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| The effects of transcutaneous electrical nerve stimulation in patients with severe angina pectoris |
| Mannheimer C, Carlsson CA, Emanuelsson H, Vedin A, Waagstein F, Wilhelmsson C |
| Circulation 1985 Feb;71(2):308-316 |
| clinical trial |
| 6/10 [Eligibility criteria: Yes; Random allocation: Yes; Concealed allocation: No; Baseline comparability: Yes; Blind subjects: No; Blind therapists: No; Blind assessors: Yes; Adequate follow-up: Yes; Intention-to-treat analysis: No; Between-group comparisons: Yes; Point estimates and variability: Yes. Note: Eligibility criteria item does not contribute to total score] *This score has been confirmed* |
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The pain-relieving effects of transcutaneous electrical nerve stimulation (TENS) were investigated in patients with severe angina pectoris first with respect to systemic and coronary hemodynamics and myocardial metabolism during pacing-induced angina and second in a controlled long-term study. Two series of patients with severe angina pectoris (NYHA class III to IV) were studied (13 patients in the pacing study and 23 in the long-term study). In the pacing-induced angina study there was increased tolerance to pacing (142 +/- 23 compared with 124 +/- 20 beats/min tolerated, p < 0.001), improved lactate metabolism (2 +/- 36% compared with -18 +/- 43%, p < 0.01), and less pronounced ST segment depression (2.3 +/- 1.1 compared with 2.9 +/- 2.6 mm, p < 0.05) with TENS. In the long study the effects of TENS were measured by means of repeated bicycle ergometer test, frequency of anginal attacks, and consumption of short-acting nitroglycerin. TENS was used regularly for 1 hr three times per day. The TENS treatment group had increased work capacity (637 +/- 308 versus 555 +/- 277 W/min, p < 0.001), decreased ST segment depression (2.3 +/- 1.1 versus 3.6 +/- 1.6 mm, p < 0.001), reduced frequency of anginal attacks (p < 0.05), and reduced consumption of short-acting nitroglycerin per week (p < 0.05) compared with the control group. The observed effects were mainly due to decreased afterload resulting from systemic vascular dilatation.
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