A 71-year-old woman with a history of hypertension and intermittent atrial fibrillation was referred for evaluation of shortness of breath (New York Heart Association II-III) and atypical chest pain. The resting electrocardiogram was normal. Transthoracic echocardiogram demonstrated normal systolic left ventricular function and moderate concentric hypertrophy. The patient underwent Technetium-99m myocardial perfusion scintigraphy, which showed a large reversible defect of the anterior wall (Figure 1A) associated with chest tightness during recovery. Coronary angiogram showed minor diffuse atheroma with some plaque in the proximal left anterior descending (LAD) coronary artery (Figures 1B and 1C, white arrows). The hemodynamic significance of the LAD stenosis was excluded using the pressure wire (Certus, St. Jude Medical; Figure 2A), which revealed a fractional flow reserve (FFR) of 0.89 (>0.8, gradient was 0.98 at baseline) with maximal hyperaemia (adenosine 140 µg/kg/min in right femoral vein). Assessment of the coronary microcirculation was then performed using the same wire, which demonstrated a severely decreased coronary flow reserve (1.1; normal, >2.0) and a pathologic index of microcirculatory resistance (48; normal, <25) (Figure 2B). The diagnosis of severe coronary microcirculatory dysfunction was made and no percutaneous coronary intervention was performed.
This case demonstrates the advantage of multi-modal assessment of patients with coronary artery disease. A significant obstructive stenosis of the LAD was excluded using FFR. Evaluation of the microcirculation was done during the same procedure and this demonstrated severely depressed CFR and a high IMR, suggesting that the defect seen on the myocardial perfusion scintigraphy was due to severe microcirculatory dysfunction. The diagnosis of severe microcirculatory dysfunction gave a pathophysiologic explanation for her findings and prevented the implantation of an unnecessary coronary stent in the proximal LAD.
When performing CFR and IMR calculations using the Pressure Wire, it is important to place the wire at least 2/3 down the vessel to avoid miscalculation of transit times (Figure 2A). Additionally, it is crucial to induce adequate hyperemia.1 In our patient, the gradient between distal coronary pressure and aortic pressure was 0.98 at baseline and it dropped to 0.89 after intravenous adenosine was administered, clearly demonstrating that hyperemia was achieved. The fact that in our case evidence of myocardial ischemia was established using a perfusion scan and FFR remained normal despite adequate response to adenosine strongly supports the diagnosis of coronary microcirculatory dysfunction.
Treatment options. It is known that reduced estrogen production plays an important role in coronary vasomotion and small studies have shown that transdermal estrogen improves endothelium-dependent coronary vasomotion.2 Calcium antagonists, endothelin-antagonists,3 and other medications are additional options, but large prospective studies with clinical endpoints are needed before these agents can be recommended for the treatment of coronary microcirculatory dysfunction.
The invasive assessment of the coronary microcirculation using the Pressure Wire is feasible and should be strongly considered in the case of discrepancy between the angiographic appearance and the perfusion scanning.
- McGeoch RJ, Oldroyd KG. Pharmacological options for inducing maximal hyperaemia during studies of coronary physiology. Catheter Cardiovasc Interv. 2008;71(2):198-204.
- Roque M, Heras M, Roig E, et al. Short-term effects of transdermal estrogen replacement therapy on coronary vascular reactivity in postmenopausal women with angina pectoris and normal results on coronary angiograms. J Am Coll Cardiol. 1998;31(1):139-143.
- Reriani M, Raichlin E, Prasad A, et al. Long-term administration of endothelin receptor antagonist improves coronary endothelial function in patients with early atherosclerosis. Circulation. 2010;122(10):958-966. Epub 2010 Aug 23.
From the Oxford Heart Centre, John Radcliffe Hospital, Oxford, United Kingdom.
Disclosure: The author has completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The author reports no conflicts of interest regarding the content herein.
Manuscript submitted April 26, 2011, provisional acceptance given May 31, 2011, final version accepted June 13, 2011.
Address for correspondence: Dr. Adrian P. Banning, Consultant Cardiologist, The John Radcliffe, Headley Way, Oxford OX3 9DU, United Kingdom. Email: firstname.lastname@example.org