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The effects of transcutaneous electrical nerve stimulation in patients with severe angina pectoris.
Author(s) -
Clas Mannheimer,
C. Carlsson,
Håkan Emanuelsson,
A Vedin,
Finn Waagstein,
Claes Wilhelmsson
Publication year - 1985
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/01.cir.71.2.308
Subject(s) - medicine , angina , transcutaneous electrical nerve stimulation , cardiology , hemodynamics , stimulation , anesthesia , afterload , myocardial infarction , alternative medicine , pathology
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 less than .001), improved lactate metabolism (2 +/- 36% compared with -18 +/- 43%, p less than .01), and less pronounced ST segment depression (2.3 +/- 1.1 compared with 2.9 +/- 2.6 mm, p less than 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 vs 555 +/- 277 W . min, p greater than .001), decreased ST segment depression (2.3 +/- 1.1 vs 3.6 +/- 1.6 mm, p less than .001), reduced frequency of anginal attacks (p less than .05), and reduced consumption of short-acting nitroglycerin per week (p less than .05) compared with the control group. The observed effects were mainly due to decreased afterload resulting from systemic vascular dilatation.

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