Mean Right Ventricular Pressure Research Articles

Study of the JAK inhibitors antifibrotic activity for the prevention and treatment of chronic thromboembolic pulmonary hypertension

Introduction. Chronic thromboembolic pulmonary hypertension (CTEPH) is the most common complication of pulmonary thromboembolism (PE). Fibrous remodeling of the pulmonary circulation vessels against the background of CTEPH leads to an irreversible increase of the vessel wall stiffness and the ineffectiveness of CTEPH treatment. The involvement of Janus kinase (JAK) in the regulation of vascular wall and lung tissue inflammation and fibrosis allows for the possible effectiveness of JAK 1,2 inhibitors (iJAK) in the course of CTEPH. Purpose – to study the antifibrotic effect of iJAK for the prevention and treatment of CTEPH. Materials and methods. The study was conducted on male Wistar rats. Modeling of CTEPH was performed by sequential embolization of the vascular bed with partially biodegradable sodium alginate microspheres. 2 weeks after the last administration of the microspheres, low, medium and high doses of iJAK were initiated. To assess the effectiveness of the substance, the following tests were used: treadmill test, echocardiography, cardiac catheterization with right ventricular (RV) manometry, histological examination of the lungs. Results. Animals undergone vascular embolization demonstrated decreased exercise tolerance at all observation points compared to healthy animals. The placebo group, in contrast with the group getting treatment and iJAK, was found to have an increased mean RV pressure compared to healthy animals. There was an increase in mean RV pressure in the placebo group (15.5±7.7 mmHg) and in the low dose and iJAK group (13.4±6.4 mmHg) compared with healthy animals (9.4±2.2 mmHg). Vascular hypertrophy of the pulmonary artery branches was lower in group getting average dosages and iJAK compared with the placebo group (54.9±19.0 and 68.9±23.1 %, respectively). Thus, the suppression by iJAK of aseptic inflammation and following fibrosis leads to the decreasing of severity of pulmonary circulation remodeling in the experimental model of CTEPH. This approach can be used in the comprehensive bypass and prevention of CTEPH.

Prognostic relevance of the right ventricular myo-mechanical index (RV-MMI) in patients with precapillary pulmonary hypertension

ObjectiveThe aim of the prospective New-RV study was to evaluate a parameter for non-invasive quantification of right ventricular (RV) dysfunction in patients with precapillary pulmonary hypertension (PH) that yields prognostic...

Abstract 12945: A Novel Index for Quantification of Interventricular Septal Flattening in Pediatric Patients With Right Ventricular Hypertension

Introduction: Systolic flattening of the inter-ventricular septum (IVS) is a marker of elevated right ventricular pressure (RVp). It can be non-invasively quantified by a left ventricular eccentricity index (LVEI), RV to left ventricular (LV) ratio and a novel index - the systolic flattening angle (SFA). Data evaluating the relationship between these indices and invasive RVp in pediatrics are limited. Methods: Patients referred for right and left heart cardiac catheterizations (CC) were enrolled and underwent echocardiograms after induction of anesthesia. The SFA, RV:LV ratio and LVEI were measured in end-systole. Peak systolic RVp and aortic pressure (pAo) were measured simultaneously during CC. The likelihood of SFA to predict an RVp:pAo ratio of > 0.5 was assessed using receiver-operator curve (ROC) analysis. Bland-Altman plots were used to assess inter-observer agreement. Results: Forty-one unique subjects were enrolled [56% female, median age 2.7 years (0.7, 7.1) and median weight 12.1kg (6.0, 22.3)]. The median mid-ventricular (MV), apical, and sub-costal LVEI was 1.18 (0.9, 1.7), 1.18 (1.0, 1.7), and 1.13 (1.0, 1.5), respectively. The mean SFA was 8.5±9.6°, the median RV:LV ratio was 0.71 (0.46, 1.23), and the mean RVp:pAo ratio was 0.68 ± 0.5. There was a significant negative correlation (r = -0.75, p <0.001) between SFA and RVp:pAo ratio and a modest correlation with other non-invasive indices (Figure). ROC analysis demonstrated an area under the curve = 0.90 for prediction of RVp:pAo > 0.50 by SFA. An SFA < 10.6 had a sensitivity of 88% and specificity of 79% in predicting RVp:pAo > 0.50. SFA was modestly reproducible with a Bland-Altman plot demonstrating a bias of 4.14 and limits of agreement of -7.8 and 16.1. Conclusions: SFA has the best correlation with RVp:pAO, good sensitivity and specificity, but relatively high inter-observer variability. Taken together, these non-invasive measures may help minimize the need for invasive assessment of RVp.

Study of Cardiac Arrest Caused by Acute Pulmonary Thromboembolism and Thrombolytic Resuscitation in a Porcine Model.

Background:The success rate of resuscitation in cardiac arrest (CA) caused by pulmonary thromboembolism (PTE) is low. Furthermore, there are no large animal models that simulate clinical CA. The aim of this study was to establish a porcine CA model caused by PTE and to investigate the pathophysiology of CA and postresuscitation.Methods:This model was induced in castrated male pigs (30 ± 2 kg; n = 21) by injecting thrombi (10–15 ml) via the left external jugular vein. Computed tomographic pulmonary angiography (CTPA) was performed at baseline, CA, and return of spontaneous circulation (ROSC). After CTPA during CA, cardiopulmonary resuscitation (CPR) with thrombolysis (recombinant tissue plasminogen activator 50 mg) was initiated. Hemodynamic, respiratory, and blood gas data were monitored. Cardiac troponins T, cardiac troponin I, creatine kinase-MB, myoglobin, and brain natriuretic peptide (BNP) were measured by enzyme-linked immunosorbent assay. Data were compared between baseline and CA with paired-sample t-test and compared among different time points for survival animals with repeated measures analysis of variance.Results:Seventeen animals achieved CA after emboli injection, while four achieved CA after 5–8 ml more thrombi. Nine animals survived 6 h after CPR. CTPA showed obstruction of the pulmonary arteries. Mean aortic pressure data showed occurrence of CA caused by PTE (Z = −2.803, P = 0.002). The maximal rate of mean increase of left ventricular pressure (dp/dtmax) was statistically decreased (t = 6.315, P = 0.000, variation coefficient = 0.25), and end-tidal carbon dioxide partial pressure (PetCO2) decreased to the lowest value (t = 27.240, P = 0.000). After ROSC (n = 9), heart rate (HR) and mean right ventricular pressure (MRVP) remained different versus baseline until 2 h after ROSC (HR, P = 0.036; MRVP, P = 0.027). Myoglobin was statistically increased from CA to 1 h after ROSC (P = 0.036, 0.026, 0.009, respectively), and BNP was increased from 2 h to 6 h after ROSC (P = 0.012, 0.014, 0.039, respectively).Conclusions:We established a porcine model of CA caused by PTE. The dp/dtmax and PetCO2 may be important for the occurrence of CA, while MRVP may be more important in postresuscitation.

The effect of sildenafil on right ventricular remodeling in a rat model of monocrotaline-induced right ventricular failure.

PurposePulmonary arterial hypertension (PAH) leads to right ventricular failure (RVF) as well as an increase in pulmonary vascular resistance. Our purpose was to study the effect of sildenafil on right ventricular remodeling in a rat model of monocrotaline (MCT)-induced RVF.MethodsThe rats were distributed randomly into 3 groups. The control (C) group, the monocrotaline (M) group (MCT 60 mg/kg) and the sildenafil (S) group (MCT 60 mg/kg+ sildenafil 30 mg/kg/day for 28 days). Masson Trichrome staining was used for heart tissues. Western blot analysis and immunohistochemical staining were performed.ResultsThe mean right ventricular pressure (RVP) was significantly lower in the S group at weeks 1, 2, and 4. The number of intra-acinar arteries and the medial wall thickness of the pulmonary arterioles significantly lessened in the S group at week 4. The collagen content also decreased in heart tissues in the S group at week 4. Protein expression levels of B-cell lymphoma-2 (Bcl-2)-associated X, caspase-3, Bcl-2, interleukin (IL)-6, matrix metalloproteinase (MMP)-2, endothelial nitric oxide synthase (eNOS), endothelin (ET)-1 and ET receptor A (ERA) in lung tissues greatly decreased in the S group at week 4 according to immunohistochemical staining. According to Western blotting, protein expression levels of troponin I, brain natriuretic peptide, caspase-3, Bcl-2, tumor necrosis factor-α, IL-6, MMP-2, eNOS, ET-1, and ERA in heart tissues greatly diminished in the S group at week 4.ConclusionSildenafil alleviated right ventricular hypertrophy and mean RVP. These data suggest that sildenafil improves right ventricular function.

The Effect of Umbilical Cord Blood Derived Mesenchymal Stem Cells in Monocrotaline-induced Pulmonary Artery Hypertension Rats.

Pulmonary arterial hypertension (PAH) causes right ventricular failure due to a gradual increase in pulmonary vascular resistance. The purposes of this study were to confirm the engraftment of human umbilical cord blood-mesenchymal stem cells (hUCB-MSCs) placed in the correct place in the lung and research on changes of hemodynamics, pulmonary pathology, immunomodulation and several gene expressions in monocrotaline (MCT)-induced PAH rat models after hUCB-MSCs transfusion. The rats were grouped as follows: the control (C) group; the M group (MCT 60 mg/kg); the U group (hUCB-MSCs transfusion). They received transfusions via the external jugular vein a week after MCT injection. The mean right ventricular pressure (RVP) was significantly reduced in the U group after the 2 week. The indicators of RV hypertrophy were significantly reduced in the U group at week 4. Reduced medial wall thickness in the pulmonary arteriole was noted in the U group at week 4. Reduced number of intra-acinar muscular pulmonary arteries was observed in the U group after 2 week. Protein expressions such as endothelin (ET)-1, endothelin receptor A (ERA), endothelial nitric oxide synthase (eNOS) and matrix metalloproteinase (MMP)-2 significantly decreased at week 4. The decreased levels of ERA, eNOS and MMP-2 immunoreactivity were noted by immnohistochemical staining. After hUCB-MSCs were administered, there were the improvement of RVH and mean RVP. Reductions in several protein expressions and immunomodulation were also detected. It is suggested that hUCB-MSCs may be a promising therapeutic option for PAH.

Tanshinone IIA sulfonate upregulated pulmonary artery smooth muscle peroxisome proliferator-activated receptor γ expression in monocrotaline induced pulmonary hypertension rat

To investigate the effect of sodium tanshinone IIA sulfonate (STS) on rat right ventricular systolic pressure (RVSP), mean right ventricular pressure (MRVP), right ventricular hypertrophy index [RV/(LV+S)], pulmonary vascular remodeling, and PPARγ protein expression in pulmonary artery smooth muscle of monocrotaline (MCT) induced rat pulmonary hypertension model. The pulmonary hypertension model was established by subcutaneously injection of MCT, and the rats were treated with or without STS for 21 days. After that, RVSP, mRVP and RV/(LV+S) were measured. Lung histopathological sections were prepared, and the lumen area, the wall thickness and arterial radius of pulmonary arteries were quantified using the Image Pro Plus 6.0 software. PPARγ protein expression in rat pulmonary artery smooth muscle was detected by Western blot. Compared with control group, the RVSP, mRVP were significantly increased in MCT group (P < 0.05), while in the MCT+STS group, it was decreased from (81.2 ± 1.9) and (28.6 ± 2.0) mmHg to (35.4 ± 8.3) and (14.1 ± 5.4) mmHg, respectively (P < 0.05). The RV/(LV+S) of MCT group was (0.57 ± 0.04), markedly higher than those of control group and control+STS group (0.33 ± 0.02) and (0.34 ± 0.02) , respectively, P < 0.05, while in MCT+STS group, the RV/(LV+S) was (0.43 ± 0.02), lower than that of MCT group (P < 0.05) ;The luminal area/total area of MCT group decreased to (27 ± 6)%compared with control rats (56.00 ± 3.00) % (P < 0.05) . The wall thickness/artery radius (WT%) of MCT group increased from (20 ± 4) % (control group) to (40 ± 3) % (P < 0.05) .In MCT+STS treated rats, luminal area/ total area and WT% were (39.0 ± 2.0) %and (31.0 ± 2.0) %, both statistically different from MCT group (P < 0.05) . The level of PPARγ protein in pulmonary artery smooth muscle of MCT group was (48 ± 4) %, lower than control group (100 ± 0) % (P < 0.05) .In the MCT+STS group, PPARγ protein expression was recovered (102 ± 3) %, (P < 0.05) . STS markedly decreased RVSP,MRVP, RV/(LV+S) and pulmonary vascular remodeling in MCT induced pulmonary hypertension rat, and PPARγ might be targeted as a key molecule during STS treatment.

NFATc3 is required for chronic hypoxia‐induced pulmonary hypertension: role of BKα and β subunits

Chronic hypoxia (CH)‐induced pulmonary arterial remodeling and right ventricular (RV) hypertrophy require NFATc3 activation. Hence, we hypothesized that NFATc3 is also required for CH‐induced pulmonary hypertension. Mean RV pressure (MRVP mmHg) was measured in anesthetized wild type (WT) mice treated with cyclosporine A (CsA, 25 mg/Kg/day, NFAT inhibitor) or vehicle (V)‐containing food, and in NFATc3 heterozygote (HET) and knockout (KO) mice exposed to normoxia (N) or CH (380 mmHg; 21 days). CsA significantly attenuated CH‐induced increases in MRVP.CH increased MRVP in WT and HET but not in KO mice (NWT: 11.8±2.3; NHET: 10.4±1.8; NKO: 15.5±3.6; CHWT: 20.0±4.4*; CHHET: 16.1±4.7*; CHKO: 17.8±5.9; n=5‐10; *p&lt;0.05 vs. N).BK channels regulate membrane potential and contractility, and NFATc3 regulates its expression in smooth muscle. A reduction in BKα and/or ? expression in pulmonary arteries via NFATc3 could underlie the increased pressure. There was no change in BK ? expression. KO mice showed less BKα mRNA than WT in N. As expected, CH induced a decrease in BKα that was not different from CHKO. Consistently, NFAT activation induced an increase in BKα promoter activity in human PASM cells that was prevented by CsA. This response was lost in cells exposed to 2% O2 for 24 h but basal activity was reduced compared to N. These data demonstrate that NFATc3 is required for CH‐induced pulmonary hypertension and basal BKα mRNA expression. In addition, a reduction in BKα mRNA may be involved in the development of hypertension independently of NFATc3. 1R01HL088151‐01A1/NIH.

Right Ventricular Pressure Changes During Induced Ventricular Tachycardias Predict Clinical Symptoms of Cerebral Hypoperfusion: Implications for a Reduction of Unnecessary, Painful ICD Shocks

ICD shocks occurring in conscious patients (as in the case of well-tolerated arrhythmias, electromagnetic interference, or oversensing) have a deleterious impact on the quality of life. We evaluated if a hemodynamic parameter, calculated from the right ventricular pressure (RVP) or systemic arterial pressure (AP) signals, could predict early clinical symptoms of cerebral hypoperfusion during induced ventricular tachycardias (VTs). We analyzed 42 tolerated (no symptoms) and 30 untolerated (syncope or severe symptoms within 30 seconds from the onset) VTs, induced during electrophysiological study. The cycle length (CL) and the hemodynamic data (mean AP and RVP, arterial pulse pressure and RV pulse pressure, and maximum AP and RVP dP/dT) were automatically sampled in two VT epochs: the "detection" window, from beat 24 to 32, and the "preintervention" window, immediately before the first therapeutic attempt. Although the CL and all the hemodynamic parameters (expressed as % change versus pre-VT values) were significantly lower in untolerated versus tolerated VTs both at detection and preintervention (with the exception of the mean RVP which progressively increased in both groups), ROC analysis demonstrated that only the preintervention RV pulse pressure showed no overlap between groups, providing 100% sensitivity and positive predictive value. The reduction of the RV pulse pressure is a better predictor of early cerebral symptoms than CL or other hemodynamic indexes during induced VTs. Since long-term RVP monitoring is feasible, this parameter could be incorporated into ICDs decisional path, in the perspective of reducing unnecessary, painful shocks.

Right ventricular contractility in systemic sclerosis-associated and idiopathic pulmonary arterial hypertension

Since systemic sclerosis (SSc) also involves the heart, the aim of the present study was to evaluate possible differences in right ventricular (RV) pump function between SSc-associated pulmonary arterial hypertension (PAH; SScPAH) and idiopathic PAH (IPAH). In 13 limited cutaneous SScPAH and 17 IPAH patients, RV pump function was described using the pump function graph, which relates mean RV pressure ((RV)) and stroke volume index (SVI). Differences in pump function result in shift or rotation of the pump function graph. (RV) and SVI were measured using standard catheterisation. The hypothetical isovolumic (RV) ((RV,iso)) was estimated using a single-beat method. The pump function graph was approximated by a parabola: (RV) = (RV,iso)[1-(SVI/SVI(max))(2)], where SVI(max )is the hypothetical maximal SVI at zero (RV), enabling calculation of SVI(max). There were no differences in SVI and SVI(max). Both (RV) and (RV,iso) were significantly lower in SScPAH than in IPAH ((RV) 30.7+/-8.5 versus 41.2+/-9.4 mmHg; (RV,iso) 43.1+/-12.4 versus 53.5+/-10.0 mmHg). Since higher pressures were found at similar SVI, the difference in the pump function graph results from lower contractility in SScPAH than in IPAH. Right ventricular contractility is lower in systemic sclerosis-associated pulmonary arterial hypertension than in idiopathic pulmonary arterial hypertension.

Assessment of right ventricular function during exercise with quantitative Doppler tissue imaging in children late after repair of tetralogy of Fallot

Doppler tissue imaging (DTI) has been developed to assess ventricular wall-motion velocity quantitatively for patients with various types of heart disease. This technique has a possibility of assessing right ventricular (RV) function reserve during exercise. To investigate RV function during exercise using DTI, 21 patients (9.3 ± 3.3 years) who had undergone operation for tetralogy of Fallot at 1 to 3 years of age and 19 age-matched healthy children were studied. Echocardiography combined with DTI was performed at rest and during supine bicycle submaximal exercise. DTI of tricuspid annulus movement during systole (Sa) was obtained from a 4-chamber view. RV pressure was estimated by maximal tricuspid regurgitation (TR) velocity. The peak value of the first derivation of RV pressure (peak dP/dt) was measured from the continuous wave Doppler-derived TR profile. Adequate spectral Doppler recordings of TR were obtained in all participants. However, 9 healthy children and 2 patients with tetralogy of Fallot were excluded from the study because of an inability to determine the entire spectral TR velocity envelope during exercise. Therefore, data were analyzed in 29 participants. At rest, the mean RV pressure for patients was higher than that in control subjects (27 ± 4 vs 18 ± 3 mm Hg, P < .01). The mean Sa and RV peak dP/dt for patients were lower than those in control subjects (6.7 ± 1.6 vs 8.8 ± 1.7 cm/s and 464 ± 77 vs 550 ± 80 mm Hg/s, P < .01, respectively). Sa and RV peak dP/dt in the two groups increased significantly during exercise. However, the magnitude of increases in Sa and peak dP/dt was significantly less for patients than in control subjects (37 ± 16 vs 66 ± 19% and 42 ± 10 vs 80 ± 13%, P < .01, respectively). The magnitude of increase in Sa correlated with that in RV peak dP/dt ( r = 0.84, P < .01). Results of DTI show high correlation with RV peak dP/dt during exercise. This technique has a potential as a useful indicator of the effect of exercise on RV systolic function. An insufficient increase in Sa suggests impaired response to exercise of RV in patients with tetralogy of Fallot.

Right Ventricular Stiffness Measured by a New Method Without Volume Estimation in Coronary Artery Disease

This study was designed to measure the right ventricular (RV) stiffness (ΔP/ΔV) with a new method without estimating the RV volume itself. RV stiffness has rarely been measured due to the difficulty in estimating the RV volume. Without measuring RV volume itself, stiffness can be determined by measuring its volume change (ΔV). Tricuspid filling flow volume, which is the diastolic RV ΔV, is measurable by using Doppler echocardiography. Thus, RV stiffness may possibly be obtained from Doppler echocardiography combined with high-fidelity RV pressure. Subjects consisted of 8 controls, 8 patients with angina pectoris, 8 with anterior, 8 with posterior, and 8 with inferior prior myocardial infarction. Tricuspid annular dimension was measured by 2-dimensional echocardiography and the tricuspid annular area was calculated. Velocity-time integral of the tricuspid filling flow during the late diastole was measured by pulsed Doppler echocardiography. Then, the late diastolic RV ΔV was obtained as the product of the tricuspid annular area and the integral. The late diastolic RV pressure rise (ΔP) was also measured with a micromanometer catheter. The RV elastic chamber stiffness constant ([ΔP/ΔV]/P) was obtained by dividing simple stiffness by the mean RV pressure during late diastole. The RV elastic chamber stiffness constant did not significantly differ among controls, patients with angina pectoris, and those with anterior and posterior myocardial infarction (0.0054 ± 0.0009 vs 0.0057 ± 0.0018 vs 0.0064 ± 0.002 vs 0.0052 ± 0.0019 ml −1). However, it was significantly increased in patients with inferior myocardial infarction (0.010 ± 0.004 ml −1, p <0.01 or 0.05) compared with those in the other 4 groups. These results suggest (1) that RV stiffness can be measured with a new method without RV volume estimation, and (2) that this new method is useful in evaluating RV diastolic pathophysiology in patients with coronary artery disease. (Am J Cardiol 1996;78:298–303)

Ventricle works as a converting organ of atrial blood flow: Physiological significance of mean ventricular pressure

The roles and characteristics of the ventricle were examined using mean ventricular pressure (MVP) in ventricular-vascular association. One hundred and two patients with congenital heart diseases who had undergone cardiac catheterization were studied. They were divided into five groups: Group 1, atrial septal defect without pulmonary hypertension (PH); Group 2, ventricular septal defect (VSD) without PH; Group 3, VSD with PH; Group 4, pulmonary valvular stenosis; and Group 5 as a control group. Then, we examined the relationships between mean pulmonary artery pressure (MPAP) and mean right ventricular pressure (MRVP), and also between mean systemic arterial pressure (MSAP) and mean left ventricular pressure (MLVP) among the five groups. Furthermore, we defined new indicators to express the ease of blood flow through each ventricle. They were referred to as a conductance of the right ventricle (CDR) and a conductance of the left ventricle (CDL), respectively. Then they were compared among the five groups. The values of MPAP/MRVP and MSAP/MLVP were kept constant to be about 1.3 and 1.7, respectively. Furthermore, CDR was different between each group according to the property of the pulmonary vascular bed, whereas CDL took almost the same value among the five groups. The ventricle works as a converter of atrial blood flow so that it can achieve efficient blood transport.

Postoperative assessment of porcine-valved right ventricular-pulmonary artery conduits

Insertion of extracardiac right ventricular (RV)-pulmonary artery (PA) conduits for repair of severe forms of RV-PA discontinuity has become a widely used technique. During a 10-year period, 76 patients had open heart repair with a porcine-valved RV-PA external conduit. The most common diagnoses were truncus arteriosus (15%) and pulmonary atresia with ventricular septal defect (15%). The patients were 18 days to 37 years old (median 7 years). The postoperative median follow-up period was 4 years. Four patients (8%) have been lost to follow-up. Nineteen patients (25%) died in the early postoperative period and there were 10 late deaths (13%). Calculated probability of survival was 66% at 8 years. Thirty-six patients have undergone late hemodynamic studies. A residual shunt was present in 14% of the patients;moderate to severe PA hypertension was present in 25% and significant RV-PA gradients (> 30 mm Hg) in 50%. The mean RV pressure for the group was 78.5 ± 38 mm Hg. The severity of the gradients appeared to be greater in patients who had been followed longer. Ten patients have undergone reoperation because of conduit obstruction or residual shunting;6 are alive and well. Of the surviving patients, 95 % are acyanotic and without significant exercise intolerance and only 5 % have cardiovascular symptoms. Thus, open heart repair using an external RV-PA conduit provides a marked improvement in the quality of life in patients who survive.

The drop of residual right ventricular pressure 24 hours after conservative infundibulectomy in repair of tetralogy of Fallot

Because of late complications such as right ventricular (RV) dysfunction and sudden death after tetralogy repair, a modification in the technique of total repair of tetralogy of Fallot is sought. In this study a shorter than usual conal incision and limited division of only the parietal muscle bands were utilized in 17 patients. The mean RV pressure at the end of the operation was 84 mm Hg; 24 hours later it had dropped to 55 mm Hg. The mean RV/LV pressure ratio at the end of the operation was 0.85, and 24 hours later it was 0.48. Pressure measurements were also taken at the end of the operation, at four predetermined points along the RV outflow tract. It was found that 40% of the average residual obstruction was located at the level of the infundibular ostium, 50% at the level of the conus, and 10% at the pulmonary valve. It is concluded that a 40% drop in the RV/LV pressure ratio can be anticipated to occur in less than 24 hours in cases in which (1) the contractility of the infundibular ostium and conus is preserved by conservative infundibulectomy and (2) there is a residual obstruction at a muscular level. This is on condition that the passage between the crista and the anterior conal wall is of adequate size.