Noninvasive prediction of the exercise-induced elevation in left ventricular filling pressure in post-heart transplant patients with normal left ventricular ejection fraction

OBJECTIVES:

At present, there are conflicting data on the ability of echocardiographic parameters to predict the exercise-induced elevation of left ventricular (LV) filling pressure. The purpose of the present study was to validate the ratio of early diastolic transmitral (E) to mitral annular velocity (e′) obtained at peak exercise in its capacity to determine the exercise-induced elevation of pulmonary capillary wedge pressure (PCWP) and to reveal new noninvasive parameters with such capacity.

METHODS:

Sixty-one patients who had undergone heart transplantation with normal LV ejection fraction underwent simultaneous exercise echocardiography and right heart catheterization.

RESULTS:

In 50 patients with a normal PCWP at rest, exercise E/e′ ≥8.5 predicted exercise PCWP ≥25 mmHg with a sensitivity of 64.3% and a specificity of 84.2% (area under the curve [AUC]=0.74). A comparable or slightly better prediction was achieved by exercise E/peak systolic mitral annular velocity (s′) ≥11.0 (sensitivity 79.3%; specificity 57.9%; AUC=0.75) and exercise E/LV systolic longitudinal strain rate ≤−105 cm (sensitivity 78.9%; specificity 78.6%; AUC=0.87). Combined, exercise E/s′ and exercise E/e′ resulted in a trend toward a slightly more precise prediction (sensitivity 53.6%; specificity 89.5%; AUC=0.78) than did either variable alone.

CONCLUSIONS:

Exercise E/e′, used as a sole parameter, is not sufficiently precise to predict the exercise-induced elevation of PCWP. Exercise E/s′, E/LV systolic longitudinal strain rate or combinations of these parameters may represent further promising possibilities for predicting exercise PCWP elevation.     

Pericardial syndromes: an update after the ESC guidelines 2004

Despite a myriad of causes, pericardial diseases present in few clinical syndromes. Acute pericarditis should be differentiated from aortic dissection, myocardial infarction, pneumonia/pleuritis, pulmonary embolism, pneumothorax, costochondritis, gastroesophageal reflux/neoplasm, and herpes zoster. High-risk features indicating hospitalization are: fever >38 °C, subacute onset, large effusion/tamponade, failure of non-steroidal anti-inflammatory drugs (NSAIDs), previous immunosuppression, trauma, anticoagulation, neoplasm, and myopericarditis. Treatment comprises 10–14-days NSAID plus 3 months colchicine (2 × 0.5 mg; 1 × 0.5 mg in patients <70 kg). Corticosteroids are avoided, except for autoimmunity, as they facilitate the recurrences. Echo-guided pericardiocentesis (±fluoroscopy) is indicated for tamponade and effusions >2 cm. Smaller effusions are drained if neoplastic, purulent or tuberculous etiology is suspected. In recurrent pericarditis, repeated testing for autoimmune and thyroid disease is appropriate. Pericardioscopy and pericardial/epicardial biopsy may clarify the etiology. Familial clustering was recently associated with tumor necrosis factor receptor-associated periodic syndrome (TNFRSF1A gene mutation). Treatment includes 10–14 days NSAIDs with colchicine 0.5 mg bid for up to 6 months. In non-responders, low-dose steroids, intrapericardial steroids, azathioprine, and cyclophosphamide can be tried. Successful management with interleukin-1 receptor antagonist (anakinra) was recently reported. Pericardiectomy remains the last option in >2 years severely symptomatic patients. In constriction, expansion of the heart is impaired by the rigid, chronically inflamed/thickened pericardium (no thickening ~20 %). Chest radiography, echocardiography, computerized tomography, magnetic resonance imaging, hemodynamics, and endomyocardial biopsy indicate the diagnosis. Pericardiectomy is the only treatment for permanent constriction. Predictors of poor survival are prior radiation, renal dysfunction, high pulmonary artery pressures, poor left ventricular function, hyponatremia, age, and simultaneous HIV and tuberculous infection.     

Isolated bilateral ostial coronary stenosis with proximal right coronary artery occlusion

The incidence of coronary ostial stenosis in patients undergoing coronary arteriography has been found to range between 0.07 and 0.25%. A slightly higher incidence has been observed in patients with angiographically confirmed coronary artery disease: between 0.13 and 2.7%. Bilateral ostial stenosis is even less common. longer a prominent condition, it must be considered in the differential diagnosis since it carries a very high risk (50%) of cardiovascular complications if left untreated. Ostial coronary stenosis occurs in 26% of patients with syphilitic aortitis. This paper reports on a 41-yearold Wasserman (WR)-positive woman with progressive angina caused by bilateral ostial coronary stenosis. (Int J Cardiovasc Although cardiovascular syphilis is no Intervent 2000; 3:47–49)     

Neutralizing and protective epitopes of the 2009 pandemic influenza H1N1 hemagglutinin

Aims and Methods To facilitate antigenic characterization of the influenza A 2009 pandemic H1N1 [A(H1N1)pdm09] hemagglutinin (HA), we generated a panel of murine monoclonal antibodies (mAbs) using as the immunogen mammalian‐derived virus‐like particles containing the HA of the A/California/04/2009 virus. The antibodies were specific for the A/California/04/2009 HA, and individual mAbs suitable for use in several practical applications including ELISA, immunofluorescence, and Western blot analysis were identified. Results and Conclusions As the panel of mAbs included antibodies with hemagglutination inhibition (HI) and virus neutralizing activities, this allowed identification and characterization of potentially important antigenic and neutralizing epitopes of the A/California/04/2009 HA and comparison of those epitopes with the HAs of other influenza viruses including seasonal H1N1 viruses as well as the A/South Carolina/1918 and A/New Jersey/1976 H1N1 viruses. Three mAbs with the highest HI and neutralizing titers were able to provide passive protection against virus challenge. Two other mAbs without HI or neutralizing activities were able to provide partial protection against challenge. HA epitopes recognized by the strongest neutralizing mAbs in the panel were identified by isolation and selection of virus escape mutants in the presence of individual mAbs. Cloned viruses resistant to HI and antibody neutralization were sequenced to identify mutations, and two unique mutations (D127E and G155E) were identified, both near the antigenic site Sa. Using human post‐vaccination sera, however, there were no differences in HI titer between A/California/04/2009 and either escape mutant, suggesting that these single mutations were not sufficient to abrogate a protective antibody response to the vaccine.     

Pulmonary thromboembolism in congenital heart defects with severe pulmonary arterial hypertension

IntroductionCongenital heart defect (CHD) with shunt can lead to severe, even irreversible pulmonary arterial hypertension (PAH); in extreme form to Eisenmenger syndrome (ES). Despite relatively good long-term survival, these patients often suffer from cyanosis and multisystemic dysfunction, where pulmonary artery thrombosis can be a potentially fatal complication. Together with bleeding these are the most frequent causes of non-cardiac death in patients with severe PAH due to CHD.Patients and methodsProspective study of 40 patients with severe PAH due to CHD (28 female/12 male, median age 41.5 years) was performed, with the aim to analyze the presence of pulmonary artery thrombosis and correlating anatomical and laboratory risk factors.ResultsPrevious thrombosis and/or thromboembolic event was found in 7 patients (17.5%). Significant differences in cyanotic vs non-cyanotic patients were in red blood count parameters: median hemoglobin level 195 vs 141 (p<0.0001), median erythrocytes count 6.62 vs 4.88×10¹²/l (p<0.0001), median hematocrit 0.58 vs 0.44 (p<0.0001). Laboratory findings causing increased risk for thrombosis were increased thrombocytes aggregation in 15 patients (37.5%), hypercoagulation in 5 patients (12.5%) and endothelial dysfunction in 8 patients (20%). Anatomical risk factor—severe pulmonary artery dilatation (>40 mm in female and >45 mm in male) was found in 19 patients (51.4%).ConclusionsPatients with severe PAH due to CHD represent a high-risk group for pulmonary artery thrombosis with morphological and flow pathology combined with secondary erythrocytosis and coagulation abnormalities. A relatively high incidence of platelet hyperaggregability shown in our study would propose that aspirin therapy might be considered in some highly selected patients with severe PAH due to CHD. Further studies though are needed to support this data.