The relationship between lactate production in the myocardium and the development of chest pain in patients with coronary artery disease (CAD)

Abstract

Silent myocardial ischemia (SMI) was recognized as early as the beginning of the 20th century. The consequences of silent ischemia can be grave because lack of symptoms and lack of symptom recognition. Early detection of SMI may prevent many episodes of sudden cardiac death annually. However, the role and behavior of the factors determining the occurrence of silent myocardial ischemia have not been fully established. To detect if there is a relationship between the level of lactate production in the myocardium and the development of chest pain in patients with coronary artery disease (CAD). This study was carried out in cardiology and biochemistry departments, Zagazig University on 46 patients (38 males) with coronary artery significant disease (>70% stenosis) including left anterior descending artery disease. Cannulation of coronary sinus with Amplatz left catheter was done and a pigtail catheter was introduced into the mid LV cavity. Right atrial pacing was done and the heart rate was increased stepwise 10 bpm/1 min until a maximum of 150 bpm or chest pain occurs or significant S–T segment depression occurs. LV gram for assessment of systolic function and blood samples were withdrawn from the LV and coronary sinus before and after pacing induced ischemia and the patients were classified into two groups according to development of chest pain (angina group; 28 patients) during pacing induced tachycardia or not (silent group; 18 patients). 24-h Holter ECG monitoring was done to all patients. Myocardial lactate production was significantly very high in angina group than in silent ischemia group; 10 patients (35.7%) had lactate diminished extraction and 18 patients (64.3%) had lactate production in response to pacing induced tachycardia in group 1 (angina group). All 18 patients (100%) in group 2 (silent ischemia group) had lactate diminished extraction in response to pacing induced tachycardia (<0.001). LV systolic function reduction in response to pacing induced ischemia was non significant between the 2 groups. Silent ischemic attacks represented >80% of total ischemic episodes during 24 h Holter ECG study and it occurred at lower heart rate than angina attacks ( P = 0.03). The magnitude of S–T segment depression was non significant between the two groups. In patients with coronary artery disease, myocardial lactate production is significantly higher in patients with angina than in patients with silent ischemia and as lactate is known (with other metabolic agents) to cause chest pain and this is considered an explanation (mechanism) for the occurrence of silent myocardial ischemia.