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Coronary angioplasty and left ventricular function in single vessel coronary artery disease.
  1. Y C Najm,
  2. A D Timmis,
  3. M N Maisey,
  4. L M Pinies,
  5. A Salinas,
  6. P V Curry,
  7. E Sowton
  1. Department of Cardiology, Guy's Hospital, London.


    Left ventricular function was investigated in 86 patients with single vessel coronary artery disease before and three to six months after successful angioplasty. Before angioplasty thallium-201 perfusion scintigraphy and technetium-99m gated equilibrium ventriculography in most patients showed that stress testing (exercise and ice water stimulation and isometric handgrip respectively) induced myocardial perfusion defects that were associated with a mean (SD) drop in left ventricular ejection fraction from 64 (6)% to 56 (7)%. After angioplasty there was residual coronary stenosis of less than or equal to 20% of the diameter of the vessel in 78 patients (group 1) and of between 20 and 50% in eight patients (group 2). After the procedure the perfusion defects seen during stress resolved in 86% of group 1 and in 87% of group 2. Despite the apparent improvement in myocardial perfusion left ventricular dysfunction persisted in group 2--that is during stress the left ventricular ejection fraction fell from 65% (6) to 56% (5). In group 1, on the other hand, the improvement in myocardial perfusion was associated with significant improvement in left ventricular function with a normal increase in ejection fraction from 63 (5) at rest to 67 (6) during stress. Radionuclide studies, one to six weeks after angioplasty in 30 group 1 patients showed continuing left ventricular decompensation during stress in nine (30%) of them despite correction of perfusion defects. But reinvestigation three to six months after the procedure showed recovery of left ventricular function with an increase in ejection fraction from 66 (5) at rest to 69 (7) during stress. These data indicate that coronary angioplasty procedures that give a residual stenosis of </= 20% improve myocardial perfusion and the response of the left ventricle to stress. The functional improvement may be delayed for up to three months, however, possibly because arterial healing at the angioplasty site is delayed. On the other hand, when the residual stenosis is between 21 and 50% of the diameter of the vessel subclinical left ventricular dysfunction during stress may persist indefinitely.

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