slowly enlarge in size, sometimes threatening the patient's life. These observations underline the importance of continuous surveillance and the potential benefits of any medical treatment in this patient population.     

Portal hypertension: Pre-primary and primary prophylaxis of variceal bleeding

In liver cirrhosis, variceal bleeding is the last in a chain of events initiated by the increase in portal pressure (estimated in clinical practice by the hepatic venous pressure gradient). When hepatic venous pressure gradient goes above 10 mmHg the patient is at risk of developing varices, and when hepatic venous pressure gradient reaches 12 mmHg variceal bleeding might develop. Currently, there is not any effective therapy for the prevention of the development of varices. When varices are small, beta-adrenergic blockers might prevent the enlargement of the varices, and may reduce the risk of variceal bleeding. In patients with medium to large varices, beta-blockers are clearly effective in reducing the risk of variceal bleeding. Endoscopic band ligation might be more effective than beta-blockers, but available evidence is still very weak.