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A Further Response to Shah Ebrahim

Posted by plosmedicine on 30 Mar 2009 at 23:42 GMT

Author: Michael Makover
Institution: New York University School of Medicine, New York, New York, United States
Submitted Date: April 27, 2005
Published Date: April 27, 2005
This comment was originally posted as a “Reader Response” on the publication date indicated above. All Reader Responses are now available as comments.

Shah Ebrahim says, in his answer to my statement in our debate, that plaque is so common that it makes sense to treat only those likely to have an acute event in the near future. Not everyone has a heart attack but everyone ages, nor can we be sure who will be lucky and who not. Anyone with an LDL above 70 is at risk [1]. Narrowing of arteries must certainly contribute to decline in aging. He says that most plaque is stable and does not rupture. The one half million yearly heart attack victims and the hundreds of thousands of stroke sufferers in the United Sates alone would disagree. Waiting decades more for yet more studies will not help all those now succumbing, as long as all the components have already been well vetted, as they have been. His statement that most [plaques] are stable and unlikely to rupture is based on his own study published in Stroke [2], but reviewing that paper finds no data as to how many of those found to have thickened intimal wall thickness (IMT) or plaque actually had heart attacks or strokes. It did find that intimal wall changes were highly associated with ischemic heart disease.

It is correct that risk factors can predict heart disease and stroke to some degree, though I have many patients for whom that approach fails but intimal wall thickness detects the risk otherwise missed, but that is not enough. Smoking, diet, weight, blood pressure and such are all targets for treatment, but how does the doctor know whether he has controlled them adequately? If the IMT increases, more control is required. If IMT stabilizes or reverses a little, then it means that control is at goal. Family history of premature CAD is a major but under-utilized risk factor. The causative factors are not yet elucidated by research, so we do not know what the goals are. However, IMT provides a highly satisfactory parameter by which to judge effectiveness of treatment in familial CAD: IMT stabilization and reversal are good, progression is bad and requires more intensive measures.

Epidemiology and public health planning correctly look at policies to apply to large populations. However, the practice of medicine is patient by patient, accomplished in the face-to-face doctor-patient relationship. Policy can be useful as a resource, but each patient should have the maximum individualized care and access a doctor can provide. Patients should be able to make their own informed choices, and not be dictated to by policies meant for masses. Should not everyone with thickening of their intimal wall at least be informed of the option to act to limit it rather than waiting until acute events or advanced narrowing occur? It would be best to start a healthy lifestyle from birth, but fortunately by adulthood there is still time to make an enormous difference in practical terms if we detect change at the stage in which intimal widening is detectable with the highly sensitive ultrasound described in my article.

1. OKeefe JH, Cordain L, Harris WH, Moe RM, Vogel R, (2004) Optimal Low-Density Lipoprotein is 50 to 70 mg/dl; Lower is Better and Physiologically Normal. JACC 43:2142-6.

2. Ebrahim S., Papacosta O, Whincup P, Wannamethee G, Walker M, et. al. (1999) Carotid plaque, intimal media thickness, cardiovascular risk factors, and prevalent cardiovascular disease in men and women. The British Regional Heart Study. Stroke 30:841-850.

No competing interests declared.