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Diagnosis and prognosis of right ventricular infarction.

The values of several non-invasive methods for the diagnosis of right ventricular necrosis in inferior myocardial infarction were compared in 51 consecutive patients who underwent serial radionuclide ventriculography, pyrophosphate scintigraphy, and cross sectional echocardiography. In addition a unipolar electrocardiographic lead V4R was recorded on admission, daily, and during episodes of further pain. Profound right ventricular dysfunction was evident in 50% of patients studied by radionuclide methods after inferior myocardial infarction but recognition on clinical groups alone was poor. Functionally important right ventricular infarction was best detected and followed serially by radionuclide ventriculography. Echocardiographic methods for evaluating right ventricular ejection fraction correlated poorly with radionuclide methods. Increased uptake of radioactivity by the right ventricle on pyrophosphate scintigraphy usually indicated poor right ventricular function, but a scan that was negative in the right ventricular territory did not exclude dysfunction. ST segment elevation in V4R was not specific for right ventricular infarction and its routine use may lead to overdiagnosis of this condition. Serial measurements suggest that profound right ventricular dysfunction persists after acute inferior infarction and is associated with considerable morbidity and mortality. Of 25 patients with severe right ventricular dysfunction, six died in the late hospital period. In the remaining 19 patients mean right ventricular ejection fraction over a two month period did not improve; six patients had persistent right ventricular dyskinesia and features of chronic right ventricular failure developed in three survivors.

Adult↗

Reversed closure sequence of the mitral and tricuspid valves in congestive heart failure.

OBJECTIVES: The purpose of this study was to evaluate functional and hemodynamic factors that determine the mitral-tricuspid and aortic-pulmonary valve closure sequence in patients with dilated cardiomyopathy. BACKGROUND: The physiologic factors determining closure sequence of cardiac valves in various forms of heart disease have been found to be complex. Few data exist for dilated cardiomyopathy, particularly for differentiating the effects of a conduction delay versus changes in ventricular performance. METHODS: A group of 64 patients were compared with 36 control subjects. Timing of valve closure and electromechanical intervals were determined by combined M-mode echocardiography, phonocardiography and apexcardiography. Hemodynamic data from right heart catheterization were available in 46 patients. RESULTS: In all control subjects, the aortic valve closed before the pulmonary valve and the mitral valve closed before the tricuspid valve. In the study group, 30 patients (49%) had reversed aortic-pulmonary valve closure and 27 (90%) of these had a left-sided conduction delay. There were 38 patients (60%) who had reversed mitral-tricuspid valve closure, but this was unrelated to the presence of a left-sided conduction delay. The presence of high ventricular filling pressures and poor systolic function was associated with delayed closure of both the mitral and the tricuspid valve. This caused the closure sequence to be related to the size of the difference between mean pulmonary artery wedge pressure and mean central venous pressure and also the magnitude of right ventricular dysfunction. Patients with a low wedge pressure (< 16 mm Hg) and a low central venous pressure (< 10 mm Hg) had a low prevalence of mitral-tricuspid valve closure reversal (30%). Those with a high wedge pressure (> 16 mm Hg) but a low central venous pressure had a high prevalence (86%) of reversal of mitral-tricuspid valve closure. Patients with high wedge and central venous pressures had a moderate prevalence (47%) of mitral-tricuspid valve closure reversal. Similar findings were observed for right ventricular dysfunction. If the right ventricle was normal or severely dysfunctional, a reversed closure sequence was less common (52% and 41%, respectively) than if moderate dysfunction was present (78%). CONCLUSIONS: Aortic-pulmonary valve closure sequence is strongly related to the presence of a left-sided conduction delay. The mitral-tricuspid valve closure sequence is unrelated to a conduction delay but can be reversed by relative differences in the severity of systolic dysfunction and filling pressures between the two ventricles.

Adolescent↗

The evaluation of right ventricular function in acute myocardial infarction by xenon-133.

Right ventricular performance was assessed in 37 patients with acute myocardial infarction within two hours of admission to Coronary Care and compared to results in 21 normal volunteers and 12 patients undergoing coronary arteriography. Right ventricular ejection fraction (RVEF) was measured from gated xenon-133 scans. The normal range of RVEF (42.8 +/- 5.1%) was significantly higher than in the 30 patients with inferior infarction (26.3 +/- 10.9%; p less than 0.001) and was similar to that in patients with anterior infarct (40.6 +/- 5.4%; ns) and patients undergoing coronary arteriography (39.3 +/- 4.9%; ns). Fifteen of the patients with inferior infarct had clinical evidence of right ventricular dysfunction with a mean RVEF of 18.9 +/- 7.9%, significantly below the fifteen patients with no clinical evidence of right ventricular dysfunction (34.3 +/- 8.3%; p less than 0.001).

Adult↗

High dose and short-term streptokinase infusion in patients with pulmonary embolism: prospective with seven-year follow-up trial.

BACKGROUND: High dose and short-term streptokinase infusion has proved to improve survival among few patients with pulmonary embolism and cardiogenic shock, without increasing hemorrhagic complications. However its efficacy and safety in terms of long follow-up and in major number of patients requires to be established. METHODS: Patients with pulmonary embolism proved through high probability V/Q lung scan, suggestive echocardiogram, or deep venous thrombosis were enrolled. All were assigned to receive 1,500,000 IU in one-hour streptokinase infusion. The primary end point was efficacy and safety of streptokinase regimen in terms of pulmonary arterial hypertension, right ventricular dysfunction, perfusion abnormalities, recurrence, mortality and hemorrhagic complications. In long-term follow-up, we assessed functional class, recurrence, chronic pulmonary arterial hypertension, postthrombotic-syndrome and mortality. RESULTS: A total of 40 consecutive patients (47.3+/-15.3 years of age) with large or massive pulmonary embolism were enrolled. In 35 patients high dose and short-term streptokinase regimen reversed acute pulmonary arterial hypertension, clinical and echocardiographic evidence of right ventricular dysfunction and improved pulmonary perfusion without increasing hemorrhagic complications. In acute phase 5 patients died, necropsy study performed in 4 patients showed massive pulmonary embolism and right ventricular myocardial infarction, without significant coronary arterial obstruction. Risk factors for mortality and recurrence were: right ventricular global hypokinesis (p<0.0001), 6 hours or over between onset symptoms and streptokinase regimen (p=0.02), severe systolic pulmonary arterial hypertension (p=0.001) right ventricular hypokinesis (p=0.001), hypoxemia (p=0.02) and right ventricular acute myocardial infarction (p<0.0001). Right ventricular hypokinesis (p=0.02) was the only independent risk factor for recurrence. In a seven-year follow-up of the original 35 patients who survived in acute phase, 2 patients were lost and 33 are alive, in functional class I, without recurrence or chronic pulmonary arterial hypertension. CONCLUSIONS: Our report indicates that among properly selected high-risk PE patients, short-term streptokinase infusion is effective and safe.

Adult↗

Ebstein's anomaly: one and a half ventricular repair.

Patients with Ebstein's anomaly can present after childhood or adolescence with cyanosis, arrhythmias, severe right ventricular dysfunction and frequently with left ventricular dysfunction secondary to the prolonged cyanosis and to the right ventricular interference. At this point conventional repair is accompanied by elevated mortality and morbidity and poor functional results. We report our experience with three patients (8, 16 and 35 years of age) with Ebstein's anomaly, very dilated right atrium, severe tricuspid valve regurgitation (4/4), bi-directional shunt through an atrial septal defect and reduced left ventricular function (mean ejection fraction = 58%, mean shortening fraction = 25%). All underwent one and a half ventricular repair consisting of closure of the atrial septal defect, tricuspid repair with reduction of the atrialised portion of the right ventricle and end-to-side anastomosis of the superior vena cava to the right pulmonary artery. All patients survived, with a mean follow-up of 33 months. In all there was complete regression of the cyanosis and of the signs of heart failure. Postoperative echocardiography showed reduced degree of tricuspid regurgitation (2/4) and improvement of the left ventricular function (mean ejection fraction = 77%, mean shortening fraction = 40%). In patients with Ebstein's anomaly referred late for surgery with severely compromised right ventricular function or even with reduced biventricular function, the presence of a relatively hypoplastic and/or malfunctioning right ventricular chamber inadequate to sustain the entire systemic venous return but capable of managing part of the systemic venous return, permits a one and a half ventricular repair with good functional results.

Adolescent↗

[Effects of restored blood flow on the contractile function of the right ventricle in patients with acute myocardial infarct: data of two-dimensional computerized echocardiography].

The volumes of the right and left ventricles were measured in 78 patients with first acute transmural myocardial infarction at days 1, 3, 7, 14, and 28 of the disease. Thirty four patients were diagnosed as having anterior myocardial infarction, 35 presented with inferior myocardial infarction, and 9 had a concurrent right and left ventricular inferior wall myocardial infarction. A high incidence of right ventricular dysfunction was confirmed both in anterior and inferior myocardial infarction. The most profound right ventricular contractile dysfunctions were detected in patients with proximal right coronary occlusion in the absence of reperfusion. Successful thrombolytic therapy for myocardial infarction was found to affect right ventricular function to a lesser extent than left function.

Adult↗

Right ventricular diastolic dysfunction in heart failure.

BACKGROUND: Left ventricular (LV) diastolic dysfunction is common in heart failure and is an important predictor of prognosis and mortality. Less attention has been paid to right ventricular (RV) diastolic function. In this study, we compared RV diastolic function in a large cohort of patients with heart failure (HF) with two groups: patients with pulmonary hypertension and normal LV function (the PHT group) and normal subjects. METHODS AND RESULTS: Transtricuspid and pulmonary artery flow were assessed by two-dimensional Doppler echocardiography at maximum inspiration and expiration in 185 subjects: 114 symptomatic HF patients (ejection fraction < 0.5), 31 PHT patients (pulmonary artery systolic pressure > 40 mm Hg), and 40 normal subjects. A subset was matched for age and heart rate. The results showed a high prevalence of RV diastolic abnormalities: HF patients had lower tricuspid E-A ratios, lower peak E-wave velocity, and prolonged RV isovolumic relaxation time (all P< .0001). Tricuspid E-wave deceleration time was significantly shorter only in those who had an LV restrictive filling pattern. The PHT group had similar findings. Compared with a normal range, more than half of the patients had lower tricuspid E-A ratios (HF, 55%; PHT, 69%), and 61% of HF and 58% of PHT patients had a prolonged RV isovolumic relaxation time. In the PHT group, RV diastolic parameters (E-wave deceleration time, E-A ratio, and isovolumic relaxation time) correlated significantly with pulmonary artery systolic pressure (P< .05). In the HF group, however, only tricuspid E-wave deceleration time correlated significantly with pulmonary artery systolic pressure, and HF patients with normal pulmonary artery systolic pressures had significantly lower tricuspid E-A ratios and prolonged RV isovolumic relaxation times compared with normal subjects. A close correlation existed between individual RV and LV diastolic parameters, suggesting that LV diastolic dysfunction may directly affect RV function, but there was no relation between LV size or systolic function and RV diastolic dysfunction. CONCLUSIONS: RV diastolic function is frequently abnormal in HF patients, and this is not related to elevated pulmonary artery systolic pressure alone, although high pulmonary artery pressure by itself also is associated with impaired RV diastolic function. Assessment of the role of right ventricular diastolic function in determining the symptoms and prognosis of heart failure is warranted.

Diastole↗

[Functional state of the right and left heart at different stages of anesthesia in patients with ischemic heart disease during myocardial revascularization surgery].

57 ischemic heart disease (IHD) patients entered the study of right and left heart function at different stages of anesthesia and operation to reveal possible reasons of myocardial dysfunction and to propose effective prevention of this dysfunction. All the patients were operated on under multicomponent balanced anesthesia (relanium, fentanyl, arduan, nitric oxide with oxygen 1:1). Left ventricular function was assessed at Doppler echocardiography, right ventricular function--at catheterization of the lung artery with a Swan-Ganz catheter with low time constant. Hemodynamic monitoring was made with a domestic MX-04 monitor. It was found that in the preperfusion period diastolic function of the right and left ventricles is impaired much more than the systolic one. The conditions of anesthesia and operation affect right ventricular function more than the left one. Diastolic and systolic right ventricular dysfunctions were observed at all stages and three stages of the operation, respectively. Diastolic and systolic left ventricular dysfunction was observed at four and one stages, respectively. Basic causes of the above systolic and diastolic disorders in the preperfusion period may be tachycardia, arterial hypertension, reduction of the preloading and increased postloading (for the right ventricle) in artificial lung ventilation.

Anesthesia↗

Preservation of the pulmonary valve complex in tetralogy of fallot: how small is too small?

BACKGROUND: Surgical repair of congenital lesions associated with right ventricular outflow tract obstruction frequently requires the destruction of pulmonary valve (PV) components including the valve annulus. The resultant pulmonary insufficiency may lead to late functional deterioration of right ventricular performance. Acute right ventricular dysfunction has been associated with poor pulmonary runoff, tricuspid valve regurgitation, and pulmonary hypertension. Preservation of PV competence may prevent both early and late right ventricular failure. However, the recent trend towards earlier repair of tetralogy of Fallot (TOF) may preclude preservation of the PV in favor of a transannular patch. We reviewed our experience with surgical repair of TOF to determine if age and/or body size affected the ability to repair the PV. METHODS: We reviewed the clinical records of 50 consecutive children who underwent surgical repair of TOF by one surgeon. The latter 27 patients underwent repair with an intention to preserve their pulmonary valve. In total, 28 patients underwent repair with preservation of their pulmonary valve, and form the basis of this study. Serial echocardiographic assessments were performed early (3 to 6 months) and late (12 months) after surgery. RESULTS: Pulmonary valve preservation was possible in the majority of children (89%) in whom it was intended. Pulmonary valve competence was observed in 68% of children, with only 5 (16%) children demonstrating severe insufficiency at follow-up. Residual right ventricular outflow tract obstruction was present in only 1 child who underwent repair with pulmonary valve preservation at greater than 2 years of age. CONCLUSIONS: Our data suggest that earlier repair of TOF does not preclude preservation of the pulmonary valve and may indeed facilitate repair. The pulmonary valve remains competent at 12 months, with acceptable gradients, and should participate in somatic growth. Pulmonary valve preservation during repair of TOF may prevent free pulmonary insufficiency, progressive right ventricular dilation, and the need for future prosthetic pulmonary valve replacement.

Age Factors↗

[Epidemiology, diagnosis, and treatment of pulmonary embolism].

Pulmonary embolism (PE) is a frequent pathology, the mortality of which remains elevated despite the efficacy of anticoagulation. This is mainly due to diagnostic difficulty, resulting from the low sensibility and specificity of clinical signs and routine exams in PE. The best diagnostic approach relies on decision making algorithms based on the determination of a clinical probability, which in turn dictates the choice of specialized exams (C-scan/scintigraphy, venous duplex, angiography and D-dimers). Risk stratification, which is based on the presence of hemodynamic alterations (right ventricular dysfunction, shock) is essential to guide therapy. In case of shock (massive embolism), treatment relies on systemic thrombolysis. In the presence of right ventricular dysfunction without shock (sub-massive embolism), the advantage of thrombolysis over anticoagulation alone has not been clearly demonstrated. In all other cases, as long as no contraindication exists, therapeutic anticoagulation with heparin must be initiated as soon as PE is suspected, since the mortality of this condition is highest in the two first hours following presentation.

Algorithms↗

[Influence of pulmonary hemodynamics on right ventricular ejection fraction in chronic obstructive pulmonary disease].

Right ventricular dysfunction is common in patients with chronic obstructive pulmonary disease. Right ventricular function might be influenced by the afterload, which depends on pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR). To evaluate the influence of the right ventricular afterload on right ventricular performance, we investigated 30 patients with chronic obstructive pulmonary disease without clinical signs or history of left heart failure or coronary heart disease. The study includes lung function tests, analysis of blood gases and right heart catheterisation. RV function was assessed by a thermodilution technique using a pulmonary artery catheter equipped with a rapid response thermistor (produced by Baxter, USA). There are 9 patients with normal, 12 with latent and 9 with fixed pulmonary hypertension. Median RVEF was measured to be 33.3% (19-44%). There was a significant correlation between RVEF and PAP (r = -0.66; p < 0.0001) and RVEF and PVR (r = -0.54; p < 0.0018). RVEF was not directly influenced by lungfunction or pulmonary capillary wedge pressure (PCWP). Under treadmill exercise RVEF and cardiac index increased without a change of PCWP. A low RVEF at rest seems to be a predictive value for a reduced exercise capacity. A reduced RVEF has a predictive value of pulmonary hypertension with a sensitivity of 66% in patients with unstable and 89% in patients with lasting pulmonary hypertension. In a subgroup of 6 cases treadmill exercise led to a RVEF decrease. These patients showed no difference in afterload, blood gases or lung function-tests compared with the total group. In conclusion, right ventricular ejection fraction seems to be influenced by PVR and PAP which determinate the right ventricular afterload. The validity of the method depends on the severity of pulmonary hypertension, and hence measurement of RVEF might not provide a reliable estimation of pulmonary arterial pressure in patients suffering from mild to moderate pulmonary hypertension.

Female↗

Right ventricular infarction: identification by hemodynamic measurements before and after volume loading and correlation with noninvasive techniques.

To evaluate the potential occurrence of right ventricular infarction, 53 patients with acute inferior transmural myocardial infarction were studied within 36 hours of symptoms by right heart catheterization, equilibrium radionuclide angiography and two-dimensional echocardiography. Technetium-99m pyrophosphate myocardial scintigraphy was performed 3 days after the onset of symptoms. The hemodynamic standard for right ventricular infarction was defined as both a right atrial pressure of 10 mm Hg or more and a right atrial/pulmonary artery wedge pressure ratio of 0.8 or more. Eight (15%) of the 53 patients had hemodynamic measurements at rest characteristic of right ventricular infarction, and 6 (11%) additional patients met these criteria after volume loading (p less than 0.05). Nineteen (37%) of the 51 patients who had radionuclide angiography had right ventricular dysfunction manifested by both a reduced right ventricular ejection fraction (less than 40%) and right ventricular regional wall motion abnormalities (akinesia or dyskinesia). An abnormal radionuclide angiogram was observed in 12 of 13 patients with hemodynamic measurements indicating right ventricular infarction. In 12 patients with an abnormal radionuclide angiographic study, right ventricular ejection fraction improved 6 to 12 weeks after infarction (27 +/- 7 to 36 +/- 9%, p less than 0.01). Twenty-two (49%) of the 45 patients with adequate two-dimensional echocardiograms had a right ventricular regional wall motion abnormality. An abnormal two-dimensional echocardiogram was seen in 9 of 11 patients with hemodynamic measurements characteristic of right ventricular infarction. Technetium-99m pyrophosphate scintigraphy was positive for right ventricular infarction in 3 of 12 patients who had hemodynamic measurements indicating right ventricular infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Clinical usefulness and prognostic value of elevated cardiac troponin I levels in acute pulmonary embolism.

BACKGROUND: Right ventricular myocardial ischemia and injury contribute to right ventricular dysfunction and failure during acute pulmonary embolism. The objective of this study was to evaluate the clinical usefulness of cardiac troponin I (cTnI) in the assessment of right ventricular involvement and short-term prognosis in acute pulmonary embolism METHODS: Thirty-eight patients with acute pulmonary embolism were included in the study. Clinical characteristics, right ventricular involvement, and clinical outcome were compared in patients with elevated levels of serum cTnI versus patients with normal levels of serum cTnI. RESULTS: Among the study population (n = 38 patients), 18 patients (47%) had elevated cTnI levels (mean +/- SD 1.6 +/- 0.7 ng/mL, range 0.7-3.7 ng/mL, median, 1.4 ng/mL), and comprised the cTnI-positive group. In the other 20 patients, the serum cTnI levels were normal (< or =0.4 ng/mL), and they comprised the cTnI-negative group. In the cTnI-positive group (n = 18 patients), 12 patients (67%) had right ventricular dilatation/hypokinesia, compared with 3 patients (15%) in the cTnI-negative group (n = 20 patients, P =.004). Right ventricular systolic pressure was significantly higher in the cTnI-positive group (51 +/- 8 mm Hg vs 40 +/- 9 mm Hg, P =.002). Cardiogenic shock developed in a significantly higher number of patients with elevated serum cTnI levels (33% vs 5%, P =.01). In patients with elevated cTnI levels, the odds ratio for development of cardiogenic shock was 8.8 (95% CI 2.5-21). CONCLUSIONS: Patients with acute pulmonary embolism with elevated serum cTnI levels are at a higher risk for the development of right ventricular dysfunction and cardiogenic shock. Serum cTnI has a role in risk stratification and short-term prognostication in patients with acute pulmonary embolism.

Adult↗

Senning plus arterial switch operation for discordant (congenitally corrected) transposition.

BACKGROUND: Congenitally corrected transposition of the great arteries is a complex cardiac lesion, usually associated with ventricular septal defect, left ventricular outflow tract obstruction, and tricuspid valve abnormalities. A subset of patients without left ventricular outflow tract obstruction have undergone Senning plus arterial switch operation in an attempt to place the left ventricle in the systemic circuit and the right ventricle in the pulmonary circuit. METHODS: Fourteen patients have had the operation performed since July 1989. Age and weight medians were 12 months (range, 0.5 to 120 months) and 8.2 kg (range, 3.2 to 34 kg). All but 1 patient had a left ventricular to right ventricular pressure ratio greater than 0.7, due to a large ventricular septal defect (with or without a previous pulmonary artery band), severe congestive heart failure caused by right ventricular dysfunction and tricuspid insufficiency, or a pulmonary artery band for left ventricular retraining. At least 10 patients had strong contraindications to "classic" repair, including right ventricular hypoplasia (n = 2), moderate to severe right ventricular dysfunction (n = 5), or moderate to severe tricuspid insufficiency (n = 9). RESULTS: There was one hospital death, occurring in a neonate (7%; 95% confidence interval = 0% to 34%). Actuarial survival beyond 10 months is 81% (95% confidence interval = 42% to 95%), currently with 389 patient-months of total follow-up time. The median grade of tricuspid insufficiency fell from 3/4 preoperatively to 1/4 postoperatively (p = 0.003). Right ventricular function is normal in 11/12 current survivors, all but 1 of whom are in New York Heart Association class I or II. CONCLUSIONS: Senning plus arterial switch operation is a good option for selected patients with congenitally corrected transposition of the great arteries with a similar or lower early risk (as compared with classic repairs). Some of the long-term problems associated with congenitally corrected transposition of the great arteries may be avoided with this strategy.

Cardiac Surgical Procedures↗

[Arrhythmogenic right ventricular dysplasia].

Arrhythmogenic right ventricular dysplasia is a cardiomyopathy with autopsy evidence of fibrous and fatty infiltration of the right ventricular. The disease, which shows familial clustering, causes electrical instability that may place affected subjects at risk of sudden death. It is characterized by ECG changes and right ventricular dysfunction. Death can occur due to ventricular arrhythmia. We describe a 46-year-old female Cypriot who presented with recurrent syncope and palpitation due to ventricular tachycardia with the LBBB pattern; T waves were inverted in V1-V3. Echocardiogram and cardiac catheterization revealed severe right ventricular dysfunction. Her sister had died several years before of a similar syndrome, including ventricular tachycardia. Family members should be screened for right ventricular dysplasia. Those currently asymptomatic should be given prophylactic therapy to prevent sudden death. Treatment is either medical: sotalol, beta-blockers or verapamil; or surgical: ablation of the arrhythmogenic focus in the right ventricle, total disconnection of the right ventricular free wall; or implantation of a cardioverter defibrillator.

Cardiac Catheterization↗

Effects of CPAP on right ventricular myocardial performance index in obstructive sleep apnea patients without hypertension.

OBJECTIVES: Obstructive sleep apnoea (OSA) might cause right ventricular dysfunction and pulmonary hypertension. We aimed to determine the effects of nasal continuous positive airway pressure (CPAP) therapy on right ventricular myocardial performance index (MPI) in OSA patients without hypertension. METHODS: 49 subjects without hypertension, diabetes mellitus, any cardiac and pulmonary disease had overnight polysomnography and echocardiography. In 18 moderate-severe OSA (apnea-hypopnea index > or = 15) patients, right ventricular free wall diameter (RVFWD) was measured by M-mode, and right ventricular MPI was calculated as (isovolumic contraction time+ isovolumic relaxation time) / pulmonary ejection time using Doppler at baseline and after 6 months CPAP therapy. RESULTS: Mean age was 46.5 +/- 4.9 year. Patients had high body mass index (BMI: 30.6 +/- 4,0 kg/m2), but there was no change in either BMI or blood pressures after 6 months. Right ventricular end-diastolic and end-systolic diameters were in normal limits at baseline, and did not change after CPAP usage. Baseline RVFWD (7.1 +/- 2.1 mm) significantly decreased after CPAP therapy (6.2 +/- 1.7 mm, p < 0.001). 15 of patients (83%) had right ventricular diastolic dysfunction at baseline, and it was completely improved in 11 of them (73%) by CPAP usage. Right ventricular global dysfunction was shown in 11 patients (61%) with a high MPI (62.2 +/- 9.3%) at baseline; and MPI was significantly decreased after CPAP therapy (47.3 +/- 8.4%, p < 0.0001), and it was completely corrected in 4 of them (36%). CONCLUSION: CPAP therapy significantly decreases RVFWD and improves right ventricular diastolic and global functions (MPI) in OSA patients without hypertension.

Adult↗

[The hemodynamic status and right ventricular diastolic function of bronchial asthma patients].

Doppler echocardiographic study of ventricular diastolic function in 90 BA patients gave evidence for diastolic left and right ventricular dysfunction in patients with moderately and gravely running BA. The above disorders were noted by changes in the speed of transmitral and transtricuspid flows: early filling rate (E) slowing, atrial systole filling rate (A) acceleration, E/A decrease. The degree of right ventricular diastolic dysfunction depends on right ventricular hypertrophy and total pulmonary resistance. Left ventricular diastolic function is related to right ventricular after-load.

Adolescent↗

The vectorcardiogram in 4 children undergoing the arterial switch repair.

Four children with complete transposition (concordant atrioventricular and discordant ventriculo-arterial connections), aged 1.2 to 16.4 years, underwent a delayed repair by the arterial switch procedure from March 1985 to October 1986. Three children had undergone previous atrial diversion repairs in early childhood. Two of these children had developed right ventricular dysfunction with tricuspid incompetence as well as having recurrent and symptomatic supraventricular tachyarrhythmias. They underwent banding of the pulmonary trunk 0.7 and 1 year prior to the final repair. The third child had dynamic obstruction of the left ventricular outflow tract and prior banding was not performed. A fourth child had right ventricular dysfunction on initial assessment in early infancy and then had banding of the pulmonary trunk. Two patients survived the arterial switch operation. Vectorcardiograms were performed on these 4 children before arterial switch repair. The left maximal spatial voltage did not correlate with elevated left to right ventricular pressure ratio at cardiac catheterization before arterial switch repair nor did it relate to survival after operation. The horizontal loop was clockwise in all patients preoperatively. The vectorcardiogram in these children was not a useful indicator that the left ventricle was suitably prepared for the arterial switch repair.

Adolescent↗