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PubMed1999

Losartan improves exercise tolerance in patients with diastolic dysfunction and a hypertensive response to exercise.

OBJECTIVES: The aim of the study was to test the hypothesis that angiotensin II (Ang II) blockade would improve exercise tolerance in patients with diastolic dysfunction and a marked increase in systolic blood pressure (SBP) during exercise. BACKGROUND: Diastolic dysfunction may be exacerbated during exercise, especially if there is a marked increase in SBP. Angiotensin II may contribute to the hypertensive response to exercise and impair diastolic performance. METHODS: We performed a randomized, double-blind, placebo-controlled, crossover study of two weeks of losartan (50 mg q.d.) on exercise tolerance and quality of life. The subjects were 20 patients, mean age 64 +/- 10 years with normal left ventricular systolic function (EF >50%), no ischemia on stress echocardiogram, mitral flow velocity E/A <1, normal resting SBP (<150 mm Hg), and a hypertensive response to exercise (SBP >200 mm Hg). Exercise echocardiograms (Modified Bruce Protocol) and the Minnesota Living With Heart Failure questionnaire were administered at baseline, and after each two-week treatment period, separated by a two-week washout period. RESULTS: Resting blood pressure (BP) was unaltered by placebo or losartan. During control, patients were able to exercise for 11.3 +/- 2.5 (mean +/- SD) min, with a peak exercise SBP of 226 +/- 24 mm Hg. After two weeks of losartan, baseline BP was unaltered, but peak SBP during exercise decreased to 193 +/- 27 mm Hg (p < 0.05 vs. baseline and placebo), and exercise time increased to 12.3 +/- 2.6 min (p < 0.05 vs. baseline and placebo). With placebo, there was no improvement in exercise duration (11.0 +/- 2.0 min) or peak exercise SBP (217 +/- 26 mm Hg). Quality of life improved with losartan (18 +/- 22, p < 0.05) compared to placebo (22 +/- 26). CONCLUSIONS: In patients with Doppler evidence of diastolic dysfunction at rest and a hypertensive response to exercise, Ang II receptor blockade blunts the hypertensive response to exercise, increases exercise tolerance and improves quality of life.

Adult↗
PubMed1999

Role of transesophageal echocardiography in assessing diastolic dysfunction in a large clinical practice: a 9-year experience.

BACKGROUND: Two-dimensional transthoracic echocardiography with respiratory monitoring has been used to characterize diseases that impair diastolic function. Transesophageal echocardiography (TEE) has emerged as a complementary technique to evaluate patients with these diseases. The purpose of this study was to evaluate in a large clinical practice the utility of TEE with respiratory monitoring for classification of patients with diastolic dysfunction. METHODS: Over a 9-year period TEE was used to examine 192 patients referred to an echocardiography laboratory for additional evaluation of abnormal diastolic function. We performed pulsed-wave Doppler TEE of the left ventricular inflow and pulmonary veins and respiratory monitoring to categorize patients as showing restrictive physiologic features, constriction with or without effusion, mixed constriction and restriction, abnormal relaxation, pseudonormalization, large pericardial effusion or tamponade, or normal diastolic function. RESULTS: Patients with diastolic dysfunction underwent 3% of the total number of transesophageal studies conducted during the study period. Among the 192 patients referred for TEE, abnormal diastolic function was found in 181 (94%); 11 (6%) had normal diastolic function. Seventy-one (39%) of the 181 patients had restrictive physiologic features. Constrictive pericarditis was found in 54 (30%) of the patients and was confirmed for all 31 patients who underwent pericardiectomy. Mixed constriction and restriction was present in 21 (12%) of the patients. The other 35 patients (19%) had abnormal relaxation, pseudonormalization, or large pericardial effusion or tamponade. The cause of diastolic dysfunction was idiopathic for 32% of the patients, previous cardiac operation for 26%, cardiac amyloidosis for 23%, radiation therapy for 11%, and hypertension or advanced ischemic heart disease for 8%. CONCLUSION: Two-dimensional and Doppler TEE with respiratory monitoring is useful in categorizing patients with impaired diastolic function, primarily into those with restrictive physiologic features or constrictive pericarditis.

Adult↗
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↗
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↗
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↗
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↗
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↗
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↗
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↗
PubMed1997

Role of MgADP in the development of diastolic dysfunction in the intact beating rat heart.

Sarcomere relaxation depends on dissociation of actin and myosin, which is regulated by a number of factors, including intracellular [MgATP] as well as MgATP hydrolysis products [MgADP] and inorganic phosphate [Pi], pHi, and cytosolic calcium concentration ([Ca2+]c). To distinguish the contribution of MgADP from the other regulators in the development of diastolic dysfunction, we used a strategy to increase free [MgADP] without changing [MgATP], [Pi], or pHi. This was achieved by applying a low dose of iodoacetamide to selectively inhibit the creatine kinase activity in isolated perfused rat hearts. [MgATP], [MgADP], [Pi], and [H+] were determined using 31P NMR spectroscopy. The [Ca2+]c and the glycolytic rate were also measured. We observed an approximately threefold increase in left ventricular end diastolic pressure (LVEDP) and 38% increase in the time constant of pressure decay (P < 0.05) in these hearts, indicating a significant impairment of diastolic function. The increase in LVEDP was closely related to the increase in free [MgADP]. Rate of glycolysis was not changed, and [Ca2+]c increased by 16%, which cannot explain the severity of diastolic dysfunction. Thus, our data indicate that MgADP contributes significantly to diastolic dysfunction, possibly by slowing the rate of cross-bridge cycling.

Adenosine Diphosphate↗
PubMed1999

Diastolic dysfunction and collagen structure in canine pacing-induced heart failure.

Heart failure is characterized not only by systolic, but also by diastolic dysfunction. The present study tested whether or not diastolic dysfunction is associated with changes in tissue properties and collagen network structure. Heart failure was induced in seven chronically instrumented, conscious dogs by rapid left ventricular pacing (2 50 min(-1)). After 2-5 [mean: 4+/-1 (S.D.)] weeks pacing, heart failure was apparent from clinical symptoms (ascites, cachexia, edema, exercise intolerance) and hemodynamic parameters (significant increases of heart rate and left ventricular end-diastolic pressure and decreases of left ventricular maximal pressure, dP/dtmax and systolic wall thickening). The left ventricle was dilated, as indicated by a decrease of end-diastolic wall thickness (6.3+/-2.0 v 7.2+/-2.1 mm; P<0.05; sonomicrometry). The left ventricular end-diastolic pressure-strain relation (strain: relative change of end-diastolic wall thickness) was obtained during alterations of loading conditions by inferior caval vein and descending thoracic aortic occlusion. The slope of this relation increased from 85+/-20 to 428+/-188 in heart failure, indicating an increase of left ventricular stiffness. Collagen was stained with picrosirius red and analyzed using polarized light microscopy. In heart failure, the collagen volume fraction remained unchanged (1.9+/-1.2 v 2.3+/-1.3%; N.S.), while the nonuniformity of collagen orientation, as reflected by its standard deviation, was increased (11.1+/-1.8 v 6.1+/-0.4 o; P<0.05). The nonuniformity of collagen fiber orientation correlated with left ventricular stiffness [r=0.75].

Animals↗
PubMed1993

Discrepancy between systolic and diastolic dysfunction of the left ventricle in patients with Duchenne muscular dystrophy.

To assess the systolic and diastolic dysfunction of the left ventricle (LV) in relation to age and the severity of impairment in Duchenne muscular dystrophy (DMD), we performed M-mode, two-dimensional and pulsed-wave Doppler echocardiography in 45 male subjects with DMD aged 8 to 25 years and in 40 age-matched healthy controls. Systolic dysfunction started in the first decade of life, with some patients showing severe systolic dysfunction in their early teens. This dysfunction, however, did not always depend on the severity of the skeletal muscle disease. No patients with DMD showed an increase in peak atrial velocity and time-velocity integrals of the atrial contraction velocity curve, findings frequently reported to precede the abnormalities in many cardiac diseases; it was thought therefore that these patients had no increase in left atrial compensation. Diastolic dysfunction may not routinely precede or accompany the systolic dysfunction in DMD, in contrast with what is reported in patients with ischaemic or hypertensive heart disease. DMD patients usually show a predominant systolic dysfunction.

Adolescent↗
PubMed2000

Diastolic dysfunction in patients with congenital heart disease.

As noted in the introduction of this article, a comprehensive evaluation of diastolic function in all known congenital heart defects is not feasible; however, by demonstrating several representative anatomic and genetic abnormalities where diastolic dysfunction may have clinical significance, it is hoped that scaffolding has been established which will provide structure for further study on this intriguing and influential component of function in patients with CHD. Understanding the contribution of diastole to overall ventricular function may be shown to have important implications in the recommendations for timing or potential benefit of surgical intervention. Or, to state differently, if diastolic dysfunction precedes that of systolic, would a rigorous analysis of diastole in the presurgical patient provide a more sensitive algorithm for intervention? The means for noninvasive assessment of diastolic function, primarily by spectral Doppler echocardiography, or using echocardiography in conjunction with other modalities, should allow for a comprehensive accrual of data in this patient population.

Diastole↗
PubMed1989

Diastolic dysfunction of perfused rat hearts induced by hydrogen peroxide. Protective effect of selenium.

Oxidant substances such as hydrogen peroxide are postulated to cause cardiac dysfunction and injury in a number of pathological conditions. Selenium is an essential nutrient which serves as an oxidant defense through the selenoenzyme glutathione peroxidase. This enzyme metabolizes hydrogen peroxide; its activity in rat heart is reduced to 5% of control by selenium deficiency. Left ventricular function of selenium-deficient and control rat hearts was studied in a Langendorff preparation under isovolumic conditions. A stabilization period of 20 min was followed by a 70 min infusion of hydrogen peroxide at 375 or 1500 nmol/min. When no hydrogen peroxide was infused, perfusion for 90 min had no effect on systolic or diastolic function and no effect of selenium deficiency was detected. Hydrogen peroxide infusion into selenium-deficient hearts at 375 nmol/min led to impaired isovolumic relaxation and a substantial increase in end-diastolic pressure after 45 min which worsened progressively until the experiment was terminated. By contrast no effect was observed on systolic contractile function as assessed by peak pressure or developed pressure. Infusion of this dose of hydrogen peroxide into control hearts had no significant effect on diastolic or systolic function. However, infusion of 1500 nmol hydrogen peroxide/min into control hearts caused diastolic dysfunction after 30 min without affecting systolic function. These results indicate that hydrogen peroxide injury to the perfused rat heart is manifested by diastolic dysfunction before systolic dysfunction occurs. Selenium deficiency lowers the dose of hydrogen peroxide needed to cause diastolic dysfunction. This suggests that the selenoenzyme glutathione peroxidase protects the heart against hydrogen peroxide injury.

Animals↗
PubMed2000

Worsening of left ventricular diastolic dysfunction during exercise causes decreased exercise tolerance in hypertension.

BACKGROUND: Exercise tolerance is reduced in hypertension. Hypertension affects left ventricular (LV) diastolic filling by causing abnormal relaxation and decreasing compliance. HYPOTHESIS: This study was designed to determine whether worsening of LV diastolic dysfunction during exercise causes decreased exercise tolerance in hypertension. METHODS: Left ventricular diastolic filling parameters were examined at mitral valve by Doppler echocardiography at rest and at peak exercise in hypertensive patients and were compared with those of age- and gender-matched normotensive individuals. Treadmill exercise stress test was performed according to the Bruce protocol and the exercise time was recorded. RESULTS: Exercise time was significantly shorter in the hypertensive group than that in the normotensive group (320 +/- 29 vs. 446 +/- 38 s, p 0.03). The hypertensive group demonstrated abnormal relaxation pattern of diastolic mitral inflow at rest, which became pseudonormal at peak exercise (E/A velocity ratio, rest 0.86 +/- 0.06 vs. exercise 1.19 +/- 0.09, p < 0.001). The diastolic mitral inflow pattern remained normal at peak exercise in the normotensive group. The deceleration time and the pressure half time of early mitral inflow at peak exercise were significantly shorter in the hypertensive group than those in the normotensive group (deceleration time, 182 +/- 20 vs. 238 +/- 22 ms, p 0.02: pressure half time, 54 +/- 5 vs. 70 +/- 12 ms, p 0.01). CONCLUSIONS: This study demonstrates that reduced exercise tolerance in hypertension is associated with worsening of diastolic dysfunction during exercise consistent with an increase in left atrial pressure.

Compliance↗
PubMed1995

Is diastolic dysfunction associated with thrombogenesis? A study of circulating markers of a prothrombotic state in patients with coronary artery disease.

Clinical data on the contributory role of heart failure to thromboembolic risk does not differentiate between systolic and diastolic left ventricular dysfunction. We therefore conducted a population-controlled cross-sectional study to determine levels of plasma fibrinogen (associated with thromboembolism), fibrin D-dimer (a marker of fibrin turnover) and von Willebrand factor (a marker of endothelial dysfunction) in patients with ischaemic heart disease (a common cause of diastolic dysfunction) in whom left ventricular diastolic function was defined by echocardiography. We studied 106 patients: those with normal left ventricular function (n = 42, Group 1); those with left ventricular dysfunction but without aneurysms (n = 34, Group 2); and those with left ventricular aneurysm formation (n = 30, Group 3). Each of these groups was subdivided into those with (a) and without (b) diastolic dysfunction. Diastolic dysfunction was present in over 60% of patients, irrespective of left ventricular systolic impairment. There were no significant differences in median levels of plasma fibrinogen, fibrin D-dimer or von Willebrand factor in each group of patients with ischaemic heart disease, whether or not left ventricular diastolic dysfunction was present (Mann-Whitney test; P = N.S.). Systolic (rather than diastolic) dysfunction was the main correlate of these (analysis of variance, general linear model--ANOVA-GLM--P < 0.05) and the greatest abnormalities of fibrinogen, endothelial dysfunction and intravascular fibrin turnover were seen in patients with left ventricular aneurysms whether or not diastolic dysfunction was present. This study demonstrates that there is no evidence of a significant additional contribution to thrombotic risk (as assessed by plasma fibrinogen, von Willebrand factor and fibrin D-dimer) for patients with left ventricular diastolic dysfunction. A relationship is noted between some prothrombotic factors and Doppler indices of flow, which suggests a possible association between cardiac haemodynamics and thrombogenesis.

Analysis of Variance↗