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PubMed1990

Diastolic dysfunction of the left ventricle: importance to the clinician.

Diastolic dysfunction is a relatively common problem that may be mild and asymptomatic or may present with severe disabling symptoms. It is frequently due to coronary artery disease and/or LV hypertrophy and it is especially common in the older population. Patients with diastolic dysfunction and normal systolic function are best treated with calcium channel blocking agents or beta-blocking agents (drugs that are generally avoided in patients with significant systolic dysfunction). These drugs are used in the same dosage as is used in patients with angina or hypertension. Most treatment is based on symptomatic relief, and therefore periods of cautious trial and error are the rule. When diastolic dysfunction is associated with systolic dysfunction, it may be necessary to treat both conditions, but in general, positive inotropic agents and arterial vasodilators are not useful in patients with diastolic dysfunction.

Cardiomegaly↗
PubMed1988

The physiological basis of left ventricular diastolic dysfunction.

Overall cardiac pump function requires adequate ventricular diastolic filling as well as normal systolic ejection. Abnormalities of the rate or extent of myocardial relaxation (diastolic dysfunction) have been described in a large variety of clinical conditions, including hypertrophy, ischemia, and after cardiac surgery. Diastolic and systolic dysfunction can be readily distinguished by analysis of pressure volume loops and utilization of echocardiography or nuclear cardiology gated blood pool scans. The mechanisms by which diastolic dysfunction can occur may be structural (hypertrophy, fibrosis) or dynamic (hypoxia, ischemia, alteration of diastolic cytosolic calcium levels). Hypertrophied myocardium is particularly susceptible to diastolic dysfunction by virtue of both structural changes (increased LV mass and interstitial fibrosis) and greater susceptibility to develop impaired myocardial relaxation during hypoxia or ischemia than nonhypertrophied myocardium.

Cardiomegaly↗
PubMed1992

Effects of enalapril on heart failure in hypertensive patients with diastolic dysfunction.

Ten hypertensive patients with symptoms of heart failure and normal systolic function but with diastolic dysfunction were treated with 10 mg enalapril twice a day for 9 +/- 3 months to evaluate the effects of this agent alone on heart failure induced by diastolic dysfunction. After therapy, all patients improved and echocardiographic parameters of diastolic dysfunction became normalized. It is concluded that enalapril appears to be useful in the treatment of heart failure in hypertensive patients with normal systolic function and diastolic dysfunction.

Adult↗
PubMed1996

Doppler echocardiographic detection of left ventricular diastolic dysfunction in patients with pulmonary sarcoidosis.

STUDY OBJECTIVE: To determine the prevalence of left ventricular diastolic dysfunction in patients with biopsy specimen-proved pulmonary sarcoidosis without clinical evidence of cardiac disease. DESIGN: A cross-sectional study. SETTING: A large tertiary care university teaching hospital. PATIENTS AND CONTROL SUBJECTS: Fifty consecutive subjects had biopsy specimen-proved pulmonary sarcoidosis without suspected cardiac involvement. Those with other conditions known to affect diastolic function were excluded. The control group comprised 30 healthy hospital workers. INTERVENTIONS: Clinical examination, 12-lead ECG, and combined echocardiographic/phonocardiographic examination. MEASUREMENTS: Indexes of left ventricular diastolic function, including isovolumic relaxation time, peak velocity of early (E) and late (A) ventricular filling, deceleration rate of early diastolic flow, and the sum of the time velocity integrals of E and A were obtained in each patient and control subject. Systolic function was determined using a modification of Simpson's rule. RESULTS: Diastolic dysfunction was present in 7 (14%) patients, 6 of whom had normal systolic function and normal two-dimensional echocardiographic examination. Those with diastolic dysfunction had a longer duration of illness (15 +/- 7 vs 6 +/- 5 years; p = 0.0004), were significantly older (52 +/- 11 vs 38 +/- 9 years; p = 0.0009), and had higher systolic BP (130 +/- 13 vs 117 +/- 12 mm Hg; p = 0.01) than the sarcoid patients with normal diastolic function. CONCLUSIONS: These results demonstrate a significant prevalence of left ventricular diastolic dysfunction in patients with pulmonary sarcoidosis. The cause of this abnormality may be a subclinical sarcoid cardiomyopathy.

Adult↗
PubMed1992

The natural history of isolated left ventricular diastolic dysfunction.

STUDY OBJECTIVE: To assess the natural history of isolated left ventricular diastolic dysfunction. PATIENTS AND METHODS: Follow-up (average duration, 68 months) was obtained in 51 patients with isolated left ventricular diastolic dysfunction at cardiac catheterization, characterized by (1) an elevated left ventricular end-diastolic pressure; (2) normal left ventricular end-diastolic and end-systolic volumes; (3) normal left ventricular ejection fraction; (4) no coronary artery disease; and (5) no valvular disease. RESULTS: During follow-up, seven patients died, but only one died of cardiac causes. Of the 44 living subjects, 20 (45%) noted new-onset symptoms of congestive heart failure, with 11 (25%) of these requiring hospitalization, and 12 (27%) required hospitalization for recurrent chest pain. CONCLUSIONS: Isolated left ventricular diastolic dysfunction is associated with a low cardiac mortality; at the same time, however, it is associated with substantial morbidity.

Adult↗
PubMed1995

Intraventricular dispersion of early diastolic filling: a new marker of left ventricular diastolic dysfunction.

Mitral flow velocity patterns are frequently "normalized" by the alteration in the loading condition even in the presence of left ventricular (LV) diastolic dysfunction. In addition, a simple index, the ratio of mitral peak early diastolic flow velocity to mitral peak flow velocity at atrial contraction, is not obtainable in patients with atrial fibrillation (Af). Thus these limitations hamper the value of analyzing the mitral flow velocity pattern in the assessment of abnormal LV diastolic characteristics. This study was designed to elucidate the hypothesis that peak early diastolic flow velocity decreases progressively from the base to the apex in patients with LV diastolic dysfunction. Regional diastolic flow velocity patterns at 1, 2, or 3 cm from the mitral tip toward the apex were simultaneously recorded with the mitral flow velocity pattern by using multigate pulsed Doppler echocardiography in 42 subjects with normal LV function (31 normal volunteers and 11 patients with Af only), 17 patients with hypertensive heart disease, and 22 patients with dilated cardiomyopathy. In the normal subjects early diastolic flow velocity at the mitral tip was maintained at the positions 1 to 3 cm away from the tip into the LV cavity. In contrast, regional peak early diastolic flow velocity progressively decreased toward the apex in patients with hypertensive heart disease and dilated cardiomyopathy. These findings were observed even in patients with a normalized mitral flow velocity pattern or those with Af. Thus the assessment of the intraventricular decrease in peak early diastolic flow velocity may be useful in detecting LV diastolic dysfunction, particularly in patients with Af or a "normalized" mitral flow velocity pattern.

Adult↗
PubMed1993

Assessment and treatment of diastolic dysfunction.

Congestive heart failure almost invariably includes a component of diastolic dysfunction, and in many patients impaired diastolic filling is the predominant functional abnormality. Failure of myocardial relaxation depends on abnormalities of calcium uptake as well as on the systolic and diastolic loads, the nonuniformity of load and the passive elastic characteristics of the ventricle. The availability of noninvasive diagnostic testing has led to an increasing interest in the study of diastolic function and its clinical implications. Recent echo-Doppler techniques (transesophageal pulmonary venous velocity recording, automatic endocardial borders detection, 3D cardiac reconstruction) demonstrated abnormal left ventricular filling patterns in patients with various cardiac disorders. It is possible that the diastolic abnormalities of heart failure may be a more appropriate target for new therapeutic interventions and several classes of pharmacologic agents may be effective in the management of diastolic dysfunction.

Diastole↗
PubMedDate not supplied

Angiotensin-converting enzyme and angiotensinogen genes in patterns of left ventricular hypertrophy and in diastolic dysfunction.

1. The association of different patterns of left ventricular hypertrophy and diastolic dysfunction with angiotensin converting enzyme (ACE) genotypes or angiotensinogen dinucleotide repeat alleles were studied in human subjects. 2. Three abnormal patterns of hypertrophy (remodelled, eccentric and concentric) were associated with a history of hypertension. The presence of remodelled or concentric hypertrophy was associated with diastolic dysfunction. 3. There was no difference between the frequencies of the ACE genotypes in normotensive and hypertensive subjects, in subjects with normal ventricles and those with different patterns of left ventricular hypertrophy, nor in subjects with normal and abnormal diastolic function. Similarly, there was no difference between the relative frequencies of AGT alleles in the same clinical subgroups. 4. We conclude that in this population of hospital patients, variants of the ACE and AGT genes do not contribute to the presence of different patterns of hypertrophy or to diastolic dysfunction.

Adult↗
PubMed1992

Reduced vascular excitatory responses to cardiopulmonary unloading in hypertensive patients with left ventricular diastolic dysfunction.

Physiological consequences of altered peak left ventricular diastolic filling rate in hypertension have not yet been fully assessed. The hypothesis that altered left ventricular diastolic filling rate interferes with inhibitory cardiopulmonary reflexes was tested. Normalized peak left ventricular diastolic filling rate was calculated from radionuclide ventriculography. Haemodynamic changes during lower body negative pressure (-5 to -40 mmHg) in nine hypertensive patients with slow normalized left ventricular filling rate (Group A) were compared with 16 hypertensive patients with normal normalized peak left ventricular diastolic filling rate and ten normal volunteers of the same age group. Baseline total peripheral resistance was higher in essential hypertension compared to normals but did not differ significantly between the two hypertensive groups. For data analysis, the levels of lower body negative pressure were grouped as low levels of -5 to -10, and -15 to -20 mmHg, an intermediate level of -25 mmHg, and high levels of -30 to -40 mmHg; the change in total peripheral resistance (from baseline) was less prominent in Group A compared to Group B and to normals (-1.4 +/- 1.7 [SE], -0.06 +/- 1.4, 1.1 +/- 1.2 and 4.5 +/- 2 u.M2 in Group A at the four consecutive levels of lower body negative pressure vs. 0.9 +/- 0.7, 3.8 +/- 0.9, 7.2 +/- 1.6, and 8.2 +/- 1.4 in Group B, and 2.0 +/- 0.7, 3.3 +/- 0.8, 4.9 +/- 0.8, and 5.6 +/- 1.0 in normals). The reductions in central venous pressure and in pulmonary wedge pressure were not significantly different among the three groups at the different levels of lower body negative pressure, but the reduction in cardiac output was smaller in patients with reduced dv/dt ratio than in the other two groups. The responses to the cold pressor test were similar in all subjects. We conclude that patients with essential hypertension and diastolic dysfunction have impaired total peripheral resistance responses to lower body negative pressure. This abnormality may reflect an alteration in cardiac baroreflexes secondary to left ventricular diastolic dysfunction, an influence of baseline sympathetic activity on the observed vascular responsiveness to lower body negative pressure, or primary differences among groups in the changes in cardiac output induced by similar levels of lower body negative pressure.

Adult↗
PubMed1995

Left ventricular hypertrophy and diastolic dysfunction: their relation to coronary heart disease.

Diastolic dysfunction is an early sign in the temporal sequence of ischemic events in coronary heart disease. The ischemic cascade, beginning with an oxygen demand supply imbalance and metabolic alterations, identifies diastolic disorders of the left ventricle (LV) as an early phenomenon, sometimes before systolic dysfunction, electrocardiographic changes, or chest pain occur. Although the physiology of diastolic function is complex, the factors contributing to diastolic disturbances can be differentiated into intrinsic and extrinsic LV abnormalities. Intrinsic mechanisms include (a) impaired LV relaxation, (b) the complex of LV hypertrophy, and (c) increased LV asynchrony. Myocardial hypertrophy leads to an increase of the myocardial mass/volume ratio, and the degree of hypertrophy is the main determinant of chamber stiffness. The main, if not unique, determinant of myocardial diastolic tissue distensibility is the structure and concentration of the collagen. Consequently, tissue stiffness is increased in coronary disease by reparative interstitial fibrosis or scar following myocardial infarction. In myocardial hypertrophy the LV collagen concentration is elevated due to reactive fibrosis. An increase in regional asynchrony of LV contraction and relaxation is a result of regional ischemia as well as of LV hypertrophy and tissue fibrosis. Factors extrinsic to the LV causing diastolic disorders include (a) increased central blood volume, which will increase left ventricular pressure without altering the LV pressure-volume relation, and (b) ventricular interaction mediated by pericardial restraint, which may cause a parallel upward shift of the diastolic LV pressure-volume relation. Improved insight into the mechanisms of LV relaxation and filling characteristics help in the treatment of LV diastolic dysfunction.

Coronary Disease↗
PubMed1994

Diagnosis and treatment of heart failure based on left ventricular systolic or diastolic dysfunction.

Data from large and small clinical trials reflect major differences in the pathophysiology, treatment, and prognosis of left ventricular (LV) systolic and diastolic dysfunction. These studies also indicate that medical therapy can benefit patients with LV dysfunction regardless of whether or not they are symptomatic. Because the descriptive term congestive heart failure does not provide for these important distinctions, a new classification of LV dysfunction has been developed in which patients with LV dysfunction are categorized on the basis of normal or abnormal systolic function. This classification is based on a simple assessment of LV function, it is applicable to patients without symptoms, and it reflects differences in treatment and prognosis. Those with clinically significant LV systolic dysfunction (ie, an LV ejection fraction < 40%) benefit from therapy whether or not they have symptoms of heart failure. Those with LV dysfunction and a normal LV ejection fraction (ie, diastolic dysfunction) also benefit from medical therapy. Annual mortality is higher in those with systolic dysfunction than in those with diastolic dysfunction, but within each of these categories mortality is higher in those with symptoms than in those without. This classification can be useful in the diagnosis and treatment of individual patients as well as in epidemiologic surveys designed to assess medical practice patterns.

Diastole↗
PubMed1993

Reversible left ventricular diastolic dysfunction resulting from frequent supraventricular tachycardia.

In two patients with frequent supraventricular tachycardia, echocardiograms revealed remarkable left ventricular systolic and diastolic dysfunction, associated with an absence of left ventricular filling during the early diastolic phase. This dysfunction was detected during normal sinus rhythm as well as tachycardia. By treatment with propafenone, both patients showed dramatic and rapid improvement of symptoms and the left ventricular dysfunction. Left ventricular diastolic dysfunction as well as systolic dysfunction were detected in patients with supraventricular tachycardia, suggesting that frequent supraventricular tachycardia results in severe left ventricular diastolic dysfunction which is reversible after control of the tachycardia.

Aged↗
PubMed1995

Diastolic dysfunction in patients on thyroid-stimulating hormone suppressive therapy with levothyroxine: beneficial effect of beta-blockade.

Thyroid-stimulating hormone (TSH) suppressive therapy with levothyroxine (L-T4) may cause adverse cardiac effects such as rhythm disturbances and ventricular hypertrophy. The latter is a predisposing condition to diastolic dysfunction. Thus, this study was designed to assess the effect of long-term TSH suppressive therapy on cardiac diastolic function. Because beta-blockade is known to reduce ventricular hypertrophy in patients on L-T4 therapy, we also tried to determine whether the addition of a beta-blocker to L-T4 improved diastolic function. Twenty-five patients (21 female and 4 male; mean age 41 +/- 10 yr) on TSH suppressive therapy for 3-9 yr (9 for differentiated carcinoma and 16 for nontoxic goiter) and 20 control subjects were studied. A subgroup of 10 patients, selected for the presence of symptoms and signs of adrenergic overactivity, was treated for 4 months with the beta-blocker bisoprolol (4.25 +/- 1.2 mg/day), and their maintaining L-T4 therapy was unchanged. In the patient group, left ventricular mass was significantly increased (P < 0.001), isovolumic relaxation time was prolonged (P < 0.001), and early diastolic filling velocity was markedly reduced (P < 0.001), whereas late diastolic filling was increased (P < 0.005). Consequently, the early-to-late diastolic flow velocity ratio was markedly decreased (P < 0.001). These alterations were more pronounced in the subgroup of patients with evidence of adrenergic overactivity. In these patients, beta-blockade induced a significant regression of cardiac hypertrophy and improved diastolic dysfunction. In particular, isovolumic relaxation time decreased (P < 0.01) and the early-to-late flow velocity ratio increased significantly (P < 0.01). Both indices reached values after beta-blockade that were no longer different from those of asymptomatic patients. It is concluded that long-term L-T4 therapy increases myocardial mass and causes relevant diastolic dysfunction, particularly in those patients with evidence of mild hyperthyroidism and adrenergic overactivity. Both myocardial hypertrophy and diastolic dysfunction are significantly improved by adrenergic beta-blockade.

Adult↗
PubMed1993

Isolated diastolic dysfunction of the myocardium and its response to CoQ10 treatment.

Symptoms of fatigue and activity impairment, atypical precordial pain, and cardiac arrhythmia frequently precede by years the development of congestive heart failure. Of 115 patients with these symptoms, 60 were diagnosed as having hypertensive cardiovascular disease, 27 mitral valve prolapse syndrome, and 28 chronic fatigue syndrome. These symptoms are common with diastolic dysfunction, and diastolic function is energy dependent. All patients had blood pressure, clinical status, coenzyme Q10 (CoQ10) blood levels and echocardiographic measurement of diastolic function, systolic function, and myocardial thickness recorded before and after CoQ10 replacement. At control, 63 patients were functional class III and 54 class II; all showed diastolic dysfunction; the mean CoQ10 blood level was 0.855 micrograms/ml; 65%, 15%, and 7% showed significant myocardial hypertrophy, and 87%, 30%, and 11% had elevated blood pressure readings in hypertensive disease, mitral valve prolapse and chronic fatigue syndrome respectively. Except for higher blood pressure levels and more myocardial thickening in the hypertensive patients, there was little difference between the three groups. CoQ10 administration resulted in improvement in all; reduction in high blood pressure in 80%, and improvement in diastolic function in all patients with follow-up echocardiograms to date; a reduction in myocardial thickness in 53% of hypertensives and 36% of the combined prolapse and fatigue syndrome groups; and a reduced fractional shortening in those high at control and an increase in those initially low.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Left ventricular diastolic dysfunction as a cause of congestive heart failure. Mechanisms and management.

OBJECTIVE: To define the mechanisms underlying left ventricular diastolic dysfunction in patients with congestive heart failure and normal systolic function and to identify the patients at risk for this syndrome. STUDY SELECTION: Studies were selected that describe the clinical observations of congestive heart failure with normal systolic function and that provide experimental and clinical insights into the mechanisms responsible for ventricular diastolic dysfunction. DATA SYNTHESIS: Recent studies indicate that a large number of patients (up to 40% in some series) presenting with congestive heart failure have preserved left ventricular systolic function. The factors contributing to altered left ventricular diastolic function include fibrosis, hypertrophy, ischemia, and increased afterload. The latter three factors, alone or in combination, predispose to impaired left ventricular relaxation, an active energy-requiring process. Thus, decreased left ventricular diastolic distensibility (increased diastolic pressure at any level of diastolic volume) may arise not only from altered passive elastic properties stemming from fibrosis or increased muscle mass but also from derangements in the dynamics of ventricular relaxation. RESULTS: In patients with essential hypertension, all four of the above mechanisms may be operative. Considering the prevalence of hypertension in the general population, hypertension appears to be an important underlying factor in many patients with heart failure on the basis of diastolic mechanisms. In the patient presenting with dyspnea and elevated filling pressures, but with a nondilated, normally contracting ventricle, treatment with standard heart failure medications (such as digitalis, diuretics, and vasodilators) is often ineffective and may be deleterious. Such patients may respond more favorably to beta-blockers and calcium-channel blockers. CONCLUSIONS: Diastolic dysfunction should be considered in the patient presenting with heart failure symptoms but with normal systolic function, particularly in hypertensive patients with left ventricular hypertrophy.

Diastole↗
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↗
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↗