Diastolic Intraventricular Pressure Research Articles

Relationship Between Left Ventricular Deformation and Early Diastolic Intraventricular Pressure Difference During Rest and Exercise

Objective: The aim of this study was to investigate the mechanism underlying the increase in intraventricular pressure difference (IVPD) during exercise. Background: Although left ventricular sucking force during early diastole plays an important role in exercise tolerance, the mechanism by which sucking force increases during exercise remains unclear. Methods: Twenty-two healthy men (age range, 22-37 years) underwent echocardiography at rest and while performing “supine bicycle” exercises that included four workload stages at 25 W, 50 W, 75 W, and 100 W. IVPD was calculated with a one-dimensional Euler equation using color Doppler M-mode data, and its relationship with ventricular wall motion patterns was assessed. Results: Peak IVPD observed at early diastole increased from 2.83± 0.65 mmHg at rest to 5.31± 0.78 mmHg at 100-W loading (p<0.001). Peak IVPD correlated positively with heart rate and cardiac output and negatively with isovolumic relaxation time and diastolic duration (p<0.001 for all). Only lengthening of circumferential strain during early diastole correlated with IVPD at rest (p=0.046). In all loading conditions, all deformation parameters except for left ventricular length strain significantly correlated with IVPD. Conclusions: IVPD plays an important role in generating diastolic sucking force to adjust to loading conditions during exercise. At rest, only circumferential dilatation generated a pressure gradient, but during exercise, torsional deformation also played an important role in causing IVPD. These results provide new insight into diastolic function during exercise.

Does the Intraventricular Pressure Gradient Increase following Acute High Intensity Interval Exercise in Heart Failure?

An increase in the diastolic intraventricular pressure gradient (IVPG) is an important mechanism that aids in left ventricular filling during exercise. Prior work has shown that individuals with severe heart failure have impairment in IVPG at peak exercise (Am J Physiol Heart Circ Physiol 2005; 289: H2081-H2088). We have previously shown in the present study cohort (J Appl Physiol 2011; 110: 398-406) that left ventricular peak twist reserve is blunted, but that left ventricular peak untwisting rate, due to an increase in peak basal rotation rate and not peak apical rotation rate, is enhanced following acute high intensity interval (HIT) exercise in patients with mild heart failure. It is unclear whether regional differences in rotational properties of the ventricle in heart failure (i.e., base versus apex) that we have observed affect the IVPG post-HIT. PURPOSE: To determine if the IVPG immediately following acute HIT would be increased despite impaired apical contribution to left ventricular untwisting. METHODS: Nine patients (49 ± 16 years; 6 male) with mild heart failure (NYHA Class I/II = 7/2; left ventricular ejection fraction = 36 ± 7%; peak VO2 = 27 ± 9 ml/kg/min) performed 1 session of HIT (4 × 4 min at 96 ± 10% peak heart rate with a 3 min recovery period between bouts). Cardiac MRI (1.5 T scanner) was performed at rest prior to HIT and 6 ± 2 min following HIT. Rotational mechanics and IVPG were analyzed using in-house techniques with custom software. Analyses were performed using 2-tailed paired t-testing with p<0.05 being significant. RESULTS: Our novel finding is that the IVPG from pre-HIT (1.8 ± 1.0 mmHg) to post-HIT (1.6 ± 0.7 mmHg) remained effectively unchanged (p>0.05), despite a significant 24% increase in untwisting rate (p<0.05) that was modulated primarily by an increase in peak basal and not peak apical rotation rate. CONCLUSION: The maintenance of, but not the increase in, IVPG may aid in diastolic filling following HIT in patients with mild heart failure. Impairment in apical rotational mechanics likely account for the poor IVPG reserve of the left ventricle in mild heart failure.

Salt Overload During Postnatal Period Promotes Neurogenic‐mediated Increase of Arterial Blood Pressure in Adult Rats

The present study evaluated the effects of salt (NaCl) overload during the postnatal phases on cardiovascular parameters, cardiac function and cardiovascular responses induced by MnPO blockade in adulthood. 21 days‐old male Wistar rats were maintained on 0.3 M NaCl solution and food for 60 days (experimental group; EG); the control group was maintained on tap water and food. Later, both groups were maintained on tap water and food for 15 days (recovery). After the recovery period, baseline mean arterial pressure (MAP) and heart rate (HR) were recorded in unanaesthetized rats. The EG presented increased MAP (118.3 ± 2.7 mmHg vs. 98.6 ± 2.6 mmHg) and HR (398.2 ± 7.5 bpm vs. 365.4 ± 12.2 bpm) when compared to control group. To evaluate the cardiac function, the isolated hearts were perfused using the Langendorff technique in constant flow; after the basal recording, the hearts were submitted to ischemia/reperfusion. The salt overload did not affect the cardiac function in basal conditions. However, during the reperfusion, the hearts from EG presented increased intraventricular diastolic pressure (20.5 ± 5.16 mmHg vs. 11.5 ± 1.6 mmHg) and increased duration of reperfusion arrhythmias (208.8 ± 32.9 s vs. 75.0 ± 7.8 s), when compared to control group. Muscimol nanoinjections into MnPO promoted a decrease of MAP in both control and experimental rats, however, the decrease was greater in the EG (‐23.68 ± 1.46 mmHg vs. ‐15.58 ± 1.57 mmHg). These results demonstrate that postnatal salt overload alters cardiovascular regulation in adulthood. However, other studies are required to clarify the mechanisms by which the changes occur.Sponsors: Fapeg, Capes, CnPq

Influence of anesthetic agent, depth of anesthesia and body temperature on cardiovascular functional parameters in the rat

Sedating animals is sometimes necessary in experimental research. This paper presents and discusses the influence of four of the most common anesthetic agents on cardiovascular parameters in rats. We also studied the influence of body temperature. Ten-week-old Sprague-Dawley rats were anesthetized with either isoflurane, pentobarbital, ketamine/xylazine or tiletamine/zolazepam (n = 12 in each group). A pressure-sensing catheter was placed in the right carotid artery for the continuous measurement of arterial pressure, and echocardiography was performed. Indices of cardiac function were significantly higher in the tiletamine/zolazepam rats compared with the other groups. Heart rate was highest but stroke volume lowest with pentobarbital. Left ventricular diastolic dimension was lower in the pentobarbital and tiletamine/zolazepam rats compared with the isoflurane or ketamine/xylazine rats. Intraventricular diastolic pressure was similar in all groups whereas intraventricular systolic pressure, as well as both systolic and diastolic aortic pressures, was significantly higher in the tiletamine/zolazepam rats compared with the other groups. No hemodynamic indices differed significantly among the isoflurane, pentobarbital and ketamine/xylazine rats. Lowering body temperature significantly reduced heart rate and cardiac output but had no apparent effect on hemodynamic parameters. In conclusion, although cardiac functional parameters differed between the different anesthetic agents in ways that could be of relevance to the researcher, they may all have a role in experimental cardiology. Importantly, tiletamine/zolazepam anesthesia resulted in significantly higher indices of cardiac function and elevated blood pressures compared with the other anesthetic agents, a finding that should be kept in mind when interpreting data obtained in rats sedated on this regimen.

Intraventricular pressure gradients: the often ignored question of how and why does the ventricle suck

Intraventricular pressure gradients: the often ignored question of how and why does the ventricle suck

Evaluation of LV Diastolic Function From Color M-Mode Echocardiography

this study evaluated early diastolic filling dynamics using a semiautomated objective analysis of filling velocities obtained from color M-mode echocardiography. diastolic function can be evaluated from color M-mode echocardiography by measuring the early diastolic flow propagation velocity (Vp) from the slope of a single linear approximation of an isovelocity contour. However, this method has limitations and may not accurately represent diastolic filling. we used a semiautomated objective analysis of color M-mode echocardiograms from a development cohort of 125 patients with varying diastolic function to quantify left ventricular filling velocities. Early diastolic filling was not accurately described with a single propagation velocity; instead, the rapid initial filling velocity abruptly decelerated to a slower terminal velocity. Then, we evaluated a new measure of diastolic function in a separate group of 160 patients. compared with normal filling, diastolic dysfunction with restricted filling had a lower initial velocity (53 ± 21 cm/s vs. 87 ± 29 cm/s, p < 0.001), and the deceleration point occurred closer to the mitral annulus (2.4 ± 0.6 cm vs. 3.1 ± 0.7 cm, p < 0.05). The product of the initial velocity and the distance to the deceleration point from the mitral annulus, indicating the strength of the early filling (Vs), was progressively reduced with diastolic dysfunction. In a separate validation cohort of 160 patients, Vs better recognized diastolic dysfunction (classified by reduced diastolic intraventricular pressure gradient, elevated pulmonary capillary wedge pressure, or elevated B-type natriuretic peptide) than Vp did. early diastolic flow propagation occurs with an initial rapid velocity that abruptly decelerates to a terminal velocity. With diastolic dysfunction, the initial velocity is slower and the deceleration point occurs closer to the mitral annulus than with normal filling. A new parameter that combines these 2 effects (Vs) provides a more accurate assessment of diastolic function than the conventional propagation velocity.

Comments on Point:Counterpoint: Left ventricular volume during diastasis is/is not the physiological in vivo equilibrium volume and is/is not related to diastolic suction

Comments on Point:Counterpoint: Left ventricular volume during diastasis is/is not the physiological in vivo equilibrium volume and is/is not related to diastolic suction

Echocardiographic Evaluation of Diastolic Function Can Be Used to Guide Clinical Care

For normal cardiac performance, the left ventricle (LV) must be able to eject an adequate stroke volume at arterial pressure (systolic function) and fill without requiring an elevated left atrial (LA) pressure (diastolic function). These systolic and diastolic functions must be adequate to meet the needs of the body both at rest and during stress. Response by Tschope and Paulus on p 809 Systolic function is conveniently (although not always accurately) measured as the ejection fraction (EF), calculated as stroke volume divided by end-diastolic volume.1 The LV EF is easily interpreted. The lower limit of normal is ≈50%. The lower the EF is, the greater the reduction in systolic function. Diastolic function has been more difficult to evaluate.2 Traditionally, invasive measures of LV diastolic pressure-volume relations and the rate of LV pressure fall during isovolumetric relaxation have been used. However, these methods are not practical for routine clinical use and do not adequately evaluate all aspects of diastolic filling.3 Comprehensive echocardiographic evaluation of the dynamics of LV filling using blood pool and tissue Doppler has now progressed so that it provides clinically important information that can be used to direct patient care. We present data that support the use of echocardiographic evaluation of diastolic function to recognize cardiac dysfunction in patients with heart failure, especially those with preserved EF; to guide the management of patients by identifying those with and without elevated left filling pressures regardless of underlying EF; and to determine prognosis in a wide variety of patient populations. Although the LV end-diastolic pressure-volume relation describes the passive properties of the LV, LV filling is not a passive or slow process.3 In fact, the peak flow rate across the mitral valve is equal to or greater than the peak flow rate across the aortic valve. …

Relationship Between Ventricular Contractility and Early Diastolic Intraventricular Pressure Gradients: A Diastolic Link to Systolic Function

Early diastolic intraventricular pressure gradient (IVPG), as derived by color M-mode echocardiography, has been proposed to correlate with left ventricular (LV) elastic recoil. However, any relationship to quantifiable indices of LV contractility is poorly defined. To relate IVPG with invasive and noninvasive indices of contractility, 6 closed-chest dogs each had a high-fidelity conductance catheter placed into the LV for continuous determination of end-diastolic pressures, volumes, +dP/dt(max), and the time constant of LV relaxation (tau) under baseline conditions and 4 different stages of beta-receptor modulation. At each stage, IVPGs were determined from color M-mode echocardiography images. Doppler-derived strain rate (epsilon') and myocardial systolic myocardial velocities (S(m)) were also measured. E(max) was obtained from the slope of the end-systolic pressure-volume relationship during caval occlusion. Results of contractility indices were compared to IVPG with regression analysis. IVPG ranged from 0.72 to 3.95 mm Hg whereas E(max) ranged from 0.66 to 14.9 mm Hg/mL and end-systolic volume ranged from 1.9 to 59.7 mL. IVPG correlated with epsilon' (r = 0.71), S(m) (r = 0.67), end-systolic volume (r = 0.53), and invasive indices (+dP/dt(max), r = 0.71, and E(max), r = 0.82). Early diastolic IVPGs are associated with LV contractility. These findings may explain the proposed mechanism in which potential energy stored during systole is released during diastole to provide for adequate ventricular filling, even under low filling pressures.

Role of Tissue Doppler and Color M‐Mode Imaging for Evaluation of Diastolic Function in Ambulatory Patients with LV Systolic Dysfunction

Tissue Doppler imaging (TDI) and color M-mode (CMM) indices provide assessment of left ventricular (LV) relaxation when combined with pulse-wave Doppler (PWD)-derived transmitral inflow, allows for estimation of LV filling pressures. However, use of these indices in patients with LV systolic dysfunction (LVSD) has not been well characterized. The study included 115 patients (age 58 +/- 11 years, 67% male) with LVSD (LV ejection fraction [LVEF] < 55%). Patients were grouped according to the diastolic LV filling pressure assessed by E/Em(septal) ratio as follows: 1) Normal (NFP), E/Em(septal) < 8; 2) Intermediate (IFP), E/Em(septal): 8-15; and 3) High (HFP), E/Em(septal) >15. Age-, gender-, and LVEF-adjusted analyses were performed. LV volumes and LVEF were significantly different between the groups (P < 0.01). PWD-derived E-wave velocity showed a significant stepwise increase across the three groups and the Em(septal) velocity demonstrated a stepwise decrease (P < 0.01 for both). CMM-derived diastolic intra-ventricular pressure gradient (IVPG) was significantly lower in the HFP compared to the other 2 groups (P < 0.01 for both); Vp was increased in the HFP compared to the other 2 groups (P < 0.01 for both), and Vp exhibited a U-shape relationship to LVEF. In patients with LVSD, abnormal LV relaxation is uniformly observed regardless of LV filling pressure. PWD-derived E-wave velocity and the TDI-derived Em velocity are important measurements to identify elevated LV filling pressures. CMM-derived Vp and IVPG were of limited incremental value for the evaluation of diastolic function in patients with LVSD.

Issue Highlights

HomeCirculationVol. 113, No. 21Issue Highlights Free AccessIn BriefPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessIn BriefPDF/EPUBIssue Highlights Originally published30 May 2006https://doi.org/10.1161/circ.113.21.2473Circulation. 2006;113:2473IMPACT OF TRANSFORMING GROWTH FACTOR-β1 ON ATRIOVENTRICULAR NODE CONDUCTION MODIFICATION BY INJECTED AUTOLOGOUS FIBROBLASTS IN THE CANINE HEART, by Bunch et al.Pharmacological treatment of atrial fibrillation using antiarrhythmic agents or ventricular rate control is challenging because of variable success and medication side effects. Catheter ablation also is not 100% successful and carries the risk of procedural complications. In this issue of Circulation, Bunch and colleagues describe a technique of percutaneously injecting cultured fibroblasts from skin biopsies to modulate atrioventricular (AV) nodal conduction and rate control in a canine model. Using electroanatomic mapping and intracardiac echocardiography to guide delivery, they injected fibroblasts (with or without transforming growth factor-β1) through a NOGA catheter at several AV nodal input regions. Regulation of AV nodal conduction and ventricular rate reduction during induced atrial fibrillation was observed and was more pronounced in dogs receiving transforming growth factor-β1–treated fibroblast injections. There were no major complications or long-term high-grade AV block. Local cell delivery may eventually be a potential therapeutic option, perhaps combined with medication and/or device therapy to modulate ventricular rate control during atrial arrhythmias. See p 2485 (and editorial on p 2474).ENHANCED VENTRICULAR UNTWISTING DURING EXERCISE: A MECHANISTIC MANIFESTATION OF ELASTIC RECOIL DESCRIBED BY DOPPLER TISSUE IMAGING, by Notomi et al.Classical concepts of myocardial function learned by all cardiologists center around pressure-volume relationships in the right and left ventricles. It is important to realize, however, that the sequence and pattern of contraction of the 2 ventricles is different: The right ventricle contracts more like a bellows, but the left ventricle undergoes a complex cycle of twisting and untwisting in systole and diastole. Notomi et al provide a detailed analysis of left ventricular (LV) untwisting both at rest and during exercise using Doppler tissue imaging. Although healthy volunteers enhance the rate of untwisting during exercise, thus increasing the diastolic intraventricular pressure gradient (facilitating LV “suction”), patients with hypertrophic cardiomyopathy have a blunted untwisting response to exercise. The new insights into the dynamic relationship between LV systolic and diastolic function described in this paper offer new tools for evaluating diastolic LV function in a variety of cardiovascular disease states and potentially monitoring the response to therapy. See p 2524.PERCUTANEOUS TREATMENT WITH DRUG-ELUTING STENT IMPLANTATION VERSUS BYPASS SURGERY FOR UNPROTECTED LEFT MAIN STENOSIS: A SINGLE-CENTER EXPERIENCE, by Chieffo et al.Coronary artery bypass grafting (CABG) is the preferred revascularization strategy for left main coronary artery (LMCA) disease. Improvements in results with percutaneous coronary intervention (PCI) with drug-eluting stents (DES) have led interventional cardiologists to perform unprotected LMCA procedures. Clinical trial evidence supporting such an approach is lacking, however. In this issue of Circulation, Chieffo et al report the single-center retrospective experience in patients with LMCA stenosis treated with PCI and DES (n=107) or CABG (n=142). At 1 year, there was no difference in the degree of protection against death, stroke, myocardial infarction, and revascularization between PCI with DES and CABG for LMCA disease. These results support the need for randomized trials with longer clinical follow-up to define optimal revascularization strategies for LMCA disease. See p 2542.Visit http://circ.ahajournals.org:Images in Cardiovascular MedicineUntreated 37-Year-Old Homozygous Familial Hypercholesterolemic Smoker. See p e777.Near Sudden Death From Cardiac Lipoma in an Adolescent. See p e778.Left Ventricular Pseudoaneurysm: A Late Complication of Low-Energy DC Ablation. See p e780. Download figureDownload PowerPointCorrespondenceSee p e782. Previous Back to top Next FiguresReferencesRelatedDetails May 30, 2006Vol 113, Issue 21 Advertisement Article InformationMetrics https://doi.org/10.1161/circ.113.21.2473 Originally publishedMay 30, 2006 PDF download Advertisement

Scaling of diastolic intraventricular pressure gradients is related to filling time duration

In early diastole, pressure is lower in the apex than in the base of the left ventricle (LV). This early intraventricular pressure difference (IVPD) facilitates LV filling. We assessed how LV diastolic IVPD and intraventricular pressure gradient (IVPG), defined as IVPD divided by length, scale to the heart size and other physiological variables. We studied 10 mice, 10 rats, 5 rabbits, 12 dogs, and 21 humans by echocardiography. Color Doppler M-mode data were postprocessed to reconstruct IVPD and IVPG. Normalized LV filling time was calculated by dividing filling time by RR interval. The relationship between IVPD, IVPG, normalized LV filling time, and LV end-diastolic volume (or mass) as fit to the general scaling equation Y = kM beta, where M is LV heart size parameter, Y is a dependent variable, k is a constant, and beta is the power of the scaling exponent. LV mass varied from 0.049 to 194 g, whereas end-diastolic volume varied from 0.011 to 149 ml. The beta values relating normalized LV filling time with LV mass and end-diastolic volume were 0.091 (SD 0.011) and 0.083 (SD 0.009), respectively (P < 0.0001 vs. 0 for both). The beta values relating IVPD with LV mass and end-diastolic volume were similarly significant at 0.271 (SD 0.039) and 0.243 (SD 0.0361), respectively (P < 0.0001 vs. 0 for both). Finally, beta values relating IVPG with LV mass and end-diastolic volume were -0.118 (SD 0.013) and -0.104 (SD 0.011), respectively (P < 0.0001 vs. 0 for both). As a result, there was an inverse relationship between IVPG and normalized LV filling time (r = -0.65, P < 0.001). We conclude that IVPD decrease, while IVPG increase with decreasing animal size. High IVPG in small mammals may be an adaptive mechanism to short filling times.

Relationship among diastolic intraventricular pressure gradients, relaxation, and preload: impact of age and fitness

Diastolic intraventricular pressure gradients (IVPGs) are a measure of the ability of the ventricle to facilitate its filling using diastolic suction. We assessed 15 healthy young but sedentary subjects, aged <50 yr (young subjects; age, 35 +/- 9 yr); 13 healthy but sedentary seniors, aged >65 yr with known reductions in ventricular compliance (elderly sedentary subjects; age, 70 +/- 4 yr); and 12 master athletes, aged >65 yr, previously shown to have preserved ventricular compliance (elderly fit subjects; age, 68 +/- 3 yr). Pulmonary capillary wedge pressure (PCWP) and echocardiography measurements were performed at baseline, during load manipulation by lower body negative pressure at -15 and -30 mmHg, and after saline infusion of 10 and 20 ml/kg (elderly) or 15 and 30 ml/kg (young). IVPGs were obtained from color M-mode Doppler echocardiograms. Baseline IVPGs were lower (1.2 +/- 0.4 vs. 2.4 +/- 0.7 mmHg, P < 0.0001), and the time constant of pressure decay (tau(0)) was longer (60 +/- 10 vs. 46 +/- 6 ms, P < 0.0001) in elderly sedentary than in young subjects, with no difference in PCWP. Although PCWP changes during load manipulations were similar (P = 0.70), IVPG changes were less prominent in elderly sedentary than in young subjects (P = 0.02). Changes in stroke volume and IVPGs during loading manipulations correlated (r = 0.96, P = 0.0002). PCWP and tau(0) were strong multivariate correlates of IVPGs (P < 0.001, for both). IVPG response to loading interventions in elderly sedentary and elderly fit subjects was similar (P = 0.33), despite known large differences in ventricular compliance. The ability to regulate IVPGs during changes in preload is impaired with aging. Preserving ventricular compliance during aging by lifelong exercise training does not prevent this impairment.

A Noninvasive Method for Assessing Impaired Diastolic Suction in Patients With Dilated Cardiomyopathy

Diastolic suction is a major determinant of early left ventricular filling in animal experiments. However, suction remains incompletely characterized in the clinical setting. First, we validated a method for measuring the spatio-temporal distributions of diastolic intraventricular pressure gradients and differences (DIVPDs) by digital processing color Doppler M-mode recordings. In 4 pigs, the error of peak DIVPD was 0.0+/-0.2 mm Hg (intraclass correlation coefficient, 0.95) compared with micromanometry. Forty patients with dilated cardiomyopathy (DCM) and 20 healthy volunteers were studied at baseline and during dobutamine infusion. A positive DIVPD (toward the apex) originated during isovolumic relaxation, reaching its peak shortly after mitral valve opening. Peak DIVPD was less than half in patients with DCM than in control subjects (1.2+/-0.6 versus 2.5+/-0.8 mm Hg, P<0.001). Dobutamine increased DIVPD in control subjects by 44% (P<0.001) but only by 23% in patients with DCM (P=NS). DIVPDs were the consequence of 2 opposite forces: a driving force caused by local acceleration, and a reversed (opposed to filling) convective force that lowered the total DIVPD by more than one third. In turn, local acceleration correlated with E-wave velocity and ejection fraction, whereas convective deceleration correlated with E-wave velocity and ventriculo:annular disproportion. Convective deceleration was highest among patients showing a restrictive filling pattern. Patients with DCM show an abnormally low diastolic suction and a blunted capacity to recruit suction with stress. By raising the ventriculo:annular disproportion, chamber remodeling proportionally increases convective deceleration and adversely affects left ventricular filling. These previously unreported mechanisms of diastolic dysfunction can be studied by using Doppler echocardiography.

Intraventricular Pressure Differences

Like all fluids, blood tends to flow from areas of high pressure to low pressure. This seemingly trite observation hides a great deal of sophisticated pathophysiology that we are only beginning to exploit diagnostically and potentially therapeutically. In this issue of Circulation , Yotti and colleagues have exploited a new noninvasive technique to measure the small pressure differences generated within the normal left ventricular outflow tract in systole, demonstrating the utility of such measurements in quantifying ventricular systolic function.1 Because the fluid dynamics concepts behind these methods remain obscure to many cardiologists, it is worth reviewing the theoretical underpinnings in the hope that they will be more widely applied on the basis of articles like those of Yotti et al and others. See p 1771 Cardiologists have become comfortable with the use of the Gorlin equation in the cardiac catheterization laboratory and the simplified Bernoulli equation in the echocardiography laboratory to characterize the severity of valvular stenosis. Both equations are based on the principle of conservation of energy, relating the pressure drop (potential energy) across the valve to the rise in velocity (kinetic energy) as blood rushes through it. Several special circumstances combine to make these simple equations particularly applicable to flow through a restrictive orifice, including lack of a significant friction factor (viscosity) and a lack of pressure recovery as the blood rushes out of the abrupt obstruction. One of the most important simplifications is the absence of a significant “inertial” component to flow through a restrictive orifice. That is, the amount of blood actually moving at high velocity is tiny compared with the volume of the overall column of blood in the left ventricular outflow tract. Thus, very little pressure is expended in getting that small mass moving, and all of the potential energy lost across the …

Relationship of diastolic intraventricular pressure gradients and aerobic capacity in patients with diastolic heart failure

We sought to elucidate the relationship between diastolic intraventricular pressure gradients (IVPG) and exercise tolerance in patients with heart failure using color M-mode Doppler. Diastolic dysfunction has been implicated as a cause of low aerobic potential in patients with heart failure. We previously validated a novel method to evaluate diastolic function that involves noninvasive measurement of IVPG using color M-mode Doppler data. Thirty-one patients with heart failure and 15 normal subjects were recruited. Echocardiograms were performed before and after metabolic treadmill stress testing. Color M-mode Doppler was used to determine the diastolic propagation velocity (Vp) and IVPG off-line. Resting diastolic function indexes including myocardial relaxation velocity, Vp, and E/Vp correlated well with VO2max (r = 0.8, 0.5, and -0.5, respectively, P < 0.001 for all). There was a statistically significant increase in Vp and IVPG in both groups after exercise, but the change in IVPG was higher in normal subjects compared with patients with heart failure (2.6 +/- 0.8 vs. 1.1 +/- 0.8 mmHg, P < 0.05). Increase in IVPG correlated with peak VO2max (r = 0.8, P < 0.001) and was the strongest predictor of exercise capacity. Myocardial relaxation is an important determinant of exercise aerobic capacity. In heart failure patients, impaired myocardial relaxation is associated with reduced diastolic suction force during exercise.

RV instantaneous intraventricular diastolic pressure and velocity distributions in normal and volume overload awake dog disease models.

Intraventricular diastolic right ventricular (RV) flow field dynamics were studied by functional imaging using three-dimensional (3D) real-time echocardiography with sonomicrometry and computational fluid dynamics in seven awake dogs at control with normal wall motion (NWM) and RV volume overload with diastolic paradoxical septal motion. Burgeoning flow cross section between inflow anulus and chamber walls induces a convective pressure rise, which represents a "convective deceleration load" (CDL). High spatiotemporal resolution dynamic pressure and velocity distributions of the intraventricular RV flow field revealed time-dependent, subtle interactions between intraventricular local acceleration and convective pressure gradients. During the E-wave upstroke, the total pressure gradient along intraventricular flow is the algebraic sum of a pressure decrease contributed by local acceleration and a pressure rise contributed by a convective deceleration that partially counterbalances the local acceleration gradient. This underlies the smallness of early diastolic intraventricular gradients. At peak volumetric inflow, local acceleration vanishes and the total adverse intraventricular gradient is convective. During the E-wave downstroke, the strongly adverse gradient embodies the streamwise pressure augmentations from both local and convective decelerations. It induces flow separation and large-scale vortical motions, stronger in NWM. Their dynamic corollaries on intraventricular pressure and velocity distributions were ascertained. In the NWM pattern, the strong ring-like vortex surrounding the central core encroaches on the area available for flow toward the apex. This results in higher linear velocities later in the downstroke of the E wave than at peak inflow rate. The augmentation of CDL by ventriculoannular disproportion may contribute to E wave and E-to-A ratio depression with chamber dilatation.

Mechanisms of diastolic intraventricular regional pressure differences and flow in the inflow and outflow tracts

ObjectivesWe sought to investigate the mechanisms of left ventricular (LV) intracavitary early diastolic flow during changes in contractility and loading. BackgroundThere is limited understanding of how intracavitary flow velocities relate to intraventricular driving pressures. MethodsIn 12 anesthetized dogs, we measured pressures in the left atrium (LA), LV at the mitral tip, apex, and subaortic region; intraventricular velocities by color M-mode Doppler echocardiography (CMD); and volume by sonomicrometry. We also investigated responses to isoprenaline, ischemic failure, and volume loading. ResultsDuring rapid, early filling, the mitral to apical pressure gradient (LVPmitral-apex) correlated with the peak mitral to apical velocity (r = 0.92). The LVPmitral-apex increased from 1.4 ± 0.6 (SD) to 3.2 ± 1.8 mm Hg during isoprenaline (p < 0.05) and decreased to 0.6 ± 0.5 during ischemic failure (p < 0.01). The pressure gradient correlated positively with the time constant of isovolumic relaxation (tau) (r = 0.82) and negatively with LV end-systolic volume (ESV) (r = −0.77). Volume loading increased LA pressure, tau, and ESV, but caused no significant change in LVPmitral-apex. At baseline and during isoprenaline, tau was shorter (p < 0.05) at the apex than at the base. When the mitral to apical gradient approached zero, filling velocities were directed toward the LV outflow tract, and a pressure gradient was established between the apex and subaortic region. ConclusionsChanges in LVPmitral-apex induced by inotropic stimuli, loading, and ischemia appeared to reflect dependency of the pressure gradient on the rate of relaxation, ESV, and LA pressure. Regional differences in the rate of relaxation may also contribute to intraventricular pressure gradients. These findings have implications for how to interpret intraventricular filling in a clinical context.

Relationship Between Early Diastolic Intraventricular Pressure Gradients, an Index of Elastic Recoil, and Improvements in Systolic and Diastolic Function

Background Early diastolic intraventricular pressure gradients (IVPGs) have been proposed to relate to left ventricular (LV) elastic recoil and early ventricular “suction.” Animal studies have demonstrated relationships between IVPGs and systolic and diastolic indices during acute ischemia. However, data on the effects of improvements in LV function in humans and the relationship to IVPGs are lacking. Methods and Results Eight patients undergoing CABG and/or infarct exclusion surgery had a triple-sensor high-fidelity catheter placed across the mitral valve intraoperatively for simultaneous recording of left atrial (LA), basal LV, and apical LV pressures. Hemodynamic data obtained before bypass were compared with those with similar LA pressures and heart rates obtained after bypass. From each LV waveform, the time constant of LV relaxation (τ), +dP/dt max , and −dP/dt max were determined. Transesophageal echocardiography was used to determined end-diastolic (EDV) and end-systolic (ESV) volumes and ejection fractions (EF). At similar LA pressures and heart rates, IVPG increased after bypass (before bypass 1.64±0.79 mm Hg; after bypass 2.67±1.25 mm Hg; P &lt;0.01). Significant improvements were observed in ESV, as well as in apical and basal +dP/dt max , −dP/dt max , and τ (each P &lt;0.05). Overall, IVPGs correlated inversely with both ESV (IVPG=−0.027[ESV]+3.46, r =−0.64) and EDV (IVPG=−0.027[EDV]+4.30, r =−0.70). Improvements in IVPGs correlated with improvements in apical τ (Δτ =5.93[ΔIVPG]+4.76, r =0.91) and basal τ (Δτ =2.41[ΔIVPG]+5.13, r =−0.67). Relative changes in IVPGs correlated with changes in ESV (ΔESV=−0.97[%ΔIVPG]+23.34, r =−0.79), EDV (ΔEDV=−1.16[%ΔIVPG]+34.92, r =−0.84), and EF (ΔEF=0.38[%ΔIVPG]−8.39, r =0.85). Conclusions Improvements in LV function also increase IVPGs. These changes in IVPGs, suggestive of increases in LV suction and elastic recoil, correlate directly with improvements in LV relaxation and ESV.

Estimation of diastolic intraventricular pressure gradients by Doppler M-mode echocardiography.

Previous studies have shown that small intraventricular pressure gradients (IVPG) are important for efficient filling of the left ventricle (LV) and as a sensitive marker for ischemia. Unfortunately, there has previously been no way of measuring these noninvasively, severely limiting their research and clinical utility. Color Doppler M-mode (CMM) echocardiography provides a spatiotemporal velocity distribution along the inflow tract throughout diastole, which we hypothesized would allow direct estimation of IVPG by using the Euler equation. Digital CMM images, obtained simultaneously with intracardiac pressure waveforms in six dogs, were processed by numerical differentiation for the Euler equation, then integrated to estimate IVPG and the total (left atrial to left ventricular apex) pressure drop. CMM-derived estimates agreed well with invasive measurements (IVPG: y = 0.87x + 0.22, r = 0.96, P < 0.001, standard error of the estimate = 0.35 mmHg). Quantitative processing of CMM data allows accurate estimation of IVPG and tracking of changes induced by beta-adrenergic stimulation. This novel approach provides unique information on LV filling dynamics in an entirely noninvasive way that has previously not been available for assessment of diastolic filling and function.