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PubMed1992

Exacerbation of left ventricular ischemic diastolic dysfunction by pressure-overload hypertrophy. Modification by specific inhibition of cardiac angiotensin converting enzyme.

Hearts with compensatory pressure-overload hypertrophy show an increased intracardiac activation of angiotensin II that may contribute to ischemic diastolic dysfunction. We studied whether pressure-overload hypertrophy in response to aortic banding would result in exaggerated diastolic dysfunction during low-flow ischemia and whether the specific inhibition of the cardiac angiotensin converting enzyme by enalaprilat would modify systolic and diastolic function during ischemia and reperfusion in either hypertrophied or nonhypertrophied hearts. Isolated, red blood cell-perfused isovolumic nonhypertrophied and hypertrophied rat hearts were subjected to enalaprilat (2.5 x 10(-7) M final concentration) infusion during 20 minutes of baseline perfusion and during 30 minutes of low-flow ischemia and 30 minutes of reperfusion. Coronary flow per gram was similar in nonhypertrophied and hypertrophied hearts during baseline perfusion, ischemia, and reperfusion. At baseline, left ventricular developed pressure was higher in hypertrophied than nonhypertrophied hearts in untreated groups (224 +/- 8 versus 150 +/- 9 mm Hg; p less than 0.01) and in enalaprilat-treated groups (223 +/- 9 versus 145 +/- 8 mm Hg; p less than 0.01). During low-flow ischemia, left ventricular developed pressure was depressed but similar in all groups. All groups showed deterioration of diastolic function; however, left ventricular end-diastolic pressure increased to a significantly higher level in untreated hypertrophied than in nonhypertrophied hearts (65 +/- 7 versus 33 +/- 3 mm Hg; p less than 0.001). Enalaprilat had no effect in nonhypertrophied hearts, but it significantly attenuated the greater increase in left ventricular end-diastolic pressure in hypertrophied hearts treated with enalaprilat compared with no drug (65 +/- 7 versus 50 +/- 5 mm Hg; p less than 0.01). The beneficial effect could not be explained by differences in coronary blood flow per gram left ventricular weight, glycolytic flux as reported by lactate production, myocardial water content, oxygen consumption, and tissue levels of glycogen and high energy phosphate compounds. During reperfusion, all hearts showed a partial recovery of developed pressure to 70-74% of initial values. No effect of enalaprilat could be detected during reperfusion on systolic and diastolic function or restoration of tissue levels of high energy compounds. In conclusion, our experiments show that hypertrophied red blood cell-perfused hearts manifest a severe impairment of left ventricular diastolic relaxation in response to low-flow ischemia in comparison with control hearts. Further, our experiments support the hypothesis that the enhanced conversion of angiotensin I to angiotensin II in rats with pressure-overload hypertrophy contributes to the enhanced sensitivity of hypertrophied hearts to diastolic dysfunction during low-flow ischemia.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2002

Coronary flow reserve and myocardial diastolic dysfunction in arterial hypertension.

The aim of this study was to assess the relation between coronary blood flow and left ventricular (LV) myocardial diastolic dysfunction in arterial hypertension. The study population included 30 hypertensive patients who were free of coronary artery disease and pharmacologic therapies. They underwent standard Doppler echocardiography and color tissue Doppler of the middle posterior septum at baseline and with high-dose dobutamine, and second-harmonic Doppler flow analysis of the distal left anterior descending coronary artery at baseline and after vasodilation by dipyridamole (0.56 mg/kg IV in 4'). Coronary flow reserve (CFR) was estimated as the ratio of hyperemic and baseline diastolic flow velocities. According to CFR, hypertensives were divided into 2 groups: 15 patients with normal CFR (>/=2) and 15 patients with reduced CFR (<2). The 2 groups were comparable for sex, age, body mass index, baseline heart rate, and blood pressure. LV mass index was greater in hypertensives with reduced CFR (p <0.01). By color tissue Doppler, baseline and high-dose dobutamine septal systolic velocities did not differ between the 2 groups. The ratio between myocardial velocities in early diastole and at atrial contraction (E(m)/A(m) ratio) was lower in patients with reduced CFR, both at baseline (p <0.05) and with high-dose dobutamine (p <0.00001). After adjusting for age, body mass index, LV mass index, and both high-dose dobutamine diastolic blood rate and heart rate by a multiple linear regression analysis, E(m)/A(m) ratio at high-dose dobutamine was independently associated with CFR in the overall population (beta 0.62, p <0.0005) (cumulative R(2) 0.38, p <0.0005). In conclusion, this study provides evidence of an independent association between CFR and myocardial diastolic function. In hypertensive patients without coronary artery stenosis, CFR alteration may be a determinant of myocardial diastolic dysfunction or diastolic impairment that should be taken into account as possibly contributing to coronary flow reduction.

Adult↗
PubMed2000

Reversal of left ventricular diastolic dysfunction after kidney-pancreas transplantation in type 1 diabetic uremic patients.

OBJECTIVE: Diastolic function is frequently impaired in diabetic patients. Our aim was to evaluate the effects of glycometabolic control achieved by pancreas transplantation on left ventricular function in uremic type 1 diabetic patients. RESEARCH DESIGN AND METHODS: Left ventricular systolic and diastolic functions were evaluated using radionuclide ventriculography in 42 kidney-pancreas transplant patients and 26 kidney-alone recipients who had similar clinical characteristics before transplantation. Patients were grouped according to 6, 24, and 48 months of follow-up. Control subjects consisted of 20 type 1 diabetic patients. RESULTS: The left ventricular ejection fraction was normal in all of the patients. However, kidney-pancreas transplant patients with 4 years of graft function had a higher ejection fraction (75.7 +/- 1.8%) than kidney-alone patients with 4 years of graft function (65.3 +/- 2.8%, P = 0.02) and type 1 diabetic patients (61.3 +/- 3.7%, P = 0.004). In patients with 4 years of graft function, normal diastolic parameters were evident in kidney-pancreas but not in kidney-alone or in type 1 diabetic patients (peak filling rate: 4.46 +/- 0.15 end diastolic volume (EDV)/s in kidney-pancreas patients vs. 2.73 +/- 0.24 EDV/s [P < 0.01] and 3.39 +/- 0.30 EDV/s [P < 0.01] in kidney-alone and type 1 diabetic patients, respectively; time-to-peak filling rate: 141.9 +/- 7.8 ms in kidney-alone patients vs. 209.4 +/- 13.5 ms in kidney-alone patients [P < 0.01]; peak filling rate/peak ejection rate ratio: 1.10 +/- 0.04 in kidney-pancreas patients vs. 0.81 +/- 0.08 in kidney-alone patients [P < 0.01]). A significant reduction in diastolic dysfunction rate was observed only in kidney-pancreas patients. CONCLUSIONS: Kidney-pancreas transplantation results in complete insulin independence, a better glycometabolic pattern and blood pressure control, an improvement of left ventricular function, and a reversal of diastolic dysfunction.

Adult↗
PubMed2006

Lack of inertia force of late systolic aortic flow is a cause of left ventricular isolated diastolic dysfunction in patients with coronary artery disease.

OBJECTIVES: We investigated whether a lack of inertia force of late systolic aortic flow and/or apical asynergy provoke early diastolic dysfunction in patients with coronary artery disease (CAD). BACKGROUND: Left ventricular (LV) isolated diastolic dysfunction is a well-recognized cause of heart failure. METHODS: We evaluated LV apical wall motion and obtained left ventricular ejection fraction (LVEF) by left ventriculography in 101 patients who underwent cardiac catheterization to assess CAD. We also computed the LV relaxation time constant (Tp) and the inertia force of late systolic aortic flow from the LV pressure (P)-first derivative of left ventricular pressure (dP/dt) relation. Using color Doppler echocardiography, we measured the propagation velocity of LV early diastolic filling flow (Vp). Patients with LVEF > or =50% (preserved systolic function [PSF], n = 83) were divided into 2 subgroups: patients with inertia force (n = 53) and without inertia force (n = 30). No patient with systolic dysfunction (SDF) (LVEF <50%) had inertia force (n = 18). RESULTS: The Tp was significantly longer in patients with SDF (85.7 +/- 21.0 ms) and with PSF without inertia force (81.1 +/- 23.6 ms) than in those with PSF with inertia force (66.3 +/- 12.8 ms) (p< 0.001). The Vp was significantly less in the former 2 groups than in the last group. In patients with PSF, LV apical wall motion abnormality was less frequently observed in those with inertia force than in those without (p < 0.0001). CONCLUSIONS: An absence of inertia force in patients with PSF is one of the causes of isolated diastolic dysfunction in patients with CAD. Normal LV apical wall motion is substantial enough to give inertia to late systolic aortic flow.

Aged↗
PubMed2005

Diastolic dysfunction in volume-overload hypertrophy is associated with abnormal shearing of myolaminar sheets.

Diastolic dysfunction in volume-overload hypertrophy by aortocaval fistula is characterized by increased passive stiffness of the left ventricle (LV). We hypothesized that changes in passive properties are associated with abnormal myolaminar sheet mechanics during diastolic filling. We determined three-dimensional finite deformation of myofiber and myolaminar sheets in the LV free wall of six dogs with cineradiography of implanted markers during development of volume-overload hypertrophy by aortocaval fistula. After 9 +/- 2 wk of volume overload, all dogs developed edema of extremities, pulmonary congestion, elevated LV end-diastolic pressure (5 +/- 2 vs. 21 +/- 4 mmHg, P < 0.05), and increased LV volume. There was no significant change in systolic function [dP/dt(max): 2,476 +/- 203 vs. 2,330 +/- 216 mmHg/s, P = not significant (NS)]. Diastolic relaxation was significantly reduced (dP/dt(min): -2,466 +/- 190 vs. -2,076 +/- 166 mmHg/s, P < 0.05; time constant of LV pressure decline: 32 +/- 2 vs. 43 +/- 1 ms, P < 0.05), whereas duration of diastolic filling was unchanged (304 +/- 33 vs. 244 +/- 42 ms, P = NS). Fiber stretch and sheet shear occur predominantly in the first third of diastolic filling, and chronic volume overload induced remodeling in lengthening of the fiber and reorientation of the laminar sheet architecture. Sheet shear was significantly increased and delayed at the subendocardial layer (P < 0.05), whereas magnitude of fiber stretch was not altered in volume overload (P = NS). These findings indicate that enhanced filling in volume-overload hypertrophy is achieved by enhanced sheet shear early in diastole. These results provide the first evidence that changes in motion of radially oriented laminar sheets may play an important functional role in pathology of diastolic dysfunction in this model.

Animals↗
PubMed1986

Alpha-adrenergic mechanisms in the pathophysiology of left ventricular heart failure--an analysis of their role in systolic and diastolic dysfunction.

Alpha-adrenoceptor (alpha-AR) mechanisms may contribute to systolic and diastolic dysfunction of the left ventricle. Centrally acting alpha 2-AR agonist drugs, including methyldopa, clonidine, and guanabenz, activate brainstem alpha 2-AR and this activation results in a decrease in overall sympathetic tone and an increase in parasympathetic tone. Peripherally acting alpha 1-AR antagonists, such as prazosin, inhibit the actions of catecholamines at post-synaptic receptor sites. Heart failure is characterized by hyperactivity of sympathetic pathways and parasympathetic withdrawal. In this situation, alpha 2-agonists reduce sympathetic activity and improve hemodynamic parameters of cardiac function; both acute and chronic administration of alpha 2-AR have been demonstrated to reduce serum catecholamine levels, heart rate, and arterial blood pressure, and to improve exercise performance. Diastolic dysfunction of the left ventricle is characterized by a marked decrease in ventricular compliance, often a result of hypertension and left ventricular hypertrophy; the end result is an increase in left ventricular filling pressure and pulmonary venous pressure. Treatment with alpha 2-AR, by decreasing sympathetic tone and blood pressure, and alpha 1-AR antagonists, by reducing blood pressure and by directly inhibiting the actions of catecholamines at alpha 1-AR, may produce a reduction in the degree of ventricular hypertrophy and improve diastolic performance of the left ventricle. Thus, therapeutic intervention in heart failure with either alpha 2-AR agonists or alpha 1-AR antagonists may favorably modulate these alterations in sympathetic tone and improve ventricular function.

Adrenergic alpha-Antagonists↗
PubMed2002

Fasting plasma glucose is an independent determinant of left ventricular diastolic dysfunction in nondiabetic patients with treated essential hypertension.

Left ventricular (LV) hypertrophy and LV diastolic dysfunction are common cardiac changes in hypertensive patients, and these changes are modified by various factors other than blood pressure. The present study was conducted to investigate the influence of mild abnormalities in glucose metabolism on LV structure and function in essential hypertension. In 193 nondiabetic patients with treated essential hypertension, two-dimensional and Doppler echocardiographic examinations were performed, and relative wall thickness (RWT), LV mass index (LVMI), fractional shortening, and the ratio of the peak velocity of atrial filling to early diastolic filling (A/E) were calculated. Fasting plasma glucose (FPG) and HbA1c levels were positively correlated with the A/E ratio and the deceleration time of the E wave. However, these plasma levels had no correlation with RWT, LVMI, or fractional shortening. Peak A wave velocity and the A/E ratio were significantly higher in patients who had FPG of > or = 100 mg/dl (and <126 mg/dl) than those who had FPG of <100 mg/dl, although age, blood pressure, RWT, LVMI, and fractional shortening did not differ between the two groups. In a multiple regression analysis of all subjects, only FPG and age were independent determinants of the A/E ratio. These observations suggest that FPG is a sensitive predictor for LV diastolic dysfunction in nondiabetic patients with treated hypertension. Since a slight increase in plasma glucose levels is associated with abnormalities in diastolic function independent of LV hypertrophy, an early stage of impaired glucose metabolism in hypertensive patients may specifically deteriorate cardiac diastolic function.

Adult↗
PubMed1988

Effects of increasing afterload on early diastolic dysfunction in hypertrophic non-obstructive cardiomyopathy.

The effects of increasing afterload on early diastolic dysfunction in 10 patients with hypertrophic non-obstructive cardiomyopathy were studied by computer assisted analyses of digitised M mode echocardiograms. Infusion of angiotensin II increased the end systolic pressure by a mean (SD) of 36.2 (10.3) mm Hg. As the afterload increased early diastolic dysfunction tended to become more normal: the interval and the change in dimension between minimal cavity dimension and mitral valve opening decreased and the duration of rapid diastolic filling and the accompanying change in dimension increased. None the less, the end diastolic dimension and thus the overall diastolic filling remained unchanged. Impaired early diastolic function in hypertrophic cardiomyopathy is at least partly caused by altered loading conditions.

Adult↗
PubMed2004

Left ventricular diastolic dysfunction: risks, identification, and treatment.

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

Adrenergic beta-Antagonists↗
PubMed2000

[Effect of left ventricular diastolic dysfunction on pathogenesis of angina decubitus].

OBJECTIVE: To investigate the effect of left ventricular diastolic dysfunction on the pathogenesis of angina decubitus. METHODS: The study population consisted of three groups: (1) group 1, 31 patients with angina decubitus who had ejection fraction > 50%; (2) group 2, 20 patients with coronary artery disease but without angina decubitus; group 2 and 1 were matched for age, EF and extent of coronary artery disease; (3) group 3, 20 patients without cardiovascular diseases. RESULTS: Left ventriculography (LVG) showed that LV first 1/3 filling fraction (1/3 FF) and LV late 1/3 FF were 0.30 +/- 0.12, 0.41 +/- 0.12, 0.46 +/- 0.07 and 0.36 +/- 0.09, 0.31 +/- 0.08, 0.29 +/- 0.06 in groups 1 to 3 respectively. LV first 1/3 FF was significantly lower in group 1 than in group 2 and 3 (both P < 0.001), but LV late 1/3 FF was much higher in group 1 than in groups 2 and 3 (P < 0.05 and P < 0.01, respectively). Left ventricular end-diastolic pressure (LVEDP) was markedly increased before and after LVG in groups 1 and 2 as compared with group 3 (P < 0.001 and P < 0.05, respectively). The difference of LVEDP caused by left atrial contraction (LACD) was much higher before and after LVG in group 1 than in group 3 (P < 0.01 and P < 0.001, respectively). However, there were significant differences in LVEDP and LACD tested between before and after LVG in group 1 (both P < 0.01). No statistical differences were found in LVEDP and LACD tested between before and after LVG in both group 2 and group 3. CONCLUSION: Patients with angina decubitus have LV diastolic dysfunction, which may be closely related to the pathogenesis of angina decubitus.

Adult↗
PubMed2003

Diastolic dysfunction.

Although the annual mortality rate for diastolic heart failure is better than that for systolic heart failure, it is still greater than that for age-matched controls. Five-year mortality rates are about 50% for patients with systolic heart failure and are about 25% for patients with diastolic heart failure. In elderly patients (over 65 years of age), the outcome with systolic and diastolic dysfunction may be more comparable. In contrast to systolic heart failure, the effect of therapy in patients with diastolic heart failure has not been evaluated in large clinical controlled trials. Guidelines for managing heart failure with preserved systolic function broadly suggest the direction for management, but specific treatments are currently based on expert consensus, clinical experience, and scientific elucidation of diastolic mechanics. Although evidence-based guidelines are not available for all aspects of management of diastolic heart failure, future research will increase the knowledge of this disorder and improve treatment strategies.

Diastole↗
PubMed1996

Echocardiographic assessment of left ventricular hypertrophy diastolic dysfunction and pericardial disease in patients on maintenance haemodialysis.

Echocardiographic study of sixty patients on maintenance haemodialysis (MHD) was undertaken to determine the prevalence and factors associated with left ventricular (LV) hypertrophy (LVH), LV diastolic dysfunction and pericardial disease. The mean age was 34.4 (standard deviation 13.0), range 14-66 years with 31 (51.7%) men. LVH was found in 41 (68%) patients. Of the factors analysed, serum calcium and calcium-phosphate product were significantly associated with LVH (t = 2.01, df = 58, p = 0.046; t = 2.18, df = 58, p = 0.032 respectively). Hypertension in this study was not significantly associated with LVH (p = 0.169). LV diastolic dysfunction was found in 23/41 (56%) patients with LVH, and in 9/19 (47%) patients without LVH (difference is not statistically significant, X2 = 0.12, df = 1, p = 0.725). Small pericardial effusions were detected in 4/60 (7%) patients and two patients had pericardial thickening. We conclude that in our MHD patients LVH, is very common and that diastolic dysfunction is observed equally in patients with and without LVH. However, haemodynamically significant pericardial effusions are rare in patients who have been on dialysis for at least six months.

Adolescent↗
PubMed2006

Association of obesity with left ventricular remodeling and diastolic dysfunction in patients without coronary artery disease.

Obese patients frequently complain of dyspnea. Deconditioning and altered left ventricular (LV) systolic or diastolic function with elevated filling pressures may contribute to dyspnea. This study analyzed 4,281 patients who underwent diagnostic coronary angiography from January 1, 1995, to December 31, 2000. No patients had coronary artery stenoses >50% of the luminal diameter, and all underwent echocardiography within the same 6-year period. The association between body mass index (BMI) and LV structure and systolic and diastolic function was examined. All analyses controlled for age and gender, with the effect size for BMI expressed using a standardized coefficient (SC). A higher BMI was associated with greater LV mass (SC 0.18, p <0.001), wall thickness (SC 0.17, p <0.001), and end-diastolic diameter (SC 0.07, p <0.001). Stroke volume increased with a higher BMI (SC 0.12, p = 0.001), but there was no association between BMI and the ejection fraction (SC 0.003, p = 0.81). Hemodynamic data from invasive studies showed an association between a higher BMI and increased LV end-diastolic pressure (mean 17 mm Hg for BMI <25 kg/m(2) vs 24 mm Hg for BMI >or=40 kg/m(2); SC 0.18, p <0.001), which persisted after controlling for end-diastolic volume (SC 0.22, p <0.001). Obesity was associated with ventricular remodeling, which may normalize wall stress while increasing stroke volume to match metabolic demand. Obesity was not associated with decreased systolic function. However, obesity was associated with increased LV end-diastolic pressure, which suggests an association between obesity and diastolic dysfunction. In conclusion, ventricular remodeling, LV diastolic dysfunction, and elevated filling pressures may contribute to the prevalence of heart failure in obese patients.

Blood Pressure↗
PubMed1991

Doppler echocardiographic evaluation of diastolic dysfunction.

Recently, considerable effort has been directed toward the application of Doppler methods for detecting diastolic dysfunction. Recordings of transmitral filling velocity as obtained from pulsed-wave Doppler have been extensively investigated as a noninvasive method for determining left ventricular diastolic filling properties. Although Doppler parameters appear to reflect volumetric transmitral flow, close correlations with invasive descriptors of diastolic performance have not been found. Furthermore, Doppler transmitral velocities are sensitive to changes in ventricular preload, afterload, and heart rate. However, at least two distinct Doppler spectral patterns have been identified that are associated with impaired ventricular relaxation and restrictive physiology. Thus, Doppler recordings have proven to be of value in identifying the presence and type of diastolic dysfunction, and in the future they may be helpful in following the response to therapeutic interventions. The purpose of this paper is to review the available information relating Doppler transmitral recordings with catheterization and clinical descriptors of diastolic function. Additionally, the aim is to provide an understanding of the value and limitations of these noninvasive measurements in identifying and treating patients with diastolic abnormalities.

Amyloidosis↗
PubMed1993

Diastolic dysfunction as a cause of heart failure.

Diastolic dysfunction is an important cause of symptoms in patients with various types of cardiac disease. Increased left ventricular diastolic pressure may lead to pulmonary congestion, even in the setting of normal left ventricular systolic function. Although the physiology of diastolic function is complex, left ventricular diastolic pressure may become elevated through one of three broad mechanisms. Abnormalities intrinsic to the left ventricle may include 1) impaired left ventricular relaxation, a finding that is common in most cardiac diseases and may be particularly important during ischemia; 2) increased left ventricular wall thickness relative to cavity volume, which will shift the diastolic pressure-volume relation such that the same volume is associated with a higher pressure; and 3) increased myocardial stiffness, which is thought to be associated with interstitial fibrosis or scar tissue formation. In addition, diastolic pressures may become elevated because of factors extrinsic to the left ventricle. These may include 1) increased central blood volume, which will increase left ventricular pressure without altering the left ventricular pressure-volume relation; and 2) ventricular interaction mediated by pericardial restraint, which may cause a parallel upward shift of the diastolic pressure-volume relation. Treatment of the factors extrinsic to the left ventricle tends to be much more successful than treating abnormalities that are intrinsic to the ventricle. Improved understanding of myocardial relaxation at the cellular level and delineation of the molecular regulation of myocyte hypertrophy and fibroblast proliferation may lead to new and innovative approaches to the treatment of heart failure.

Animals↗
PubMed2005

Ankylosing spondylitis and heart abnormalities: do cardiac conduction disorders, valve regurgitation and diastolic dysfunction occur more often in male patients with diagnosed ankylosing spondylitis for over 15 years than in the normal population?

The objective of this study was to determine the rate of selected cardiac pathologies (conduction disorders, valve regurgitation and diastolic dysfunction) in patients with long-standing ankylosing spondylitis (AS) and compare the results with the prevalence in the normal population. A rheumatologic (structured questionnaire interview) and cardiac evaluation (resting electrocardiography and echocardiography) was performed in 100 male subjects with AS and a disease duration of more than 15 years. The rates for conduction disorders, aortic and mitral valve regurgitation and diastolic dysfunction were compared with the corresponding results in the literature among the normal population. In patients with long-standing AS there was no increased rate for valve regurgitation (mitral and aortic valve) and for arrhythmia. Diastolic dysfunction occurred more often in patients with long-standing AS. However, this might be caused by the presence of other cardiovascular risk factors such as age and hypertension. According to these results, a cardiologic evaluation with echocardiography should not be recommended routinely in patients with long-standing AS. To confirm these results, a large prospective study with patients with long-standing AS and with a matched control group should be performed in the future.

Adult↗
PubMed1992

Comparison of simultaneous Doppler echo and apexcardiogram in detecting left ventricular diastolic dysfunction in patients with systemic hypertension.

Patient with systemic hypertension have often abnormalities of left ventricular (LV) diastolic function. Although pulsed Doppler echocardiography (PDE) is at present time the only simple widely used noninvasive method for evaluating such LV diastolic dysfunction, LV apexcardiogram (ACG) reflecting LV pressure curve changes can also be useful for evaluating LV diastolic events. In order to compare the validity of these two methods in assessing LV diastolic dysfunction, PDE and ACG were simultaneously obtained in 29 patients with chronic systemic hypertension and in 61 controls. As diastolic indices of PDE served the peak early (E) and late atrial (A) diastolic transmitral flow velocities, the A/E ratio and the deceleration time; and of the ACG the relative A-wave to total height (A/H), the total relaxation time (TART), the heart rate corrected TART and the combined index DATI (= diastolic amplitude time index). In patients with hypertension, from the PDE only A and A/E ratio were significantly different from the controls, whereas all mentioned ACG indices showed an abnormal mean value. Thus, the less widely used ACG appears to be a more accurate method in the noninvasive evaluation of diastolic mechanical events than the routinely used PDE in patients with chronic hypertension.

Chronic Disease↗
PubMed2001

Effects of verapamil in normal elderly individuals with left ventricular diastolic dysfunction.

Treatment with oral verapamil for 3 to 4 days has been found to enhance left ventricular (LV) diastolic filling in elderly subjects as assessed by radionuclide angiography. However, there are no Doppler echocardiographic studies to assess the long-term effect of verapamil in normal elderly subjects. Thirteen healthy elderly subjects (mean age, 64 +/- 7 years; 8 men and 5 women) with LV diastolic dysfunction underwent this placebo-controlled cross-over trial. The effect of verapamil on LV diastolic function was assessed by treadmill exercise test and Doppler echocardiography at baseline, and after each 3-month treatment period (placebo or verapamil 120 mg once daily), separated by a 1-week washout period before cross-over. Blood pressure, heart rate, LV ejection fraction, LV mass, and cardiac output were unaltered by placebo or verapamil. The exercise time was similar at baseline (11.4 +/- 2.4 min) and after placebo treatment (11.4 +/- 2.3 min) but significantly increased (P < 0.05) after verapamil treatment (12.3 +/- 2.0 min). The ratio of mitral A wave duration/pulmonary venous atrial systolic reversal duration increased after verapamil treatment (1.12 +/- 0.08) compared to placebo (0.93 +/- 0.06, P < 0.05) and baseline (0.89 +/- 0.09), which had similar durations. The isovolumic relaxation time (IVRT) was significantly decreased (P < 0.05) from 85 +/- 13 msec at baseline and 87 +/- 13 msec with placebo to 73 +/- 9 msec with verapamil. The results of this study suggest that in normal elderly patients with Doppler evidence of diastolic dysfunction, 3 months treatment with verapamil can increase exercise tolerance and improve LV diastolic function.

Aged↗