PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 1828021

Transient prolonged postischemic ventricular dilatation documented by 99mTc MIBI scan.

M Galli·R Giubbini·L Tavazzi
View original source ↗Export metadata ↓

Abstract

We describe two cases of prolonged postischemic ventricular dilatation during myocardial scintigraphy with 99mTc MIBI, the new perfusion tracer that has only negligible redistribution. Ventricular dilatation, caused by true chamber dilatation and/or subendocardial ischemia, was still present over two hours after the induced ischemic episode, suggesting a prolonged duration of such a commonly believed fleeting scintigraphic finding.

Explore related subjects

CardiomegalyCoronary DiseaseHumansMaleMiddle AgedNitrilesOrganotechnetium CompoundsRadionuclide ImagingTechnetium Tc 99m SestamibiTime FactorsCase ReportsJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

M Galli, R Giubbini, L Tavazzi. 1991. Transient prolonged postischemic ventricular dilatation documented by 99mTc MIBI scan.. https://doi.org/10.1378/chest.99.6.1536

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Obesity, hypothyroidism, craniosynostosis, cardiac hypertrophy, colitis, and developmental delay: a novel syndrome.

We describe in two brothers an apparently novel syndrome comprising obesity, congenital hypothyroidism, neonatal colitis, cardiac biventricular hypertrophy, craniosynostosis, and developmental delay. The first brother presented with neonatal colitis and congenital hypothyroidism and died at age 5 weeks of fulminant colitis. The second brother presented neonatally with the same condition, but survived and subsequently developed severe obesity, sagittal and coronal synostosis, and developmental delay. Both pregnancies had been complicated by hemolysis, elevated liver enzymes, and low platelets (HELLP syndrome). Exhaustive genetic and metabolic investigations have failed to provide a unifying pathogenesis. This unique combination of manifestations appears to represent a new syndrome with probable autosomal recessive or X-linked recessive inheritance.

Cardiomegaly↗
PubMed2006

The relationship between myocardial extracellular matrix remodeling and ventricular function.

Elevations in myocardial stress initiate structural remodeling of the heart in an attempt to normalize the imposed stress. This remodeling consists of cardiomyocyte hypertrophy and changes in the amount of collagen, collagen phenotype and collagen cross-linking. Since fibrillar collagen is a relatively stiff material, a decrease in collagen can result in a more compliant ventricle while an increase in collagen or collagen cross-linking results in a stiffer ventricle. If continued elevations in wall stress exceed the ability of the heart to compensate, then the ventricular wall thickness is disproportionately reduced compared to chamber volume and diastolic and systolic dysfunction ensues. This review describes the structural organization of collagen within the myocardium, discusses its effect on ventricular function and considers whether therapy aimed at reducing fibrosis is efficacious in heart failure. The evidence indicates that chamber stiffness can clearly be affected by alterations in both collagen quantity and quality, with the effect of changes in collagen concentration being modified by the extent of collagen cross-linking. The limited evidence available regarding the effects of collagen on systolic function indicates that pharmacological attempts to reduce interstitial collagen have a negative impact. Accordingly, a shift in treatment strategies directed more specifically at affecting collagen cross-linking, rather than reducing the concentration of collagen, may be warranted in the prevention of the adverse impact of collagen alterations on myocardial remodeling.

Cardiomegaly↗