Contribution of hypertension to left ventricular diastolic function in patients with asymmetrical apical hypertrophy

This study was designed to ascertain the contribution of hypertension to the early diastolic time intervals in asymmetrical apical hypertrophy (AAH). Eighteen patients with untreated AAH were categorized as those with (n = 13) and without (n = 5) hypertension. Isovolumic relaxation time and early diastolic filling were determined in four groups: normotensive subjects (n = 20), patients with essential hypertension (n = 20), AAH with hypertension, and AAH without hypertension. Early diastolic function was measured by the interval from the aortic closure sound (IIA, phonocardiography) to the opening of the mitral valve (MVO, echocardiography) and the interval from MVO to the O point of the apexcardiogram. The IIA-O interval was also calculated. Peak velocities in the rapid filling phase (R) and atrial contraction phase (A) were measured using two-dimensional Doppler echocardiography in the center of the mitral orifice in diastole. The MVO-O/IIA-MVO and A/R ratios were also calculated. 1. In the AAH with and without hypertension groups, the IIA-O, IIA-MVO, and MVO-O intervals were significantly prolonged. The IIA-O and MVO-O intervals in the AAH without hypertension group were more prolonged than were those in the AAH with hypertension group. In patients with essential hypertension, the IIA-O and the IIA-MVO intervals were prolonged, but there was no prolongation of the MVO-O interval. 2. The MVO-O/IIA-MVO ratio was lower in essential hypertension and in the AAH with hypertension groups, and significantly higher in the AAH without hypertension group. 3. There was no significant change of the R, A, and A/R in each group. These results indicated that prolonged left ventricular relaxation was distinguished in essential hypertension. In AAH with hypertension, the same prolongation was observed, but the disturbance of early diastolic filling was mild. It is suggested that apical hypertrophy has a possible association with hypertension, though it may more properly belong to cardiomyopathy.     

Effects of calcium antagonists or beta-blockade on left ventricular diastolic function in essential hypertension

This study was performed to assess the effect of a calcium channel blocker (nifedipine) and beta-blockade (atenolol) on left ventricular early diastolic function and filling in essential hypertension (WHO stage I, II; HT). Twenty-two untreated patients were randomly divided as nifedipine (11 patients) and atenolol (11 patients) treatment groups and both the groups had complete echocardiographic and Doppler studies. Twenty normotensive cases served as controls. Clinical and echo-Doppler data obtained at baseline and four weeks after initiation of each therapy showed no difference between the two HT groups as to mean blood pressure (before therapy, 119 +/- 3 vs 117 +/- 11 mmHg; after therapy, 106 +/- 3 vs 110 +/- 3 mmHg), left ventricular dimension, left atrial dimension, and wall thickness. To evaluate early diastolic function, the interval from the aortic closure sound (IIA, phonocardiography) to the opening of the mitral valve (MVO, echocardiography) and that from MVO to the O point of the apexcardiogram were measured. The IIA-O interval was also calculated. The peak velocities in the rapid filling (R) and atrial contraction phases (A) were measured using pulsed Doppler echocardiography at the center of the mitral orifice. The MVO-O/IIA-MVO and A/R ratios were also calculated. Compared with the controls, the IIA-O interval (143.9 +/- 6.8 msec) and the IIA-MVO interval (81.5 +/- 4.9 msec) were significantly prolonged in HT (p less than 0.01). There was no significant difference between the MVO-O interval and R. Velocity A (54.2 +/- 2.7 cm/sec) and the A/R ratio (1.01 +/- 0.11) increased significantly in HT (p less than 0.05). The IIA-O interval (before therapy, 153.3 +/- 7.6 vs after therapy, 134.3 +/- 6.2 msec) and IIA-MVO interval (87.3 +/- 6.3 vs 77.8 +/- 5.9 msec) decreased and R (43.7 +/- 3.8 vs 49.1 +/- 3.0 cm/sec) increased significantly with nifedipine. The IIA-O interval (135.7 +/- 11.3 vs 150.4 +/- 7.6 msec) and the MVO-O (58.4 +/- 3.9 vs 66.5 +/- 4.7 msec) interval were significantly prolonged with atenolol, however the IIA-MVO interval, R, and A/R did not change. A (57.5 +/- 4.0 vs 50.2 +/- 2.9 cm/sec) was also significantly decreased with atenolol. There was a significant correlation between reduction in velocity A and prolongation in the MVO-O interval (r = -0.62, p less than 0.05) with atenolol. These results suggested that the prolongation of the diastolic closure rate of the mitral valve by atenolol was related to increased ventricular filling and decreased atrial contraction.(ABSTRACT TRUNCATED AT 400 WORDS)     

Difference in myocardial characteristics between hypertrophic cardiomyopathy and myocardial hypertrophy due to essential hypertension

To investigate the qualitative difference in myocardial hypertrophy that exists between hypertrophic cardiomyopathy (HCM) and essential hypertension (HT), we measured the mean wall thickness (MWT), the early diastolic time intervals (IIA-MVO time: from the second heart sound to the point of mitral valve opening, MVO-O time: from MVO to the O point of apexcardiogram) and the MVO-O/IIA-MVO ratio. The MWT in HCM and HT was measured by biventriculogram and echocardiogram, respectively. The MWT showed no significant difference between HT (13.1 +/- 3.0 mm) and non-obstructive type of HCM (14.8 +/- 3.7), but the MWT in obstructive type (1.08 +/- 0.24) was significantly thinner than that in HT. As the MWT increased, both IIA-MVO and MVO-O time were prolonged in both groups. But the mode of prolongation was quite different. In HT, the prolongation of the IIA-MVO time was almost always greater than that of the MVO-O time. In HCM, the prolongation of the latter was greater than that of the former. The MVO-O/IIA-MVO ratio in HT was significantly less than that in normal subjects, but those in HCM were significantly greater. These findings suggest that the differences in the early diastolic time intervals between HCM and HT are not due to the magnitude of the left ventricular hypertrophy, but due to myocardial characteristics.     

Comparative effects of calcium-channel blockers and beta-adrenergic blocker on early diastolic time intervals and A-wave ratio in patients with hypertrophic cardiomyopathy

To compare the effects of calcium-channel blockers with those of beta-adrenergic blockers in patients with hypertrophic cardiomyopathy (HCM), diastolic time intervals (IIA-O time, from the second heart sound to the O point of apexcardiogram, IIA-MVO time, from IIA to the mitral valve opening, and MVO-O time, from the MVO to the O point of apexcardiogram), and A-wave ratio measured from apexcardiogram were evaluated before and after more than three months of treatment. In both groups, heart rate significantly decreased after treatment. The IIA-MVO time was not affected by either drug. The IIA-O and the MVO-O times were significantly shortened by calcium-channel blockers (from 234.6 +/- 77.4 ms to 204.6 +/- 39.2 ms; p less than 0.01, and from 133.1 +/- 66.4 ms to 100.3 +/- 34.0 ms; p less than 0.01, respectively). However, they were not affected by beta-adrenergic blocker. A-wave ratio significantly decreased after calcium-channel blockers (from 18.0 +/- 9.8% to 13.7 +/- 7.3%; p less than 0.01) and beta-adrenergic blocker (from 21.7 +/- 12.6% to 17.2 +/- 8.0%; p less than 0.01). From these observations, it is suggested tht calcium-channel blockers improved the early diastolic filling rate, whereas beta-adrenergic blocker did not affect it. It is concluded that the effects of calcium-channel blockers and beta-adrengergic blocker on early diastolic time intervals were different in patients with HCM.     

Clinical significance of early diastolic time intervals for the differentiation of idiopathic dilative cardiomyopathy from ischemic cardiomyopathy

In order to differentiate idiopathic dilative cardiomyopathy from ischemic cardiomyopathy noninvasively, systolic time intervals (STIs) and early diastolic time intervals were investigated in patients with idiopathic dilative cardiomyopathy (n = 11), patients with ischemic cardiomyopathy (n = 8), and normal controls (n = 17). Minimal left ventricular pressure and pulmonary capillary wedge pressure (PCWP) were also measured to clarify the relationship between early diastolic time intervals and early diastolic hemodynamics. Cardiac function estimated by STIs was markedly depressed both in idiopathic dilative cardiomyopathy and ischemic cardiomyopathy, and there was no difference between the two diseases. In early diastolic time intervals, IIA-O time (the interval from the aortic component of the second heart sound to the O point of apexcardiogram) was significantly prolonged both in idiopathic dilative cardiomyopathy (144 +/- 31 (SD); p less than 0.01) and ischemic cardiomyopathy (153 +/- 15; p less than 0.01) compared to normal controls (126 +/- 11). IIA-MVO time (the interval from IIA to the mitral valve opening) in idiopathic dilative cardiomyopathy (49 +/- 23) was significantly shorter than that in normal controls (70 +/- 8; p less than 0.05). On the contrary, IIA-MVO time in ischemic cardiomyopathy (126 +/- 11) was markedly prolonged compared with normal controls (p less than 0.01) and idiopathic dilative cardiomyopathy (p less than 0.01). MVO-O time was significantly prolonged in idiopathic dilative cardiomyopathy (94 +/- 18; p less than 0.01). However, it was conversely shortened in ischemic cardiomyopathy (25 +/- 15) compared with normal controls (54 +/- 7; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Doppler-Derived Myocardial Performance Index in Patients with Impaired Left Ventricular Relaxation and Preserved Systolic Function

Background: The Doppler-derived myocardial performance index (MPI) has been used in the evaluation of left ventricular (LV) function in several diseases. In patients with isolated diastolic dysfunction, the diagnostic utility of this index remains unclear. The aim of this study was to determine the diagnostic utility of MPI in patients with systemic hypertension, impaired LV relaxation, and normal ejection fraction. Methods: Thirty hypertensive patients with impaired LV relaxation were compared to 30 control subjects. MPI and its components, isovolumetric relaxation time (IRT), isovolumetric contraction time (ICT), and the ejection time (ET), were measured from LV outflow and mitral inflow Doppler velocity profiles. Results: MPI was higher in patients than in control subjects (0.45 ± 0.13 vs 0.37 ± 0.07 P < 0.0029). The increase in MPI was due to the prolongation of IRT without significant change of ICT and ET. MPI cutoff value of ≥0.40 identified impaired LV relaxation with a sensitivity of 63% and specificity of 70% while an IRT >94 ms had a sensitivity of 67% and specificity of 80%. Multivariate analysis identified relative wall thickness, mitral early filling wave velocity (E), and systolic myocardial velocity (Sm) as independent predictors of MPI in patients with hypertension. Conclusions: MPI was increase in patients with hypertension, diastolic dysfunction, and normal ejection fraction but was not superior to IRT to detect impaired LV relaxation.     

Quantitative analysis of global and regional cardiac performance in normal subjects and patients with coronary artery disease by rest/exercise radionuclide blood-pool study

This study was undertaken to assess regional and diastolic left ventricular (LV) function in relation to LV asynchronous contraction during exercise (Ex). Rest and serial Ex (25w-75w) gated blood-pool study (Tc-99m-RBC) of 6 normal subjects (N), 12 patients with stable angina pectoris (AP) and 8 with LV aneurysm (LVan) were evaluated in regional LV ejection fraction (EF) and Fourier analysis using higher-order harmonics. In the patients with Ex and regional EF showed various responses to Ex. Global LVEF in the patients with AP indicated almost no change during Ex and regional EF declined apparently in anteroseptal segment, corresponding to stenotic left anterior descending artery. Diastolic indices of regional and global cardiac performance, PFR (peak filling rate), TPF (time to PFR) and standard deviation (SD) of TPF histogram, were obtained by Fourier analysis using two-order harmonics. Patients with coronary artery disease (CAD) showed significantly lower PFR, longer TPF and higher SD of TPF than normal group, suggesting asynchronous relaxation. We conclude that regional EF response and diastolic indices of cardiac performance to exercise provide useful and sensitive information detecting the severity of CAD.     

Afterload induced changes in myocardial relaxation: a mechanism for diastolic dysfunction.

BACKGROUND: Diastolic left ventricular (LV) dysfunction manifests as an upward shift of the diastolic pressure-volume relation. One of the possible causes of diastolic LV dysfunction is incomplete myocardial relaxation. It is well known that high afterload slows myocardial relaxation. This contribution investigated to what extent afterload elevation could also affect LV filling pressures including end-diastolic LV pressure (LVP). METHODS: Selective, beat-to-beat elevations of afterload were induced in anaesthetised open-chest rabbits (n = 9) by abrupt narrowing of the ascending aorta during the diastole of the preceding heartbeat. This was performed with physiological heart rate and blood pressure. RESULTS: These interventions increased systolic LVP from 90 +/- 3 mm Hg at baseline to 103 +/- 4, 123 +/- 5, 139 +/- 5 and 154 +/- 6 mm Hg. The last intervention was a total aortic occlusion inducing a first beat isovolumetric contraction. Smaller afterload elevations decreased tau (accelerated LVP fall) and did not elevate diastolic pressure-internal diameter relation (P-ID). Larger afterload elevations increased tau (decelerated LVP fall), induced an upward shift of the diastolic P-ID and increased end-diastolic LVP. Effects of afterload on end-diastolic LVP were correlated with effects on tau (r = 0.89; P < 0.01). Incomplete relaxation or load-dependent residual active state appeared to be the mechanism for this diastolic dysfunction. Similar findings were made retrospectively in dogs instrumented with circumferential segment length gauges (n = 16). CONCLUSIONS: Diastolic LV dysfunction was induced by elevated afterload in healthy hearts of rabbits and dogs. If this mechanism could be shown to be operative in the failing heart, reversal of diastolic dysfunction should contribute to the beneficial effects of vasodilating and inotropic therapy on pulmonary congestion.     

Relaxation and diastolic filling precisely evaluated in patients with left ventricular dysfunction]

To assess left ventricular (LV) diastolic function in patients with LV dysfunction, LV pressures (manometer tip) and biplane angiograms were analyzed for 27 patients with LV systolic dysfunction (EF < or = 0.45) (dilated cardiomyopathy or coronary artery disease) and 18 normal controls. LV volumes were obtained from frame-by-frame analyses of angiograms. LV relaxation was assessed by the time constant (T) of LV pressure decay. LV relaxation was impaired in patients with LV dysfunction, however, early diastolic filling assessed by the peak filling rate (PFR) and mean filling rate (MFR) during the rapid filling phase was maintained. Compared to the control group, early diastolic filling was significantly decreased in patients with LV dysfunction without mitral regurgitation (MR), but not in those with LV dysfunction with MR. In conclusion, although diastolic filling may be modified by MR, LV relaxation and early diastolic filling are essentially impaired in patients with LV dysfunction.     

Is the blood flow in the left ventricle during the isovolumic relaxation period a useful parameter of left ventricular systolic and early diastolic performance?

Left ventricular (LV) early diastolic performance is determined by LV behavior in the late systole to early diastole and may relate to the physical potential of patients. Isovolumic relaxation flow (IRF) velocity was obtained by continuous Doppler echocardiography in the left ventricle from the apex in 26 patients with atypical chest pain and 63 patients with coronary artery disease (CAD) with or without prior myocardial infarction (MI) who underwent cardiac catheterization. In each patient, a time constant of LV relaxation (tau) was calculated from the LV pressure waves obtained by a catheter-tipped micromanometer. The LV end-systolic volume index was measured using contrast left ventriculography. IRF velocity in patients having CAD with prior MI (24.8 +/- 5.4 cm/s) was significantly less than in those with atypical chest pain (41.2 +/- 9.6 cm/s). It was also significantly less than in patients having CAD without prior MI (37.3 +/- 6.8 cm/s). IRF velocity significantly correlated with the time constant tau (r = -0.42, p < 0.001) and LV end-systolic volume index (r = -0.84, p < 0.001). This study indicates that IRF velocity obtained by continuous Doppler echocardiography in the left ventricle provides important information regarding LV systolic performance and early diastolic performance.     

Effects of calcium-channel blocking agents on left ventricular diastolic function in hypertrophic cardiomyopathy and in coronary artery disease

Abnormal left ventricular (LV) diastolic performance is a characteristic feature of hypertrophic cardiomyopathy (HC) and an important contributor to the development of symptoms. Impaired diastolic filling of the hypertrophied left ventricle results from both diminished distensibility and prolonged or incomplete relaxation. LV distensibility is not only influenced by fixed anatomic abnormalities (such as fibrosis or hypertrophy) that determine the passive elastic properties of the left ventricle, but also is modulated by the dynamics of myocardial relaxation: prolonged or incomplete LV relaxation may restrict the rate and extent of LV filling and result in altered pressure-volume relations throughout diastole. Several studies indicate that impaired LV relaxation and filling in HC may be modified favorably by verapamil or nifedipine administered on a short-term basis in the catheterization laboratory, associated with improved diastolic pressure-volume relations. Verapamil also improves LV filling during oral therapy. Improved indexes of LV filling correlate with symptomatic improvement, both short-term and long-term: Approximately 80% of patients having a persistent increase in peak LV filling rate have persistent improvement in objective exercise tolerance compared with preverapamil values. Altered LV relaxation and filling are also often observed in patients with coronary artery disease (CAD) after myocardial infarction or during acute ischemia. Moreover, impaired filling occurs under resting conditions in many patients who have normal systolic function and no evidence of previous infarction. Nifedipine improves indexes of LV relaxation and distensibility during pacing-induced ischemia and verapamil improves indexes of LV filling at rest and during exercise-induced ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Improved left ventricular diastolic filling in patients with coronary artery disease after percutaneous transluminal coronary angioplasty

Left ventricular (LV) diastolic filling is abnormal at rest in many patients with coronary artery disease (CAD), even in the presence of normal resting LV systolic function. To determine the effects of improved myocardial perfusion on impaired. LV diastolic filling, we studied 25 patients with one-vessel CAD by high-temporal-resolution radionuclide angiography before and after percutaneous transluminal coronary angioplasty (PTCA). No patient had ECG evidence of previous myocardial infarction. Despite normal regional and global LV systolic function at rest in all patents, LV diastolic filling was abnormal (peak LV filling rate [PFR] less than 2.5 end-diastolic volumes (EDV)/sec or time to PFR greater than 180 msec) in 17 of 25 patients. Twenty-three patients had abnormal LV systolic function during exercise. After successful PTCA, LV ejection fraction and heart rate at rest were unchanged, but LV ejection fraction during exercise increased, from 52 +/- 8% (+/- SD) to 63 +/- 5% (p less than 0.001). LV diastolic filling at rest improved: PFR increased from 2.3 +/- 0.6 to 2.8 +/- 0.5 EDV/sec (p less than 0.001) and time to PFR decreased from 181 +/- 22 to 160 +/- 18 msec (p less than 0.001). Thus, a reduction in exercise-induced LV systolic dysfunction after PTCA, reflecting a reduction in reversible ischemia, was associated with improved LV diastolic filling at rest. These data suggest that in many CAD patients with normal resting LV systolic function and without previous infarction, abnormalities of resting LV diastolic filling are not fixed, but appear to be reversible manifestations of impaired coronary flow.     

Diastolic vibration improves systolic function in cases of incomplete relaxation.

BACKGROUND. Incomplete relaxation of the left ventricle (LV) affects LV filling, but the subsequent effect on LV systolic function remains unclear. We attempted to improve relaxation by applying oscillatory mechanical perturbation during diastole (diastolic vibration) and examined the extent to which systolic function improved. METHODS AND RESULTS. Using 10 open-chest canine preparations, pacing tachycardia and administration of propranolol were imposed to induce various levels of incomplete relaxation. Myocardial length perturbation was induced with an oscillator attached to the LV surface (50 Hz, 1-mm amplitude) and was restricted to the period from the beginning of isovolumic relaxation to end diastole. At resting heart rates, diastolic vibration caused an immediate decrease in the time constant (T) of LV pressure fall without any influence on heart rate, LV peak systolic pressure (peak LVP), stroke volume (SV), LV peak positive dP/dt, and total systemic vascular resistance. With pacing tachycardia, diastolic vibration increased both peak LVP and SV at 160 beats per minute (before) and 120 beats per minute (after propranolol), simultaneously decreasing both T and LV diastolic pressures and increasing end-diastolic segment length. The increase in peak LVP and SV caused by diastolic vibration correlated with the T/diastolic interval (r = 0.82), the assumed index of severity of incomplete relaxation. CONCLUSIONS. These results suggest that diastolic vibration accelerates the LV relaxation rate and that this increased relaxation improves systolic function through the Frank-Starling mechanism.     

Relation of regional asynchrony to global left ventricular systolic and diastolic function in patients with angina pectoris without previous myocardial infarction

To assess left ventricular (LV) systolic and diastolic function globally and regionally and to study the relationship between regional asynchrony and global LV function in patients with stable effort angina pectoris (AP) without previous myocardial infarction, we conducted a resting gated radionuclide ventriculographic study in 15 control subjects (N group) and 22 AP patients with isolated disease of the left anterior descending coronary artery (LAD). In nine of these 22 AP patients, LV systolic and diastolic function before surgical revascularization (Aorto-Coronary Bypass) were compared with those after surgical revascularization. A computer program subdivided the image of the LV into four regions (septal, basal, lateral and apical) by our previously reported method. The time-activity and first-derivative curves of the global LV and three regions (septal, lateral, apical; the basal region was not computed) LV were computed. In the global LV, the peak filling rate (PFR) normalized to LV end-diastolic volume (EDV) and the ratio of increment of filling volume at 100 msec from global end-systole (ES) to the EDV (%EFV), which was correlated with the time constant of LV pressure decay during isovolumic relaxation, decreased (p less than 0.01, p less than 0.001, respectively) and time to PFR (time interval from global ES to PFR) was greater (p less than 0.001) in the AP group than that in the N group. However, in the AP group, the ejection fraction (EF), normalized peak ejection rate (PFR) and %1/3SV, which was defined as the percent stroke volume ejected during the first third of the global LV ejection phase, were not different from these in the N group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Proinflammatory cytokine levels in patients with diastolic heart failure

BACKGROUND: The role of cytokines in the pathogenesis of systolic heart failure (HF) has been well established whereas in diastolic HF it remains uncertain. AIM: To define levels of Tumor Necrosis Factor-a (TNFa) and Interleukin-6 (IL-6) in patients with diastolic HF and to reveal their association with functional class and types of left ventricular (LV) diastolic dysfunction. METHODS: We examined 26 patients with diastolic HF. The control group consisted of 10 healthy persons. Commonly used echocardiographic parameters of systolic and diastolic function of the LV, thickness of the interventricular septum (IVS), posterior LV wall thickness (PWLV), end-diastolic size of the LV (EDSLV) and left atrial (LA) volume were assessed. Serum levels of TNFa and IL-6 were measured with highly sensitive enzyme-linked immunosorbent assay. RESULTS: The TNFa and IL-6 levels were significantly higher in the group with diastolic HF than in the control group. TNFa and IL-6 levels in groups with impaired LV relaxation and restriction/pseudonormalisation were significantly higher than in the control group. TNFa level was significantly higher in the restriction/pseudonormalisation group than in the group with impaired relaxation, whereas the IL-6 level was similar. The TNFa level was significantly higher in the group with NYHA class III-IV in comparison to the group with NYHA class II. The IL-6 level in these groups was similar. Of the echocardiographic parameters, only LA volume significantly correlated with the TNF+/- level. No relationship between the IL-6 level and echocardiographic parameters was found. CONCLUSIONS: In diastolic HF, serum levels of TNFa and IL-6 are elevated. The magnitude of TNF+/- elevation is associated with the severity of HF, assessed by NYHA classification, LV diastolic dysfunction level or LA volume.     

Relation between exercise capacity and left ventricular systolic versus diastolic function during exercise in patients after myocardial infarction

BACKGROUND: It is known that left ventricular systolic function at rest does not correlate well with exercise capacity of patients with heart failure. However, the contribution of left ventricular diastolic dysfunction, especially during exercise, to exercise capacity of cardiac patients remains to be determined. OBJECTIVE: To determine the impact of left ventricular systolic and diastolic function during exercise on exercise capacity of patients with left ventricular dysfunction after myocardial infarction. METHODS: A symptom-limited exercise test was performed with measurements for hemodynamics and uptake of oxygen (Vo2) of 26 men who had previously suffered myocardial infarction. These patients were divided into two groups according to their peak Vo2 (group 1 with peak Vo2 > or = 16 ml/kg per min, n= 13; and group 2 with peak Vo2 < 16 ml/kg per min, n= 13). Pulmonary arterial pressure, left ventricular and systemic arterial pressure, and cardiac output were measured at rest and during exercise. RESULTS: At rest, there was no difference between the two groups in terms of hemodynamic parameters except for minimal dP/dt, minimal left ventricular pressure (LVP) and time constant for decay of left ventricular pressure (tau). During peak exercise, cardiac output, left ventricular end-diastolic pressure (EDP), minimal dP/dt, minimal LVP, and tau for the two groups were significantly different. Furthermore, peak Vo2 was significantly correlated with T, minimal LVP, minimal dP/dt, EDP, and maximal dP/dt during peak exercise for the whole group of patients. CONCLUSION: Left ventricular diastolic function during exercise, i.e. diastolic reserve, may be an important determinant of exercise capacity of patients with left ventricular dysfunction after myocardial infarction.     

Longitudinal changes and prognostic implications of left ventricular diastolic function in first acute myocardial infarction

BACKGROUND: Left ventricular (LV) diastolic dysfunction contributes to signs and symptoms of clinical heart failure and may be related to prognosis in heart diseases. LV diastolic dysfunction is reported to be present in acute myocardial infarction (MI); however, little is known about the time course of changes in LV diastolic function and its relation to prognosis after acute MI. METHODS AND RESULTS: Two-dimensional and Doppler echocardiographic examinations were performed in 58 consecutive patients with first acute MI. The patients were studied serially within 1 hour and at days 5, 90, and 360 after arrival to the coronary care unit. LV diastolic function was assessed by Doppler measurements of transmitral and pulmonary venous flow. On the basis of mitral inflow, patients with MI were stratified at baseline to 3 LV diastolic filling patterns: normal, impaired relaxation, or pseudonormal/restrictive. Patients with MI were observed for development of congestive heart failure (Killip class >I) during hospitalization and for death during 1-year follow-up, and these complications were related to LV diastolic function. LV diastolic dysfunction was present in the very early phase of acute MI, with signs of impaired relaxation or restrictive LV filling dynamics in 38% and 24% of the patients, respectively, whereas 38% had normal LV filling characteristics. Impaired relaxation of the LV was most pronounced and found in 60% after 1-year follow-up. In-hospital congestive heart failure (Killip class >I) was found in 50% of the patients with initial impaired LV relaxation and in 71% of the patients with initially pseudonormal or restrictive LV filling dynamics, whereas patients with normal LV filling were free of heart failure. Patients with initial impaired relaxation and restrictive LV filling dynamics demonstrated a significant LV dilation during 1-year follow-up. Patients with initial pseudonormal/restrictive LV filling pattern were more frequently readmitted to the hospital for heart failure and had significant higher New York Heart Association class score compared with patients with normal or impaired relaxation during follow-up. Cardiac death was (n = 6) only observed in patients with pseudonormal or restrictive LV filling pattern. In a multivariate stepwise regression analysis, mitral E deceleration time 相似文献   

Left ventricular relaxation abnormality is detectable by analysis of the relaxation time constant in patients with atrial fibrillation.

Left ventricular (LV) contractility is constantly changing during atrial fibrillation (AF), which is dependent on the force-interval relationships. However, no information has been available on LV relaxation in patients with both AF and impaired LV systolic function. LV pressure was measured with a catheter-tipped micromanometer and the time constant of isovolumic LV pressure decline (tau(bf)) was calculated with best exponential fitting from more than 10 consecutive beats. Patients with AF (5 with mitral valvular disease, 6 with idiopathic dilated cardiomyopathy, and 1 with no underlying disease) were subdivided into 2 groups: group A, with ejection fraction (EF) <0.5 (n=7); and group B, with EF > or =0.5 (n=5). Linear correlation coefficients (r) between tau and RR2, RR2/RR1, LV peak systolic pressure (peak LVP) were calculated. Although tau did not show a discrepancy between the 2 groups, tau(bf) correlated better with RR2/RR1 only in the group A patients. The relation between tau and peak LVP showed a good correlation with a steep slope (R, Deltatau/Deltapeak LVP) only in the group A patients (accentuated afterload-dependence). R was significantly different between the 2 groups. Thus, a beat-to-beat analysis of tau may be a practical and feasible way for detecting LV relaxation abnormality in patients with AF.     

Chronic and acute effects of smoking on left and right ventricular relaxation in young healthy smokers

BACKGROUND: Left ventricular (LV) diastolic dysfunction has been observed in cigarette smokers with coronary artery disease. The aim of the study was to assess LV and right ventricular (RV) diastolic function in healthy, young, and slim smokers before and after smoking one cigarette. MATERIAL AND METHODS: The participants were 66 healthy volunteers (age < 40 years; body mass index < 25 kg/m(2)): 33 smokers (study group [HS]) and 33 nonsmokers (control group). Echocardiographic examination was done in the HS before smoking one cigarette (HS-1) and after smoking one cigarette (HS-2). To assess diastolic function of LV and RV mitral valve flow (MVF), pulmonary venous flow (PVF) and tricuspid valve flow (TVF) were evaluated. RESULTS: MVF early to late phase ratio (E/A) was significantly lower in HS-1 and HS-2 than in the control group. The PVF systolic to diastolic phase ratio (S/D) was significantly higher in HS-1 and HS-2 than in the control group. These changes suggest LV diastolic function impairment in the HS, but the MVF pattern remained within the normal range. PVF S/D showed systolic dominance (S/D > 1) typical for impaired LV relaxation and abnormal for this age group. TVF E/A was significantly lower in HS-2 than in HS-1 and control subjects and suggests RV diastolic dysfunction. CONCLUSIONS: The following conclusion are made: (1) MVF and PVF demonstrate LV relaxation impairment in healthy smokers before and after smoking one cigarette; (2) the assessment of PVF is a good method reflecting LV diastolic function changes, even when MVF remains normal; and (3) TVF shows RV relaxation impairment after smoking one cigarette in healthy smokers.     

Exercise-induced ischemia: the influence of altered relaxation on early diastolic pressures

Left ventricular pressure (LVP) decay and early diastolic pressures were studied at rest and during exercise in three groups of patients. Patients in the ischemia group (n = 15) had coronary artery disease and developed new regional wall motion abnormalities documented by biplane LV cineangiography during exercise. Patients in the control group (n = 4) had a normal exercise response. Patients in the scar group (n = 5) had prior infarction, akinetic scars and no ischemia with exercise. Isovolumic pressure data were used to compute the time constant (T) of LVP decay (from the linear relation of LVP and negative dP/dt) and an extrapolated baseline pressure (PB) at dP/dt = 0. During exercise in the ischemia group, minimal LV diastolic pressure (PL) increased from 9 +/- 3 to 21 +/- 5 mm Hg (p less than 0.001), end-systolic volume increased from 38 +/- 7 to 55 +/- 8 ml/m2 (p less than 0.001) and PB rose from -10 +/- 7 to 11 +/- 8 mm Hg (p less than 0.001); T decreased (from 55 +/- 9 to 37 +/- 8 msec, p less than 0.001), although inadequately, compared with the decrease in the control group (from 49 +/- 15 to 22 +/- 2 msec, p less than 0.01). Relaxation at PL during exercise was incomplete in the ischemia group (2.2 +/- 0.4 T) and complete in the control group (3.8 +/- 0.7 T, p less than 0.05). The time course of LVP fall was extrapolated from the isovolumic period into the passive LV filling phase. The extrapolated pressure at the time PL occurred (PE) rose from 0 +/- 4 to 20 +/- 7 mm Hg with ischemia (p less than 0.001). Thus, the characteristics of LVP decay can account for the elevated early diastolic pressures during ischemia. In contrast, the scar group maintained a low PL during exercise (11 +/- 3 to 8 +/- 3 mm Hg), even though T decreased inadequately (from 66 +/- 10 to 36 +/- 5 msec, p less than 0.01), because PB did not shift upward. Ischemia-related pressure elevations involve both delayed relaxation and a pressure baseline shift. During exercise, LVP decay is normally adjusted to maintain low diastolic pressures; with exercise-induced ischemia, LVP decay is abnormal and early diastolic pressures are severely elevated.