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At least 829 records · Page 46Linked to original sources
PubMed2005

Spironolactone improves diastolic function in the elderly.

BACKGROUND: Diastolic dysfunction is common in the elderly. Increased myocardial fibrosis, a major determinant of diastolic function, has been observed with advancing age. Spironolactone prevents age-related increases in myocardial fibrosis in old normotensive rats. HYPOTHESIS: Spironolactone, via its antifibrotic activity, can improve diastolic function in the elderly with isolated diastolic dysfunction. METHODS: The study was a prospective, double-blind, randomized, placebo-controlled trial. Thirty elderly subjects between 60 and 85 years of age with isolated diastolic dysfunction and no contraindications for spironolactone were randomized to 25 mg/day of spironolactone or placebo for 4 months. Mitral E/A and deceleration time, plasma levels of carboxy-terminal of procollagen type I (PICP), and brain natriuretic peptide (BNP) were measured at baseline and at the end of 4 months. Plasma level of potassium was also monitored to prevent clinically significant hyperkalemia. RESULTS: There was no serious adverse event or clinically significant hyperkalemia in the spironolactone group. Compared with baseline values, spironolactone significantly improved mitral E/A ratio (0.71 +/- 0.08 vs. 0.84 +/- 0.19, p = 0.025) and deceleration time (285.5 +/- 73.1 vs. 230.0 +/- 54.7, p = 0.035). There were no significant differences in the magnitude of change in the levels of PICP and BNP between the two treatment groups. CONCLUSION: Spironolactone may improve diastolic function in the elderly.

Aged↗
PubMed2003

Decreased left ventricular longitudinal contraction in normotensive and normoalbuminuric patients with Type II diabetes mellitus: a Doppler tissue tracking and strain rate echocardiography study.

Type II diabetes mellitus is associated with congestive heart failure with preserved ejection fraction. This group of patients has been assumed to have isolated diastolic dysfunction; however, the longitudinal systolic contraction of the left ventricle has not been studied previously. The objective of the present study was to investigate the longitudinal contraction of the left ventricle in normotensive Type II diabetes mellitus patients with normal ejection fraction. We examined 32 normotensive patients with Type II diabetes mellitus with ejection fraction >0.55 and fractional shortening >0.25. Exclusion criteria were angina pectoris, cardiac valve disease, albuminuria, retinopathy or neuropathy. Normal subjects (n =32) served as controls. A 16 segment model of motion amplitude assessed left ventricular longitudinal contraction and the average of the segments was calculated as the tissue tracking score index. Peak systolic velocity and strain rate was also obtained in each segment. Patients with Type II diabetes mellitus had a significantly lower tissue tracking score index compared with normal subjects (5.8+/-1.6 mm compared with 7.7+/-1.1 mm; P <0.001). Mean peak systolic velocity was also significantly lower (4.3+/-1.5 cm/s compared with 5.4+/-1.0 cm/s; P <0.001), as well as peak systolic strain rate (-1.2+/-0.3 s(-1) compared with -1.6+/-0.4 s(-1); P <0.001). Patients with Type II diabetes mellitus and preserved diastolic function had a significantly lower tissue tracking score index compared with normal subjects (6.6+/-1.5 mm; P <0.001), but patients with diastolic dysfunction had an even more profound decrease in tissue tracking score index compared with patients without diastolic dysfunction (4.9+/-0.9 mm; P <0.01). In conclusion, the longitudinal systolic contraction was significantly decreased in normotensive patients with Type II diabetes mellitus with normal ejection fraction, which was most profound in patients with concomitant diastolic dysfunction.

Case-Control Studies↗
PubMed2005

Lateral vs medial mitral annular tissue Doppler in the echocardiographic assessment of diastolic function and filling pressures: which should we use?

Tissue Doppler echocardiography (TDE) is used in the assessment of diastolic function, however, it is unclear whether the medial (E' med) or lateral (E' lat) annulus should be used. Our aim was to compare the diagnostic utility of E' med and E' lat. In 232 subjects left ventricular (LV) systolic and diastolic function was assessed via transthoracic echocardiography with TDE measurements obtained from both annuli. LV function was normal in 91 subjects (39%), with diastolic dysfunction found in 141 subjects (61%). TDE velocities decreased with age and progressive diastolic dysfunction for either annulus. E' med recorded significantly lower myocardial velocities than E' lat. Receiver operator curves showed improved area under the curve (AUC) for E' med than E' lat. Furthermore the AUC was significantly improved compared to E/A ratio and deceleration time. For diagnosing diastolic dysfunction, an E' med<11cm/s provided a sensitivity of 78%, specificity of 67% and positive predictive value of 70%. Whilst for diagnosing elevated filling pressures an E/E' medial ratio>8 provided values of 56%, 93% and 91%, respectively. In conclusion, although either annulus can be used, E' med provides better diagnostic utility.

Aged↗
PubMed1996

[From left hypertrophy to heart insufficiency: hemodynamic and clinical findings].

The pathophysiology of left-ventricular hypertrophy is characterized by structural remodeling with increasing content of collagen and development of ventricular dilatation ('Gefügedilatation'). According to recent clinical view points, three stages may be distinguished: first stage, compensation, second stage, diastolic dysfunction with delayed relaxation and decrease of the passive-elastic properties, third stage, systolic and diastolic dysfunction with decreasing pump function and signs of left-ventricular failure. Diastolic dysfunction is linked to delayed rotation during isovolumetric relaxation (delayed 'untwisting') which leads to decreased ventricular filling. These changes of the myocardial adaptation process may be prevented and the vicious circle interrupted by appropriate therapeutic strategies.

Adaptation, Physiological↗
PubMed2000

Heart failure with preserved LV function: pathophysiology, clinical presentation, treatment, and nursing implications.

The syndrome of congestive heart failure occurring secondary to diastolic dysfunction accounts for the major pathophysiologic mechanism in up to one-third of patients who present with dyspnea on exertion and pulmonary congestion. Diastolic dysfunction is characterized by an alteration in the normal diastolic pressure-volume relationship while systolic function may be normal. It is manifested by impairment in the left ventricle's ability to relax and fill completely during diastole at normal low ventricular pressures. This subset of heart failure is most commonly associated with concentric left ventricular hypertrophy and ischemic states. Symptom presentation is similar to that associated with systolic dysfunction as are rates of rehospitalization. Diagnosis is made based on data obtained from invasive and noninvasive procedures. Unlike in the setting of systolic dysfunction, however, there are no large-scale randomized clinical trials evaluating drug efficacy that could be used to guide treatment for the management of diastolic dysfunction. Treatment recommendations, therefore, are empiric. Identifying and aggressively treating potentially reversible causes is a priority. Many of the same drugs used in the management of heart failure associated with systolic dysfunction are also used in the setting of diastolic impairment; however, dosages and rationale for administration may differ. Nursing interventions too are similar. Monitoring response to medications, especially in the acute setting, and comprehensive patient education are paramount. Much is yet to be learned about the management of diastolic dysfunction.

Cardiovascular Agents↗
PubMed1997

Prevalence of sleep-disordered breathing in diastolic heart failure.

OBJECTIVE: Sleep-disordered breathing (SDB) is common in congestive heart failure. While isolated diastolic heart failure (DHF) accounts for up to a third of all cases of congestive heart failure, the prevalence of SDB in DHF is unknown. We aim to determine the prevalence and characteristics of SDB in a group of patients with symptomatic DHF. METHODS: Twenty subjects with symptomatic DHF (New York Heart Association class II or III) and isolated diastolic dysfunction on echocardiography were assessed with lung function tests, modified sleep and health questionnaire, and overnight polysomnography. Significant SDB was defined as an apnea/hypopnea index (AHI) > 10. RESULTS: Thirteen female and seven male subjects (mean age, 65+/-6.0 years; mean body mass index (BMI), 28+/-3.2) were evaluated, of whom 17 (85%) had a diagnosis of hypertension. Overall sleep quality was poor, with fragmentation and frequent arousals associated with respiratory events. Fifty-five percent of the patients had significant SDB, mainly obstructive apneas. BMI and the prevalence of hypertension were similar in patients with and without SDB. The deceleration time, an index of diastolic dysfunction, was more prolonged in the group with SDB (236+/-40 ms vs 282+/-31 ms; p<0.05). As a group, a lower minimum percentage arterial oxygen saturation during sleep, but not the AHI was associated with more severe degree of diastolic dysfunction on echocardiogram, including a lower ratio between the early peak transmittal flow velocity and the late peak atrial systolic velocity (rho=0.57; p<0.05) and a prolonged isovolumic relaxation time (rho=-0.54; p<0.05). CONCLUSIONS: SDB is common in patients with DHF. Patients with DHF and SDB may be associated with worse diastolic dysfunction than those without SDB, although a causal relationship remains to be established.

Aged↗
PubMed2001

[Interaction between load and beta-adrenergic stimulation in the modulation of diastolic function].

INTRODUCTION AND OBJECTIVES: Excessive afterload induces an upward shift of the diastolic pressure-volume relation. This diastolic dysfunction was attributed to the concomitant slowing of relaxation. The present study investigated to what extent beta-adrenergic stimulation could influence this effect. METHODS: Beat-to-beat afterload elevations were induced in anaesthetised open-chest rabbits (n = 7) by narrowing the ascending aorta, to increase peak left ventricular pressure (LVPmax) from control up to isovolumetric. Afterload elevations were performed at baseline and during infusion of isoproterenol (0.15 mg/kg/min). RESULTS: At baseline, LVPmax increased from 84 +/- 7 in the control beat to 154 +/- 10 mmHg in the isovolumetric beat, while during isoproterenol it increased from 88 +/- 4 to 184 +/- 11 mmHg (p < 0.01). After an isovolumetric beat, diastolic dysfunction was 7.9 +/- 1.5 mmHg at baseline and 2.6 +/- 0.5 mmHg during isoproterenol (p < 0.01). At all afterload levels, isoproterenol accelerated LVP fall (decreased the time constant tau), decreased the predicted time to completion of relaxation but did not influence the time available for the ventricle to relax. CONCLUSIONS AND IMPLICATIONS: Afterload induced diastolic dysfunction was attenuated by beta-adrenergic stimulation. These results, along with the inotropic and lusitropic effects of isoproterenol, may contribute to the acute improvement of cardiac function induced by beta-adrenergic stimulation. It may also help to explain the response to physical exercise and the pathophysiology of diastolic dysfunction in heart failure.

Animals↗
PubMed2005

Impaired systolic dysfunction of left ventricular longitudinal fibers: a sign of early hypertensive cardiomyopathy.

BACKGROUND: Atrioventricular plane displacement (AVPD) study by M-mode echocardiography can supply useful clinical information about left ventricular (LV) long-axis function. HYPOTHESIS: We assessed the hypothesis that AVPD estimation could be used to detect early hypertensive cardiomyopathy. METHODS: The study population included 81 hypertensive patients with normal LV ejection fraction and fractional shortening, and 50 age- and gender-matched healthy controls. By utilizing M-mode and apical views, the following parameters were estimated: early mitral flow peak velocity (E) and deceleration time (DT), peak velocity of late mitral flow (A), A/E ratio, isovolumic relaxation time (IVRT), total AVPD, AVPD motion during atrial systole (At), systolic AVPD (total AVPD-At), and At/total AVPD ratio. RESULTS: Of 81 hypertensive patients, 16 (19.7%) had a normal (Group 1) and 65 (80.3%) an impaired LV relaxation filling pattern (Group 2). Mean total AVPD-At was significantly lower in Group 2 than in Group 1 (7.1 +/- 2 vs. 10.3 +/- 3 mm, p<0.001) and in Group 1 compared with healthy subjects (10.3 +/- 3 vs. 13.1 +/- 1 mm, p<0.001). Mean At and At/total AVPD were significantly higher in Group 2 than in Group 1 (46.9 +/- 8.6 vs. 37.7 +/- 8.7%, p<0.001), but not in Group 1 compared with healthy subjects (37.7 +/- 8.7 vs. 36 +/- 6%, p>0.05). CONCLUSIONS: Hypertensive patients without overt systolic dysfunction demonstrate LV long-axis systolic dysfunction, while long-axis diastolic dysfunction always coexists with abnormal diastolic filling patterns. This suggests that long-axis systolic dysfunction precedes diastolic dysfunction at the same axis in hypertensive patients.

Adult↗
PubMedDate not supplied

Diastolic heart failure in older people--myth or lost tribe?

Left ventricular diastolic dysfunction occurs due to a variable combination of abnormal myocardial relaxation and reduced ventricular compliance. The diagnosis of diastolic congestive heart failure is controversial. Some studies suggest that up to one-third of older people with symptomatic congestive heart failure (CHF) have echocardiograph evidence of diastolic dysfunction. Other authors have suggested the comorbid diseases often found in persons with suspected diastolic CHF explain the patient's symptoms and hence diastolic CHF is a misdiagnosis in many cases. Many of the characteristic echo features of diastolic dysfunction occur in normal ageing hearts. Unlike in systolic CHF, evidence for disease modifying treatment is lacking. Clinical trials currently in progress to determine the effectiveness of ACE inhibitors and angiotensin II receptor antagonists in the management of diastolic CHF may clarify the prognosis and management of this condition.

Aged↗
PubMed2003

[Longitudinal global and regional left ventricular function in patients with hypertensive disease (tissue Doppler echocardiography data)].

Impulse tissue doppler study was carried out in 154 patients with hypertensive disease (age 35-60 years) and 39 practically healthy volunteers (mean age 43.4+/-5.5 years). According to left ventricular geometry the following groups of patients were distinguished (after A.Ganau): with normal geometry (n=47), with concentric remodeling (n=12), with concentric hypertrophy (n=53), and with eccentric hypertrophy (n=42). Tissue doppler spectrum was registered from mitral annulus and 15 left ventricular segments. The following characteristics were obtained: in each annular spectrum - maximal velocities of peaks s(m), e(m), a(m), ratio e(m)/a(m), isovolumic relaxation time (ivrt) and their average values (from 6 measurements); in each left ventricular segmental spectrum - maximal velocities of waves s, e, a, ratio e/a and segmental ivrt. Compared with healthy persons patients with hypertension had lowered longitudinal global systolic function of the left ventricle. Patients with concentric left ventricular hypertrophy had least values of e(m), e(m)/a(m), ivrt(m) and greatest number of dysfunctional (e/a<1.0 and ivrt>90 ms) segments. Some hypertensive patients with normal values of transmitral blood flow had signs of segmental diastolic dysfunction. Among patients with normal left ventricular geometry isolated segmental diastolic dysfunction was revealed according to e/a in 12 of 20 (60%), according to ivrt in 11 of 22 (50%). All patients with concentric and eccentric left ventricular hypertrophy had segmental diastolic dysfunction. Thus impulse tissue doppler study is indicated to patients with hypertension and normal parameters of transmitral flow for assessment of longitudinal segmental diastolic left ventricular function.

Adult↗
PubMed1997

Effect of regional myocardial perfusion abnormalities on regional myocardial early diastolic function in patients with hypertrophic cardiomyopathy.

Nonuniform hypertrophy of the left ventricle is an important factor in regional diastolic dysfunction in patients with hypertrophic cardiomyopathy (HCM). However, the effect of myocardial perfusion abnormalities on regional diastolic dysfunction has not been established in patients with HCM. We investigated the relationship between regional myocardial perfusion abnormalities and regional early diastolic function in 31 patients with HCM and 8 control patients. Short-axis images of the left ventricle recorded by cine magnetic resonance imaging were divided into ten blocks. The time-to-peak-wall-thickness-thinning rate (TPWR) and the wall thickness were measured in each block. Of the 310 blocks from the patients with HCM, 242 (78%) showed normal thallium-201 uptake (group 1), 40 (13%) showed slightly decreased uptake (group 2), and 28 (9%) showed markedly decreased uptake (group 3). There was no difference in the regional wall thickness among the three groups. The TPWR was longer in patients with HCM than in control patients. It was significantly longer in group 3 (190+/-45ms) than in group 1 (167+/-36 ms) and group 2 (160+/-31 ms). (P < 0.01). The linear regression slope of the relationship between the TPWR and the regional wall thickness was significantly steeper in group 3 than in groups 1 and 2 (P < 0.05). In conclusion, abnormalities in regional myocardial perfusion, in addition to regional hypertrophy, contributed to the regional early diastolic dysfunction in patients with HCM.

Adult↗
PubMed2005

Genetic deletion of the A1 adenosine receptor limits myocardial ischemic tolerance.

Adenosine receptors may be important determinants of intrinsic ischemic tolerance. Genetically modified mice were used to examine effects of global A1 adenosine receptor (A1AR) knockout (KO) on function and ischemic tolerance in perfused mouse hearts. Baseline contractile function and heart rate were unaltered by A1AR KO, which was shown to abolish the negative chronotropic effects of 2-chloroadenosine (A1AR-mediated) without altering A2 adenosine receptor-mediated coronary dilation. Tolerance to 25 minutes global normothermic ischemia (followed by 45 minutes reperfusion) was significantly limited by A1AR KO, with impaired contractile recovery (reduced by 25%) and enhanced lactate dehydrogenase (LDH) efflux (increased by 100%). Functional effects of A1AR KO involved worsened systolic pressure development with little to no change in diastolic dysfunction. In contrast, cardiac specific A1AR overexpression enhanced ischemic tolerance with a primary action on diastolic dysfunction. Nonselective receptor agonism (10 micromol/L 2-chloroadenosine) protected wild-type and also A1AR KO hearts (albeit to a lesser extent), implicating protection via subtypes additional to A1ARs. However, A1AR KO abrogated effects of 2-chloroadenosine on ischemic contracture and diastolic dysfunction. These data are the first demonstrating global deletion of the A1AR limits intrinsic myocardial resistance to ischemia. Data indicate the function of intrinsically activated A1ARs appears primarily to be enhancement of postischemic contractility and limitation of cell death.

Animals↗
PubMed1993

Failure of calcium channel blockers to improve ventricular relaxation in humans.

OBJECTIVES: The objective of this study was to ascertain whether the reversal of low peak filling rates after administration of calcium channel blockers in patients with diastolic dysfunction indicates true improvement in the rate of ventricular relaxation and left ventricular end-diastolic pressure measured by invasive indexes. BACKGROUND: Depressed filling rates measured noninvasively have been associated with diastolic dysfunction, specifically abnormal relaxation of the left ventricle. There is a reversal of these low peak filling rates after administration of calcium channel blockers. METHODS: Doppler echocardiographic measurements of peak filling rates were made and invasive high fidelity manometer-tipped pressures were measured before and after administration of verapamil (0.1 mg/kg body weight) in 20 patients with coronary artery disease who had an ejection fraction > 40% and decreased peak filling rates. RESULTS: Verapamil caused significant increases in the peak filling rate, as measured by early transmitral (E) flow velocity, from 0.57 +/- 0.16 m/s to 0.77 +/- 0.15 m/s (p < 0.01), indicating reversal of decreased peak filling rates. Concomitantly, left ventricular end-diastolic pressure increased from 18.0 +/- 7.7 mm Hg to 24.1 +/- 9.0 mm Hg (p < 0.001). The time constant of relaxation was variable, with an overall significant increase from 45.8 +/- 10.4 ms to 53.2 +/- 14.6 ms (p = 0.01). CONCLUSIONS: Verapamil administered intravenously produced reversal of decreased peak filling rates in patients with coronary artery disease and normal ventricular function. However, there was an increase in left ventricular end-diastolic pressure as well as an overall prolongation of the time constant of relaxation. Therefore, changes in peak filling rates do not accurately reflect the response of ventricular relaxation to drug interactions. Thus, calcium channel blockers should be used cautiously in the empiric treatment of patients with diastolic dysfunction.

Aged↗
PubMed2004

Hypothyroidism as a risk factor for cardiovascular disease.

The cardiovascular risk in patients with hypothyroidism is related to an increased risk of functional cardiovascular abnormalities and to an increased risk of atherosclerosis. The pattern of cardiovascular abnormalities is similar in subclinical and overt hypothyroidism, suggesting that a lesser degree of thyroid hormone deficiency may also affect the cardiovascular system. Hypothyroid patients, even those with subclinical hypothyroidism, have impaired endothelial function, normal/depressed systolic function, left ventricular diastolic dysfunction at rest, and systolic and diastolic dysfunction on effort, which may result in poor physical exercise capacity. There is also a tendency to increase diastolic blood pressure as a result of increased systemic vascular resistance. All these abnormalities regress with L-T4 replacement therapy. An increased risk for atherosclerosis is supported by autopsy and epidemiological studies in patients with thyroid hormone deficiency. The "traditional" risk factors are hypertension in conjunction with an atherogenic lipid profile; the latter is more often observed in patients with TSH >10 mU/L. More recently, C-reactive protein, homocysteine, increased arterial stiffness, endothelial dysfunction, and altered coagulation parameters have been recognized as risk factors for atherosclerosis in patients with thyroid hormone deficiency. This constellation of reversible cardiovascular abnormalities in patient with TSH levels <10 mU/L indicate that the benefits of treatment of mild thyroid failure with appropriate doses of L-thyroxine outweigh the risk.

Cardiovascular Diseases↗
PubMed2006

Cardiotoxicity of anthracycline in young breast cancer female patients: the possibility of detection of early cardiotoxicity by TDI.

Tissue Doppler imaging (TDI) was investigated for its applicability for detecting cardiac function and early cardiotoxicity in breast cancer patients treated with anthracyclines. A total of 40 women (age range 18 to 65 years) were enrolled, who had not received anthracyclines previously and had normal systolic and diastolic cardiac function. All healthy patients in the control group were of the same age. Each patient underwent not only standard echocardiographic measurements (ventricular dimensions and wall thickness, ejection fraction, E-wave deceleration time (DT), E/A ratio), but also specific imagings (E-septum separation, pulmonary venous flow), and in addition the myocardial velocity of many segments of mitral anulus obtained with pulsed wave tissue Doppler imaging were performed during the one year of observation period. Based on the results we found that systolic left ventricular function did not change significantly - neither in the study nor in the control group. Diastolic left ventricular function was impaired in 39 patients (97.5%), and 30 (75%) of these showed clear changes by means of both the traditional E/A ratio and TDI. Diastolic dysfunction in 9 patients (22.5%), however, could be detected only with TDI. The analysis of myocardial velocity in different segments showed that diastolic dysfunction does not develop in a homogeneous way but in a different way in segments. Diastolic function was intact in the control group during the study. The detectable myocardial damage occurred in the study group of young female patients without risk factors as a result of one year anthracycline therapy was so severe that the possible outcome might be serious congestive heart failure or death. Our results confirmed our assumptions that TDI is a more precise and useful examination method than traditional ones (E/A ratio or deceleration time) to demonstrate isolated diastolic dysfunction as a result of chemotherapy. Relevant extra information might be given by TDI compared to parameters describing diastolic functions depending on several changing values. TDI may become a regularly and more widely used noninvasive method to detect subclinical cardiotoxicity emerging after chemotherapy.

Adult↗
PubMed2005

Detection of early systolic dysfunction with strain rate imaging in a patient with light chain cardiomyopathy.

Congestive heart failure (CHF) in cardiac amyloidosis has been attributed to the development of diastolic dysfunction, because severe CHF symptoms have been observed despite a normal or only mildly reduced LV ejection fraction (EF). An early impairment of longitudinal systolic function has been described by means of tissue Doppler-derived myocardial deformation imaging ('strain rate imaging', SRI). Our patient presented with signs of CHF and significantly increased brain-natriuretic peptide (BNP) levels. Conventional measures of systolic contractile function were within the normal range and mitral inflow Doppler showed only moderate diastolic dysfunction. Histopathological examination by endomyocardial biopsy revealed interstitial deposition of amyloid fibers. Quantitative assessment of myocardial velocities (TDI) and deformation properties (Strain) from the apical view demonstrated a significant impairement of systolic longitudinal myocardial function. In patients with isolated diastolic dysfunction detected by conventional Doppler echocardiography, the quantitative assessment of myocardial strain and strain rate can be helpful in the early detection of systolic dysfunction.

Amyloidosis↗
PubMed1985

Early diastolic left ventricular function in children and adults with aortic stenosis.

Pressure overload hypertrophy of the left ventricle is associated with abnormal left ventricular early diastolic filling. The roles of the extent of cardiac hypertrophy, depressed left ventricular systolic function and aging in the pathogenesis of left ventricular diastolic dysfunction have not, however, been fully defined. To determine the relative importance of these factors in the pathogenesis of diastolic dysfunction in pressure overload hypertrophy, 16 children and 25 adults with aortic stenosis were compared with 48 normal children and adults, using rates of left ventricular early diastolic filling and wall thinning derived from M-mode echocardiography. Left ventricular early diastolic filling and wall thinning rates were significantly depressed in both children and adults with aortic stenosis as compared with values in normal subjects. Filling and thinning rates correlated negatively with age, left ventricular peak systolic pressure and wall thickness in all subjects. Furthermore, the effect of age on diastolic function appeared to be mediated by age-related increases in systolic pressure and wall thickness. In adults with aortic stenosis, early diastolic filling and wall thinning rates were depressed to a similar extent in subjects with normal and abnormal systolic function; thus, diastolic dysfunction does not appear to be a manifestation of abnormal systolic loading and ejection performance. These results suggest that extent of hypertrophy itself plays a dominant role in the mechanism of impaired left ventricular early diastolic filling in pressure overload due to aortic stenosis.

Adolescent↗