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PubMed1984

Comparison of the influence of acute transmural and nontransmural myocardial infarction on ventricular function.

In order to assess the relative impact on left and right ventricular function of nontransmural and transmural acute myocardial infarction (AMI), we performed radionuclide ventriculography in 86 patients (54 men and 32 women) within 16 hours after a first infarct. Nontransmural infarction was present in 19 patients (11 anterior and 8 inferior). Transmural infarction was found in 67 patients (30 anterior and 37 inferior). Left ventricular ejection fractions were higher (0.57 +/- .014 vs 0.46 +/- 0.14, p less than 0.005) and left ventricular end-systolic volume lower (29 +/- 11 vs 42 +/- 20 ml/m2, p = 0.013) in patients with nontransmural infarction compared to those with transmural infarction. Right ventricular ejection fraction also may have been different in the two groups (0.63 +/- 0.15 vs 0.55 +/- 0.13, p = 0.057). In patients with inferior infarction, left and right ventricular ejection fractions were similar in patients with nontransmural and transmural infarction (0.60 +/- 0.09 vs 0.55 +/- 0.10, p = 0.119 and 0.58 +/- 0.14 vs 0.51 +/- 12, p = 0.226). On the other hand, patients with anterior transmural infarction had lower left ventricular ejection fractions (0.36 +/- 0.12 vs 0.54 +/- 0.17, p = 0.003) but similar right ventricular ejection fractions (0.60 +/- 0.13 vs 0.66 +/- 0.14, p = 0.14) compared to those with nontransmural anterior infarction. In 29 additional patients with a history of previous infarction, no differences in any of the parameters studied were found between those with transmural and those with nontransmural infarcts.(ABSTRACT TRUNCATED AT 250 WORDS)

Electrocardiography↗
PubMed1986

Right and left ventricular performance in acute hypoxemic respiratory failure.

We examined biventricular performance on two occasions in 28 patients with acute hypoxemic respiratory failure (ARF), using a combination of invasively determined pressures and flows as well as radionuclide scintigraphy to measure the right and left ventricular ejection fractions (RVEF and LVEF, respectively). From the EF and concurrently measured thermodilution stroke volumes, we calculated right and left ventricular end-diastolic and end-systolic volume indices (EDVI and ESVI, respectively). Regression analysis demonstrated that changes (delta) in global right ventricular function (RVEF) were inversely correlated with concurrent changes in the mean pulmonary arterial pressure (MPAP): delta RVEF = 0.015-0.015 delta MPAP (r2 = 0.60; p less than .005), while an increase in right ventricular preload (RVEDVI) was positively correlated with changes in MPAP: delta RVEDVI = 2.68 +/- 6.27 delta MPAP (r2 = 0.46; p less than .005). Global left ventricular function (LVEF) was related to changes in systemic pressures as well as to right-sided events: delta LVEF = -0.01-0.0015(delta RVESVI) + 0.001(delta BP systolic)-0.42(CVP/RVEDVI) (r2 = 0.35; p less than .01). These data confirm the significant influence of right ventricular afterload on RVEF in ARF patients and an apparent interrelationship between altered right ventricular systolic function and global left ventricular performance.

Acute Disease↗
PubMed1999

Right ventricular dysfunction after cardiac transplantation: primarily related to status of donor heart.

BACKGROUND: It is unclear whether right ventricular dysfunction after transplantation is due to donor brain death-related myocardial injury or recipient pulmonary hypertension. METHODS: A canine donor model of brain death and a monocrotaline pyrrole-induced chronic pulmonary hypertension recipient model were established, and used for 30 orthotopic bicaval cardiac transplantations divided into three groups: Controls (group A, normal donor/recipient), group B (brain-dead donors/normal recipient), and group C (normal donor/recipients with pulmonary hypertension). Right ventricular function was measured before transplant and brain death, 4 hours after brain death, and after transplant (1 hour off bypass) by load-independent means plotting stroke work versus end-diastolic volume during caval occlusion. Right ventricular total power and pulmonary vascular impedance were determined by Fourier analysis. RESULTS: In comparison to the control group right ventricular preload-recruitable stroke work and total power decreased significantly after brain death and transplant in group B (from 22.7 x 10(3) erg (+/-1.2) at baseline to 15.6 x 10(3) (+/-0.9) after brain death and to 11.3 x 10(3) (+/-0.9) after transplant). In group C there was a significant increase in pulmonary artery pressure, impedance, right ventricular preload-recruitable stroke work, total power after transplant. CONCLUSIONS: Normal donor hearts adapt acutely to the recipient's elevated pulmonary vascular resistance by increasing right ventricular power output and contractility. Brain death caused significant right ventricular dysfunction and power loss, which further deteriorated after graft preservation and transplantation. The effects of donor brain death on myocardial function contribute to right ventricular dysfunction after cardiac transplantation.

Animals↗
PubMed1997

Doppler echocardiography in cardiac transplant patients: allograft rejection and its relationship to diastolic function.

Right ventricular endomyocardial biopsy has been the traditional gold standard for determining cardiac transplant rejection. Although endomyocardial biopsy has proved useful in guiding rejection therapy, this procedure is not without risk. The objective of the present study was to determine whether a noninvasive method for assessing cardiac diastolic function would be of value in predicting biopsy scores. Doppler echocardiographic indices of left ventricular function were compared with biopsy scores in 43 studies from 23 patients (age 50 +/- 8 years). The average time from transplant to echocardiographic study was 1.5 years. Standard clinical indices of diastolic function failed to predict biopsy results. The A-Ar interval, evaluated in 36 studies, was found to significantly decrease (p < 0.003) with increasing biopsy scores. Preliminary results suggest that this echocardiographic parameter may prove useful in predicting biopsy results.

Biopsy, Needle↗
PubMed2006

Results of staged palliation for hypoplastic left heart syndrome: a complete population-based series.

AIM: To study the outcome of staged palliation for classic hypoplastic left heart syndrome. METHODS: Retrospective chart review. Risk factors for mortality were analysed using Cox's proportional hazard regression modelling. RESULTS: From 1993 to 2004, 55 infants underwent Norwood stage I procedure at a median age of 8 d (range 1-19 d). Hospital survival was 39/55 (71%), and there were six late deaths (before stage II). Birthweight, circulatory arrest time and cardiopulmonary bypass time were independent risk factors for stage I hospital mortality (p=0.029, p=0.001 and p=0.003, respectively). Poor right ventricular function prior to stage I was a significant predictor for interstage mortality (p=0.02). Thirty-two patients underwent bidirectional cavopulmonary anastomosis, at a median age of 6.5 mo (range 2.0-9.5 mo), with seven late deaths. Two patients had a heart transplant after stage II. Total cavopulmonary connection (TCPC) was performed in 13 patients, at a median age of 33 mo (range 21-45 mo), without mortality. Kaplan-Meier survival was 58%, 52% and 45% at 6, 12 and 48 mo, respectively. CONCLUSION: Low birthweight, long time on circulatory arrest and cardiopulmonary bypass were risk factors for stage I mortality. Poor right ventricular function was detrimental to intermediate outcome.

Child, Preschool↗
PubMed1999

Right ventricular systolic function and ventricular interaction during acute embolisation of the left anterior descending coronary artery in sheep.

OBJECTIVE: Regional LV ischemia involving the septum affects LV systolic function and geometry. We investigated the effects of these changes on RV function and geometry. METHODS: In six closed-chest sheep end-systolic pressure-volume relationships (ESPVRs) were constructed from ventricular volumes, measured with magnetic resonance imaging (MRI) and matching intraventricular pressures, before and after selective embolisation of the left anterior descending coronary artery (LAD). The extent of myocardial ischemia was assessed post-mortem by coronary perfusion with Evans-Blue. Alterations in septal geometry were studied by measuring the curvature, segmental length and thickness of the septum in two midventricular (short-axis) MRI slices before and during ischemia. From these data, changes in LV and RV free wall segmental lengths were calculated. RESULTS: Selective embolisation of the LAD resulted in left ventricular ischemia (15 +/- 2.1% of the total LV) with 23% of the septum involved. Stroke volume did not change significantly, while LV systolic pressure decreased by 24 mmHg (p < 0.05). Although RV systolic function decreased to a significantly lesser extent than LV function (p < 0.01), systolic function of both ventricles diminished significantly as indicated by substantial rightward shifts of the ESPVRs: 121% for LV and 41% for RV (both p < 0.01). At mid-ventricular level and end-systole, the septum showed significant increases in its radius of curvature and segmental length (both p < 0.05), and a significant wall thinning (p < 0.01). Calculated end-systolic lengths of LV and RV free walls also increased, by 57 and 14% respectively. CONCLUSIONS: LAD embolisation not only results in a significantly diminished LV systolic function but also causes RV systolic function to decline significantly. Regional dysfunction by necessity entails global dysfunction as well. Analysis of ventricular geometry reveals that both the septum and the RV free wall increase their length, which plays an important role in the pathophysiology of diminished RV systolic function concomitant with reduced LV function.

Animals↗
PubMed2000

Patients with pulmonary fibrosis: cardiac function assessed with MR imaging.

PURPOSE: To detect abnormalities in cardiac function by using magnetic resonance (MR) imaging in patients with mild to moderate pulmonary fibrosis and to evaluate the relationship between pulmonary function and cardiac function. MATERIALS AND METHODS: Sixteen patients were compared with 16 sex- and age-matched healthy control subjects. Systolic function was assessed by using multisection multiphase cine MR imaging. Diastolic function was assessed with flow-sensitive MR imaging across the mitral and tricuspid valves. MR imaging results were compared with the severity of impairment in pulmonary function. RESULTS: Biventricular systolic function and left ventricular diastolic function were normal in patients, but right ventricular diastolic function was significantly impaired versus that of control subjects, with a ratio of peak flow during early diastolic (E) filling to peak flow during atrial contraction (A) of 0.85 +/- 0.40 versus 1.28 +/- 0.50 (P =.035). Biventricular E/A ratios were strongly correlated to age in patients and control subjects. The right ventricular E/A ratio in patients corresponded with values that are normally expected in people 20 years older. Diastolic left and right ventricular functions were significantly correlated with each other. There was no relationship between pulmonary function and cardiac function. CONCLUSION: Impairment of right ventricular diastolic function was found by using MR imaging in patients with mild to moderate pulmonary fibrosis, whereas left ventricular diastolic function and biventricular systolic function were preserved.

Adult↗
PubMed1994

Cardiopulmonary actions of intravenously administered enalaprilat in trauma patients.

OBJECTIVE: To determine the cardiopulmonary actions of the intravenous administration of the angiotensin-converting enzyme inhibitor enalaprilat in hypertensive trauma patients. DESIGN: Prospective, before/after trial. SETTING: Intensive care unit (ICU) of a university hospital. PATIENTS: Twenty critically injured and hypertensive ICU patients. All patients were receiving continuous sedation (fentanyl and midazolam) for at least 2 days before the injection of enalaprilat and had a mean arterial pressure (MAP) of > 95 mm Hg. "Responders" were defined as having a decrease in MAP of > 15% within 30 mins after enalaprilat injection. INTERVENTIONS: Intravenous administration of 0.06 mg/kg of the angiotensin-converting enzyme inhibitor enalaprilat. Repeated doses were given when no sufficient response (decrease of MAP of > 15% within 30 mins after injection) was seen ("nonresponders"). MEASUREMENTS: In addition to standard hemodynamic monitoring, right ventricular hemodynamics and oximetric variables were also documented. Measurements were carried out before enalaprilat injection (during hemodynamic steady state [baseline values]) and at 1, 5, 10, 20, 30, 60, and 120 mins after enalaprilat administration. MAIN RESULTS: MAP was successfully controlled in 17 of 20 patients (maximum decrease -27 mm Hg [-26%]). In the three other patients, even reinjection of enalaprilat (0.06 mg/kg) did not sufficiently reduce MAP. In the 17 responders, heart rate did not increase, whereas central venous pressure, pulmonary arterial pressure, and pulmonary artery occlusion pressure decreased significantly after intravenous administration of enalaprilat. Cardiac index changed only slightly (mean maximum +0.70 L/min/m2 [+18%]). Right ventricular ejection fraction increased from 36% to 45% (p < .05); right ventricular end-diastolic and end-systolic volume index decreased significantly. Both systemic and pulmonary vascular resistance indices decreased within the investigation period (-31% and -16%, respectively). Pao2/FIO2, intrapulmonary right-to-left shunting, and oxygen extraction ratio were not altered. Oxygen delivery index (+17%) and oxygen consumption index (+20%) increased during the investigation period (p < .04). CONCLUSIONS: The intravenous administration of enalaprilat successfully decreased blood pressure in most of our patients. Mechanisms other than the renin-angiotensin system also appear to be involved in hypertensive, critically ill patients. Pulmonary function was not altered; right ventricular function, and both oxygen consumption and oxygen delivery improved in the enalaprilat responder group. Thus, the availability of intravenous enalaprilat seems to enlarge our armamentarium for treating hypertension in the critically ill patient.

Acute Disease↗
PubMed2005

Hemodynamic assessment of critically ill patients using echocardiography Doppler.

PURPOSE OF REVIEW: The evaluation of hemodynamic status in critically ill patients is a leading recommended indication of transesophageal echocardiography in the intensive care unit. Advantages and diagnostic yield of transesophageal echocardiography in this setting are particularly relevant when considering limitations and questioned prognostic impact of pulmonary artery catheterization. RECENT FINDINGS: Recent clinical studies have been performed to validate and assess the value of transesophageal echocardiography in determining cardiac output, cardiac preload dependence, right ventricular function, and left ventricular filling pressure. In addition, diagnostic capacity and therapeutic impact of transesophageal echocardiography have been widely reported in various intensive care unit settings. SUMMARY: Transesophageal echocardiography appears well suited for the determination of cardiac index and to track its variations after therapeutic interventions. Although repeated measurements of left ventricular end-diastolic dimension allows to accurately track preload variations, a single determination is not reliable to predict fluid responsiveness in intensive care unit patients. Identification of preload dependence in hemodynamically unstable patients currently tends to rely mainly on dynamic parameters that use cardiopulmonary interactions under mechanical ventilation. Transesophageal echocardiography also allows to adequately assess right ventricular function and left ventricular filling pressure using combined Doppler modalities. Adequate education and training of intensivists and anesthesiologists is crucial to further develop the use of transesophageal echocardiography in the intensive care unit setting. Despite the absence of randomized controlled studies documenting transesophageal echocardiography benefits on patient outcome, present evidence and experience strongly recommend a larger use of echocardiography Doppler for a comprehensive functional hemodynamic assessment of critically ill patients with circulatory failure.

Blood Pressure↗
PubMed2007

Impaired NO-mediated vasodilation with increased superoxide but robust EDHF function in right ventricular arterial microvessels of pulmonary hypertensive rats.

Pulmonary hypertension (PH) causes right ventricular (RV) hypertrophy and, according to the extent of pressure overload, eventual heart failure. We tested the hypothesis that the mechanical stress in PH-RV impairs the vasoreactivity of the RV coronary microvessels of different sizes with increased superoxide levels. Five-week-old male Sprague-Dawley rats were injected with monocrotaline (n=126) to induce PH or with saline as controls (n=114). After 3 wk, coronary arterioles (diameter = 30-100 microm) and small arteries (diameter = 100-200 microm) in the RV were visualized using intravital videomicroscopy. We evaluated ACh-induced vasodilation alone, in the presence of N(omega)-nitro-L-arginine methyl ester (L-NAME), in the presence of tetraethylammonium (TEA) or catalase with or without L-NAME, and in the presence of SOD. The degree of suppression in vasodilation by L-NAME and TEA was used as indexes of the contributions of endothelial nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF), respectively. In PH rats, ACh-induced vasodilation was significantly attenuated in both arterioles and small arteries, especially in arterioles. This decreased vasodilation was largely attributable to reduced NO-mediated vasoreactivity, whereas the EDHF-mediated vasodilation was relatively robust. The suppressive effect on arteriolar vasodilation by catalase was similar to TEA in both groups. Superoxide, as measured by lucigenin chemiluminescence, was significantly elevated in the RV tissues in PH. SOD significantly ameliorated the impairment of ACh-induced vasodilation in PH. Robust EDHF function will play a protective role in preserving coronary microvascular homeostasis in the event of NO dysfunction with increased superoxide levels.

Acetylcholine↗
PubMed1992

Right ventricular assist devices and the surgical treatment of right ventricular failure.

Treatment of patients with severe right ventricular dysfunction follows a continuum of progressive therapies. If optimization of volume status and inotropic support do not adequately improve right ventricular function, higher levels of mechanical circulatory support are required. A right-sided intraaortic balloon pump has been helpful in such circumstances. The centrifugal pump and the artificial ventricle provide the most effective long-term circulatory support for patients with right ventricular or biventricular failure after cardiopulmonary bypass, myocardial infarctions, or as a bridge to cardiac transplantation. All of these support measures still carry a high morbidity and mortality. Survival in approximately one third of these high-risk patients can be expected with the use of right ventricular assist devices. Cardiopulmonary bypass has also been effective for circulatory support of patients with massive pulmonary emboli.

Cardiopulmonary Bypass↗
PubMed1996

Intracardiac echocardiography: in vitro and in vivo validation for right ventricular volume and function.

To determine the feasibility and accuracy of intracardiac ultrasonography (ICUS) for the measurement of right ventricular (RV) volumes and function, a 10 MHz ICUS catheter was used in an in vitro and in vivo model. In the in vitro study, 16 sheep hearts were imaged. Sequential cross-sectional images from RV apex to base were recorded during a calibrated pullback. Volumes were calculated by applying Simpson's algorithm. ICUS-obtained volumes correlated well with actual volumes (standard error of estimate [SEE] = 2.3 ml, r = 0.98). For the in vivo study, a beating-heart canine model was used (31 hemodynamic stages in six dogs). Actual volumes were measured by an intracavitary balloon connected to an external column. Sequential cross-sectional images were recorded during the ICUS catheter pullback from apex to base of the RV, and volumes calculated by Simpson's algorithm. Good correlations were observed between ICUS and actual values for diastolic (SEE = 4.1 ml, r = 0.97), systolic (SEE = 3.4 ml, r = 0.96), and ejection fraction (SEE = 3.1%, r = 0.87) values. This new technique can accurately quantitate RV volumes, can function both in vitro and in vivo, and has the potential for increasing applications to questions of clinical and research interest.

Algorithms↗
PubMed1998

Venous return and right ventricular diastolic function in ARED flow fetuses.

The absence or reversal of end-diastolic flow in the umbilical artery (UA) is widely accepted as an ominous sign of fetal compromise. However, in these high-risk pregnancies, the significance of sequentially appearing changes of the venous return is poorly established. Doppler blood flow waveforms were longitudinally assessed in the inferior vena cava (IVC), ductus venosus (DV), umbilical vein (UV) and tricuspid valve, along with the UA, middle cerebral artery and descending aorta. Thirty-two serial Doppler studies were performed in six fetuses with intrauterine growth-retardation (IUGR). In the cases of absent or reversed UA endodiastolic flow, changes in the venous return were found following the same sequence: presence of dicrote pulsations in the UV, increase of retrograde flow in the IVC and reduction or inversion of DV velocity during atrial contraction. Transtricuspid flow patterns changed from normal to a restrictive pattern of ventricular filling. There were two intrauterine deaths and one early neonatal death. Our preliminary results suggest that the evaluation of the venous compartment of hemodynamically disturbed preterms fetuses along with right ventricular filling appears to be a useful model for investigating the physiopathology of fetal deterioration and, therefore, may yield indirect discriminatory signs of severe compromise.

Adult↗
PubMed1996

Age related dilatation of the right ventricle in arrhythmogenic right ventricular dysplasia-cardiomyopathy.

'Progression' in typical arrhythmogenic right ventricular dysplasia cardiomyopathy could be mainly demonstrated in case reports and generally implies decreasing left ventricular function; systematic follow-up data are only available on clinical features such as recurrent arrhythmias, late potentials or left ventricular ejection fraction. Due to methodological problems, continuous data on structural and functional right ventricular performance are not available. In order to get some more information about basic mechanisms of possible progression in arrhythmogenic right ventricular dysplasia-cardiomyopathy, the age-dependency of right ventricular enddiastolic volume, right ventricular ejection fraction, number of bulges, left ventricular involvement and the form of tachycardias was analysed at a single examination after having made the diagnosis of arrhythmogenic right ventricular dysplasia-cardiomyopathy. In the whole cohort of patients (n = 66), age-dependency of right ventricular volume could be demonstrated using linear regression analysis, chi-square-test and paired t-test (P < 0.01); global right ventricular ejection fraction and the number of right ventricular bulges did not differ significantly in younger and older patients. The same was true for mild left ventricular impairment and sustained or non-sustained ventricular tachycardias, respectively. In a follow-up, two older patients developed dramatic left ventricular dilatation and reduction of left ventricular function requiring heart transplantation. A third older patient died from isolated right heart failure. Increasing age-related right ventricular dilatation is possibly a marker of disease progression as a basis for right heart failure. Dramatic left heart involvement seems to be an event with abrupt onset in most cases due to acute or chronic myocarditis.

Adolescent↗
PubMed2006

Right ventricular hypertrophy causes impairment of left ventricular diastolic function in the rat.

Right ventricular (RV) pressure overload causes right ventricular hypertrophy in several types of pulmonary and congenital heart diseases. The associated cardiac dysfunction has generally been attributed to alterations in RV function. However, due to global neurohormonal adaptations and mechanical ventricular interaction left ventricular (LV) function could be affected as well.Therefore,LV function, RV function and their interaction were studied in rats with monocrotaline (MCT)-induced RV hypertrophy and control rats. MCT (30 mg/kg) was used to induce pulmonary hypertension, which resulted, after 28 days, in marked RV hypertrophy (RV-weight: control 220 +/- 15,MCT 437 +/- 34mg,p < 0.05). In Langendorff-perfused hearts with balloons inserted in both the LV and the RV, the diastolic pressure-volume relations showed increased stiffness, and relaxation was prolonged in the LV and RV in the MCT group compared to controls. In the MCT group, developed pressures were increased only in the RV. An increase of LV volume increased RV diastolic pressure to a similar extent in both groups. However, an increase in RV volume did not affect LV diastolic pressure in controls, but significantly increased LV diastolic pressure in the MCT group. LV and RV developed pressure-volume relations were not affected. Calculated circumferential end-diastolic wall stresses (sigma) were larger in the MCT group (LV-sigma: 0.55 +/- 0.02, RV-sigma: 1.94 +/- 0.30 kN/m(2), both p< 0.05 to control) compared to controls (LV-sigma: 0.34 +/- 0.06,RV-sigma: 1.23 +/- 0.46 kN/m2). In the MCT group, collagen content was increased in the LV, septum and RV compared to controls. In conclusion, structural changes of the RV and LV result in depressed LV diastolic function during RV hypertrophy.

Animals↗
PubMedDate not supplied

Stress echocardiography for evaluation of hemodynamics: valvular heart disease, prosthetic valve function, and pulmonary hypertension.

A broad variety of diseases can affect dynamic cardiac function and contribute to exertional symptoms. Although hemodynamic data at rest may be sufficient to guide therapy in some patients with cardiovascular disease, medical and surgical decisions may be impacted by the cardiac response to stress and the ability to associate exertional symptoms with cardiac hemodynamic response. Stress echocardiography/ Doppler provides a unique noninvasive means to evaluate cardiovascular function and ehmodynamic responses during increased cardiac work. Specifically, stress echocardiographic/Doppler imaging allows assessment of the response to exercise of left and right ventricular function, transvalvular and prosthetic valve gradients, and right ventricular systolic pressure. It has substantial clinical use in the evaluation of patients with equivocal evidence of mitral stenosis, suspicion of dynamic mitral insufficiency or prosthetic valve dysfunction, aortic stenosis and impaired left ventricular systolic function, diseases associated with pulmonary hypertension or cor pulmonale, and among patients with dyspnea of unknown origin. The dynamic nature of cardiovascular disease and the broad spectrum of diseases that affect cardiac function make exercise echocardiography/Doppler an ideal tool ideal for the noninvasive assessment of patients with symptoms of exertional dyspnea.

Echocardiography↗
PubMed2003

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.

Animals↗
PubMed1984

[Function and interaction of the right and left ventricle in patients with mitral valve stenosis].

In 17 patients with mitral stenosis functional class III (NYHA) and chronic pulmonary hypertension, volumes and function of the right (RV) and left ventricle (LV) were analysed. Biplane cineventriculography of the right and left ventricle was performed subsequently and repeated 3 min after application of 1.6 mg nitroglycerin (NTG), which was given sublingually to decrease pre- and afterload. Pulmonary artery (PAP) and wedge pressures (PCW) were measured continuously. RV ejection fraction (EF) was 62.8 +/- 7.2% before and did not change significantly after NTG. RV enddiastolic volume index (EDVI) and endsystolic volume index (ESVI) was 80.7 +/- 27.2 ml/m2 and 31.7 +/- 11.9 ml/m2, respectively, and did not change significantly after NTG. Volumes and function of the LV were normal (LVEDVI: 66.5 +/- 13.5 ml/m2, LVESVI: 23.0 +/- 7.1 ml/m2, LVEF: 62.4 +/- 9.5%). Systolic PAP decreased significantly from 43.4 +/- 11.1 mm Hg before to 37.8 +/- 9.1 mm Hg after NTG (p less than 0.025) as well as total pulmonary resistance from 243 +/- 51 to 209 +/- 50.8 dynes . sec . cm-5 (p less than 0.05). No significant correlation was found between function and volumes of both ventricles. In 4 patients, however, the decrease in LV ejection fraction was associated with a considerable increase of right ventricular enddiastolic volume. Thus, the right ventricle compensates moderate pulmonary hypertension completely maintaining normal right ventricular function. If, however, septal dysfunction occurs, right ventricular insufficiency will develop in a shorter period of time.

Blood Pressure↗