Case Report

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A 61-year-old white woman with diabetes was hospitalized for evaluation of chest pain induced by hypoglycemia. She had had myocardial infarctions in 1974 and 1980; she had been diagnosed with diabetes at age 47 and had been receiving insulin since that time. Her only other cardiac risk factor was hyperlipidemia; she had stopped smoking in 1980.

The patient reported exertional chest pain after 15 minutes of yard work; the pain was relieved by sublingual nitroglycerin and the patient dealt with the problem by reducing her workload. Of more concern for her was chest pain during episodes of hypoglycemia. Since her second myocardial infarction, which had occurred at approximately the same time that her diabetes was diagnosed, the patient had begun to have chest pain associated with low blood glucose levels (typically less than 3.9 mmol/L [70 mg/dL]). The patient had never had typical symptoms of hypoglycemia, such as lightheadedness or shaking. In the absence of physical exertion, her chest pain was always associated with a low blood glucose level. Concomitantly, she had shortness of breath, but did not have nausea, diaphoresis, or lightheadedness. The chest pain always stopped within minutes after carbohydrate intake; the patient did not take nitroglycerin in these cases. In the months preceding admission, the episodes of hypoglycemia-associated chest pain had been increasing in frequency to a maximum of one per week.

The patient was admitted for blood glucose control and cardiac evaluation. On the second hospital day, she awoke with chest pain. Her blood glucose level, measured by portable meter, was 2.8 mmol/L (51 mg/dL). An electrocardiogram showed new ST depression in leads V2 to V6, II, III, and aVF (Figure 1). The patient was given orange juice, which corrected the hypoglycemia, and the chest pain resolved within minutes. A follow-up electrocardiogram obtained approximately 6 to 8 hours after the episode showed complete resolution of the changes seen on the previous electrocardiogram (Figure 1).

View larger version (89K): [in this window] [in a new window]   Figure 1. Hypoglycemia-induced electrocardiographic changes. Top. Baseline electrocardiogram obtained at admission. Middle. Electrocardiogram obtained during episode of hypoglycemia and chest pain. Bottom. Electrocardiogram obtained 6 to 8 hours after resolution of chest pain.

An exercise thallium test was done, during which the patient had chest pain relieved by sublingual nitroglycerin. The stress test was markedly positive, showing 0.3 mV of ST depression in leads V3 to V6, II, III, and aVF. The perfusion scan showed ischemia in the lower anterior wall and anteroapex. A cardiac catheterization showed a left dominant system and the following coronary anatomy: normal right coronary artery, left-anterior descending artery with proximal stenosis of 75% and mid-stenosis of 95% (proximal lesion very close to left main artery), and first circumflex marginal artery with 95% stenosis proximally. A two-vessel coronary artery bypass was done.

The operation had no complications, and the patient recovered quickly. During recovery, however, she had another episode of hypoglycemia, with a blood glucose level of 2.4 mmol/L (44 mg/dL). She had no chest pain; however, she described being lightheaded, diaphoretic, and extremely hungry during the episode. Six months after discharge from the hospital, she remains free of chest pain despite occasional episodes of symptomatic hypoglycemia.

Discussion

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The phenomenon of hypoglycemia-induced angina pectoris in patients with diabetes mellitus and coronary artery disease has received little attention in the recent literature. A patient with coronary artery disease shown on angiography was described with hypoglycemia-associated silent myocardial ischemia documented by Holter monitoring [1]. Another patient had hypoglycemia-induced angina pectoris in the absence of both electrocardiographic changes and coronary artery disease [2].

The patient we describe had episodes of hypoglycemia-induced angina pectoris associated with ischemic electrocardiographic changes. These changes correlated well with the distribution of her coronary artery disease. That hypoglycemia could induce ischemia and angina in a patient with coronary artery disease is not surprising; there are two potential mechanisms by which this could occur. The sympathetic response to hypoglycemia, resulting in a substantial increase in plasma epinephrine levels, would increase myocardial oxygen consumption and simultaneously reduce myocardial oxygen supply by coronary vasoconstriction. In addition, hypoglycemia and coronary vasoconstriction might limit the delivery of substrate (glucose and free fatty acids) to the myocardium, consequently contributing to an imbalance of myocardial energy supply and demand.

It is interesting that our patient had classic hypoglycemic symptoms for the first time after successful coronary revascularization. Conceivably, the elimination of chest pain, which had been the patient's previous "early warning system" for hypoglycemia, resulted in delayed treatment for hypoglycemia, allowing adequate time for the development of symptoms.

We have described a patient with diabetes mellitus and coronary artery disease in whom hypoglycemia was the major stimulus of angina. Conversely, angina was the only manifestation of hypoglycemia. Hypoglycemia-induced angina was the primary clue to the extensive coronary artery disease in this patient. It is possible that the same may be true in other patients with diabetes and coronary artery disease. It is also important for clinicians to consider the prevalence of silent ischemic myocardial disease in patients with diabetes mellitus and to periodically reassess the cardiac status of such patients, particularly if they are prone to hypoglycemia.