Heart Failure in Acute Ischemic Stroke


Heart failure (HF) is a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood. HF is characterized by specific symptoms (dyspnea and fatigue) in the medical history and signs (edema, rales) during physical examination.

The clinical syndrome of HF may result from disorders of the pericardium, myocardium, endocardium, or great vessels, but the majority of patients with HF have symptoms due to an impairment of left ventricle (LV) myocardial function. Coronary artery disease (CAD), hypertension, valvular disease and dilated cardiomyopathy are the main causes of HF in the western world [4]. Cardiomyopathies (CM) are a heterogeneous group of diseases of the myocardium associated with mechanical and/or electrical dysfunction; there is a variety of causes, frequently genetic. Inappropriate ventricular hypertrophy or dilatation is usually exhibited [5,6].

The classification system most commonly used to quantify the degree of functional limitation was developed by the New York Heart Association (NYHA). This system assigns patients to a functional class based on the degree of effort needed to elicit symptoms: Class I- symptoms of HF only at activity levels that would limit normal individuals; Class II- symptoms of HF with ordinary exertion; Class III- symptoms of HF with less than ordinary exertion; and Class IV- symptoms of HF at rest.

However, there is a poor relationship between measures of cardiac performance and the symptoms produced by the disease. Patients with a very low EF may be asymptomatic, whereas patients with preserved LVEF may have severe disability. In fact, it is estimated that although 2.9% of the USA population has an EF≤30%, only half of these individuals have symptomatic HF [7].

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HF is a progressive disorder. Its development has been characterized by 4 stages: Stage A- High risk for HF without structural heart disease or symptoms; Stage B- Heart disease with asymptomatic LV dysfunction; Stage C- Prior or current symptoms of HF; Stage D- Refractory end stage HF. In contrast to NYHA classification, this staging system emphasizes the progressive nature of HF and defines the appropriate therapeutic approach for each stage.

The principal manifestation of the progression is a change in the geometry and structure of the LV, such that the chamber dilates and/or hypertrophies and becomes more spherical—a process referred to as cardiac remodeling. Cardiac remodeling generally precedes the development of symptoms (occasionally by months or even years), continues after the appearance of symptoms, and contributes substantially to worsening of symptoms despite treatment. The activation of endogenous neurohormonal systems plays an important role in cardiac remodeling and thereby in the progression of HF.

Patients with HF have elevated circulating or tissue levels of norepinephrine, angiotensin II, aldosterone, endothelin, vasopressin, and cytokines, which can act (alone or in concert) to adversely affect the structure and function of the heart. These neurohormonal factors not only increase the hemodynamic stresses on the ventricle by causing sodium retention and peripheral vasoconstriction but may also exert direct toxic effects on cardiac cells.

Heart failure has been traditionally classified as “diastolic” (preserved EF) or “systolic” (reduced EF). However, this nomenclature has become the subject of controversy [8] and some have suggested that the phenotypic expression of HF occurs on a continuum, with underlying myocardial dysfunction present in the early stages of the syndrome when diastolic abnormalities predominate [9]. Since 2005 the American College of Cardiology-American Heart Association (ACC/AHA) guidelines for the diagnosis and management of heart failure have used the term “heart failure with preserved or normal ejection fraction” (HFNEF) rather than “diastolic heart failure” [1]. Depending on the criteria used to delineate HF and the accepted cutoff for defining preserved LVEF, it is estimated that as many as 20% to 60% of patients with HF have a relatively normal LVEF and, in the absence of valvular disease, are believed to have reduced ventricular compliance as a major contributor to the clinical syndrome [10,11]. In HFNEF, clinical presentation can be as dramatic as that in patients with low LVEF, for example in patients admitted with acute pulmonary edema [12].

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In general, a definitive diagnosis of HFNEF can be made when the rate of ventricular relaxation is slowed according to some diagnostic criteria [13]. In practice, the diagnosis is generally based on the finding of typical symptoms and signs of HF in a patient who is shown to have a normal LVEF and no valvular abnormalities (aortic stenosis or mitral regurgitation, for example) on echocardiography.

In the Acute Decompensated Heart Failure National Registry (ADHERE) database [14], among 52 187 patients admitted to hospital for acute decompensated HF, patients with HFNEF (n = 26 322) were more likely to be older and female, and less likely to have CAD or a previous myocardial infarction. The HFNEF group was more likely to have comorbidities such as hypertension and diabetes than patients with HF and low EF. Atrial fibrillation (AF) and obesity have also been associated with HFNEF more frequently than HF with low EF [10,15].

HF is the end stage of a cardiac disease and therefore prognosis is poor. The 1-year mortality rate for HF is high (20%) and 5-year survival is lower in men than in women: 59% of men and 45% of women will die within 5 years of HF diagnosis [3].

The ADHERE registry [14] also revealed a lower overall mortality in HFNEF patients compared with low EF patients, whereas symptom burden, duration of intensive care unit stay, overall length of hospital stay, and long-term mortality were similar between the two groups.

Most, but not all, series of patients with HFNEF have shown better survival than is seen in patients with HF and reduced LVEF [10,11,16]. Moreover, secular trends have revealed slightly improved survival in patients with HF and low EF over the past 20 years, attributed to recent therapeutic advances in the treatment of systolic HF. Nevertheless, death rates from HFNEF remained unchanged. [10,11,16] These studies highlight a change in HF epidemiology, with HFNEF prevalence increasing along with increasing age of the population, and the inadequacy of current therapeutic options for this disease.

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