Time To Prognosticate...
NATIONAL JOURNAL OF HOMOEOPATHY 2002 Jul / Aug VOL 4 NO 4.
Dr C H Asrani
Enough has been said about Stable Angina, Unstable Angina, Myocardial Infarction and Angina equivalent symptoms. For the practicing physician, whether allopath or homoeopath, emphasis should be on prognosticating a case of Coronary Artery Disease. Bluntly put, it means trying to assess the chances of complications like Infarction or LVF in a diagnosed case of CAD. To do this would require an in-depth understanding of the risk factors as well as monitoring parameters.
CAD is the commonest cause of Cardio vascular disability and mortality. Male to female overall ratio of those afflicted is 4:1, the ratio is 8:1 before age 40, and it is 1:1 beyond age 70. In men, the peak incidence of clinical manifestations is at age 50-60; and in women at age 60-70.
Risk Factors for Coronary Heart Disease:
A number of important risk factors have been identified for premature
coronary heart disease. These include a positive family history (particularly
when onset is before age 50), age, male gender, blood lipid abnormalities,
hypertension, physical inactivity, cigarette smoking, diabetes mellitus,
elevated blood homocysteine levels, and hypoestrogenemia in women. There is
overwhelming evidence to show that abnormalities of lipid metabolism play a
direct role in the pathophysiology of CAD. We all know that in today’s times
just asking of Total Cholesterol and Triglycerides would be real foolish as one
may have near normal Total Cholesterol with very high LDL Cholesterol. Risk
increases progressively with higher levels of LDL cholesterol and declines with
higher levels of HDL cholesterol. The ratio of LDL to HDL cholesterol provides a
composite marker of risk, with ratios below 3 indicating a lower risk and ratios
above 5 indicating higher risk. Patients presenting with clinical manifestations
of CAD before age 50 often have predisposing risk factors. These risk factors
are important for delaying/ identifying early onset of disease but less closely
linked to the onset of coronary disease in later years
It is now known that other abnormalities of lipids are also important in the pathogenesis of CAD, and these are looked for in patients with otherwise unexplained premature coronary atherosclerosis. Noteworthy amongst these are elevated levels of apolipoprotein(a) and of small, dense LDL lipoprotein particles. Evidence also suggests that hypertriglyceridemia is an independent risk factor for CAD. Elevated triglyceride levels often occur in association with other lipid abnormalities, including low levels of HDL cholesterol and elevated concentrations of lipoprotein(a).
One of the newer markers is Homocysteine. Elevated levels of serum homocysteine and non-specific markers of inflammation, such as cross-reactive protein (CRP), fibrinogen and ferritin, correlate with the occurrence of coronary disease. Hyperhomocysteinemia is known to increase the risk of thrombosis.
Pathophysiology:
Much is known today concerning the pathophysiology of
atherosclerosis and the clinical presentations of CAD. Abnormal lipid metabolism
or excessive intake of cholesterol and saturated fats - especially when
superimposed on a genetic predisposition - initiates the atherosclerotic
process. Low-density lipoproteins (LDLs) are the major atherogenic lipid.
High-density lipoproteins (HDLs), in contrast, are protective and probably
assist in the mobilization of LDLs. The pathogenetic role of other lipids,
including triglycerides, is less clear. LDLs undergo in-situ-oxidation, which
makes them more difficult to mobilize as well as locally cytotoxic. LDL thus is
more important marker of progression of CAD.
Primary & Secondary Prevention Of Ischemic Heart Disease
Although many risk factors for coronary artery disease are
non-modifiable (gender, age, family history), active intervention in the
modifiable ones like cessation of smoking, treatment of dyslipidemia and
lowering of blood pressure can both prevent coronary disease and delay its
progression and complications even after the disease is manifested. Treatment of
lipid abnormalities delay the progression of atherosclerosis and in some cases
produces regression. Even if there is no regression, fewer new lesions develop
and coronary event rates are markedly reduced in patients with clinical evidence
of atherosclerosis.
The importance of elevated LDL cholesterol in the pathogenesis of CAD - as well as stroke and peripheral arterial diseases - is substantiated by a series of trials. The substantial benefit of treating hyperlipidemia in preventing these conditions has also been proven beyond doubt. Trials have demonstrated improved outcomes even in patients who have already had myocardial infarction. The reductions were found in non-fatal cardiac events and cardiovascular deaths and the reductions occurred regardless of age, race or the presence of hypertension.
Aggressive lipid-lowering therapy should be implemented in all patients with Dyslipidemia and coronary artery or peripheral vascular disease. There is now clear evidence that reduction of LDL cholesterol can prevent coronary events & stroke in patients without clinically manifesting atherosclerosis (primary prevention) and LDL levels as low as 130 mg/dL. A European study enrolled high risk patients with a mean LDL of 192 mg/dL and demonstrated a reduction of coronary death and nonfatal myocardial infarction.
Since oxidation of LDL appears to play a role in the atherogenicity of lipid molecules that have passed into the vessel wall, antioxidant therapy1 has been advocated as a preventive measure.
Elevated plasma homocysteine levels are associated with an increased risk of vascular events. Although homocysteine levels can be reduced with dietary supplements of folic acid (1 mg/day) in combination with vitamin B6 and vitamin B12, it is not clear that this reduces clinical events in individuals with coronary artery disease.
Another preventive measure is aspirin prophylaxis.
The effect of hormone replacement therapy in postmenopausal women is uncertain. Epidemiologic data suggest that oestrogen protects against the development of coronary artery disease. However, the HERS trial, a prospective evaluation of estrogen use in women with coronary artery disease, showed no benefit in reducing mortality or preventing subsequent cardiac events. This issue should be considered unresolved.
Control of blood pressure has now been shown to prevent infarctions in older patients. Although unproved, it seems likely that control of blood pressure in younger individuals also prevents subsequent coronary events. The role of exercise remains controversial. Although individuals who exercise for at least 30 minutes a week are at lower risk for subsequent coronary events, it is difficult to be certain that this outcome relates specifically to exercise rather than a generally healthy lifestyle.
The decrease in number of coronary deaths over the last 2 decades may be due to a decrease in the prevalence of risk factors but probably also reflects improvements in medical therapy, the role of coronary care units, better treatment of angina, arrhythmias and heart failure, and improved survival after coronary revascularization in some patient subsets.
Even at risk of insulting your intelligence, I would repeat the same for sake of completing the article.
