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A case of right and left ventricular myocardial infarction in infectious endocarditis of the aortic valve in an injected drug abuser is reported. The infarction was diagnosed only in autopsy. Diagnostic difficulties are discussed. The literature on the problem is listed.
Two patients died following heart transplantation from failure of the donor right ventricle. Histological examination of the lungs showed occlusion of pulmonary veins. A more reliable method is required to predict the outcome for potential heart transplant recipients with a "borderline" pulmonary vascular resistance.
To determine whether diastolic ventricular interdependence mechanisms would act in the presence of an open pericardial sac, as during cardiac surgery, moderate acute right ventricle afterload increases were applied to eight dogs with the chest and pericardium open while left ventricular filling dynamics were being assessed by Doppler echocardiography. Dogs were studied under basal conditions and after acute banding of the main pulmonary artery tightened to produce a 100% increase in right ventricular systolic pressure. With banding, the left ventricular filling velocity ratio (E/A), as assessed by Doppler echocardiography of mitral inflow, changed from a baseline value of 1.32 +/- 0.05 to 1.16 +/- 0.03 (p < 0.02), suggesting a restrictive pattern to early left ventricular filling, which is differed to that during the second half of diastole. Isovolumic relaxation time, measured as the time interval between aortic valve closure and mitral valve opening, assessed by M-mode echocardiography of both valves, was prolonged, though not significantly, from 63.3 +/- 2.5 ms to 69.4 +/- 2.9 ms, by banding of the pulmonary artery. E wave deceleration time, a filling variable influenced by chamber pressure/volume relations, was shortened by pulmonary artery banding, changing from 75.1 +/- 1.7 ms to 68.0 +/- 1.8 ms (p < 0.01). It was concluded that pressure loads applied to the right ventricle restricted early left ventricular filling. Prolonged relaxation and altered pressure-volume chamber relations were the diastolic interdependence mechanisms involved that proved to be acting even under open pericardium conditions.
Angiotensin II causes pulmonary vasoconstriction in man and in animals, and angiotensin-converting enzyme (ACE) inhibitors have prevented the development of chronic pulmonary hypertension in animals models. Angiotensin II may contribute to lung vascular remodeling in pulmonary hypertensive disease, since cilazapril, an inhibitor of ACE, reduces pulmonary vascular medical thickening in chronically hypoxic rats with established pulmonary hypertension. Furthermore, the ACE DD genotype, which has been associated with increased circulating and tissue ACE activity, has been associated with left ventricular hypertrophy in human hypertensive disorders. The ACE DD genotype may also 'permit' a greater hypertrophic adaptation of the pressure-over-loaded right ventricle. In fact, we have shown that pulmonary hypertension patients with maintained cardiac output and less right-heart failure fall into the group with the DD genotype and that patients with a low cardiac output and more severe right-heart failure fall into the group with the non-DD genotype, supporting the hypothesis. We assessed cardiopulmonary hemodynamics in patients with primary (unexplained) pulmonary hypertension and segregated the patients based on their ACE genotype. For similar mean pulmonary artery pressures in the DD and non-DD groups, the cardiac output was substantially lower in the patients with the non-DD genotype, whereas the values for mean right atrial pressure and pulmonary vascular resistance were double when compared with the DD group. Our data show that the ACE DD genotype is prevalent in patients with severe pulmonary hypertension and is a marker of maintained right ventricular function.
A three-year-old boy presented with generalized edema, respiratory distress, prominent right ventricular impulse and hepatosplenomegaly. He had undergone Senning repair at one year of age. On his echocardiography, there were numerous prominent trabeculations and deep intertrabecular recesses measuring approximately 5 mm in depth along the free wall and right ventricular apex. Echogenicity of the endocardial surface was increased suggesting a fibrotic process in progress. Intertrabecular recesses were observed to be filling from the ventricle by color Doppler which is consistent with noncompaction. Various semilunar valve obstructions were shown to be responsible for the persistence of deep endomyocardial spaces surrounded by exeggerated hypertrophy of the trabeculae. This report presents the echocardiographic findings of right ventricular cardiomyopathy associated with dextroposition of the great arteries following Senning operation resembling noncompaction. Thus, this rare entity needs to be clarified regarding morphological criteria in distinction from other cardiomyopathies.
PURPOSE: To evaluate some features of ventricular arrhythmias in patients with mitral valve prolapse. METHODS: We studied 25 patients (female: 19; mean age: 37 +/- 13 years) with ventricular arrhythmias, mitral valve prolapse and normal ventricular function. All patients underwent a 24h Holter and high resolution ECG (HRECG). The Qtc intervals were measured in lead II (normal < 0.44 s). In order to define the possible origin of the ventricular focus, the morphology of the ectopic beats were analysed in leads I, II, aVF, V1 using the following criteria: 1) LBBB morphology with left axis deviation in the frontal plane (FP): origin at the inflow tract of the right ventricle (RV); 2) LBBB morphology with right axis deviation in the FP: origin at the outflow tract of the RV; 3) RBBB morphology with left axis deviation in the FP: origin at the posterior region of the left ventricle (LV). RBBB morphology with right axis deviation in the FP: origin at the anterior region of the LV. RESULTS: Twenty three (92%) patients showed > 720 isolated ventricular ectopic beats/24 h. Paired ventricular response was detected in 18 (72%) patients and non-sustained VT in 15 (60%). HRECG was positive in six (24%) patients and Qtc interval was prolonged in 13 (52%). RV was the site of origin of the ventricular ectopic beats in 85% of the patients (outflow: 85%; inflow: 15%). Only five (20%) patients had arrhythmias from the LV. CONCLUSION: There was a high incidence of ventricular arrhythmias with a low incidence of positive HRECG tests, suggesting that the mechanisms of the arrhythmias do not correlate with slow intramyocardial conduction. It was noted a strong association between mitral valve prolapse, arrhythmogenic right ventricular disease and Qtc prolongation. It is possible that in some of this patients the finding could represent a global myocardial disease.
OBJECTIVES: We report a series of patients with severe tricuspid valve regurgitation due to a permanent pacemaker (PPM) or implantable cardioverter-defibrillator (ICD) lead. BACKGROUND: Severe tricuspid regurgitation caused by a PPM or ICD lead is an under-recognized but treatable etiology of severe right heart failure. METHODS: We reviewed the records of 41 patients who underwent tricuspid valve operation for severe tricuspid regurgitation caused by previously placed PPM or ICD leads. RESULTS: During surgery, severe tricuspid regurgitation was found to be caused by the PPM or ICD leads in all 41 patients. There was a perforation of the tricuspid valve leaflet by the PPM or ICD lead in 7 patients, lead entanglement in the tricuspid valve occurred in 4 patients, lead impingement of the tricuspid valve leaflets occurred in 16 patients, and lead adherence to the tricuspid valve occurred in 14 patients. The septal leaflet was most often perforated (6 of 7). In the preoperative evaluation, valve malfunction due to the PPM or ICD lead was diagnosed preoperatively in only 5 of 41 (12%) patients by transthoracic echocardiography. All patients underwent successful tricuspid valve operation (22 tricuspid valve replacement), with one perioperative death occurring. During follow-up (range, 1 to 99 months), there was one patient who died from left-sided heart failure and three patients died of other causes. The remaining patients showed improvement in signs and symptoms of heart failure. CONCLUSIONS: Damage to the tricuspid valve by PPM or ICD leads may result in severe symptomatic tricuspid regurgitation and may not be overtly visualized by echocardiography. This etiology should be considered when evaluating patients with severe right heart failure after PPM or ICD implantation.
PURPOSE: In congenital heart disease, the exact determination of the right ventricular function is of high importance for therapeutic and especially surgical planning. The aim of this study was to correlate the parameters of the right ventricular function in MRI and 3D echocardiography to determine the agreement of both modalities. MATERIALS AND METHODS: In 18 patients suffering from congenital heart disease, 3D echocardiography was performed using a Philips Sonos 7500 system. In MRI short axis slices with a 4-mm distance were acquired using an SSFP sequence on a Siemens Sonata or Symphony System. Volumetry for both modalities was performed on an external workstation (Tomtec) using the EchoView software. RESULTS: Enddiastolic and endsystolic volumes showed a highly significant correlation with coefficients of 0.996 and 0.990, respectively. In echocardiography there was a systematic slight underestimation of enddiastolic volumes and overestimation of endsystolic volumes. The Wilcoxon test did not show significant differences between the volumes and ejection fractions assessed by both modalities. CONCLUSION: There is an excellent correlation in the quantification of right ventricular volumes in MRI and 3D echocardiography, which allows a comparison of acquired volumes in clinical follow-up.
Acute pulmonary embolism (PE) is a potentially life-threatening condition, with an overall 3-month mortality rate of 15% and with right ventricular failure as the most common cause of early death. Risk stratification facilitates identification of high-risk patients and may be helpful in guiding the initial and long-term management. In patients with massive PE and hemodynamic instability, rapid risk assessment is paramount and bedside echocardiography and multislice chest computed tomography (CT) are useful for identifying patients who may benefit from thrombolysis or embolectomy. Cardiac biomarkers, including troponin and the natriuretic peptides, are sensitive markers of right ventricular function. Low levels of troponin, B-type natriuretic peptide (BNP), and NT-terminal proBNP are all highly sensitive assays for identifying patients with an uneventful clinical course. Multislice chest CT is not only useful to diagnose or exclude PE; it also is useful for risk assessment. A right-to-left ventricular dimension ratio > 0.9 on the reconstructed CT four-chamber view identifies patients at increased risk of early death. This article focuses on risk stratification tools, including the clinical examination, electrocardiography, echocardiography, cardiac biomarkers, and chest CT.
Isolated acute right ventricular (RV) infarction is rare, and ECG diagnosis may be difficult. We report two cases of acute myocardial infarction with ST-segment elevation in anterior precordial leads caused by such an RV involvement. Potential mechanisms for the relationship are given.
Right ventricular myocardial infarction (RVMI) occurs rather rarely, under the mask of various diseases and is not easy to detect. Hypo-vate prognosis. Intravital diagnosis of RVMI was successful in 4 patients. Location of the lesion and its extent were determined. This article reports two cases of the four. The disease onset manifested with dyspnea, dry cough, attacks of night asphyxia then symptoms of right ventricular failure arose and intensified. The clinical picture, typical ECG signs suggested the RVMI diagnosis. However, its verification, precise localization and estimation of the lesion size were possible only after balanced radioventriculography.
Primary neoplasia of the heart is rare and often diagnosed postmortem (with a prevalence < 0.2% at postmortem examinations) due to the lack of specific clinical symptoms and signs. Among benign cardiac tumors, cavernous hemangioma has a prevalence of 2.8%. Less invasive diagnostic techniques such as transthoracic echocardiography allow for the diagnosis to be made during life with definitive surgical treatment. We report a representative case of right ventricular cavernous hemangioma, which mimicked right ventricular failure associated with systolic pulmonary flow tract obstruction. Surgical treatment was indicated for symptom severity and for the unpredictable behavior of the large neoplasm.
Iloprost inhalation has recently emerged as an alternative therapy for severe primary pulmonary hypertension. In the studies documenting the effect of iloprost inhalation therapy, hemodynamic variables have been measured invasively. We have followed a patient with primary pulmonary hypertension receiving iloprost inhalation therapy for 5 years using echocardiography to monitor changes in pulmonary artery pressure and right ventricular function. Echocardiography was also used to evaluate the initial response to iloprost inhalation therapy. This case illustrates the feasibility and utility of echocardiography in the testing and follow-up of iloprost inhalation therapy in patients with pulmonary hypertension.
BACKGROUND: The development of pulsatile ventricular assist devices for children has been limited mainly by size constraints. The purpose of this study was to evaluate the MEDOS trileaflet-valved, pulsatile, pediatric right ventricular assist device (stroke volume = 9 mL) in a neonatal lamb model of acute right ventricular failure. METHODS: Right ventricular failure was induced in ten 3-week-old lambs (8.6 kg) by right ventriculotomy and disruption of the tricuspid valve. Control group 1 (n = 5) had no mechanical support whereas experimental group 2 (n = 5) had right ventricular assist device support for 6 hours. The following hemodynamic parameters were measured in all animals: heart rate and right atrial, pulmonary arterial, left atrial, and systemic arterial pressures. Cardiac output was measured by an electromagnetic flow probe placed on the pulmonary artery. RESULTS: All results are expressed as mean +/- standard deviation and analyzed by Student's t test. A p value less than 0.05 was considered statistically significant. Base-line measurements were not significantly different between groups and included systemic arterial pressure, 80.6 +/- 12.7 mm Hg; right atrial pressure, 4.6 +/- 1.6 mm Hg; mean pulmonary arterial pressure, 15.6 +/- 4.2 mm Hg; left atrial pressure, 4.8 +/- 0.8 mm Hg; and cardiac output, 1.4 +/- 0.2 L/min. Right ventricular injury produced hemodynamics compatible with right ventricular failure in both groups: mean systemic arterial pressure, 38.8 +/- 10.4 mm Hg; right atrial pressure, 16.8 +/- 2.3 mm Hg; left atrial pressure, 1.4 +/- 0.5 mm Hg; and cardiac output, 0.6 +/- 0.1 L/min. All group 1 animals died at a mean of 71.4 +/- 9.4 minutes after the operation. All group 2 animals survived the duration of study. Hemodynamic parameters were recorded at 2, 4, and 6 hours on and off pump, and were significantly improved at all time points: mean systemic arterial pressure, 68.0 +/- 13.0 mm Hg; right atrial pressure, 8.2 +/- 2.3 mm Hg; left atrial pressure, 6.4 +/- 2.1 mm Hg; and cardiac output, 1.0 +/- 0.2 L/min. CONCLUSIONS: The results demonstrate the successful creation of a right ventricular failure model and its salvage by a miniaturized, pulsatile right ventricular assist device. The small size of this device makes its use possible even in small neonates.
It was previously shown that body surface QRST isointegral maps of the anterior chest were abnormal in patients with right ventricular overload and that the abnormalities varied with hemodynamic status. The QRST isointegral maps were first characterized by using a departure index map for normal controls. The study group consisted of 14 patients with pulmonary stenosis (PS), 20 with tetralogy of Fallot, (TOF) and 43 with atrial septal defect (ASD). The QRST isointegral maps of these three groups were compared with the data on 23 to 65 age-matched normal children. In mean departure index maps, the patients with right ventricular pressure overload (PS or TOF) showed an increase in departure index on the anterior midchest, while those of right ventricular volume overload (ASD) showed two maxima on the anterior and left lateral chest, with a trough-like negative area between them. Since the abnormal findings were seen on the anterior chest, we evaluated the diagnostic usefulness of QRST time integral values for precordial leads of the routine electrocardiogram (ECG) in a second part of this study. The precordial QRST time integral values from 9 patients with PS and 11 with TOF (0-2 years of age, mean 1.1 years) and 22 ASD patients (6-15 years, mean 10.1 years) were compared with those of the age-matched control children. The QRST time integral values of the precordial leads in right ventricular pressure overload were significantly increased in the right precordial leads (V1, V2). In right ventricular volume overload, the QRST time integral values of the V1, V2, V4, and V6 leads demonstrated a significant deviation from those of the control group. Therefore, a discrimination formula was constructed by using the values of these leads, and the criteria derived from this formula revealed good (98%) diagnostic accuracy. In detection of right ventricular overload, the QRST time integral values of the precordial lead ECG, if confirmed in a larger data set, may be useful as a simple screening method.
Implantable left-ventricular assist devices (LVAD) are successfully used as a bridge to transplant if the patient's condition is worsening and no donor organ is available. They allow recovery of compromised organ function. However, postoperative bleeding, thrombemboelism, and right-heart failure may jeopardize the important improvement of organ function and may even lead to death. We introduce our strategy for implantation of the Novacor LVAD system, which aims at minimal bleeding and maintained right-heart function. The Novacor LVAD was implanted with the heart beating during extracorporeal circulation in 8 patients, 3 of whom had previous cardiac surgery. Postoperatively, no patient developed right heart failure or had to undergo redo thoracotomy.
Pulmonary regurgitation (PR) following nonvalved reconstruction of the right ventricular outflow tract is usually well tolerated. However, a small percentage of patients develop progressive right ventricular dilatation and failure due to long-standing PR. When this group of patients becomes refractory to medical management, pulmonic valve replacement (PVR) may offer symptomatic relief and hemodynamic improvement. From a cumulative experience, the pulmonary homograft may be the optimal choice for PVR due to its very low transvalvular gradient assuring optimal hemodynamics, the absence of anticoagulation-related and thromboembolic complications, and the excellent mid-term results when compared to other valved conduit, including the aortic homograft. We report our experience in two patients who have been operated upon at the BWH between March and August 1995 for severe pulmonary valve insufficiency and right heart failure, who received cryopreserved pulmonary homografts. We also describe our technique of PVR using a pulmonary homograft as an orthotopic root replacement.
Ebstein's anomaly is a rare congenital heart defect in which the hinges of the septal and/or posterior leaflets are displaced downward to the right ventricle. The anterior leaflet is usually not displaced but is enlarged and sail-like and valve closure is likewise displaced downwards. Since 1988 we have operated on 22 patients with Ebstein's anomaly using a modified repair technique of the tricuspid valve. This technique restructures the valve mechanism at the level of the true tricuspid annulus by using the most mobile leaflet for valve closure without plication of the atrialized chamber. We evaluated our long-term results with regard to functional capacity (New York Heart Association functional class), tricuspid valve function, rhythm disturbances and re-operation rate. We quantified the right ventricular function by measuring flow velocity integral of the pulmonary artery (VTIPA). All patients survived the operation. There were two hospital deaths (9%) and the late mortality was 4.5%. The mean followup period was 9 years (range, 1.5 to 13 years) for 19 patients. So far no re-operation has been necessary. Preoperatively, the majority of all patients were in NYHA classes III and IV (79%). After the first postoperative follow-up examination (2.9 months), 17 patients were in NYHA class II. Long-term follow-up examinations showed an additional improvement of 11 patients to NYHA class I. Echocardiographic studies demonstrated a significant improvement of tricuspid valve function. No tricuspid valve stenosis was observed. Significant improvement of VTI(PA) was observed. Analysis of the postoperative deaths demonstrated that all patients were in NYHA class III or IV and had a cardiothoracic ratio of 0.65 or more. A severe reduction in functional capacity seems to be an additional risk factor for mortality beside a cardiothoracic ratio greater than 0.65. We conclude that reconstruction of the tricuspid valve without ventricle plication not only achieves good functional results immediately after the operation but that follow-up examinations demonstrate stable or improved functional capacity in the long term. We postulate that incorporation of the atrialized chamber into the right ventricle may contribute to right ventricular contraction and thereby account for the improved functional capacity of the patients.