Mean Left Ventricular Diastolic Pressure Research Articles

Impaired left ventricular global longitudinal strain is associated with elevated left ventricular filling pressure after myocardial infarction.

Left ventricular (LV) global longitudinal strain (GLS) has emerged as a significant prognostic marker in patients after myocardial infarction (MI). Although elevated LV filling pressure after MI might alter GLS, direct evidence for this is lacking. This study aimed to clarify the association between GLS and LV filling pressure in a large animal MI model. A total of 104 Yorkshire pigs underwent both echocardiographic and hemodynamic assessments 1-4 wk after induction of large anterior MI. GLS was measured in the apical four-chamber view using a semiautomated speckle-tracking software. LV pressure-volume relationship was invasively measured using a high-fidelity pressure-volume catheter. GLS >-14% was considered impaired. Compared with pigs with LV ejection fraction (LVEF) >40% and preserved GLS (n = 29), those with LVEF >40% and impaired GLS (n = 37) and those with LVEF ≤40% (n = 38) had significantly higher LV end-diastolic pressure (15.5 ± 5.5 vs. 19.7 ± 5.8 and 19.6 ± 6.6 mmHg; P = 0.008 and P = 0.026, respectively) and higher LV mean diastolic pressure (7.1 ± 2.9 vs. 10.4 ± 4.5 and 11.1 ± 5.4 mmHg; P = 0.013 and P = 0.002, respectively). GLS was modestly correlated with τ (r = 0.21, P = 0.039) and slope of LV end-diastolic pressure-volume relationship (r = 0.43, P < 0.001). Impaired GLS was associated with higher LV end-diastolic and mean-diastolic pressures after adjusting for LVEF and baseline characteristics (P = 0.026 and P = 0.001, respectively). Impaired GLS assessed by speckle-tracking echocardiography was associated with elevated LV filling pressure after MI. GLS has an incremental diagnostic value for detecting elevated LV filling pressure and may be particularly useful for evaluating post-MI patients with preserved LVEF.NEW & NOTEWORTHY Strain analysis was performed in 104 pigs after MI, and its relationship to invasive hemodynamic measurements was studied. Impaired longitudinal strain was associated with high ventricular filling pressure independent of LVEF in post-MI setting. Global longitudinal strain is a potential prognostic marker after MI.

Ginsenoside Rb1 pretreatment attenuates myocardial ischemia by reducing calcium/calmodulin-dependent protein kinase II-medicated calcium release

Objective: The aim of this study was to investigate the protective effects of ginsenoside Rb1 and assess whether these protective effects are related to calcium/calmodulin-dependent protein kinase II (CaMKII).Methods: A myocardial ischemia (IS) rat. model and a myocardial H9C2 cell hypoxia model were established. MI was induced by occluding the left anterior descending artery for 120 min. Ginsenoside Rb1 (10 mg/kg) was administered 30 min before ischemia induction, and the treatment continued for 7 days. Results: In the rat IS injury model, ginsenoside Rb1 reduced myocardial infarct size, mean left ventricular diastolic pressure, incidence of arrhythmia, and levels of serum creatine kinase, lactate dehydrogenase, and malondialdehyde. However, the mean left ventricular systolic pressure, and maximal rising and falling rates of ventricular pressure (±dp/dtmax) increased. In the myocardial H9C2 cell hypoxia model, ginsenoside Rb1 reduced intracellular calcium concentrations ([Ca2+ ]i) during hypoxia, and markedly reversed the hypoxia-induced decrease in cell survival. Ginsenoside Rb1 was involved in the downregulation of CaMKII and the ryanodine receptor, as well as hypoxia-induced H9C2 cell survival. Conclusion: The findings of the present study suggest that ginsenoside Rb1 attenuates MI injury in rats, partially through the downregulation of CaMKII expression.

Estimation of Mean Left Atrial Pressure in Patients with Acute Coronary Syndromes: A Doppler Echocardiographic and Cardiac Catheterization Study

Doppler echocardiography, including the ratio of transmitral E to tissue Doppler e' velocities (E/e'), is widely used to estimate mean left atrial pressure (mLAP). This method, however, has not been validated in patients with acute coronary syndromes. Fifty-seven patients with acute coronary syndromes who underwent left heart catheterization and transthoracic echocardiography within 8hours of each other were retrospectively analyzed. Forty-two of the patients (74%) were men, with a mean age of 65±11years. Patients with known cardiomyopathy, atrial fibrillation, or left-sided valvular disease were excluded. Doppler mLAP was estimated using Nagueh's formula (1.24×[E/e']+1.9). Invasive mLAP was estimated using the formula of Yamamoto etal. (1.20×mean left ventricular diastolic pressure - 0.82), wherein we averaged left ventricular diastolic pressure starting from the isovolumic relaxation phase to the post-A inflection point. Subanalyses were performed in groups with reduced or normal left ventricular ejection fraction (EF). There was stronger agreement between the two techniques to estimate mLAP in the reduced EF group (r=0.73, r2=0.53, P<.001) compared with the normal EF group (r=0.33, r2=0.11, P=.08). The κ statistic for agreement was 0.34 for the overall study cohort, suggesting fair agreement according to partition values of mean mLAP: <8, 8 to 15, and >15mm Hg. Left atrial volume index did not correlate with invasively estimated mLAP in this cohort. In patients with acute coronary syndromes, Doppler- and catheter-derived estimates of mLAP correlate well in patients with reduced EFs. In the acute setting, echocardiographic evaluation is a reliable adjunct to clinical examination in assessment of heart failure in this subgroup of patients.

Indexing peak rapid filling velocity to both relaxation and filling volume to estimate left ventricular filling pressures.

The peak transmitral velocity/peak mitral annular velocity (E/e') ratio has been used as a left ventricular (LV) filling pressure (LVFP) correlate. However, the E/e' and its changes with haemodynamic alterations have not always correlated with changes in LVFP's. We hypothesized that indexing E/e' to a measure of LV filling volume may enhance the correlation with LVFP and LVFP changes. We summarized previously obtained haemodynamic and Doppler echo data in 137 dogs with coronary microsphere embolization induced-chronic LV dysfunction prior to and following haemodynamic induced alterations in LVFP's. E/e' values were obtained as E*tau where tau is the inverse logarithmic LV pressure decay. E*tau was indexed to LV filling volume by dividing by the diastolic time velocity integral (DVI) and correlated with LV mean diastolic pressure (LVmDP). Similarly, the relationship of E/e' and E/e'/DVI to LV pre A wave pressure was evaluated in 84 patients by invasive haemodynamics and Doppler echo. Combining data from all interventions, LVmDP correlated with E*tau (r = 0.408) but more strongly with E*tau/DVI (r = 0.667, z = 3.03, P = 0.0008). The change in LVmDP correlated with the change in E*tau/DVI (r = 0.742) more strongly than E*Tau (r = 0.187, Z = 4.01, P < 0.0001). In the patient cohort, E/e' was modestly correlated with LV pre A wave pressure (r = 0.301) but more strongly correlated with E/e'/DVI (r = 0.636, z = 2.36, P = 0.0161). Indexing E to both LV relaxation and filling volume results in a more robust relation with LVFP's and with LVFP changes.

Left Ventricular Mass Influences Relationship Between Filling Pressure and Early-Diastolic Ratio of Inflow Velocity to Mitral Annular Velocity (E/e').

Early-diastolic mitral annular velocity (e') and the ratio of early-diastolic left ventricular (LV) inflow velocity (E) to e' (E/e') have been widely used as indexes of LV relaxation and filling pressure, respectively. However, many recent studies have demonstrated that they are not reliable in various clinical settings. We thus investigated the factors influencing these echocardiographic parameters in a multicenter study.Methods and Results:The study group comprised 69 patients, referred for cardiac catheterization, and enrolled in 5 university hospitals. Time constant (τ) and LV mean diastolic pressure (LVMDP) were measured using a micromanometer-tipped catheter. Although e' only weakly correlated with τ (r=-0.35, P<0.01), E/e' modestly correlated with LVMDP (r=0.48, P<0.001). Multivariable analysis revealed that hypertension (β=-0.33, P<0.01) and LV ejection fraction (LVEF) (β=0.44, P<0.001) were the independent determinants of e', and LV mass index (LVMI) (β=0.37, P<0.001) and LVMDP (β=0.47, P<0.001) were those of E/e'. Additionally, E/e' significantly correlated with LVMDP in patients with normal LVMI (r=0.74, P<0.001) but not in those with increased LVMI. The coincidence of hypertension and LVEF affected the relationship between LV relaxation and e', whereas LVMI altered the relationship between LV filling pressure and E/e'. Thus, clinical conditions associated with an increase in LVMI, such as LV hypertrophy and LV dilatation, should be considered when estimating the filling pressure from E/e'.

Echocardiographic Assessment of Diastolic Function

The stepwise approach in evaluation of left ventricular (LV) diastolic function is essential in any patients with dyspnea on exertion or heart failure. Many of them have normal to near-normal ejection fractions (EFs). These subsets of patients are labeled as diastolic heart failure or heart failure with preserved EF. It is important to differentiate diastolic dysfunction from dyspnea of pulmonary origin for further management and future prognosis. LV filling pressures is usually synonymous with pulmonary capillary wedge pressure (PCWP), mean left atrial pressure (LAP), mean LV diastolic pressure, and LV end-diastolic pressure (LVEDP). PCWP on the other hand is also an indirect estimate of LV diastolic pressures. LVEDP is often elevated in early diastolic dysfunction because of a large atrial pressure wave, while mean PCWP and LAP remain normal. While mean PCWP and LAP increased during tachycardia and where there is increased LV afterload which is the basis for the diastolic stress test. It is essential that certain Doppler variables correlate well with an increase in LVEDP only and not reflecting the increase in either LAP or LVEDP. Therefore, early evaluation of LV filling pressures and LVEDP are more important than mean LA pressure which is elevated later. Echocardiography is the best evaluation tool to evaluate LV diastolic function. The purpose of this article is to provide the simplest stepwise approach of different diastolic parameters which are used as routine protocol with minimal use of the newer modalities at various clinical settings.

Abstract 12824: Comparison of Tissue Doppler-Derived and Speckle Tracking-Derived Parameters for the Estimation of Left Ventricular Filling Pressure: A Multicenter Study in Japan

Background: We conducted a multicenter study in Japan to compare tissue Doppler echocardiography-derived and speckle tracking echocardiography (STE)-derived parameters of left ventricular (LV) diastolic function for the estimation of LV filling pressure. Methods: Seventy-eight patients (age 59±14 years, 59 male) with structural heart diseases including angina pectoris (n=34), old myocardial infarction (n=15), dilated cardiomyopathy (n=13), hypertrophic cardiomyopathy (n=8), and hypertensive heart disease (n=8) were studied according to the same protocol in 5 university hospitals in Japan. LV mean diastolic pressure (MDP) was measured by using a micromanometer-tipped catheter. Early-diastolic mitral annular velocity (e′) was measured at septal and lateral side of the annulus and averaged, and the ratio of early-diastolic transmitral velocity to e′ (E/e′) was calculated. Global longitudinal strain was measured using STE in 3 apical views and averaged on a frame-by-frame basis to construct a time-strain curve as well as a time-strain rate (SR) curve. Then, the absolute value of peak longitudinal strain (LS), early-diastolic peak SR (LSR E ), and that during isovolumic relaxation (IVR) period (LSR IVR ) were measured. Similarly, peak circumferential strain (CS), early-diastolic peak circumferential SR (CSR E ), and that during IVR (CSR IVR ) were measured from 3 short-axis views. Results: E/e′ weakly correlated with MDP (r=0.50, p&lt;0.001). E/LSR IVR and E/CSR IVR did not correlate with MDP, whereas there was a significant but weak correlation between E/LSR E and MDP (r=0.50, p&lt;0.001) or between E/CSR E and MDP (r=0.41, p&lt;0.001). In contrast, there was a good correlation between E/LS and MDP (r=0.70, p&lt;0.001) or between E/CS and MDP (r=0.62, p&lt;0.001). Especially, the correlation between E/LS and MDP was statistically better than that between E/e′ and MDP (p&lt;0.01). Conclusions: STE-derived longitudinal parameters better correlated with MDP than circumferential parameters. Especially, E/LS was better than E/e′ for estimating LV filling pressure.

Novel Acute Collateral Flow Index in Patients With Total Coronary Artery Occlusion During ST-Elevation Myocardial Infarction

The effect of collaterals to occluded coronary arteries during ST-elevation myocardial infarction (STEMI) is unclear. The conventional CVP-based formula to calculate collateral flow index during STEMI yields values higher than in elective patients, which prompted derivation of a modified formula, pertinent in STEMI when left ventricular mean diastolic pressure (LVMDP) is the extravascular pressure limiting collateral flow. We aimed to evaluate this new LVMDP-based acute collateral flow index (ACFI). The pressure distal to coronary artery occlusion (P(d)) was measured during intervention in 111 consecutive STEMI patients, 67 (61%) of whom underwent primary intervention, followed for 58 months. ACFI (0.18 ± 0.17, median 0.15) correlated with both P(d) and collateral grade (P<0.0001). Higher creatine kinase levels and white cell counts were measured in the lowest ACFI tertile compared with the highest tertile group (P<0.012). ACFI correlated slightly with early regional but not with global left ventricular ejection fraction or with long-term coronary events and mortality. The ACFI is appropriate for evaluating collateral function during STEMI. Collateral flow during STEMI may marginally limit myocardial damage but had no effect on left ventricular contraction or long-term mortality, most likely because of the low flow provided by emerging collaterals and the high proportion of patients undergoing intervention before the beneficial effect of collaterals could be realized.

Dobutamine Stress Echocardiography Doppler Estimation of Cardiac Diastolic Function: A Simultaneous Catheterization Correlation Study

Doppler echocardiography using the ratio of early diastolic transmitral velocity to early diastolic mitral annular tissue velocity (E/E') is routinely used to evaluate left ventricular (LV) filling pressures at rest. We tested the hypothesis that measurement of E/E' in patients undergoing dobutamine stress echocardiography (DSE) will detect changes in LV filling pressures. In this prospective study, 16 patients with normal LV ejection fraction and normal coronary arteries by angiography underwent a standard DSE protocol with simultaneous LV filling pressure monitoring with a fluid filled pigtail catheter. Doppler echocardiographic assessment of LV diastolic function was performed using E/E' at rest and during DSE. The average age of the study participants was 57 ± 8 years. Average heart rate was 61 ± 11 bpm at baseline and 141 ± 12 bpm at peak stress. LV mean diastolic pressure decreased from 12.3 ± 2.6 mmHg at baseline to 9.0 ± 2.3 mmHg at peak stress (P = 0.0001). Baseline E/E' at the septum and lateral annulus were 8.7 ± 2.2 and 7.5 ± 1.9 and during peak stress were 8.3 ± 3.1 and 7.9 ± 3.5, respectively. There was no significant change in E/E' at either the septum or the lateral annulus (P = 0.55, P = 0.66). There was no significant correlation between LV mean diastolic pressure and E/E' with dobutamine stress. In patients with normal LV ejection fraction and no significant coronary artery disease undergoing DSE, the ratio of early diastolic transmitral velocity to early diastolic tissue velocity (E/E') at peak stress with dobutamine does not predict changes in LV filling pressures.

Hemodynamic Effects of Tachycardia in Patients with Relaxation Abnormality: Abnormal Stroke Volume Response as an Overlooked Mechanism of Dyspnea Associated with Tachycardia in Diastolic Heart Failure

Prevention of tachycardia is an important therapeutic strategy in patients with relaxation abnormality. Eleven patients with stable relaxation abnormality (group 1) and 8 healthy individuals (group 2) were enrolled. Left ventricular (LV) mean diastolic pressure, LV dimensions, stroke volume (SV), and LV ejection, filling, and isovolumic times between right atrial pacing rates of 80 and 120/min were compared. Both groups 1 and 2 showed significant decreases in LV mean diastolic pressure when heart rate (HR) increased. At a HR of 80/min, no significant difference was noted between groups 1 and 2 in SV (51.4 +/- 13.0 vs 45.2 +/- 9.0 mL, P = .35). However, a decrement in SV between a HR of 80 and 120/min was significantly greater for group 1. Therefore, group 1 showed a significantly lower SV (30.2 +/- 7.1 vs 40.1 +/- 6.9 mL, P < .05) at a HR of 120/min. In terms of time intervals between HRs of 80 and 120/min, group 1 showed a significantly greater reduction in LV ejection time (84.5 +/- 20.1 vs 30.0 +/- 34.6 milliseconds, P < .005) and a smaller reduction in LV filling time (106.4 +/- 38.5 vs 166.3 +/- 30.7 milliseconds, P < .005) than group 2. Results of our study suggest that an inadequate SV response to tachycardia may play an important role in the production of dyspnea associated with tachycardia in these patients.

The usefulness of tissue Doppler imaging in the determination of left ventricular diastolic filling pressure. Comparison with other techniques

The further examination of left ventricular diastolic function (LVDF) is important in terms of early diagnosis, therapy and follow-up of heart failure. Although cardiac catheterization is considered as the most accurate method in the evaluation of diastolic function, since it is invasive, noninvasive methods are preferred.This study was undertaken to examine whether mitral annular velocities assessed by pulsed tissue Doppler imaging (PTDI) were associated with invasive measures of diastolic LV pressure and whether additional information was gained over traditional transmitral and pulmonary venous flow velocity parameters. Doppler examination was performed in 102 patients referred to our clinic for cardiac catheterization. Doppler signals from the mitral inflow, pulmonary venous inflow, and PTDI of the mitral annulus were obtained. Mean left ventricular diastolic pressure (M-LVDP) was measured. The relationship between echocardiographic parameters and M-LVDP was investigated.A significant correlation was observed between M-LVDP and E/septal Em (r = 0.52, p < 0.000), E/lateral Em (r = 0.45, p < 0.0001), E/posterior Em (r = 0.46, p < 0.0001) E/anterior Em (r = 0.49, p < 0.0001), E/mean Em (r = 0.49, p < 0.0001), PVadur – MVadur (r = 0.51, p < 0.0001). The best echocardiographic parameters correlating with M-LVDP were E/septal Em and PVa-dur – MVa-dur.In conclusion, PTDI could be used in the assessment of LVDP. However, the combination of transmitral flow and pulmonary venous flow velocities with annular velocity can be proposed as the best method for assessing LV filling pressure that combines the influence of transmitral driving pressure and myocardial relaxation.

Independent and incremental prognostic value of early mitral annulus velocity in patients with impaired left ventricular systolic function

This study sought to investigate the incremental prognostic value of non-invasive measures of early myocardial relaxation and left ventricular diastolic pressure (LVDP) in patients with impaired left ventricular (LV) systolic function. The early diastolic mitral annulus velocity (Em) reflects myocardial relaxation, and the combined ratio of the early transmitral flow velocity (E) to Em (E/Em) >15 correlates well with elevated mean LVDP. It is unknown if these new indexes will predict poorer survival in patients with LV systolic dysfunction. Echocardiograms were prospectively obtained in 182 patients with impaired LV systolic function, defined as an LV ejection fraction <0.50. The end point was cardiac mortality. The majority of this patient sample (80%) has been reported on in a previous publication. After a median 48 months' follow-up, Em emerged as an independent predictor of survival (hazard ratio 0.61, 95% confidence interval 0.45 to 0.82). An Em <3 cm/s was associated with a significantly excess mortality (log-rank statistic 9.36, p = 0.002), and this measurement added incremental prognostic value to standard indexes of systolic or diastolic function, including a deceleration time <140 ms and an E/Em >15 (p = 0.038). Early diastolic mitral annulus velocity is a powerful predictor of cardiac mortality in patients with LV systolic impairment; Em <3 cm/s emerged as the best prognosticator in long-term follow-up, incremental to other clinical or echocardiographic variables, including the ratio E/Em.

Noninvasive estimation of left ventricular filling pressure by e/e′ is a powerful predictor of survival after acute myocardial infarction

ObjectivesThe aim of this study was to assess the prognostic value of a noninvasive measure of left ventricular diastolic pressure (LVDP) early after acute myocardial infarction (MI). BackgroundThe early diastolic velocity of the mitral valve annulus (e′) reflects the rate of myocardial relaxation. When combined with measurement of the early transmitral flow velocity (E), the resultant ratio (E/e′) correlates well with mean LVDP. In particular, an E/e′ ratio >15 is an excellent predictor of an elevated mean LVDP. We hypothesized that an E/e′ ratio >15 would predict poorer survival after acute MI. MethodsEchocardiograms were obtained in 250 unselected patients 1.6 days after admission for MI. Patients were followed for a median of 13 months. The end point was all-cause mortality. ResultsSeventy-three patients (29%) had an E/e′ >15. This was associated with excess mortality (log-rank statistic 21.3, p < 0.0001) and was the most powerful independent predictor of survival (risk ratio 4.8, 95% confidence interval 2.1 to 10.8, p = 0.0002). The addition of E/e′ >15 improved the prognostic utility of a model containing clinical variables and conventional echocardiographic indexes of left ventricular systolic and diastolic function (p = 0.001). ConclusionsE/e′ is a powerful predictor of survival after acute MI. An E/e′ ratio >15 is superior, in this respect, to other clinical or echocardiographic features. Furthermore, it provides prognostic information incremental to these parameters.

Effects of a New Cardiomyoplasty Technique on Cardiac Function

Objective: The current cardiomyoplasty technique was modified to maintain the resting tension of the latissimus dorsi muscle and to prevent lateral movement of the heart during muscle stimulation. The aim of this study is to compare the short term hemodynamic effects of the new cardiomyoplasty wrap (W1) with those of the clinically applied cardiomyoplasty wrap (W2). Preliminary indications of the long-term hemodynamic effects of W1 are presented. Methods: In three acute experiments in sheep mean central venous pressure (MCVP), mean arterial pressure (MAP), mean cardiac output (MCOP), mean left ventricular systolic pressure (MLVSP). and mean left ventricular diastolic pressure (MLVDP) were measured for 30 s before and five minutes after applying each procedure with and without stimulation of the muscle graft. The same parameters were also recorded 5 min after removing each muscle wrap. Hemodynamic changes associated with unstimulated muscle wraps were compared to the baseline data. Hemodynamic effects of muscle stimulation were determined by comparing the assisted to the preceding unassisted cardiac cycle. The long-term effects of W1 on the hemodynamics of another three sheep were studied at 6–12 months after the operation. The viability of the muscles used in the chronic experiments were evaluated by morphometric analysis. Results: Unstimulated W2 significantly increased mean central venous pressure and reduced mean cardiac output. It also increased mean left ventricular diastolic pressure and reduced peak negative dP/dt. Unstimulated W1 had no deleterious effect on mean central venous pressure, mean left ventricular diastolic pressure or peak — dP/dt, but it also reduced mean cardiac output and increased mean left atrial pressure (MLAP). Synchronised muscle stimulation, in both techniques, augmented the mean arterial pressure, mean cardiac output and mean left ventricular systolic pressure. In W2, however, myostimulation was also associated with a significant increase of the mean left ventricular diastolic pressure. In two long-term experiments significant hemodynamic assistance was observed at 6 months and at 1 yr after W1. In those sheep 68% of the cross-sectional area of the muscle was well preserved. Conclusions: Unstimulated cardiomyoplasty wraps acutely impair left ventricular function in sheep. The new technique, however, may offer significant long-term hemodynamic assistance and adequate preservation of the structural and functional integrity of the muscle flap for up to 1 yr.

Effects of a new cardiomyoplasty technique on cardiac function

Objective: The current cardiomyoplasty technique was modified to maintain the resting tension of the latissimus dorsi muscle and to prevent lateral movement of the heart during muscle stimulation. The aim of this study is to compare the short term hemodynamic effects of the new cardiomyoplasty wrap (W1) with those of the clinically applied cardiomyoplasty wrap (W2). Preliminary indications of the long-term hemodynamic effects of W1 are presented. Methods: In three acute experiments in sheep mean central venous pressure (MCVP), mean arterial pressure (MAP), mean cardiac output (MCOP), mean left ventricular systolic pressure (MLVSP), and mean left ventricular diastolic pressure (MLVDP) were measured for 30 s before and five minutes after applying each procedure with and without stimulation of the muscle graft. The same parameters were also recorded 5 min after removing each muscle wrap. Hemodynamic changes associated with unstimulated muscle wraps were compared to the baseline data. Hemodynamic effects of muscle stimulation were determined by comparing the assisted to the preceding unassisted cardiac cycle. The long-term effects of W1 on the hemodynamics of another three sheep were studied at 6–12 months after the operation. The viability of the muscles used in the chronic experiments were evaluated by morphometric analysis. Results: Unstimulated W2 significantly increased mean central venous pressure and reduced mean cardiac output. It also increased mean left ventricular diastolic pressure and reduced peak negative dP/dt. Unstimulated W1 had no deleterious effect on mean central venous pressure, mean left ventricular diastolic pressure or peak −dP/dt, but it also reduced mean cardiac output and increased mean left atrial pressure (MLAP). Synchronised muscle stimulation, in both techniques, augmented the mean arterial pressure, mean cardiac output and mean left ventricular systolic pressure. In W2, however, myostimulation was also associated with a significant increase of the mean left ventricular diastolic pressure. In two long-term experiments significant hemodynamic assistance was observed at 6 months and at 1 yr after W1. In those sheep 68% of the cross-sectional area of the muscle was well preserved. Conclusions: Unstimulated cardiomyoplasty wraps acutely impair left ventricular function in sheep. The new technique, however, may offer significant long-term hemodynamic assistance and adequate preservation of the structural and functional integrity of the muscle flap for up to 1 yr.

Quantification of effect of pericardium on LV diastolic PV relation in dogs

The aim of the present study was to quantify the effect of the pericardium on the left ventricular (LV) diastolic pressure-volume relation. The experiments were done in 10 anesthetized closed-chest dogs. Pericardial and cardiac volumes were determined by computed tomography. Pericardial effusion (n = 5) and volume loading (6% dextran iv; n = 5) were used to increase pericardial volume. Volumes were normalized as multiples of the LV volume measured when LV transmural pressure was 6 mmHg (VLV6). Using the data from the pericardial effusion experiments, we calculated the best-fit exponential equations for the pericardial pressure-volume relations. From these equations we calculated that the changes in pericardial volume necessary to shift the LV diastolic pressure-volume curve upward by 2, 5, 10, and 20 mmHg were 0.6 +/- 0.1, 1.1 +/- 0.2, 1.6 +/- 0.2, and 2.2 +/- 0.3 times VLV6, respectively. Using the data from the volume loading experiments, we also calculated the degree of upward shift of the LV pressure-volume relation caused by volume loading, which increased LV mean diastolic pressure by 12 mmHg. (The upward shift is that increment in pericardial pressure caused by the total increase in volume of the extra-LV contents of the pericardium, i.e., the atria, the right ventricle, and any pericardial effusion.) This volume loading increased the total volume of the right ventricle and the atria by 1.0 +/- 0.1 VLV6, which, in itself, increased pericardial pressure by 3.6 +/- 0.8 mmHg. We conclude that in situations in which heart or pericardial volume increases acutely, the pericardium shifts the diastolic pressure-volume relation of the LV upward by a significant amount.

Effect of diltiazem on coronary reactive hyperemia in patients with flow-limiting coronary artery stenosis

The acute effects of diltiazem on coronary reactive hyperemia were studied in 12 patients with flow-limiting coronary stenosis. Reactive hyperemia was elicited by injection of 8 ml contrast medium into the left coronary artery, while coronary sinus blood flow and left ventricular and aortic pressures were continuously recorded. Relative magnitude of hyperemia was estimated by the ratio of coronary flow at peak hyperemia to baseline flow (hyperemic ratio). Coronary resistance was calculated as the ratio between mean aortic pressure minus left ventricular mean diastolic pressure and coronary sinus blood flow. The 12 patients studied had flow-limiting coronary stenosis since their hyperemic ratio was significantly restrained when compared to that of seven control subjects (1.45 ± 0.17 vs 2.02 ± 0.24, respectively; < 0.001). The intravenous infusion of ditiazem (0.30 mg · kg −1) reduced heart rate, mean aortic pressure, and myocardial oxygen consumption (all p < 0.001). After diltiazem the hyperemic ratio was blunted when compared to the basal state (1.36 ± 0.15 vs 1.45 ± 0.17, respectively; p < 0.05), and hyperemia volume was reduced (−33%; p < 0.001). The decrease in coronary resistance at peak hyperemia was also reduced from −30 ± 8% to −25 ± 8% ( p < 0.05). We conclude that diltiazem blunts coronary reactive hyperemia in patients with demonstrated flow-limiting coronary stenosis. This reduction of coronary flow response to a hyperemic stimulus could favorably influence blood flow distribution in patients with significant coronary stenosis.

Improvement of reduced left ventricular diastolic compliance in ischemic heart disease after successful coronary artery bypass surgery

To determine the effects of myocardial revascularization on decreased left ventricular diastolic compliance consequent to chronic stable coronary artery disease, 15 patients with patent coronary artery bypass grafts (Group I) were compared with 8 patients with occluded grafts (Group II) studied before and after operation. In addition, eight normal patients served as controls. Left ventricular diastolic compliance was assessed by: (1) total observed diastolic compliance: stroke volume (V) related to left ventricular diastolic pressure (P) change (ΔV/ΔP) normalized for end-systolic volume; (2) left ventricular stiffness index of passive elastic modulus (a = slope of ΔV/ΔP related to mean left ventricular diastolic pressure); and (3) fractional pattern of left ventricular filling. All patients had normal sinus rhythm and none had preoperative or postoperative mitral regurgitation. The two groups with coronary disease were well matched preoperatively for ventricular function, volumes, mass, segmental contraction and compliance. Ejection fraction increased in Group I (0.56 preoperatively to 0.65 postoperatively, P < 0.05) but was unchanged in Group II (0.63 to 0.61, P > 0.05). Postoperative indexes of left ventricular compliance improved in Group I: (1) 0.110 to 0.150 (P < 0.05); (2) 0.030 to 0.019 (P < 0.05); and (3) 37 to 30 percent filling during last one third of diastole (P < 0.05). These indexes were unchanged postoperatively in Group II: (1) 0.109 to 0.102 (P > 0.05); (2) 0.033 to 0.039 (P > 0.05); and (3) 36 to 41 percent (P > 0.05). Compliance indexes were not altered (P > 0.05) in a subset of seven patients in Group I with preoperative or intercurrent myocardial infarction. Thus, this investigation demonstrates the relatively reversible nature of abnormal left ventricular compliance after successful coronary artery bypass surgery in certain patients with ischemic heart disease.

Effect of l-norepinephrine on left ventricular diastolic pressures in man.

Left ventricular systolic pressure, left ventricular diastolic pressure, left ventricular end-diastolic pressure, left ventricular cardiac output, systemic vascular resistance, and central blood volume were specifically measured in seven patients with normal cardiovascular systems before and during the tenth minute of an infusion of <i>l</i>-norepinephrine and the emergence of a `square wave9 pattern in the peripheral arterial blood pressure during Valsalva9s manœuvre. At that time point the mean left ventricular systolic pressure exceeded the resting level. The mean left ventricular diastolic pressure rose by 6 mm. Hg, and the mean left ventricular end-diastolic pressure rose by 5·5 mm. Hg. The left ventricular output remained unchanged. A reduction in the heart rate of 13 beats/minute was found, and the calculated mean systemic vascular resistance, mean left ventricular stroke volume, and left ventricular stroke work continued to be above resting levels. No change was apparent in the central blood volume. The results indicate that the left ventricular diastolic pressure and left ventricular end-diastolic pressure rise significantly in the course of a prolonged infusion of <i>l</i>-norepinephrine coinciding with left ventricular after-loading. The magnitude of this elevation affects all diastolic pressures passively throughout the lesser circulation, including the central venous pressure. <i>l</i>-Norepinephrine is markedly inotropic when released within the myocardium. In the usual clinical dose and during a period of 10 minutes9 infusion its efferent vagal, peripheral, arteriolar constrictor, and left ventricle after-load effects reduce the initial inotropy.