Search

Abstract: This American Society of Hypertension position paper focuses on the importance of out-of-office blood pressure (BP) measurement for the clinical management of patients with hypertension and its complications. Studies have supported direct and independent associations of cardiovascular risk with ambulatory BP and inverse associations with the degree of BP reduction from day to night. Self-monitoring of the BP (or home BP monitoring) also has advantages in evaluating patients with hypertension, especially those already on drug treatment, but less is known about its relation to future cardiovascular events. Data derived from ambulatory BP monitoring (ABPM) allow the identification of high-risk patients, independent from the BP obtained in the clinic or office setting. While neither ABPM nor self-BP monitoring are mandatory for the routine diagnosis of hypertension, these modalities can enhance the ability for identification of white-coat and masked hypertension and evaluate the extent of BP control in patients on drug therapy. [Copyright &y& Elsevier]

Because most of myocardial perfusion takes place during diastole, reducing the heart rate is likely to have anti-ischaemic effects. The present paper reviews the role of heart rate in relation to coronary artery disease outcome, as well as ways to reduce heart rate in the clinical setting. Nonpharmacological intervention, and particularly exercise training, has a definite effect on both heart rate reduction and the prevention of myocardial ischaemia. The protective role of β-blockers after acute myocardial infarction is amply documented; their anti-ischaemic efficacy appears to be attributable to their effect on heart rate, but also to their role in cardiac inotropism. Recently, the If (funny) current inhibitor ivabradine, which has a potent heart rate reduction effect without any haemodynamic effect has demonstrated anti-ischaemic efficacy in a randomised trial versus placebo, as well as in trials where it showed an effect similar to that of the conventional anti-ischaemic agents amlodipine and atenolol. In addition, such an agent, which does not influence myocardial contractility, might be particularly valuable in the setting of myocardial stunning or acute left ventricular failure at the acute stage of myocardial infarction. However, only future studies will determine whether isolated heart rate reduction will have the same protective efficacy as that of β-blocking agents in secondary prevention after myocardial infarction. Keywords: heart rate, myocardial ischaemia, β-blockers, If current, ivabradine Résumé La perfusion myocardique a lieu principalement pendant la période diastolique. Dans cette revue, les liens entre fréquence cardiaque et maladie coronaire sont rappelés et les traitements utilisables pour abaisser la fréquence cardiaque en clinique humaine sont passés en revue. Parmi ceux-ci, certains sont de nature non médicamenteuse, comme l’entraînement à l’effort, et ont démontré un effet à la fois sur le ralentissement de la fréquence cardiaque, tant au repos qu’à l’effort, et sur l’ischémie myocardique. Parmi les traitements médicamenteux anti-ischémiques, les β-bloquants représentent le chef de file incontesté. Outre leur impact sur la fréquence cardiaque, ils ont une action de prévention secondaire établie dans le post-infarctus. Leur action anti-ischémique est cependant vraisemblablement à la fois la résultante de la bradycardie qu’ils induisent, mais aussi de la baisse de contractilité. Les résultats récemment obtenus avec l’ivabradine, inhibiteur sélectif des canaux If (dits de pacemaker), sont à cet égard particulièrement intéressants car ils démontrent qu’un médicament agissant uniquement en réduisant la fréquence cardiaque et n’ayant aucun effet hémodynamique a une action anti-ischémique vérifiée contre placebo chez le coronarien stable, et comparable à l’effet anti-ischémique de l’amlodipine ou de l’aténolol. Par ailleurs, un tel médicament pourrait avoir un intérêt tout particulier dans les situations aiguës telles que la sidération myocardique ou les décompensations ventriculaires gauches aiguës au stade aigu de l’infarctus. Il faudra cependant attendre avant de savoir si la simple réduction de fréquence cardiaque permet d’obtenir la même efficacité de prévention secondaire que les β-bloquants. Mots clés : fréquence cardiaque, ischémie myocardique, β-bloquants, courant If, ivabradine [ABSTRACT FROM AUTHOR]

Summary: A recent analysis by the Blood Pressure Lowering Treatment Trialists’ Collaboration revealed that any commonly-used blood pressure (BP)-lowering regimen reduced the risk of total major cardiovascular events, and larger reductions in BP produced larger reductions in the risk. These observations suggest that most of the differences among treatment regimens in their effects on cardiovascular outcomes could be explained by the differences in achieved BP level. However, it may also be true that some treatment regimen is superior or inferior to others with regard to the risk reduction of cardiovascular events. Indeed, the data from dihydropyridine-based calcium antagonist (DHP) trails are consistent in that they could not protect against new-onset heart failure or progression of renal disease in patients with left-ventricular systolic dysfunction or overt proteinuria, respectively. However, a multicenter, randomized, placebo-controlled, double-blind ACTION trial, which compared the effect of long-acting nifedipine or placebo on mortality and cardiovascular morbidity in patients with stable angina, revealed that nifedipine reduced the risk for new-onset overt heart failure by 29%. Further, an open-label, randomized prospective J-MIND trial, which compared the effect of long-acting nifedipine or enalapril, an angiotensin-converting enzyme inhibitor on onset and progression of nephropathy in hypertensive patients with type 2 diabetes, showed that long-acting nifedipine had an equipotent reoprotective effect on diabetic nephropathy. In this paper, we would like to propose our hypothesis that nifedipine may be unique and superior in its effects on heart failure and proteinuria compared with various DHPs. For ensuring our hypothesis, the following clinical issues would be addressed. Does nifedipine treatment alone decrease the progression of renal disease with overt proteinuria? If these answers are yes, are these beneficial effects of nifedipine superior to that of other DHPs with equihypotensive properties? Does nifedipine treatment also reduce oxidative stress markers? Are these unique effects of nifedipine correlated with its anti-oxidative properties? These prospective studies will provide further valuable information whether nifedipine may be a preferred DHP to achieve BP goals in hypertensive patients with systolic dysfunction or overt proteinuria. [Copyright &y& Elsevier]