Coronary hemodynamics in simulated paroxysms of ventricular tachycardia: role of myocardial impairment and of extravascular resistance.

In 6 patients with healthy hearts (controls), 17 with coronary artery disease (CAD) and 6 with left ventricular hypertrophy due to aortic valvular disease, aortic pressure, coronary sinus blood flow (CSF) and lactate extraction were determined before and after the sudden onset of a paced ventricular tachycardia of 170 bpm (VT 170 = simulated paroxysmal ventricular tachycardia). Comparison to parameter changes during dipyridamol vasodilation revealed reduced coronary vascular reserve for CAD and hypertrophy. While VT induced a reduction of aortic pressure (stabilized by an average of 22%, and most excessively for CAD; p less than 0.05) and CSF remained at/or slightly above control levels (by an average of 31%; p greater than 0.05) equally for all groups (p greater than 0.05), lactate production in the groups with CAD and hypertrophy indicated myocardial impairment by ischemia. Excessively greater increases of CSF during dipyridamol vasodilation (vs. VT) for all groups suggested VTs extravascular resistance increase to have limited the extent of the potential of coronary vascular decrease. With one variable being kept constant (i.e. 'clamping' the vascular component of coronary resistance at its limit by dipyridamol), tachycardia during dipyridamol (D) vasodilation (VT 170+D and VT 140+D) in the controls and in the CAD group resulted in a linear decrease of CSF, allowing quantification of impaired coronary reserve for CAD. We concluded from the observations that: (1) paroxysmal VT demands fast therapeutic action foremost in the impaired myocardium, and (2) tachycardia per se acts as limiting factor for coronary blood flow via increase in extravascular resistance (aside from a shortened diastole).