TACHYCARDIA-INDUCED CARDIOMYOPATHY - EFFECTS ON BLOOD-FLOW AND CAPILLARY STRUCTURE

Chronic supraventricular tachycardia (SVT) causes a dilated cardiomyopathy. A potential factor contributing to the development of SVT-induced cardiomyopathy is abnormal myocardial blood flow (MBF). The purpose of this study was to relate changes in left ventricular (LV) function, MBF, and capillary structure with the development of SVT-induced cardiomyopathy. LV function and MBF were measured in two groups of conscious pigs: sham control (CON; n = 8) and after 3 wk of atrial pacing (SVT; 240 beats/min; n = 8) using echocardiography-catheterization and microspheres. Measurements were made under three states: 1) at rest with a basal heart rate, 2) during rapid atrial pacing (240 beats/min), and 3) during adenosine infusion (1.5-mu-M.kg-1.min-1) without pacing. LV capillary density, diameter, wall thickness, and capillary-myocyte distance were measured in four additional pigs from each group. LV fractional shortening was lower, and left atrial pressure was significantly higher in the SVT group compared with CON at rest, during pacing, and with adenosine (P < 0.05). In the CON group, average LV-MBF at rest was 2.0 +/- 0.2 ml.min-1.g-1, increased with pacing to 3.0 +/- 0.2 ml.min-1.g-1 (P < 0.05), and increased further with adenosine to 4.1 +/- 0.3 ml.min-1.g-1 (P < 0.05). In all states, SVT LV-MBF was significantly reduced vs. CON (P < 0.05); SVT LV-MBF was 0.8 +/- 0.2 ml.min-1.g-1 at rest, increased to 1.3 +/- 0.3 ml.min-1.g-1 with rapid pacing (P < 0.05), and remained unchanged during adenosine (1.3 +/- 0.4 ml.min-1.g-1). Coronary vascular resistance was significantly higher in the SVT group in all three states (P < 0.05). Capillary density remained unchanged with SVT, however, luminal diameter decreased (P < 0.05) and capillary-myocyte distance increased (P < 0.05). These changes in MBF and capillary structure may have played a contributory role in the development of SVT-induced cardiomyopathy.