静息心率加快增加健康人心衰发生风险(71)

心率增快有窦速与慢性心率增快两种,前者指心率>100bpm,患者常伴症状而能较早诊断与治疗。相反,心率80～100bpm的慢性心率增快,虽经Holter检查能获诊断,但多数患者症状轻,不被察觉而使其长期存在,进而对人体产生显著危害。研究证实,静息心率增快能增加高血压及心血管事件的发生率,在心衰发展中也能起重要作用。最近欧洲的一项     

血管导管相关血流感染

血管导管广泛用于临床，20世纪70年代美国报道放置血管导管后并发导管相关血流感染（CRBSI）的发生率为8％，估计每年发生CRBSI2．5万例，20世纪90年代美国估计每年放置各类血管导管〉1．5亿次，中心静脉导管〉500万次，院内血流感染20万次，约40％与各种血管导管相关，特别与非隧道化中心静脉导管相关。2006年欧洲分析ICU中心静脉导管感染者28％伴脓毒症（发热、心率增快、呼吸增快及白细胞增多），     

肾上腺髓质素与神经肽Y在慢性心率增快心力衰竭患者中的变化及临床意义

目的　观察存在慢性心率增快的慢性心力衰竭患者血浆肾上腺髓质素（ADM）、神经肽Y（NPY）水平变化及临床意义,进一步探讨其在慢性心率增快中的作用。方法　将2011～2012年收住我院的慢性心力衰竭患者,根据患者入院时24　h动态心电图结果分为慢性心率增快组：80例,平均心率≥80次/分；非慢性心率增快组：80例,平均心率＜80次/分。使用酶联免疫吸附法测定两组慢性心力衰竭患者的血浆ADM、NPY、脑钠肽水平，用超声心动图测量左心房内径、左心室舒张末内径、左心室射血分数、左心室短轴缩短率。结果　慢性心率增快组慢性心力衰竭患者的血浆ADM、NPY水平均高于非慢性心率增快组（P<0.05）,随NYHA分级逐级增高，差异有统计学意义（P<0.01）。单因素分析显示ADM、NPY水平与左心房内径呈正相关（P<0.001），与左心室射血分数、左心室短轴缩短率呈负相关（P<0.001）。结论　ADM、NPY可能参与了慢性心力衰竭中慢性心率增快的病理生理过程，是心力衰竭恶化的危险因素。     

酚妥拉明用于特发性肥厚性主动脉瓣下狭窄激发试验时的评价

特发性肥厚性主动脉瓣下狭窄(IHSS)的特征是左室流出道呈动力性梗阻,系由于肥厚的室间隔与二尖瓣前叶在收缩期对合而造成,梗阻程度随在室收缩力、心室容量及后负荷的大小而改变。Val-salva氏动作正压期时静脉回流减少,可使左室流出道压力阶差增加。吸入亚硝酸异戊酯导致周围血管阻力降低、心率增快、心脏指数及喷血速度增加,可加重左室流出道梗阻。酚妥拉明亦可引起周围血管阻力降低、心室收缩力增强和心率轻度增快,因此亦可用作激发左室流出道梗阻的诊断试验。本文目的是:(1)比较酚妥拉明与亚硝酸异戊酯对IHSS患者左心室流出道梗阻的作用;(2)IHSS患者在用心得     

心率控制的新认识

近年研究显示,心率与心血管疾病的死亡率呈正相关,心率增快是心血管疾病的危险因素。现综述正常心率及其波动节律的进展,包括正常心率范围、勺形心率、心率变异、心率震荡、心率控制、恢复节律及心率控制的J或U型曲线等。     

心率：一个独立的危险因子——现有的证据及基本机制

很多的流行病学研究提示快心率在一般人群及各种心血管疾病人群中都联系着不良预后，这种联系在心率〉80次min。的时候已经比较明显。随着特异降心率药物的出现，单纯降低心率带来的获益也已经得到证实，另外，很多实验也已表明快的心率可能联系着血流动力学的改变、血管顺应性的下降、血管内皮功能受损、血管炎症反应并可能增加急性冠脉事件的发生。这些证据都表示，心率应该被列入心血管疾病的危险因子。     

高危心血管病人的心率与尿微量白蛋白的关系:评估高血压病人尿微量白蛋白的国际研究

尿微量白蛋白（MAU）是肾脏损害和心血管事件的预测指标。心率增加与心血管死亡率密切相关。评估高血压病人MAU的国际研究（I-SEARCH）对21050名合并有心血管危险因素的高血压病人进行调查，其中18900例窦性心律的高血压病人进入最后的研究，分析心率增快与MAU发生率的关系.     

有关控制心率重要性的探讨

流行病学研究表明：快速的静息心率与心血管病的发病率、心血管病及其他原因所致的死亡有关。心率增快是死亡、特别是心血管病所致死亡的独立危险因子。本文对有关控制心率的重要性作一探讨。     

新型血管扩张剂——多噻唑嗪的临床应用

周围性α受体阻滞剂已广泛应用于临床。非选择性α受体阻滞剂酚妥拉明具有明显的扩张血管作用,但由于同时阻滞了α_1和α_2两种受体,去甲肾上腺素释放增加,故使心率增快和扩血管作用减弱。近年来,出现了哌唑嗪(Prazosin)、曲马唑嗪(Trimazosin)     

有关控制心率重要性的探讨

流行病学研究表明快速的静息心率与心血管病的发病率、心血管病及其他原因所致的死亡有关.心率增快是死亡、特别是心血管病所致死亡的独立危险因子.本文对有关控制心率的重要性作一探讨.     

Association of heart rate with microalbuminuria in cardiovascular risk patients: data from I-SEARCH

BACKGROUND: Microalbuminuria (MAU) is an indicator of impaired renal function and a relevant risk predictor for cardiovascular events. An increased heart rate is closely correlated with increased cardiovascular mortality. The International Survey Evaluating Microalbuminuria Routinely by Cardiologists in Patients with Hypertension (I-SEARCH) investigated 21 050 patients with hypertension and risk factors for cardiovascular disease. In patients in sinus rhythm (n = 18 900) the relationship between increased heart rate and the prevalence of MAU was analysed. METHODS AND RESULTS: The study was performed in 26 countries worldwide from September 2005 to March 2006. Heart rate, blood pressure, urine albumin and serum creatinine were measured as key parameters. With increasing heart rate (> 80 bpm to < 120 bpm) the proportion of patients with MAU increased from 63 to 69% (P < 0.0001). The odds ratio (OR) for MAU increased with increasing heart rate [heart rate 80-100 bpm compared with 60 bpm: OR, 1.47; 95% confidence interval (CI), 1.29-1.68; P < 0.0001; and heart rate 100-120 bpm compared with 60 bpm: OR, 1.56; 95% CI, 1.22-1.99; P = 0.0004]. The prevalence of MAU was similar whether or not patients were receiving beta-blockers; but MAU was significantly reduced in physically active patients compared with sedentary patients (OR, 0.78; 95% CI, 0.73-0.84; P < 0.0001). SUMMARY: These results show that heart rate is an independent predictor for the prevalence of MAU in hypertensive patients with cardiovascular risk factors. In contrast to beta-blocker therapy, physical activity markedly decreased MAU with increasing heart rates. Further controlled and prospective studies are needed to show that lowered heart rates in combination with MAU can significantly reduce kidney damage, as well as cardiovascular events.     

Resting heart rate and the risk of death and cardiovascular complications in patients with type 2 diabetes mellitus

Aims/hypothesis

An association between resting heart rate and mortality has been described in the general population and in patients with cardiovascular disease. There are, however, few data exploring this relationship in patients with type 2 diabetes mellitus. The current study addresses this issue.

Methods

The relationship between baseline resting heart rate and all-cause mortality, cardiovascular death and major cardiovascular events (cardiovascular death, non-fatal myocardial infarction or non-fatal stroke) was examined in 11,140 patients who participated in the Action in Diabetes and Vascular Disease: Preterax and Diamicron Modified Release Controlled Evaluation (ADVANCE) Study.

Results

A higher resting heart rate was associated with a significantly increased risk of all-cause mortality (fully adjusted HR 1.15 per 10?bpm [95% CI 1.08, 1.21], p?p?=?0.001).

Conclusions/interpretation

Among patients with type 2 diabetes, a higher resting heart rate is associated with an increased risk of death and cardiovascular complications. It remains unclear whether a higher heart rate directly mediates the increased risk or is a marker for other factors that determine a poor outcome.     

Long-term prognostic value of resting heart rate in patients with suspected or proven coronary artery disease.

AIMS: Heart rate reduction is the cornerstone of the treatment of angina. The purpose of this study was to explore the prognostic value of heart rate in patients with stable coronary artery disease (CAD). METHODS AND RESULTS: We assessed the relationship between resting heart rate at baseline and cardiovascular mortality/morbidity, while adjusting for risk factors. A total of 24 913 patients with suspected or proven CAD from the Coronary Artery Surgery Study registry were studied for a median follow-up of 14.7 years. All-cause and cardiovascular mortality and cardiovascular rehospitalizations were increased with increasing heart rate (P<0.0001). Patients with resting heart rate > or =83 bpm at baseline had a significantly higher risk for total mortality [hazard ratio (HR)=1.32, CI 1.19-1.47, P<0.0001] and cardiovascular mortality (HR=1.31, CI 1.15-1.48, P<0.0001) after adjustment for multiple clinical variables when compared with the reference group. When comparing patients with heart rates between 77-82 and > or =83 bpm with patients with a heart rate < or =62 bpm, the HR values for time to first cardiovascular rehospitalization were 1.11 and 1.14, respectively (P<0.001 for both). CONCLUSION: Resting heart rate is a simple measurement with prognostic implications. High resting heart rate is a predictor for total and cardiovascular mortality independent of other risk factors in patients with CAD.     

Vascular pathophysiology in response to increased heart rate

This review summarizes the current literature and the open questions regarding the physiology and pathophysiology of the mechanical effects of heart rate on the vessel wall and the associated molecular signaling that may have implications for patient care. Epidemiological evidence shows that resting heart rate is associated with cardiovascular morbidity and mortality in the general population and in patients with cardiovascular disease. As a consequence, increased resting heart rate has emerged as an independent risk factor both in primary prevention and in patients with hypertension, coronary artery disease, and myocardial infarction. Experimental and clinical data suggest that sustained elevation of heart rate-independent of the underlying trigger-contributes to the pathogenesis of vascular disease. In animal studies, accelerated heart rate is associated with cellular signaling events leading to vascular oxidative stress, endothelial dysfunction, and acceleration of atherogenesis. The underlying mechanisms are only partially understood and appear to involve alterations of mechanic properties such as reduction of vascular compliance. Clinical studies reported a positive correlation between increased resting heart rate and circulating markers of inflammation. In patients with coronary heart disease, increased resting heart rate may influence the clinical course of atherosclerotic disease by facilitation of plaque disruption and progression of coronary atherosclerosis. While a benefit of pharmacological or interventional heart rate reduction on different vascular outcomes was observed in experimental studies, prospective clinical data are limited, and prospective evidence determining whether modulation of heart rate can reduce cardiovascular events in different patient populations is needed.     

Heart rate and cardiovascular mortality: the Framingham Study

The relation of resting heart rate on biennial ECG examinations to mortality rates over 30 years of follow-up of the Framingham cohort was examined based on 1876 total deaths and 894 cardiovascular deaths, evolving out of 5070 subjects free of cardiovascular disease at entry into the study. In both sexes, at all ages, all-cause, cardiovascular, and coronary mortality rates increased progressively in relation to antecedent heart rates determined biennially. A more impressive association to cardiovascular disease was observed in men than in women, which was independent of associated cardiovascular risk factors. Case fatality rates following coronary events also increased with antecedent heart rate and the fraction of coronary deaths as sudden death increased strikingly with heart rate in men 35 to 64 years of age. There was also a substantial excess of noncardiovascular deaths at high heart rates, and the proportion of all deaths resulting from cardiovascular disease did not increase with heart rate. The excess cardiovascular deaths with more rapid heart rates were also noted, excluding those with interim overt cardiovascular disease, suggesting an effect independent of preexisting cardiac damage.     

The heart rate hypothesis: ready to be tested

There is increasing evidence that increased heart rate may be an independent risk factor for cardiovascular morbidity and mortality both in patients with ischaemic heart disease and in the general population. Elevated heart rate in coronary artery disease is a major determinant of oxygen consumption and appears to evoke most episodes of ischaemia. Increased resting heart rate may also contribute to the development of atherosclerosis, facilitate plaque destabilisation and initiate arrhythmias, leading to acute coronary events and sudden death. Reducing heart rate is a central aim in the treatment of stable angina pectoris; this therapeutic approach may have an essential role in lowering the incidence of cardiovascular morbidity and mortality in patients with pre-existing ischaemic heart disease. However, this heart rate hypothesis has not thus far been proven. Evidence suggests that the use of heart rate-lowering drugs may have a beneficial effect; however, most treatments for angina have additional negative inotropic effects on the heart. This hypothesis can now be tested following the recent development of selective heart rate drugs.     

脑钠素对老年人心力衰竭诊断和预后评估的价值

目的探讨脑钠素(BNP)对老年人心力衰竭诊断和预后评估的价值。方法选择老年无症状性心力衰竭患者21例(aSHF组)和老年症状性心力衰竭患者42例(SHF组),另选18例健康老年人作为对照组,采用放射免疫分析法测定各组血浆BNP水平;比较各组血浆BNP水平和心功能状况及心血管事件发生的关系。结果血浆BNP水平在对照组、aSHF组、SHF组呈递增趋势,且随着纽约心功能分级(NYHA)增高而增加;血浆BNP为70 ng/L时,对诊断aSHF的灵敏度、特异度分别为90.48%、94.44%;根据左心室射血分数值、NYHA、BNP水平3种分级法与专家分级法符合率分别为81.9%、73.0%、85.7%;NYHAⅢ级和NYHAⅣ级患者心血管事件的发生率明显高于aSHF组和NYHAⅡ级患者,发生心血管事件患者的血浆BNP水平高于而LVEF值低于未发生心血管事件的患者。结论血浆BNP水平能反映心力衰竭的严重程度,与左心室的结构和功能相关,检测血浆BNP水平对于aSHF的诊断和鉴别诊断有重要的临床价值,且对于心力衰竭患者近期发生心血管事件具有重要的预测意义。     

Elevated heart rate and nondipping heart rate as potential targets for melatonin: a review

Elevated heart rate is a risk factor for cardiovascular and all‐cause mortalities in the general population and various cardiovascular pathologies. Insufficient heart rate decline during the night, that is, nondipping heart rate, also increases cardiovascular risk. Abnormal heart rate reflects an autonomic nervous system imbalance in terms of relative dominance of sympathetic tone. There are only a few prospective studies concerning the effect of heart rate reduction in coronary heart disease and heart failure. In hypertensive patients, retrospective analyses show no additional benefit of slowing down the heart rate by beta‐blockade to blood pressure reduction. Melatonin, a secretory product of the pineal gland, has several attributes, which predict melatonin to be a promising candidate in the struggle against elevated heart rate and its consequences in the hypertensive population. First, melatonin production depends on the sympathetic stimulation of the pineal gland. On the other hand, melatonin inhibits the sympathetic system in several ways representing potentially the counter‐regulatory mechanism to normalize excessive sympathetic drive. Second, administration of melatonin reduces heart rate in animals and humans. Third, the chronobiological action of melatonin may normalize the insufficient nocturnal decline of heart rate. Moreover, melatonin reduces the development of endothelial dysfunction and atherosclerosis, which are considered a crucial pathophysiological disorder of increased heart rate and pulsatile blood flow. The antihypertensive and antiremodeling action of melatonin along with its beneficial effects on lipid profile and insulin resistance may be of additional benefit. A clinical trial investigating melatonin actions in hypertensive patients with increased heart rate is warranted.     

Depression: treating the patient with comorbid cardiac disease

Depressed patients develop symptomatic and fatal ischemic heart disease at a higher rate than nondepressed patients, even after studies are controlled for known cardiovascular risk factors. Changes in sympathetic and parasympathetic tone appear to make depressed patients more vulnerable to ventricular fibrillation. Tricyclic antidepressants share the electrophysiologic profile of type 1A antiarrhythmic compounds and therefore may carry a risk of increased mortality when given to patients with ischemic heart disease. Serotonin reuptake inhibitors have shown no antiarrhythmic effect in depressed patients with serious cardiovascular disease, but studies to date have been small and short-term.     

Effect of posture on spontaneous and thermally stimulated cardiovascular oscillations

STUDY OBJECTIVE--The aim of the study was to investigate the effect of posture on thermally stimulated cardiovascular oscillations. DESIGN--The effect of increased gravitational stress (rising from sitting to standing position) on the thermally stimulated cardiovascular oscillations was measured in young male volunteers. Extensive cardiovascular function data were obtained using a cardiovascular investigation protocol. SUBJECTS--The volunteers were five fit young men, aged 20-21 years. EXPERIMENTS AND MAIN RESULTS--Cardiovascular changes from sitting to standing indicated increased sympathetic and decreased parasympathetic influence on heart and skin blood vessels; mean heart rate increased, beat to beat heart rate variability diminished, high frequency periodic heart rate variability decreased, low frequency heart rate oscillations and ratio of low frequency to high frequency heart rate variability increased, mean skin blood flow and oscillations of skin blood flow decreased (all p less than 0.05). Thermal skin stimulation at 0.01-0.10 Hz frequency increased both sitting and standing 0.10 Hz periodic heart rate variability (p less than 0.05), and 0.10 Hz thermal stimulation entrained the heart rate oscillations in sitting and standing subjects (p less than 0.05). In contrast, skin blood flow oscillations in sitting subjects decreased, while in standing subjects it increased during 0.10 Hz thermal stimulation compared to the corresponding prestimulus values (p less than 0.04). CONCLUSIONS--On the basis of previous physiological experiments, these results suggest coupling between thermoregulatory and 0.10 Hz reflex activities.