Hypertension and cardiac arrhythmias

Transcription

1 CardioPulse 223 doi: /eurheartj/ehw664 Hypertension and cardiac arrhythmias A consensus document from the European Heart Rhythm Association (EHRA) and European Society of Cardiology (ESC) Council on Hypertension, endorsed by the Heart Rhythm Society (HRS), Asia-Pacific Heart Rhythm Society (APHRS), and Sociedad Latinoamericana de Estimulacion Cardıaca y Electrofisiologıa (SOLEACE) Hypertension has been recognized as the principal and most common risk factor responsible for death and disability of noncommunicable diseases worldwide. Indeed, high blood pressure leads to heart failure, coronary artery disease, stroke, peripheral artery disease, and chronic renal failure. The heart contributes to blood pressure and suffers the consequences. Focussed on the heart, different cardiac arrhythmias have been recognized as clinical manifestations of hypertensive heart disease, related to structural and functional pathophysiological changes of the myocardium, which may predispose to arrhythmias. Left ventricular hypertrophy (LVH) is one of the clearest manifestations of hypertensive target organ damage, and several supraventricular and ventricular arrhythmias may occur in hypertensive patients, especially in those with LVH or heart failure. Also, some of the antihypertensive drugs commonly used to reduce blood pressure, such as thiazide diuretics, may result in electrolyte abnormalities further contributing to arrhythmias. Effective blood pressure reduction and sustained BP control over years may prevent the development of these arrhythmias and its complications. In recognizing this close relationship between hypertension and arrhythmias, the EHRA and the Council on Hypertension of the ESC convened a Task Force, with representation from the HRS, APHRS, and SOLEACE, with the remit to comprehensively review the available evidence and publish a joint consensus document on hypertension and cardiac arrhythmias providing up-to-date consensus recommendations for use in clinical practice. The consensus statement has been written by 15 authors chaired by Prof. Gregory Lip representing the EHRA and Prof. Antonio Coca representing the ESC Council on Hypertension. In addition, a group of 15 external official reviewers co-ordinated by Prof. G.A. Dan revised the manuscript introducing more than 400 suggestions and criticisms, which contributed to improve the document. The full version of this important consensus document is published in the Europace journal, with an executive summary published simultaneously in the European Heart Journal: Cardiovascular Pharmacotherapy. The aim of the Task Force has been to prepare an expert consensus and evidence-based document reviewing the best available scientific evidence on this issue and to update the current knowledge in this field, not only for the cardiology community but also for other specialists who see patients with hypertension, particularly general internists, nephrologists, endocrinologists, and general practitioners, all of whom have to take decisions in the clinical evaluation and treatment of these patients. We hope to achieve this aim through this comprehensive consensus document, which has been written in a comprehensive way based in the best available evidence. The ultimate judgment regarding care of a particular patient must be made by the healthcare provider and the patient considering all the circumstances presented by that patient, in a holistic approach. The major consensus statements are listed as follows Assessment, screening, and approach to management Patients with frequent supraventricular premature beats (SVPBs) and LVH have a higher probability of atrial fibrillation (AF) and prolonged ECG monitoring for AF detection may be considered. Majority of patients with SVPBs can be managed by lifestyle changes including addressing precipitants relevant to some patients (e.g. alcohol, caffeine) and optimizing BP control especially where LVH is present Atrial fibrillation should be considered as a manifestation of hypertensive heart disease. Given that stroke prevention is central to the management of AF patients, detection of hypertension and good blood pressure control is essential in minimizing the risk of stroke and thromboembolism, as well as bleeding whilst on antithrombotic therapy Silent AF is common, and opportunistic screening for underlying AF amongst hypertensive patients should be considered. In hypertensive patients with symptoms suggestive of a cardiac rhythm disorder, documentation of the presence and type of arrhythmia is essential for adequate management of the arrhythmia. Both sinus node and atrioventricular conduction disturbances (particularly in patients with LVH) can occur in hypertensive patients as a consequence of sleep apnoea and sleep disordered breathing is more common in hypertensive patient Conduction delays occur both at the atrial and ventricular level in hypertensive patients, particularly in those with LVH, leading to AF

2 224 CardioPulse or sudden cardiac death (SCD), respectively. The presence of left bundle branch block in hypertension, especially with LVH identifies patients at increased cardiovascular risk. An increased resting heart rate (>80 85 b.p.m.), portends an adverse prognosis not only in patients with coronary artery disease and heart failure, but in hypertensive patients as well. Intervention trials have not convincingly demonstrated that lowering the heart rate with use of beta-blockers or other agents is beneficial in hypertensive subjects uncomplicated by other comorbidities (e.g. impaired left ventricular (LV) function). Patients with hypertension are prone to bradyarrhythmias, mostly due to drug-related effects conferred by use of beta-blockers or non-dihydropyridine calcium channel blockers or more commonly their combination, which should be used with caution. Particular attention should be paid to those with chronic kidney disease leading to drug or active metabolite accumulation. Specific management issues (a) Supraventricular arrhythmias Oral amiodarone may be considered for ongoing management in patients with symptomatic supraventricular tachycardia (SVT) who are not candidates for, or prefer not to undergo, catheter ablation and in whom beta blockers, diltiazem, flecainide, propafenone, sotalol, or verapamil are ineffective or contraindicated. The priority in the treatment of patients with AF is stroke prevention, and AF patients with hypertension have a CHA 2 DS 2 -VASc score of at least 1; thus, effective stroke prevention should be considered with oral anticoagulation (OAC) as well as good BP control. With additional stroke risk factors CHA2 DS 2 -VASc score 2, OAC is recommended, as well controlled vitamin K antagonist (VKA) [Time in Therapeutic Range (TTR) >70%] or a nonvitamin K antagonist oral anticoagulants (NOAC), with a preference for the latter. Bleeding risk is assessed with focus on the modifiable bleeding risk factors, most of which can be identified using the HAS-BLED score. The HAS-BLED score should be used to identify those high risk patients (score 3) for more careful review and follow-up, and to address the reversible bleeding risk factors (e.g. uncontrolled hypertension). A high HAS-BLED score alone is not a reason to withhold OAC. AF ablation is recommended in hypertensive patients with symptomatic recurrences of AF on antiarrhythmic drug therapy who prefer further rhythm control therapy, and may be considered as first therapy in selected individuals as an alternative to antiarrhythmic drug therapy depending on patient choice, benefit, and risk. In patients with re-entrant SVT and isthmus dependent flutter, catheter ablation is recommended and is associated with a high success and low complication rate (b) Ventricular arrhythmias Frequent ventricular premature beats (VPBs), couplets, or nonsustained ventricular arrhythmias (NSVA) should prompt a careful clinical history and examination, blood chemistry, a 12-lead ECG, and a 24-h Holter recording. Transthoracic echocardiography should be considered when assessing hypertensive patients with arrhythmias to assess for signs of hypertensive or structural heart disease. Exercise testing or other functional testing for ischaemia may be considered for patients with suspected coronary disease and frequent VPBs or associated symptoms, both for assessing suppression or worsening of VPBs and for evaluating the presence of myocardial ischaemia. Further non-invasive testing or coronary angiography may be considered if necessary/needed. Serological studies including electrolyte levels, glucose, and thyroid studies should be checked to assess for reversible, secondary causes of increased ventricular ectopy. Identification of non-prescription or non-pharmacologic sources of increased adrenergic stimulation, including intake of alcohol, caffeine, other stimulants including recreational drugs, should be documented through history taking in order to provide appropriate counselling and/or assistance as needed Finding of frequent VPBs and/or non-sustained ventricular tachycardia should prompt investigation for structural heart disease, including with transthoracic echocardiography or cardiac MRI In patients with severe structural heart diseases, such as severe LVH, history of myocardial infarction and heart failure, a haemodynamically significant valvular disease, flecainide, or propafenone should be avoided. Sotalol should be avoided in LVH patients. Diltiazem and verapamil are contraindicated in heart failure with reduced ejection fraction. Miscellaneous considerations Achieving and maintaining adequate BP control remain the primary goals in management of patients with hypertension and ventricular arrhythmias, especially if severe LV systolic dysfunction [Ejection fraction (EF)<35%] is present Beta blockers are recommended for management of hypertension in the setting of coronary artery disease and heart failure Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are also recommended for hypertension management in patients at high risk for SCD Avoiding hypokalaemia or QT prolonging drugs in the context of HTN and LVH may be important In patients with sustained ventricular arrhythmias or frequent NSVA with LV systolic dysfunction antiarrhythmic drugs, catheter ablation, and/or implantable cardioverter defibrillator (ICD) implantation should be considered in addition to antihypertensive therapy Persistent, severe LV systolic dysfunction, despite adequate blood pressure and other heart failure management, with frequent VPBs in patients thought to have a premature ventricular complexes induced cardiomyopathy, ICD implantation may be considered, if coronary disease is evident. In patients with symptomatic systolic heart failure not caused by coronary artery disease ICDs do not significantly lower long-term mortality compared to usual clinical care Using anticoagulants for stroke prevention in hypertensive patients with AF The use of OAC to reduce the risk of stroke should be considered in most AF patients with hypertension, including those with AF in whom hypertension is the single additional stroke risk factor. Shared, informed decision-making regarding the risks and benefits of OAC therapy should be used, especially where hypertension is the single additional risk factor for stroke. Well-controlled anticoagulation intensity (i.e. a TTR of 65 70%) is crucial for achieving the optimal risk/benefit ratio with VKA therapy. Compared to VKAs, NOACs offer additional safety benefit provided that there is good adherence to treatment.

3 CardioPulse 225 Optimal blood pressure control is of key importance for minimizing the risks of AF-related stroke and OAC-related bleeding. Until more data are available, target BP values in AF patients taking OAC should be below 140mmHg for systolic BP and below 90mmHg for diastolic BP. OAC should be used with caution in patients with persistent uncontrolled hypertension (systolic BP 180mmHg and/or diastolic BP 100mmHg) but strenuous efforts to control BP should be made. Antonio Coca (Spain, representing ESC Council on Hypertension) Task Force co-chair On behalf of the Task Force Hypertension and Vascular Risk Unit. Department of Internal Medicine. Hospital Clínic (IDIBAPS), University of Barcelona. Barcelona, Spain Gregory Y.H. Lip (UK, representing EHRA) Task Force chair On behalf of the Task Force University of Birmingham Institute of Cardiovascular Science, City Hospital, Birmingham, United Kingdom Aalborg Thrombosis Research Unit, Department of Clinical Medicine, Aalborg University, Aalborg, Denmark. Reference 1. Lip GYH, Coca A, Marin F, et al. Hypertension and cardiac arrhythmias: A consensus document from the European Heart Rhythm Association (EHRA) and ESC Council on Hypertension, endorsed by the Heart Rhythm Society (HRS), Asia- Pacific Heart Rhythm Society (APHRS) and Sociedad Latinoamericana de Estimulacion Cardıaca y Electrofisiologıa (SOLEACE). Europace 2017; in press. doi: /eurheartj/ehw665 Evolving concepts for the Long QT Syndrome As in the history of earth with the Mesozoic and the Pleistocene Periods, there have been different epochs in the history of the long QT syndrome (LQTS). Someone with fantasy and no modesty may identify three such epochs, starting from 1957 to the mid-70s, from the late 70s to the mid-90s, and from the new millennium to the present. The milestones marking the beginnings and ends of these epochs would then be represented by (1) The ground-breaking report by Prof. Jervell of the first family with the LQTS variant with congenital deafness; 1 (2) The experimental reproduction of both QT prolongation and macroscopic T wave alternans in cats by stimulation of the left stellate ganglion, which highlighted the critical role of the left cardiac sympathetic nerves in triggering life-threatening arrhythmias; 2 (3) The institution of the international registry for LQTS, which has provided key information about the natural history and response to therapy and, by the identification of carefully phenotyped large LQTS families, paved the way to the genetic discoveries; 3 (4) The discovery of the 1st three major LQTS genes 4 6, one of the most dramatic turning points ever in clinical cardiology and genetics; (5) The realization of how tight the genotype-phenotype relationship can be, thus opening the initial approaches to gene-specific management and therapy; 7 (6) The current efforts toward the unravelling of the role and mechanism(s) of action of modifier genes, as described below. It goes without saying that the epochs just described represent my personal, and unabashedly biased, point of view. Here, I will focus the discussion on what the recent and ongoing studies on modifier genes have been showing so far and what their potential impact for the understanding and better management of LQTS may be. First things 1st familiar with LQTS have always known that within families with several affected members one always finds the patient with syncope and cardiac arrest and the patient who, despite a similarly prolonged QTc, goes through life without a single symptom. In the genetic era, it has become evident that this occurs also when the asymptomatic subject and the one with severe symptoms share the same, identical, disease-causing mutation. It is this realization that has forced the development of the concept that this dramatic phenotype variability is likely due to the presence, by chance, of genetic variants usually referred to as modifier genes capable of modifying in either direction the arrhythmic risk directly associated with the consequences of the specific mutation. This concept is exemplified by Figure 1. Once born, any concept like a plant needs water to develop and grow. In this case, the water is represented by the studies aiming to identify genetic variants that might, with reason, be considered to Figure 1 Illustration of the potential impact on outcome (survival vs sudden death) of the interaction between two arrhythmogenic substrates (acute myocardial infarction or heart failure, and mutations causing arrhythmogenic diseases) and a predominantly protecting or damaging clusters of common genetic variants (SNPs). As the cluster of SNPs of a given individual reflects the inheritance by the parents, this interaction is clearly governed by chance. (From Wellens et al. Eur Heart J 2014;35: with permission).

4 2017 专家共识 : 高血压和心律失常 左心室肥厚是高血压靶器官损害的最明确表现之一, 高血压患者 ( 尤其是左心室肥厚或心衰患者 ) 可能会出现室上性和室性心律失常 此外, 一些降压药物, 例如噻嗪类利尿剂, 有可能造成电解质异常而导致心律失常 有效降压和保持血压平稳可以帮助预防这些心律失常及并发症的发生 鉴于高血压和心律失常的密切关系, 欧洲心律学会 (EHRA) 和欧洲心脏病学会 (ESC) 高血压委员会组成了一个工作组, 同时集合了心律协会 (HRS) 亚太心律学会 (APHRS) 和拉丁美洲皇家学会 (SOLEACE) 的专家, 全面审查现有证据, 于 2017 年 2 月份发表了关于高血压和心律失常的联合共识 我们摘录了部分共识声明内容进行了整理 评估 筛查和管理路径 1 频发室上性早博和左心室肥厚患者发生房颤的可能性高, 或许可考虑持续 ECG 监测及时发现房颤 2 大多数室上性早博患者可通过改变生活方式 ( 例如限制酒精 咖啡因摄入 ) 和优化血压控制来管理, 尤其是当患者存在左心室肥厚时 3 出现房颤时, 应该考虑到可能是高血压性心脏病的一种表现 4 卒中预防对于房颤患者的管理至关重要, 高血压检测以及良好血压控制对于 降低卒中和血栓栓塞的风险起着重要的作用, 也可以降低抗栓治疗的出血风险

5 5 无症状性房颤比较常见, 应该考虑对高血压患者进行机会性筛查以发现潜在 的房颤 6 高血压患者有提示心律失常疾病的症状, 记录心律失常的发生以及类型对于 心律失常的充分治疗至关重要 7 高血压患者 ( 尤其是左心室肥厚患者 ) 有可能出现窦房结和房室传导阻滞, 高血压患者睡眠呼吸暂停和睡眠呼吸障碍后更易出现 8 心房和心室传导阻滞都有可能在高血压患者 ( 尤其是左心室肥厚患者 ) 中发 生, 可分别导致房颤和心源性猝死 高血压患者 ( 尤其是左心室肥厚患者 ) 存在 左束支传导阻滞, 提示患者的心血管风险增加 9 静息心率增加(>80-85bpm) 不仅预示冠脉疾病和心衰患者的预后不良, 同样也预示着高血压患者的预后不良 对于无其他并发症 ( 如左室功能受损 ) 的高血压患者, 干预试验没有得出明确的证据表明使用 β 受体阻滞剂或其他降低心率的药物可带来获益 10 高血压患者易发生缓慢性心律失常, 主要是由于药物相关的副作用, 如使用 β- 受体阻滞剂或非二氢吡啶类钙通道阻断剂, 两药联用更易导致上述副作用, 因此在使用时要谨慎 慢性肾病患者的药物或活性代谢物易在体内蓄积, 需要特别关注 具体问题室上性心律失常

6 1 有症状室上性心动过速的患者出现以下情况, 或许可以考虑口服胺碘酮进行 长期管理 : 不适合或者不愿意进行导管消融的患者 ;β 受体阻滞剂 地尔硫卓 氟卡尼 普罗帕酮 索他洛尔和维拉帕米等药物治疗无效或者有禁忌者 2 治疗房颤优先考虑的事情是预防卒中, 因为患有高血压的房颤患者的 CHA2DS2-VASc 评分至少为 1, 因此应考虑使用口服抗凝剂 (OAC) 以及良 好控制血压来有效预防卒中 3 如果卒中危险因素 CHA2DS2-VASc 评分 2, 推荐使用 OAC, 选择容易 控制的维生素 K 拮抗剂 ( 治疗窗内时间 TTR>70%) 或者非维生素 K 拮抗剂 口服抗凝药物, 后者是优选 4 对出血风险的评估主要集中在可改变的出血风险因素, 大多数可以通过 HAS-BLED 评分来确认 (1)HAS-BLED 评分应被用于确认 高危 患者 ( 评分 3), 可进行更仔细 的检查和随访, 以解决可逆的出血风险因素 ( 例如, 未控制的高血压 ) (2) 仅仅是 HAS-BLED 评分高, 不能成为停止 OAC 的原因 (3) 对于服用抗心律失常药物的高血压患者, 出现有症状房颤复发, 患者希望 能加强节律控制治疗, 推荐进行房颤消融治疗 房颤消融治疗也可作为某些患者 的首选治疗, 取决于患者的意愿 益处和风险

7 (4) 折返性室上性心动过速和峡部依赖性房补患者, 推荐进行导管消融治疗, 成功率高且并发症低 室性心律失常 1 频发室性早搏, 成对早搏, 或非持续性室性心律失常的患者, 应该仔细询问 病史和体检, 进行血液生化检查,12 导联 ECG 检查, 以及 24 小时动态心电 图检查 2 在评估有高血压的心律失常患者时, 考虑经胸超声心动图来发现高血压性或 结构性心脏病的迹象 3 疑似冠心病和有频发室性早搏或相关症状的患者, 或许可以考虑运动试验或 其他针对缺血的功能性试验, 以评估室性早搏的抑制或加重情况, 以及是否存在 心肌缺血 如果有必要 / 需要, 可以考虑非侵入性检测或冠脉造影 (1) 血清学检查, 包括电解质水平 葡萄糖和甲状腺等检查, 可用于评估心室 异位活动增加的可逆性继发原因 (2) 确认刺激肾上腺素分泌增加的非医疗性原因, 包括酒精 咖啡因 兴奋剂 的摄入等 采集病史后进行记录, 在需要时可提供适当的咨询和 / 或救助 (3) 发现患者有频发室性早搏和 / 或非持续性室性心动过速, 应该检查是否有 结构性心脏病, 包括经胸超声心动图或心脏 MRI

8 4 严重结构性心脏病的患者 ( 例如严重左心室肥厚, 心肌梗死和心衰史, 血流 动力学改变明显的瓣膜病 ), 应避免使用氟卡尼或普罗帕酮 左心室肥厚患者应 避免使用索他洛尔 射血分数降低的心衰患者, 禁用地尔硫卓和维拉帕米