Page 452 - Textbook of Pathology, 6th Edition

436 7. Pericarditis. Sterile pericarditis appearing on about the ii) An alternate concept of development of myocardial
second day is common over transmural infarcts. It is fibrosis is healing of minute areas of focal myocytolysis—
characterised by fibrinous pericarditis and may be associated the myocardial fibres in a small area undergo slow
with pericardial effusion. Often, it is of no functional degeneration due to myocardial ischaemia. These fibres lose
significance and resolves spontaneously. their myofibrils but nuclei remain intact. These foci are
8. Postmyocardial infarction syndrome. About 3 to 4% of infiltrated by macrophages and eventually are replaced by
patients who suffered from acute MI develop postmyocardial proliferating fibroblasts and collagen.
infarction syndrome or Dressler’s syndrome subsequently. It MORPHOLOGIC FEATURES. Grossly, the heart may be
usually occurs 1 to 6 weeks after the attack of MI. It is normal in size or hypertrophied. The left ventricular wall
characterised by pneumonitis. The symptoms are usually generally shows foci of grey-white fibrosis in brown
mild and disappear in a few weeks. The exact pathogenesis myocardium. Healed scars of previous MI may be present.
of this syndrome is not known. It may be due to autoimmune Valves of the left heart may be distorted, thickened and
reaction as evidenced by circulating anti-heart antibodies in show calcification. Coronary arteries invariably show
the serum of these patients. But these antibodies are also pre- moderate to severe atherosclerosis.
sent in patients with acute MI who do not develop this Microscopically, the characteristic features are as follows
syndrome.
(Fig. 16.22):
CHRONIC ISCHAEMIC HEART DISEASE i) There are scattered areas of diffuse myocardial fibrosis,
especially around the small blood vessels in the interstitial
Chronic ischaemic heart disease, ischaemic cardiomyopathy tissue of the myocardium.
or myocardial fibrosis, are the terms used for focal or diffuse ii) Intervening single fibres and groups of myocardial
fibrosis in the myocardium characteristically found in elderly fibres show variation in fibre size and foci of myocytolysis.
patients of progressive IHD. Such small areas of fibrous iii) Areas of brown atrophy of the myocardium may also
scarring are commonly found in the heart of patients who be present.
have history of episodes of angina and attacks of MI some
years back. The patients generally have gradually developing iv) Coronary arteries show atherosclerotic plaques and
CHF due to decompensation over a period of years. Occasio- may have complicated lesions in the form of super-
nally, serious cardiac arrhythmias or infarction may imposed thrombosis.
supervene and cause death.
SECTION III
SUDDEN CARDIAC DEATH
ETIOPATHOGENESIS. In majority of cases, coronary
atherosclerosis causes progressive ischaemic myocardial Sudden cardiac death is defined as sudden death within 24
damage and replacement by myocardial fibrosis. A small hours of the onset of cardiac symptoms. The most important
percentage of cases may result from other causes such as cause is coronary atherosclerosis; less commonly it may be
emboli, coronary arteritis and myocarditis. due to coronary vasospasm and other non-ischaemic causes.
The mechanism of development of myocardial fibrosis These include: calcific aortic stenosis, myocarditis of various
can be explained by one of the following concepts: types, hypertrophic cardiomyopathy, mitral valve prolapse,
i) Myocardial fibrosis represents healing of minute infarcts endocarditis, and hereditary and acquired defects of the
involving small scattered groups of myocardial fibres. conduction system. The mechanism of sudden death by

Systemic Pathology

Figure 16.22 Chronic ischaemic heart disease. There is patchy myocardial fibrosis, especially around small blood vessels in the interstitium.
The intervening single cells and groups of myocardial cells show myocytolysis.