Number 42, 2009
Chronic ischemic heart disease

Changing ischemic symptoms despite stable coronary anatomy

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Mario Marzilli, Alda Huqi
Division of Cardiovascular Medicine, Cardiothoracic Department, University of Pisa, Pisa, Italy
Correspondence: Professor Mario Marzilli, Division of Cardiovascular Medicine, Cardiothoracic
Department, University of Pisa, Via Paradisa 2, 56100 Pisa, Italy.
E-mail: marzilli@med.unipi.it

Introduction
Chronic total coronary occlusions are observed in 35–50% of patients with significant coronary disease undergoing diagnostic angiography [1,2]. It is expected that the extent of the corresponding ischemic region remains essentially unchanged unless a significant progression of atherosclerotic lesions in other vessels occurs, but, as often documented, there is no close relationship between the severity of epicardial coronary stenosis and that of the ischemic syndrome. We report here the case of a patient with chronic total occlusion of the right coronary artery, who presented with a worsening of his ischemic syndrome despite no appreciable changes in coronary angiographic features.

Case report
A 67-year-old man was admitted to our Cardiology Department in October 2008. His cardiac history had begun in 2002, when he was admitted after an acute myocardial infarction. Subsequently, he presented occasional episodes of chest pain and, in January 2007, he underwent an exercise stress test, as part of a preoperative evaluation for abdominal surgery. At peak exercise ST-segment depression was present in anterior leads from V4 to V6 and in the inferior leads, in the absence of any symptom (125 W, 6.5 metabolic equivalent of task units [METS], maximal heart rate 131 beats/min; maximal blood pressure 210/100 mm Hg) (Figure 1).

Comment
In patients with chronic angina, changes in ischemic threshold are commonly attributed to progression of coronary atherosclerotic lesions. Here, however, we have reported a case of changing severity of ischemia, in the absence of significant progression of coronary atherosclerosis in other vessels.
At the time of the first exercise stress test, the patient was almost asymptomatic for angina or dyspnea; the onset of his symptoms was associated with an extension of ischemic signs in a control exercise stress testing. Indeed, a similar pattern on the electrocardiogram was present at lower working load, lower METS, and lower double-product values. We hypothesized that a revascularization procedure might improve the collateral circulation and myocardial perfusion, and therefore we performed percutaneous transluminal coronary angioplasty and stenting on the only treatable lesion. Nevertheless, the exercise stress test undertaken after this “successful” percutaneous coronary intervention showed a similar electrocardiographic pattern at equivalent METS and double-product values, confirming the absence of any obvious link between coronary anatomy and progression of the ischemia over time.
This case report emphasizes that we frequently adopt the position of passive bystander in the management of chronic ischemic heart disease. For this reason, we perhaps need to see beyond the plaque and have the confidence to leave plaques alone; alternative mechanisms, including microvascular dysfunction and coagulation abnormalities, may be important determinants of chronic ischemic heart disease. The awareness of several underlying mechanisms could help us to avoid ineffictive, expensive, and possibly harmful revascularization procedures and to optimize treatment by other means.

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