Cardiac Left Ventricular Hypertrophy [antikvár]

VII INTRODUCTION Left ventricular hypertrophy (LVH) is usually considered to be a compensatory 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 f death. Most cases of LVH show focal degenerative tissue changes including cellular atrophy, myofibriliar 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 correct ion of hypertension. Interstit ial fibrosis, intracellular changes of musele cells, and loss of contractile 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. fi Epidemiologic studies conducted in the Framingham population in the early 1950' s demonstrated LVH according to electrocardiographic criteria in [j 1.5% of the population; 2% of the population had LVH according to chest r X-ray criteria. Recently, a study in second-generation offspring of the ^.J original cohort, now at the same age as the original cohort in the early p- 1950's, showed a dec line to 0.2% and 1% respect ively. In the recent p/ study, echocardiography was used in addition to electrocardiography and chest X-ray to detect LVH. In the offspring population, 6% had LVH and of .//j the original cohort 22% now had LVH according to echocardiographic criteria. Echocard iography is far more sens11 ive in detecting LVH than ECG or chest X-ray. LVH with typical electrocardiographic changes carries an unfavorable prognosis It is found in 45% of all cardiovascular deaths and five-