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Heart and brain matters in heart failure: a literature review.

Abstract

Heart failure (HF) patients are reported to have twice the risk of having cognitive deficits compared to the general population. Cognitive impairment in this population may cause non-compliance to prescribed self-care regimens and delay in seeking care that may potentially lead to frequent readmissions. Although cognitive deficit is common among people with HF, cognitive screening is not routinely performed due to lack of a simple screening tool and the misconception that cognitive changes are part of normal aging. Therefore, future research needs to focus on identifying a simple screening tool that nurses can use to screen for subtle changes in cognition including forgetfulness and delayed recall. Early identification of subtle cognitive changes has the potential to guide healthcare providers to formulate feasible strategies to understand and/or prevent a low cardiac output state before major cognitive impairment becomes evident.

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Despite the decline in the incidence of other cardiovascular diseases, the incidence of heart failure (HF) remains unchanged, with more than 550,000 new cases diagnosed annually in the United States (American Heart Association, 2006). The prevalence and incidence of HF varies with age, gender, and ethnicity, presenting at higher rates among older adults (Barker, Mullooly, & Getchell, 2006), females (Levy et al., 2002), and African Americans (Wolinsky, Overhage, Strump, Lubitz, & Smith, 1997). In the 1950s, the most common causes of HF in the United States and other western nations were hypertension and valvular heart diseases (Braunwald & Bristow, 2000; Ho, Anderson, Kannel, Grossman, & Levy, 1993). Currently, the most common causes for HF are ischemic heart disease among older men, idiopathic dilated cardiomyopathy among young adults, and hypertension among older adults and females (Braunwald & Bristow, 2000; Ho et al., 1993). According to the American Heart Association (AHA), HF currently represents the single most costly cardiovascular illness in the United States, with an estimated direct and indirect cost of $29.6 billion for the year 2006 compared to $27.9 billion in 2005, of which $14.7 billion was paid in the year 2005 towards hospitalization alone (AHA, 2006; Heywood & Saltzberg, 2005). The cost for managing HF depends on the complexity of the disease and the complexity of services delivered (Galbreath et al., 2004).

Cognitive deficit in HF

Among the general population in the United States, the prevalence of dementia doubles with every 5 years of increase in age (Jorm, Scott, Cullen, & MacKinnon. 1991). Alarmingly, HF patients are reported to have twice (RR = 1.96) the risk of having cognitive dysfunction compared to the general population of those 65 years or older, with an increased prevalence of cognitive decline among older females (Cacciatore et al., 1998). Cognitive impairment was more prevalent in patients with HF 28.0% compared to those with cancer 25.8% (Corsonello et al., 2005). HF patients with cognitive dysfunction have a 66% increased relative risk of mortality compared to people with diabetes mellitus, myocardial infarction, stroke, cancer, and hip fractures (Finkel, 2003). The prevalence of cognitive dysfunction among HF patients ranges from 53% to 58%, with increasing prevalence among older adults (Zuccala et al., 2001). These figures are impressive when one considers the estimated prevalence of HF as 5 million in the United States.

Normal brain aging

Cognitive deficits without dementia are commonly considered a normal consequence of brain aging (Ritchie & Touchon, 2000). A number of clinical labels have been proposed to describe cognitive deficits that are considered part of the normal aging process. An early label for cognitive impairment was benign or malignant senescent forgetfulness (Kral, 1972). This early label was criticized and classified as age-associated memory impairment by Crooks in 1986 (Goldman & Morris, 2001), age-associated cognitive decline (Levy, 1994), and age-related cognitive decline in the DSM IV Criteria (Celsis, 2000), all of which fall within the limits of normal aging. Not all cognitively impaired people have dementia, and those who do not meet the current criteria for dementia have received less attention by researchers.

Cardiac dementia

The so-called cardiac dementia, a subtype of vascular dementia, recently has been introduced as a concept to explain cognitive deficits in HF (Rockwood, Bowler, Erkinjuntti, Hackinski, & Wallin, 1999). In contrast to the dementia related to many of the neurodegenerative illnesses, patterns of cognitive impairment arising from cardiac origin are subtle, with changes in memory and reasoning (Rockwood, Dobbs, Rule, Howlett, & Black, 1992). Multiple ischemic episodes due to atherosclerosis (Wallin & Blennow, 1993), chronic intermittent or diurnal ischemia due to cerebral infarcts (Erkinjuntti, 1997; Tatemichi, 1990), and atrial fibrillation (Sulkava & Erkinjuntti, 1987) resulting in embolic stroke have been identified as subsets of vascular dementia.

The type of cognitive deficit seen among people with HF differs in its pathology due to chronic cerebral hypoperfusion related to impaired cardiac function (Acanfora et al., 1996). Cardiac dementia as a sub-type of vascular dementia was originally identified in cases of cardiac dysarhythmias, such as third-degree atrio-ventricular block and sick sinus syndrome (Sulkava & Erkinjuntti, 1987). These conditions also cause chronic hypoperfusion due to hypotension or bradycardia that result in low cardiac output. Improved cognitive function has been reported after pacemaker implantation for symptomatic bradycardia (Koide, Kobayashi, Kitani, Tsunematsu, & Nakazawa, 1994). Similarly, improved cognitive function had been reported after heart transplant (Bornstein, Starling, Myerowitz, & Hass, 1995; Roman, Kubo, Ormaza, Francis, Bank, & Shumway, 1997; Scahll, Petrucci, Brozena, Cavarocchi, & Jessup, 1989), implantation of ventricular assistive device (Zimpfer et al., 2006), and cardiac resynchronization (Auricchio et al., 2002), A 30% improvement in cognitive performance was demonstrated with the use of ACE inhibitors (Zuccala, Onder et al., 2005). The findings of reversible cognitive deficit suggest that the type of cognitive deficit seen in chronic HF is cardiogenic dementia related to chronic cerebral hypoperfusion.

Cerebral hypoperfusion

By definition, HF is a disorder that results in inadequate tissue and organ perfusion (Braunwald & Bristow, 2000), and the brain is the vital organ that requires large amounts of oxygen for adequate function (Lezak, 1994). HF is classically defined by hemodynamic concepts. The pathophysiology of cognitive deficits in HF is the result of inadequate cerebral perfusion to the areas of brain due to impaired cardiac function in HF (Pullicino & Hart, 2001). Significant impairment in hemodynamic measures such as low cardiac output, left ventricular ejection fraction (LVEF) and left ventricular filling pressures causes inadequate supply of oxygen to all tissues and organs (Cohn, Ferrari, & Sharpe, 2000). Decline in cognitive function has been associated with diminished ejection fraction, low cardiac output, and/or cardiac index and supports the role of reduced cerebral blood flow and cerebral perfusion among HF patients as an explanation of cognitive deficit (Gorkin et al., 1993; Roman et al., 1997; Zuccala, Marzetti et al, 2005). On the contrary, a nurse-based interventional study on HF reported no correlation between mini mental state examination (MMSE) score and left ventricular ejection fraction (Karlsson et al., 2005).

A similar pathophysiology of chronic cerebral hypoperfusion-induced progressive brain injury has been reported in animal models (Dijkhuizen et al., 1998; Sarti, Pantoni, Bartolini, & Inzitari, 2002; Tanaka, Wada, & Ogawal, 2000), among stroke survivors (Patel, Coshall, Rudd, & Wolfe, 2003), and sudden cardiac arrest survivors (Sauve, Doolittle, Walker, Paul, & Scheinman, 1996). Moreover, the episodic decompensation of HF symptoms resulting in hypoxia may predispose to autoneurotoxicity or neural cell death throughout the nervous system due to loss of brain plasticity resulting in cognitive dysfunction (Kolb, Gibb, & Robinson, 2003). It is clearly evident from the literature that the impaired cardiac function that causes cerebral hypoperfusion is the common etiology for cognitive deficits among HF patients (Almeida & Flicker, 2001). Collectively, it has been suggested that cerebral hypoperfusion might account for the disproportionate prevalence of cognitive impairment among patients with HF (Putzke, Williams, Rayburn, Kirklin, & Boll, 1998).

Mild cognitive impairment

The cognitive deficits seen in HF are subtle. The subtle cognitive changes in HF mimic mild cognitive impairment (MCI) by character and pathology. MCI refers to the clinical state of individuals who have memory impairment but are otherwise functioning normally (Petersen et al., 2001). MCI has been increasingly recognized as a neurologic transition stage between normal cognitive function that progresses to dementia or Alzheimer's disease (Petersen et al., 2006).

Similarly, in HF the cognitive dysfunctions are subtle transient impairment affecting verbal memory, forgetfulness, delayed recall, and impaired learning (Antonelli et al., 2003). Most often, these subtle cognitive changes are not identified by practitioners until the person displays inability to carry out everyday activities or are reported by family members (Antonelli et al., 2003).

Meyer, Rauch, Rauch, & Haque (2000) followed a total of 224 normal subjects for a mean period of 5.8 years who were at increased risk for cognitive decline and reported a decreased cortical perfusion in patients with MCI suggesting a decreased brain perfusion as an etiology for MCI. A similar reduction in brain perfusion to the posterior cortical area was associated with HF, suggesting that persons with MCI and HF manifest similar pathological changes in the brain due to hypoperfusion that manifests in subtle cognitive dysfunction (Alves et al., 2005; Skoog, Palmertz, & Anderson, 1994).

Impact of cognitive dysfunction in HF Poor adherence to self-care

Wehby and Brenner (1999) found that patients with HF find it difficult to retain information and do not appreciate the relevance of the information provided by their clinicians resulting in non-compliance to prescribed self-care regimens for management of HF. Cline and colleagues (1999) found that only 55% of HF patients could correctly name their prescribed medications and 27% were not following their HF treatment regimens (Cline, Bjorck-Linne, Israelsson, Willenheimer, & Erhardt, 1999). Several authors have reported similar deficits in memory, forgetfulness, and other cognitive abilities that affect adherence to HF self-care practices (Almeida & Flicker, 2001; Antonelli et al, 2003; Grubb, Simpson, & Fox, 2000; Lackey, 2004; Leventhal, Riegel, Carlson, & DeGeest, 2005).

Delay in seeking care

Deaton and Grady (2004) reported that symptom monitoring in HF is difficult for patients and multiple factors such as older age, lower education, and lack of social support are associated with inadequate self-care behavior, non-compliance to self-care practices, and delay in seeking treatment for HF symptoms. Similarly, Friedman (1997) reported that older adults experienced symptoms of HF for a relatively longer time than younger adults before obtaining health care. Recently, Jurgens (2006) developed a model combining physical and cognitive aspects of the HF symptom experience to examine delay in care-seeking among HF patients. She found that cognitively impaired HF patients have poor somatic awareness for HF symptoms that predict delay in seeking care.

Increased readmission rates

The economic impact of HF is driven largely by high hospital readmission rates: 2%, 15%20%, and 50% within 2 days, 1 month, and 6 months of initial diagnosis, respectively (Aghababian, 2002; Foote, 2003). Older adults with HF have the highest hospital readmission rates, ranging from 29% to 47% of all hospitalized adult patients, primarily in the first few weeks after discharge (Hammer & Ellison, 2005). Approximately 50% of the readmissions of people with HF have been attributed to lack of knowledge and adherence to self-care recommendations (Clark, Tu, Weiner, & Murray, 2003). Knox and Mischike (1999) reported that HF exacerbation due to non-compliance with diet (18%), noncompliance to medication (15%), lack of social support (21%), and failure to seek prompt medical attention (20%) led to hospital readmission. Similarly, lack of compliance to HF self-care regimen increased hospital readmission rates by 20-64% (Leventhal et al., 2005; Stromberg, Matensson, Fridlund, Levin, Karlsson, & Dahlstron, 2003). Lack of knowledge alone, however, was not a predictor for readmission among HF patients (Bennett, Baker, & Huster, 1998). Until recently, researchers have focused on providing cost-effective management such as: tailored education (Sethares & Elliott, 2004); family support (Dunbar, Clark, Deaton, Smith, De, & O'Brien, 2005); individual peer support (Riegel & Carlson, 2004); enhanced discharge planning (Pugh, Haven, Xie, Robinson, & Blaha, 2001); disease management programs (Rich et al., 1995); specialized nurse management programs (Stewart & Horowitz, 2003); home visiting, education, and support intervention (Krumholz et al., 2002); team management (Grady et al., 2000); and comprehensive discharge planning (Naylor et al., 1999) in an effort to reduce readmissions. To date, cognitive deficits among people with HF have not been examined as a factor influencing hospital readmissions.

Increased mortality rates

Cognitive impairment is associated with a fivefold increase in mortality of HF patients, with a relative risk of 4.9 (Zuccala et al., 2003). Even taking into account other co-morbidities that are associated with increased mortality among patients with HF such as stroke (Tatemichi, Desmond, Stern, Paik, Sano, Bagiella, 1994), diabetes (Croxson & Jagger, 1995), atrial fibrillation (Kilander, Andren, Nyman, Lind, Boberg, & Lithell, 1998), and anemia (Beard, 2003). Of all comorbidities, 38% was related to cognitive impairment (Lien, Gillespie, Struthers & McMurdo, 2002), thus making cognitive deficit an independent prognostic marker among patients with HF.

Impaired quality of life

Severity of HF associated with NYHA functional classification of III or IV predicted worse health-related quality of life (Bennett, Cordes, Westmoreland, Castro, & Donnelly, 2000). Poor self-reported cognitive function also has been correlated with poor health-related quality of life among patients with HF, particularly regarding emotional aspects (Juenger et al., 2002). In addition, being older and having HF have been identified as factors that limit functional abilities and impair quality of life among NYHA class III HF patients (DeJong, Moser, & Chung, 2005). Cognitive screening in HF Although cognitive deficit among HF patients is common and can be reversed with therapies, cognitive screening is not routinely performed in the outpatient setting. An extensive literature review on cognitive deficit in HF showed that HF researchers have used a variety of neuropsychological instruments, anywhere from 4-10 in a single study (Antonelli et al., 2003; Bornstein et al., 1995, Trojano et al., 2003). However, no simple screening instrument that identifies subtle cognitive changes is available for use in the clinical arena (Riegel et al., 2002). Researchers have mainly focused on (a) understanding the etiology of cognitive dysfunction in HF (Pullicino, Mifsud, Wong, Graham, Ali, & Smajlovic, 2001), (b) describing the types of subtle cognitive dysfunction in HF (Grubb et al., 2000; Putzke et al., 1998; Trojano et al., 2003), and (c) explaining reversibility of cognitive dysfunction following interventions such as heart transplant (Roman et al., 1997; Schall et al., 1989). The inconsistencies in the use of neuropsychological instruments among HF researchers limit the ability to make comparisons across studies. In addition, the HF literature indicates that a global neuropsychological measure, such as the MMSE is not sensitive enough to capture the early subtle cognitive changes manifested by HF patients due to hypoperfusion (Cupples & Stilley, 2005).

Although cognitive dysfunction is reversible in HF, it is apparent that sustained reduction in cardiac output may lead to permanent, nonreversible cognitive impairment when the hypoperfusion state reaches its neural threshold, called the "ischemic penumbra" (Heiss, 2000; Saita et al., 2004). The ischemic penumbra represents part of the hypoperfused region associated with focal brain ischemia that potentially can be salvaged by timely intervention. Therefore, early identification of the subtle cognitive changes in HF patients is important before they cross this ischemic threshold, to prevent permanent cognitive impairment. In addition, the U.S. Preventive Service Task Force Guidelines calls for routine screening for cognitive changes among all older adults to identify reversible causes for cognitive deficits (Boustani, Peterson, Hanson, Harris, & Lohr, 2003). Thus, a routine cognitive screening among HF patients is necessary.

Implications for practice

Because of the high incidence of HF, it is important to recognize the incidence of potential cognitive impairment in this population that may cause non-compliance to prescribed HF regimen, delay in seeking care for HF symptoms, and potential frequent readmissions to hospitals and emergency room visits. Currently, no simple cognitive screening tool to assess early cognitive changes among HF patients is available for use by nurses in the clinic or home care setting. Riegel and colleagues (2002) have tested four cognitive screening instruments among people with HF, including the MMSE. Riegel reported varied effectiveness among the screening tools, with only 2.4% of their participants scoring below the clinical cutoff score of 24 on the MMSE, confirming low sensitivity of the MMSE in picking up subtle cognitive changes among their HF participants. Riegel recommended further research to identify a simple cognitive measurement tool to pick up early changes. Using several cognitive screening tools takes time and is not feasible to do routinely in an outpatient setting. Future research may need to focus on identifying a simple cognitive screening tool that will help nurses screen for early cognitive changes during their encounter in the clinic or during home visiting. Often, family members report early cognitive changes such as forgetfulness and delayed recall in their loved ones to nurses and nurse practitioners more than to physicians. Early identification of these subtle cognitive changes has the potential to guide healthcare providers to formulate feasible strategies to understand and/ or prevent low cardiac output state before the cerebral perfusion pressure crosses the ischemic threshold resulting in permanent non-reversible cognitive deficits. Early identification of potential cognitive dysfunction by nursing staff may enable healthcare providers to make appropriate referrals for neuropsychological testing as warranted. Early screening of cognitive deficit may enhance adherence to heart failure regimen by HF patients and thus reduce hospital and ICU admissions. Lastly, addressing cognitive function may improve quality of life in HF patients.

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Ponrathi Athilingam, PhD, RN, ACNP

Kathleen B. King, PhD, RN, FAHA, FAAN

Ponrathi Athilingam is a nurse practitioner at Strong Memorial Hospital, University of Rochester Medical Center in Rochester, NY. Kathleen B. King is a professor emeritus at the University of Rochester School of Nursing, Rochester, NY.
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Author:Athilingam, Ponrathi; King, Kathleen B.
Publication:Journal of the New York State Nurses Association
Article Type:Clinical report
Geographic Code:1U2NY
Date:Sep 22, 2007
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