Background and hypothesis: Systemic hypertension is the leading cause of left ventricular (LV) hypertrophy. The present study aimed to investigate the mechanism of left atrial (LA) enlargement in patients with hypertensive heart disease during cardiac catheterization.
Methods: Data were obtained from eight control subjects and seven patients with hypertensive heart disease. Left atrial and LV pressures from catheter-tip micromanometer, and LA and LV volumes from biplane cineangiograms were analyzed during the same cardiac cycle.
Results: Left atrial maximal volume were 93 +/- 26 ml in patients with hypertensive heart disease and 63 +/- 12 ml in control subjects (p < 0.05). In patients with hypertensive heart disease, time constant of LV relaxation was significantly greater than that in controls (54 +/- 18 vs. 31 +/- 16 ms, respectively; p < 0.01). Left atrial maximal volume correlated with time constant of LV relaxation (r = 0.86, p < 0.01). The ratio of LV filling volume before LA contraction to LV stroke volume in patients with hypertensive heart disease was significantly lower than that in control subjects (65 +/- 13 vs. 76 +/- 7%, respectively; p < 0.05). On the other hand, the ratio of LV filling volume during LA contraction to stroke volume in patients with hypertensive heart disease was significantly higher than that in controls (35 +/- 13 vs. 24 +/- 7%, respectively; p < 0.05). Left atrial volume before LA contraction in patients with hypertensive heart disease was significantly larger than that in controls (74 +/- 22 vs. 47 +/- 10 ml, respectively, p < 0.01). During LA contraction, LA work was significantly increased in patients with hypertensive heart disease compared with that in controls (274 +/- 101 vs. 94 +/- 42 mmHg. ml, respectively; p < 0.001). Left atrial work showed significant correlation with LA volume before LA contraction (r = 0.75, p < 0.01).
Conclusion: Left ventricular diastolic filling was impaired in patients with hypertensive heart disease. Enlargement of left atrium might be attributed to the impairment of blood flow from left atrium to left ventricle due to the increased LV stiffness.