Uncomplicating the Diagnosis of Coronary Artery Diseases

Humans have a complicated circulatory system; we need to understand some of its peculiar characteristics, to understand how to deal with coronary artery disease (CAD). Coronary arteries are not end-arteries. They grow extensive collaterals when the need arises. There are two of them, left and right, each taking origin from a sinus of Valsalva at the aortic root. The left main coronary artery quickly divides into the anterior descending and the circumflex arteries that run around the heart at the level of the atrio-ventricular grove. Of the two coronaries, the one which feeds the posterior descending artery is called the dominant coronary artery.

Coronary arteries feed only during the diastolic phase of the cardiac cycle while the rest of the arteries in the body feed during the full cardiac cycle. That is why we should not try and reduce diastolic pressures to very low levels. Coronary arteries have no rest during life. As a result, there are thousands of small perforating coronary arteries that take origin from the two main vessels and dip into the heart muscle perpendicularly.

In a healthy state, these perforating vessels have the capacity to dilate five times their normal lumen to accommodate extra blood when needed. This is called coronary reserve. As age advances, this reserve goes down in most of us, making us more vulnerable to coronary ischemia on exertion. The main coronary vein that runs in the atrio-ventricular grove always has 30% oxygen left behind during rest or exertion. Congenital abnormalities or ectatic dilations are seen occasionally in coronary arteries.

Everyone has atherosclerosis. The question is: Do you have unstable plaque? One function of the body’s repair system is to clear cholesterol from the cells lining the artery wall, a role that falls to cellular garbage trucks called macrophages. They swoop in and suck up the cholesterol from the plaque and haul it away. But, when the plaque is fatty, the immune-system macrophages can become engorged with so much cholesterol that they can’t do their job effectively. They turn into, what we call, foam cells, because they are full of fat. Unable to perform their duties, they die and add their contents to the cauldron of plaque bubbling under the fibrous cap. This lays the groundwork for the plaque to rupture.

Diagnosis

With all the advances in the field of cardiac diagnosis, myocardial ischemic heart disease diagnosis depends only on good bedside history and examination. In fact, there was a plea to control coronary angiography to prevent unnecessary coronary interventions which, today, are one of the main avoidable causes of intervention and death. Resting ECG can, in almost all cases, give a suggestive clue and, in some cases, a clear cut diagnosis of CAD. The usual stress tests (tread mill or cycle test) are not conclusive and unnecessary. The specificity and sensitivity of those tests are less than 50%, thus making them unreliable, to say the least.

Investigations

The diagnosis of chest pain could tax the best medical brain. Most chest pains that are vague are not due to coronary artery disease. Angiographically blocked coronary artery is not symptomatic of CAD. Even healthy young adults have significant blocks in the coronary arteries, as was seen in American soldiers in Korea and Vietnam. Intra-luminal blocks are but an attempt at sealing a damaged vessel. The vulnerable plaque can only be seen angioscopically.

Apart from chest pain, confirmation could come from thallium scanning, to map the area of ischemia. Tests like C-reactive protein, leucocytosis and serum CRP levels—tests that reveal the presence of intra-mural inflammation—would be of additional help in deciding who needs interventions like a bypass surgery. The last will have to be done only for the rarest of the rare cases. Because atherosclerosis is a systemic, multi-genic, and multi-focal disease, optimal care is likely to require systemic and multi-focal diagnosis and therapy, including local plaque therapy, in some patients.

(Professor Dr BM Hegde, a Padma Bhushan awardee in 2010, is an MD, PhD, FRCP (London, Edinburgh, Glasgow & Dublin), FACC and FAMS.)