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PubMed1991

[Diastolic dysfunction].

Diastolic dysfunction is characterized by an abnormal function of one or both ventricles which is manifested by an increased resistance to diastolic filling. The pathophysiology of diastolic dysfunction includes relaxation disturbances, abnormal diastolic filing and/or abnormal passive elastic properties. In 1/5 to 1/3 of all patients with congestive heart failure, diastolic dysfunction is found to be the sole cause of heart failure. The etiology is most commonly severe myocardial hypertrophy and less often coronary artery disease. The prognosis in patients with isolated diastolic dysfunction is good; the annual mortality rate is 8% and 5-year survival approximately 70%. Therapy is based on a reduction of circulating blood volume to reduce diastolic filling pressure and improvement of relaxation and diastolic filling by the administration of calcium antagonists.

Cardiomegaly↗

PubMed1991

Congestive heart failure in patients with normal left ventricular systolic function: a manifestation of diastolic dysfunction.

Diastolic dysfunction is a relatively common problem that may be mild and asymptomatic or may present with congestive heart failure and severe disabling symptoms. It is frequently due to coronary artery disease or left ventricular hypertrophy and it is especially common in the older population. The pathophysiology is related to increased left ventricular passive stiffness and impaired or slowed myocardial relaxation. Patients with diastolic dysfunction are best treated with calcium channel blocking agents or beta-blocking agents (drugs that are generally avoided in patients with significant systolic dysfunction). Most treatment is based on symptomatic relief, and therefore periods of cautious trial and error are the rule. Congestive symptoms are treated with agents that reduce pulmonary venous pressure; in general positive inotropic agents and arterial vasodilators are not useful in heart failure that is due to diastolic dysfunction.

Adrenergic beta-Antagonists↗

PubMed1989

Left ventricular diastolic dysfunction: early diastolic relaxation and late diastolic compliance.

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Coronary Disease↗

PubMed1991

Prevalence of unsuspected mitral regurgitation and left ventricular diastolic dysfunction in patients with coronary artery disease and acute pulmonary edema associated with normal or depressed left ventricular systolic function.

To define the prevalence and role of left ventricular (LV) systolic dysfunction, LV diastolic dysfunction and mitral regurgitation (MR) in patients with acute pulmonary edema, 40 patients with coronary artery disease and acute pulmonary edema were prospectively evaluated within 36 hours of presentation. LV ejection fraction and 3 parameters of LV diastolic function were measured with radionuclide ventriculography, whereas MR was assessed with Doppler echocardiography. LV ejection fraction was normal in 11 (27%) and depressed in 29 (73%) patients. Moderate or severe MR without LV diastolic dysfunction was common and equally prevalent in patients with and without LV systolic dysfunction (33 vs 38%; difference not significant). Diastolic dysfunction without MR was less frequent but equally prevalent in patients with and without systolic dysfunction (17 vs 27%; difference not significant). Two (18%) of 11 patients without and 12 (33%) of 36 patients with LV systolic dysfunction had both MR and LV diastolic dysfunction. Furthermore, MR was clinically silent and unsuspected in two-thirds of all patients with MR, regardless of a normal or depressed systolic function. These data show that there is a high prevalence of unrecognized moderate to severe MR in patients with acute pulmonary edema, regardless of the presence or absence of LV systolic dysfunction. Furthermore, the prevalence of LV diastolic dysfunction without MR is relatively low even in patients with normal LV systolic function and pulmonary edema. Thus, unrecognized MR may be an important contributor to the syndrome of acute pulmonary edema in patients with normal or depressed LV systolic function.

Aged↗

PubMed2026

Cine-derived mitral annular relaxation velocity for detection of preclinical left ventricular diastolic dysfunction.

OBJECTIVES: Imaging diastolic dysfunction in pre-clinical heart failure (HF) is challenging. We evaluated a novel cardiac MRI (CMR) biomarker, CMR e-prime (CMR-MARV), in patients at risk of HF. METHODS: In this substudy of the PARABLE trial (NCT04687111), 236 patients (71.6 ± 7.7 years, 61.6% male) fulfilling trial-defined ALVDD citeria underwent CMR with measurement of mitral annular relaxation velocity (CMR-MARV) at four mitral annular anchor points. Diastolic strain rates from FT were also assessed. Twenty-five age- and sex-matched controls were included (73.8 ± 3.1 years, 52% male). Group differences were tested with t-tests, diagnostic accuracy with ROC analysis, and predictors of diastolic dysfunction with adjusted logistic regression. RESULTS: Compared with controls, patients had significantly higher indexed maximal left atrial volume (LAVimax), LV end-diastolic and end-systolic volumes, and LV mass (all p < 0.001). Of FT variables, only peak diastolic longitudinal velocity differed between groups (p < 0.001). In multivariate models, CMR-MARV correlated with radial, circumferential, and longitudinal diastolic strain rates, radial and longitudinal diastolic velocities (all p < 0.001), echocardiographic e' (r = 0.20, p = 0.007), LV mass (r = -0.18, p = 0.008), LAVimax (r = -0.18, p = 0.008), and NT-proBNP (r = -0.30, p < 0.0001). LAVimax and CMR-MARV were strongly independently associated with ALVDD (AUC 0.89 and 0.76, respectively; p < 0.0001). A combined model (LAVimax + CMR-MARV) achieved excellent discrimination (AUC 0.91, 95% CI 0.86-0.97, p < 0.0001). Independent predictors included LAVimax, CMR-MARV, and peak diastolic longitudinal velocity (all p < 0.001). CONCLUSION: CMR-MARV provides a simple cine-derived measure of longitudinal relaxation that correlates with established structural and biochemical markers of diastolic burden. Within an at-risk population, it offers incremental functional information beyond conventional parameters and may support multiparametric CMR phenotyping of preclinical diastolic dysfunction.

Aged↗

PubMed1991

Significance of diastolic dysfunction of the heart.

Diastolic dysfunction is an important cause of the clinical syndrome of congestive heart failure. Traditionally, the syndrome of pulmonary congestion due to the elevation of left heart filling pressure has been attributed to the depressed ability of the heart to eject blood during systole, with a secondary increase in left ventricular volume. However, heart failure can also occur when the left ventricle fails to receive blood during diastole at low filling pressures. With a mild degree of resistance of the left ventricle to diastolic filling, the initial hemodynamic manifestation may just be the elevation of left ventricular diastolic pressure and pulmonary venous pressure. More severe resistance to left ventricular filling may cause an inadequate extent of diastolic filling and insufficient myofiber stretch, which results in the depression of stroke volume. In this review, the factors contributing to diastolic dysfunction are discussed, with a particular focus on the role of diastolic heart failure in patients with ischemic heart disease or hypertrophy.

Animals↗

PubMed1991

Diastolic dysfunction in congestive heart failure.

The available literature on the evaluation of diastolic function, the importance of diastolic dysfunction in congestive heart failure (CHF), and the effects of therapeutic agents on diastolic dysfunction are summarized. The normal cardiac cycle consists of two components: systole (contraction; ventricular emptying) and diastole (dilation; ventricular filling). Recent studies have shown that 30-40% of patients with CHF have normal systolic function; the majority of these patients have diastolic dysfunction as the underlying disorder. As a result, the role of diastolic dysfunction in CHF is currently an area of interest for researchers. The two primary causes of diastolic dysfunction are left ventricular hypertrophy and ischemic heart disease. Patients with CHF caused by diastolic dysfunction and patients with CHF caused by systolic dysfunction have nearly identical clinical presentations. Therapy with diuretics, vasodilators, angiotensin-converting-enzyme inhibitors, beta-agonists, the partial beta-agonist xamoterol, phosphodiesterase III inhibitors, or calcium-channel blockers may be beneficial in patients with diastolic dysfunction. Therapy with digitalis glycosides would be of no benefit, and could theoretically be detrimental, in patients with predominant diastolic dysfunction. Available data indicate that beta blockers have neither an important beneficial effect nor an important detrimental effect on diastolic function. Continued studies into diastolic dysfunction and the diastolic properties of agents that are used in the treatment of CHF should enhance the understanding of this clinical syndrome and the drugs used to treat it.

Diastole↗

PubMed1990

Diastolic dysfunction and congestive heart failure.

Diastolic heart failure is characterized by increased resistance to diastolic filling of one or both cardiac ventricles. Although some degree of diastolic failure exists in most patients presenting clinically with heart failure, a substantial subset of patients have relatively pure diastolic heart failure with normal systolic function. Diastolic heart failure can be due to structural abnormalities that increase resistance to ventricular inflow, and these structural abnormalities can be extramyocardial (e.g., constrictive pericarditis and mitral stenosis) or intramyocardial (e.g., fibrosis and amyloidosis). In addition to structural abnormalities, physiological derangement of myocardial inactivation and relaxation can contribute importantly to diastolic dysfunction in patients with heart failure. There is mounting evidence that advanced myocardial hypertrophy is associated with increased resistance to ventricular diastolic inflow due to both structural alteration (increased wall thickness and altered collagen matrix) and impaired diastolic relaxation of the hypertrophied myocardium. Physiological mechanisms for impaired relaxation in advanced hypertrophy remain controversial but can include disordered function of myocardial sarcoplasmic reticulum, subendocardial ischemia, and altered adenylate cyclase function. Diastolic dysfunction can play an important role in the genesis of flash pulmonary edema seen in patients with ischemic heart disease because myocardial ischemia is associated with a decline in relaxation rate, increased resistance to early diastolic filling, and in some cases, a striking upward shift in the left ventricular diastolic pressure-volume relation.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Output↗

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↗

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↗

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↗

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↗

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↗