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Left ventricular hypertrophy (LVH) is usually considered to be a
compen satory adjustment of heart muscle to an inreased work load.
LVH develops in the course of valvular or congenital heart disease,
or when part of the myocardium is damaged by long-standing ischemia
or infarction. In the hypertrophied heart the muscle fibers
increase in size, not in number. The fibers are found to contain a
larger number of myofibrils and the cell organelles are larger.
From epidemiologic studies it is known that even mild LVH is
associated with myocardial ischemia, ventricular arrhythmias, and
sudden cardiac death. Most cases of LVH show focal degenerative
tissue changes including cellular atrophy, myofibrillar
disorganization, interstitial fibrosis, and loss of intracellular
connections. Myocardial dysfunction develops and, unlike the
functional adaptive changes found in pure hypertrophy, is not
reversible by surgical treatment of the valvular heart disease or
medical correction of hypertension. Interstitial fibrosis,
intracellular changes of musc Ie cells, and loss of contract ile
tissue lead to poor mechanical function and undoubtedly increase
the risk of ischemia, arrhythmias, or sudden death, a
well-recognized problem in patients with a variety of heart
diseases. Even When successfully treated, the patients may remain
at risk if the compensatory hypertrophy is not fully reversed.
Epidemiologic studies conducted in the Framingham population in the
early 1950' s demonstrated LVH according to electrocardiographic
criteria in 1. 5% of the population; 2% of the population had LVH
according to chest X-ray criteria."
1 Introduction, history and contents.- 2 Isolation procedure.- 3
Perfusion box.- 4 Cardiac metabolism, electrolyte shifts and
acid-base problems.- 5 Haemolysis and pulmonary edema.- 6
Electrical measurements.- 7 Haemodynamics.- 8 Coronary flow and
oxygen consumption.- Layout of Perfusion Box and Equipment
(enclosure at the back of the book).
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