INTRODUCTION: To clarify the mechanisms of abnormal Q waves in hypertrophic cardiomyopathy (HCM), local epicardial electrical activities were assessed by intracoronary electrocardiography (ECG). METHODS AND RESULTS: Unipolar intracoronary ECG was recorded by introducing a guide wire for angioplasty into the left anterior descending artery (LAD) in 20 patients with HCM and 10 control subjects. Intracoronary ECG showed no Q waves in any control subjects. Intracoronary ECG showed no Q waves in 8 HCM patients without abnormal Q waves on surface ECG. In 12 HCM patients with abnormal Q waves on surface ECG, 4 showed Q waves on intracoronary ECG associated with regional wall-motion abnormalities, suggesting Q waves are formed by loss of electrical forces due to transmural myocardial fibrosis. The remaining 8 patients, who did not have Q waves on intracoronary ECG, showed greater thickening of the basal free wall than the apical free wall, with no wall-motion abnormalities. Intracoronary ECG was characterized by increased R or R' waves and prolonged R peak times at the proximal LAD, suggesting Q waves are formed by increased electrical forces of hypertrophied basal septal and/or ventricular free wall, unopposed by apical forces. CONCLUSION: The study findings provide evidence for two mechanisms of abnormal Q waves in HCM: (1) loss of electrical forces due to transmural myocardial fibrosis, and (2) altered direction of resultant initial QRS vector due to increased electrical forces of disproportionate hypertrophy of the basal septal and/or ventricular free wall, unopposed by apical forces.
INTRODUCTION: To clarify the mechanisms of abnormal Q waves in hypertrophic cardiomyopathy (HCM), local epicardial electrical activities were assessed by intracoronary electrocardiography (ECG). METHODS AND RESULTS: Unipolar intracoronary ECG was recorded by introducing a guide wire for angioplasty into the left anterior descending artery (LAD) in 20 patients with HCM and 10 control subjects. Intracoronary ECG showed no Q waves in any control subjects. Intracoronary ECG showed no Q waves in 8 HCM patients without abnormal Q waves on surface ECG. In 12 HCM patients with abnormal Q waves on surface ECG, 4 showed Q waves on intracoronary ECG associated with regional wall-motion abnormalities, suggesting Q waves are formed by loss of electrical forces due to transmural myocardial fibrosis. The remaining 8 patients, who did not have Q waves on intracoronary ECG, showed greater thickening of the basal free wall than the apical free wall, with no wall-motion abnormalities. Intracoronary ECG was characterized by increased R or R' waves and prolonged R peak times at the proximal LAD, suggesting Q waves are formed by increased electrical forces of hypertrophied basal septal and/or ventricular free wall, unopposed by apical forces. CONCLUSION: The study findings provide evidence for two mechanisms of abnormal Q waves in HCM: (1) loss of electrical forces due to transmural myocardial fibrosis, and (2) altered direction of resultant initial QRS vector due to increased electrical forces of disproportionate hypertrophy of the basal septal and/or ventricular free wall, unopposed by apical forces.