Artigo Revisado por pares

AMERICAN SOCIETY FOR PREVENTIVE CARDIOLOGY

2007; Wiley; Volume: 10; Issue: 1 Linguagem: Inglês

10.1111/j.1520-037x.2007.05976.x

ISSN

1751-7141

Autores

Douglas D. Schocken,

Tópico(s)

Cardiovascular Function and Risk Factors

Resumo

Since the American College of Cardiology/American Heart Association (ACC/AHA) Guidelines for the Evaluation and Management of Chronic Heart Failure made its appearance in 2001 and was subsequently updated in 2005, a revolution has been afoot in the medical community. The long-respected (but often misused) New York Heart Association classification system for heart failure (HF) based on symptomatic functional status using classes I through IV was joined by a new system of staging based on pathophysiology and clinical picture. This staging classification system places new emphasis on 2 new concepts: consideration of risk (stage A) and consideration of structural disease in the absence of symptoms (stage B). I'd like to focus here on stage A HF, an enormous problem with a big identity crisis. Stage A HF in patients is defined as a high risk for HF but without structural heart disease or symptoms of HF. Obviously, this is a huge population. Many individuals have the traditional risk factors for heart disease: hypertension, dyslipidemia, tobacco use, diabetes mellitus, obesity, and sedentary lifestyle. I speak to audiences of generalists throughout the country and they tell me repeatedly, “I don't treat heart failure.” On the other hand, many of my cardiology colleagues tell me, “This [stage A disease] isn't heart failure.” Each of these responses couldn't be further from the truth. As caregivers, we need to come together to connect the dots. In the present era, it is apparent that for practical purposes we should assume that adult cardiac myocytes are not a self-renewing resource. Therefore, preservation of as many properly working myocytes—functional myocyte reserve—is key to both avoiding HF and sustaining functional capacity in a whole-body context. At the core of preventing stages B, C, and D HF through aggressive approaches to stage A disease is the prevention of loss of myocytes through infarction or accelerated apoptosis, prevention of abnormal myocyte growth through ventricular hypertrophy, and prevention of the maladaptive ventricular remodeling that leads to altered geometry and altered ventricular function inherent to stage B, C, and D disease. The evidence to connect the dots is more apparent when one examines stage B disease. This point is a good one to both peer down the slippery slope to stage C and D as well as up the slope to the “gate house” at stage A. It is abundantly clear that patients with stage B disease have decreased survival when compared with disease-free population controls. Similarly, stage B disease represents the initiation of the maladaptive remodeling phenomenon more likely to move down the slope to stage C and symptomatic HF, since we've already progressed irreversibly from stage A (in this present era when we understand little about the process or product of reverse remodeling). At least a dozen clinical trials have conclusively demonstrated that intervention in conventional risk factors in patients at variable risk with structural disease based on clinical documentation but without prevalent HF symptoms (stage B) prevents the development of HF end points. Whether management of hypertension (Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial [ALLHAT]), dyslipidemia (Heart Protection Study [HPS]), or diabetes and hypertension (UK Prospective Diabetes Study [UKPDS]), these and other trials have demonstrated the robust impact of risk factor intervention in preventing clinical HF. What about preventing risk or addressing “sub-clinical” risk? Here is the crux of stage A intervention. Data are beginning to accrue to support the hypothesis that effective prevention begins earlier than we previously imagined feasible or relevant. The publication of the Diabetes Prevention Program in 2002 was an important landmark in this regard. The investigators convincingly established that metformin could prevent the development of diabetes in a population of at-risk individuals. Even more impressive, however, was the ability of lifestyle intervention (diet and exercise) to prevent diabetes in a similarly at-risk sample drawn from the same group of trial subjects. More recently, the Diabetes Reduction Approaches With Ramipril and Rosiglitazone Medications (DREAM) trial has shown that rosiglitazone, a drug in the thiazolidinedione family used to manage diabetes, is able to prevent the development of diabetes in a population of patients with impaired glucose tolerance. Therapeutic lifestyle change remains at the core of managing hypertension, with well-documented efficacy in lowering both systolic and diastolic blood pressures. On the other hand, the publication of the Trial of Preventing Hypertension (TROPHY) earlier in 2006 demonstrated that hypertension could be prevented from appearing in prehypertensive patients by treatment with the angiotensin receptor blocker candesartan when compared with a placebo control group. It follows from the goals of the ACC/AHA guidelines that the preservation of functional myocyte reserve is also dependent on avoiding cardiotoxic agents such as exposure to tobacco and excess alcohol ingestion. The above paragraphs help underscore the beginning of what should be a growing movement to act earlier in the prevention of cardiovascular disease with preemptive approaches to the risk factors themselves. Stage A HF appears to be, indeed, ready for prime time. In other news, the Society is busily making plans for the coming year. Rollout of a new (and improved) American Society for Preventive Cardiology (ASPC) Web page should be forthcoming. Stay tuned. The AHA Council on Cardiovascular Disease Epidemiology and Prevention will be holding its 47th Annual Scientific Conference in Orlando on February 28–March 3, 2007, in association with the Council on Nutrition, Physical Activity and Metabolism. Make plans to attend. The highly anticipated (and always entertaining) ASPC-sponsored debate promises to again be a hit. Please also plan to attend the ASPC annual membership dinner while at the meeting in Orlando (details to follow). The Joseph Stokes Award will be presented at that time. Registration and housing forms for the AHA Council on Epidemiology and Prevention Meeting are available at my.americanheart.org. The coming year should mark even more changes for the ASPC. Please join us. Membership forms are in this issue of Preventive Cardiology.

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