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Gram-negative bacteremia produces both severe systolic and diastolic cardiac dysfunction in a canine model that simulates human septic shock.

A canine sepsis model that simulates the human cardiovascular response to septic shock was produced in 10 conscious unsedated dogs by implanting an Escherichia coli-infected clot into the peritoneum, resulting in bacteremia. By employing serial, simultaneous measurements of radionuclide scan-determined left ventricular (LV) ejection fraction (EF) and thermodilution cardiac index (CI), the end-diastolic volume index (EDVI) was calculated (EDVI = stroke volume index divided by EF). By using three different methods of quantifying serial ventricular performance (EF, shifts in the Starling ventricular function curve using EDVI vs. stroke work index, and the ventricular function curve response to volume infusion), this study provides evidence (P less than 0.01) that septic shock produces a profound, but reversible, decrease in systolic ventricular performance. This decreased performance was not seen in controls and was associated with ventricular dilatation (P less than 0.01); the latter response was dependent on an adequate volume infusion. Further studies of EDVI and pulmonary capillary wedge pressure during diastole revealed a significant, though reversible, shift (P less than 0.001) in the diastolic volume/pressure (or compliance) relationship during septic shock.

Animals↗

Effect of Losartan on left ventricular diastolic function in patients with nonobstructive hypertrophic cardiomyopathy.

In hypertrophic cardiomyopathy (HC), diastolic dysfunction of the left ventricle is a prominent feature caused by myocardial hypertrophy and fibrosis. Angiotensin II has trophic and profibrotic effects on the heart, and the blockade of angiotensin II receptors reverses hypertrophy and fibrosis in human cardiac diseases and in animal HC. This study investigated the short-term (6 months) effects of losartan 100 mg/day in 20 patients with nonobstructive HC, with an emphasis on left ventricular (LV) diastolic dysfunction, compared with 10 patients with HC who were not treated. At the final evaluation, significant changes were observed in the losartan group: a left atrial diameter decrease (p<0.0001), a tissue Doppler early (Ea) mitral annulus diastolic velocity increase (p=0.003) and an E/Ea ratio decrease (p=0.0002), and a significant decrease in plasma levels of the aminoterminal fragment of pro-brain natriuretic peptide (NT-pro-BNP) from a median of 860 to 606 pg/ml (p=0.001). A significant correlation was found between percentage changes in NT-pro-BNP and the E/Ea ratio from baseline to 6 months (r=0.61, p=0.002). In the 2 groups, echocardiographic LV wall and cavity measures did not change. In conclusion, in selected patients with nonobstructive HC, losartan during a 6-month period improved LV diastolic function.

Adolescent↗

Relation of aneurysmectomy in patients with advanced left ventricular remodeling to postoperative left ventricular filling pressure, redilatation with ischemic mitral regurgitation.

Left ventricular (LV) volume, mitral E deceleration time, and mitral regurgitation (MR) fraction were measured by echocardiography in 14 patients with surgical LV aneurysmectomy. Late MR developed 3 to 6 months after surgery in 5 of the 14 patients (36%). Compared with patients without late MR, those with late MR had a significantly greater preoperative LV end-diastolic volume index (LVEDVI) (134 +/- 21 vs 93 +/- 19 ml/m(2), p <0.01), surgical reduction in LVEDVI (-51 +/- 14 vs -20 +/- 16 ml/m(2), p <0.01), early postoperative LV diastolic dysfunction with shortened mitral E deceleration time (106 +/- 23 vs 141 +/- 24 ms, p <0.01), and a late postoperative reincrease in LVEDVI (+28 +/- 4 vs +3 +/- 8 ml/m(2), p <0.01), suggesting that surgical LV aneurysmectomy in patients with advanced preoperative LV remodeling may result in postoperative LV diastolic dysfunction, promoting later LV redilation with ischemic MR.

Aged↗

The perindopril in elderly people with chronic heart failure (PEP-CHF) study.

AIMS: Many patients who receive a diagnosis of heart failure have neither a low left ventricular (LV) ejection fraction nor valve disease. Few substantial randomized controlled trials have been conducted in this population, none has focussed on patients with evidence of diastolic dysfunction and none has shown clear benefit on symptoms, morbidity, or mortality. METHODS AND RESULTS: This was a randomized double-blind trial, comparing placebo with perindopril, 4 mg/day in patients aged > or =70 years with a diagnosis of heart failure, treated with diuretics and an echocardiogram suggesting diastolic dysfunction and excluding substantial LV systolic dysfunction or valve disease. The primary endpoint was a composite of all-cause mortality and unplanned heart failure related hospitalization with a minimum follow-up of 1 year. A total of 850 patients were randomized. Their mean age was 76 (SD 5) years and 55% were women. Median follow-up was 2.1 (IQR 1.5-2.8) years. Enrollment and event rates were lower than anticipated, reducing the power of the study to show a difference in the primary endpoint to 35%. Many patients withdrew from perindopril (28%) and placebo (26%) after 1 year and started taking open-label ACE-inhibitors. Overall, 107 patients assigned to placebo and 100 assigned to perindopril reached the primary endpoint (HR 0.919: 95% CI 0.700-1.208; P = 0.545). By 1 year, reductions in the primary outcome (HR 0.692: 95% CI 0.474-1.010; P = 0.055) and hospitalization for heart failure (HR 0.628: 95% CI 0.408-0.966; P = 0.033) were observed and functional class (P < 0.030) and 6-min corridor walk distance (P = 0.011) had improved in those assigned to perindopril. CONCLUSION: Uncertainty remains about the effects of perindopril on long-term morbidity and mortality in this clinical setting since this study had insufficient power for its primary endpoint. However, improved symptoms and exercise capacity and fewer hospitalizations for heart failure in the first year were observed on perindopril, during which most patients were on assigned therapy, suggesting that it may be of benefit in this patient population.

Aged↗

Therapeutic effects of angiotensin II type 1 receptor blocker at an advanced stage of hypertensive diastolic heart failure.

OBJECTIVE: Angiotensin II type 1 receptor blocker (ARB) is increasingly prescribed for the treatment of systolic heart failure with a growing body of clinical evidence. The roles of ARB, however, remain to be clarified in the treatment of diastolic heart failure (DHF), particularly at its advanced stage. This experimental study investigated the effects of ARB administered at an advanced stage of hypertensive DHF. METHODS: Dahl salt-sensitive rats fed an 8% NaCl diet from age 7 weeks represent overt DHF at age 20 weeks, as noted in previous studies (hypertensive DHF model). The DHF model rats were randomly divided into two groups at age 17 weeks when left ventricular diastolic dysfunction, hypertrophy, fibrosis, macrophage infiltration and reactive oxygen species generation were already augmented; six rats treated for 3 weeks with a subdepressor dose of ARB (olmesartan 0.6 mg/kg per day), and six untreated rats. RESULTS: The 3-week administration of ARB significantly decreased the left ventricular end-diastolic pressure in association with attenuation of left ventricular hypertrophy, fibrosis and diastolic dysfunction. Macrophage infiltration was attenuated with decreased gene expression of transforming growth factor-beta1 and monocyte chemoattractant protein-1 in the left ventricular myocardium of the ARB-treated rats. The production of reactive oxygen species also decreased with NADPH oxidase activity. CONCLUSIONS: ARB provides beneficial effects in hypertensive DHF independent of its antihypertensive effects even if initiated at an advanced stage. The beneficial effects are at least partly attributed to the attenuation of inflammatory changes and oxidative stress through the suppression of cytokine and chemokine production and of NADPH oxidase activity.

Angiotensin II Type 1 Receptor Blockers↗

Time course of sympathovagal imbalance and left ventricular dysfunction in conscious dogs with heart failure.

To elucidate the time course of sympathovagal balance and its relationship to left ventricular function in heart failure, we serially evaluated left ventricular contractility and relaxation and autonomic tone in 11 conscious dogs with tachycardia-induced heart failure. We determined a dynamic map of sympathetic and parasympathetic modulation by power spectral analysis of heart rate variability. The left ventricular peak +dP/dt substantially fell from 3,364 +/- 338 to 1,959 +/- 318 mmHg/s (P < 0.05) on the third day and declined gradually to 1,783 +/- 312 mmHg/s at 2 wk of rapid ventricular pacing. In contrast, the time constant of left ventricular pressure decay and end-diastolic pressure increased gradually from 25 +/- 4 to 47 +/- 5 ms (P < 0.05) and from 10 +/- 2 to 21 +/- 3 mmHg (P < 0.05), respectively, at 2 wk of pacing. The high-frequency component (0.15-1.0 Hz), a marker of parasympathetic modulation, decreased from 1,928 +/- 1,914 to 62 +/- 68 x 10(3) ms2 (P < 0.05) on the third day and further to 9 +/- 12 x 10(3) ms2 (P < 0.05) at 2 wk. Similar to the time course of left ventricular diastolic dysfunction, plasma norepinephrine levels and the ratio of low (0.05- to 0.15-Hz)- to high-frequency component increased progressively from 135 +/- 50 to 532 +/- 186 pg/ml (P < 0.05) and from 0.06 +/- 0.06 to 1.12 +/- 1.01 (P < 0.05), respectively, at 2 wk of pacing. These cardiac and autonomic dysfunctions recovered gradually toward the normal values at 2 wk after cessation of pacing. Thus a parallel decline in left ventricular contractility with parasympathetic influence and a parallel progression in left ventricular diastolic dysfunction with sympathoexcitation suggest a close relationship between cardiac dysfunction and autonomic dysregulation during development of heart failure.

Animals↗

Differentiating constrictive pericarditis from restrictive cardiomyopathy.

Constrictive pericarditis and restrictive cardiomyopathy are 2 forms of diastolic dysfunction with similar presentation but different treatment options. Whereas constrictive pericarditis has the potential of being cured with pericardiectomy, restrictive cardiomyopathy is usually incurable. It is therefore crucial to differentiate between the 2 disorders. In the last few years, new diagnostic techniques have become available to differentiate these causes of diastolic dysfunction from each other. This review provides a complete, in-depth comparison of the 2 disorders with regard to their symptoms and clinical features, etiology, pathophysiology, hemodynamics, echocardiographic presentation, and finally the different available management options.

Cardiomyopathy, Restrictive↗

Reduced left ventricular diastolic function in asymptomatic patients with non-insulin-dependent diabetes mellitus.

AIMS: This prospective study was performed to assess the provalence of diastolic dysfunction of the lelt ventricle (LV) in patients with noninsulin-dependent diabetes mellitus (NIDDM), and the effect of patients' age and the duration of diabetes in the appearance of this dysfunction. METHODS AND RESULTS: We studied 103 patients with NIDDM (group I) and 103 subjects without diabetes (group 2). SF and EF were lower in patients with NIDDM as compared with the control group (32.7+/-5.5%, vs. 34.2+/-5.2%, p=0.04 and 61+/-8.7% vs. 64.4+/-8.1, p<0.01, respectively). The EA ratio <1 is found in 71 (68.9%) patients with NIDDM, and in 36 (34.9%) subjects of the control group (p<0.01). The age of patients had significant correlation with E/A ratio of transmitral Doppler flow (r = -0.38, p<0.01). The duration of diabetes had significant correlation with EF (r = -0.26, p<0.01) and with E/A ratio (r= -0.295, p<0.01). Body mass index and waist/hip ratio did not have significant correlation with EF and with E/A ratio. CONCLUSIONS: In asymptomatic NDDM patients there was a more frequent reduction of systolic and diastolic function of the LV, as compared with healthy subjects. The presence of diastolic dysfunction of the LV in NDDM patients is dependent on the age of the patients and duration of diabetes.

Diabetes Mellitus, Type 2↗

[Echocardiography methods in the diagnosis of cardiomyopathies in children].

We investigated 59 children with cardiomyopathy (CMP) by echocardiographic methods (ECHO). 29 children with dilated CMP showed typical enlargement of the left ventricle 159 +/- 31%, xxx; (% of normal value +/- SD) and of the left atrium (143 +/- 27%, xxx). Systolic and diastolic function of the left ventricle were decreased, systolic change in size of the left ventricle % delta D = 16 +/- 7%; xxx; systolic change in area of the left ventricle % delta A = 20 +/- 8%; xxx; maximum filling rate of the left ventricle in the phase of quick filling E max = 0.37 +/- 0.09 m. sec-1, xxx; the percentage of filling in the first third of diastole 0.33 DA = 37 +/- 9%, xx. Mitral insufficiency was found by us in 81% of children. In 25 children with hypertrophic CMP the size of left ventricle was decreased (81 +/- 13%, xxx). Asymmetric septal hypertrophy was found by us in 69% of children, symmetric hypertrophy in 27%, local hypertrophy of the apex in 4%. Systolic function of the left ventricle was increased (% delta D = 47 +/- 10%, xxx; % delta A = 70 +/- 10%, xxx). Diastolic dysfunction manifested itself by reduced E max (0.71 +/- 0.19 m.sec-1, xx) and 0.33 DA (45 +/- 12%, x). Mitral insufficiency was found in 54% of the children. In the case of the 5 children with restrictive CMP an extreme enlargement of left atrium (195 +/- 41%, xxx) was typical, as well as diastolic dysfunction of the left ventricle (0.33 DA = 67 +/- 6%, x).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Dominant-negative effect of a mutant cardiac troponin T on cardiac structure and function in transgenic mice.

Hypertrophic cardiomyopathy (HCM) is a disease of sarcomeric proteins. The mechanism by which mutant sarcomeric proteins cause HCM is unknown. The leading hypothesis proposes that mutant sarcomeric proteins exert a dominant-negative effect on myocyte structure and function. To test this, we produced transgenic mice expressing low levels of normal or mutant human cardiac troponin T (cTnT). We constructed normal (cTnT-Arg92) and mutant (cTnT-Gln92) transgenes, driven by a murine cTnT promoter, and produced three normal and five mutant transgenic lines, which were identified by PCR and Southern blotting. Expression levels of the transgene proteins, detected using a specific antibody, ranged from 1 to 10% of the total cTnT pool. M-mode and Doppler echocardiography showed normal left ventricular dimensions and systolic function, but diastolic dysfunction in the mutant mice evidenced by a 50% reduction in the E/A ratio of mitral inflow velocities. Histological examination showed cardiac myocyte disarray in the mutant mice, which amounted to 1-15% of the total myocardium, and a twofold increase in the myocardial interstitial collagen content. Thus, the mutant cTnT-Gln92, responsible for human HCM, exerted a dominant-negative effect on cardiac structure and function leading to disarray, increased collagen synthesis, and diastolic dysfunction in transgenic mice.

Animals↗

Myocardial hypertrophy and left ventricular diastolic function in hypertensive patients: an echo Doppler evaluation.

The presence and the characteristics of left ventricular diastolic dysfunction in mild to moderate systemic hypertension were evaluated in 13 normotensive subjects (Group I), in 12 hypertensive subjects without (Group II) and 28 with (Group III) LV hypertrophy who underwent two-dimensional Doppler echocardiographic study. Among Group III patients, a subset (n = 12) with a dilated left ventricle was identified. Diastolic filling parameters were impaired in Group III patients while, in Group II, they were intermediate between Groups I and III. In all Group III patients normalized peak filling rate (nPFR) correlated directly with mean velocity of circumferential fibre shortening (mVCF) (r = 0.55; P less than 0.001) and inversely with left ventricular mass index (LVM) (r = -0.60; P less than 0.001), left ventricular end-diastolic diameter (LVIDd) (r = -0.63; P less than 0.001), LV peak systolic stress (LVWST) (r = -0.64; P less than 0.01). A separate analysis showed that these correlations were also present in patients without left ventricular dilation; in the subset with left ventricular dilation nPFR correlated only with LVWST (r = -0.73; P less than 0.01), but not with LVM, mVCF, LVIDd. Thus, left ventricular hypertrophy is one of the major determinants of diastolic dysfunction in hypertensives; other factors influence nPFR values in hypertensive patients when the left ventricle dilates.

Adult↗

Characterization of cardiopulmonary function and cardiac muscarinic and adrenergic receptor density adaptation in C57BL/6 mice with chronic Trypanosoma cruzi infection.

Circulating antibodies in chagasic patients interact with myocardial beta adrenergic and muscarinic cholinergic receptors, triggering intracellular signals that alter cardiac function along the course of the disease. However, until now, experimental data in models of chronically infected chagasic mice linking the effects on myocardial beta adrenergic and muscarinic receptors to cardiopulmonary dysfunction is lacking. Thus, we studied C57BL/6 mice 8 months after intraperitoneal injection of 100 trypomastigote forms of the Colombian strain of T. cruzi. Uninfected mice, matched in age, were used as controls. Histopathological analyses (inflammation and fibrosis) and radio-ligand binding assays for estimation of muscarinic and adrenergic receptor density were performed in myocardium tissue samples. When compared to controls, infected mice had electrical conduction disturbances, diastolic dysfunction, lower O2 consumption and anaerobic threshold. In addition, hearts of chronic chagasic mice had intense inflammation and fibrosis, and decreased beta adrenergic and increased muscarinic receptor densities than normal controls. Our data suggest that chronic T. cruzi infection causes alterations in cardiac receptor density and fibrosis deposition which can be associated with cardiac conduction abnormalities, diastolic dysfunction and lower exercise capacity, associating for the first time all these functional and histopathological alterations in chagasic mice.

Animals↗

Wave-intensity analysis: a new approach to left ventricular filling dynamics.

In order to explore a new approach to the analysis of diastolic dysfunction, we adapted wave-intensity analysis (WIA), a time-domain analysis that provides information regarding both upstream and downstream events, to left ventricular (LV) filling. WIA considers the pressure and flow waves as summations of successive wavelets, characterised by the direction they travel and by the sign of the pressure gradient associated with them. Wave intensity is the product, dPdU, calculated from the incremental differences in LV pressure (dP) and mitral velocity (dU) and, during the diastolic filling interval, yields up to five dPdU peaks. Peak 1 is caused by backward-travelling expansion waves that accelerate the blood while LV pressure falls, and may be related to "diastolic suction". Peak 2 is caused by forward-travelling compression waves which occur if acceleration continues after LV pressure begins to increase. Peak 3 is caused by backward compression waves and is associated with rising LV pressure and deceleration. Peak 4 is caused by forward compression waves and is associated with the increasing LV pressure and acceleration caused by atrial contraction. Peak 5 is caused by backward compression waves and is associated with increasing pressure and deceleration. These preliminary observations suggest that WIA can be useful in describing the mechanics of LV filling and, after much further work has been accomplished, it might prove useful in the detection and characterization of diastolic dysfunction.

Aorta↗

Utility of the amino-terminal fragment of pro-brain natriuretic peptide in plasma for the evaluation of cardiac dysfunction in elderly patients in primary health care.

BACKGROUND: The aims of this study were to measure the N-terminal fragment of pro-brain natriuretic peptide (proBNP) in plasma in medical conditions commonly found in primary care and to evaluate the utility of these measurements in identifying impaired cardiac function in elderly patients with symptoms associated with heart failure. METHODS: We studied 415 patients (221 men and 194 women; mean age, 72 years) who had contacted a primary healthcare center for dyspnea, fatigue, and/or peripheral edema. One cardiologist evaluated the patients in terms of history, physical examination, functional capacity, electrocardiography, and suspicion of heart failure. Plasma N-terminal proBNP was measured by an in-house RIA. An ejection fraction < or =40% by Doppler echocardiography was regarded as reduced cardiac function. Abnormal diastolic function was defined as an abnormal mitral inflow defined as reduced ratio of peak early diastolic filling velocity to peak filling velocity at atrial contraction (E/A ratio), or as abnormal pulmonary venous flow pattern. RESULTS: Patients with impaired functional capacity, impaired systolic function, and/or impaired renal function had significantly increased N-terminal proBNP concentrations. By multiple regression analysis, N-terminal proBNP concentrations were also influenced by ischemic heart disease, cardiac enlargement, and certain medications but not by increased creatinine. No gender differences were observed. Patients with isolated diastolic dysfunction attributable to relaxation abnormalities had lower concentrations than those with normal cardiac function, whereas those with pseudonormal E/A ratios or restrictive filling patterns had higher concentrations. CONCLUSIONS: Plasma N-terminal proBNP concentrations increase as a result of impaired systolic function, age, impaired renal function, cardiac ischemia and enlargement, and certain medications. Values are high in diastolic dysfunction with pseudonormal patterns, but not in patients with relaxation abnormalities. An increase in plasma N-terminal proBNP might be an earlier sign of abnormal cardiac function than abnormalities identified by currently used echocardiographic measurements.

Aged↗

Diabetic cardiomyopathy. A unique entity or a complication of coronary artery disease?

The increased incidence of congestive heart failure and the increased mortality and morbidity in the diabetic patient following myocardial infarction or coronary artery bypass graft can be explained by the presence of diabetic cardiomyopathy. Noninvasive studies in young diabetic patients show no cardiac abnormality, but in older diabetic patients mild cardiac diastolic dysfunction is detectable. This mild cardiomyopathy can become clinically detectable in the presence of hypertension and can be severe in the presence of myocardial ischemia. Microvascular disease is unlikely to cause diabetic cardiomyopathy. Cellular changes, including defects in calcium transport and fatty acid metabolism, may lead to myocellular hypertrophy and myocardial fibrosis, initially causing diastolic dysfunction that may advance to systolic dysfunction. Glycemic control, energetic detection and treatment of hypertension with appropriate antihypertensive agents, and early detection and treatment of ischemic heart disease are essential in preventing and treating diabetic cardiomyopathy.

Animals↗

Thermal therapy for congestive heart failure: estimation by TEI index.

Systolic dysfunction commonly coexists with diastolic dysfunction in patients with congestive heart failure due to myocardial disease. Also, right ventricular dysfunction is frequently associated with left ventricular dysfunction. The Doppler total ejection isovolume (TEI) index, a combined measurement of systolic and diastolic myocardial performance, is more reflective of overall cardiac function than systolic or diastolic function alone in both ventricles, and provides a conceptually new measure of global cardiac function. Single sauna bathing improves acute hemodynamics and repeated sauna therapy improves cardiac function and clinical symptoms in patients with heart failure. More recently, improvement of vascular endothelial function were observed by repeated sauna therapy in patients with heart failure. The TEI index, combining systolic and diastolic myocardial function, is a promising tool for the quantitative assessment of global cardiac function before and after thermal therapy.

Diastole↗

[Early diagnosis of pulmonary hemodynamic disorders in patients with pulmonary sarcoidosis].

A hundred and eleven patients with pulmonary sarcoidosis (PS) were examined to detect early impairments of pulmonary hemodynamics and myocardial function. A package of examinations included Doppler echocardiography at rest and with the Valsalva test, as well as electrocardiography and myocardial scintigraphy. In patients with early PS, right ventricular diastolic dysfunction is shown to be preceded by systolic dysfunction, as manifested itself in the altered ratio of different phases of right ventricular filling. As a method for early diagnosis of latent hypertension, the authors propose to use the Valsalva test to create a short-term volume overload of the right cardiac cavities. The study has indicated that left cardiac dilatation, decreased ejection fraction, left ventricular diastolic dysfunction, and the presence of large focal portions of fibrosis in the ventricular myocardium, interventricular septum, and papillary muscles can be considered to be early Doppler echocardiographic signs of sarcoidosis of the heart in patients with PS.

Acute Disease↗

Pulmonary regurgitation end-diastolic gradient is a Doppler marker of cardiac status: data from the Heart and Soul Study.

BACKGROUND: Echocardiograms routinely sample pulmonary regurgitation signals from which it is possible to measure end diastolic gradients; these correlate with pulmonary artery diastolic pressures. METHODS: We performed echocardiograms in 741 ambulatory adults with coronary artery disease who were recruited for the Heart and Soul Study. We compared indicators of cardiac status among individuals with normal (0-5.0 mm Hg) and elevated (> 5.0 mm Hg) end diastolic pulmonary regurgitation (EDPR) gradients. RESULTS: Of the 481 participants with measurable EDPR gradients, 21% had elevated EDPR gradients (> 5.0 mm Hg). EDPR gradients > 5.0 mm Hg were associated with higher New York Heart Association functional class (P = .002), higher brain natriuretic peptide (P = .002), fewer metabolic equivalents achieved on treadmill testing (P < 0.001), and higher left ventricular mass (P < 0.001). The EDPR gradient > 5.0 mm Hg had a sensitivity of 25% (95% confidence interval 20-30%) and a specificity of 86% (80-91%) for detecting at least one of the following: systolic dysfunction, diastolic dysfunction, or abnormal wall motion score. The EDPR gradient > 5.0 mm HG was statistically equivalent to the tricuspid regurgitation (TR) gradient > 30 mm Hg in terms of diagnostic value (area under the receiver operating characteristic curve equaled 0.58 for each test). The EDPR gradient increased the yield of pulmonary artery pressures from 61% (TR gradient alone) to 84% (P < .0001). CONCLUSION: The EDPR gradient provides valuable information independent of the TR gradient in evaluating pulmonary artery pressures and cardiac dysfunction.

Aged↗