The natural history of CAD is very important from the prcvcntive point or view.Though the usual manifestations of angina ancl heart attoclcs tend to occur at the nliddle age, numerous studies have shown that the process starts very early in life,even as early as threc years of age. Evidence ii-on1 various autopsy studies, ~unimal experiments, and long-term epiden~iological studies supports the concept that secd of atherosclerosis is sown in childhood a ~ i d it has also becn shown that cosonory risk factors which accelerate the process may also originnle in the same age g~.oup.Post ~norlem analysis of hearts of young US casualties (mean age 22 years) in thc Korean and Vietnam conflicts showed the incidence of coronary atl~ei.o~clcrotic lesions to be 77 pcr ccnt and 45 per cent, respectively. The Boga1us:l I-IearL St~~cly clearly showed a positive correlation between childhood risk fi~ctors and coronary ai-tery lesion. More recently, the notion thal coronary atherosclerosis begins at a young age was confirmed by an in vivo intravascular ultrasound (IVUS) study appeariilg in the June 5, 2001 issue of Circ-ulution where one in sixteens were found to have atllcrosclerotic plaque in their coronary arteries. Young Anlericans who have risk factors for clinical coronary heart disease - in particular high LDL-cholesterol levels and obesity - have a high prevalence of advanced athcrosclerolic plaques in their arteries that contain qualities indicating vulnerability to rupture,according to the Pathobiological Determinants of Atllcrosclerosis in Youth (PDAY) Research Group reporting in the July 25, 2000 issue of Circulation.
Developmental Periods
The development of coronary artery disease like many other diseases can be divided into the following periods:
i)Incubation period: which begins in infancy and continue into adolescence.Here the genetic or hereditary factors interplay with environ~nental conditions to start the process and sustain it. The presence of various risk factors accentuates and accelerates the pathogenetic mechanism, but the disease does not become evident.
ii) Preclinical and latent period: when the disease is present in varying degrees of severity but the person remains asymptomatic. Presence of disease can be ascertained by various tests.
iii) Clinical period: when signs and synmptonis appear. Though the typical sympto~n is angina of effort because of inyocardial ischaernia, many patients do develop myocardial infarction without any preceding angina. For some the only manifestation will be sudden death coming without any waning, mostly because of malignant ventricular arrhythmias. It is to be noted that the sylnptonlatic period is the tip of the iceberg and the vast majority of patients remain asy~imptoinatic, until some catastrophe strikes them.
Stages sf Atherosclerosis
The process of atherosclerosis which gives rise to CAD nmmches in stages. The earliest recognizable pathologic lesions are the fatty streaks, slnall yellvwish focal lesions, whiclm make their appearance in the aorta and big vessels even before three years of age, The fatty slreaks are composed of intracellular collection of lipid materials with elastin and other fibre protein in the intima and inner media of blood vessels. These linear streaks increase in number, size and distribution during the second decade and become evident in coronay arteries. Gradually in the third decade, the fatty streaks progress to fibrous plaques - a firm raised white lesion containiilg increased nlnounts of lipids, collagen and fibrous tissue. As the fibrous plaque grows in bulk wi tll more and more fatty substances, cel1ul:u infiltrates and coimnect~ve tissue proliferation, it bulges into the lumen of thc artery in the for111 of 'atheroma'. Tlmere are varying amounts of lipid in the core and a fibrous cap covers the inner core. This happens around the fourth decade in life. Subsequently there ]nay be plaque fissure, rupture, lmaemorrl~age, clot fornmation - the 'complicated' atheroma giving risc to acculc coronary syndrome, heart attacks etc. The rate by which the lesion progresses through different stages varies in diflelcnl ethnic groiipfiand individuals depending on various risk hlctors. New fatty strcalcs continue to foi~n't1~1'0~1gImo~t adult life and athel.osclerotic lcsions in different stages of devcloprnent may be present in the same inclividunl. The plaques ]nay be 'stable' or 'unstable' depending on the amount of lipid core tlnd the thickness and hardness of the cap covering the plaque. While the stable plaqucs are respotlsible for tlme ischaenlia and anginal symptoms, ~t is the soft unstable plaques which usually ruptures aiicl initiates clotting process resulling in unstable angina, acute coronary syndrolnes and myocardial infarction. Atherosclerosis is not conl'ined to the coronary arteries only; almost all nlcdiuin sized arteries including arta-ies to the brains almcl lilnbs may b.: involved.
Understanding the natural history and stages of athe~.osclerosis is important from the point of preventing and reversing the coronary artery disease. While lifestyle modification and drug treatment can reverse the process with decrease in the size of the small soft newer plaques, it is u;lliltely that the older, hard, encrusted plaques with gross remodclling of the vessel wall will be changed even with aggressive treatment. Preventive measures should therefore stast early in life and lollowed lor the rest of the life for long-term benefit.
Developmental Periods
The development of coronary artery disease like many other diseases can be divided into the following periods:
i)Incubation period: which begins in infancy and continue into adolescence.Here the genetic or hereditary factors interplay with environ~nental conditions to start the process and sustain it. The presence of various risk factors accentuates and accelerates the pathogenetic mechanism, but the disease does not become evident.
ii) Preclinical and latent period: when the disease is present in varying degrees of severity but the person remains asymptomatic. Presence of disease can be ascertained by various tests.
iii) Clinical period: when signs and synmptonis appear. Though the typical sympto~n is angina of effort because of inyocardial ischaernia, many patients do develop myocardial infarction without any preceding angina. For some the only manifestation will be sudden death coming without any waning, mostly because of malignant ventricular arrhythmias. It is to be noted that the sylnptonlatic period is the tip of the iceberg and the vast majority of patients remain asy~imptoinatic, until some catastrophe strikes them.
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| Stagcs of athcrosclcrosis |
Stages sf Atherosclerosis
The process of atherosclerosis which gives rise to CAD nmmches in stages. The earliest recognizable pathologic lesions are the fatty streaks, slnall yellvwish focal lesions, whiclm make their appearance in the aorta and big vessels even before three years of age, The fatty slreaks are composed of intracellular collection of lipid materials with elastin and other fibre protein in the intima and inner media of blood vessels. These linear streaks increase in number, size and distribution during the second decade and become evident in coronay arteries. Gradually in the third decade, the fatty streaks progress to fibrous plaques - a firm raised white lesion containiilg increased nlnounts of lipids, collagen and fibrous tissue. As the fibrous plaque grows in bulk wi tll more and more fatty substances, cel1ul:u infiltrates and coimnect~ve tissue proliferation, it bulges into the lumen of thc artery in the for111 of 'atheroma'. Tlmere are varying amounts of lipid in the core and a fibrous cap covers the inner core. This happens around the fourth decade in life. Subsequently there ]nay be plaque fissure, rupture, lmaemorrl~age, clot fornmation - the 'complicated' atheroma giving risc to acculc coronary syndrome, heart attacks etc. The rate by which the lesion progresses through different stages varies in diflelcnl ethnic groiipfiand individuals depending on various risk hlctors. New fatty strcalcs continue to foi~n't1~1'0~1gImo~t adult life and athel.osclerotic lcsions in different stages of devcloprnent may be present in the same inclividunl. The plaques ]nay be 'stable' or 'unstable' depending on the amount of lipid core tlnd the thickness and hardness of the cap covering the plaque. While the stable plaqucs are respotlsible for tlme ischaenlia and anginal symptoms, ~t is the soft unstable plaques which usually ruptures aiicl initiates clotting process resulling in unstable angina, acute coronary syndrolnes and myocardial infarction. Atherosclerosis is not conl'ined to the coronary arteries only; almost all nlcdiuin sized arteries including arta-ies to the brains almcl lilnbs may b.: involved.
Understanding the natural history and stages of athe~.osclerosis is important from the point of preventing and reversing the coronary artery disease. While lifestyle modification and drug treatment can reverse the process with decrease in the size of the small soft newer plaques, it is u;lliltely that the older, hard, encrusted plaques with gross remodclling of the vessel wall will be changed even with aggressive treatment. Preventive measures should therefore stast early in life and lollowed lor the rest of the life for long-term benefit.
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