Transcutaneous electrical nerve stimulation (TENS) in angina pectoris.
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Biomedical subjects
Publications and source records attributed to C Wilhelmsson.
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The aim of this study was to investigate menstrual history, reproductive functions, fertility regulation and gynaecological operations is a representative sample of middle-aged women. A sample consisting of 1746 women aged 40-66 was randomly selected. Of those initially selected, a total of 1413 (81%) were investigated. Gynaecological data were acquired by means of questionnaires. Eighty-six percent of menstruating women reported a cycle length of 22-30 days and menstrual flows lasting 4-7 days. The median age at natural menopause was 50.9 yr. The oldest menstruating women were 57 yr old. Curettage had been performed in 53%, and 9% were hysterectomised. Every fourth woman had had three or more children, and 15% were nulliparous. Abortion (spontaneous or induced) was reported by 28% of the women. Of 714 menstruating women, 62% were utilising contraceptive methods, among which barrier or natural methods predominated. Nine percent of women aged 40-44 used combined oral contraceptives. Previous or current use of contraceptive pills was reported by 32% of all the women, and of these 20% had been on the pill for 10 or more yr.
A wealth of evidence supports the use of beta-blockers in stable angina pectoris and myocardial infarction, both early and late. The situation in unstable angina is less well illuminated, but forthcoming results of trials will hopefully close some of this gap.
Among 262 women with a first myocardial infarction discharged alive from hospital in Göteborg, Sweden between 1968 and 1977, 161 (61%) were smokers at the time of infarction. Postinfarction smoking was established after three months. In relation to smoking status three months after the infarction, subsequent survival and reinfarction rate were calculated by comparing those who smoked before infarction and later stopped (52%) with those who continued to smoke after the infarction (48%). There were no differences in preinfarction characteristics between quitters and continuing smokers. Women who stopped smoking after the infarction had higher serum enzymes during the acute phase than those who continued to smoke. The cumulative five-year survival rate was 85% among those who stopped smoking compared to 73% among those who continued to smoke (p less than 0.05). No significant difference was found in the cumulative reinfarction rate between the two groups with different smoking habits.
1306 men below 68 years of age who survived a first myocardial infarction (MI) during 1968-1977 were followed up between 2 and 12 years after discharge from hospital. The mean follow-up time was 6.5 years. The patients were unselected and paid regular visits to a Post-MI Clinic where treatment was standardized. The diagnosis of a non-fatal reinfarction was based on conventional clinical criteria, and the diagnosis of a fatal reinfarction on autopsy findings of a recent myocardial injury and/or a fresh coronary thrombus. The autopsy rate was high and the follow-up of endpoints was complete. The total cumulative rate of endpoint free patients was 64% at 5 years and 50% at 10 years follow-up. The total mortality rate was 19% at 5 years and 33% at 10 years follow-up. The total cumulative rate of a first reinfarction was 28% at 5 years and 37% at 10 years follow-up (80% non-fatal and 20% fatal). 63 patients suffered more than one reinfarction. The mortality rate was strongly associated with age. In contrast the rate of non-fatal reinfarctions was independent of age.
1306 men less than 68 years of age who survived a first myocardial infarction (MI) during 1968-1977 were followed up between 2 and 12 years. The mean follow-up time was 6.5 years. The patients were unselected and paid regular visits to a Post-MI Clinic where treatment was standardized. The autopsy rate was high and the follow-up of endpoints was complete. The diagnosis of a non-fatal reinfarction was based on conventional clinical criteria, and the diagnosis of a fatal reinfarction on autopsy findings of a recent myocardial injury and/or a fresh coronary thrombus. The patients were randomly assigned to two halves. One was used only for derivation of the predictive models, and the other only for validation. Common clinical variables judged to be prognostically important were selected. Among variables available at discharge from hospital a history of hypertension, angina pectoris or diabetes before the MI and the maximal serum ASAT during the MI were independently related to reinfarctions during the follow-up. A predictive index was formed and validated. The rate of reinfarction among risk quartiles in the validation sample increased from 24 to 38% (P = 0.003). The aetiologic fraction (the percent of reinfarctions predicted by the index) was 24%. Among variables from the follow-up only cessation of smoking after the MI had independent predictive power. A new predictive index including this variable was formed and validated. The reinfarction rate in the risk quartiles increased from 15 to 39% (P less than 0.001). The aetiologic fraction was 44%. When only reinfarctions occurring before the median follow-up time of 21 months were considered, the aetiologic fraction was 62%.
In the present study 27 post-myocardial infarction patients were treated with Persantin capsules (Depot-Kapseln, sustained release form), containing 200 mg dipyridamole, b.i.d. over a period of 3 weeks. Baseline levels for plasma beta-thromboglobulin (BTG), platelet factor 4 (PF4), and serum thromboxane B2 (TXB2) were obtained on day 0 and subsequently on days 1, 3, 5, 7, 14 and 21. The baseline levels for plasma BTG and PF4 as well as for serum TXB2 significantly exceeded those for a control group consisting of healthy subjects. The plasma values for BTG and PF4 remained unchanged during the whole study period. During the first week of study the levels for serum X TXB2 were unchanged; however, on days 14 and 21 the means for TXB2 dropped significantly. There is experimental work to suggest that dipyridamole may exert an inhibitory effect on platelet thromboxane biosynthesis. The present results support this concept.
Adenosine diphosphate (ADP)-induced platelet aggregation was studied in 35 young female survivors of acute myocardial infarction (AMI) 14-46 (median 30) months after the infarction. The results were compared to those obtained for 35 control females of comparable age. Five different final ADP concentrations (0.2-1.0 microM) were employed, and the object was to assess the slope for the primary wave of aggregation as well as the threshold ADP concentration for secondary aggregation. The results showed that AMI patients and control subjects did not differ with respect to the primary wave of aggregation. However, secondary platelet aggregation was recorded to a significantly higher extent (p less than 0.02) in AMI patients than in their controls. The results therefore support the concept that enhanced platelet reactivity is present in patients with documented ischemic heart disease.
The dose-response relationship of enalapril was evaluated in a double-blind, balanced, two-period, incomplete-block study in 91 patients with mild to moderate essential hypertension. Patients were randomly assigned to two of six treatments: placebo, 2.5, 5, 10, 20 and 40 mg/day of enalapril maleate. There were two 3-week treatment periods, each preceded by a 4-week, single-blind placebo washout. Each dose of enalapril produced significant decreases in standing and supine systolic and diastolic blood pressure after 2 and 3 weeks of treatment. There were no significant changes on placebo. There was a significant linear dose response relationship for both mean blood pressure and mean change from baseline in blood pressure (P less than 0.01 for systolic and mean arterial pressure, and P less than 0.05 for diastolic pressure). Enalapril was associated with an increasing dose-response relationship across the 2.5-40 mg/day range. The 2.5 mg/dose is effective in some patients; however, doses greater than or equal to 10 mg/day may be necessary to achieve satisfactory blood pressure control.
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.
Men (1306) who survived a first myocardial infarction (MI) were studied. The mean follow-up time was 6.5 yr, and at the end of the follow-up period survival status was known for all patients. By the time of the MI the prevalence of diabetes was 5.6%. Patients with and without diabetes were compared. There were no differences in the estimated primary or secondary risk. The cumulative survival rate 1, 2, and 5 yr after the MI was 82, 78, and 58% among the diabetic subjects compared with 94, 92, and 82% among the nondiabetic subjects (P less than 0.001). The difference remained even after allowance for age and estimated secondary risk in a multivariate regression analysis. There were no differences in mortality rates among patients with type I diabetes compared with type II diabetes, nor among patients treated with diet alone, sulfonylurea, or insulin, but the numbers were small. The cumulative rate of reinfarctions after 1, 2, and 5 yr was 18, 28, and 46% in diabetic subjects and 12, 17, and 27% in nondiabetic subjects (P = 0.004). A history of diabetes was an independent secondary risk factor among male survivors of a first MI with respect to deaths and reinfarctions.
Following a myocardial infarction any residual symptoms are likely to remind the patient of a possible fatal outcome and be detrimental to successful rehabilitation. Negative psychological attitudes need to be identified early. Intervention to improve the mental state should be introduced to restore self-confidence.
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The effect of metoprolol on chest pain was compared with that of placebo in all randomized patients. The pain score before and 15 minutes after the injection of trial medication was registered and a reduction in chest pain was observed in the metoprolol group. Increasing chest pain after blind injection was observed in only 16 and 9 patients from the placebo and metoprolol groups, respectively. Comparison with the placebo as well as detailed analysis of clinical data revealed that in these patients the increasing pain could not be explained by coronary spasm evoked by beta-blockade. Similarly, metoprolol did not exhibit any unfavorable effect on the 14 patients who were withdrawn (together with the 28 patients given placebo) from blind treatment due to angina pectoris. Either metoprolol does not induce coronary vasospasm or spasm does not play a role in these patients with definite and suspected acute myocardial infarction as well as unstable angina pectoris. Metoprolol reduced the need for analgesics during the first 4 days and shortened the duration of pain. The effects were similar in patients with early and late treatment, but may depend on initial heart rate, blood pressure and site of infarction.
Heart rate, systolic blood pressure and rate-pressure product were analyzed during the first 18 hours and 4 days after intravenous metoprolol or placebo. On injection of metoprolol there was an immediate decrease in mean heart rate from 72.9 +/- 0.6 to 62.7 +/- 0.4 beats/min, but no change was found in the placebo group. The difference in heart rate remained during the first 4 days. Systolic blood pressure was reduced from 144.1 +/- 0.9 to 134.6 +/- 0.9 mm Hg after intravenous metoprolol and was lower than that in the placebo group during 4 days of follow-up. Indirect signs of congestive heart failure tended to be less severe in patients given metoprolol within 12 hours of the onset of symptoms than in those given placebo. The duration of hospitalization also tended to be shorter in patients given early metoprolol treatment than in those given placebo early.
During a 3-month follow-up, 131 patients (19.1%) withdrew from blind treatment in both metoprolol- and placebo-treated groups. More metoprolol-treated than placebo-treated patients withdrew because of cardiovascular adverse experience mainly during the very early phase. In all, 45 (6.5%) metoprolol-treated vs 14 (2.0%) placebo-treated patients were not given either a full intravenous dose or a full oral dose 15 minutes later. Bradycardia and hypotension were more common in the metoprolol group, whereas severe atrioventricular block did occur in a similar number of patients in both groups and severe congestive heart failure was more common in the placebo group. Results indicate that tolerance is generally good after intravenous and oral treatment with metoprolol in patients with suspected acute myocardial infarction.
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