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Impact of pulmonary regurgitation and right ventricular dysfunction on oxygen uptake recovery kinetics in repaired tetralogy of Fallot.

BACKGROUND: Patients with repaired tetralogy of Fallot (ToF) featuring severe pulmonary regurgitation (PR) and/or right ventricular (RV) dysfunction have reduced exercise tolerance. AIMS: To assess the impact of PR and of RV function on the ability to recover from exercise in ToF patients. METHODS: 61 consecutive patients aged 23.1+/-12.1 years underwent maximal cardiopulmonary exercise test (CPX), transthoracic echocardiography and magnetic resonance imaging. This data was compared to those of 153 matched healthy subjects. RESULTS: 19 patients (31%) had severe PR. RV dysfunction was noted in 19 patients (31%). Nine patients (15%) had both severe PR and RV dysfunction. Patients had lower peak oxygen uptake (VO2), VO2 slope, carbon dioxide production (VCO2) slope and O2 pulse slope (p < 0.0001), especially those with severe PR and RV dysfunction (p < 0.0001). Heart rate slope was similar between groups. No patient with severe PR and RV dysfunction had a predicted peak VO2 > 40%. CPX had a high sensitivity and specificity to identify patients with severe PR and RV dysfunction. CONCLUSIONS: In ToF patients, severe PR and RV dysfunction lead to delayed recovery from exercise. CPX can identify patients with severe PR and RV dysfunction and may be useful to guide the pulmonary valve replacement decision-making process.

Adolescent↗

Right Ventricular Dysfunction Secondary to Myocardial Ischemia Provoked by Stress Testing.

We present the cases of two patients, aged 59 and 85 years, who were evaluated with stress echocardiography for chest pain. Both patients developed dramatic echocardiographic findings consisting of severe right ventricular enlargement and hypokinesis, as well as enlargement of the right atrium at relatively low-level exercise. One patient collapsed with severe sinus bradycardia, junctional rhythm, ST elevation in the inferior leads, marked hypotension, and neck vein congestion. The other patient developed staggering and symptoms of hypoperfusion. In both patients, correction of critical proximal right coronary artery stenosis by angioplasty resulted in complete resolution of the right ventricular dysfunction on repeat stress testing. We conclude that in some patients, stress-induced myocardial ischemia may involve primarily the right ventricle with little or no evidence of ischemic changes in the left ventricle. An assessment of right ventricular function should be included in stress echocardiographic studies.

Journal Article↗

Plasma brain natriuretic peptide levels increase in proportion to the extent of right ventricular dysfunction in pulmonary hypertension.

OBJECTIVES: This study sought to investigate the influence of right ventricular (RV) hemodynamic variables and function on the secretion of brain natriuretic peptide (BNP) in patients with isolated RV overload. BACKGROUND: Plasma BNP is known to increase in proportion to the degree of left ventricular (LV) overload. However, whether BNP secretion is also regulated in the presence of RV overload remains unknown. METHODS: Plasma BNP and atrial natriuretic peptide (ANP) levels in the pulmonary artery were measured in 44 patients with RV overload: 18 with RV volume overload (RVVO) due to atrial septal defect and 26 with RV pressure overload (RVPO) due to primary or thromboembolic pulmonary hypertension. Right heart catheterization was performed in all patients. RV and LV ejection fraction, myocardial mass and volume of the four chambers were determined by using electron beam computed tomography. RESULTS: Although both plasma BNP and ANP levels were significantly elevated in patients with RV overload compared with values in control subjects, plasma BNP and the BNP/ANP ratio were significantly higher in patients with RVPO than with RVVO (BNP 294 +/- 72 vs. 48 +/- 14 pg/ml; BNP/ANP 1.6 +/- 0.2 vs. 0.8 +/- 0.2, both p < 0.05). Plasma BNP correlated positively with mean pulmonary artery pressure (r = 0.73), total pulmonary resistance (r = 0.79), mean right atrial pressure (r = 0.79), RV end-diastolic pressure (r = 0.76) and RV myocardial mass (r = 0.71); it correlated negatively with cardiac output (r = -0.33) and RV ejection fraction (r = -0.71). Plasma BNP significantly decreased from 315 +/- 120 to 144 +/- 54 pg/ml with long-term vasodilator therapy (total pulmonary resistance decreased from 23 +/- 4 to 15 +/- 3 Wood U). CONCLUSIONS: Plasma BNP increases in proportion to the extent of RV dysfunction in pulmonary hypertension.

Adult↗

Early reversal of right ventricular dysfunction in patients with acute pulmonary embolism after treatment with intravenous tissue plasminogen activator.

To assess abnormalities of right heart function and their reversal with thrombolysis in pulmonary embolism, serial imaging and Doppler echocardiographic studies were performed before and after a 6 hour intravenous infusion of 80 to 90 mg of recombinant tissue-type plasminogen activator (rt-PA) in seven patients with segmental or lobar acute pulmonary embolism. None of the five men and two women had known prior pulmonary hypertension. Substantial clot lysis and improvement in pulmonary blood flow, as determined by serial pulmonary angiography and perfusion lung scanning, were achieved in all. Coincident with clot lysis, pulmonary artery systolic pressure decreased (from 42 +/- 11 to 26 +/- 7 mm Hg, p less than 0.005), right ventricular diameter decreased (from 3.9 +/- 1.0 to 2.0 +/- 0.5 cm, p less than 0.005) and left ventricular diameter increased (from 3.7 +/- 0.9 to 4.4 +/- 0.6 cm, p less than 0.01). Right ventricular wall movement, initially mildly, moderately or severely hypokinetic in one, two and four patients, respectively, normalized in five and improved to mild hypokinesia in two. Tricuspid regurgitation was present before lytic therapy in six patients. In five, flow velocity in the tricuspid regurgitant jets indicated a peak systolic right ventricular minus right atrial pressure gradient of 25 to 52 mm Hg. Tricuspid regurgitation was detected early after lytic therapy in only two patients. Systolic septal flattening was noted before but not after lysis. These findings confirm that pulmonary emboli may result in appreciable right ventricular dysfunction and dilation, resultant tricuspid regurgitation, abnormal septal position and decreased left ventricular size.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

Right ventricular dysfunction in acute inferoposterior myocardial infarction. An echocardiographic and isotopic study.

We analyzed right ventricular (RV) regional wall motion by two-dimensional echocardiographic (2D echo) and multigated acquisition radionuclear (MUGA) studies in 104 patients with acute inferoposterior myocardial infarction (AIPMI). Sixty-eight patients (65 percent) had 2D echo RV regional wall motion abnormalities (RV dysfunction(RVD) group) while 36 patients showed no 2-D echo RV regional wall motion abnormalities (no-RVD group). The RVD group had a higher incidence of jugular venous engorgement (p less than 0.05), Kusmaul's sign, (p less than 0.05) complete atrio-ventricular block (p less than 0.05), and in-hospital death (p less than 0.02). The RVD group had significantly higher 2-D echo RV end-systolic dimensions (p less than 0.005) and lower values of percentage of fractional shortening (%FS) (p less than 0.005) in the long and short axis of the RV four-chamber view than patients in the no-RVD group and a control group of 20 patients with normal hearts. There was no statistical significant difference in the 2-D echo RV end-diastolic dimensions among the three groups. Patients in the RVD group had a lower MUGA derived RV ejection fraction (EF) than patients in the no-RVD and control groups (26.5 +/- 13.2 vs. 46.3 +/- 7 and vs. 50.6 +/- 4, respectively; p less than 0.05). RVD was diagnosed by both 2-D echo and MUGA in 60 of 104 patients (57.7 percent) with a sensitivity for 2-D echo of 92 percent and 79 percent specificity (when compared to the MUGA study). The predictive value for a positive test was 88 percent and for a negative test 86 percent. The accuracy was 87.5 percent. Recognition of regional wall motion abnormalities by 2-D echo permits a prompt and accurate bedside identification of right ventricular dysfunction (RVD) within the first 72 hours of clinical onset. An enlarged RV 2D echo end-diastolic dimension was not a sensitive parameter for the diagnosis of this pathology, whereas an increased end-systolic RV diameter and decreased RV %FS were better indicators of RV dysfunction in patients with acute inferoposterior wall myocardial infarction.

Aged↗

The short-term effects of digoxin in patients with right ventricular dysfunction from pulmonary hypertension.

OBJECTIVE: Studies on the effects of digoxin in patients with right ventricular failure and normal left ventricular function have not been performed. We evaluated the short-term effects of digoxin administration in patients with primary pulmonary hypertension on hemodynamics, neurohormones, and baroreceptor responsiveness. DESIGN: This was a prospective study with patients serving as their own controls. SETTING: University Hospital Intensive Care Unit with central monitoring. PATIENTS: Seventeen patients with primary pulmonary hypertension and symptomatic heart failure were enrolled. INTERVENTIONS: Following baseline hemodynamics, neurohormonal samples were drawn and the heart rate response to change in blood pressure following a challenge of phenylephrine and nitroprusside were recorded. One mg of intravenous digoxin was given and the measurements repeated after 2 hours. RESULTS: Following digoxin there was a significant increase in cardiac output (3.49+/-1.2 to 3.81+/-1.2 L/min., p=0.028), a significant fall in norepinephrine (680+/-89 to 580+/-85 pg/ml, p=.013), and a significant increase in atrial natriuretic peptide (311+/-44 to 421+/-9 pg/ml, p=0.01). All of the patients had changes in heart rate and blood pressure following phenylephrine and nitroprusside challenge, but there was no significant difference in the change in heart rate response to change in blood pressure when rechallenged after digoxin treatment. CONCLUSION: Digoxin produces a modest increase in cardiac output in patients with pulmonary hypertension and right ventricular failure, as well as a significant reduction in circulating norepinephrine. No detectable effects of digoxin on baroreceptor responsiveness were apparent. The use of digoxin in pulmonary hypertension is warranted.

Adult↗

Heterozygous deficiency of hypoxia-inducible factor-2alpha protects mice against pulmonary hypertension and right ventricular dysfunction during prolonged hypoxia.

Chronic hypoxia induces pulmonary vascular remodeling, leading to pulmonary hypertension, right ventricular hypertrophy, and heart failure. Heterozygous deficiency of hypoxia-inducible factor-1alpha (HIF-1alpha), which mediates the cellular response to hypoxia by increasing expression of genes involved in erythropoiesis and angiogenesis, has been previously shown to delay hypoxia-induced pulmonary hypertension. HIF-2alpha is a homologue of HIF-1alpha and is abundantly expressed in the lung, but its role in pulmonary hypertension remains unknown. Therefore, we analyzed the pulmonary response of WT and viable heterozygous HIF-2alpha-deficient (Hif2alpha(+/-)) mice after exposure to 10% O(2) for 4 weeks. In contrast to WT mice, Hif2alpha(+/-) mice were fully protected against pulmonary hypertension and right ventricular hypertrophy, unveiling a critical role of HIF-2alpha in hypoxia-induced pulmonary vascular remodeling. Pulmonary expression levels of endothelin-1 and plasma catecholamine levels were increased threefold and 12-fold respectively in WT but not in Hif2alpha(+/-) mice after hypoxia, suggesting that HIF-2alpha-mediated upregulation of these vasoconstrictors contributes to the development of hypoxic pulmonary vascular remodeling.

Animals↗

Right ventricular dysfunction detected by gated scintiphotography in patients with acute inferior myocardial infarction.

Twenty-seven patients with acute myocardial infarction not complicated by cardiogenic shock and ten normal volunteers were studied with gated cardiac blood pool scans. The ratio right vetricular area/left ventricular area (RVA/LVA) determined from the left anterior oblique end-diastolic scans was examined. The ratio was 1.11 +/- .06 in the normal volunteers. In patients with anterior infarction the ratio fell to 0.75 +/- .12 (P less than .05) due to left ventricular enlargement. In those with inferior infarction the ratio was 1.12 +/- .23 which was greater than in those with anterior infarction (P less than .05) due to enlargement of both the left and right ventricles. Six patients with cardiogenic shock, three with inferior and three with anterior infarction were studied. The three with anterior infarction had left ventricular enlargement and a decrease in the ratio of RVA/LVA to 0.62 while the three with inferior infarction had an increase in the ratio to 2.05 suggesting right ventricular dilatation and dysfunction. These studies suggest a high incidence of right ventricular dysfunction in patients with inferior myocardial infarction.

Aged↗

Right ventricular dysfunction in acute thermal injury.

The elevated cardiac output (CO) and pulmonary artery hypertension (PAH) observed in thermal injury offers a unique opportunity to study the effects of a combined pressure-flow load on the right ventricle in previously healthy persons. Potential responses include a diminished right ventricular ejection fraction (RVEF), increased right ventricular end-diastolic volume index (RVEDVI), and augmented myocardial oxygen consumption because of increased systolic wall tension. We investigated these factors in 15 nonhypoxic patients without sepsis having 15--75% body surface area burns using flow directed catheters and the thermodilution technique. All patients increased their CO in response in fluid resuscitation, but six patients with an elevated mean pulmonary artery pressure (greater than 20 mmHG and increased pulmonary vascular resistance (greater than 1.2 mmHg/min/L) had right ventricular dysfunction as evidenced by an increase (188 +/- 15 ml/M2) in RVEDVI and a decreased (0.26 +/- 4 ml/M2) RVEF. Patients without PAH had a smaller RVEDVI (115 +/- 4 ML/M2) and larger RVEF (0.39 +/- 0.02). Patients with PAH and RV dysfunction were older, had larger body surface area burns, lower systemic diastolic artery pressures (63 +/- 4 mmHg) and higher heart rates (114 +/- 7 beats/min); RV end-diastolic pressures were minimally elevated (9.5 +/- 1.4 mmHg). The decrease in RVEF and increase in RVEDVI may limit the hemodynamic response to fluid volume replacement and survival.

Acute Disease↗

A case series of systemic right ventricular dysfunction post atrial switch for simple D-transposition of the great arteries: the impact of beta-blockade.

BACKGROUND: Patients with atrial switch (Mustard or Senning) repair of D-transposition of the great arteries (D-TGA) are at increased risk for atrial arrhythmias, systemic right ventricular (RV) dysfunction and late mortality. OBJECTIVES: To evaluate case series from a single-centre experience with beta-blocker use in adult, post atrial switch, simple D-TGA patients. METHODS: The Adult Congenital Heart Disease Clinic (Halifax, Nova Scotia) database was used to identify patients with post atrial switch, simple D-TGA. Treatment effect of beta-blockade was evaluated. RESULTS: Eight patients were treated with beta-blockers for systemic RV dysfunction (n=2), arrhythmia (n=2) or both (n=4). Median follow-up was three years, at which time seven of eight patients were still on beta-blockade. Of those patients with complete data, two of five had improved systemic ventricular dysfunction, two of four had improved tricuspid regurgitation and four of six had improved functional capacity, as determined by history or exercise testing. Beta-blockade was well tolerated in seven of eight patients without any significant clinical deterioration. CONCLUSIONS: Beta-blockade was used infrequently in patients with a prior Mustard procedure. When beta-blockade was prescribed to patients with a prior atrial switch procedure, the drugs were well tolerated and were associated with trends toward improved symptoms, less tricuspid regurgitation and improved functional status in patients with reduced systemic RV function. These data support the need for a randomized trial of beta-blockade in patients with a previous Mustard or Senning operation and RV dysfunction.

Adrenergic beta-Antagonists↗

Association of right ventricular dysfunction and Cheyne-Stokes respiration in patients with chronic heart failure.

Cheyne-Stokes respiration (CSR) is present in up to 40% of patients with congestive heart failure (CHF) and is an independent risk factor for increased overall mortality. We examined whether CSR is associated with right ventricular (RV) dysfunction in CHF patients. Parameters of RV function were assessed by two-dimensional echocardiography and tissue velocity imaging in 42 patients (aged 23-75 years) with a left ventricular (LV) ejection fraction below 40%. Respiratory polygraphy revealed CSR with an central apnea-hypopnea index (CAHI) >10 h-1 in 13 of the 42 patients (31%). Demographic characteristics did not differ among the patient groups. The velocity of the tricuspid annular systolic motion (TASM), a parameter reflecting systolic RV function, was significantly reduced in CHF patients with CSR (10.5 +/- 2.3 cm s-1) compared with those without CSR (15.0 +/- 5.1 cm s-1, P = 0.004), and was inversely associated with the CAHI (y = 15.2-0.2x; r = 0.46, P = 0.003). The RV dimensions were significantly increased and the fractional RV area changes significantly reduced in CHF patients with CSR (33 +/- 17 versus 48 +/- 20%; P = 0.04). Doppler parameters of pulmonary artery flow indicate higher pulmonary artery pressures in CSR patients compared with patients without CSR, which is also reflected by an increased RV free-wall thickness in CSR patients (6.5 +/- 1.1 vs. 5.3 +/- 1.3 mm; P = 0.05). Parameters of systolic LV function, forced expiratory volume in 1 s (FEV1), and PaO2 and PaCO2 were not different among patients with or without CSR. In conclusion, CSR is associated with depressed systolic RV function and increased RV dimensions in CHF patients. Future studies will show whether optimized treatment of CSR will improve RV function.

Adult↗

[Effectiveness and limitations of IABP or LVAD in right ventricular dysfunction].

IABP and well functioning left ventricular assist device for a failing left ventricle have potential for altering the loading condition of the right heart. Depending on the extent of myocardial damage and the pulmonary vascular resistance, IABP and LVAD can have different degree of hemodynamic effect on the right ventricle. We examined 20 clinical cases who required IABP support to wean from cardiopulmonary bypass. In 10 cases (group I), CVP rose up above 20 cmH2O within 12 hrs of post operative period. In another 10 cases (group II), CVP rose less than 20 cm H2O. Then we compared hemodynamic change (m-PAP, PVR, CVP, PAWP, CI and RVSWI) between two groups until 72 hrs of post operative period. No significant differences were noted in PVR and CI between two groups, but CVP, m-PAP, PAWP and RVSWI were markedly higher in I group. Reduction of RV afterload produced with an IABP may probably be due to degree of recovery of failing left ventricular function. It is though that IABP has less favorable effect on right ventricular in the cases whose CVP elevate above 20 mmH2O within 12 hrs after operation than in those with CVP below 20 cmH2O. Clinical studies were made on 4 cases with biventricular failure in our experiences of 8 LVAD cases (LV aneurysmectomy + VSP closure, MVR + AVR + CABG + LV aneurysmectomy, CABG + LV aneurysmectomy and MVR + CABG). LVAD seems to have more beneficial effect on RV afterload, than IABP right ventricular dysfunction, however, is likely to continue in the cases whose CVP elevates above 30 mmH2O even if LVAD is used.

Adult↗

Serial echocardiographic findings early after heart transplantation: evidence for reversible right ventricular dysfunction and myocardial edema.

Serial M-mode and two-dimensional echocardiograms were performed on 10 patients at 1 week, 1 month, and 3 months after heart transplantation to determine early structural and functional changes in the allograft. Standard M-mode echocardiographic measurements of at least five cardiac cycles were averaged. Right ventricular size and function were assessed by mid-ventricular diameter and the right ventricular apex to lateral tricuspid anulus shortening fraction, respectively, on the two-dimensional apical four-chamber view. There were no consistent differences in left ventricular end-diastolic dimension or fractional shortening between study periods. Left ventricular posterior wall thickness decreased from 15 +/- 2 to 11 +/- 1 mm (p = 0.001), and septal thickness decreased from 15 +/- 2 to 12 +/- 2 mm (p = 0.0006) between the 1-week and 3-month studies. Right ventricular cross-sectional dimension increased from 34 +/- 6 to 39 +/- 6 mm (p = 0.047), and right ventricular fractional shortening increased from 13% +/- 3% to 21% +/- 5% (p = 0.0051) between the 1-week and 3-month studies. There were no correlations between any of the above changes and rejection episodes. There was a weak correlation (r = 0.53) between ischemic time and change in posterior wall thickness. Right ventricular dysfunction and increased left ventricular wall thickness presumably caused by interstitial edema appear to be normal findings early after heart transplantation.

Adult↗

Selective right ventricular dysfunction after coronary artery bypass grafting.

Preoperative and postoperative right (RVEF) and left ventricular ejection fractions (LVEF) were studied by means of radionuclide techniques in 15 patients undergoing coronary bypass operations. Three of them, all with right coronary artery lesions, had postoperative depression of RVEF without concomitant decrease in LVEF. In contrast to those with left ventricular dysfunction, the patients with selective RVEF depression did not have significant elevation of myocardial injury index calculated from creatine kinase isoenzyme (CK-MB) curves.

Cardiac Output↗

Relation of right ventricular free wall mechanical delay to right ventricular dysfunction as determined by tissue Doppler imaging.

Several well-established echocardiographic parameters used in the assessment of right ventricular (RV) performance, as well as tissue Doppler imaging (TDI) to investigate RV free wall mechanical events, were prospectively obtained from a heterogenous group of 20 patients with varying degrees of pulmonary hypertension (mean age 51 +/- 13 years; World Health Organization class average 2.8, mean pulmonary systolic pressure 78 +/- 24 mm Hg) and compared with similar data retrospectively obtained from 20 healthy volunteers (mean age 45 +/- 15 years). Patients with varying degrees of pulmonary hypertension had worse RV performance parameters than healthy volunteers (RV fractional area change 37 +/- 13% vs 52 +/- 5%, p < 0.0001; RV myocardial performance index 0.76 +/- 0.31 vs 0.29 +/- 0.11, p < 0.0001; and eccentricity index 1.41 +/- 0.57 vs 0.98 +/- 0.06, p < 0.005). Similarly, in these patients with abnormal RV performance, TDI showed statistically significant smaller peak longitudinal RV free wall strain (-21.5 +/- 9.0% vs -28.0 +/- 4.1%, p < 0.01) and significantly delayed time to peak strain (459 +/- 76 vs 388 +/- 29 ms, p < 0.0005) values than in healthy volunteers; a very strong correlation between RV mechanical delay and RV fractional area change (r = -0.89) was noted.

Adult↗

The impact of right ventricular dysfunction on the prognosis and therapy of normotensive patients with pulmonary embolism.

The prognosis and optimal therapy of patients with pulmonary embolism (PE) are strongly influenced by the presence or absence of associated hemodynamic derangements. Patients with normal systemic arterial pressure have a relatively low risk of recurrent PE and death when treated promptly with therapeutic anticoagulation. Those who present with hypotension, shock, or cardiac arrest, however, have a much higher mortality rate and often receive thrombolytic therapy. Recent evidence indicates that the presence of right ventricular (RV) dysfunction identifies a subgroup of normotensive patients with a much more guarded prognosis who may benefit from more intensive therapy with thrombolytic agents. This article reviews our current understanding of the pathophysiology and diagnosis of RV dysfunction and its impact on the prognosis and therapy of normotensive patients with PE.

Humans↗

Effects of reperfusion on ischemic right ventricular dysfunction. Disparate mechanisms of benefit related to duration of ischemia.

BACKGROUND: Right ventricular free wall (RVFW) ischemia impairs global RV performance and may result in acute hemodynamic compromise. However, RV function and hemodynamic performance typically improve spontaneously over time. This study was designed to determine whether reperfusion facilitates recovery of function in the ischemic right ventricle. METHODS AND RESULTS: Closed chest dogs underwent right coronary balloon occlusion for 1 hour (n = 9), 4 hours (n = 6), or 8 hours (n = 7). In all animals, occlusion depressed RVFW function and global RV performance. After 1 hour of ischemia, reperfusion led to immediate improvement in RVFW function and consequently global RV performance, with complete recovery over 4 weeks and scar in < 1% of total RVFW area. Reperfusion after 4- and 8-hour occlusions resulted in acute improvement in global RV performance but to a lesser extent and by different mechanisms, since RVFW contraction remained severely impaired. This disproportionate recovery of global RV function was attributable to diminished RVFW dyskinesis associated with reperfusion-induced increments in RVFW diastolic thickness (characterized histopathologically in 6 additional animals subjected to 4-hour occlusions but killed 1 hour after reperfusion by interstitial edema, contraction band necrosis, and hemorrhage). Although later reperfusion was associated with a slower pace and lesser extent of recovery, RVFW contraction improved markedly over time. At 4 weeks, there was trivial RVFW scar in 4-hour animals (2% of total RVFW area), and, although fibrosis was significantly greater in 8-hour animals (7% of RVFW area), infarction was minimal relative to the extent of jeopardized myocardium. CONCLUSIONS: The responses of ischemic RV myocardium to reperfusion are complex, with disparate effects according to the duration of preceding ischemia. Early reperfusion results in prompt improvement in and subsequent complete recovery of RVFW contraction and global RV performance, with trivial or no RVFW scar. Late reperfusion leads to little acute recovery of RVFW function, but global performance improves owing to diminished RVFW dyskinesis associated with reperfusion-induced increments in RVFW diastolic thickness. Nevertheless, RVFW function improves over time, with minimal evidence of infarction. Therefore, reperfusion facilitates recovery of RV function and minimizes the extent of infarction even after prolonged ischemia.

Acute Disease↗

Nesiritide for treatment of heart failure due to right ventricular dysfunction.

Little information exists regarding the use of nesiritide for treatment of right-sided heart failure. Similarly, little information is available regarding routine use of combination nesiritide and diuretics as initial therapy to relieve edema due to heart failure. Nesiritide may be beneficial in combination with diuretics because it reduces activity of the renin-angiotensin-aldosterone system. It is unclear how potent nesiritide is as a diuretic. Patients exhibit wide variability in clinical response from the diuretic effects of the drug. Two patients were given a combination of nesiritide and diuretics as initial treatment of right-sided heart failure; both experienced significant diuresis and weight loss. Further literature is needed to clarify the role of nesiritide in the treatment of right-sided heart failure.

Adult↗