Decrease In Right Atrial Pressure Research Articles

Rivero-Carvallo Sign in Bioprosthetic Tricuspid Valve Stenosis

In a case with bioprosthetic tricuspid stenosis, simultaneous phonocardiogram and Doppler recordings revealed that the louder diastolic rumble in inspiration (Rivero-Carvallo sign) is related to increased tricuspid gradient caused by less prominent decrease of right atrial pressure compared with that of the right ventricle in inspiration caused by tricuspid stenosis. (Level of Difficulty: Intermediate.)

Haemodynamic effects of initial combination therapy in pulmonary arterial hypertension: a systematic review and meta-analysis.

BackgroundAlthough the initial use of combination treatment has been proven to be beneficial for patients’ clinical outcomes, there are scarce data on its haemodynamic effects. The objective of the present study was to evaluate the effect of an initial combination of pulmonary arterial hypertension (PAH)-targeted therapies on haemodynamic parameters in treatment-naïve PAH patients.MethodsA systematic search of PubMed, Cochrane Central Register of Controlled Trials and Web of Science was performed. We considered eligible studies with an intervention of initial PAH-targeted combination therapy in treatment-naïve PAH patients with or without monotherapy control. A random-effects meta-analysis was performed for the difference between baseline and follow-up in pulmonary vascular resistance (PVR) and other haemodynamic parameters.ResultsIn 880 patients receiving initial combination therapy PVR was reduced by −6.5 Wood Units (95% CI −7.4–−5.7 Wood Units) or by −52% (95% CI −56%–−48%, I2=0%) compared to baseline. Initial triple therapy including a parenteral prostanoid resulted in significantly greater PVR reduction (−67% versus −50% with all other combination therapies, p=0.01). The effect was more pronounced in younger patients (p=0.02). Compared to baseline, there was −12.2 mmHg (95% CI −14.0–−10.4 mmHg) decrease in mean pulmonary artery pressure, 0.9 L·min−1·m−2 (95% CI 0.8–1.1 L·min−1·m−2) increase in cardiac index, −3.2 mmHg (95% CI −4.1–−2.3 mmHg) decrease in right atrial pressure and 8.6% (95% CI 6.9–10.3%) increase in mixed venous oxygen saturation. In the controlled studies, initial combination therapy reduced PVR by −4.2 Wood Units (95% CI −6.1–−2.4 Wood Units) compared to monotherapy.ConclusionInitial combination therapy leads to remarkable haemodynamic amelioration. Parenteral prostanoids should be considered early, especially in more severely affected patients, to enable right ventricular reverse remodelling.

Inferior Vena Cava Diameter Measurement Provides Distinct and Complementary Information to Right Atrial Pressure in Acute Decompensated Heart Failure

Inferior vena cava (IVC) measurements correlate only modestly with right atrial pressure (RAP). Part of this inaccuracy is due to the high compliance of the venous system, where a large change in blood volume may result in only a small change in pressure. As such, the information provided by the IVC may be different rather than redundant. We analyzed patients in the ESCAPE (Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness) trial who had both pulmonary artery catheter and IVC measurements at baseline (n = 108). There was only a modest correlation between baseline RAP and IVC diameter (r = 0.41; P < 0.001). Hemoconcentration, defined as an increase in hemoglobin levels between admission and discharge, was correlated with decrease in IVC diameter (r = 0.35; P = 0.02) but not with a decrease in RAP (r = 0.01; P = 0.95). When patients had both IVC and RAP measurements that were below the median, survival rates were superior to the rates of those who had only 1 measurement below the median, and when both rates were above the median, patients fared the worst (P = 0.002). IVC and RAP have limited correlation with each another, and changes in intravascular volume appear to correlate better with IVC diameter rather than with RAP. Furthermore, complementary information is provided by pressure and volume assessments in acute decompensated heart failure.

Abstract 14595: The Clinical Impact of Portal Vein Pulsatility on the Prognosis of Hospitalized Acute Heart Failure Patients

Introduction: Heart failure (HF) especially right-heart failure causes hepatic portal system congestion. The Portal vein (PV) pulsatility can be influenced by right atrial pressure (RAP). However, the association between PV pulsatility and the condition of HF remains unclear. Hypothesis: In this study, we aim to evaluate usefulness of PV pulsatility as a prognostic marker as well as a therapeutic indicator for hospitalized acute HF patients. Methods: We enrolled 54 patients with acute HF and 17 patients without HF served as controls. PV flow velocity was measured by ultrasonography at admission and discharge phase. PV pulsatility ratio (PVPR) was calculated by dividing minimal velocity by peak velocity. The primary endpoint for prognostic analysis was cardiac death and unexpected re-hospitalization for recurrent HF. The observation period was one year from first hospitalization for HF. Results: On admission, PVPR was significantly higher in controls compared to acute HF patients (0.91±0.08 vs. 0.71±0.04, p&amp;lt0.01).PVPR did not change during the hospitalization in controls (admission 0.91±0.08 vs discharge 0.93±0.06, p=0.31). However, in acute HF patients, PVPR was significantly elevated after the improvement of HF (admission 0.71±0.04 vs discharge 0.82±0.02, p&amp;lt0.05) due to the increase in minimal velocity (admission 12.6±4.5 cm/s vs. discharge 14.6±4.6 cm/sec, p&amp;lt0.05), indicating the decrease in RAP. To elucidate the association between PVPR and primary endpoint, the patients were divided into three groups according to the tertile of PVPR at discharge (PVPR-Q1:0.92&amp;ltPVPR&amp;lt1, PVPR-Q2: 0.73&amp;ltPVPR&amp;lt0.92, PVPR-Q3:PVPR&amp;lt0.73). Kaplan-Meier analysis found that the patients with higher PV pulsatility at discharge had significantly higher event rate among the groups (Figure). Conclusions: PVPR at discharge would reflect the condition of HF. It also can be a novel prognostic marker for hospitalized acute HF patients.

FIRST ATRIAL SEPTOSTOMY IN THE PHILIPPINES FOR IDIOPATHIC PULMONARY HYPERTENSION

SESSION TITLE: Respiratory Care SESSION TYPE: Original Investigation Posters PRESENTED ON: 10/10/2018 01:00 PM - 02:00 PM PURPOSE: Despite significant advances in pharmacological treatments, PAH remains to be an incurable disease with high morbidity and mortality. Although specific pharmacotherapies have shifted the survival curves of patients and improved exercise endurance as well as quality of life, it is also true that these pharmacological interventions are not always accessible and perhaps most importantly, not all these patients respond similarly to these drugs. Furthermore, many patients will continue to deteriorate and will eventually require an additional, non pharmacologic intervention such as Atrial Septostomy. METHODS: This is a case of a 38 year old female, known case of idiopathic pulmonary arterial hypertension diagnosed in 2007 through Right Heart Catheterization. She is currently maintained on Sildenafil, Bosentan, Furosemide, Amiodarone and Warfarin. Despite compliance to medications patient remained to be in Functional Class IV with PAP of 125mmHg. Patient also had recurrent hospitalizations due to dyspnea, chest pain and grade 3 bipedal edema. Hence patient was offered Atrial Septostomy as a treatment option. RESULTS: Hemodynamics post procedure showed a significant decrease in right atrial pressure to 10mmHg from 15mmHg and an increase in the left atrial pressure of 10mmhg from 8mmHg. The final size of the defect was 10mm. 2D echocardiogram done one year post Atrial Septostomy showed a Pulmonary Artery Pressure of 75mmHG which was the lowest pressure recorded in the course of her disease. Her functional Class also improved to II from IV. CONCLUSIONS: PAH remains a severe, life limiting condition, despite the introduction of multiple PAH specific therapies. Atrial Septostomy can provide hemodynamic and functional improvements and possibly survival benefits despite being previously known as only palliative or bridge to more definitive treatment for PAH. However with recent studies showing improved survival rates in severe PAH refractory to medical therapy, atrial septostomy may be life saving in our setting where lung transplantation is still unavailable.This is the first successfully performed atrial septostomy in the Philippines as a therapeutic option for severe, refractory end stage Pulmonary Arterial Hypertension. Although there are several areas for further study, our current thought is that this procedure is underutilized, which is probably related to overestimation of its risks and underestimation of its benefits. CLINICAL IMPLICATIONS: In view of poor prognosis and limited therapeutic options in our country, Atrial Septostomy becomes an alternative treatment option to patients with Pulmonary Hypertension. DISCLOSURES: No relevant relationships by Gracielle May Mendoza-Yu, source=Web Response

Time courses of central hemodynamics during rapid changes in posture

Changes in posture cause blood volume redistribution, affecting cardiac filling and stroke volume (SV). We hypothesized that the time courses of ventricular filling would differ between the right and left ventricle during a rapid (2 s) tilt and that changes in right ventricular filling pressure would be more swift because of the direct coupling to the systemic circulation. We further hypothesized that the transient imbalance between right and left ventricular filling pressure would influence left ventricular SV changes. Right atrial pressure (RAP), pulmonary capillary wedge pressure (PCWP), left ventricular stroke volume, heart rate, and arterial pressure were recorded beat-by-beat during rapid tilts from supine to upright positions and back again, during rest and dynamic 100-W leg exercise. RAP changes had a faster time course than PCWP during down-tilts, both during rest and exercise (1 ± 1 vs. 6 ± 2 s and 2 ± 2 vs. 6 ± 2 s, respectively; P < 0.05). This discrepancy caused a transient decrease in the end-diastolic pressure difference between the right and left ventricle. The decreased pressure difference in diastole impeded left ventricular filling because of ventricular interdependence, causing SV to fall transiently. The mechanisms of ventricular interdependence were also involved in reverse during up-tilt, where SV was maintained for 2-3 s despite falling PCWP. Furthermore, the decrease in RAP during up-tilt in the resting condition was biphasic with an initial fast and a second slower component, which might suggest the effect of venous valves. This was not seen during dynamic leg exercise where blood pooling is prevented by the venous muscle pump.

A modified Glenn shunt reduces venous congestion during acute right ventricular failure due to pulmonary banding: a randomized experimental study

Right ventricular failure after left ventricular assist device implantation is a serious complication with high rates of mortality and morbidity. It has been demonstrated in experimental settings that volume exclusion of the right ventricle with a modified Glenn shunt can improve haemodynamics during ischaemic right ventricular failure. However, the concept of a modified Glenn shunt is dependent on a normal pulmonary vascular resistance, which can limit its use in some patients. The aim of this study was to explore the effects of volume exclusion with a modified Glenn shunt during right ventricular failure due to pulmonary banding, and to study the alterations in genetic expression in the right ventricle due to pressure and volume overload. Experimental right ventricular failure was induced in pigs (n = 11) through 2 h of pulmonary banding. The pigs were randomized to either treatment with a modified Glenn shunt and pulmonary banding (n = 6) or solely pulmonary banding (n = 5) as a control group. Haemodynamic measurements, blood samples and right ventricular biopsies for genetic analysis were sampled at baseline, at right ventricular failure (i.e. 2 h of pulmonary banding) and 1 h post-right ventricular failure in both groups. Right atrial pressure increased from 10 mmHg (9.0-12) to 18 mmHg (16-22) (P < 0.01) and the right ventricular pressure from 31 mmHg (26-35) to 57 mmHg (49-61) (P < 0.01) after pulmonary banding. Subsequent treatment with the modified Glenn shunt resulted in a decrease in right atrial pressure to 13 mmHg (11-14) (P = 0.03). In the control group, right atrial pressure was unchanged at 19 mmHg (16-20) (P = 0.18). At right heart failure, there was an up-regulation of genes associated with heart failure, inflammation, angiogenesis, negative regulation of cell death and proliferation. Volume exclusion with a modified Glenn shunt during right ventricular failure reduced venous congestion compared with the control group. The state of right heart failure was verified through genetic expressional changes.

Electrocardiographic Changes in Patients Responding to Treatment with Group I Pulmonary Arterial Hypertension

Various changes in conductivity as reflected in the electrocardiogram (ECG) have been associated with the onset and progression of pulmonary arterial hypertension (PAH). Little data exist as to whether the ECG can be used to identify patients responding to treatment. A retrospective chart review of patients diagnosed by right-sided cardiac catheterization as having group I PAH within the past 5 years was performed. A total of 121 patients were reviewed, of whom 36 were found to be responders to treatment and were included in our study. Patients were defined as responders by evidence of symptomatic improvement and decrease in right ventricular systolic pressure by at least 15%. Of 36 patients included, the majority were women (n = 26, 72%) with an average age of 59.6 years. Significant differences in right-sided heart pressures based on echocardiogram were noted between the pretreatment and posttreatment subsets, with a decrease in right atrial pressure from 12.7 to 7.6 mm Hg (P = 0.0035), right ventricular systolic pressure from 83.2 to 55.3 mm Hg (P < 0.0001), and estimated pulmonary arterial mean pressure from 53.8 to 38.9 mm Hg (P < 0.0001). Electrocardiographic parameters, including resting heart rate (80 vs 76 bpm; P = 0.3683), QRS duration (98 vs 99 msec; P = 0.8444), calculated QT interval (461 vs 454 msec; P = 0.4386), premature ventricular contractions (n = 0 vs 2; P = 0.1558), right axis deviation (n = 14 versus 14; P = 1.00), right bundle branch block (n = 13 vs 7; P = 0.1176), and various measurements of right ventricular hypertrophy showed no difference. Although the ECG may be useful in helping to evaluate the onset and progression of PAH, its utility is limited in assessing appropriate response to treatment in this patient population.

Fluid loss, venous congestion, and worsening renal function in acute decompensated heart failure

To investigate the relationship between decongestion, central venous pressure, and risk of worsening renal function (WRF) in patients with acute decompensated heart failure (ADHF). We studied 475 patients with ADHF, of whom 238 underwent right heart catheterization. Right atrial pressure (RAP) was measured at baseline and at 24 h. Net fluid loss was recorded in the first 24 h. WRF was defined as a >0.3 mg/dL increase in serum creatinine above baseline. WRF occurred in 84 catheterized patients (35.3%). There was a weak correlation between baseline RAP and baseline estimated glomerular filtration rate (r = -0.17, P = 0.009). The amount of fluid removed during the first 24 h did not correlate with the magnitude of RAP reduction (r = 0.06, P = 0.35). No association was observed between WRF and baseline RAP [odds ratio (OR) 1.06, 95% confidence interval (CI) 0.80-1.41, P = 0.68 per 6.6 mmHg] or the decrease in RAP (adjusted OR 1.13, 95% CI 0.85-1.49, P = 0.40 per 5.3 mmHg reduction in RAP). In contrast, smaller net fluid loss was strongly associated with increased WRF risk. Compared with the first net fluid loss tertile, the adjusted OR was 1.85 (95% CI 0.90-3.80, P = 0.10) and 2.58 (95% CI 1.27-5.25; P = 0.009) for the second and third tertile, respectively (P for trend <0.0001). Smaller early net fluid loss is associated with increased risk for WRF. RAP is not a reliable surrogate of the magnitude of decongestion and risk of WRF. Future research is necessary to determine if targeting congestion may help prevent WRF.

Infant Gasps 8 Minutes After Birth

Please read the following vignette and watch the video clip (Fig 1). Figure 1. A 32 2/7-weeks’-gestation male is born by emergent cesarean delivery secondary to suspected abruption. The infant is lifeless, without respirations or detectable heart rate, after birth. The Neonatal Resuscitation Program (NRP) is initiated and followed according to the algorithm. The infant is successfully intubated at 60 seconds after birth; chest compressions are initiated after establishing effective ventilation; an umbilical venous catheter is placed and 0.01 mg/kg of epinephrine is administered via the umbilical venous catheter; 10 mL/kg of normal saline is then infused over 5 minutes. The infant remains lifeless without a heartbeat. A second dose of UV epinephrine is administered 3 minutes after the first dose. The infant gasps for the first time 8 minutes after birth (depicted in video); the heart rate returns, but remains less than 60 beats per minute. The correct intervention at this time is which of the following? 1. Administer sodium bicarbonate 2 mEq/kg intravenously. 2. Continue positive pressure ventilation. 3. Extubate the infant. 4. Discontinue chest compressions. 5. Provide continuous positive airway pressure via the endotracheal tube. Correct Response B. Continue positive …

Understanding Guyton's venous return curves

Based on observations that as cardiac output (as determined by an artificial pump) was experimentally increased the right atrial pressure decreased, Arthur Guyton and coworkers proposed an interpretation that right atrial pressure represents a back pressure restricting venous return (equal to cardiac output in steady state). The idea that right atrial pressure is a back pressure limiting cardiac output and the associated idea that "venous recoil" does work to produce flow have confused physiologists and clinicians for decades because Guyton's interpretation interchanges independent and dependent variables. Here Guyton's model and data are reanalyzed to clarify the role of arterial and right atrial pressures and cardiac output and to clearly delineate that cardiac output is the independent (causal) variable in the experiments. Guyton's original mathematical model is used with his data to show that a simultaneous increase in arterial pressure and decrease in right atrial pressure with increasing cardiac output is due to a blood volume shift into the systemic arterial circulation from the systemic venous circulation. This is because Guyton's model assumes a constant blood volume in the systemic circulation. The increase in right atrial pressure observed when cardiac output decreases in a closed circulation with constant resistance and capacitance is due to the redistribution of blood volume and not because right atrial pressure limits venous return. Because Guyton's venous return curves have generated much confusion and little clarity, we suggest that the concept and previous interpretations of venous return be removed from educational materials.

Age-Related Decrease in Inferior Vena Cava Diameter Measured with Echocardiography

The diameter of the inferior vena cava (IVC) measured with echocardiography is clinically used as a parameter to estimate right atrial pressure, which reflects dehydration or overhydration. Because elderly patients fall easily into dehydration, normal values for IVC diameters in elderly patients may be helpful for geriatric medicine. However, normal values of IVC diameter in relation to age have not been investigated. The purpose of this study was to elucidate age-related changes in IVC diameter using echocardiography. Enrolled in the study were 200 patients (67 ± 15 yrs: range 17-94 yrs) with cardiovascular risk factors but no overt cardiac diseases. IVC diameters throughout the respiratory cycle were measured as maximum and minimum IVC diameters (IVC(max), IVC(min)) using M-mode echocardiography. To assess IVC collapsibility, the respirophasic variation of IVC diameter was calculated as (IVC(max) - IVC(min))/(IVC(max)) ×100. Maximum IVC diameter was decreased with advancing age (r = -0.221, p = 0.002). The respirophasic variation of the IVC diameter was increased with advancing age (r = 0.244, p = 0.001). Stepwise multiple regression analysis showed that age was an independent determinant for both maximum IVC diameter (ß coefficient = -0.249, p < 0.001) and respirophasic variation of the IVC diameter (ß coefficient = 0.268, p < 0.001). Age-related decrease in maximum IVC diameter and increase in the respirophasic IVC collapsibility may indicate the decrease in right atrial pressure in some elderly patients. Therefore, elderly patients with decreased maximum IVC and increased respirophasic IVC collapsibility may need prevention for dehydration.

Patent Foramen Ovale and Cryptogenic Stroke: To Close or Not to Close? Closure: What Else!

A 39-year-old mother of 2 teenage boys complained of severe migraine with aura for >10 years. Otherwise healthy, she suffered an ischemic stroke that rendered her permanently aphasic. Diagnostic evaluation revealed no evidence of atherosclerosis of the carotid arteries or plaques of the ascending aorta and the aortic arch. The ECG showed normal sinus rhythm, and the patient denied any history of palpitations or arrhythmias. Echocardiography documented normal ventricular function without wall motion abnormalities or evidence of thrombus and normal-appearing valves but a large patent foramen ovale (PFO). The most likely clinical diagnosis is stroke due to paradoxical embolism. The patient’s neurologist recommended PFO closure. However, guidelines regarding PFO closure from professional societies remain ambiguous because of insufficient evidence regarding therapeutic measures (Table 1).1,2 View this table: Table 1. Guidelines From Professional Societies 1,2 Response by Messe and Kasner p 1998 Stroke is the third leading cause of mortality and the most important cause of serious, long-term disability in developed countries.3 The presented case is testimony to the sad sequelae of stroke that may deprive someone permanently of speech, an emotional and mental tragedy. A classic etiology is not found in up to 40% of ischemic strokes despite an extensive diagnostic evaluation. This is referred to as cryptogenic stroke , a term that strangely ignores the role of the PFO.4 The foramen ovale is an opening in the atrial septum secundum, with the septum primum functioning as a 1-way valve allowing right-to-left shunt during in utero development. The postnatal decrease in right atrial pressure results first in functional followed by anatomic closure in the ensuing months. Autopsy studies show that fusion of the 2 septae fails to occur in ≈1 of 4 people.5 This is referred to as PFO and represents the most common congenital abnormality.6 Paradoxical …

Sympathetic Overactivity in Patients with Pulmonary Stenosis and Improvement after Percutaneous Balloon Valvuloplasty

Percutaneous balloon valvulotomy (PBV) is the procedure of choice for the treatment of valvular pulmonary stenosis (PS) with similar results comparable to surgical valvotomy but less invasive. Twenty-seven consecutive patients with PS being evaluated for PBV were enrolled in the study. Peak instantaneous transvalvular gradient, right ventricle (RV) diameter, mean atrial pressures, RV systolic pressure (RVSP), pro-brain natriuretic peptide (proBNP) levels significantly decreased immediately after PBV. Regarding heart rate variability (HRV) parameters, mean HR (heart rate), LF (low frequency) day and night, LF/HF day and night significantly decreased and standard deviation of all NN intervals (SDNN), root mean square of successive differences (RMSSD), P number of NN intervals that differed by more than 50 ms from adjacent interval divided by the total number of all NN intervals (PNN50), HF (High frequency) day and night significantly increased 1 day after PBV and these changes were shown to be preserved at the first month. The increase in SDNN was correlated with the decrease in right atrial pressure (RAP) (r =-0.5, P = 0.04); the increase in standard deviation of the 5-minute mean RR intervals (SDANN) was correlated with the decrease in proBNP (r =-0.4, P = 0.03). Sympathetic overactivity and increased proBNP levels were associated with the symptomatic status of patients with PS. Associated with a decrease in atrial pressures and proBNP levels, PBV yielded a decrease in adrenergic overactivity in the patients with PS.

An HDL‐mimetic peptide improves cardiac performance and lipoprotein profiles in septic rodents

Background: Cardiac failure is a common cause of death in septic patients, and elevating plasma HDL reduces sepsis complications.Objective: We tested the hypothesis that the apoA‐I mimetic peptide L‐4F improves cardiac function in rats undergoing cecal ligation and puncture (CLP).Methods: Male Sprague‐Dawley rats were randomized to undergo CLP or sham surgery. CLP rats were further subdivided to receive saline (n=11) or L‐4F (10mg/kg, n=12) by ip. injection 6 hours after sepsis induction. Sham‐operated rats received saline (n=8).Results: There was a significant decrease in right atrial pressure, left ventricular end‐diastolic volume, stroke volume and cardiac output 24hrs after CLP. L‐4F blunted changes in these parameters in CLP rats and improved ejection fraction. Lipoprotein profiles were altered by CLP surgery after 24 hrs. Total cholesterol (TC) was reduced from 96± 4 to 51± 4 mg/dl in CLP rats and was principally characterized by a reduction in HDL (80± 3 to 23± 3). L4F administration to CLP rats attenuated this shift in lipoproteins (TC: 67± 5/HDL: 43± 3).Conclusion: L‐4F treatment improved cardiac performance in CLP rats compared to saline‐treated controls. This was associated with an increase in HDL cholesterol and a decrease in plasma and cardiac cytokines. It is hypothesized that HDL reduces sepsis complications by neutralizing pathogens, such as endotoxin, in CLP rats. Supported by NIH DK070040.

Cardiovascular effects of enoximone in isoflurane anaesthetized ponies

ObjectiveEnoximone is a phosphodiesterase III inhibitor frequently used to improve cardiac output (CO) in man. As the use of enoximone has not been reported in horses, the effects of this inodilator were examined in isoflurane anaesthetized ponies. Study designProspective, randomised, experimental study.Animals Six healthy ponies, weighing 286 (212–367) ± 52 kg, aged 5.0 ± 1.6 years (4–6.5). MethodsAfter sedation with romifidine [80 μg kg−1 intravenously (IV)], general anaesthesia was induced with midazolam (0.06 mg kg−1 IV) and ketamine (2.2 mg kg−1 IV) and maintained with isoflurane in oxygen (Et Iso 1.7%). The ponies were ventilated to maintain eucapnia (PaCO2 4.66–6.00 kPa). Each pony was anaesthetized twice with an interval of 3 weeks; receiving enoximone 0.5 mg kg−1 IV (E) or saline (S) 90 minutes post-induction. Heart rate (HR), arterial (AP) and right atrial pressure (RAP) were measured before treatment, every 5 minutes between T0 (treatment) and T30 and then every 10 minutes until T120. Cardiac output measurements (lithium dilution technique) and blood gas analysis (arterial and central venous samples) were performed before T0 and at T5, T10, T20, T40, T60, T80, T100 and T120. Stroke volume (SV), systemic vascular resistance (SVR), venous admixture ( Q˙s/ Q˙t) and oxygen delivery ( D˙O2) were calculated. ResultsEnoximone induced significant increases in HR, CO, SV, Q˙s/ Q˙t and D˙O2 and a significant decrease in RAP. No significant differences were detected for AP, SVR and blood gases. No cardiac arrhythmias or other side effects were observed. Conclusions and Clinical relevanceThe present results suggest that in isoflurane anaesthetized ponies, enoximone has beneficial effects on CO and SV without producing significant changes in blood pressure. Despite an increase in Q˙s/ Q˙t, D˙O2 to the tissues was improved.

Atrial Septostomy Decreases Sympathetic Overactivity in Pulmonary Arterial Hypertension

We have reported previously that the sympathetic nervous system is activated in patients with pulmonary arterial hypertension (PAH), and that this is only partly explained by a decrease in arterial oxygenation. Possible causes for increased muscle sympathetic nerve activity (MSNA) in patients with PAH include right atrial distension and decreased cardiac output. Both may be improved by atrial septostomy, but this intervention also further decreases arterial oxygenation. In the present study, we wanted to investigate the effect of atrial septostomy on MSNA in patients with PAH. We recorded BP, heart rate (HR), arterial O2 saturation (SaO2), and MSNA before and after atrial septostomy in PAH patients (mean [+/- SE] age, 48 +/- 5 years) and in closely matched control subjects. Measurements were also performed after septostomy, while SaO2 was brought to the preprocedure level by supplemental O2 therapy. Compared to the control subjects (n = 10), the PAH patients (n = 11) had a lower mean BP (75 +/- 2 vs 96 +/- 3 mm Hg, respectively; p < 0.001), lower mean SaO2 (92 +/- 1% vs 97 +/- 0%, respectively; p < 0.001), increased mean HR (84 +/- 4 vs 68 +/- 3 beats/min; p < 0.01), and markedly increased mean MSNA (76 +/- 5 vs 29 +/- 2 bursts per minute; p < 0.001). Atrial septostomy decreased mean SaO2 (to 85 +/- 2%; p < 0.001) and mean MSNA (to 69 +/- 4 bursts per minute; p < 0.01), but did not affect HR or BP. Therapy with supplemental O2 did not affect MSNA, BP, or HR. The decrease in MSNA was correlated to the decrease in right atrial pressure (r = 0.62; p < 0.05). Atrial septostomy in PAH patients decreases sympathetic hyperactivity despite an associated decrease in arterial oxygenation, and this appears to be related to decreased right atrial distension.

Effects of an endothelin receptor antagonist and nitroglycerin on digital vascular function in horses during the prodromal stages of carbohydrate overload-induced laminitis

To evaluate changes in digital vascular function in horses with carbohydrate overload (CHO)-induced laminitis and determine the effects of an endothelin (ET) receptor antagonist and nitroglycerin on laminitis-associated vascular dysfunction. 20 adult horses without abnormalities of the digit. Hemodynamic variables were recorded before (baseline) and hourly after all horses were administered a CHO ration via nasogastric tube. In 4 groups of 5 horses each, saline (0.9% NaCl) solution or ET receptor antagonist (10(5)M in digital blood) was administered into the digital arterial circulation according to 1 of 2 schedules. During anesthesia, blood flow; arterial, venous, and capillary pressures; and total, precapillary, and postcapillary resistances were measured in an isolated perfused digit of each horse. In all groups, nitroglycerin was infused (10(5)M in digital blood), and digital microvascular assessments were repeated. The CHO caused a significant decrease in right atrial pressure by 14 hours that was not affected by administration of saline solution or ET receptor antagonist. In isolated digits of anesthetized horses, CHO resulted in a significant decrease in digital blood flow associated with a significant increase in total and postcapillary resistances. Treatment with the ET receptor antagonist and nitroglycerin caused a significant decrease in total resistance. Postcapillary resistance was significantly decreased following treatment with the ET receptor antagonist but was not altered by treatment with nitroglycerin. Treatment with an ET receptor antagonist and nitroglycerin resulted in significant improvement in vascular resistance in isolated perfused digits of anesthetized horses with CHO-induced laminitis.

Effects of ramipril on renal function during progressive overpacing-induced heart failure in dogs

To investigate the effects of preventive angiotensin converting enzyme inhibitor treatment with ramipril in dogs with progressively severe experimentally induced heart failure. 20 dogs. Dogs were randomly allocated to receive no treatment (control) or ramipril (0.125 mg/kg, PO, daily) for 7 weeks. Physical examination, repetitive catheterization of the right side of the heart, and echocardiography were performed before the study (day 0) and weekly for 7 weeks. Renal plasma flow (RPF) as determined by para-aminohippuric acid clearance and glomerular filtration rate (GFR) as determined by creatinine and iohexol clearances were measured on day 0 and at weeks 4 and 7. Overpacing induced a progressive increase in right atrial pressure (RAP) and pulmonary artery pressure, occluded (PAPO), with a decrease in systemic arterial pressure. There were progressive alterations of echocardiographic indices of diastolic and systolic ventricular function. The RPF and GFR decreased before cardiac output decreased, and filtration fraction increased. The logarithm of the urinary sodium-to-potassium concentration ratio (log(10)[Na(+)/K(+)]) decreased. Significant effects of ramipril included a delay in clinical signs of heart failure, a late decrease in RAP and PAPO, and increases in the sodium excretion fraction and log(10)(Na(+)/K(+)). There was a satisfactory agreement between the creatinine and iohexol clearance measurements. Results suggest that, in this rapid-evolving, dilated cardiomyopathy, activation of the renin-angiotensin system contributes to the pathophysiology of heart failure late in the disease and essentially by an activation of renal salt and water retention.

Direct myocardial effects of OPC-18790 in human heart failure: beneficial effects on contractile and diastolic function demonstrated by intracoronary infusion with pressure-volume analysis.

We sought to determine the precise myocardial effects of OPC-18790 as demonstrated by intracoronary administration. Although previous studies have determined the cardiovascular effects of a novel intravenous inotrope, OPC-18790, the observed benefits on contractile and diastolic function may have been confounded by the marked changes in peripheral loading associated with this drug when given intravenously. Eight heart failure patients received intracoronary OPC-18790 at 31.25 microg/min for 20 min, and then at 62.5 microg/min for another 20 min. Hemodynamic variables and pressure-volume indexes using the conductance catheter method were determined at baseline and then after the two doses. There were no significant effects on heart rate, cardiac output or loading conditions, including afterload as determined by systemic vascular resistance and arterial elastance (Ea) and preload as determined by end-diastolic volume (EDV). There were significant increases in end-systolic elastance (Ees) from 0.74+/-0.11 to 0.90+/-0.16 mm Hg/ml at 31.25 microg/min and to 137+/-0.33 mm Hg/ml at 62.5 microg/min (p < 0.05 by analysis of variance [ANOVA]). Diastolic function improved, as determined by the time constant for isovolumetric relaxation tau, which decreased significantly from baseline to 31.25 microg/min (94+/-9 to 79+/-9 ms, p < 0.05), and did not shorten further at 62.5 microg/min (78+/-8 ms, p=NS). There were significant decreases in right atrial pressure (9+/-1 to 7+/-1 mm Hg, p < 0.01 by ANOVA) and mean pulmonary artery wedge pressure (21+/-3 to 16+/-2 mm Hg, p < 0.05 by ANOVA). This fall in filling pressures was not accompanied by any change in EDV. Inspection of the diastolic portion of the pressure-volume curve confirmed a downward shift consistent with pericardial release in five of the eight patients. Intracoronary administration of OPC-18790 demonstrates that the direct myocardial effects of this agent include a modest increase in inotropy and improvement in diastolic function, both of which occur without increases in heart rate, indicating that this agent may be beneficial for the intravenous treatment of congestive heart failure.