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PubMed1990

Hemodynamic importance of systolic ventricular interaction, augmented right atrial contractility and atrioventricular synchrony in acute right ventricular dysfunction.

To delineate the determinants of right ventricular performance with acute right ventricular dysfunction, surgical electrical isolation of the right ventricular free wall was produced in 13 dogs. During atrioventricular (AV) pacing, hemodynamic and wall motion measurements were normal. When not paced, the right ventricular free wall became asystolic, resulting in a depressed and bifid right ventricular systolic pressure (33 +/- 5 to 18 +/- 4 mm Hg) and decreased left ventricular systolic pressure (100 +/- 18 to 80 +/- 18 mm Hg) and stroke volume (14 +/- 4 to 10.3 +/- 3.5 ml) (all p less than 0.05). Ultrasound demonstrated right ventricular free wall dyskinesia, increased right ventricular end-diastolic size (155 +/- 13% of control), but decreased left ventricular size (69 +/- 11% of control) (both p less than 0.05). Right atrial pressure increased (5.8 +/- 2.5 to 7.6 +/- 2.8 mm Hg, p less than 0.05) with an augmented A wave and blunted Y descent, indicating pandiastolic right ventricular dysfunction. The septum demonstrated reversed curvature in diastole and bulged paradoxically into the right ventricle during early systole, generating the initial peak of right ventricular pressure and reducing its volume. Later, posterior septal motion coincided with maximal left ventricular pressure and the second peak of the right ventricular waveform. Left ventricular pacing alone led to further decreases in right ventricular systolic pressure and size, left ventricular systolic pressure and stroke volume. The previously augmented A wave was replaced by a prominent V wave. Therefore, when contractility of its free wall is acutely depressed, right ventricular performance is dependent on left ventricular-septal contractile contributions transmitted by the septum.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Exercise-induced STV1 elevation: a sign of right ventricular dysfunction in recent inferior myocardial infarction.

BACKGROUND: Little is known about exercise-induced electrocardiographic ST segment shift in right-sided precordial leads, especially elevated ST in patients with subacute inferior myocardial infarction. OBJECTIVE: To test the clinical significance of exercise-induced STV1 deviation with special regard to right ventricular function and right ventricular involvement. DESIGN: Sixty-eight patients with recent inferior myocardial infarction (without having a left descending arterial lesion) aged 30 to 73 years (mean +/- SD, 59.1 +/- 10.0) were investigated with respect to biventricular function observed in radionuclide ventriculography and treadmill stress electrocardiographic findings. RESULT: STV1 shift during exercise (delta STV1) had a negative linear logarithmic relationship only with the right ventricular ejection fraction (RVEF) and no correlation with the left ventricular ejection fraction (delta STV1 = 6.7604-1.7528xlnRVEF, r = 0.709, P = 0.0001). Significant STV1 elevation (delta STV1 of 0.5 mm or more) predicted right ventricular dysfunction (RVEF of 40% or less) and right ventricular infarction with sensitivities of 76% and 77%, specificities of 88% and 92%, and accuracies of 84% and 77%, respectively. Twenty patients with STV1 elevation (0.5 mm or more) showed nearly identical rest and exercise electrocardiographic findings, exercise capacities and similar stenotic lesions on coronary angiography, to 43 patients without significant STV1 elevation. Elective balloon angioplasty reduced the delta STV1 during exercise in only three of six patients (50%) with right ventricular infarction. CONCLUSION: Exercise-induced STV1 elevation may be a useful indicator of global right ventricular dysfunction and/or right ventricular infarction in the subacute phase of myocardial inferior infarction.

Adult↗

PubMed1995

Prognostic significance of right ventricular dysfunction in patients with acute inferior myocardial infarction and right ventricular involvement.

Little is known about the influence of right ventricular (RV) dysfunction on prognosis of patients with acute inferior myocardial infarction (IMI) and RV involvement. Therefore, 99 consecutive patients (mean age 56.6 +/- 3.4 years) with RV involvement during acute IMI were followed for a 12-month period to clarify the influence of acute RV dysfunction on short- and long-term survivals. Forty-one patients with IMI evolved with severe arterial hypotension due to RV dysfunction, while 58 patients had no hemodynamic impairment due to RV involvement. Basal hemodynamic data (mean +/- SD) for patients with RV dysfunction were blood pressure (BP) 92/59 +/- 22/20 mmHg, systemic vascular resistance (SVR) 2314 +/- 252 dynes.s.cm-5, and cardiac index (CI) 1.3 +/- 0.3 l/min/m2. Patients without RV dysfunction demonstrated BP 113/74 +/- 20/16 mmHg (p < or = 0.05), SVR 1324 +/- 354 dynes.s.cm-5 (p < or = 0.01), and CI 2.6 +/- 0.5 l/min/m2 (p < or = 0.05). Angiographic differences noted were that hemodynamically compromised patients showed lower RV ejection fractions (0.27 +/- 0.08) than patients without hemodynamic disturbance [0.41 +/- 0.11 (p < or = 0.05)]; however, left ventricular ejection fractions were 0.48 +/- 0.10 and 0.52 +/- 0.12, respectively. Short- and long-term mortality rates were assessed during the follow-up period. Patients with hemodynamic impairment due to RV infarction had a higher mortality rate for the first month and for 11 subsequent months post MI than patients without hemodynamic impairment, that is 24.4 vs. 6.9 and 14.6 (p <or = 0.05) vs. 3.4 (p < or = 0.05), respect ively.(ABSTRACT TRUNCATED AT 250 WORDS)

Creatine Kinase↗

PubMed1995

Right ventricular dysfunction in low output syndrome after cardiac operations: assessment by transesophageal echocardiography.

BACKGROUND: Low output syndrome after cardiac operations is associated with high morbidity and mortality rates. The contribution of right ventricular dysfunction to this syndrome has not been fully characterized. The purpose of this study was to evaluate the utility of transesophageal echocardiography to identify the frequency and the in-hospital mortality from right ventricular dysfunction in patients with this syndrome. METHODS: Seventy-five consecutive patients undergoing transesophageal echocardiography for low output syndrome early after cardiac operations were evaluated. The findings from transesophageal echocardiography were correlated with the type of surgical procedure, cross-clamp time, right heart hemodynamics, and coronary angiography. RESULTS: Right ventricular systolic dysfunction occurred in 36 patients (42%); in 17 patients it was isolated and in 19 patients it occurred in combination with left ventricular dysfunction. Postoperative right ventricular dysfunction was not uniformly associated with important right coronary artery disease or with prolonged ischemic time during cardiopulmonary bypass. Hemodynamic data were not useful to distinguish the group with postoperative right ventricular dysfunction. Patients with right ventricular dysfunction had a high (44%) in-hospital mortality rate. CONCLUSIONS: Right ventricular dysfunction occurs frequently in patients with low output syndrome after cardiac operations and is associated with a high in-hospital mortality rate. Better understanding of the mechanisms causing postoperative right ventricular dysfunction may provide insight for preventing this complication.

Adult↗

PubMed1987

Selective right ventricular dysfunction following doxorubicin therapy.

Cardiotoxicity is one of the major side effects of doxorubicin therapy. The side effect presents in an acute and chronic form. It has been observed mainly when the cumulative dosage exceeds 450 mg/m2 of body surface. The cardiotoxicity presents with a low left ventricular ejection fraction. We report three patients who developed selective right ventricular dysfunction, expressed by low right ventricular ejection fraction as measured by radionuclide angiography. This complication was observed with rather low cumulative dosages of the drug (105 to 318 mg/m2). Two of the patients received concurrent mitomycin-C chemotherapy and the third patient underwent prior mediastinal irradiation. The possible mechanism for this selective cardiotoxicity is discussed. Monitoring of right ventricular performance by radionuclide angiography during doxorubicin therapy is recommended so that therapy can be discontinued before the left ventricle is damaged.

Adult↗

PubMed1996

Mechanisms of right ventricular dysfunction after pulmonary resection.

BACKGROUND: Significant right ventricular (RV) dysfunction as measured by increased end-diastolic volume and reduced ejection fraction has been documented in the postoperative period after pulmonary resection. We hypothesized that changes in RV contractile state or afterload may contribute to this RV pump dysfunction. METHODS: In part one of the study, RV preload was altered on postoperative day 2 (n = 6) by rapid infusion of Hespan to a total of 250, 500, and 1,000 mL. The relationship between RV stroke work and end-diastolic volume was plotted using linear regression. This preload recruitable stroke work relation had been previously validated as a load-insensitive index of RV contractility. The slopes of the preoperative relation (n = 35) and postoperative relation were compared. In part two of the study, RV afterload was reduced by continuous infusion of prostaglandin E1 (n = 6) through postoperative day 2 and RV pump function was assessed. RESULTS: Comparison of the slopes of the preload recruitable stroke work relation plotted preoperatively and on postoperative day 2 revealed no significant difference, indicating no change in RV contractile state. Infusion of prostaglandin E1 in the postoperative period (n = 6) significantly reduced pulmonary vascular resistance (3.67 +/- 0.19 versus baseline 5.72 +/- 0.19 dyne . s . cm-5/ m2; p < 0.05). However, RV ejection fraction remained significantly reduced (0.34 +/- 0.01 versus baseline 0.42 +/- 0.01; p < 0.05) and end-diastolic volume significantly increased (105 +/- 5 versus baseline 93 +/- 2 mL/m2; p < 0.05). Heart rate was increased compared with baseline throughout the postoperative period. CONCLUSIONS: The present study suggests that RV dysfunction after pulmonary resection is not caused by primary alterations in contractility or immediate changes in afterload. Better control of heart rate with minimal effect on inotropy may enhance RV pump function.

Alprostadil↗

PubMed1997

Right ventricular dysfunction during coronary artery occlusion: pressure-volume analysis using conductance catheters during coronary angioplasty.

OBJECTIVE: To study the effects of coronary artery occlusion on the pressure-volume relations of the right ventricle. DESIGN: Right ventricular pressure-volume cycles were studied using conductance catheters and micromanometers in 19 subjects undergoing coronary angioplasty in a tertiary referral cardiac centre. RESULTS: Catheter occlusions of either the left anterior descending coronary artery or the right coronary artery were associated with a decline in stroke work (mean change (SD): left-13.3 (15.8)%, p = 0.008; right -13.5(16.5)%, p = 0.04). Two patterns of change were evident: an upward shift usually associated with occlusion in the left coronary artery, and a rightward shift in the right coronary artery. In the former there was an increase in maximum ventricular volume (mean change: 3.0(2.7)%, p = 0.004) and in minimum ventricular volume (mean change: 2.3(2.7)%, p = 0.01) and a fall in peak pressure (mean change: -4.8 (5.1)%, p = 0.04). In the latter there was an increase in peak pressure (mean change 9.9(16.3)%, p = 0.04) and an increase in minimum ventricular volume (mean change 3.7(5.0)%, p = 0.02) leading to a fall in stroke volume (mean change -13.3(15.8)%, p = 0.008). CONCLUSIONS: Occlusion of the left anterior descending coronary artery or the right coronary artery is associated with a decline in right ventricular work. However, different patterns of change in indices of preload and afterload lead to different effects on overall right ventricular pump function.

Angioplasty, Balloon, Coronary↗

PubMed1995

Right ventricular dysfunction after acute pulmonary embolism: pathophysiologic factors, detection, and therapeutic implications.

Acute PE may lead to right ventricular dilatation and failure. Through ventricular interdependence and decreased left ventricular filling, cardiac output and systemic circulation also may be compromised. The associated decrease in coronary perfusion pressure to the acutely overloaded right ventricle may produce ischemia and worsening right heart failure. This downward cycle of right ventricular failure and ischemia may ultimately progress to right ventricular infarction, circulatory arrest, and death. Certain clinical findings, hemodynamic values, and, particularly, echocardiographic signs can identify right ventricular dysfunction after PE. Detection of right ventricular hypokinesis helps to stratify patients' risk, because right ventricular dysfunction confers a worse prognosis than does normal right ventricular function after PE. The concept of "hemodynamic instability" after PE should be expanded to include right ventricular dilatation and wall motion abnormalities, even among normotensive patients. Aggressive intervention with thrombolytic therapy, vasoactive agents, or mechanical embolectomy may improve right ventricular function and clinical outcome.

Electrocardiography↗

PubMed1980

Right myocardial infarction with predominant right ventricular dysfunction.

Two patients with right ventricular myocardial infarction are described. In both cases, the hemodynamic criteria established for this diagnosis were fulfilled, namely, right-side pressure values (central venous pressure and right atrial pressure) equal to or higher than left-side pressure values (pulmonary capillary wedge pressure and left ventricular end-diastolic pressure). ECG tracings showed acute diaphragmatic myocardial infarction. The lungs were clear both clinically and radiologically. The diagnosis of right ventricular myocardial infarction was confirmed in the first patient by hemodynamic studies and at autopsy, and in the second patient, by hemodynamic and echocardiographic studies. Only in the second care was the administration of massive quantities of fluids and dopamine followed by good results. The importance of establishing a precise diagnosis of right ventricular myocardial infarction is emphasized, since therapy for this condition is different than that for left ventricular myocardial infarction.

Aged↗

PubMed1985

A prospective clinical, scintigraphic, angiographic and functional evaluation of patients after inferior myocardial infarction with and without right ventricular dysfunction.

To elucidate the functional and prognostic significance of right ventricular dysfunction after acute inferior wall myocardial infarction, 74 consecutive patients with inferior infarction were prospectively evaluated with gated equilibrium blood pool imaging at rest, submaximal exercise thallium-201 scintigraphy and coronary angiography before hospital discharge. In addition, symptom-limited stress thallium-201 scintigraphy was performed in 61 patients at 3 months, and all patients were followed up clinically for 23 +/- 15 months. Utilizing predetermined radionuclide angiographic criteria, 47 patients (Group I) had normal right ventricular function, 12 patients (Group II) had mild to moderate dysfunction and 15 patients (Group III) had severe right ventricular dysfunction. There were no significant differences among the groups with regard to age, history of prior myocardial infarction, peak creatine kinase values, maximal Killip functional class, number or type of in-hospital complications, left ventricular ejection fraction, prevalence of multivessel disease or the distribution and severity of disease affecting the infarct-related vessel. Exercise tolerance as assessed by treadmill time, blood pressure-heart rate product and peak work load in METS was comparable among the three groups, both before hospital discharge and at 3 month follow-up. No differences in indicators of exercise-induced ischemia were noted among the groups, including the prevalence of redistribution thallium-201 defects, ST segment depression or symptoms of chest pain. Finally, cardiac mortality, reinfarction rate and the incidence of medically refractory angina pectoris were similar in the three groups. Thus, right ventricular dysfunction after acute inferior wall myocardial infarction does not appear to limit exercise tolerance or identify a subgroup of patients at higher risk for recurrent cardiac events.

Adult↗

PubMed2025

Identification of Biomarkers for Right Ventricular Dysfunction in Idiopathic Dilated Cardiomyopathy Via Urinary Proteomics and Machine Learning.

BACKGROUND: Right ventricular dysfunction (RVD) is a common complication of idiopathic dilated cardiomyopathy linked to poor outcomes. However, reliable noninvasive biomarkers for RVD remain lacking. This study aimed to identify urinary proteomic markers using mass spectrometry and machine learning. METHODS: In this prospective cohort, patients with idiopathic dilated cardiomyopathy were classified by cardiac magnetic resonance imaging into groups with RVD (RV ejection fraction <45%) and without RVD groups. Baseline urine samples were profiled by data-independent acquisition mass spectrometry. Differentially expressed proteins were identified and selected by least absolute shrinkage and selection operator regression to build a diagnostic model, developed in a training set, and validated in a test set. The primary end point was a composite of cardiovascular death, heart failure rehospitalization, left ventricular assist device implantation, or heart transplantation. RESULTS: The study enrolled 147 patients with idiopathic dilated cardiomyopathy (64 with RVD, 83 without), with a median follow-up of 19.3 months. Of 3579 quantified urinary proteins, 46 were differentially expressed between groups. A 3-protein panel (RARRES1 [retinoic acid receptor responder protein 1], MVB12B [multivesicular body subunit 12B], GSK3A [glycogen synthase kinase 3 alpha]) was identified and showed excellent diagnostic accuracy (training area under the curve 0.946; validation area under the curve0.935), outperforming both NT-proBNP (N-terminal pro-brain natriuretic peptide) and tricuspid annular plane systolic excursion. The risk score derived from this panel effectively stratified patients, with the high-risk group exhibiting significantly worse outcomes than the low-risk group (hazard ratio, 3.24 [95% CI, 1.56-6.71], P=0.002). CONCLUSIONS: The urinary proteomic panel developed in this study demonstrates diagnostic and prognostic potential for identifying RVD in idiopathic dilated cardiomyopathy, providing a promising noninvasive tool for precise detection and clinical risk stratification.

Humans↗

PubMed1996

Right ventricular dysfunction in obstructive sleep apnoea: reversal with nasal continuous positive airway pressure.

The incidence and pathogenesis of right ventricular dysfunction in obstructive sleep apnoea (OSA) remains controversial. Using nuclear ventriculography, the prevalence of right ventricular dysfunction (RVD) was therefore determined in obese patients with OSA, as well as their clinical characteristics, arterial blood gas values, spirometry and sleep parameters. The reversibility of RVD was evaluated after long-term use of nasal continuous positive airway pressure (nCPAP). We studied 112 obese patients with OSA by nuclear ventriculography, 35 with RVD (Group 1), 77 without RVD (Group 2), and 14 patients without OSA as controls (Group 3). Repeat nuclear ventriculography was performed in seven patients who used nCPAP nightly for 6-24 months. The mean right ventricular ejection fractions (RVEF) were 31%, 47% and 44% in Groups 1, 2 and 3, respectively. Group 1 also had a lower left ventricular ejection fraction (LVEF) of 55 vs 63% in Group 2. The OSA groups did not differ in mean spirometric or arterial blood gas values. Group 1 had a lower mean nocturnal arterial oxygen saturation (Sa,O2) of 82 vs 87% in Group 2, and a longer apnoea duration of 22.3 vs 19.2 s. All but two patients in Group 1 had either awake alveolar hypoventilation or an apnoea + hypopnoea index > 40 disordered breathing events.h-1. Repeat nuclear ventriculography after nCPAP revealed an increase in RVEF from 30 to 39%. In conclusion, right ventricular dysfunction is common in obstructive sleep apnoea, but it is reversible with nasal continuous positive airway pressure treatment and appears to be related to nocturnal oxygen desaturation.

Adult↗

PubMed1989

Right ventricular dysfunction in septic shock: assessment by measurements of right ventricular ejection fraction using the thermodilution technique.

Right ventricular ejection fraction (RVEF) was measured by the thermodilution technique in a series of 127 consecutive critically ill patients monitored with a modified pulmonary artery (PA) catheter equipped with a fast response thermistor. Thermodilution RVEF was significantly lower in septic shock (23.8 +/- 8.2%, 93 measurements) than in sepsis without shock (30.3 +/- 10.1%, 118 measurements) or in the absence of sepsis or cardiopulmonary impairment (32.5 +/- 7.1%, 62 measurements). Both myocardial depression and pulmonary hypertension could account for this impairment of RV function. RVEF decreased from 35.1 +/- 9.8 to 24.2 +/- 10.4% (P less than 0.01) during development of septic shock and increased from 25.0 +/- 7.6 to 29.8 +/- 8.5% (P less than 0.05) during recovery (14 patients). Initial RVEF in septic shock was 27.8 +/- 8.6% in 11 patients who survived but only 20.9 +/- 6.7% (P less than 0.02) in the 23 patients who eventually died. Thus, RV dysfunction is common during septic shock, is directly related to its severity, and can easily be recognized in patients monitored with a PA catheter.

Adult↗

PubMed1986

High-frequency ventilation versus conventional ventilation in dogs with right ventricular dysfunction.

A randomized crossover protocol was used to compare conventional mechanical ventilation (CMV) and high-frequency ventilation (HFV) in mongrel dogs experiencing right ventricular dysfunction after right ventriculotomy. When inspired oxygen, pH, PCO2, core temperature, and preload were held constant, cardiac output increased significantly (p less than .05) from 1.16 +/- 0.24 to 1.38 +/- 0.25 L/min and pulmonary vascular resistance decreased significantly (p less than .05) from 734 +/- 257 to 554 +/- 169 dyne X sec/cm5 during HFV relative to CMV. We also noted a significant (p less than .05) increase in mean arterial pressure from 116 +/- 27 to 124 +/- 23 mm Hg and a significant (p less than .05) increase in left ventricular stroke work from 10.2 +/- 3.5 to 12.3 +/- 2.6 g X m during HFV. During the inspiratory phase of CMV there were increases in CVP, pulmonary artery pressure, and systemic arterial pressure, and decreases in pulmonary artery flow which did not occur during HFV. HFV may be preferable to CMV in the presence of right ventricular dysfunction.

Animals↗

PubMed1997

[Clinical, echocardiographic and Doppler outcome in ischemic right ventricular dysfunction associated with inferior wall infarction].

Right ventricular involvement during inferior wall myocardial infarction does not seem to alter long-term clinical prognosis but its specific outcome has not been clearly studied. We have previously demonstrated that pulmonary regurgitant (PR) flow tracings doppler analysis allows the accurate diagnosis of RV involvement, especially when the pressure half-time of PR was < or = 150 ms and the ratio of the minimal velocity to the maximal velocity was < or = 0.5. We studied 40 patients with acute inferior wall myocardial infarction and with PR flow. Doppler echocardiography was obtained during the first day, before discharge (early control) and between 12 and 24 months follow-up (late control). Among 22 patients with RV involvement defined with PR-derived doppler parameters (RVIPR). 8 had right ventricular enlargement and/or wall motion abnormalities, observed in 6 cases at early control and in 4 at late control. Doppler analysis showed remnant RVIPR parameters in 9 patients at early control and 8 among these at late contorl, with no relation with pulmonary artery pressure or other echocardiographic parameters. No clinical, angiographic or therapeutic data predicted these distinct echocardiographic and doppler patterns and the long-term prognosis was not different. At late control, among 12 RVIPR patients which PR-derived doppler parameters were normal at early control, two patients had still RVIPR pattern at late control and described ischemic recurrence. PR flow doppler analysis is a useful tool for diagnosis and outcome evaluation of RV involvement and shows a remnant diastolic dysfunction in half of the patients with acute RV involvement.

Aged↗

PubMed1990

[Right ventricular dysfunction of mitral valve stenosis].

Right ventricular function was studied in 9 patients with mitral valve stenosis who underwent mitral valve replacement (St. Jude Medical valve 29-31 mm) (MVR). The right ventricular systolic pressure/end-systolic volume index (RVSP/ESVI) correlated well with right ventricular ejection fraction (RVEF) in the normal control group thus it considered to be a index of right ventricular contractility. At rest, RVEF in the MVR group was significantly lower than that in the control group. However there was no difference in the RVSP/ESVI between both groups. In the MVR group, the total pulmonary resistance index (TPRI) and mean pulmonary arterial pressure (mPAP) were higher than those in the control group. During exercise, the RVSP/ESVI became higher in both groups, but RVEF did not increase in the MVR group. In the control group, RVEF became higher during exercise. In addition, TPRI and mPAP increased in the MVR group but the control group did not show significant changes during exercise. In conclusion, low RVEF after MVR, which reflects pump function of the right ventricle, was not caused by contractile dysfunction of the right ventricle but mainly by excess afterload due to irreversible pulmonary vascular resistance persisting after operation as a result of chronic pulmonary vascular hypertension.

Adult↗

PubMed1986

Effect of beta-blockade on right ventricular performance in patients with and without right ventricular dysfunction due to coronary artery disease.

To assess the effects of beta-blockade on right ventricular performance in patients with and without right ventricular dysfunction due to coronary artery disease, we performed radionuclide ventriculography on eight patients with normal right ventricular ejection fraction (RVEF greater than or equal to 35%) and 14 patients with mild to moderate right ventricular dysfunction (RVEF less than 35%) at rest. All patients had chronic stable angina pectoris, and nine patients had prior myocardial infarction. Radionuclide ventriculography was performed on placebo and during clinical beta-blockade (heart rate, 50 to 60 beats per minute and less than or equal to 20% increase in heart rate over baseline during stage I treadmill exercise, Bruce protocol) with the oral, cardioselective beta-blocking agent, betaxolol. The resting RVEF (mean +/- 1 SD) was 33% +/- 7% on placebo and 34% +/- 7% during clinical beta-blockade. Mean exercise RVEF was 40% +/- 8% on placebo and 39% +/- 8% during clinical beta-blockade. These differences were not statistically significant. Resting left ventricular ejection fraction ranged from 22% to 60% (mean, 42% +/- 8%). On placebo, one of eight patients with a resting RVEF greater than or equal to 35% had a normal exercise RVEF response (greater than or equal to 5% increment) whereas nine of 14 patients with resting RVEF less than 35% had normal exercise response. The discordant relationship between baseline RVEF and exercise response on placebo became less marked during clinical beta-blockade. We conclude that beta-blockade does not produce significant deterioration of right ventricular systolic function or right ventricular reserve either in patients with normal or in those with mild to moderately impaired resting right ventricular systolic function.

Adrenergic beta-Antagonists↗

PubMed1997

Nitric oxide inhalation in the treatment of right ventricular dysfunction following left ventricular assist device implantation.

BACKGROUND: Following left ventricular assist device (LVAD) implantation in end-stage heart failure, the management of right ventricular dysfunction presents a therapeutic problem unresolved by conventional drug therapy (catecholamines, nitrates, and prostacyclin). This study was performed to investigate the effects of supplemental inhalation of nitric oxide (NO), a selective pulmonary vasodilator, postoperatively and prospectively. METHODS AND RESULTS: Intraindividual dose titration of NO was performed (0 to 40 ppm) according to a standardized protocol. Thereafter treatment was continued with the individually most effective dose of NO (25 to 40 ppm). In 8 consecutive male patients presenting with right ventricular dysfunction postoperatively, a significant dose-dependent improvement in hemodynamic function was observed: pulmonary vascular resistance decreased from 336+/-110 to 210+/-59 dynes x s x cm(-5) (P<.0001), cardiac index rose from 2.0+/-0.4 to 2.7+/-0.4 L x min(-1) x m(-2) (P<.003) at 40 ppm; doses of >20 ppm were effective in increasing cardiac index (P<.05). With continuous NO inhalation up to 48 hours, pulmonary vascular resistance decreased further to 155+/-33 dynes x s x cm(-5) (P<.0001) as the cardiac index increased to 3.3+/-0.6 L x min(-1) x m(-2) (P<.003). Pulmonary artery pressure decreased (P<.0001) as did systemic vascular resistance with hemodynamic improvement (P<.01). Central venous pressure and mean arterial pressure remained unchanged. Right ventricular ejection fraction at transesophageal echocardiography increased from 24+/-7% to 44+/-7% (P<.01) at the end of the study, and right ventricular end-diastolic volume decreased (P<.05). Weaning from NO therapy was successful at 2 to 8 days, and all patients were extubated. Right ventricular function remained stable thereafter. CONCLUSIONS: In the treatment of right ventricular dysfunction following LVAD implantation, inhalation of NO markedly decreased right ventricular afterload by its selective vasodilating effects on the pulmonary circulation without producing systemic hypotension; this merits further evaluation.

Administration, Inhalation↗