Heart Disease and Atrial Fibrillation

In: Disease

21 Apr 2010

Heart DiseaseINTRODUCTION

Traditionally, chronic heart failure (HF) has been attributed to a reduced systolic left ventricular (LV) function, accompanied by an increase in LV filling pressures and volumes (also called “systolic HF”). The important role of neuro-hormones in the pathophysiology of chronic HF is well recognized. Chronic HF is characterized by an increased activity of the neurohormonal system, such as the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS).

Beta-adrenergic blocking agents (beta blockers) and angio-tensin-converting enzyme (ACE)-inhibitors or angiotensin II receptor blockers (ARBs) are well known as keystones in the medical treatment of systolic HF because of their ability to suppress sympathetic drive and the RAAS. However, during the past decade, it has become clear that about 50% of all patients with chronic HF have preserved LV systolic function (also called “diastolic HF”). Diastolic HF is suspected in patients with signs and symptoms of HF and a normal or mildly reduced systolic LV ejection fraction (LVEF) greater than 40% and normal LV end-diastolic volumes.┬áDiastolic HF may arise as a consequence of various underlying conditions that result in a modification of the physical properties of the myocardium. These conditions (e.g., hypertension, ischemic heart disease, atrial fibrillation [AF], and valvular heart disease) can cause a structural impairment of the heart.

One study identified many patients with isolated AF or valvular heart disease, or both, who had dyspnea and normal or near-normal LV function. There is no doubt today that diastolic HF is a pathophysiological clinical condition, distinct from or concomitant with systolic HF. However, many questions remain, not the least of which concerns methods of treatment, because these two syndromes are not identical.

Previous studies have confirmed that the sympathetic nervous system is activated prior to the RAAS during the development of chronic HF, and plasma norepinephrine is one of the most powerful predictors of mortality in early chronic HF. The Metoprolol CR/XL Randomized Intervention in Congestive Heart Failure (MERIT-HF) trial demonstrated consistent and similar improvement in outcomes of patients receiving con-trolled-release or extended-release when combined with either a high or low dose of an ACE-inhibitor or digitalis or no digitalis at all.

Long-term beta-blocker treatment in chronic HF patients who have already been treated with ACE-inhibitors showed plasma renin levels comparable to those without ACE-inhibitors. Indeed, the suppression of angiotensin II by an ACE-inhibitor is more effiective in patients who are also receiving a beta blocker, and the escape (inhibitive effect) of angiotensin II from ACE-inhibitors is attenuated in such patients. Beta blockers have a renin-inhibiting effect and therefore hinder the sympathetic nervous system as well as the RAAS. These results suggest that beta blockers probably have a more pronounced protective effect than ACE-inhibitors against elevations in neurohormones.

Rheumatic heart disease (RHD) often results in two main pathophysiological changes: mitral valve stenosis and AF. AF is the most common cause of chronic HF resulting from a loss of atrial contraction and an associated rapid ventricular rate in patients with RHD. Both mitral stenosis and AF result in a low cardiac output that activates the sympathetic nervous system. Ozdemir et al. noted increased sympathetic activity in patients with RHD, especially in patients whose disease was complicated by AF. AF was an independent predictor of a higher risk of diastolic HF in patients hospitalized with chronic HF.

Several studies have shown important differences in efficacy among different agents. Metoprolol canadian succinate (e.g., AstraZeneca) and (e.g., Concor®, Merck) are both selective beta1 antagonists, whereas canadian carvedilol (GlaxoSmithKline) is a nonselective beta blocker with additional beta1-blocking and antioxidant properties. A selective beta1 blocker without a vasodilatory effect can decrease the ventricular rate by suppressing sympathetic drive and without having a deteriorative effect on low cardiac output. Therefore, we thought that a selective beta1 blocker might be more feasible for treating chronic HF related to RHD concomitant with AF. However, the effects and mechanisms of this agent in this subgroup of patients remain to be explored.

The aim of our study was to analyze the effects of bisopro-lol therapy for six to 12 months on the clinical symptoms and prognosis in patients with chronic HF and normal or near-normal systolic function related to RHD and AF.


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