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76 LINKING SYMPTOMATOLOGY TO INDIVIDUAL CORONARY STENOSIS: COMPLEMENTARY INFORMATION FROM ANATOMY AND PHYSIOLOGY TO PROVIDE APPROPRIATE REVASCULARIZATION.
  1. D. G. Patel1,
  2. V. Robinson1
  1. 1Medical College of Georgia, August, GA.

Abstract

Introduction Recently, there is an increasing trend of using noninvasive tests to define coronary anatomy; the importance of physiology has been minimized. We report a case of angina treated based on the anatomic information, which was only cured after revascularization of the flow deficit related coronary artery identified by myocardial perfusion imaging. This case provides insight into the importance of the physiologic flow and the inability of coronary anatomy to determine flow impairment.

Case A 55-year-old obese male with a history of diabetes, hypertension, and dyslipidemia presented with complaints of chest discomfort and dyspnea on exertion. He was a long-time smoker. Myocardial perfusion imaging (MPI) showed 15% reversible defect involving the anteroapical and distal anterolateral segments of the left ventricle. Coronary angiography showed 80% stenosis in the midportion of the left circumflex (LCX) and equivocal proximal stenosis of the dominant right coronary artery (RCA). Intravascular ultrasonography (IVUS) of the RCA confirmed 62% area stenosis, and two stents were deployed with 0% residual stenosis. After 2 months, he presented with worsening of dyspnea. Repeat MPI showed 20% reversible defect of the lateral, anterolateral, inferolateral, and adjacent apices. Cardiac catheterization showed patent stents in the RCA and mid-80 to 90% stenosis of the nondominant LCX. The patient underwent cutting balloon coronary angioplasty of the LCX with 40% residual stenosis. Up to 3 years of follow-up, he has sustained relief in symptoms.

Discussion In this case, initially, the decision of which coronary vessel to dilate was taken based on the anatomic information provided by IVUS assessment of coronary stenosis. Even though the dominant stenosed RCA was reopened successfully, the patient continued to have symptoms, which only improved after balloon angioplasty of the nondominant LCX. This case illustrates that the severity of anatomic stenosis does not determine the coronary flow reserve deficit.

Conclusion Considering coronary anatomic information now available noninvasively, such as with computed tomographic angiography, inappropriate coronary angioplasties, as in our case, may become an increasing occurrence. This can be avoided if the importance of physiologic flow measurement can be imparted to intervening cardiologists.

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