Search PubMed⌕ Search
Home/Archive/PubMed

PubMed · 1267527

Constrictive pericarditis.

J S Simon·J R Pluth
View original source ↗Export metadata ↓

Abstract

A patient with constrictive pericarditis following an open-heart operation without sepsis is discussed. In the absence of sepsis, it has been widely held that this complication does not develop following an open-heart procedure. The fatal outcome in this patient could have been avoided had such an association been known.

Explore related subjects

Aortic ValveAortic Valve StenosisCardiac Surgical ProceduresDiagnostic ErrorsFemaleFollow-Up StudiesHeart Valve ProsthesisHumansMiddle AgedMitral ValveMitral Valve StenosisPericarditis, ConstrictivePericardiumPleural EffusionRadiographyTissue AdhesionsCase ReportsJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

J S Simon, J R Pluth. 1976. Constrictive pericarditis.. https://doi.org/10.1016/s0003-4975(10)63895-7

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

KEEP EXPLORING

Related citations

PubMed1996

[Long term results of the use of Björk-Shiley convex-concave heart valves. Ullevol hospital 1978-83].

In recent years, Björk-Shiley CC-valves have become the object of suspicion after several reports of strut fracture with embolization of the tilting disk and acute heart failure. At Ullevål Hospital Björk-Shiley CC-valves were used in 341 patients during the period October 1978 to March 1983. Strut fracture occurred in four cases, three of the patients died and one survived an emergency heart operation with replacement of the valve. In four patients, prophylactic replacement of the valves was performed. During the observation period concluded in September 1995 a total of 187 patients died. These included 26 operative deaths (7.6%). Of the late deaths, 40% were due to heart failure and 21% were sudden deaths. Strut fracture was the cause of death in 2% of the late deaths.

Aortic Valve↗
PubMed1996

Normalization of left ventricular nonuniformity late after valve replacement for aortic stenosis.

The aim of the present study was to evaluate nonuniformity in pressure overload hypertrophy due to aortic stenosis. Twenty patients were included in the present analysis. Ten patients with severe aortic stenosis were studied preoperatively as well as early (21 +/- 8 months) and (89 +/- 21 months) after aortic valve replacement (AVR) using left ventricular biplane angiograms, high-fidelity pressure measurements and endomyocardial biopsies. Ten normal subjects served as controls. LV systolic function was assessed from biplane ejection fraction, and diastolic function from the time constant of relaxation, the peak filling rate and the constant of myocardial stiffness. Nonuniformity was evaluated from the coefficient of variation of the time to end-systole (systolic asynchrony) and peak filling rate (diastolic asynchrony) of 12 regions in right anterior oblique and left anterior oblique projection. Ejection fraction was comparable in patients with aortic stenosis and in controls, whereas preoperatively diastolic dysfunction with prolonged relaxation and increased stiffness was present in patients with aortic stenosis and was normalized late after AVR. LV systolic asynchrony was present (>25D of controls) in 7 and diastolic asynchrony in 10 of 10 patients with aortic stenosis. Early as well as late after AVR systolic asynchrony was normalized in 9 of 10 patients. Diastolic asynchrony was present early AVR in all but one patient, although there was a significant improvement with respect to the preoperative evaluation. Late after AVR there was a normalization of diastolic asynchrony in 9 of 10 patients with aortic stenosis. Thus, it is concluded that systolic asynchrony is normalized early after AVR probably due to its load-sensitivity, whereas diastolic asynchrony persists probably due to residual LV hypertrophy with increased interstitial fibrosis and myocardial stiffness. Late after AVR, diastolic asynchrony is normalized due to structural remodeling with regression of both myocardial hypertrophy and interstitial fibrosis.

Aortic Valve↗