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Hypertension and Cardiac Arrhythmias: a Review of the Epidemiology, Pathophysiology and Clinical Implications

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Hypertension and Cardiac Arrhythmias: a Review of the Epidemiology, Pathophysiology and Clinical Implications Journal of Human Hypertension (2008) 22, 380–388 & 2008 Nature Publishing Group All rights reserved 0950-9240/08 $30.00 www.nature.com/jhh REVIEW Hypertension and cardiac arrhythmias: a review of the epidemiology, pathophysiology and clinical implications K-H Yiu and H-F Tse Division of Cardiology, Department of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong, China Hypertension is commonly associated with cardiac cular ectopy and sudden cardiac death. Recent arrhythmias in patients with and without concomitant prospective clinical trials reveal that antihyper- cardiovascular disease. Experimental and epidemiolo- tensive therapy may delay or prevent the occurrence gical studies have demonstrated potential links of cardiac arrhythmias and sudden cardiac death in between hypertension and atrial and ventricular arrhyth- patients with hypertension. Although antihypertensive mias, although the underlying pathophysiological me- agents that block the renin–angiotensin–aldosterone chanism remains unclear. Nonetheless, the importance system appear to protect against cardiac arrhythmias, of hypertension as a cause of atrial and ventricular this needs to be confirmed by current ongoing clinical arrhythmias is not well recognized. In particular, trials. the occurrence of left ventricular hypertrophy is a Journal of Human Hypertension (2008) 22, 380–388; strong predictor for the development of AF, ventri- doi:10.1038/jhh.2008.10; published online 13 March 2008 Keywords: atrial fibrillation; arrhythmia; sudden cardiac death Introduction Epidemiology Concomitant cardiac arrhythmias are commonly Atrial fibrillation seen in patients with hypertension, although the Atrial fibrillation is the most common sustained mechanism of this association is unclear. The arrhythmia in adults and is associated with an contribution of hypertension to the development of increased risk for cardiovascular morbidity, mortality atrial and ventricular arrhythmias is unrecognized and stroke.1,2 The incidence of AF increases with age; and thus undertreated. Recent clinical trials have a prevalence of 0.1% in adults younger than 55 years demonstrated the possible preventive role of anti- increases to 9% in adults older than 80 years.3,4 In hypertensive agents, in particular those that induce the Framingham Heart Study, the lifetime risk for blockade of the renin–angiotensin–aldosterone sys- developing AF was one in four in men and women tem (RAAS). The aim of this paper is to review the aged 40 years or above.5 Among different risk epidemiology, underlying mechanisms and clinical factors, hypertension is one of the important implications of atrial and ventricular arrhythmias independent risk factors for the development of in hypertensive patients. We searched MEDLINE AF.6 In the Cardiovascular Health Study of subjects using the following terms individually and/or in older than 65 years of age, the risk for developing combination: ‘atrial fibrillation (AF)’, ‘left ventricu- new-onset AF was higher in hypertensive patients: lar hypertrophy (LVH)’, ‘hypertension’, ‘ventricular the relative risk was 1.11 after adjustment for age arrhythmias’ and ‘sudden cardiac death (SCD)’. In and other covariates.7 addition, abstracts from international cardiovascular The Framingham Study cohort8 also demonstrated meetings were studied to identify unpublished that hypertension and diabetes were the only studies. cardiovascular risk factors that were responsible for the development of new-onset AF. Hypertension was responsible for more AF in the population (14%) than any other risk factor due to its high Correspondence: Professor H-F Tse, Division of Cardiology, prevalence. After adjusting for age, hypertension Department of Medicine, Queen Mary Hospital, The University increased the risk of AF by 80% in female patients of Hong Kong, Room 1928, Block K, Hong Kong, China. E-mail: [email protected] and 70% in male patients. In addition, evidence of Received 28 November 2007; revised 19 January 2008; accepted LVH on ECG was associated with at least a threefold 26 January 2008; published online 13 March 2008 increased risk for AF. In the Progetto Ipertensione Hypertension and cardiac arrhythmias K-H Yiu and H-F Tse 381 Umbria Monitoraggio Ambulatoriale (PIUMA) Study, age and left ventricular (LV) mass as measured by echocardiogram were independent predictors for new-onset AF after a mean follow-up period of 5.3 years.9 The high prevalence of coexistent hypertension and AF is also reflected by the high proportion of hypertensive patients who require antihypertensive treatment (470%) and who are participating in major clinical trials on AF, such as the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) Study10 and the Stroke Prevention Using an Oral Thrombin Inhibitor in Atrial Fibrillation (SPORTIF III) Study.11 Ventricular arrhythmia In patients with hypertension, the most important Figure 1 Potential mechanisms of atrial fibrillation related to determinant for the occurrence of ventricular ar- hypertension. rhythmia is the presence of LVH. Several studies have shown that hypertensive patients with LVH Renin–angiotensin–aldosterone system. It has been have an increased frequency of premature ventricu- well demonstrated that activation of the RAAS lar ectopic beats and ventricular arrhythmias.12–15 In occurs in patients with hypertension21 and is the Framingham Heart Study, echocardiographic strongly implicated in the development of AF.22 evidence of LVH was associated with ventricular Evidence is accumulating that explains the link arrhythmia independent of conventional cardio- vascular risk factors.12 In untreated hypertensive between RAAS and AF: there are two receptor subtypes that act as binding sites for angiotensin patients, non-sustained ventricular arrhythmia II, namely AT1 and AT2. Most of the known effects was observed in up to 5% of patients during 24-h of angiotensin II in adult tissue are attributable to Holter monitoring.14 the actions AT1 receptor and acts antagonistically by the action of AT2.23 In addition to its known Sudden cardiac death physiological effects (vasoconstriction, aldosterone The presence of LVH is strongly correlated with and vasopressin release, sodium and water retention SCD, although a direct causal relationship has not and sympathetic facilitation), AT1 also induces been identified.16,17 In the Framingham Heart atrial myocyte hypertrophy and fibrosis that predis- Study,17 an incremental increase in LV mass by pose an individual to development of AF.24 Upre- 50 g mÀ2 conferred a 45% higher risk of SCD in gulation of the AT1 receptor in the left atrium in hypertensive subjects aged 440 years. Increased LV patients with AF, but not the AT2 receptor, has been mass and LVH were also associated with a long-term demonstrated.25 In contrast, there is downregulation risk of sudden death. The presence of asymptomatic of AT1 and upregulation of AT2 in the right complex or frequent ventricular arrhythmia in the atrium.26 Angiotensin II is known to induce pro- absence of coronary artery disease was also asso- liferation of fibroblasts and extracellular matrix ciated with a 62% increase in mortality.18 Electro- protein accumulation via activation of the mitogen- physiological studies in hypertensive patients with activated protein kinases.27 Experimental studies LVH have nonetheless yielded conflicting show that inhibition of this angiotensin II pathway results.19,20 In symptomatic hypertensive patients, attenuates the formation of fibrosis and diminishes the presence of LVH increased susceptibility to the the incidence of AF.28 In a hypertensive rat heart development of malignant ventricular arrhythmia model, the degree of atrial fibrosis correlated with during programmed ventricular stimulation.20 the susceptibility for development of atrial tachy- cardia.29 Structural remodelling of the atria related to the activation of RAAS can thus contribute to the Pathophysiology development of AF in hypertension. In an animal model, rapid atrial pacing resulted in The development of atrial and ventricular arrhyth- atrial electrical remodelling, characterized by short- mias in hypertensive patients and patients with LVH ening of the atrial effective refractory period and appears to be complex. It is, nonetheless, clearly loss of the normal rate adaptation of refractoriness.30 evident that hypertension and LVH exert a robust Blockade of RAAS can prevent the development of proarrhythmic effect on the heart. electrical remodelling for short (3 h),31 but not long periods of time (1–5 weeks).32 It has been postulated Atrial fibrillation that an increased angiotensin II level is proarrhyth- In patients with hypertension, several mechanisms mic due to increased intracellular calcium. The may contribute to the development of AF (Figure 1). latter is due to increased intake of extracellular Journal of Human Hypertension Hypertension and cardiac arrhythmias K-H Yiu and H-F Tse 382 calcium and increased release from the sarcoplas- mic reticulum through the activation of membrane L-type calcium channels or phosphatidylinositol– phospholipase C pathways.33,34 In addition, activa- tion of RAAS may lead to inflammation: this has also been implicated in the pathogenesis of AF.35 Experimental studies have shown that angiotensin II possesses proinflammatory properties, inducing the production of reactive oxygen species, inflammatory cytokines and adhesion molecules.36 In accordance with this observation, angiotensin II receptor block- ade
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