EFFECTS OF NIFEDIPINE AND NITROGLYCERIN ON LEFT-VENTRICULAR SYSTOLIC DYSFUNCTION AND IMPAIRED DIASTOLIC FILLING AFTER EXERCISE-INDUCED ISCHEMIA IN HUMANS

Objectives. This study sought to determine whether calcium antagonist, compared with nitroglycerin, administration attenuates left ventricul ar dysfunction after exercise-induced ischemia in humans. Background. Exercise-induced ischemia impairs left ventricular systolic function a nd diastolic filling after exercise. The mechanism of this phenomenon is unknown but may relate to intracellular calcium overload. Methods. Echocardiography was performed in 131 patients before and 30 min, 2 h and 4 h after exercise stress test. Ischemia was defined as a reversib le thallium stress defect; No medication, sublingual nitroglycerin or nifedipine was randomly given to each patient at peak exercise. Result s. Isovolumetric relaxation time was significantly prolonged from rest (100 +/- 19 ms [mean +/- SD]) to 30 min (118 +/- 20 ms, p < 0.0005), 2 h (117 +/- 18 ms, p < 0.0005) and 4 h (110 +/- 22 ms, p < 0.05) afte r exercise in 21 patients with exercise-induced ischemia who received no medication (ischemia-none group), Isovolumetric relaxation time sim ilarly increased after exercise in 23 patients who received nitroglyce rin and had exercise induced ischemia (ischemia-NTG group) but was unc hanged in 20 patients with exercise induced ischemia who received nife dipine (ischemia-nifedipine group). Peak early filling velocity decrea sed in the ischemia-none and ischemia-NTG groups from rest to 30 min a nd 2 h after exercise, but peak early filling velocity was unchanged i n the ischemia-nifedipine group. Ejection fraction decreased from rest to 30 min after exercise in the ischemia-none group (59 +/- 12% vs. 5 1 +/- 13%, p < 0.025) and ischemia-NTG group (59 +/- 14% vs. 49 +/- 14 %, p < 0.005) but was unchanged in the ischemia- nifedipine group (60 +/- 19% vs. 64 +/- 18%, p = NS). A new regional left ventricular wall motion abnormality occurred more frequently 30 min after exercise in t he ischemia-none group (11 [52%] of 21) and ischemia-NTG group (9 [39% ] of 23) compared with the ischemia-nifedipine group (2 [10%] of 20, b oth p < 0.05). No change occurred in left ventricular systolic functio n and diastolic filling after exercise in the control groups. Conclusi ons. Exercise induced ischemia impairs systolic function and diastolic filling after exercise. Sublingual nifedipine but not nitroglycerin a ttenuates this process and suggests that altered calcium homeostasis m ay play a role in left ventricular dysfunction that occurs after exerc ise-induced ischemia.