心血管病人性功能障碍的康复(下)

因为心血管病人伴性功能障碍者更常见，性功能障碍的治疗出现突破，心血管医师的治疗勃起功能障碍的住方已处于非泌尿科医师的领先地位，心脏康复医师应掌握与此有关知识和技术，改善患者的生活质量，因篇幅关系，分次刊登本文的，一，性功能障碍；二，心血管病人性活动减少，三，心血管病人性活动危险分层；四主血管病人恢复性活动的指征；五，降低性生活危险性的治疗；六，恢复性功能；，七，附录，勃起功能国际指数问卷等。本刊今年第4期291－296页刊登了本文的第一，二部分，现续登其它部分，供参考。     

50岁时危险因子对终生心血管病的预警意义

治疗危险因子，预防心血管病应当及早进行。50岁以前的人很少有心血管病，但是可能已经有危险因子。过去评估这些危险因子对心血管病的影响，都只研究10年内有多少百分数发生心血管病（CVD），这种做法对中年人来说评估时间太短（Circulation，2006，113：791-998）。该文报道参加Framingham研究，50岁时没有心血管病的3564名男性与4362名女性，在111777人年的随访期间，有1757人患CVD（心肌梗死、冠心病死亡、心绞痛、缺血性脑中风、间歇性跛行），1641名因CVD死亡。研究计算出50岁的人假如男的再活30年，女的再活36年，52％的男性及40％女性会得CVD。     

关于老年心血管病人抑郁症的临床研究

目的：研究老年心血管病人抑郁症的患病率和对策。方法：以汉密尔顿抑郁量表对200例老年心血管病人，50例正常人（对照组）进行问卷调查。老年人心血管病人中冠心病人145例（心绞痛患40例，无心绞痛患85例，陈旧性心肌梗死患20例），高血压病人55例（2级20例，3级35例）。结果：与对照组比较，各种心血管病人的抑郁症患病率显增加（P＜0．05－0．01），病程越长，抑郁症发病率越高，病程＞10年组的抑郁症发病率显高于＜5年组的（P＜0．01）。结论：老年心血管病人抑郁症的患病率显增加，应重视其治疗。     

心率对老年急性心肌梗死患者预后的影响

静息心率是独立于其它危险因子之外的心血管病的危险因子（Eur Heart J，2000，21：116）。但对于急性心肌梗死（AMI）患入院心率与预后的关系却了解较少，本旨在探讨趼段抬高的AMI老年患的入院心率快慢对预后的影响。     

心脏病患者的性生活问题

性交活动相当于轻至中等度的日常活动。在冠心病患者，性交可能成为心肌梗死的诱发因素。多种心血管病治疗药物可引起性功能障碍，且较为常见。治疗勃起功能障碍的药物如西地那非可使全身血流动力学发生改变，其体内清除时间又可因服用其它心血管病药物而延迟，在服用心血管病药物的患者，应减少西地那非的剂量。医生应关注冠心病患者的性生活问题并给予指导。     

糖尿病和高血压

约70％糖尿病人发生高血压，近于无糖尿病者之2倍。不同人种、种族、社会人群各不相同。重要的是，兼患此两病的病人心血管并发症危险增高，易患慢性肾脏病。两病并存者缺血性心血管病、眼底病、性功能不正常的危险有一定程度增加。Ⅱ型糖尿病是冠心病的一个独立的危险因子，兼患高血压时，危险明显增加。     

降压治疗中左房大小与主要心血管事件危险的关系

该文是氯沙坦对糖尿病病人心血管事件减少试验（LIFE）研究中881名高血压病人每年观察超声心电图左房大小与心血管病的关系的研究结果。平均随访4．8年，首要终点（心血管病死亡、心肌梗死或脑卒中）88例，COX回归分析发现矫正Framingham评分与房颤史后入选时左房大小／身高比可预测心血管病发病率（左房大小／身高比每增加1cm／m危险比1．98；CI为1．02～3．83，P=0．042）；随访期间氯沙坦治疗左室肥厚减轻较多，     

前期高血压及心肌梗死后血压水平对高危心肌梗死患者预后的影响

血压水平对高危心肌梗死患者的预后影响仍不清楚。该文对缬沙坦心肌梗死试验中14703例伴心力衰竭和（或）左室收缩功能不全的急性心肌梗死患者进行分析，探讨血压和心血管事件危险的相关性。评估前期高血压，心肌梗死后血压升高（SBP〉140mmHg）或血压降低（SBP〈100mmHg）与心肌梗死后6月及随后24．7月期间心血管事件的关系。结果发现前期高血压显著增加心力衰竭危险比（OR：1．19，95％CJ为1．08～1．32）、脑卒中危险（OR：1．27，95％CJ为1．02～1．58）、心血管病死亡（OR：1．11，95％CI为1．01～1．22）及死亡、心肌梗死、心力衰竭、脑卒中或心脏猝死联合终点的风险（OR：1．13，95％CI 1．06～1．21）。     

美国新的心血管病二级预防指南修订：要更加积极地治疗心血管病危险因子

最新临床研究结果提示已有心血管病的病人应当更加积极治疗危险因子，更积极的二期预防能减少心肌梗死与脑中风。美国心脏病学会（AHA）与美国心脏病学学会（ACC）2006—05—16发布修订的指南，呼吁对已有冠心病及其他动脉粥样硬化性血管病的病人，包括周围动脉病，主动脉及颈动脉动脉粥样硬化性的病人，采取更积极地减少危险因子措施（JAMA，2006，296：30—31）。该指南在1995年AHA与ACC治疗心血管病危险因子的建议，以及2001年修订的基础上，今年又作了进一步修订。     

n-3脂肪酸用于有多种危险因子病人的临床试验

正背景:多项临床试验反映n-3多价不饱和脂肪酸用于心肌梗死(简称心梗)或心力衰竭(简称心衰)史的患者有效。作者评估它对具有多种心血管病危险因子或未发生过心梗的粥样硬化性心血管病人的可能裨益。方法:这是项双盲、安慰剂对照的临床试验,选入意大利860名执业医师随访的一个网络的队列。选入条件为有多种心血管危险因子或动脉粥样硬化性心血管病(但未有心梗)和非致命性脑卒中的男、女病人。事件率低于预期的一年后,第一终点     

Should the patient with coronary artery disease use sildenafil?

Since the etiology of erectile dysfunction is frequently related to endothelial dysfunction, a problem in common with much vascular disease, erectile dysfunction disproportionately affects patients with cardiovascular disease. With the development of phosphodiesterase 5 inhibitors, the first of which was sildenafil (Viagra), an effective oral medication became available. The question of safety of these drugs, especially in patients with latent or overt coronary artery disease, is of concern. Sildenafil relaxes smooth muscle and therefore lowers systolic and diastolic blood pressure slightly. With organic nitrates, the drop in blood pressure is potentiated, at times dangerously, thereby making it contraindicated to take nitrates within 24 hours of using sildenafil. In double-blind, placebo-controlled trials, there was no difference between sildenafil subjects and control patients in the incidence of myocardial infarction, cardiovascular, and total deaths. Coronary disease patients with stable angina, controlled on medications, were included in the trials. Therefore, sildenafil, as a drug, is safe in such patients. With a patient with coronary artery disease suddenly engaging in the physical exercise associated with sexual intercourse, there is the danger of increased risk of precipitating myocardial infarction or death. The cardiovascular metabolic cost of sexual activity is reviewed and appears to be approximately at the level of 3-5 metabolic equivalents of exercise. Sexual activity occurs within 2 hours of the onset of an acute myocardial infarction in <1.0% of patients. Although sexual intercourse is estimated to increase the risk of myocardial infarction by a factor of 2x, there is still only a very small increase in risk, a risk acceptable to patients who feel their quality of life will be markedly improved by their ability to engage in sexual activity.     

Underutilization and clinical benefits of angiotensin-converting enzyme inhibitors in patients with asymptomatic left ventricular dysfunction

Despite evidence of therapeutic benefit of angiotensin-converting enzyme (ACE) inhibitors for congestive heart failure and asymptomatic left ventricular (LV) dysfunction, recent studies suggest that in heart failure patients, rates of ACE inhibitor usage in clinical practice remain low. In this study, the medical records of 107 patients with documented LV dysfunction were investigated for patterns of ACE inhibitor usage; 6-month and 1-year outcomes and event rates were evaluated. At index admission, 48% patients did not receive ACE inhibitor treatment, 32% were initiated on treatment, 19% continued on a prior regimen, and 1% were discontinued. Patients seen by a cardiologist were more likely to receive ACE inhibitor treatment (53% vs 35%, p = 0. 172), as were patients with histories of hypertension (60% vs 40%, p = 0.044) or myocardial infarction (56% vs 44%, p = 0.221). Significantly shorter hospitalizations (5.9 vs 9.5 days, p = 0.001) were noted for patients with on-going ACE inhibitor treatment compared with those receiving newly initiated treatment or no treatment. At time of hospital discharge, 102 patients were alive. Of 54 patients who received ACE inhibitors, 67% received an insufficient dose. At a 6-month follow-up, of 51 patients on ACE inhibitors, 23% died or were readmitted to hospital compared with 55% of nonusers (p = 0.001). At 1 year, this event rate was 31% among ACE inhibitor users versus 71% among nonusers (p < 0.0001). Bivariate and multivariate analysis revealed absence of ACE inhibitor use as the only significant variable associated with the event rate (p < 0.0011). Thus, about half of patients with asymptomatic LV dysfunction received ACE inhibitors; 2/3 of these did not receive a sufficient dose. ACE inhibitor usage increased with involvement of a cardiologist, presence of coexistent hypertension, or prior myocardial infarction. Ongoing ACE inhibitor therapy was associated with shorter hospitalizations and fewer hospital readmissions or deaths.     

Early preventive treatment of left ventricular dysfunction following myocardial infarction: optimal timing and patient selection.

Treatment for clinical congestive heart failure is effective, but because severe ventricular dysfunction is often present at the time of clinical presentation, it may only be palliative. Recent clinical studies indicate that treatment of symptomless left ventricular dysfunction from 1 week following myocardial infarction or later may prevent further ventricular dilation and possibly reduce the occurrence of heart failure. Considering the potential for progressive ventricular dilation that exists from the time of myocardial infarction, early intervention following myocardial infarction may provide greater benefit. In a double-blind study, 100 patients with Q-wave myocardial infarction, but without clinical heart failure, were randomized to treatment with captopril 50 mg twice daily or placebo, 24-48 hours following onset of symptoms. During 3 months of treatment, the placebo group showed significant increases in left ventricular end-diastolic and end-systolic volume indices with ejection fraction unchanged. In contrast, the captopril group showed a slight but insignificant increase in left ventricular end-diastolic volume index and a significant reduction in end-systolic volume index with ejection fraction increased. Thus, early treatment of patients following Q-wave myocardial infarction with converting enzyme inhibition is effective in preventing ventricular dilation and provides an advantage over later treatment. Selection of patients with Q-wave infarction at 24 hours, after thrombolysis, provides therapy for those most likely to benefit, which is well tolerated without risk of hypotension.     

Patients treated by cardiologists have a lower in-hospital mortality for acute myocardial infarction

Objectives. We sought to determine the effect of specialty care on in-hospital mortality in patients with acute myocardial infarction.Background. There has been increasing pressure to limit access to specialists as a method to reduce the cost of health care. There is little known about the effect on outcome of this shift in the care of acutely ill patients.Methods. We analyzed the data from 30,715 direct hospital admissions for the treatment of acute myocardial infarction in Pennsylvania in 1993. A risk-adjusted in-hospital mortality model was developed in which 12 of 20 clinical variables were significant independent predictors of in-hospital mortality. To determine whether there were factors other than patient risk that significantly influenced in-hospital mortality, multiple logistic regression analysis was performed on physician, hospital and payer variables.Results. After adjustment for patient characteristics, a multiple logistic regression analysis identified treatment by a cardiologist (odds ratio = 0.83 [confidence interval {CI} = 0.74 to 0.94] p < 0.003) and physicians treating a high volume of acute myocardial infarction patients (odds ratio = 0.89 [CI = 0.80 to 0.99] p < 0.03) as independent predictors of lower in-hospital mortality. Treatment by a cardiologist as compared to primary care physicians was also associated with a significantly lower length of stay for both medically treated patients (p < 0.01) and those undergoing revascularization (p < 0.01).Conclusions. Treatment by a cardiologist is associated with approximately a 17% reduction in hospital mortality in acute myocardial infarction patients. In addition, patients of physicians treating a high volume of patients have approximately an 11% reduction in mortality. This has important implications for the optimal treatment of acute myocardial infarction in the current transformation of the health care delivery system.     

Management of sexual dysfunction in patients with cardiovascular disease: recommendations of The Princeton Consensus Panel

Sexual dysfunction is highly prevalent in both sexes and adversely affects patients' quality of life and well being. Given the frequent association between sexual dysfunction and cardiovascular disease, in addition to the potential cardiac risk of sexual activity itself, a consensus panel was convened to develop recommendations for clinical management of sexual dysfunction in patients with cardiovascular disease. Based upon a review of the research and presentations by invited experts, a classification system was developed for stratification of patients into high, low, and intermediate categories of cardiac risk. The large majority of patients are in the low-risk category, which includes patients with (1) controlled hypertension; (2) mild, stable angina; (3) successful coronary revascularization; (4) a history of uncomplicated myocardial infarction (MI); (5) mild valvular disease; and (6) no symptoms and <3 cardiovascular risk factors. These patients can be safely encouraged to initiate or resume sexual activity or to receive treatment for sexual dysfunction. An important exception is the use of sildenafil in patients taking nitrates in any form. Patients in the intermediate-risk category include those with (1) moderate angina; (2) a recent MI (<6 weeks); (3) left ventricular dysfunction and/or class II congestive heart failure; (4) nonsustained low-risk arrhythmias; and (5) >/=3 risk factors for coronary artery disease. These patients should receive further cardiologic evaluation before restratification into the low- or high-risk category. Finally, patients in the high-risk category include those with (1) unstable or refractory angina; (2) uncontrolled hypertension; (3) congestive heart failure (class III or IV); (4) very recent MI (<2 weeks); (5) high-risk arrhythmias; (6) obstructive cardiomyopathies; and (7) moderate-to-severe valvular disease. These patients should be stabilized by specific treatment for their cardiac condition before resuming sexual activity or being treated for sexual dysfunction. A simple algorithm is provided for guiding physicians in the management of sexual dysfunction in patients with varying degrees of cardiac risk.     

Sexuality in patients with coronary disease and heart failure

INTRODUCTION: When a cardiologist is speaking about sexual disorder with a patient with coronary artery disease (CAD) or heart failure (HF) mostly the male sexual disorder is the point. Questions about sexual physical stress and the use of Viagra or MUSE are dominant in the first step. But usually sexual disorders of men and women are a challenge for the cardiologist: is there not another problem behind? Is sexual disorder only a "common symptom"? Is there a need for psychotherapy? There are patients with a "well functioning" of all sexual functions but however feeling unhappy and not satisfied because lacking in sexual fulfilling [32]. The most common questions in my opinion deal with male patients after CABG or valve replacement surgery or after myocardial infarction (MI) or percutaneous transluminal coronary angioplasty (PTCA). Those patients often are concerned about future sexual activity or about a diminished libido. Some fear of failing during intercourse. HOPEFUL PREMISE: The risk of having severe complications during sexual activity is far less than many of the patients and their partners or we the cardiologists would have expected. In only about 0.9% of patients with MI sexual activity was a likely contributor to the onset of MI [27]. Regular exercise reduces the risk of MI by sexual activity. Even in high risk CAD-patients the risk for MI or death are low with 20 chances per million per hour with known CAD [14]. THE PREVALENCE OF ERECTILE DYSFUNCTION (ED) IN POPULATION BASED STUDIES: One of the largest and longest during newer studies is the Massachusetts Male Aging Study (MMAS) asking men with an age of 40-69 years. There was a prevalence of ED (3 levels: mild, moderate, complete) of 39% in the 40 years old and of maximal 67% in men with 69 years of age [16]. Common risks for ED are lower education, diabetes, heart disease, hypertension, cigarette smoking, obesity [22]. As early as possible we should reinforce patients (or even "non-yet-patients") to adopt healthy lifestyles with more physical activity to modify risk for sexual malfunction and for heart disease as well [15]. THE FEMALE SEXUAL DYSFUNCTION (FSD): The prevalence seems to be the same as in men. The most common complaints depending upon their age include decreased libido, vaginal dryness, pain with intercourse, decreased genital sensation and difficulty or inability to achieve orgasm [5]. One of the most important problems for older women are the availability of a sexually active partner and the presence of concurrent illnesses. We should ask for sexual history in older women because the need of love and sexual intimacy does not diminish with age [25]. The risks for FSD are age related as well as para-aging: level of education, history of sexual abuse or sexually transmitted disease, the "integrity" of physical health as well as the overall state general happiness [19]. DEPRESSION AS A RISC FACTOR FOR CAD AND IMPAIRMENT OF SEXUALITY: As cardiologists know sexual dysfunction may be a risk indicator for arteriosclerosis and for heart disease or even a consequence of heart disease. Depression is meanwhile recognized as a independent risk factor for MI. But the connexion of depression and sexual dysfunction is a common problem for psychiatrists', gynaecologists', urologists' and cardiologists' consulting-hours [2, 3, 18, 20, 21, 23]. HEART FAILURE AND SEXUALITY: There is very little data available on this topic. Data are dealing with the need of information for patients and partners on the physical stress during sexual activity [33]. RISK STRATIFICATION FOR SEXUAL ACTIVITY DEPENDING ON THE CLINICAL STATUS OF HEART DISEASE: The examples for clinical status are given in a simple scheme of the Princeton Consensus Panel. Patients with low risk (the large majority of patients) can be safely encouraged to initiate or resume sexual activity or to receive treatment for sexual dysfunction. In group 2 patients with an intermediate risk should undergo cardiologic evaluation before restratification into low- or high-risk category. In the high-risk patients there is a precondition before resuming sexual activity: stabilisation by specific treatment [13]. CONCLUSIONS: Think on the sexual dysfunction when treating female and male cardiologic patients. Work together with other disciplines (gynaecology, psychiatry, sexual medicine, urology) when evaluating a treatment plan. As early as possible try to reinforce lifestyle change for risk factor modification. The absolute risk for death or MI during sexual activity is very low even in patients with known CAD.     

Early neurohormonal effects of trandolapril in patients with left ventricular dysfunction and a recent acute myocardial infarction: a double-blind, randomized, placebo-controlled multicentre study

Angiotensin-converting enzyme inhibitors improve long-term survival in patients with left ventricular dysfunction after a myocardial infarction, but their mechanism of action is not entirely clear. The neurohormonal effects may be important in this respect, as well as an early hemodynamic unloading induced by these drugs. The primary objective was to assess the effect of trandolapril on plasma levels of atrial natriuretic peptide. A secondary objective was to assess the effects of trandolapril on selected neurohormones, vasoactive peptides and enzymes, which may be important in the development of left ventricular remodeling and heart failure following an acute myocardial infarction. A total of 119 patients with an acute myocardial infarction and a wall motion index < or =1.2 (16-segment echocardiographic model) were randomized to double blind treatment with trandolapril or placebo within 3-7 days after the onset of infarction. Blind treatment was discontinued 21 days after the index infarction. Venous blood samples were collected at rest, before randomization and on the day after treatment was discontinued. At the end of the study, there were no differences in plasma levels of atrial natriuretic peptide between the two treatment groups. Angiotensin-converting enzyme activity was suppressed and plasma renin activity was higher in the trandolapril group. No differences in plasma levels of N-terminal pro-atrial natriuretic peptide, brain natriuretic peptide, aldosterone, noradrenaline, adrenaline, vasopressin, big endothelin-1 and neuropeptide Y were found between the two treatment groups. There were positive correlations between several markers of neurohormonal activation at baseline and variables expressing left ventricular dysfunction and clinical heart failure. Neurohormonal activation is related to left ventricular dysfunction. The effects of 2-3 weeks of angiotensin-converting enzyme inhibition on neurohormonal activation does not predict the already established beneficial long-term effects after myocardial infarction. Thus, early modulation of circulatory neurohormone levels may not be a major mechanism for the efficacy of angiotensin-converting enzyme inhibitors in these patients. Selected plasma hormone markers may still be used to identify patients who might get the greatest benefit from treatment.     

Are beta‐blockers effective in patients who develop heart failure soon after myocardial infarction? A meta‐regression analysis of randomised trials

BACKGROUND: The great majority of post-infarction studies of beta-blockers were conducted in an era when these agents were widely held to be contra-indicated for the management of heart failure. We now know that beta-blockers are highly effective for the management of patients with chronic stable heart failure. However, there remains uncertainty about their role in the setting of post-infarction heart failure and ventricular dysfunction. AIM: the primary objective in this paper, was to investigate the extent to which heart failure or evidence of major cardiac dysfunction influenced outcome in previous trials of beta-blockers in heart failure after myocardial infarction. METHODS: We assessed the extent to which the inclusion of patients with heart failure or major cardiac dysfunction influenced outcome in randomised trials of long-term use of beta-blockade after myocardial infarction. The primary analysis was to assess the extent to which the proportion of patients included in each trial with heart failure influenced the relative odds of all-cause mortality in the trials. All randomised trials without crossover with treatment lasting more than one month and with 50 or more patients were considered. All those that provided information on the proportion of patients with heart failure or major cardiac dysfunction in the original or subsequent articles were included in the analysis. RESULTS: Overall treatment with a beta-blocker was associated with a 22.6% reduction in the odds of death (95% C1 11-32.3%). There were very few data on the effects of beta-blockers after myocardial infarction in patients with documented left ventricular systolic dysfunction. In the analysis that included heart failure as a factor, treatment with a beta-blocker was associated with a non-significant interaction with the presence of heart failure. However, because the group including heart failure patients were at higher risk, the absolute benefit of treatment with beta-blockers appeared greater in this group. CONCLUSIONS: This analysis suggests that the relative benefit of beta-blockers on mortality after a myocardial infarction is similar in the presence or absence of heart failure but that the absolute benefit may be greater in the former. However, as current clinical practice has changed radically from the time when the majority of these trials were conducted, further trial evidence would be desirable.