Publications by authors named "Elstein E"

Background: Primary cardiac lymphoma (PCL) is rare and can present with a wide variety of clinical symptoms, frequently leading to a delay in diagnosis.

Case Summary: We report a case of a PCL in an 81-year-old man. Cardiac magnetic resonance imaging showed multiple masses in the right atrium and a mass in the right ventricular outflow tract extending to the pulmonary artery.

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This study compares the prevalence of titin gene mutations in patients with dilated cardiomyopathy receiving standard pharmacological therapy with and without recovery of systolic function.

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Purpose: Determine the relative risk of cancer users of commonly prescribed antihypertensive drugs with a focus on documenting risk in long-term users (>7.5 years).

Methods: We conducted a nested case-control study using the Saskatchewan Health databases.

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Purpose: Confounding by indication is common in observational studies of outcomes that treatment is intended to affect. In light of the stepped-care approach to hypertension management, we reexamined the controversy around myocardial infarction (MI) risk in relation to antihypertensive agents by considering past drug history both as a confounder and as an effect modifier.

Methods: Case-control design nested within a cohort of 19,501 adults initiating therapy with angiotensin-converting enzyme inhibitors (ACEI), calcium channel blockers (CCB) or beta-blockers in Saskatchewan (1990-93) and followed up to 1997.

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Objectives: To determine the effect of angiotensin-converting enzyme (ACE) inhibition on brachial flow-mediated vasodilation.

Background: Quinapril, an ACE inhibitor with high affinity, has been shown to improve coronary endothelial dysfunction in patients with coronary artery disease. The effectiveness of different vasoactive agents to improve human endothelial function is unknown.

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Background: Based on the excellent correlation between cyclosporine A 2-hr postdose blood levels (C2) and the area under the concentration versus time curve, we evaluated the clinical benefit of Neoral dose monitoring with C2 compared trough levels (C0) in stable heart transplant patients.

Methods: We studied 114 stable adult patients followed at the heart transplant clinic, who were >1 year after surgery. In May 1996 (period 1, follow-up 10+/-4 months), Neoral dose monitoring was based on C2 (300-600 ng/ml); while in May 1997 (period 2, follow-up 10+/-2 months), it was based on C0 (100-200 ng/ml).

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Background: Reference-based pricing is a cost-containment policy applied to prescription drugs that are in the same class and deemed to be therapeutically equivalent. Recent reference-based pricing measures have targeted several drug classes, including angiotensin-converting-enzyme (ACE) inhibitors. The objective of this study was to assess whether patients treated for hypertension with various ACE inhibitors differed in their utilization of health care services and hence, whether the various ACE inhibitors should be considered therapeutically equivalent.

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To assess the safety profile of Neoral dose adjustment using cyclosporine (CsA) trough levels (C0) compared with levels obtained 2 h after the morning dose (C2), 30 stable adult heart transplant patients 1 yr or more after surgery were converted from Sandimmune to Neoral. After a baseline visit (before conversion), initial follow-up included two visits (2 and 4-6 wk after conversion). After the first visit, patients were randomized to Group I (C0: 100-200 ng/ml) or Group II (C2: 200-400 ng/ml).

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Background: The phenotypic expression of left ventricular hypertrophy (LVH) in patients with hypertrophic cardiomyopathy (HCM) is variable. This phenotypic variability is not completely explained by the responsible mutations or other known factors. Recent data denote a role for the modifier genes and environmental factors.

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Hypertrophic cardiomyopathy has been shown to be a genetically heterogeneous disorder, linked to at least four different loci on chromosomes 14, 1, 15, and 11. Thus far, three genes have been identified that harbor mutations leading to hypertrophic cardiomyopathy. These genes--cardiac beta myosin heavy chain, alpha tropomyosin, and troponin T--code for proteins that are integral components of the sarcomere.

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In this article we review the techniques of molecular biology as they apply to the elucidation of the genetic basis of hypertrophic cardiomyopathy. We review the evidence for linkage to chromosome 14 and the specific mutations described to date. The evidence for genetic heterogeneity is presented.

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