A Country Doctor Writes:

Just in the past few months I have had three patients with crippling chest pain brought on by exercise who were dismissed as having noncardiac chest pain. All three are now essentially symptom-free on isosorbide and metoprolol – common antianginals. I may not know exactly how this treatment works, but I am passionate about providing for my patients the common medications we know work. Even a simple country doctor can do that.

Once upon a time there was only one common kind of angina and only one kind of heart failure. Now we know there are two kinds of each. For some reason doctors are all excited about the new epidemic of heart failure with preserved ejection fraction, but skeptical and uninterested in angina with normal coronaries. Both of these more recently discovered diseases turned the old definitions upside down. Doctors of my generation (and younger) have had to unlearn what they taught us in medical school. Many are still bucking.

Angina pectoris is a syndrome, a group of clinical signs and symptoms with several possible causes. When I went to school we talked of blocked coronary arteries or a rare form of angina occurring during sleep and caused by spasm, Prinzmetal‘s angina. We now know that many people, perhaps half of all angina patients, have normal coronaries as far as we can see them on catheterization but poorly functioning smaller blood vessels rather than pure spasm. This type is triggered by exertion, just like angina caused by major blockages.

Heart failure is also a syndrome. For the longest time it was believed that the problem was that the heart didn’t push the blood out well enough with each beat. Only relatively recently did it become obvious that about half of all heart failure patients have poor relaxation of the heart. We have been measuring what percentage of the blood is pumped out with each heart beat. That number should be greater than 55%. But if there is less than the normal amount of blood in the heart and you pump out only half of that, you don’t get enough pumping done for things to work.

Neither angina nor heart failure are strictly disorders of a mechanical system of plumbing. These days the term neuroendocrine pops up everywhere in the literature. Our arteries, big and small, and our heart muscles are not static but constantly changing and adapting. And our understanding of how this all works is still in the early stages.

Maybe we should trust our clinical assessment more often and not look blindly at the results of imperfect tests like Lexiscans, crude angiographies and blurry echocardiographies: If it walks like a duck and talks like a duck, maybe it really is a duck?