Baseline Left Ventricular End-diastolic Pressure Research Articles

Instantaneous wave-free ratio and fractional flow reserve: effect of variation in left ventricular end diastolic pressure

Abstract Funding Acknowledgements Type of funding sources: None. Introduction Among patients with intermediate coronary artery stenosis (50-90%), assessment of functional significance of the lesion by instantaneous wave free ratio (iFR)/ fractional flow reserve (FFR) is recommended in latest guidelines. Though iFR is not much affected by change in hemodynamics compared to FFR, the change in iFR vs FFR due to various hemodynamic factors need a validation. Left ventricular end-diastolic pressure (LVEDP) is one of the hemodynamic factors whose variation and effect on FFR vs iFR is largely unknown. In the present study we evaluated the association of change in LVEDP on the changing pattern of iFR/FFR which may hold a clinical significance especially with percutaneous coronary intervention in heart failure patients. Methods This was a prospective, investigator-initiated, single-center study involving 20 patients with stable coronary artery disease and at least one intermediate coronary lesion (50-90%). The enrolled patients were subjected to both iFR and FFR along with baseline LVEDP measurement. Subsequently, intravenous nitroglycerine infusion was given to reduce LVEDP and corresponding iFR and FFR were re-evaluated. The dynamic changes in iFR and FFR were studied in relation to changes in LVEDP using Pearson’s correlation analysis and linear regression analysis. Results The mean LVEDP was lowered from 16.20 ± 1.54 mmHg to 9.50 ± 1.10 mmHg, the mean iFR and FFR got changed from 0.80 ± 0.12 to 0.76 ± 0.12 mmHg and 0.75 ± 0.09 to 0.72 ± 0.09 mmHg respectively. On Pearson’s correlation analysis, LVEDP change did not show statistically significant correlation (linear relationship) with iFR (p = 0.105, r2 = 0.373) and FFR (p = 0.227, r2 = 0.283) changes across the entire range of stenosis severity and in all vessels. Linear regression analysis did not state any independent correlation between LVEDP and iFR and FFR changes in the study group (p >0.05). The % R2 value for iFR and FFR (as a coefficient of determination) of the regression equation were 13.9% and 8%, which means only these percentages of the total variance in iFR and FFR change were explained by LVEDP changes respectively. There was no serious adverse event related to the procedure. Conclusion To the best of our knowledge, this is the first study comparing the effect of changes in LVEDP on both iFR and FFR simultaneously. In our study, 1 mmHg change in LVEDP was associated with a change in FFR by 0.004 and change in iFR by 0.004 which didn’t reveal any significant association (p = 0.227 and 0.105 respectively). This helps us to put FFR at par with iFR under variable hemodynamics. So either of the variables may be used interchangeably with confidence in varied hemodynamic conditions including patients with heart failure. The correlation was non-significant across entire range of stenosis severity, irrespective of sex, age, diabetes and hypertension. This study sets platform for further research with larger number of heterogeneous patient population. Abstract Figure. Box whisker plot

Diagnostic usefulness of passive leg raising test for detection of heart failure with preserved ejection fraction compared to cycle ergometer exercise (invasive hemodynamic study)

Abstract Background Invasive diastolic stress test using cycle ergometer is gold standard for diagnosis of heart failure with preserved ejection fraction (HFpEF) by demonstrating elevation of left ventricular end diastolic pressure (LVEDP) during exercise. It is well known that passive leg raising increases preload and augments LVEDP in HFpEF patients. However correlation between passive leg raising induced increase of LVEDP and cycle ergometer exercise induced increase of LVEDP is not well established. Therefore we investigated whether passive leg raising test could substitute cycle exercise test for diagnosis of HFpEF. Method Forty-five patients with unexplained dyspnea and ejection fraction >50% underwent invasive exercise test. After measuring baseline LVEDP in supine position using pigtail catheter through radial artery approach, LVEDP during passive leg raising was evaluated. Then exercise LVEDP was measured after 3 minutes of 20 watt supine cycle ergometer exercise. Patients with normal resting LVEDP <16mmHg were enrolled. Patients with cycle ergometer exercise LVEDP >26mmHg were classified as HFpEF and exercise LVEDP <26mmHg were defined as noncardiac dyspnea. Results Among 45 patients with unexplained dyspnea with preserved EF, 30 patients with ergometer exercise LVEDP >26mmHg were grouped as HFpEF and 15 patients with exercise LVEDP <26mmHg grouped as noncardiac dyspnea (NCD). Resting LVEDP was higher in HFpEF than NCD (14±2mmHg vs 11±3mmHg, P=0.01) but there was substantial overlap (figure 1) showing poor differentiation power of resting LVEDP. Passive leg raising increased LVEDP in both HFpEF and NCD but this was more marked in HFpEF group than in NCD group with minimal overlap (24±4mmHg vs 17±2mmHg, P<0.001) (figure 2). Passive leg raising LVEDP was well correlated with cycle ergometer exercise LVEDP (R2=0.60, P<0.01). The best cutoff value for passive leg raising LVEDP to detect HFpEF was 20mmHg (sensitivity, 0.87; specificity, 1.00), giving an area under the curve of 0.93 (95% confidence interval, 0.80 to 0.99). Positive predictive value of passive leg raising LVEDP >20mmHg for diagnosis of HFpEF was 96% and negative predictive value was 77%. Conclusion Passive leg raising induced augmentation of left ventricular end diastolic pressure (LVEDP) was well correlated with cycle exercise induced elevation of LVEDP in HFpEF patients. Passive leg raising test may be used for detecting HFpEF with good accuracy in substitution for cycle ergometer exercise test. Funding Acknowledgement Type of funding source: None

Temporary balloon occlusion of atrial septal defects in suspected or documented left ventricular diastolic dysfunction: Hemodynamic and clinical findings.

To review our experience with balloon testing prior to atrial septal defect (ASD) closure in adults with left ventricular (LV) diastolic dysfunction. ASD closure in patients with LV diastolic dysfunction may precipitate LV failure. Temporary ASD occlusion has been used in this scenario but data are limited. Retrospective review of 27 patients age ≥ 50 years undergoing temporary ASD balloon occlusion between 2000 and 2018 for suspected LV diastolic dysfunction or elevated LV end-diastolic pressure (LVEDP). Median age was 72 years (IQR 66.7; 75.2). Atrial fibrillation was seen in 58% of patients, hypertension in 58%, and coronary artery disease in 26%; 52% were females. Median ASD size was 13 mm (10; 18) and Qp/Qs 1.8 (1.6; 2.2). Median LVEDP was 14 mmHg (12; 22); pulmonary artery wedge pressure (PAWP) 12 mmHg (9; 16.5) and left atrial pressure (LAP) 13.5 mmHg (8; 16.3). After a median of 5 min (3; 10) of balloon occlusion, patients with baseline LVEDP ≥15 mmHg had more significant increases in LVEDP (9 [6; 12] vs. 2 mmHg [0.5; 5]; p = 0.03) and LAP/PAWP (10.5 [8.3; 16.3] vs. 1.5 mmHg [-1.5; 3]; p = 0.0003) than those with baseline LVEDP <15 mmHg. None of those with a baseline LVEDP <15 mmHg had a LAP/PAWP >15 mmHg during balloon testing compared to 92% of patients with a baseline LVEDP ≥15 mmHg. LVEDP might be used to predict LAP post-ASD closure. Comorbidities typically associated with LV diastolic dysfunction are common in these patients and should be considered in their management.

Left ventricular end diastolic pressure and contrast-induced acute kidney injury in patients with acute coronary syndrome undergoing percutaneous coronary intervention

Left ventricular end-diastolic pressure (LVEDP) reflects ventricular performance and volume status. We sought to analyze the relationship between LVEDP and the incidence of contrast-induced acute kidney injury (AKI) in patients with acute coronary syndrome undergoing percutaneous coronary intervention (PCI). Between January 2006 and December 2008, a total of 254 patients presenting with an acute coronary syndrome had the LVEDP assessed prior to the intervention. Contrast-induced AKI was defined as an increase in serum creatinine ≥25% from baseline or an absolute increase of >0.5 mg/dL from baseline. Patients were divided into three groups according to baseline LVEDP (<12 mmHg, 12-20 mmHg and > 20 mmHg). Baseline clinical, angiographic and procedural characteristics, as well as serum creatinine and estimated glomerular filtration rate (eGFR) at baseline and at 24, 48 and 72 h were retrospectively collected. Baseline clinical characteristics were similar in all three groups with the exception of lower left ventricular ejection fraction in patients with elevated LVEDP (p = 0.02). Among the 17 patients with an LVEDP < 12 mmHg, only one (5.9%) developed AKI; among the 82 patients with an LVEDP = 12-20 mmHg, 15 (18.3%) developed AKI; and among the 155 patients with an LVEDP > 20 mmHg, only 22 developed AKI (13.6%). There was no correlation between LVEDP and the change in GFR at 24 h and at 48 h. Further comparison between the group of patients that developed contrast induced AKI versus those that did not, showed a that there was a significantly lower baseline left ventricular ejection fraction (LVEF) among patients that developed contrast induced AKI compared to those that did not (41.4% vs. 48.3%, p = 0.045, respectively). In patients with acute coronary syndrome undergoing PCI, baseline LVEDP was not associated with contrast-induced AKI. However patients with reduced ejection fraction seemed to be at a higher risk of developing AKI. More studies are needed to assess the relationship between LVEDP, LVEF and the risk of developing contrast induced AKI.

Left ventricular end‐diastolic pressure as an independent predictor of outcome during balloon aortic valvuloplasty

In this study, we examined the predictive value of the left ventricular end-diastolic pressure (LVEDP) in patients undergoing balloon aortic valvuloplasty (BAV). The LVEDP is a useful indicator of hemodynamic status in patients with severe aortic stenosis. In BAV, decompensated heart failure is associated with worse outcomes. We identified all consecutive patients with severe symptomatic aortic stenosis who underwent retrograde BAV at the Massachusetts General Hospital from 2004 to 2008. Patients were stratified and compared according to their baseline LVEDP into ≤15 mm Hg, 16-20 mm Hg, 21-25 mm Hg, and ≥26 mm Hg. Procedural and in-hospital outcomes and adverse events were compared. Multivariate logistic regression was used for the adjusted analysis. A total of 111 patients with a mean age of 83±11 years underwent BAV. Of these, the LVEDP was ≤15 mm Hg in 29 (26%), 16-20 mm Hg in 41 (37%), 21-25 mm Hg in 16 (14%), and ≥26 mm Hg in 25 (23%) patients. Baseline characteristics were similar among the four groups. Noticeably, patients with high LVEDP levels had significantly higher rates of the combined endpoint of in-hospital death, myocardial infarction (MI), cardiopulmonary arrest, and tamponade was P = 0.02. Periprocedural MI was more common among those with higher LVEDP (16% vs. 2.3%; P = 0.04). Multivariate analysis revealed LVEDP (OR 1.08, for each mm Hg increase in pressure, 95 % CI 1.02-1.14), small LV chamber size, and New York Heart Association class as independent predictors of adverse outcomes. The LVEDP is an important independent predictor of poor in-hospital outcome during BAV. In these patients, the immediate hemodynamic status may be more important than the baseline left ventricular systolic function. Hemodynamic optimization before or during BAV should be considered and may be beneficial.

Hemodynamic effects of iodixanol and iohexol during ventriculography in patients with compromised left ventricular function

A crossover study was performed to compare the hemodynamic effects of the iso-osmolar contrast agent iodixanol (Visipaque®) 320 mg I/ml to those of the low-osmolar iohexol (Omnipaque®) 350 mg I/ml. The main hypothesis was that iodixanol and iohexol would affect left ventricular end-diastolic pressure (LVEDP) to different degrees. In 48 patients with reduced cardiac function (mean ejection fraction 33.4%), one ventricular injection was performed with each contrast medium. Ventricular, aortic and right atrial pressures and heart rate were measured continuously. Cardiac output (using Fick's principle) and systemic vascular resistance were calculated. LVEDP increased with both agents, but significantly less after iodixanol than after iohexol (P < 0.01), also in subgroups of patients in whom baseline LVEDP was severely increased and in whom 3-vessel disease was present. Immediate changes in variables reflecting vasodilatation were similar with both agents. In conclusion, both contrast agents influenced hemodynamics during ventriculography, but iodixanol had significantly less influence on LVEDP than did iohexol. Cathet. Cardiovasc. Intervent. 50:314–321, 2000. © 2000 Wiley-Liss, Inc.

Contraction-relaxation coupling and impaired left ventricular performance in coronary surgery patients.

Dependence of left ventricular (LV) relaxation on cardiac systolic load is a function of myocardial contractility. The authors hypothesized that, if a tight coupling would exist between LV contraction and relaxation, the changes in relaxation rate with an increase in cardiac systolic load would be related to the changes in LV contraction. Coronary surgery patients (n = 120) with preoperative ejection fraction >40% were included. High-fidelity LV pressure tracings (n = 120) and transgastric transesophageal echocardiographic data (n = 40) were obtained. Hearts were paced at a fixed rate of 90 beats/min. Effects on contraction were evaluated by analysis of changes in dP/dt(max) and stroke area. Effects on relaxation were assessed by analysis of R (slope of the relation between tau and end-systolic pressure). Correlations were calculated with linear regression analysis using Pearson's coefficient r. Baseline LV end-diastolic pressure was 10+/-3 mm Hg (mean +/- SD). During leg raising, systolic LV pressure increased from 93+/-9 to 107+/-11 mm Hg. The change in dP/dt(max) was variable and ranged from -181 to +254 mm Hg/s. A similar variability was observed with the changes in stroke area, which ranged from -2.0 to +5.5 cm2. Changes in dP/dt(max) and in stroke area were closely related to individual R values (r = 0.87, P<0.001; and r = 0.81, P<0.001, respectively) and to corresponding changes in LV end-diastolic pressure (r = 0.81, P< 0.001; and r = 0.74, P<0.001, respectively). A tight coupling was observed between contraction and relaxation. Leg raising identified patients who developed a load-dependent impairment of LV performance and increased load dependence of LV relaxation.

Peripheral circulatory control of cardiac output in diabetic rats

Diabetes is believed to be associated with impaired systolic and diastolic function of the heart; however, some investigators have found that diabetic rats have increased cardiac output. We investigated changes in the peripheral circulation that could account for an increased cardiac output in diabetic rats (n = 30), 4 wk after a single tail vein injection of streptozotocin (60 mg/kg), and age-matched control rats (n = 31). Compared with controls, diabetic rats exhibited decreased (P less than 0.05) mean arterial pressure, characteristic aortic impedence, and total peripheral resistance; however, cardiac index and stroke volume index were increased. Aortic compliance, mean circulatory filling pressure, central venous pressure, pressure gradient for venous return, and venous compliance were unchanged in the diabetic rats compared with control. Baseline left ventricular end-diastolic pressure and end-diastolic volume were increased in the diabetic rats. Following a volume load of 30 ml/kg, cardiac index and stroke volume index increased less in the diabetic than in the control rats (35 vs. 102% and 69 vs. 105%, respectively). Thus, even with impaired systolic function, cardiac output is increased or maintained in diabetic rats because of the combination of decreased afterload and maintenance of preload.

Preoperative and Intraoperative Predictors of Inotropic Support and Long-Term Outcome in Patients Having Coronary Artery Bypass Grafting

The prognostic value of preoperative symptoms, preoperative left ventricular function, and intraoperative factors as related to postoperative outcome in coronary artery bypass grafting is unclear. This study was performed to identify risk factors that could be used as markers to predict immediate and long-term outcome, knowledge of which might allow physicians to modify these factors to decrease the likelihood of an adverse outcome. We retrospectively evaluated preoperative factors (including age, sex, New York Heart Association [NYHA] classification of symptoms, ejection fraction [EF], wall motion abnormalities, baseline left ventricular end-diastolic pressure [LVEDP], postradiographic contrast injection LVEDP, change in LVEDP with contrast injection, cardiac enlargement, and collateral vessels) and intraoperative factors (duration of bypass and aortic cross-clamp time) in 128 patients. The need for inotropic drug support was used as a marker of immediate outcome. A 36-mo follow-up used death and the postoperative NYHA classification of symptoms as markers of long-term outcome. The various factors associated with the use of inotropes and immediate outcome were analyzed by logistic regression. The factors related to inotrope use (and presumed adverse short-term outcome) in order of decreasing significance were lower EF, older age, cardiac enlargement, female sex, and higher baseline and postcontrast LVEDP. Patients with EF greater than or equal to 55%, but also having wall motion abnormalities and LVEDP change greater than or equal to 10 mm Hg, and all patients with EF less than 55% were more likely to require inotropic drug stimulation after cardiopulmonary bypass. Neither the change in LVEDP nor the presence of wall motion abnormalities independently predicted the need for postoperative inotropic support.(ABSTRACT TRUNCATED AT 250 WORDS)

Systolic direct ventricular interaction affects left ventricular contraction and relaxation in the intact dog circulation.

Changes in right ventricular systolic function directly influence left ventricular systolic function. Most of our knowledge of this systolic direct ventricular interaction comes from studies of isolated hearts, which suggest that changes in right ventricular size only affect left ventricular systolic function at low pressures and volumes. However, almost nothing is known about systolic direct ventricular interaction in a heart functioning in situ as a part of the intact circulation. We used sudden constriction of the pulmonary artery to assess the immediate effect of a change in right ventricular pressure and contraction pattern on left ventricular contraction and relaxation on the beat following the pulmonary artery constriction in anesthetized open-chest dogs. By focusing on this first beat, we were able to avoid the confounding effect of series ventricular interaction, which changes left ventricular filling and, thus, indirectly influences left ventricular function. At baseline left ventricular end-diastolic pressure of 9.6 +/- 2.1 mm Hg (mean +/- SD), sudden pulmonary artery constriction increased left ventricular peak systolic pressure by 3 +/- 2 mm Hg (2% change), left ventricular stroke volume by 2 +/- 2 ml (8% change), and monoexponential time constant of left ventricular pressure fall during relaxation by 9 +/- 6 msec (22% change). This increased left ventricular relaxation time constant was associated with altered regional segment length changes in the posterior and anterior left ventricular free walls during relaxation. We conclude that systolic direct ventricular interaction affects left ventricular systolic function and relaxation under normal conditions in the intact circulation.