“Men are vain authorities who can resolve nothing.”



Michel de Montaigne.







Almost every American has some degree of blocks in the coronary arteries, avers a recent editorial in a leading medical journal.1 Most blocks have been there from our childhood and are innocuous. They stimulate the growth of multiple collateral vessels that, naturally, bypass the blocks. This, to a great extent, applies to other races as well; only the degree varies. Recent studies have shown these blocks in all the major vessels in young healthy American soldiers killed in the battle front as also young kids killed in the cross fire in Los Angeles riots a few years ago.2 What, then, is the role of an angiogram in the diagnosis of coronary artery disease? Hardly any! The only role for coronary angiogram is after the diagnosis of coronary artery disease is confirmed by various other methods, most important being the patient’s clinical presentation, in the unlikely event of an intervention being considered as the best management strategy, the coronary angiogram becomes mandatory to decide the plumbing techniques.3



Does the presence of calcium indicate the nature of the plaque?



Recently, there have been attempts to establish another expensive and, to a certain degree, dangerous diagnostic test to detect calcium in the coronary blocks to indicate the risky type of blocks that are supposed to progress to plaque rupture with intravascular clots, producing myocardial infarcts. EBCT, the computed tomography (fast CT) electron beam double helical system, detects calcium in the vessel walls as a sign of atherosclerosis.4 There are two kinds of atherosclerotic plaques, the one with and another without calcium. The former is seen in elderly patients with stable angina and the calcium deficient plaques are seen in younger patients but, the presence of calcium does not mean that the plaque is active.



EBCT again is not the “Holy Grail” of coronary artery disease diagnosis. As much as 19% of patients with acute myocardial infarction, in a recent study, did not have calcium in their infarct related vessels!5 The advertisers of this machine miss this vital point deliberately. In addition, each EBCT scan gives the patient as much as six chest radiogram worth of radiation. If this is combined, as many times done, with a lung scan, it adds another six chest radiogram worth radiation and if done with abdominal scan another twelve radiographs worth of radiation. As such this is a dangerous procedure in patient follow up.



How to detect a dangerous plaque?



The best method, of course, would be intravascular angioscopy coupled with intravascular echo. It has its limitations, though and, the facility is not available routinely. It needs a great degree of skill to interpret the results. Among the various methods the one that stands out is the presence of inflammation in the plaque. Inside the coronary vessels it is very difficult to detect the four major signs of inflammation color, dolor, rubor and tumor. However, part of the chest pain could come from the inflamed plaque itself, as the heart muscle, per se, has no pain fibres, anyway. That would again be a crude denominator. Raised local temperature is a definite sign. The plaques that are going to create problems in the near future are always a couple of degrees centigrade warmer than the quiet plaques that remain dormant all through one’s life. Measuring coronary intimal temperatures is not easy.



The next best would be to look for indirect evidences. Inflammatory cells of all kinds leave their foot prints in the circulation. Most inflammatory cells produce the kind of cytokine response that stimulates the liver to generate C reactive proteins. A serial study of rising titres of the C reactive protein, in the absence of other inflammations, is a very good sign of imminent danger from the plaque.6 In addition, the macrophages, the scavenger cells that mop up the debris around the area of inflammation also leave their markers. Another new test recently approved by the American FDA is called the PLAC, which measures the macrophage markers.7



This test measures the level of lipoprotein associated phospholipase A2, the end product of macrophage degradation-the tell tale feature of a recent inflammation. Once again, if there are no other evidences of inflammation in the body and, in the presence of unstable angina, PLAC test is worth its cost. I must hasten to add here that no test should ethically be performed in clinical medicine, that too an expensive test, which does not give a new direction to get at the diagnosis nor helps plan a new management strategy. From that point of view PLAC is a good test. This, coupled with high density lipoprotein levels, and homocysteine levels might help the diagnosis of coronary artery disease in a patient with unstable angina.



Intravascular echocardiogram has helped us to get much more information about atherosclerotic plaques than all that we have believed so far. It was believed till recently that early plaques that are small usually rupture. A prospective study did show that one in a hundred such plaques only produced trouble; most of them remain quiescent for life.8 So the size of the plaque is of no consequence. The large plaques which are calcified rarely create any problem. In addition, these early plaques help remodel the coronary arteries and rarely block the flow of blood. They may induce collateral growth as well.





The “Holy Grail” of coronary disease?



Medical world has yet to find the “Holy Grail” of coronary artery disease diagnosis, leave alone drinking from it. However, recent studies have reinforced some of the well know facts that coronary artery blocks are not synonymous with coronary artery disease. The two are poles apart. This brings us to the heart of the matter. Atherosclerosis is only a band-aid that nature puts on any vessel injury. Unfortunately, Aniskov and Rokithansky found the gruel (cholesterol) inside those plaques and we have been equating serum cholesterol and all its cousins as the be all and end all of vascular disease till very recently. Similar is the story of coronary angiograms. Although they do not tell us anything about the nature and the future of the coronary plaque we still make the gullible people believe that detecting a plaque is the gold standard for diagnosing coronary artery disease and have been predicting the unpredictable to increase patient anxiety to get them into our net for interventions that are the biggest till movers in medicine today.9 Nothing could be farther from the truth, though.



Let us accept this fact and act fast before society realizes our tricks to hold us in contempt. The size or extent of the plaque has no relevance to disease but is needed to help the plumber if we chose to intervene with either angioplasty or CABG. Both these procedures are also anti-Nature. Both of them increase the original disease, the intimal damage, not to mention the other dangers. The original disease in the vessel is the intimal damage and if we could find a solution to avoid that we could win the war against this killer. The key could be in the human mind.10 It is the disturbed mind that is at the root of vessel wall damage. The urgent need now is to confine the angiography set ups to scientific research departments only and not let them mushroom on a commercial scale. The latter is a curse on man kind. There have been sane pleas for this kind of action even from the advanced west.11 Hope we will be able to practise humane medicine and be ready to walk our talk, to get back the lost glory of the medical profession.



“We do not see things as they are,

We see them as we are.”

Nin Anais.













BIBLIOGRAPHY.



1) Ewy GA. In search of the “Holy Grail” of clinically significant coronary artery disease. Arch. Intern. Med 2004; 164: 1226-67.

2) Hegde BM. Coronary artery disease-time for reappraisal. Proc. Royal Coll. Physi. Edinburgh. 1995; 26: 421-24.

3) Graboys TB, Biegelson B, Lampert S, Blatt CM, & Lown B. Second Opinion trial of Coronary angiography. JAMA 1992; 268: 2537-2540.

4) O’Malley PG, Feurstein IM, TaylorAJ, et. al. Impact of Electron Beam Computed Tomography. JAMA 2003; 289: 2215-2223.

5) Shemesh J, Stroh CL, Tenebaum A et al: Comparison of coronary calcium deposit in stable angina and first myocardial infarct using EBCT. Amer J Cardiol. 1998; 81: 271-275.

6) Pepys MB, Hirshfield GM. C-reactive protein a critical update. J. Clin. Invest. 2003; 111: 1805-1812.

7) Tyler J. New test predicts heart disease in low risk patients. 2003; vol1. http://www.bcmfindings.net

8) Davies MJ. The composition of coronary plaques. New. Engl.J. Med. 1997; 336: 1332-34.

9) Krumholz HM. Cardiac Procedures, outcomes, and accountability. N. Engl. J. Med 1997; 336; 1522-23

10) Linden.W,,,Stossel.C,and,,,,Maurice.J…Psycho-social interventions for patients with CAD. Arch. Intern. Med. 1996; 156: 745-752.

11) Treasure T. US doubts about angiography. Lancet 1993; 341: 154.