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PubMedDate not supplied

Allograft diastolic dysfunction and chronotropic incompetence limit cardiac output response to exercise two to six years after heart transplantation.

BACKGROUND: Because prolonged survival of heart transplant recipients is expected with the current immunosuppressive treatment, the functional capacity of these long-term survivors is of interest. Previous exercise studies showed no objective improvement in exercise tolerance several years after transplantation, but the extent to which chronotropic incompetence and allograft diastolic dysfunction observed early after transplantation may improve over time has not been defined. METHODS: Thirteen untrained heart transplant recipients without symptoms, between 27 and 70 months after transplantation, and 13 age-matched sedentary normal controls underwent maximal upright bicycle exercise testing with simultaneous hemodynamic, radionuclide, and expired gas measurements. RESULTS: Systolic function as measured by ejection fraction was supranormal at rest in the transplant group and normalized with exercise. Despite their maximal exercise effort, transplant recipients had a 60% reduction in their exercise capacity compared with nontransplant recipients. Peak oxygen consumption was similarly reduced by 52%. Cardiac output response to exercise was 43% lower in the transplant group because of a 78% reduction in heart rate reserve and an 18% reduction in maximal stroke volume. Ventricular volumes were similarly reduced after transplantation, but filling pressures remained normal, indicating allograft diastolic dysfunction. Despite the significantly reduced maximal cardiac output, maximal arteriovenous oxygen difference was 25% lower in the transplant recipients, suggesting a peripheral deficit in oxygen handling. CONCLUSIONS: Therefore, patients, 2 to 6 years after transplantation, continue to have a significant reduction in exercise tolerance as a result of a combination of severe chronotropic incompetence, limited stroke volume reserve caused by a reduced ventricular size and allograft diastolic dysfunction, and an abnormality in peripheral oxygen delivery or use. Efforts aimed at improving these factors may further enhance the functional capacity of these long-term survivors of heart transplantation.

Cardiac Output↗
PubMed2004

Sympathetic dysfunction in type 1 diabetes: association with impaired myocardial blood flow reserve and diastolic dysfunction.

OBJECTIVES: This study was designed to explore the relationships of early diabetic microangiopathy to alterations of cardiac sympathetic tone and myocardial blood flow (MBF) regulation in subjects with stable type 1 diabetes. BACKGROUND: In diabetes, augmented cardiac sympathetic tone and abnormal MBF regulation may predispose to myocardial injury and enhanced cardiac risk. METHODS: Subject groups comprised healthy controls (C) (n = 10), healthy diabetic subjects (DC) (n = 12), and diabetic subjects with very early diabetic microangiopathy (DMA+) (n = 16). [(11)C]meta-hydroxyephedrine ([(11)C]HED) and positron emission tomography (PET) were used to explore left ventricular (LV) sympathetic integrity and [(13)N]ammonia-PET to assess MBF regulation in response to cold pressor testing (CPT) and adenosine infusion. RESULTS: Deficits of LV [(11)C]HED retention were extensive and global in the DMA+ subjects (36 +/- 31% vs. 1 +/- 1% in DC subjects; p < 0.01) despite preserved autonomic reflex tests. On CPT, plasma norepinephrine excursions were two-fold greater than in C and DC subjects (p < 0.05), and basal LV blood flow decreased (-12%, p < 0.05) in DMA+ but not in C or DC subjects (+45% and +51%, respectively). On adenosine infusion, compared with C subjects, MBF reserve decreased by approximately 45% (p < 0.05) in DMA+ subjects. Diastolic dysfunction was detected by two-dimensional echocardiography in 5 of 8 and 0 of 8 consecutively tested DMA+ and DC subjects, respectively. CONCLUSIONS: Augmented cardiac sympathetic tone and responsiveness and impaired myocardial perfusion may contribute to myocardial injury in diabetes.

Adenosine↗
PubMed1997

Role of left ventricular hypertrophy in diastolic dysfunction in aged hypertensive patients.

OBJECTIVE: To evaluate the influence of left ventricular hypertrophy (LVH) on the diastolic dysfunction in older hypertensive patients. METHODS: In total 665 patients (58% men, 61% White, aged 55-80 years) with mild-to-moderate essential hypertension underwent Doppler echocardiography. Data included left ventricular dimensions, left ventricular mass index, body mass index, E- and A-wave mitral flow velocities, E:A ratio, deceleration time > 150 ms), impaired relaxation (E:A ratio < 1.0, prolonged deceleration time according to age), and restrictive physiology (E:A ratio > 2.1, deceleration time < 150 ms)]. Data were distributed according to age (50-59, 60-69, and 70-80 years). RESULTS: The overall prevalence of sex-adjusted LVH in this study was 65%. When we compared hypertensive patients with and without LVH, the E- and A-wave velocities, E:A ratio, and deceleration time were similar. Moreover, the prevalences of normal, impaired relaxation, and restrictive physiology patterns among patients with and without LVH did not differ significantly (20, 79.5, and 0.5 versus 24, 75.5, and 0.5%). When the mitral flow patterns were adjusted according to age, the impaired relaxation pattern increased further with age (to 73% during the fifth decade, 83% during the sixth decade, and 88% during the seventh decade). CONCLUSIONS: LVH is not an independent factor associated with abnormal flow patterns in hypertensive patients aged over 50 years with normal systolic contractility. The impaired relaxation is the predominant pattern of diastolic dysfunction in older hypertensive patients and increases further with aging.

Aged↗
PubMedDate not supplied

Effect of cardiac resynchronization therapy on diastolic dysfunction as assessed by transthoracic two-dimensional Doppler echocardiography.

Cardiac resynchronization therapy (CRT) in patients with left ventricular systolic dysfunction and electrical dyssynchrony has been shown to improve morbidity and mortality. Improvement in diastolic dysfunction may contribute to these results. In this retrospective study, the authors assessed the effect of CRT on the E/A ratio and mitral valve deceleration time, which are commonly utilized parameters of left ventricular diastolic function. In 13 patients (aged 62 +/- 11.3 years), the E/A ratio increased from 1.17 +/- 0.58 to 1.49 +/- 0.66 (p = nonsignificant) and the mitral valve deceleration time increased from 178.48+/-57.71 milliseconds to 227.70 +/- 76.18 milliseconds (p = 0.054) post-CRT. In patients without mitral regurgitation, there was a significant increase in E/A ratio, from 1.22 +/- 0.4 to 1.86 +/- 0.47 (p = 0.025), but no significant change in the mitral valve deceleration time post-CRT was observed. These data suggest improvement in diastolic dysfunction as assessed by routine two-dimensional echocardiography in patients who receive CRT devices.

Adult↗
PubMed2004

Comparison of early diastolic mitral annular velocity and flow propagation velocity in detection of mild to moderate left ventricular diastolic dysfunction.

BACKGROUND: Pulsed wave tissue Doppler echocardiography (PW-TDE) and color M-mode are new Doppler methods for left ventricular (LV) diastolic function assessment. To date, few studies have compared the data obtained by these methods in the same series of patients and compared them to the current clinical reference method of detecting LV diastolic function. AIMS: To determine the utility of PW-TDE and color M-mode parameters in the assessment of LV diastolic function in the typical patient population encountered in daily clinical practice and to compare their discriminating power. METHODS: Early diastolic septal mitral annular velocity (Em) determined by PW-TDE and color M-mode flow propagation velocity (Vp) were measured in 86 male patients and compared to LV filling patterns obtained using standard Doppler indices. Values of Em < 0.08 m s(-1) and Vp < 0.5 m s(-1) were considered as markers of abnormal LV diastolic function. RESULTS: A value of Em < 0.08 m s(-1) distinguished mild to moderate LV diastolic dysfunction with higher sensitivity and specificity than Vp < 0.5 m s(-1) (96% and 87% vs. 73% and 84%, respectively). A comparison of receiver operating characteristic curves showed a significant difference for areas under the curve in favor of Em (P < 0.01). In a stepwise multiple logistic regression analysis, a pseudonormal filling pattern and an EF > 60% were identified as significant predictors of Vp false negative results (p < 0.05). CONCLUSIONS: Em appears to be superior to Vp in the detection of mild to moderate LV diastolic dysfunction. Vp failed to detect abnormal LV diastolic function in particular in patients with preserved LV systolic function and a pseudonormal filling pattern type.

Adult↗
PubMedDate not supplied

Left ventricular diastolic dysfunction secondary to hyperglycemia in patients with type II diabetes.

Diabetes mellitus type II, a cause of preclinical left ventricular dysfunction that can progress to cardiac insufficiency ventricular dysfunction in diabetic patients, is attributed to systemic arterial hypertension, or ischemic cardiopathy. Diastolic ventricular dysfunction takes place during the course of diabetes mellitus. The purpose of the present article is to report on the influence of hyperglycemia on the left ventricular diastolic dysfunction independently of dyslipidemia, obesity, and systemic arterial hypertension, usually present in diabetic patients. Left ventricular diastolic function was studied by Doppler echocardiography in asymptomatic type II diabetic patients without ischemic or valvular cardiopathies, cardiomegaly, or systemic arterial hypertension. Two groups of patients were integrated: patients with and without left ventricular diastolic dysfunction, i.e., groups A and B, respectively. Glycemia, cholesterol, triglycerides, and body mass index (BMI) were determined in each subject. Bivariate statistical tests (Student t, chi-square, or Mann-Whitney U tests) were applied to study the influence of the previously mentioned variables on the ventricular diastolic function. To evaluate the influence of hyperglycemia on ventricular diastolic function separately from dyslipidemia, systemic arterial hypertension, and the influence of obesity, logistic regression, and multivariate statistical analysis were applied. Independently of dyslipidemia and obesity, a relationship was found between hyperglycemia and diastolic dysfunction of the left ventricle in patients belonging to group A (p <0.05, odds ratio [OR] 12.1). No statistical significance was found between glycemia and the diastolic function of the left ventricle in group B patients. Even in type II diabetic patients without cardiopathy, uncontrolled hyperglycemia provokes diastolic left ventricular dysfunction.

Adult↗
PubMed2006

Left ventricular diastolic dysfunction is related to oxidative stress and exercise capacity in hypertensive patients with preserved systolic function.

BACKGROUND: Left ventricular diastolic dysfunction and oxidative stress are important determinants in heart failure development. Peak oxygen uptake, maximal oxygen consumption, metabolic equivalents (MET), ventilatory response and time to respiratory gas exchange assess cardiopulmonary capacity. AIM: It was the aim of this study to investigate the impact of oxidative stress on diastolic indexes and cardiopulmonary exercise capacity in hypertensive patients with left ventricular diastolic dysfunction. METHODS: Mitral flow velocities (E, A), ejection fraction, left atrial and ventricular diameters were assessed by Doppler echocardiography. Superoxide dismutase (SOD) and glutathione peroxidase activity in blood were evaluated. Sixty patients (aged 49.8 +/- 9.2 years) with essential hypertension and preserved systolic function (ejection fraction 58.3 +/- 7%) performed a bicycle exercise test. Forty patients showed impaired left ventricular relaxation (E/A <1, deceleration time of E >220 ms) and were assigned to group 1, while 20 had normal relaxation (group 2). RESULTS: An increase in SOD was significantly blunted after exercise in group 1 compared with group 2 (p = 0.049). A significant difference between groups in the glutathione peroxidase level was observed before exercise (p = 0.038). There were significantly lower values of peak oxygen uptake and MET (p = 0.013 and p = 0.024, respectively) and a prolonged respiratory exchange ratio (p = 0.022) in group 1 compared with group 2. MET was significantly influenced by SOD level (p = 0.035). CONCLUSIONS: Lower antioxidative protection and impaired relaxation decrease cardiopulmonary capacity in hypertensive patients.

Aged↗
PubMed1988

Relation of left ventricular dilation during acute myocardial infarction to systolic performance, diastolic dysfunction, infarct size and location.

The quantification of left ventricular (LV) volumes and assessment of their relation to systolic and diastolic dysfunction, infarct size and anatomic location were performed in 54 patients with a first acute myocardial infarction (AMI). Blood pool radionuclide angiography was used to assess LV end-diastolic, end-systolic, and stroke volume indexes, ejection fraction and peak diastolic filling rate. Infarct size was estimated from plasma MB creatine kinase activity. Substantial LV dilation occurred within the initial 24 hours of AMI. The peak diastolic filling rate was low, even in those patients with a normal ejection fraction. In comparison with inferior AMI (n = 25), patients with anterior AMI (n = 29) had a larger end-diastolic volume index (105 +/- 8 vs 81 +/- 4 ml/m2, p less than 0.01) and end-systolic volume index (64 +/- 7 vs 37 +/- 4 ml/m2, p less than 0.001), but similar stroke volume index (41 +/- 3 vs 43 +/- 2 ml/m2, difference not significant). No significant relation was noted between infarct size estimated by MB creatine kinase and any volumetric index. On repeat study (day 10 after AMI), end-diastolic and end-systolic volume indexes increased further (p less than 0.05 vs day 1) but ejection fraction and peak diastolic filling rate were unchanged. It was concluded that: (1) LV dilation occurs within hours of AMI in both inferior and anterior AMI, but is more marked in the latter; (2) significant LV diastolic dysfunction is the rule, even in patients with preserved LV systolic function; and (3) LV dilation is an early compensatory mechanism that maintains normal stroke volume, even in patients with severely reduced LV function.

Cardiac Volume↗
PubMed2002

Assessment of diastolic dysfunction after acute myocardial infarction using Doppler echocardiography.

Doppler echocardiography (DE) is becoming a powerful noninvasive tool for assessing left ventricular diastolic dysfunction after myocardial infarction (MI). Transmitral inflow DE measurements of early and late filling velocities, early to late ratio and early deceleration time correlate well with left ventricular filling pressure. Three abnormal filling patterns (impaired relaxation, pseudonormalization and restrictive) develop after MI, depending on infarct size. Pulmonary venous inflow DE contributes important additional diagnostic data and, when combined with transmitral DE, avoids potential confusion due to the pseudonormal pattern that develops in the presence of high left atrial pressure and impaired relaxation. Several studies indicate that these DE patterns correlate with progressively increasing functional impairment, and the restrictive transmitral pattern predicts heart failure and death among MI survivors. Further studies are needed to evaluate the effects of therapy on the DE patterns of diastolic dysfunction after MI.

Diastole↗
PubMed2005

Reversible diastolic dysfunction after long-term exogenous subclinical hyperthyroidism: a randomized, placebo-controlled study.

BACKGROUND: Subclinical hyperthyroidism has been reported to affect systolic and diastolic cardiac function. However, the reversibility of these effects is not well established. OBJECTIVE: Our objective was to investigate the presence and reversibility of cardiac abnormalities in patients with long-term exogenous subclinical hyperthyroidism. DESIGN: We conducted a prospective, single-blinded, placebo-controlled randomized trial of 6 months duration with two parallel groups. SETTING: The study occurred at the Leiden University Medical Center, a tertiary referral center for thyroid carcinoma. PATIENTS: As a model for subclinical hyperthyroidism, 25 patients with a history of differentiated thyroid carcinoma with more than 10 yr of TSH suppressive therapy with L-T4 were studied. INTERVENTIONS: L-T4 dose was replaced by study medication containing L-T4 or placebo. Medication was titrated in a single-blinded fashion to establish continuation of TSH suppression (low-TSH group) or euthyroidism (euthyroid group). MEASUREMENTS: We assessed serum levels of free T4 and TSH and used echo Doppler cardiography including tissue Doppler to establish left ventricular (LV) dimensions and function as well as diastolic function. Baseline echocardiography data were compared with 24 controls. RESULTS: There were no differences in baseline cardiac parameters and TSH levels between the two groups. Although mean LV mass index was increased as compared with 24 controls, only four patients had LV hypertrophy at baseline. This was not improved by restoration of euthyroidism. At baseline, diastolic function was impaired in all patients as indicated by abnormal values for the peak flow of the early filling phase (E, 55.3 +/- 9.5 mm/sec), the ratio of E and the peak flow of the atrial filling phase (E/A ratio, 0.87 +/- 0.13), the early diastolic velocity obtained by tissue Doppler (E', 5.7 +/- 1.3 cm/sec), and the peak atrial filling velocity obtained by tissue Doppler (A', 6.8 +/- 1.4 cm/sec), prolonged E deceleration time (234 +/- 34 msec), and isovolumetric relaxation time (121 +/- 15 msec). After 6 months, significant improvements were observed in the euthyroid group in the E/A ratio (+41%; P < 0.001), E deceleration time (-18%; P = 0.006), isovolumetric relaxation time (-25%; P < 0.001), E' (+31%; P < 0.001), and the E'/A' ratio (+40%; P < 0.001). CONCLUSIONS: We conclude that prolonged subclinical hyperthyroidism is accompanied by diastolic dysfunction that is at least partly reversible after restoration of euthyroidism. Because isolated diastolic dysfunction may be associated with increased mortality, this finding is of clinical significance.

Adult↗
PubMed2002

Determinants of afterload-induced diastolic dysfunction.

Severe left ventricular (LV) afterload elevations induce diastolic dysfunction (DD). This decompensatory response, observed in both dogs and rabbits, seems to be related to cytosolic calcium levels. As rats have different calcium kinetics, we investigated the effects of acute LV afterload elevation in rats. Anaesthetized Wistar rats (n = 10) were instrumented in order to record simultaneously LV pressure and septal-free wall dimensions. Afterload was elevated through partial or total occlusions of the ascending aorta. In afterloaded heartbeats, we measured the time constant tau, the necessary (NTR) and the available (ATR) time intervals to complete LV relaxation. DD was evaluated through analysis of the position of the end-diastolic pressure-volume relation. Afterload elevations elicited acceleration of relaxation and DD was observed only in isovolumetric heartbeats. This DD could be explained by the deficit in time to complete relaxation in isovolumetric heartbeats. We conclude, therefore, that the time constant tau and ATR are the major determinants of afterload-induced DD. The calcium kinetics of the rat provide a better adaptation to afterload elevations in this than in other species.

Animals↗
PubMed1989

Exercise-induced pulmonary blood volume changes and diastolic dysfunction of the aged heart.

Impaired diastolic function has been described in healthy elderly subjects. Pulmonary blood volume (PBV) changes with exercise have been associated with left ventricular dysfunction, but not directly related to diastolic abnormalities. Exercise-induced relative changes in PBV were measured using gated blood pool imaging with count density comparisons over the lung in 20 healthy volunteers: 13 elderly, age 76 +/- 5 years and seven young, age 27 +/- 4 years. Serial (first exercise stage, peak exercise, and post exercise) PBV ratios were measured and correlated to peak early filling rate, peak late filling rate, and percent atrial filling obtained from the resting left ventricular time-activity curve analysis. PBV ratios tended to be higher in elderly subjects, but reached significance only at the first stage of exercise (1.04 +/- 0.07 vs. 0.93 +/- 0.10, p less than 0.01). Significant correlations were found between PBV ratios at first exercise stage and peak early filling rate (r = -0.64), peak late filling rate (r = 0.47), and percent atrial filling (r = 0.48). A significant correlation was found between PBV changes at peak exercise and resting diastolic parameters. Exercise-induced PBV changes are associated with left ventricular diastolic dysfunction at rest. Diastolic abnormalities of the aged heart may explain the differential PBV response early into exercise between young and elderly healthy subjects.

Adult↗
PubMed2004

Myocardial fibrosis and diastolic dysfunction in deoxycorticosterone acetate-salt hypertensive rats is ameliorated by the peroxisome proliferator-activated receptor-alpha activator fenofibrate, partly by suppressing inflammatory responses associated with the nuclear factor-kappa-B pathway.

OBJECTIVES: We sought to clarify that a peroxisome proliferator-activated receptor-alpha (PPAR-alpha) activator inhibits myocardial fibrosis and its resultant diastolic dysfunction in hypertensive heart disease, as well as to investigate whether inflammatory mediators through the nuclear factor (NF)-kappa-B pathway are involved in the effects. BACKGROUND: Patients with hypertensive heart disease often have diastolic heart failure without systolic dysfunction. Meanwhile, it has been well established in atherosclerosis that PPAR-alpha activation negatively regulates early inflammation. In hypertensive hearts, however, it is still unclear whether PPAR-alpha activation inhibits inflammation and fibrosis. METHODS: Twenty-one rats were randomly separated into the following three groups: deoxycorticosterone acetate (DOCA)-salt hypertensive rats treated with a PPAR-alpha activator, fenofibrate (80 mg/kg/day for 5 weeks); DOCA-salt rats treated with vehicle only; and uni-nephrectomized rats as normotensive controls. RESULTS: Fenofibrate significantly inhibited the elevation of left ventricular end-diastolic pressure and the reduction of the magnitude of the negative maximum rate of left ventricular pressure rise and decline, corrected by left ventricular pressure (-dP/dt(max)/P), which are indicators of diastolic dysfunction. Next, fenofibrate prevented myocardial fibrosis and reduced the hydroxyproline content and procollagen I and III messenger ribonucleic acid expression. Finally, inflammatory gene expression associated with NF-kappa-B (interleukin-6, cyclooxygenase-2, vascular cell adhesion molecule-1, and monocyte chemoattractant protein-1), which is upregulated in DOCA-salt rats, was significantly suppressed by fenofibrate. Activation of NF-kappa-B and expression of I-kappa-B-alpha in DOCA-salt rats were normalized by fenofibrate. CONCLUSIONS: A PPAR-alpha activator reduced myocardial fibrosis and prevented the development of diastolic dysfunction in DOCA-salt rats. The effects of a PPAR-alpha activator may be mediated partly by prevention of inflammatory mediators through the NF-kappa-B pathway. These results suggest that treatment with PPAR-alpha activators will improve diastolic dysfunction in hypertensive heart disease.

Animals↗
PubMed1995

Effects of left ventricular diastolic dysfunction on exercise capacity three to six weeks after acute myocardial infarction in men.

To examine the effects of left ventricular (LV) diastolic dysfunction on exercise capacity, hemodynamic and radionuclide responses were measured at rest and during exercise in 50 patients with recent myocardial infarction. The ratio of an increase in pulmonary arterial wedge pressure (PAWP) to an increase in LV end-diastolic volume (EDV) from rest to peak exercise (delta PAWP/delta EDV) was used as an index of LV diastolic function, delta PAWP/delta EDV had modest and negative correlations with peak oxygen consumption (VO2), cardiac output, and stroke volume in all patients. Among patients with peak VO2 > or = 20 ml/min/kg (group I, n = 24) and those with peak VO2 < 20 ml/min/kg (group II, n = 26), there were no differences between the 2 groups with regard to resting LV ejection fraction, EDV, PAWP, cardiac output, and stroke volume. Although there was no significant difference in LV ejection fraction at peak exercise, group II had significantly reduced EDV, increased PAWP, and decreased cardiac output and stroke volume than those in group I. As a result, delta PAWP/delta EDV was significantly higher in group II. These results suggest that LV diastolic dysfunction has a key role in determining exercise capacity in patients with reduced exercise capacity after recent myocardial infarction.

Adolescent↗
PubMed2006

Regional diastolic dysfunction in individuals with left ventricular hypertrophy measured by tagged magnetic resonance imaging--the Multi-Ethnic Study of Atherosclerosis (MESA).

BACKGROUND: Impairment of global diastolic function is considered to be the mechanism of congestive heart failure in individuals with preserved systolic left ventricular (LV) function. Left ventricular hypertrophy (LVH) is known to be a risk factor for congestive heart failure with preserved systolic function, and this process may begin as a regional process. We investigated whether regional LV diastolic function measured by magnetic resonance tagging is altered in asymptomatic participants of the MESA with LVH and preserved systolic LV function. METHODS: Regional systolic and diastolic strain rates were calculated from strain data in 218 participants of the MESA study. Circumferential strain was calculated from the midwall layer of the septum, anterior, lateral, and inferior walls at mid-LV level. Global LV function measures were studied by magnetic resonance imaging in 4291 MESA participants. Left ventricular hypertrophy for men and women was defined from the MESA population using previously established Framingham criteria. RESULTS: Global systolic function was slightly less in the LVH (ejection fraction = 0.66 +/- 0.10) versus the non-LVH group (ejection fraction = 0.69 +/- 0.07, P < .001). Stepwise regression analyses showed a direct relationship between regional diastolic dysfunction and increasing LV mass. Regional systolic strain and strain rate measures from participants with LVH were not significantly different from those without LVH. However, regional diastolic strain rate was significantly reduced in participants with LVH (1.5 +/- 1.1 s(-1)) compared with the non-LVH group (2.2 +/- 1.1 s(-1), P < .001) regardless of age or sex. CONCLUSIONS: Left ventricular hypertrophy is associated with regional diastolic dysfunction in individuals without evidence of clinical cardiovascular disease and preserved systolic function. Magnetic resonance imaging tagging provides detailed quantification of regional diastolic function noninvasively.

Aged↗
PubMed2006

Validity of revised Doppler echocardiographic algorithms and composite clinical and angiographic data in diagnosis of diastolic dysfunction.

BACKGROUND: Commonly used echocardiographic indices for grading diastolic function predicated on mitral inflow Doppler analysis have a poor diagnostic concordance and discriminatory value. Even when combined with other indices, significant overlap prevents a single group assignment for many subjects. We tested the relative validity of echocardiographic and clinical algorithms for grading diastolic function in patients undergoing cardiac catheterization. METHOD: Patients (n = 115), had echocardiograms immediately prior to measuring left ventricular (LV) diastolic (pre-A, mean, end-diastolic) pressures. Diastolic function was classified into the traditional four stages, and into three stages using a new classification that obviates the pseudonormal class. Summative clinical and angiographic data were used in a standardized fashion to classify each patient according to the probability for abnormal diastolic function. Measured LV diastolic pressure in each patient was compared with expected diastolic pressures based on the clinical and echocardiographic classifications. RESULT: The group means of the diastolic pressures were identical in patients stratified by four-stage or three-stage echocardiographic classifications, indicating that both classifications schemes are interchangeable. When severe diastolic dysfunction is diagnosed by the three-stage classification, 88% and 12%, respectively, were clinically classified as high and intermediate probability, and the mean LV pre-A pressures was >12 mmHg (P < 0.005). Conversely, the mean LV pre-A pressure in the clinical low probability or echocardiographic normal groups was <11 mmHg. CONCLUSION: Use of a standardized clinical algorithm to define the probability of diastolic function identifies patients with elevated LV filing pressure to the same extent as echocardiographic methods.

Aged↗
PubMed2004

Persistent diastolic dysfunction despite complete systolic functional recovery after reperfused acute myocardial infarction demonstrated by tagged magnetic resonance imaging.

AIMS: This study was designed to characterise both the systolic and diastolic mechanical properties of regions with different degrees of myocardial ischaemic injury after reperfused acute myocardial infarction (AMI). METHODS AND RESULTS: Fourteen dogs underwent 90-min coronary artery occlusion followed by reperfusion. Image acquisition was performed 24 h after reperfusion using three techniques: tagged, first-pass perfusion and delayed-enhancement magnetic resonance imaging (MRI). Systolic circumferential strain and both systolic and diastolic strain rates were calculated in 30 segments/animal. Transmural AMI segments displayed reduced systolic contractility when compared to subendocardial AMI segments (systolic strain = -2.5 +/- 0.5% versus -6.0 +/- 0.9%, P < 0.01 and systolic strain rate = -0.11 +/- 0.12 versus -0.82 +/- 0.16 s(-1), P < 0.01), and both exhibited significant systolic and diastolic dysfunction compared to remote. Moreover, AMI segments presenting with microvascular obstruction ("no-reflow") displayed further compromise of systolic and diastolic regional function (P < 0.05 for both). Importantly, risk region segments only exhibited diastolic impairment (diastolic strain rate = 1.62 +/- 0.14 versus 2.99 +/- 0.13 s(-1), P < 0.001), but not systolic dysfunction compared to remote 24 h after reperfusion. CONCLUSION: Reversibly injured regions can demonstrate persistent diastolic dysfunction despite complete systolic functional recovery after reperfused AMI. Moreover, the presence of no-reflow entails profound systolic and diastolic dysfunction. Finally, tagged magnetic resonance imaging (MRI) strain rate analysis provides detailed mechanical characterisation of regions with different degrees of myocardial ischaemic injury.

Animals↗
PubMed2001

Plasma nitric oxide level in heart failure secondary to left ventricular diastolic dysfunction.

Nitric oxide (NO) is a free radical that is elevated in the plasma of patients with systolic heart failure. However, its relation to diastolic function is unknown. This study investigated the relation between the level of stable end-products of plasma NO (NOx level) and diastolic function in patients with heart failure. We performed echocardiographic Doppler studies in 76 patients (mean age of 66 +/- 10 years, 75% men) with congestive heart failure. Left ventricular (LV) diastolic dysfunction was classified as either a restrictive (RFP) or nonrestrictive filling pattern (non-RFP). Same day venous total nitrite plus nitrate levels were measured by chemiluminscence. Both patients with isolated diastolic heart failure (ejection fraction >50%) (77 +/- 9 micromol/L, n = 33) and systolic failure (ejection fraction < or = 50%) (115 +/- 17 micromol/L, n = 43) had significantly higher plasma NOx levels than controls (37 +/- 2 micromol/L, both p <0.001). RFP coexists mostly in patients with systolic heart failure (15 of 18), and these patients had a higher NOx level than patients with systolic failure and a non-RFP (n = 28) (163 +/- 35 vs 88 +/- 16 micromol/L, p <0.05). Patients who were not on oral nitrate drugs had insignificant lower plasma NOx levels than those on regular nitrate therapy, although it was still higher than controls. Plasma NOx level did not correlate with LV ejection fraction. Stepwise multiple regression analysis confirmed that the presence of RFP was the only independent predictor of NOx, and hence NO production. Plasma NOx level is elevated in patients with isolated diastolic heart failure. In addition, in patients with LV systolic failure, the severity of LV diastolic dysfunction determines the amount of NO production.

Aged↗