Independent Predictors of Survival in Primary Systemic (Al) Amyloidosis, Including Cardiac Biomarkers and Left Ventricular Strain Imaging: An Observational Cohort Study

OBJECTIVES: The prognostic value of Doppler myocardial imaging, including myocardial velocity imaging, strain, and strain rate imaging, in patients with primary (AL) amyloidosis is uncertain. The aim of this longitudinal study was to identify independent predictors of survival, comparing clinical data, hematologic and cardiac biomarkers, and standard echocardiographic and Doppler myocardial imaging measures in a cohort of patients with AL amyloidosis.

METHODS: A total of 249 consecutive patients with AL amyloidosis were prospectively enrolled. The primary end point was all-cause mortality, and during a median follow-up period of 18 months, 75 patients (30%) died. Clinical and electrocardiographic data, biomarkers (brain natriuretic peptide and cardiac troponin T) and standard echocardiographic and longitudinal systolic and diastolic Doppler myocardial imaging measurements for 16 left ventricular segments were tested as potential independent predictors of survival.

RESULTS: Age (hazard ratio [HR], 1.03; P = .03), New York Heart Association class III or IV (HR, 2.47; P = .01), the presence of pleural effusion (HR, 1.79; P = .08), brain natriuretic peptide level (HR, 1.29; P = .01), ejection time (HR, 0.99; P = .13), and peak longitudinal systolic strain of the basal anteroseptal segment (HR, 1.05; P = .02) were independent predictors in the final model.

CONCLUSIONS: Multivariate survival analysis identified independent predictors of clinical outcome in patients with AL amyloidosis: New York Heart Association class III or IV, presence of pleural effusion, brain natriuretic peptide level > 493 pg/mL, ejection time < 273 ms, and peak longitudinal systolic basal anteroseptal strain less negative than or equal to -7.5% defined a high-risk group of patients.

PMID: 20434879

Comprehensive Echocardiographic Assessment of Normal Mitral Medtronic Hancock II, Medtronic Mosaic, and Carpentier-Edwards Perimount Bioprostheses Early After Implantation

OBJECTIVES: Normal Doppler-derived hemodynamic data for mitral valve bioprostheses are limited.

METHODS: To establish parameters for identifying normal function for each of the 3 types of bioprostheses examined, we conducted a comprehensive, retrospective, two-dimensional, and Doppler echocardiographic assessment of 179 patients who underwent implantation of the Medtronic Hancock II or the Medtronic Mosaic (Medtronic, Inc, Minneapolis, MN) porcine mitral valve bioprosthesis or the Carpentier-Edwards Perimount (Edwards Lifesciences LLC, Irvine, CA) bovine pericardial mitral valve bioprosthesis.

RESULTS: All bioprostheses were normal by clinical examination, intraoperative transesophageal echocardiography, and postoperative transthoracic echocardiography. Regardless of valve type and body surface area, the pressure half-time was < 124 ms in all patients. Mean gradient < 9.5 mm Hg, mitral E velocity < 2.6 m/s, mitral valve prosthesis time-velocity integral < 69 cm, and ratio of the mitral valve prosthesis time-velocity integral to the left ventricular outflow tract time-velocity integral < 3.4 were recorded in nearly all patients.

CONCLUSIONS: These cutoff values (mean + 2 standard deviation) are specific, but not sensitive, for identifying mitral valve prosthesis dysfunction. Prostheses with hemodynamic values that are higher than these cutoff values are likely dysfunctional, but in select cases, mitral valve prosthesis dysfunction may be present even when hemodynamic values are lower than these thresholds.

PMID: 20497863

The Vascular Biology of Atherosclerosis and Imaging Targets

The growing worldwide health challenge of atherosclerosis, together with advances in imaging technologies, have stimulated considerable interest in novel approaches to gauging this disease. The last several decades have witnessed a burgeoning in understanding of the molecular pathways involved in atherogenesis, lesion progression, and the mechanisms underlying the complications of human atherosclerotic plaques. The imaging of atherosclerosis is reaching beyond anatomy to encompass assessment of aspects of plaque biology related to the pathogenesis and complication of the disease. The harnessing of these biologic insights promises to provide a plethora of new targets for molecular imaging of atherosclerosis. The goals for the years to come must include translation of the experimental work to visualization of these appealing biologic targets in humans.

PMID: 20395349