[Reversible right ventricular dysfunction caused by thyrotoxicosis].
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When shock complicates an acute increase in RV afterload, initial therapy should be directed toward restoration of an adequate BP (RV coronary perfusion pressure) and CO. Current results indicate that norepinephrine, a drug with direct inotropic and pressor effects, may be an excellent agent for acute resuscitation and short-term maintenance of hemodynamic stability when frank circulatory instability complicates pulmonary embolism. Following hemodynamic stabilization, thrombolytic therapy should be initiated. Recent evidence suggests that the lytic agent can be given by bolus technique, but more work is required to determine the optimum dosing regimen. In the absence of shock, when a moderate decrease in CO complicates pulmonary embolism, isoproterenol or hydralazine may be used to improve flow. However, both of these agents may decrease systemic vascular resistance and BP. Accordingly, the latter parameter should be carefully monitored to ensure that excessive falls in BP and RV coronary perfusion pressure do not occur. Whereas in certain conditions volume expansion is appropriate therapy to increase CO, in acute pulmonary hypertension with excessive RV afterload, volume expansion may worsen RV function. Recent canine studies indicate that an increase in vascular closing pressure is the predominant mechanism explaining the increase in PAP and apparent increase in PVR complicating pulmonary embolism. Accordingly, in addition to decreasing vascular resistance, therapy to decrease RV afterload could be directed toward decreasing the vascular response producing excessive closing pressures.
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The natural history of arrhythmogenic right ventricular cardiomyopathy is determined by the electrical instability of the dystrophic myocardium, which can precipitate arrhythmic cardiac arrest any time during the course of the disease and by the progressive myocardial loss that results in ventricular dysfunction and heart failure. Sudden death accounts for the majority of the fatal events but its occurrence is mostly unpredictable. There are no prospective and controlled studies assessing clinical markers that can predict the occurrence of life-threatening ventricular arrhythmias. However, the noninvasive risk profile, which emerges from retrospective analysis of clinical and pathologic series, is characterized by history of syncope, physical exercise, spontaneous ventricular tachycardia or ventricular fibrillation, right ventricular dysfunction, left ventricular involvement, right precordial negative T wave, right bundle branch block, QT-QRS dispersion, right precordial ST-segment elevation and late potentials. At present only QRS dispersion, history of syncope and right and/or left ventricular abnormalities at radionuclide angiography proved to be independent noninvasive predictors of sudden death.
Within the course of an acute posterior wall myocardial infarction there may be involvement of the right ventricle leading to right ventricular infarction. The long-term prognosis of patients with right ventricular infarction is not meaningfully compromised provided that the left ventricular function is preserved. However, in the acute phase, there may be a threefold increase in mortality if the right ventricular infarction leads to substantial right ventricular dysfunction. Consequently, right ventricular involvement should be detected as early as possible. In addition to the clinical presentation, the ECG and echocardiogram can provide decisive information. In addition to reperfusion, specific measures are employed to address the hemodynamic derangement of right ventricular dysfunction. These include administration of fluids for volume expansion to increase filling pressure and avoidance of vasodilators and diuretics.
Forty-nine children with Kawasaki disease were included in this study. Based on the severity of carditis as determined by Tc-99m HMPAO-labeled WBC heart scan, the children were separated into two groups. Group A (n=24) had significant carditis and group B (n=25) did not have significant carditis. The left and right ventricular ejection fractions (LVEF and RVEF) were evaluated by equilibrium multigated blood pooling ventriculography. Diameters of the left and right coronary arteries (LCA and RCA) were measured by two-dimensional echocardiography. The results showed that group A had lower LVEF and RVEF, but larger diameters of the LCA and RCA than those of group B patients. The sensitivity of significant carditis to predict left ventricular dysfunction, right ventricular dysfunction, LCA dilation and RCA dilation was 88.9, 70.6, 75, and 71.4%, respectively; the specificities were 100, 100, 100, and 67.9%, respectively. Our findings suggest that significant carditis determined by Tc-99m HMPAO-labeled WBC heart scan can accurately predict impaired ventricular function and coronary artery dilation.
Doppler echocardiography was performed in 83 patients, 13-26 (median 19) years after repair of tetralogy of Fallot. Median age at repair was 7 years (range 9 months-42 years). An outflow patch restricted to the right ventricle was used in 29%, a transannular patch in 27% and the right ventricle was closed without a patch in 44%. Ninety-six percent of the patients were asymptomatic at follow-up. Patients with a transannular patch were younger, had a larger right ventricle and a higher right ventricle to pulmonary artery pressure difference than those without a patch. The average end-diastolic diameter of the right ventricle was larger than normal regardless of type of repair. The thickness of the right ventricular wall was increased in 50%. In 43% of the patients there was persistent hypertrophy of the right ventricular wall despite normalized systolic pressure. The average size and function of the left ventricle were normal although fractional shortening was reduced in 30% of the patients. The aortic root was abnormally large in 48%. Thirty-four percent had moderate or severe pulmonary valve regurgitation. Symptom-limited work capacity was 87% of predicted and was inversely related to age, systolic pressure in the right ventricle. E/A ratio of the left ventricle and use of the transannular patch. We conclude that right ventricular dysfunction and right ventricular outflow obstruction and/or incompetence were common even in asymptomatic long-term survivors after repair of tetralogy of Fallot.
Mongrel dogs underwent a large (apex to pulmonary valve) right ventriculotomy to produce right ventricular dysfunction. Right ventriculotomy decreased cardiac output from 2.47 +/- 0.43 to 1.34 +/- 0.16 L/min (p less than .01), increased CVP from 3.7 +/- 1.5 to 8.3 +/- 2.4 mm Hg (p less than .01), and decreased mean systemic arterial pressure (MAP) from 143 +/- 16 to 121 +/- 21 mm Hg (p less than .01). There was no effect on mean pulmonary artery pressure (MPAP) or pulmonary artery occlusion pressure. After stabilization a randomized crossover controlled comparison of conventional mechanical ventilation (CMV) and high-frequency oscillation (HFO) was performed. FIO2, pH, PCO2, core temperature, and preload were held constant. Mean airway pressure (Paw) was 4.8 +/- 0.7 cm H2O on CMV vs. 3.5 +/- 1.0 cm H2O on HFO (p less than .05). There was no difference in PaO2. We found no statistically significant differences between the two modes of ventilation with respect to cardiac output, MAP, MPAP, systemic vascular resistance, and pulmonary vascular resistance. Blood flows to cerebral cortex, renal cortex, adrenal, hepatic artery, left ventricular myocardium, and skeletal muscle were not different when comparing CMV to HFO. Despite the ability to attain equivalent oxygenation and ventilation at lower Paw, HFO offers no hemodynamic advantage over CMV in the presence of right ventricular dysfunction.
Initial hemodynamics were studied in 101 patients with acute myocardial infarction complicated by shock or left heart failure. 59 had anterior myocardial infarction (AMI); 42 had inferior myocardial infarction (IMI). Data were processed by univariate analysis and correspondence analysis. AMIs and IMIs were significantly different on conduction disturbances, heart rate, left ventricular filling pressure, mean pulmonary artery pressure and right ventricular function indices. Both patients and parameters were projected on the most meaningful factorial plane generated by correspondence analysis. This two-dimensional graphical representation showed that all the information was roughly distributed along the 2 orthogonal axes defining this plane. Survivors and nonsurvivors were fairly well separated along the first factorial axis (prognostic axis) which was highly correlated with both outcome and left ventricular function parameters. AMIs and IMIs were grossly separated along the second factorial axis (topographical axis) which was rather well correlated with location and right ventricular function parameters. These studies suggest that AMI and IMI hemodynamic profiles are modulated by the presence or absence of right ventricular dysfunction. Moreover right ventricular dysfunction may be held responsible of some lack of information about left ventricular function status.
We evaluated right and left ventricular function by intraoperative transesophageal echocardiography for the patients with left ventricular dysfunction (left ventricular ejection fraction (LVEF) < or = 40) who underwent isolated coronary artery bypass grafting (CABG). We divided these patients into two groups; group 1 who had difficulty of weaning from cardiopulmonary bypass due to hypotension (n = 8) and group 2 who did not have any difficulty of it (n = 17). Basement characteristics (age, gender, history of myocardial infarction, congestive heart failure, LVEF, severity of the right coronary artery disease) of both groups were not different significantly. Intraoperative characteristics (the number of distal anastomoses, duration of aortic cross-clamp and cardiopulmonary bypass, and bypass to the right coronary artery) were also not different between two groups. However, mean duration of ICU stay and in-hospital mortality were significantly longer and higher in group 1 than group 2. On the other hand, right ventricular systolic function was severely impaired, particularly postoperatively, in group 1 compared with group 2. Right and left ventricular systolic function of group 2 was fairly improved postoperatively. These results may indicate that right ventricular dysfunction is a potent predictor of postoperative morbidity and mortality for the patients with left ventricular dysfunction who undergo isolated CABG.
Right ventricular systolic dysfunction (RVSD) at baseline (pre-treatment) predicts early death in patients with pulmonary hypertension (PH). However, RVSD can only be detected reliably by prohibitively invasive or expensive techniques. N-terminal B-type natriuretic peptide concentration ([NT-proBNP]) correlates with RV function in PH; however, an [NT-proBNP] threshold that indicates RVSD in individual patients has not previously been determined. Twenty-five patients with PH (pulmonary arterial hypertension (n = 19) or chronic thromboembolic PH (n = 6)) underwent cardiovascular magnetic resonance (CMR) imaging and NT-proBNP measurement at baseline. [NT-proBNP] was correlated against RV dimensions and ejection fraction (RVEF) measured directly by CMR imaging. The ability of NT-proBNP to detect RVSD (defined as a CMR-derived RVEF >2 SDS below control values) was tested and predictors of [NT-proBNP] identified. [NT-proBNP] correlated negatively with RVEF. RVSD was present in nine out of 25 patients. An [NT-proBNP] threshold of 1,685 pg.mL(-1) was sensitive (100%) and specific (94%) in detecting RVSD. RVEF and RV mass index independently predicted [NT-proBNP]. In pulmonary hypertension, a baseline N-terminal B-type natriuretic peptide concentration of >1,685 ng.L(-1) suggests right ventricular systolic dysfunction, and thus an increased risk of early death. N-terminal B-type natriuretic peptide could prove useful as an objective, noninvasive means of identifying patients with pulmonary hypertension who have right ventricular systolic dysfunction at presentation.
UNLABELLED: The detection of right ventricular dysfunction in acute inferior myocardial infarction is important because of its potentially serious consequences which may be remediable with the appropriate therapeutic manoeuvres. A technique has been developed to assess right ventricular function using 133-xenon. This technique was applied to 26 patients who had sustained an acute inferior myocardial infarction. Right ventricular ejection fractions ranged from 7-54%, mean 30 +/- 11%, which was significantly lower than values obtained from normal volunteers (n = 21), mean 43 +/- 5%, and patients with arteriographically proven coronary artery disease without previous myocardial infarction (n = 12), mean 39 +/- 9%, P less than 0.001, and P less than 0.001, respectively. In the patients with acute inferior myocardial infarction 18 patients (69%) had evidence of right ventricular dysfunction (right ventricular ejection fraction less than 35%). 13/26 patients (50%) had clinical evidence of right ventricular dysfunction with a mean right ventricular ejection fraction 26 +/- 11% (range 7-54%) which was significantly lower than the patients without evidence of right ventricular dysfunction, mean 35 +/- 9% (range 16-49%), P less than 0.001. The clinical signs had a sensitivity of 72% (13/18), a specificity of 87.5% (7/8) and a predictive accuracy of 76% (20/26) when compared to the imaging data. IN CONCLUSION: (1) gated 133-xenon imaging provides a method for assessing right ventricular function in the setting of acute myocardial infarction; (2) a wide spectrum of right ventricular dysfunction occurs following inferior myocardial infarction which may not manifest itself clinically.
PURPOSE: As the evaluation of diastolic function can be complex in the setting of a busy cardiac operating room, its assessment may benefit from an algorithmic approach using transesophageal echocardiography. We developed a diagnostic algorithm which was then applied in a series of cardiac surgery patients to determine whether moderate to severe left ventricular diastolic dysfunction (LVDD) and right ventricular diastolic dysfunction (RVDD) can predict difficult separation from cardiopulmonary bypass (DSB). METHODS: An algorithm using pulsed-wave Doppler interrogation of the mitral and tricuspid valve, the pulmonary and hepatic venous flow, and tissue Doppler interrogation of the mitral and tricuspid annulus was developed. The study was divided in two phases involving two groups of patients undergoing cardiac surgery. In phase I, echocardiographic evaluations of patients (n = 74) were used to test the reproducibility of the algorithm and to evaluate inter-observer variability using Cohen's kappa values which were calculated in three specific periods. In phase II, the algorithm was applied to a second group of patients (validation group, n = 179) to explore its prognostic significance. The primary end-point in phase II was DSB. RESULTS: In phase I, the kappa coefficients for LVDD and RVDD algorithms were 0.77 and 0.82, respectively. In phase II, moderate or severe degrees of LVDD were observed in 29 patients (16%) and moderate to severe RVDD was observed in 18 patients (10%) before cardiac surgery. Both moderate and severe LVDD (P = 0.017) and RVDD (P = 0.049) before surgery were observed more frequently in patients with DSB. CONCLUSION: Moderate and severe LVDD and RVDD can be identified with very good reproducibility, and both degrees of diastolic dysfunction are associated with DSB.