Arterial hypertension and systolic left ventricular dysfunction: therapeutic approach

Arterial hypertension is a cardinal precursor of congestive heart failure, and diastolic dysfunction is the most frequent mechanism for it. Systolic left ventricular dysfunction, although less frequent, has a worse prognosis. Most cases of systolic dysfunction in patients with hypertension is due to acute myocardial infarction, although other mechanisms can be involved. In some studies, non-ischemic hypertensive systolic dysfunction is the etiology of chronic heart failure in up to 10% of patients with dilated cardiomyopathy. Diastolic dysfunction and left ventricular hypertrophy are also associated with a higher risk of heart failure and systolic dysfunction. Given the poor prognosis of patients with congestive heart failure and dilated cardiomyopathy, it is fundamental to try to prevent the development of left ventricular dysfunction by means of a correct control of blood pressure, regression of left ventricular hypertrophy and prevention of coronary artery disease. When systolic dysfunction is established, angiotensin converting enzyme inhibitors are the treatment of choice; diuretics and digoxin can be added in patients with overt congestive heart failure. Recent studies suggest that other drugs, such as carvedilol and losartan, can be beneficial, but current evidence is still scarce.     

Left ventricular diastolic dysfunction as a cause of congestive heart failure. Mechanisms and management.

OBJECTIVE: To define the mechanisms underlying left ventricular diastolic dysfunction in patients with congestive heart failure and normal systolic function and to identify the patients at risk for this syndrome. STUDY SELECTION: Studies were selected that describe the clinical observations of congestive heart failure with normal systolic function and that provide experimental and clinical insights into the mechanisms responsible for ventricular diastolic dysfunction. DATA SYNTHESIS: Recent studies indicate that a large number of patients (up to 40% in some series) presenting with congestive heart failure have preserved left ventricular systolic function. The factors contributing to altered left ventricular diastolic function include fibrosis, hypertrophy, ischemia, and increased afterload. The latter three factors, alone or in combination, predispose to impaired left ventricular relaxation, an active energy-requiring process. Thus, decreased left ventricular diastolic distensibility (increased diastolic pressure at any level of diastolic volume) may arise not only from altered passive elastic properties stemming from fibrosis or increased muscle mass but also from derangements in the dynamics of ventricular relaxation. RESULTS: In patients with essential hypertension, all four of the above mechanisms may be operative. Considering the prevalence of hypertension in the general population, hypertension appears to be an important underlying factor in many patients with heart failure on the basis of diastolic mechanisms. In the patient presenting with dyspnea and elevated filling pressures, but with a nondilated, normally contracting ventricle, treatment with standard heart failure medications (such as digitalis, diuretics, and vasodilators) is often ineffective and may be deleterious. Such patients may respond more favorably to beta-blockers and calcium-channel blockers. CONCLUSIONS: Diastolic dysfunction should be considered in the patient presenting with heart failure symptoms but with normal systolic function, particularly in hypertensive patients with left ventricular hypertrophy.     

Obesity and the heart

Obesity has been identified as an independent risk factor for coronary heart disease and congestive heart failure. Although congestive heart failure can be secondary to coronary heart disease, in morbid obesity these conditions can be independent. Cardiac structure and function can be altered even in the absence of systemic hypertension and underlying organic heart disease. In obese patients total blood volume increases and creates a high cardiac output state that may cause ventricular dilatation and ultimately eccentric hypertrophy of the left (and possibly the right) ventricle. Eccentric left ventricular hypertrophy produces diastolic dysfunction. Systolic dysfunction may ensue due to excessive wall stress if wall thickening fails to keep pace with dilatation. This disorder is referred to as obesity cardiomyopathy. The frequent coexistence of systemic hypertension in obese individuals facilitates development of left ventricular dilatation and hypertrophy. Congestive heart failure may occur and may be attributable to left ventricular diastolic dysfunction or to combined diastolic and systolic dysfunction. The risk of coronary heart disease seems to be more strictly correlated to central obesity than to increased body mass index. Insulin resistance seems to be the key factor that links obesity and ischaemic heart disease. In such a condition the so called Syndrome X appears. It is characterized by: obesity, systemic hypertension, diabetes mellitus, hypertriglyceridaemia and reduced HDL cholesterol levels. Considering that left ventricular hypertrophy is often present, many risk factors coexist in obese patients. Weight loss is very useful in obese patients. It may reduce mortality and morbidity for coronary heart disease and delay or avoid the appearance of congestive heart failure. It is proved that after weight loss, blood pressure, glucose, cholesterol, triglycerides and left ventricular mass decrease.     

From left ventricular hypertrophy to congestive heart failure: management of hypertensive heart disease

Other than age, left ventricular hypertrophy (LVH) is the most potent predictor of adverse cardiovascular outcomes in the hypertensive population, and is an independent risk factor for coronary heart disease, sudden death, heart failure and stroke. Although directly related to systolic blood pressure, other factors including age, sex, race, body mass index and stimulation of the renin-angiotensin-aldosterone and sympathetic nervous systems play an important role in the pathogenesis of LVH. LVH involves changes in myocardial tissue architecture consisting of perivascular and myocardial fibrosis and medial thickening of intramyocardial coronary arteries, in addition to myocyte hypertrophy. The physiologic alterations which occur as a result of these anatomical changes include disturbances of myocardial blood flow, the development of an arrhythmogenic myocardial substrate and diastolic dysfunction. The latter is directly related to the degree of myocardial fibrosis and is the hemodynamic hallmark of hypertensive heart disease. When diastolic dysfunction is present, left ventricular end-diastolic pressure increases out-of-proportion to volume and may be elevated at rest or with exertion leading to clinical heart failure. At least one third of heart failure patients in the United States can be considered to have heart failure related to diastolic dysfunction. Compared to heart failure patients with systolic dysfunction, diastolic heart failure patients are more likely to be older, female, and to be hypertensive at the time of presentation. Although it has been assumed that LVH may lead to systolic dysfunction, evidence is lacking that LVH resulting from hypertension is a major risk factor for systolic heart failure independent of coronary artery disease. Treatment of hypertension greatly attenuates the development of LVH and significantly decreases the incidence of heart failure. In patients with established LVH, regression is both possible and desirable and results in a significant reduction in adverse clinical endpoints.     

Hochdruck und Herz

Arterial hypertension often leads to diseases of kidneys, vessels and brain. Besides these end organ damages the changes of the heart are of important role. Substantial consequences of hypertension are microangiopathy, interstitial fibrosis and left ventricular hypertrophy. Hence, as an early stage diastolic dysfunction results. Due to longer persistent hypertension also systolic dysfunction develops. Clinically, patients suffer from angina pectoris, dyspnoea and cardiac arrhythmias (i.e. atrial arrhythmia, atrial fibrillation). The left ventricular hypertrophy also is associated with an increased risk of malignant ventricular arrhythmias. The risk of sudden cardiac death is raised as well, in particular in patients with dilated heart and reduced left ventricular ejection fraction. Well controlled antihypertensive therapy could lead to a regression of left ventricular hypertrophy. Hence, disorders and prognosis of the patients could be improved.     

Aspects of the Use of Angiotensin-Converting Enzyme Inhibitors and Calcium Antagonists in Treatment of Heart Failure in the Older Patient

The syndrome of congestive heart failure may result from either systolic or diastolic dysfunction of the left ventricle. Diastolic left ventricle dysfunction is particularly common in the geriatric age group, and is associated with left ventricular hypertrophy resulting from aging and hypertension. The clinical differentiation of these two patterns is important in understanding the pathophysiologic process and in selecting appropriate therapy. Angiotensin-converting enzyme (ACE) inhibitors are useful in systolic dysfunction, both in improving clinical manifestations of reduced cardiac output and in actually prolonging survival. ACE inhibitors are also beneficial in diastolic heart failure by promoting regression of left ventricular hypertrophy, thus improving diastolic physiological function. Calcium antagonists improve diastolic function by reducing blood pressure of hypertensive subjects, reducing left ventricular mass, and theoretically, by facilitating the energy-dependent transport of calcium ions from the actin-myosin complex into the sarcoplasmic reticulum. However, because of the negative inotropic properties of the calcium antagonists, they should be used cautiously, if used at all, in patients with significant systolic dysfunction, at least until the results of clinical trials using these drugs in systolic congestive heart failure are available.     

Primary diastolic heart failure

Diastolic heart failure is defined clinically when signs and symptoms of heart failure are present in the presence of preserved left ventricular systolic function (ejection fraction >45%). The incidence and prevalence of primary diastolic heart failure increases with age and it may be as high as 50% in the elderly. Age, female gender, hypertension, coronary artery disease, diabetes, and increased body mass index are risk factors for diastolic heart failure. Hemodynamic consequences such as increased pulmonary venous pressure, post-capillary pulmonary hypertension, and secondary right heart failure as well as decreased cardiac output are similar to those of systolic left ventricular failure, although the nature of primary left ventricular dysfunction is different. Diagnosis of primary diastolic heart failure depends on the presence of preserved left ventricular ejection fraction. Assessment of diastolic dysfunction is preferable but not mandatory. It is to be noted that increased levels of B-type natriuretic peptide does not distinguish between diastolic and systolic heart failure. Echocardiographic studies are recommended to exclude hypertrophic cardiomyopathy, infiltrative heart disease, primary valvular heart disease, and constrictive pericarditis. Myocardial stress imaging is frequently required to exclude ischemic heart disease. The prognosis of diastolic heart failure is variable; it is related to age, severity of heart failure, and associated comorbid diseases such as coronary artery disease. The prognosis of severe diastolic heart failure is similar to that of systolic heart failure. However, cautious use of diuretics and/or nitrates may cause hypotension and low output state. Heart rate control is essential to improving ventricular filling. Pharmacologic agents such as angiotensin receptor blockers, angiotensin-converting enzyme inhibitors, and calcium channel blockers are used in selected patients to decrease left ventricular hypertrophy. To decrease myocardial fibrosis, aldosterone antagonists have a potential therapeutic role. However, prospective controlled studies will be required to establish their efficacy in primary diastolic heart failure.     

Das Herz bei arterieller Hypertonie

The term hypertensive heart disease covers the entities of left ventricular hypertrophy, microangiopathy and endothelial dysfunction resulting in diastolic and systolic dysfunction, arrhythmias and increased cardiovascular risk. From the pathophysiological point of view, this is caused by the hypertrophy of cardiac myocytes, interstitial fibrosis and media hypertrophy of the arterioles. Microangiopathy can be diagnosed as the earliest sign of hypertensive heart disease, with diastolic dysfunction also being found as an early change. In further persisting arterial hypertension left ventricular hypertrophy develops (often asymmetric) and later a systolic dysfunction. Clinically, the patients suffer from angina pectoris, dyspnea and rhythm disorders. Left ventricular hypertrophy is associated with an increased risk of malignant ventricular arrhythmias. Thus, the main therapeutic principle should be antihypertensive therapy with the goal of regression of hypertrophy leading to decreased mortality risk.     

The clinical quandary of left and right ventricular diastolic dysfunction and diastolic heart failure

Summary

Diastolic heart failure is a common clinical entity that is indistinguishable from systolic heart failure without direct evaluation of left ventricular function. Diastolic heart failure is a clinical diagnosis in patients with signs and symptoms of heart failure but with preserved left ventricular function and normal ejection fraction, and is often seen in patients with a long-standing history of hypertension or infiltrative cardiac diseases. In contrast, diastolic dysfunction represents a mechanical malfunction of the relaxation of the left ventricular chamber that is primarily diagnosed by two-dimensional transthoracic echocardiography and usually does not present clinically as heart failure. The abnormal relaxation is usually separated in different degrees, based on the severity of reduction in passive compliance and active myocardial relaxation. The question whether diastolic dysfunction ultimately will lead to diastolic heart failure is critically reviewed, based on data from the literature. Treatment recommendations for diastolic heart failure are primarily targeted at risk reduction and symptom relief. Currently, few data only are reported on diastolic dysfunction and its progression to systolic heart failure.     

Therapy for diastolic heart failure

There is little objective to guide the therapy of patients with diastolic heart failure. Because of the similarities of pathophysiology abnormalities in diastolic and systolic heart failure, it is a reasonable inference to suggest that the proven therapy for systolic heart failure may also be of benefit in patients with diastolic heart failure. Treatment of underlying or exacerbating conditions in diastolic heart failure, such as hypertension, left ventricular hypertrophy, ischemia, diabetes, anemia, obesity and pulmonary disease is an important means of managing diastolic heart failure. Control of systolic blood pressure is effective in improving and preventing the development of diastolic heart failure. Treatment of diastolic heart failure is most effective when it is associated with hypertension. Production of systolic arterial pressure acutely reduces pulmonary congestion, ischemia, and chronically may lead to regression of left ventricular hypertrophy. Patients with diastolic heart failure in the absence of hypertension are very difficult to treat.     

Cardiovascular diseases in obstructive sleep apnea

Obstructive sleep apnea (OSA) affects approximately 5% of women and 15% of men in the middle-aged adults, and associated with adverse health outcomes. Cardiovascular disturbances are the most serious complications of OSA. These complications include heart failure, left/right ventricular dysfunction, acute myocardial infarction, arrhythmias, stroke, systemic and pulmonary hypertension. All these cardiovascular complications increase morbidity and mortality of OSA. Several epidemiologic studies have demonstrated that sleep related breathing disorders are an independent risk factor for hypertension, probably resulting from a combination of intermittent hypoxia and hypercapnia, arousals, increased sympathetic activity, and altered baroreflex control during sleep. Arterial hypertension, obesity, diabetes mellitus and coronary artery disease (CAD) which are independent predictors of left ventricular dysfunction, often have co-existence with OSA. Especially severe OSA patients having diastolic dysfunction might have an increased risk of heart failure, since diastolic dysfunction might be combined with systolic dysfunction. Early recognition and appropriate therapy of ventricular dysfunction is advisable to prevent further progression to heart failure and death. Patients with acute myocardial infarction, especially if they had apneas and hypoxemia without evident heart failure should be evaluated for sleep disorders. So, patients with CAD should be evaluated for OSA and vice versa. Early recognition and treatment of OSA may improve cardiovascular functions. Continuous positive airway pressure (CPAP) applied by nasal mask, is still the gold standard method for treatment of the disease and prevention of complications.     

From Hypertension to Heart Failure

The prevalence of heart failure is increasing in modern societies. Hypertension is a major contributor to the development of heart failure, whether through the development of left ventricular hypertrophy and diastolic dysfunction or by promoting atherosclerosis and myocardial infarction, which eventually leads to systolic dysfunction and left ventricular dysfunction. Effective therapy for hypertension can prevent more than 50% of heart failure events. Most studies done in the last three decades have used β blockers with diuretics as the modality of therapy. These agents have been shown to effectively prevent the development of heart failure. More recent comparative studies have shown that use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are also effective in preventing heart failure. Calcium channel blockers, however, seem to be less effective in preventing development of heart failure in patients with hypertension. It needs to be emphasized that the most important variable in preventing heart failure is the appropriate treatment of hypertension.     

Left Ventricular Dysfunction in Diabetes

Patients with diabetes mellitus have a greater morbidity and mortality from cardiovascular disease than patients without diabetes. Concomitant hypertension and diabetes are associated with even greater risk of coronary disease, atherosclerotic and peripheral vascular disease, and congestive heart failure. In addition, an independent left ventricular dysfunction (diabetic cardiomyopathy) exists in patients with diabetes that may manifest itself initially as abnormalities in diastolic function but ultimately in systolic function. Firm evidence for this outcome exists experimentally, and reversal of systolic and diastolic abnormalities has been noted experimentally. The Diabetes Control and Complications Trial (DCCT) indicated that intensive glycemic control ameliorates microvascular complication of neuropathy, proteinuria, and retinopathy. Little evidence exists for macrovascular complications or for left ventricular dysfunction. Preliminary results of a canine study of glycemic control and left ventricular function are presented. Clinical correlates of this study and its results are meager. Determination of the role that glycemic control plays with regard to left ventricular systolic function and congestive heart failure awaits carefully controlled and designed clinical trials.     

Prevalence of Suspected Diastolic Dysfunction in Patients with a Clinical Diagnosis of Congestive Heart Failure

Introduction: The prevalence of diastolic left ventricular (LV) dysfunction in a population presenting with a suspected diagnosis of congestive heart failure (CHF) is questionable and widely variable in the current literature. To minimize the disparity, we evaluated a large echocardiographic database to investigate the prevalence of systolic and suspected diastolic LV dysfunction in those with a suspected clinical diagnosis of CHF. Methods: We retrospectively reviewed echocardiograms performed at our institution and evaluated the prevalence of abnormal LV systolic and diastolic function in those with a suspected clinical diagnosis of CHF. Diastolic dysfunction was defined as the presence of left atrial enlargement, left ventricular hypertrophy and reverse trans-mitral inflow ratio (E/A reversal). Results: Of the 636 echocardiograms with CHF as the primary diagnosis, 461 had measured LV function. Normal LV systolic function were found in 238 of the patients (48%). Isolated diastolic LV dysfunction was found in 166 patients (36%). Twelve percent of the patients with a suspected clinical diagnosis of CHF had normal LV systolic and diastolic function. Conclusion: Normal LV systolic function was seen in nearly one-half of the echocardiograms with a suspected clinical diagnosis of CHF. Suspected LV diastolic dysfunction was observed in one-third of the echocardiograms with a suspected clinical diagnosis of CHF.     

Development of different phenotypes of hypertensive heart failure: systolic versus diastolic failure in Dahl salt-sensitive rats

OBJECTIVE: There are two phenotypes of heart failure, systolic failure and isolated diastolic heart failure with preserved left ventricular systolic function. Although isolated diastolic heart failure frequently occurs, there are only models for diastolic dysfunction unassociated with heart failure and models with overt diastolic heart failure have not been established. We attempted to develop two different models, i.e. diastolic and systolic failure models, based on hypertension. MATERIALS AND METHODS: Dahl salt-sensitive rats were placed on 8% NaCl diet from 7 weeks old (7-week starting group) or 8 weeks old (8-week starting group). As an age-matched control, Dahl salt-sensitive rats were consistently placed on normal chow. In these rats, echocardiogram was serially recorded, followed by hemodynamic and histological studies. RESULTS: The 7-week starting rats showed a steep elevation in blood pressure and progressive left ventricular hypertrophy, and fell into overt heart failure at approximately 19 weeks. The development of heart failure was not associated with a decrease in left ventricular midwall fractional shortening or an increase in left ventricular end-diastolic dimension as compared with the age-matched control, which mimics the characteristics of clinically observed isolated diastolic heart failure. The 8-week starting rats showed a gradual rise in blood pressure and less progressive left ventricular hypertrophy, and fell into heart failure at approximately 26 weeks with a decrease in mid-wall fractional shortening and an increase in left ventricular end-diastolic dimension. Hemodynamic and histological studies at failing stage revealed comparable elevation of left ventricular end-diastolic pressure and comparable left ventricular fibrosis in both groups. CONCLUSION: These two different models of overt heart failure may be useful as models of isolated diastolic heart failure and systolic heart failure based on the same hypertensive heart disease, respectively, and may contribute to discrimination of the mechanisms of the development of the two different phenotypes of heart failure.     

Diastolic dysfunction

Opinion statement Heart failure is a leading cause of hospital admissions in North America. Approximately half of patients with symptoms of heart failure have normal or minimally impaired systolic function and are therefore diagnosed, by exclusion, with diastolic dysfunction. The therapy of diastolic dysfunction to date is largely unsatisfactory. There have been few outcome-based clinical trials to guide clinicians, and most treatments have been empirically derived from the data from systolic heart failure studies. In general, acute management consists of central volume reduction with loop diuretics and long-acting nitrates. In some cases improvement in left ventricular filling can be achieved by reducing heart rate, usually with either β blockers or calcium channel blockers. The role of digoxin is unclear and it should be used with caution. Theoretically, it has the capacity to further impair ventricular function, but one of the few trials in diastolic heart failure suggested that it improves symptoms and reduces hospitalization. Renin-angiotensin system blockade is a very attractive therapeutic avenue; angiotensin-converting enzyme inhibitors and angiotensin receptor blockers effectively reduce afterload, induce regression of left ventricular hypertrophy in excess of their blood pressure-lowering effect, and confer survival benefits to patients at high risk for cardiovascular death. Although the results of a recent trial using an angiotensin receptor blocker in patients with primarily diastolic heart failure were unimpressive, renin-angiotensin system blockade should still be considered because of its aforementioned benefits. The long-term management of these patients includes a careful assessment for and treatment of myocardial ischemia, treatment of hypertension, and reduction in left ventricular hypertrophy. For the treatment of ischemia, long-acting nitrates and calcium channel blockers may be particularly useful. The results of new trials in this area are expected soon, and hopefully therapy that directly targets the pathophysiologic pathways of this important disease is on the horizon.     

Hypertension--still an important cause of heart failure?

Hypertension has been the single most important risk factor for heart failure until the last few decades. Now, it is frequently claimed that atherosclerotic coronary artery disease dominates as the major underlying cause, and hypertension is of lesser importance. We here review evidence regarding the contribution of hypertension to heart failure in the recent decades. It is not possible, in our view, to be confident of the relative importance of hypertension and coronary artery disease since there are significant limitations in the available data. The often-questionable diagnostic criteria used in defining heart failure is one such limitation. The absence or inadequacy of blood pressure recordings over the years prior to a diagnosis of heart failure seriously hinders the reaching of firm conclusions in many reports. Extrapolations from aetiological observations in one racial group to those in other racial groups, and from highly selected study groups in tertiary referral centres to patients with heart failure in primary and secondary care, may not be justified. Finally, the situation of heart failure primarily due to impaired left ventricular diastolic function, where hypertension is a frequent precursor, is often ignored in discussions of aetiology. Our view is that hypertension remains and probably is the single most, important modifiable risk factor for cardiac failure in some races and countries, where the dominant cardiac abnormality is left ventricular diastolic dysfunction. The situation is less clear for patients with heart failure primarily due to left ventricular systolic dysfunction.     

Diastolic dysfunction in exercise and its role for exercise capacity

Diastolic dysfunction is frequent in elderly subjects and in patients with left ventricular hypertrophy, vascular disease and diabetes mellitus. Patients with diastolic dysfunction demonstrate a reduced exercise capacity and might suffer from congestive heart failure (CHF). Presence of symptoms of CHF in the setting of a normal systolic function is referred to as heart failure with normal ejection fraction (HFNEF) or, if evidence of an impaired diastolic function is observed, as diastolic heart failure (DHF). Reduced exercise capacity in diastolic dysfunction results from a number of pathophysiological alterations such as slowed myocardial relaxation, reduced myocardial distensibility, elevated filling pressures, and reduced ventricular suction forces. These alterations limit the increase of ventricular diastolic filling and cardiac output during exercise and lead to pulmonary congestion. In healthy subjects, exercise training can enhance diastolic function and exercise capacity and prevent deterioration of diastolic function in the course of aging. In patients with diastolic dysfunction, exercise capacity can be enhanced by exercise training and pharmacological treatment, whereas improvement of diastolic function can only be observed in few patients.     

Diastolic heart failure in the elderly

Heart failure with preserved left ventricular function is a common problem among elderly patients.Given that diastolic heart failure(DHF)occurs in up to 50% of all heart failure admissions,and that incidence increases with age,knowledge of current recommendations for its diagnosis and treatment are extremely important for the elderly population.Causes of DHF include the aging process itself,hypertension,left ventricular hypertrophy,aortic stenosis,and hypertrophic obstructive cardiomyopathy.The patient with DHF may present with signs and symptoms similar to those observed in systolic heart failure.Treatment goals for the patient with DHF include achieving normal volume status,improving relaxation of the left ventricle,regression of hypertrophy if possible,and management of any co-morbidities that may aggravate the clinical status of patients with DHF.Hopefully,in the future,further data from randomized clinical trials will allow a more defined approach to care in these patients.     

Left ventricular diastolic dysfunction: risks, identification, and treatment

Risk factors of cardiovascular disease, such as hypertension, diabetes, and myocardial infarction, if left untreated, will increase the risk of the development of chronic heart failure. Much is known about the pathophysiology and effective treatments of chronic heart failure from left ventricular systolic dysfunction; however, little clinical trial evidence exists concerning benefits of treating patients with chronic heart failure and preserved systolic function, also known as left ventricular diastolic dysfunction. Rather, an understanding of the pathophysiology and patient signs and symptoms has usually dictated choice of treatments. With the results of ongoing trials, as well as the Candesartan in Heart Failure: Assessment of Reduction in Mortality and Morbidity (CHARM)-Preserved and the Digitalis Investigation Group (DIG) trials, clinical evidence is accumulating to support effective treatments in patients with left ventricular diastolic dysfunction. The focus of this review is to discuss the risks of, identification of, and rationale for therapeutic choices being employed for treating left ventricular diastolic dysfunction and implications from studies that may support these choices.