I'm a 53 year old female, nonsmoker, no cardiac risk factors, excellent lipid profile, quite fit. History of MVP w/ trace MR and RVOT PVCs. Meds: Verapamil SR 180 mg. b.i.d. Going through very stressful period after losing both parents late last year. This winter had several bouts of severe, prolonged chest pain, diffuse and nonradiating, not exercise-related. EKG normal during symptoms. In March I had a Cardiolite treadmill test to rule out ischemia. 12:51, went to 171 bpm with no symptoms, 14.8 mets. No ischemic EKG changes, no arrhythmias, bp response normal. Scan showed a small, mild, reversible anterior wall defect that "does not meet criteria for abnormality by quantitative analysis". Motion corrected scan but not attenuation corrected. Cardiologist reading the scan said the defect could be an attenuation artifact but suggested a stress echo as followup. My cardiologist prefers to wait a year and repeat unless my symptoms come back, saying that clinically he believes I do not have obstructive CAD. His dx is possible vasospasm brought on by grief/stress.
1. In your opinion, is it reasonable to take a wait and see approach given my history?
2. How often does a reversible "defect" prove to be an artifact? From what I've read, if it was attenuation artifact over the anterior wall, it would likely be breast attenuation which usually causes a fixed defect unless the breasts are large. My breasts are small and dense, so I don't understand how they could move enough between scans to cause an apparent reversible defect.
3. Could this "small mild defect" be showing an area of lesser perfusion from a plaque not severe enough to cause actual ischemia directly, but that could make me prone to focal vasospasm?
4. Sensitivity of stress echo vs nuclear stress?
5. Are there any other tests that you would recommend?
BTW I had a 2D echo in Feb 2008 that showed normal valves and chamber sizes except for a mildly dilated RA. EF 60%.
Given you exercise capacity you are at low risk for developing significant heart disease in the near future and I feel is OK to wait before retesting. A single area of mild perfusion defect is also not a significant finding that increases your risk for developing heart disease or death. This may however be causing you pain with exertion, so treatment with verapamil, aspirin and a lipid lowering medication is appropriate at this time. You goal LDL should be 70 mg/dl.
Stress Echocardiograms and stress nuclear tests have similar sensitivities for obstructive CAD, but the tests give different aspects of heart function: the stress echocardiogram probably would be better in you case because of the valvular heart problem, and the ability to look at the mitral regurgitation and right ventricular function with stress.
Doctor, thanks for your answers. I'm confused, though, if the perfusion defect is due to a stenosis and this degree of stenosis could cause pain with exertion, why isn't that already considered significant heart disease? Also, my LDL is 48 mg/dl, HDL 76, total cholesterol 134. Would lipid lowering meds provide any additional protection in my case?
I have never had pain with exertion, but yesterday I had (first time in my life) episode of prolonged chest pressure (elephant on chest feeling) starting 5 minutes after exercise, lasting an hour, with no unusual symptoms during. I'm not sure if this could be related. I have also had some kind of lingering URI for a few weeks that has left me feeling very run down. Yes, I will be seeing my doctor about it! Just wondered if you or anyone else has any thoughts (also posted in community forum).
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