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PubMed2006

Utility of N terminal pro brain natriuretic peptide in elderly patients.

OBJECTIVE: To evaluate the utility of N terminal pro brain natriuretic peptide (NT-proBNP) as a diagnostic marker for diastolic dysfunction or failure, systolic dysfunction, and significant valve disorders in patients over 75 years. DESIGN: Cohort study. SETTING: Outpatient echocardiography service in a district general hospital. PARTICIPANTS: 100 consecutive patients. MAIN OUTCOME MEASURES: Sensitivity, specificity, positive predictive values, negative predictive values, and area under receiver operating characteristic curve for NT-proBNP assay in the diagnosis of left ventricular diastolic dysfunction or failure, systolic dysfunction, and significant valve disorders. RESULTS: For diagnosis of systolic dysfunction NT-proBNP level of 424 pg/ml had a sensitivity of 96%, specificity of 45%, positive predictive value of 36%, and negative predictive value of 96%. The area under the curve was 0.71 (95% confidence intervals: 0.69 to 0.89). In valve heart disease, level of 227 pg/ml had sensitivity of 91%, specificity of 43%, positive predictive value of 40%, and negative predictive value of 92%. Patients with diastolic dysfunction/failure had lower plasma concentrations. CONCLUSIONS: This study showed that NT-proBNP had excellent negative predictive value for systolic dysfunction and significant valve disorders in very elderly patients. It increased significantly in systolic dysfunction, valve heart disease, and atrial fibrillation. NT-proBNP is not useful in the diagnosis of diastolic dysfunction or diastolic heart failure using standard echocardiography criteria.

Aged↗
PubMedDate not supplied

Impact of obstructive sleep apnea on right ventricular global function: sleep apnea and myocardial performance index.

BACKGROUND: Obstructive sleep apnea (OSA) is characterized by repetitive upper airway obstructions during sleep, and it might cause cardiovascular complications such as heart failure, arrhythmias, myocardial infarction, systemic and pulmonary hypertension. OBJECTIVES: To determine right ventricular diameters and myocardial performance index (MPI) reflecting ventricular global function in uncomplicated OSA patients. METHODS: 49 subjects without hypertension, diabetes mellitus, or any cardiac or pulmonary disease referred for evaluation of OSA had overnight polysomnography and complete echocardiographic assessment. According to the apnea-hypopnea index (AHI), subjects were divided into three groups: group 1: control subjects (AHI <5, n = 20), group 2: patients with mild OSA (AHI: 5-14, n = 11), and group 3: moderate-severe OSA (AHI > or = 15, n = 18). Right ventricular free wall diameter was measured by M mode, and right ventricular MPI was calculated as (isovolumic contraction time + isovolumic relaxation time)/pulmonary ejection time. RESULTS: There were no differences of age, body mass index, heart rates, systolic and diastolic blood pressures among the groups (p > 0.05). Right ventricular end-diastolic and end-systolic diameters were not statistically different between the groups, and were within normal limits. Also, right ventricular free wall diameter was not significantly different between the groups of control, mild OSA and moderate-severe OSA (6.7 +/- 0.9, 6.9 +/- 1.0, 7.1 +/- 1.1 mm, p > 0.05). Right ventricular diastolic dysfunction was shown only in group 3 patients. Right ventricular MPI was statistically higher in group 3 (0.62 +/- 0.18) than in group 2 patients (0.50 +/- 0.10), and group 1 patients (0.48 +/- 0.08, p < 0.001). CONCLUSIONS: It was suggested that patients with moderate-severe OSA had a right ventricular global dysfunction, in addition to the presence of a diastolic dysfunction.

Adult↗
PubMed2005

Prognostic value of plasma brain natriuretic peptide, urea nitrogen, and creatinine in outpatients >70 years of age with heart failure.

This study analyzed the relevance of plasma brain natriuretic peptide (BNP) and echocardiography in predicting cardiovascular events in a large population >70 years old with heart failure (HF). Three hundred four outpatients with HF (51.6% men, mean age 78.6) underwent transthoracic echocardiography and plasma BNP testing shortly before hospital discharge. Echocardiography was intended to reveal systolic dysfunction (left ventricular [LV] ejection fraction [EF] <50%) or diastolic dysfunction (EF > or =50% and abnormalities of ventricular relaxation). During 6-month follow-up, all-cause death and readmission were assessed. One hundred seventeen patients had diastolic dysfunction with preserved systolic LV function, and 187 had systolic dysfunction. At 6-month clinical follow-up, 33 subjects (10.9%) had died, and 62 (20.4%) needed readmission for cardiac decompensation. In all patients, univariate logistic regression demonstrated significant correlations between age (r = 0.14, p = 0.01), plasma BNP (r = 0.36, p = 0.0001), the EF (r = 0.16, p = 0.003), urea nitrogen (r = 0.35, p = 0.0001), serum creatinine (r = 0.27, p = 0.0001), and New York Heart Association (NYHA) class (r = 0.35, p = 0.0001) and the occurrence of cardiovascular events. In patients with HF in NYHA class III or IV, a BNP cut-off level of 200 pg/ml identified different outcomes (BNP <200 pg/ml in 1 of 20 events vs BNP >200 pg/ml in 55 of 85 events, p = 0.0001). In patients with HF who were >70 years old, BNP, NYHA class, and renal function predicted adverse outcome. In patients with severe HF, BNP was better than NYHA class in predicting future events.

Aged↗
PubMed1994

Central and peripheral limitations to upright exercise in untrained cardiac transplant recipients.

BACKGROUND: Functional capacity and quality of life are subjectively improved after cardiac transplantation. However, the objective improvement in exercise tolerance after transplantation has been disappointing. The extent to which allograft diastolic dysfunction contributes to this exercise intolerance has not been defined. METHODS AND RESULTS: Thirty cardiac transplant recipients between 3 and 16 months after transplantation and 30 age-matched normal control subjects underwent maximal symptom-limited graded upright bicycle exercise testing with simultaneous radionuclide angiography, invasive hemodynamic monitoring, and breath-by-breath gas analysis. Mean blood pressure was higher in the transplant group at supine rest (112.1 versus 97.7 mm Hg), normalized with upright posture, and became lower than normal at peak exercise (121.1 versus 133.2 mm Hg). Systolic function as measured by ejection fraction was normal in both groups. However, the cardiac transplant recipients had significantly lower exercise tolerance, achieving a mean maximal work rate of 390 kilopond-meters per minute (kpm/min), compared with 825 kpm/min in the normal subjects. Peak oxygen consumption was 12.3 mL.min-1.kg-1 in the transplant group, 46% lower than the normal group's value of 22.9 mL.min-1.kg-1. The transplant patients had a resting tachycardia (94 beats per minute) and a 79% reduction in exercise heart rate reserve compared with normal. Despite this chronotropic incompetence, stroke index response to exercise was consistently lower after transplantation, accounting for a 41% reduction in cardiac index at maximal exercise. The lower stroke index was accompanied by a 32% lower end-diastolic volume index at rest and a 14% lower end-diastolic volume index at peak exercise. Despite the smaller ventricular volumes after transplantation, pulmonary capillary wedge pressure was 35% higher than normal at supine rest and 50% higher at maximal exercise. Right atrial and mean pulmonary arterial pressures were similarly elevated. The ratio of pulmonary capillary wedge pressure to end-diastolic volume index was significantly higher during the postural change and exercise, suggesting allograft diastolic dysfunction. Arteriovenous oxygen difference was similar between groups at rest and with submaximal exercise but was 24% lower at maximal exercise in the transplant group, suggesting an abnormality in peripheral oxygen uptake or utilization. CONCLUSIONS: Exercise tolerance is severely limited during the first 16 months after cardiac transplantation despite preservation of allograft left ventricular systolic function. This intolerance is due to an inadequate cardiac index response from a combination of chronotropic incompetence and diastolic dysfunction limiting the appropriate compensatory use of the Starling mechanism. In addition, there is a peripheral abnormality in oxygen transport or utilization that may partially reflect the effects of deconditioning.

Adult↗
PubMed2001

[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.

English Abstract↗
PubMed2000

The echo-Doppler evaluation of left ventricular diastolic function. A current perspective.

The role of left ventricular (LV) diastolic function in health and disease is still incompletely understood and under appreciated by most primary care physicians and many cardiologists. Physical examination, electrocardiogram, and chest radiographs are unreliable in making the diagnosis of LV diastolic dysfunction in most individuals, and invasive measurements of cardiac pressures, rates of LV relaxation, and LV compliance are costly, clinically impracticable as they carry increased risk, and require special catheters and software analysis programs. The authors address the definition of LV diastolic dysfunction, history of diastole, LV filling patterns, pulmonary venous flow velocity variables, additional ancillary data, practical echo-Doppler evaluation of LV diastolic function, and limitations.

Diastole↗
PubMed1999

[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.

Amlodipine↗
PubMed2005

[Cardiovascular end organ impairment due to hypertension].

Arterial hypertension is the most frequent cause of pressure overload on the left ventricle. Longer lasting arterial hypertension leads to hypertension-specific organ manifestations summarized as "hypertensive heart disease". Hypertensive heart disease comprise the manifestation of stenosis in epicardial arteries, hypertensive microvascular disease, ischemic cardiomyopathy, left ventricular hypertrophy, endothelial dysfunction, increased sympathetic drive and degeneration of aortic valve. Diastolic dysfunction and reduced coronary flow reserve can be evaluated as early markers of hypertensive heart disease. These alterations lead to the major clinical manifestations of hypertensive heart disease that are symptoms of reduced coronary insufficiency with typical angina pectoris, but also of symptoms of heart failure (systolic and diastolic dysfunction) and arrhythmia. Different non-invasive and invasive procedures are available for screening and follow-up of patients with hypertensive heart disease. Primary therapeutic target is, apart from lowering blood pressure, to reverse cardiac manifestations of arterial hypertension using specific therapeutic algorithms.

Humans↗
PubMed2003

Transforming growth factor beta and diastolic left ventricular dysfunction after heart transplantation: echocardiographic and histologic evidence.

BACKGROUND: The mechanism for chronic left ventricular diastolic dysfunction in the non-rejecting cardiac allograft has not been fully studied. OBJECTIVES: The purposes of this study were to analyze the significance and frequency of left ventricular diastolic dysfunction after heart transplantation and to examine the involvement of fibrotic cytokines (transforming growth factor beta [TGF-beta]) in development of clinical and echocardiographic changes in cardiac allograft recipients. METHODS: We studied 152 heart transplant recipients who had survived for at least 24 months. We compared histopathologic findings (staining of endomyocardial biopsy specimens using hematoxylin and eosin, and polyclonal antibodies expressed as TGF-beta score), left ventricular function (Doppler echocardiography), and clinical course (New York Heart Association [NYHA] status). We classified patients into Group 1 (n = 41 recipients) with a restrictive filling pattern, mitral deceleration time (MDT) <140 milliseconds, and Group 2 (n = 111 recipients), MDT >or=140 milliseconds. RESULTS: The MDT was 122 +/- 7 milliseconds in Group 1 compared with an MDT of 177 +/- 17 milliseconds in Group 2 (p = 0.0003). Group 1 showed significant immunohistochemical staining in endomyocardial biopsy specimens (a mean TGF-beta score of 9.1 +/- 1.2 for Group 1 compared with a mean TGF-beta score of 3.6 +/- 0.8 for Group 2 p = 0.001). The TGF-beta expression correlated inversely with both MDT and isovolumic relaxation time (r = -0.77, p = 0.0004, and r = -0.69, p = 0.004, respectively). Mean NYHA status in Group 1 recipients was 2.2 +/- 1.1 compared with 1.37 +/- 0.6 for Group 2 (p = 0.006). CONCLUSIONS: Transforming growth factor beta expression in cardiac allografts is associated with impaired left ventricular diastolic function. The pathogenesis of diastolic dysfunction may be an aberrant repair process after rejection-caused TGF-beta expression in the allograft.

Adult↗
PubMed1999

Alterations in cardiac flow parameters in patients with polycystic ovarian syndrome.

The aim of this study was to examine the echocardiographic profiles of patients with polycystic ovarian syndrome (PCOS). Serum concentrations of follicle stimulating hormone, luteinizing hormone, androstenedione, free testosterone, prolactin, DHEA-SO(4) and 17-OH-progesterone, lipid profile (high and low density lipoproteins, triglyceride and total cholesterol) and basal and total insulin after a glucose tolerance test were measured in 35 patients with PCOS and 35 healthy controls matched for body mass index. Doppler, two dimensional M mode echocardiography was performed for the following indices: isovolumetric relaxation time (IVRT), E wave duration time (EVT), A wave duration time (AVT), E wave deceleration time (DT), peak early diastolic flow velocity (PEV), peak late diastolic flow velocity (PAV), E wave velocity time integral (FVI-E), A wave velocity time integral (FVI-A), atrial filling fraction (AFF), ejection fraction (EF), pre-ejection time (PEP), ejection time (ET) and aortic flow velocity time integral (FVI). Androstenedione, free testosterone, low density lipoproteins and cholesterol concentrations were significantly higher in patients with PCOS. There was no difference in basal and total insulin concentrations. IVRT, AVT, FVI-A, AFF, and PEP were higher in patients with PCOS, while PEV, FVI-E, EF, ET, EVT and EVT/AVT were higher in the control group. There was a positive correlation between basal insulin values and IVRT, and between total insulin values and EF. These changes are consistent with a non-restrictive type of diastolic dysfunction and left ventricular stiffness. PCOS may lead to diastolic dysfunction via hyperinsulinaemia and male type dyslipidaemia.

17-alpha-Hydroxyprogesterone↗
PubMed2006

Rapid brain natriuretic peptide test and Doppler echocardiography for early diagnosis of mild heart failure.

BACKGROUND: The early identification of patients at risk for the development of clinical heart failure (HF) is a new challenge in an effort to improve outcomes. METHODS: We prospectively evaluated whether the combination of brain natriuretic peptide (BNP) measurements (Triage BNP test, Biosite Diagnostics) and echocardiography would effectively stratify patients with new symptoms in a cost-effective HF program aimed at early diagnosis of mild HF. A total of 252 patients were referred by 100 general practitioners. RESULTS: Among the study population, the median BNP value was 78 ng/L (range, 5-1491 ng/L). BNP concentrations were lower among patients without heart disease [median 15 ng/L (range, 5-167 ng/L); n = 96] than among patients with confirmed HF [median, 165 ng/L (22-1491 ng/L); n = 157; Mann-Whitney U-test, 12.3; P <0.001]. Patients were grouped into diastolic dysfunction [BNP, 195 (223) ng/L], systolic dysfunction [BNP, 290 (394) ng/L], and both systolic and diastolic dysfunction [BNP, 776 (506) ng/L]. In this model, a cutoff value of 50 ng/L BNP increases the diagnostic accuracy in predicting mild HF, avoiding 41 echocardiograms per 100 patients studied, with a net saving of 14% of total costs. CONCLUSIONS: Blood BNP concentrations, in a cost effective targeted screening, can play an important role in diagnosing mild HF and stratifying patients into risk groups of cardiac dysfunction.

Adult↗
PubMed1993

Obesity and the heart.

Obesity can result in alterations in cardiac structure and function even in the absence of systemic hypertension and underlying organic heart disease. Increased total blood volume 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 (LV) 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 presence of systemic hypertension in obese individuals facilitates development of LV dilatation and hypertrophy. Congestive heart failure may occur in such individuals, and may be attributable to LV diastolic dysfunction or to combined LV diastolic and systolic dysfunction. The sleep apnea/obesity hypoventilation syndrome occurs in 5% of morbidly obese individuals and is potentially life-threatening. Treatment of obesity cardiomyopathy consists of weight loss, salt restriction, and diuretics. Digitalis and vasodilators may be useful in selected cases. Central obesity is probably a risk factor for the development of coronary heart disease. Alterations in lipid and insulin metabolism may facilitate development of coronary heart disease in obese patients.

Heart Diseases↗
PubMed1995

Echocardiographic and Therapeutic Approach to Heart Failure in the Elderly.

In most elderly patients, cardiac failure is associated with multiple cardiac pathologies, and the most common underlying abnormality is ventricular systolic dysfunction with reduced ejection fraction. In patients without cardiac enlargement, diastolic dysfunction may be predominant and left ventricular ejection fraction may be normal. Echocardiography is particularly suitable to evaluate changes in cardiovascular function that accompany age either as changes in disease patterns or as changes resulting simply from aging. The effects of digitalis on systolic and diastolic dysfunction are briefly reviewed, as well as the effects of diuretics, angiotensin-converting-enzyme inhibitors, and anticoagulant drugs.

Journal Article↗
PubMed2000

Levosimendan improves diastolic and systolic function in failing human myocardium.

Ca(2+)-sensitizers increase myocardial contractility, but may worsen diastolic dysfunction. Levosimendan, through its unique troponin-C interaction, may preserve diastolic function. We investigated the effects of levosimendan (10(-7)-10(-5) M) on diastolic and systolic function in multicellular cardiac muscle preparations from end-stage failing human hearts (1 and 2.5 Hz, 37 degrees C, 1.25 mM [Ca(2+)], pH 7.4). Levosimendan improved systolic function: at 1 Hz, developed force (F(dev)) increased from 13.84+/-3.27 to 16.40+/-3.57 (10(-7) M, P<0.05), while diastolic force (F(dia)) decreased from 5.32+/-0.67 to 4.94+/-0.61 mN/mm(2) (P<0.05). Under control conditions, the increase in stimulation frequency from 1 to 2.5 Hz resulted in a decrease in F(dev) of -0.51+/-1.80 mN/mm(2) (negative force-frequency relationship). Levosimendan improved this relationship: at 10(-7) M, this change became positive (+1.81+/-2.06 mN/mm(2), P<0.05). Diastolic function was markedly improved in the presence of levosimendan; the increase in F(dia) of 1.56+/-0.42 mN/mm(2) (control) was attenuated to 0.70+/-0.19 mN/mm(2) (P<0.05). To allow for a more detailed analysis, preparations were sometimes divided into two groups, based on their force-frequency behavior. Twitch timing parameters were accelerated by levosimendan in preparations with a negative force-frequency relationship. Levosimendan improves both systolic and diastolic function in failing human myocardium. Effects are even more pronounced at higher heart rates and under prevailing diastolic dysfunction.

Cardiotonic Agents↗
PubMed2003

Effects of calcium channel antagonists on left ventricular hypertrophy and diastolic function in patients with essential hypertension.

Hypertensive patients characteristically exhibit left ventricular (LV) hypertrophy and diastolic dysfunction. The effects of antihypertensive agents on LV hypertrophy and diastolic dysfunction do not always correlate with the degree of blood pressure reduction, but their effects on the sympathetic nervous system and renin-angiotensin system (RA system) are thought to be important. We investigated the effects of amlodipine and cilnidipine, N- and L-type calcium channel antagonists that suppress both blood pressure elevation and sympathetic activities, on LV hypertrophy and diastolic function. Patients with essential hypertension were randomly assigned to receive either amlodipine, cilnidipine or nifedipine CR (which does not block N-type calcium channels) for 6 months. The LV mass index was determined using M-mode echocardiography. The E/A ratio, i.e., the ratio of maximum amplitude between the early diastolic wave (E wave) and the atrial systolic wave (A wave) in the LV inflow pattern, and the deceleration time for the E wave were determined using pulse Doppler echocardiography. Systolic and diastolic blood pressures significantly decreased from the baseline values in all three groups, with no significant differences among the groups. The LV mass index had significantly decreased when it was evaluated 3 months after the initiation of treatment in the cilnidipine group and when it was evaluated 6 months after the initiation of treatment in the amlodipine group; only a slight decrease was observed in the nifedipine CR group. A significant decrease in the deceleration time and a significant increase in the E/A ratio were observed after 3 months of treatment in the cilnidipine and amlodipine groups but not in the nifedipine CR group. Thus, the effects of long-acting calcium channel antagonists on hypertensive LV hypertrophy and LV diastolic function varied from one antagonist to the other. Left ventricular hypertrophy and diastolic function improved in the cilnidipine and amlodipine groups, but not in the nifedipine CR group. These results indicate that the suppression of sympathetic nerve activity by the blockade of N-type calcium channels contributes to the improvement of LV hypertrophy and diastolic function.

Amlodipine↗
PubMed2006

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.

Cardiovascular Diseases↗
PubMed1991

New hope for failing hearts.

Major changes in our understanding of congestive heart failure have resulted from an etiologic shift, identification of neurohormonal effects, and a realization of the importance of diastolic dysfunction. Accordingly, management has changed. Digitalis should be avoided with diastolic dysfunction. When the dysfunction is systolic, a regimen of digitalis, diuretic and ACE inhibitor may be optimal.

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