The Prevalence of Diabetic Cardiomyopathy: A Population-Based Study in Olmsted County,Minnesota

BackgroundDiabetic cardiomyopathy defined as either systolic or diastolic dysfunction in otherwise healthy diabetic persons is not clearly understood. The prevalence and outcomes of this disease in a community-based population have not been defined.Methods and ResultsCross-sectional survey of 2042 randomly selected residents of Olmsted County, Minnesota, aged 45 years or older between June 1997 and September 2000. All patients underwent Doppler echocardiographic assessment of systolic and diastolic function. Diabetic cardiomyopathy was defined in a person with diabetes and any systolic or at least moderate diastolic dysfunction without a history of coronary disease, hypertension, significant valvular disease, or congenital heart disease. The diagnosis of diabetic cardiomyopathy was made in 23 people, corresponding to a community population prevalence rate of 1.1%. Among diabetic patients, 16.9% met criteria for diabetic cardiomyopathy and 54.4% had diastolic dysfunction. Diabetes was associated with a 1.9-fold increase in risk of any left ventricular dysfunction, a 1.7-fold increase in risk of diastolic dysfunction, and a 2.2-fold increase in risk of systolic dysfunction. Among patients with diabetic cardiomyopathy, the cumulative probability of death was 18%, development of heart failure was 22%, and development of death or heart failure was 31% at 9 years.ConclusionDiabetic cardiomyopathy is relatively common in the community with a prevalence of 1.1%. The morbidity and mortality of patients with diabetic cardiomyopathy is high.     

Diabetic cardiomyopathy

Opinion statement  Diabetes mellitus is a major risk factor for the development of congestive heart failure (CHF). Diabetic cardiomyopathy has been acknowledged as a distinct disease entity that is an additional risk for diabetic patients to develop CHF, especially when they are affected by hypertension or epicardial coronary artery disease. Moreover, diabetic cardiomyopathy has been documented to lead to CHF even in the absence of other risk factors. As the combination of hypertension and diabetes has shown to be particularly detrimental, aggressive blood pressure control with a goal of less than 130/85 mm Hg is of critical importance. The first choice for pharmacologic treatment is angiotensinconverting enzyme inhibitors. Double- or triple-drug therapy is frequently required for good control. The increased risk of epicardial coronary artery disease in patients with diabetes warrants stringent treatment of dyslipidemia. If dilated cardiomyopathy with low ejection fraction is present, therapy with angiotensin-converting enzyme inhibitors, digoxin, diuretics, beta-blockers, and spironolactone (for patients with New York Heart Association class III to IV functional status) is indicated. If cardiac dysfunction consists predominantly of impaired diastolic function, heart rate control with a beta-blocker or a calcium antagonist is of particular importance. Control of blood glucose should be achieved, with hemoglobin A1c levels of less than 7%. Hyperinsulinemia should be avoided when possible; therefore, insulin-sensitizing agents are preferred over insulin-secretion-enhancing agents. Symptoms of CHF and acutely decompensated CHF should be treated no differently than nondiabetic patients. Care for patients with diabetes always includes lifestyle changes consisting of smoking cessation, decreasing obesity, regular exercise, and a heart-healthy diabetic diet.     

Diabetic cardiomyopathy

Diabetic cardiomyopathy is a myocardial disease caused by diabetes mellitus unrelated to vascular and valvular pathology or systemic arterial hypertension. Clinical and experimental studies have shown that diabetes mellitus causes myocardial hypertrophy, necrosis, and apoptosis, and increases interstitial tissue. The pathophysiology of diabetic cardiomyopathy is incompletely understood. It appears that metabolic perturbations such as hyperlipidemia, hyperinsulinemia, hyperglycemia, and changes in cardiac metabolism are involved in cellular consequences leading to increased oxidative stress, interstitial fibrosis, myocyte death, and altered intracellular ions transient and calcium homeostasis. Clinically, an early detection of asymptomatic diastolic dysfunction is possible. When patients develop signals and symptoms of heart failure, isolated diastolic dysfunction is usually detected. Systolic dysfunction is a late finding. Treatment of heart failure due to diabetic cardiomyopathy is not different from myocardiopathies of other etiologies and must follow the guidelines according to ventricular function, whether diastolic or diastolic and systolic impairment.     

Pharmacological heart rate lowering in patients with a preserved ejection fraction—review of a failing concept

Epidemiological studies have demonstrated that high resting heart rates are associated with increased mortality. Clinical studies in patients with heart failure and reduced ejection fraction have shown that heart rate lowering with beta-blockers and ivabradine improves survival. It is therefore often assumed that heart rate lowering is beneficial in other patients as well. Here, we critically appraise the effects of pharmacological heart rate lowering in patients with both normal and reduced ejection fraction with an emphasis on the effects of pharmacological heart rate lowering in hypertension and heart failure. Emerging evidence from recent clinical trials and meta-analyses suggest that pharmacological heart rate lowering is not beneficial in patients with a normal or preserved ejection fraction. This has just begun to be reflected in some but not all guideline recommendations. The detrimental effects of pharmacological heart rate lowering are due to an increase in central blood pressures, higher left ventricular systolic and diastolic pressures, and increased ventricular wall stress. Therefore, we propose that heart rate lowering per se reproduces the hemodynamic effects of diastolic dysfunction and imposes an increased arterial load on the left ventricle, which combine to increase the risk of heart failure and atrial fibrillation. Pharmacologic heart rate lowering is clearly beneficial in patients with a dilated cardiomyopathy but not in patients with normal chamber dimensions and normal systolic function. These conflicting effects can be explained based on a model that considers the hemodynamic and ventricular structural effects of heart rate changes.     

Morphological characteristics in diabetic cardiomyopathy associated with autophagy

Diabetic cardiomyopathy, clinically diagnosed as ventricular dysfunction in the absence of coronary atherosclerosis or hypertension in diabetic patients, is a cardiac muscle-specific disease that increases the risk of heart failure and mortality. Its clinical course is characterized initially by diastolic dysfunction, later by systolic dysfunction, and eventually by clinical heart failure from an uncertain mechanism. Light microscopic features such as interstitial fibrosis, inflammation, and cardiomyocyte hypertrophy are observed in diabetic cardiomyopathy, but are common to failing hearts generally and are not specific to diabetic cardiomyopathy. Electron microscopic studies of biopsy samples from diabetic patients with heart failure have revealed that the essential mechanism underlying diabetic cardiomyopathy involves thickening of the capillary basement membrane, accumulation of lipid droplets, and glycogen as well as increased numbers of autophagic vacuoles within cardiomyocytes. Autophagy is a conserved mechanism that contributes to maintaining intracellular homeostasis by degrading long-lived proteins and damaged organelles and is observed more often in cardiomyocytes within failing hearts. Diabetes mellitus (DM) impairs cardiac metabolism and leads to dysregulation of energy substrates that contribute to cardiac autophagy. However, a “snapshot” showing greater numbers of autophagic vacuoles within cardiomyocytes may indicate that autophagy is activated into phagophore formation or is suppressed due to impairment of the lysosomal degradation step. Recent in vivo studies have shed light on the underlying molecular mechanism governing autophagy and its essential meaning in the diabetic heart. Autophagic responses to diabetic cardiomyopathy differ between diabetic types: they are enhanced in type 1 DM, but are suppressed in type 2 DM. This difference provides important insight into the pathophysiology of diabetic cardiomyopathy. Here, we review recent advances in our understanding of the pathophysiology of diabetic cardiomyopathy, paying particular attention to autophagy in the heart, and discuss the therapeutic potential of interventions modulating autophagy in diabetic cardiomyopathy.     

Diabetic cardiomyopathy--fact or fiction?

Epidemiologic as well as clinical studies confirm the close link between diabetes mellitus and heart failure. Diabetic cardiomyopathy (DCM) is still a poorly understood ??entity??, however, with several contributing pathogenetic factors which lead in different stages of diabetes to characteristic clinical phenotypes. Hyperglycemia with a shift from glucose metabolism to increased beta-oxidation and consecutive free fatty acid damage (lipotoxicity) to the myocardium, insulin resistance, renin-angiotensin-aldosterone system (RAAS) activation, altered calcium homeostasis and structural changes from the natural collagen network to a stiffer matrix due to advanced glycation endproduct (AGE) formation, hypertrophy and fibrosis contribute to the respective clinical phenotypes of DCM. We propose the following classification of cardiomyopathy in diabetic patients:

1. Diastolic heart failure with normal ejection fraction (HFNEF) in diabetic patients often associated with hypertrophy without relevant hypertension. Relevant coronary artery disease (CAD), valvular disease and uncontrolled hypertension are not present. This is referred to as stage 1 DCM.
2. Systolic and diastolic heart failure with dilatation and reduced ejection (HFREF) in diabetic patients excluding relevant CAD, valvular disease and uncontrolled hypertension as stage 2 DCM.
3. Systolic and/or diastolic heart failure in diabetic patients with small vessel disease (microvascular disease) and/or microbial infection and/or inflammation and/or hypertension but without CAD as stage 3 DCM.
4. If heart failure may also be attributed to infarction or ischemia and remodeling in addition to stage 3 DCM the term should be heart failure in diabetes or stage 4 DCM.

These clinical phenotypes of diabetic cardiomyopathy can be separated by biomarkers, non-invasive (echocardiography, cardiac magnetic resonance imaging) and invasive imaging methods (levocardiography, coronary angiography) and further analysed by endomyocardial biopsy for concomitant viral infection. The role of specific diabetic drivers to the clinical phenotypes, to macro- and microangiopathy as well as accompanying risk factors or confounders, e.g. hypertension, autoimmune factors or inflammation with or without viral persistence, need to be identified in each individual patient separately. Thus hyperglycemia, hyperinsulinemia and insulin resistance as well as lipotoxicity by free fatty acids (FFAs) are the factors responsible for diabetic cardiomyopathy. In stage 1 and 2 DCM diabetic cardiomyopathy is clearly a fact. However, precise determination of to what degree the various underlying pathogenetic processes are responsible for the overall heart failure phenotype remains a fiction.     

Treatment of hypertension for patients with diastolic dysfunction

Diastolic dysfunction is a poorly understood pathophysiological entity; its importance is magnified by the increasing prevalence of diastolic heart failure. Forty-six million people in the US are experiencing heart failure and 550000 new cases are diagnosed annually. A large percentage of these patients with heart failure have a normal or nearly normal left-ventricular ejection fraction. Isolated diastolic dysfunction may be associated with an increased mortality. One of the major causes of diastolic dysfunction is hypertension. Advances in diagnosis and treatment strategies may improve the clinical outcome for patients with diastolic dysfunction.     

Diabetic cardiomyopathy: a hyperglycaemia- and insulin-resistance-induced heart disease

Diabetic cardiomyopathy is characterised in its early stages by diastolic relaxation abnormalities and later by clinical heart failure in the absence of dyslipidaemia, hypertension and coronary artery disease. Insulin resistance, hyperinsulinaemia and hyperglycaemia are each independent risk factors for the development of diabetic cardiomyopathy. The pathophysiological factors in diabetes that drive the development of cardiomyopathy include systemic metabolic disorders, inappropriate activation of the renin–angiotensin–aldosterone system, subcellular component abnormalities, oxidative stress, inflammation and dysfunctional immune modulation. These abnormalities collectively promote cardiac tissue interstitial fibrosis, cardiac stiffness/diastolic dysfunction and, later, systolic dysfunction, precipitating the syndrome of clinical heart failure. Recent evidence has revealed that dysregulation of coronary endothelial cells and exosomes also contributes to the pathology behind diabetic cardiomyopathy. Herein, we review the relationships among insulin resistance/hyperinsulinaemia, hyperglycaemia and the development of cardiac dysfunction. We summarise the current understanding of the pathophysiological mechanisms in diabetic cardiomyopathy and explore potential preventative and therapeutic strategies.     

Murine Models of Diastolic Dysfunction and Heart Failure With Preserved Ejection Fraction

Left ventricular diastolic dysfunction leads to heart failure with preserved ejection fraction, an increasingly prevalent condition largely driven by modern day lifestyle risk factors. As heart failure with preserved ejection fraction accounts for almost one-half of all patients with heart failure, appropriate nonhuman animal models are required to improve our understanding of the pathophysiology of this syndrome and to provide a platform for preclinical investigation of potential therapies. Hypertension, obesity, and diabetes are major risk factors for diastolic dysfunction and heart failure with preserved ejection fraction. This review focuses on murine models reflecting this disease continuum driven by the aforementioned common risk factors. We describe various models of diastolic dysfunction and highlight models of heart failure with preserved ejection fraction reported in the literature. Strengths and weaknesses of the different models are discussed to provide an aid to translational scientists when selecting an appropriate model. We also bring attention to the fact that heart failure with preserved ejection fraction is difficult to diagnose in animal models and that, therefore, there is a paucity of well described animal models of this increasingly important condition.     

Diastolic heart failure or heart failure with a normal ejection fraction

Nearly half of patients with symptoms of heart failure are found to have an left ventricular (LV) ejection fraction which is within normal limits. These patients have variously been labeled as having diastolic heart failure, heart failure with preserved LV function or heart failure with normal ejection fraction (HFNEF). Since recent studies have shown that systolic function is not entirely normal in these patients, HFNEF is the better term. More common in elderly females it has a mortality similar to heart failure with a reduced ejection fraction (HFREF). The exact pathophysiology of the symtpoms is still not clear and, therefore, debated. As heart failure is often episodic, the underlying abnormal mechanisms may not be completely apparent at rest. It is likely there is a mixture of systolic and diastolic dysfunction which will be different to some degree in individual patients and isolated diastolic dysfunction or primary abnormalities of relaxation are probably extremely rare. The main difference between HFNEF and HFREF is the degree of ventricular remodeling with increased ventricular volumes in HFREF. The time course of remodeling depends to some extent on the aetiology being quicker post myocardial infarction--the commonest cause of HFREF, and slower with hypertension which is the most frequent aetiological factor in HFNEF. Ventricular volumes rather than ejection fraction or the concept of a pure diastolic abnormality can be used to classify patients in a more rational manner.     

The effect of diabetes mellitus on prognosis and serial left ventricular function after acute myocardial infarction: contribution of both coronary disease and diastolic left ventricular dysfunction to the adverse prognosis. The MILIS Study Group

Patients with diabetes mellitus experience a more adverse outcome after acute myocardial infarction compared with nondiabetic patients, although the mechanisms responsible for these findings are not clear. From the Multicenter Investigation of the Limitation of Infarct Size (MILIS) study, the course of acute infarction in 85 diabetic patients was compared with that in 415 nondiabetic patients, all of whom had serial assessments of left ventricular function. The diabetic patients experienced a more complicated in-hospital and postdischarge course than did the nondiabetic patients, including a higher incidence of postinfarction angina, infarct extension, heart failure and death, despite the development of a smaller infarct size and similar levels of left ventricular ejection fraction. Although diabetic patients had a worse profile of cardiovascular risk factors at the time of the index infarction, the increased incidence of adverse outcomes among them persisted despite adjustment for these baseline imbalances. Diabetic women had a poor baseline risk profile compared with the other groups categorized by gender and diabetic status, and experienced an almost twofold increase in cardiac mortality despite development of the smallest infarct size during the index event. The duration of diabetes and the use of insulin at the time of the index infarction were associated with a better in-hospital mortality rate, but the duration of diabetes did not exert a major influence on the outcome of the diabetic patients. The factors responsible for the increased incidence of adverse outcomes among diabetic patients may be related to an acceleration of the atherosclerotic process, diastolic left ventricular dysfunction associated with diabetic cardiomyopathy or other unidentified unfavorable processes.     

糖尿病性心肌病的发病机制及治疗方法研究进展

心血管疾病是2型糖尿病的主要并发症,约占2型糖尿病患者死亡人数的2/3。血糖异常、血脂异常、胰岛素抵抗、慢性低度炎症、氧化应激、内皮功能障碍、血管钙化和高凝状态等多种病理生理过程可加快2型糖尿病患者糖尿病心脏病的进展。糖尿病性心肌病是糖尿病心脏病中较为常见的一种,可导致心功能异常并最终进展为心力衰竭、心律失常,甚至猝死。本文综述了糖尿病性心肌病的发病机制,以及当前及未来潜在的治疗方法。     

Echocardiographic evaluation of cardiac function in asymptomatic type 2 diabetes mellitus

Diabetic patients are at increased risk of cardiovascular disease. We do not have a definite data regarding the echocardiographic findings in asymptomatic type 2 diabetics in our population. The present study conducted an echocardiographic evaluation of asymptomatic type 2 diabetic patients of Kottayam district in central part of Kerala state. Hundred totally asymptomatic known type 2 diabetic patients were included in the study. Trans-thoracic echocardiography was performed in these patients and parameters were compared with age and sex matched controls. Diabetic patients were divided into three groups depending on the age, and duration of diabetes mellitus and each group was compared for E/A ratio(early diastolic flow velocity / late diastolic flow velocity), EDT(deceleration time), IVRT(Isovolumic relaxation time), EF(ejection fraction),LVmass(Left ventricular mass).The same parameters were also compared depending on the modes of therapy. Mean EDT (Early deceleration time), IVRT(Isovolumic relaxation time) , LV Mass (Left ventricular mass) ,IV septal thickness and left atrial diameter were significantly increased in the diabetic as compared with the control group. The mean E/A ratio was significantly lower in diabetic than control. There was no significant difference in ejection fraction ,LVIDD (left ventricular internal diastolic diameter), LVIDS( left ventricular internal systolic diameter) between diabetics and controls. There was a progressive increase in EDT and IVRT as the age and duration of diabetes increased. No significant difference was noted with mode of control of diabetes. Left ventricular diastolic dysfunction is much more common than previously reported in subjects with well controlled asymptomatic type 2 diabetes and clinically undetectable heart disease.     

Advanced glycation end-products, a pathophysiological pathway in the cardiorenal syndrome

The prevalence of heart failure (HF) is increasing. A distinction is made between diastolic HF (preserved left ventricular ejection fraction (LVEF)) and systolic HF (reduced LVEF). Advanced glycation end-products (AGEs) are crystallized proteins that accumulate during ageing, but are particularly increased in patients with diabetes mellitus and in patients with renal failure. Through the formation of collagen crosslinks, and by interaction with the AGE-receptor, which impairs calcium handling and increases fibrosis, AGE-accumulation has pathophysiologically been associated with the development of diastolic and renal dysfunction. Interestingly, diastolic dysfunction is a frequent finding in elderly patients, diabetic patients and in patients with renal failure. Taken together, this suggests that AGEs are related to the development and progression of diastolic HF and renal failure. In this review, the role of AGEs as a possible pathophysiological factor that link the development and progression of heart and renal failure, is discussed. Finally, the role of AGE intervention as a possible treatment in HF patients will be discussed.     

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.     

Heart failure with normal ejection fraction

Opinion statement Heart failure with normal ejection fraction, also known as diastolic heart failure, is a major problem for patients and health-care providers and is a substantial expense to society. The main pathophysiologic processes involved are increased left ventricular stiffness and abnormal relaxation, with resulting impaired left ventricular filling. These processes typically displace the pressure-volume relationship in an upward direction, resulting in increased left ventricular end-diastolic, left atrial, and pulmonary capillary wedge pressures, leading to symptoms of pulmonary congestion. The most common clinical disorders leading to diastolic heart failure are 1) hypertension with concentric left ventricular hypertrophy, 2) coronary artery disease with decreased left ventricular compliance, 3) hypertrophic cardiomyopathy, and 4) aortic stenosis with concentric left ventricular hypertrophy. Echocardiography and cardiac catheterization with magnetic resonance imaging hold promise as future diagnostic tools. The approach to the treatment of diastolic heart failure is focused on four treatment goals: 1) persistent control of elevated blood pressure, with regression of left ventricular hypertrophy, 2) careful reduction of central blood volume (diuretics), 3) maintenance of atrial contraction and control of heart rate (beta-blockers, digoxin, atrioventricular pacing); and 4) improvement of left ventricular relaxation. There is currently no drug treatment specific for abnormal relaxation, although efforts are being made to develop such compounds. A promising future therapy includes agents that lyse advanced glycation end-products as an approach to relieving increased ventricular stiffness. In addition to pharmacotherapy, maintaining ideal body weight and a regular exercise program are also helpful in the treatment of diastolic heart failure. Although the overall prognosis of patients with diastolic dysfunction is more favorable than that of patients with systolic dysfunction, the frequency of treatment failure and recurrent symptoms underscores the need for further improvement in treatment of this condition.     

Heart failure in elderly patients

Several structural and functional changes contribute to heart failure in elderly patients: an age dependent increase in sympathetic nervous activity, left ventricular wall diameter, myocardial fibrosis and apoptosis, micro- and macrovascular coronary sclerosis, aortic stiffness. As a consequence, diastolic, but also systolic heart failure is a frequent finding in elderly patients. The relation of systolic to diastolic heart failure is clearly shifted towards diastolic heart failure in elderly patients, especially in women. Mortality is increased with systolic dysfunction in elderly patients compared to younger heart failure patients. Mortality is less with diastolic dysfunction, but still higher compared to elderly without heart failure. In addition, morbidity is increased both with diastolic and systolic heart failure in elderly patients. Cognitive dysfunction is a frequent finding. After exclusion of specific cardiac and extracardiac reasons for dyspnoea, drug therapy of systolic heart failure in elderly is similar to younger patients. However, the physiological decrease of renal function and the more frequent renal impairment in elderly patients with heart failure needs to be considered. Guideline recommendations for drug therapy are based in most cases on studies conducted in younger systolic heart failure patients. A recent meta-analysis of randomized beta-blocker trials suggests improved survival with beta-blockers even in the elderly subgroup. Guidelines for the treatment of diastolic heart failure are available only recently. The term heart failure with normal left ventricular ejection fraction (LVEF) has been proposed instead of diastolic heart failure. Given the increased morbidity and mortality in elderly patients with heart failure and normal LVEF, therapy should include general measures, such as physical activity, weight reduction, volume restriction. Specific therapy includes optimal control of systolic and diastolic blood pressure, diuretics, nitrates, and frequency-control. However, randomized trials evaluating the efficacy of specific therapies in heart failure with normal LVEF are still missing.     

Congestive heart failure in the elderly: the Cardiovascular Health Study

Congestive heart failure in the elderly is recognized as a national public health priority; however, clinical diagnosis can be problematic in elderly persons, many of whom have a history of heart failure in the presence of normal or only minimally decreased ejection fraction. Findings of the Cardiovascular Health Study have underscored the common substrate and predictors underlying heart failure both with decreased ejection fraction and with normal ejection fraction (i.e., diastolic heart failure). Coronary heart disease, systolic blood pressure, and C-reactive protein (a measure of inflammation) are predictive of heart failure independent of ejection fraction. Left atrial size, arguably a marker of the effects of impaired diastolic filling over time, is increased in both systolic and diastolic heart failure of the elderly, as is atrial natriuretic peptide. The outcome of heart failure in elderly persons is poor both for systolic and diastolic heart failure. Moreover, many community-dwelling elderly persons have decreased ejection fraction without heart failure. In these persons the chance of death is similar to that of participants with diastolic heart failure. Since most clinical trials have studied younger patients with predominantly systolic heart failure, the appropriate therapy for heart failure in elderly persons remains to be determined.     

Diastolic heart failure can be diagnosed by comprehensive two-dimensional and Doppler echocardiography.

There are many myocardial and non-myocardial conditions that cause heart failure with normal left ventricular ejection fraction (LVEF). Among them, diastolic heart failure (heart failure due to diastolic dysfunction) is the most common cause of heart failure with normal LVEF. Diastolic heart failure easily can be diagnosed by comprehensive two-dimensional and Doppler echocardiography, which can demonstrate abnormal myocardial relaxation, decreased compliance, and increased filling pressure in the setting of normal LV dimensions and preserved LVEF. Therefore, diastolic heart failure should always be considered when LVEF is normal on two-dimensional echocardiography in patients with clinical evidence of heart failure. The diagnosis can be confirmed if Doppler echocardiography and myocardial tissue imaging provide evidence for impaired myocardial relaxation (i.e., decreased longitudinal velocity of the mitral annulus during early diastole and decreased propagation velocity mitral inflow), decreased compliance (shortened mitral A-wave duration and mitral deceleration time), and increased filling pressure (shortened isovolumic relaxation time and an increased ratio between early diastolic mitral and mitral annular velocities). Early identification of diastolic dysfunction in asymptomatic patients by the use of echocardiography may provide an opportunity to manage the underlying etiology to prevent progression to diastolic heart failure.     

Diastolic heart failure can be diagnosed by comprehensive two-dimensional and Doppler echocardiography

There are many myocardial and non-myocardial conditions that cause heart failure with normal left ventricular ejection fraction (LVEF). Among them, diastolic heart failure (heart failure due to diastolic dysfunction) is the most common cause of heart failure with normal LVEF. Diastolic heart failure easily can be diagnosed by comprehensive two-dimensional and Doppler echocardiography, which can demonstrate abnormal myocardial relaxation, decreased compliance, and increased filling pressure in the setting of normal LV dimensions and preserved LVEF. Therefore, diastolic heart failure should always be considered when LVEF is normal on two-dimensional echocardiography in patients with clinical evidence of heart failure. The diagnosis can be confirmed if Doppler echocardiography and myocardial tissue imaging provide evidence for impaired myocardial relaxation (i.e., decreased longitudinal velocity of the mitral annulus during early diastole and decreased propagation velocity mitral inflow), decreased compliance (shortened mitral A-wave duration and mitral deceleration time), and increased filling pressure (shortened isovolumic relaxation time and an increased ratio between early diastolic mitral and mitral annular velocities). Early identification of diastolic dysfunction in asymptomatic patients by the use of echocardiography may provide an opportunity to manage the underlying etiology to prevent progression to diastolic heart failure.