I50.2 is a non-billable ICD-10 code for Systolic (congestive) heart failure. It should not be used for HIPAA-covered transactions as a more specific code is available to choose from below. Heart failure with reduced ejection fraction [HFrEF]
Although the prevalence of stage B patients in individual studies varied from 0.9% to 12.9% in the community, adjustment for the above factors yielded 3% to 6% as a reasonable estimate for the presence of asymptomatic LVSD in the adult population. Therefore, asymptomatic LVSD, or stage B, is at least as common as symptomatic HF (stages C and D).
The resultant changes in LV shape toward a more spherical, less efficient chamber (increased sphericity) are accompanied by an increased end-diastolic volume, reduced systolic function (low LVEF), and a decrease in ventricular compliance.
Because substantial evidence indicates that pharmacological intervention may have an effect on the risk of progression to HF and death, identification of patients who are asymptomatic would then appear to be a priority. However, recognition of asymptomatic LVSD is a challenge that our present diagnostic methods have yet to answer completely.
Asymptomatic left ventricular systolic dysfunction (ALVSD) is defined as depressed LV systolic function in the absence of heart failure. Studies of asymptomatic LV systolic dysfunction have used heterogeneous criteria to identify this condition.
Asymptomatic left ventricular systolic dysfunction (ALVSD), classified as stage B heart failure, is defined as depressed left ventricular systolic function in the absence of clinical heart failure. Early initiation of therapies in patients with presumed ALVSD has been shown to lead to better outcomes.
Left ventricular systolic dysfunction (LVSD) is a common and serious complication of myocardial infarction (MI) that leads to greatly increased risks of sudden death and of heart failure. Effective and cost effective treatment is available for such patients that can reduce both morbidity and mortality.
When the provider has linked either diastolic or systolic dysfunction with acute or chronic heart failure, it should be coded as 'acute/chronic diastolic or systolic heart failure. ' If there is no provider documentation linking the two conditions, assign code I50. 9, Heart failure, unspecified.”
Numerous cardiac disorders can lead to a decline in left ventricular ejection fraction (LVEF) without heart failure (HF) symptoms, which is referred to as asymptomatic LV systolic dysfunction (ALVSD).
Right ventricular (RV) systolic dysfunction is an established prognostic factor in heart failure,1 myocardial infarction,2 and pulmonary hypertension (PH).
Left ventricular ejection fraction (LVEF) is the central measure of left ventricular systolic function. LVEF is the fraction of chamber volume ejected in systole (stroke volume) in relation to the volume of the blood in the ventricle at the end of diastole (end-diastolic volume).
Systolic dysfunction is clinically associated with left ventricular failure in the presence of marked cardiomegaly, while diastolic dysfunction is accompanied by pulmonary congestion together with a normal or only slightly enlarged ventricle.
Background. Left ventricular diastolic dysfunction (DD) is defined as the inability of the ventricle to fill to a normal end-diastolic volume, both during exercise as well as at rest, while left atrial pressure does not exceed 12 mm Hg.
Heart Failure, UnspecifiedICD-9 Code Transition: 428.0 Code I50. 9 is the diagnosis code used for Heart Failure, Unspecified. It is a disorder characterized by the inability of the heart to pump blood at an adequate volume to meet tissue metabolic requirements.
ICD-10 | Unspecified systolic (congestive) heart failure (I50. 20)
I50.2 is a non-billable ICD-10 code for Systolic (congestive) heart failure. It should not be used for HIPAA-covered transactions as a more specific code is available to choose from below.
DO NOT include the decimal point when electronically filing claims as it may be rejected. Some clearinghouses may remove it for you but to avoid having a rejected claim due to an invalid ICD-10 code, do not include the decimal point when submitting claims electronically.
Many of the patients in these trials might be correctly classified as stage B, because LVSD was commonly a primary determinant for enrollment, often without a concomitant need for HF symptoms. A review of these studies provides important insights into the role of medical therapy for patients with asymptomatic LVSD.
The assumption has been that most LVSD progresses gradually, beginning with myocardial injury of various causes, most commonly due to the loss of functioning myocytes from an acute infarction , often exacerbated by hypertension or diabetes mellitus. Depending on the extent of acute injury to the myocardium, clinical evidence of HF occurs in only 2% to 20% of patients within the first 4 weeks after an MI. 10 The initial loss of cardiac function results in the activation of compensatory mechanisms, such as peripheral vasoconstriction, salt and water retention, or enhanced contractility of noninfarcted myocardium, to maintain homeostatic levels of systemic blood flow and pressure. In the ensuing weeks and months, structural changes (remodeling) result in an increased LV chamber size (dilatation) and wall thickness (hypertrophy), accompanied by myocardial fibrosis. The resultant changes in LV shape toward a more spherical, less efficient chamber (increased sphericity) are accompanied by an increased end-diastolic volume, reduced systolic function (low LVEF), and a decrease in ventricular compliance. These remodeling forces are mediated in part by the neurohormones of the sympathetic nervous system and the renin-angiotensin-aldosterone system. The remodeling process can persist despite the absence of any further myocardial injury, producing progressive increases in LV volume and concomitant diminution of contractility. This progression of structural deterioration leads to the eventual emergence of HF symptoms in an increasing proportion of patients.
There are 2 primary challenges for clinicians in attempting to manage this group of patients: treatment compliance and a paucity of evidence-based recommendations. Patients with asymptomatic LVSD feel good and may be unwilling to take medications for an extended period of time, especially if they lead to side effects or increased healthcare costs. Also, data supporting the use of specific therapies are limited. Without a structured screening program, identification of asymptomatic patients is difficult, because they are unlikely to present for care. Unfortunately, no cost-effective screening program has been developed. In this population, most of the existing studies are in patients presenting with coronary ischemia who, in the course of their evaluation, are identified as having LVSD without symptoms of HF. Only limited data are available for patients with nonischemic cardiomyopathies, who in clinical practice are most commonly identified incidentally from an abnormal ECG or chest radiograph.
Stage B includes patients with asymptomatic abnormalities of cardiac structure. It is possible, of course, that many patients with these myocardial disorders minimize or deny their symptoms, despite demonstrable exercise intolerance. The onset of HF symptoms is gradual and may not be appreciated or acknowledged by patients. These patients may remain apparently symptom-free by unconsciously reducing activity levels to compensate for worsening exertional symptoms. Therefore, clinicians may need objective testing, including formal exercise testing, to truly differentiate stage B from stage C patients. This makes the identification of stage B patients in epidemiological or treatment trials more challenging.
As ymptomatic LVSD, as a precursor to HF and cardiovascular death, is an important contemporary health problem. The elderly, men, and those with CAD, hypertension, and diabetes mellitus are at greatest risk for developing asymptomatic LVSD. Those with a family history of nonischemic cardiomyopathy may also be at risk for the development of asymptomatic LVSD. Because HF represents the product of a progressive continuum of LVSD, initiated by myocardial injury and perpetuated by neurohormonally mediated remodeling, both ACE inhibitors and β-blockers can limit the progression of asymptomatic LVSD to HF and reduce the risk of death and hospitalization. There is no role for the use of digoxin, and the role of aldosterone antagonists remains unknown. ICD prophylactic therapy may be appropriate in post-MI patients. Treatment of underlying factors or comorbidities, such as hypertension and diabetes, may also slow HF progression. Populations at risk for the development of asymptomatic LVSD should be screened to identify those patients who might benefit from pharmacological interventions. More effort should be focused on finding appropriate treatment for populations such as women and blacks, because these groups have been underrepresented in trials that include asymptomatic LVSD. One potential, although not validated, screening strategy is measurement of plasma BNP in the high-risk population, followed by echocardiography in those patients with elevated BNP. A clinical trial to provide data leading to a consensus recommendation for screening is needed. Through diagnosis and screening, an increased identification of patients with asymptomatic LVSD may lead to the early initiation of appropriate pharmacological therapy. Appropriate therapy, in turn, can improve outcomes and decrease morbidity, mortality, and progression to clinical HF.