[Myocardial infarction--important field for control of quality of health care and therapeutic results].
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Biomedical subjects
Publications and source records attributed to L Wallentin.
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On exercise testing after an episode of unstable coronary artery disease (CAD; unstable angina or non-Q-wave myocardial infarction), a proportion of patients show ST-segment depression, indicating myocardial ischaemia, but do not report concomitant symptoms of angina. Treatment of such "silent" ischaemia aims mainly to reduce the risk of subsequent cardiac events. We have studied the effect of low-dose aspirin in patients with myocardial ischaemia defined at the predischarge test as silent (though patients might have had symptomatic ischaemia at other times) or symptomatic. 740 men with unstable CAD aged 70 years or less underwent symptom-limited exercise testing before hospital discharge; 144 showed ST depression without pain and 230 ST depression with simultaneous chest pain. Of the silent ischaemia group, 67 were randomly assigned placebo and 77 aspirin (75 mg daily); the corresponding numbers in the symptomatic group were 125 and 105. Angina symptoms were less common in the silent than in the symptomatic ischaemia group both before inclusion and during follow-up, and a greater proportion of the silent ischaemia group were included because of myocardial infarction. In both ischaemia groups aspirin treatment reduced the risk of subsequent myocardial infarction or death by 3 months' follow-up (silent 4% of aspirin-treated vs 21% of placebo-treated patients, p = 0.004; symptomatic 9% vs 18%, p = 0.05); at 12 months' follow-up a significant benefit of aspirin was still apparent in the silent ischaemia group (9% vs 28%, p = 0.005) but not in the symptomatic group (13% vs 22%, p = 0.109). Low-dose aspirin reduced the risk of subsequent myocardial infarction at least as well in silent as in symptomatic myocardial ischaemia. Since improvement of outlook is the main treatment objective in symptom-free patients, aspirin should be a mainstay of their treatment.
Two hundred five men, 40 to 70 years of age, admitted to the coronary care unit with unstable coronary artery disease (unstable angina or non-Q wave myocardial infarction), were randomized to double-blind placebo-controlled treatment with an intravenous infusion of recombinant tissue-type plasminogen activator (rTPA), 1 mg/kg body weight (maximum 100 mg) during 4 hours, in addition to aspirin, heparin, and beta-blockade. No severe complications occurred. Myocardial ischemia, defined as myocardial infarction, incapacitating angina despite medication, or signs of ischemia at the exercise test, was reduced by treatment with rTPA compared with placebo both at discharge, 53% compared with 70% (p = 0.02), and at 1 month, 61% compared with 80% (p = 0.005). Signs of myocardial ischemia during the exercise test were reduced at discharge 51.0% compared with 68% (p = 0.03) and at 1 month 48% compared with 62% (p = 0.09). Coronary angiography after 1 month showed no difference in major coronary lesions between the groups, nor was there any reduction in the number of performed coronary revascularization procedures. In conclusion, treatment with rTPA in unstable coronary artery disease in men reduced myocardial ischemia but did not significantly reduce the need for revascularization in long-term follow-up.
The prognostic value of silent ischemia during a symptom-limited predischarge exercise test (ET) was evaluated in 740 men after an episode of unstable angina or non-Q wave myocardial infarction. The 51% of patients with ST depression at the ET had a higher rate of myocardial infarction or death after 1 year (18%) compared with those without ST depression (9%; p less than 0.01). This increased risk was not influenced by the presence or absence of pain at the ET: 18.3% in patients with painful ischemia compared with 18.1% in patients with silent ischemia. However, ST depression combined with pain at the ET predicted a higher incidence of class III or IV angina at follow-up (43.9% compared with 16.7% in the group with asymptomatic ST depression; p less than 0.001). Because revascularization in addition to alleviating symptoms also enhances the prognosis in certain groups of patients, selections for coronary angiography and possible revascularization should not be made only on the basis of symptoms but also on the presence of myocardial ischemia, whether symptomatic or not.
The diagnostic and prognostic value of ST recordings in unstable coronary artery disease were evaluated in 198 men below 70 years of age admitted to the coronary care unit because of chest pain due to myocardial ischaemia but without the development of Q-wave infarction. The ST recordings were performed for 24 h in bed in the CCU (n = 75) between 6 and 66 hours after the last episode of pain, before discharge during ambulation in hospital 4-6 days after admission (n = 198), and ambulatory out of hospital 1 month later (n = 109). The long-term ECG was registered from bipolar leads corresponding to V2 and V5 using two-channel FM-recorders. Significant ST episodes were defined as ST segment deviation greater than or equal to 0.1 mV from baseline and lasting for at least 1 min. During the recordings 85-90% of the patients were treated with betablockers and 27-41% also with calcium channel blockers. In the CCU recordings, ST depression occurred in 23% of the patients, 21% had asymptomatic and 7% symptomatic episodes. Before discharge the ST recordings showed ST depression in 18% of the patients, 16% asymptomatic and 7% symptomatic. Ambulatory monitoring after 1 month showed a higher occurrence of ST depressions--33% (P less than 0.01 compared to day 5), 26% had episodes without pain and 13% painful episodes.(ABSTRACT TRUNCATED AT 250 WORDS)
It is unclear whether echocardiography at peak bicycle exercise adds information to registrations obtained recumbent immediately after the test and what factors influence image quality. Therefore, exercise echocardiography was performed consecutively and prospectively in 66 men, unselected with regard to echocardiography, one month after an episode of unstable coronary artery disease. Of 594 segments (9 x 66), 569 (96%) were adequately visualized recumbent at rest. The corresponding figures recumbent directly after exercise, seated before exercise, and seated at peak exercise were 544 (92%), 474 (80%), and 428 (72%), respectively. In the majority of our patients, acceptable images at peak exercise were obtained for the septal region, while for the anterior, lateral, and inferior segments the success rate varied from 50 to 70%. Recumbent after exercise, the success rate was acceptable for most segments, possibly with the exception of the apical and lateral segments. Fifty-five patients developed new wall motion abnormalities or worsening of wall motion in connection with exercise. Echocardiography at peak exercise provided more information than afterwards in patients with images of good quality. However, in patients with inferior image quality, the registrations obtained recumbent after the test revealed wall motion abnormalities which were not obtained seated at peak exercise. Patients with worse image quality had significantly higher respiratory rate and weight, and rated a higher degree of dyspnoea at peak exercise than those with good quality. We conclude that in middle aged men with coronary artery disease, image acquisition at peak bicycle exercise and immediately after exercise are of complementary value.
In order to elucidate the long-term alterations in cholesterol transport and esterification as a part of the changes in the carbohydrate and lipoprotein metabolism subsequent to calorific restriction, 15 obese women were investigated before and after treatment with vertical banded gastroplasty. Insulin resistance and production, lipid levels in plasma, lipoproteins and the lecithin: cholesterol acyl transferase (LCAT) rate were assessed. There was a 60% decrease in mean calorific intake six months after surgery. A slight hyperglycaemia was almost normalized concomitant with a reduction of serum insulin and C-peptide after 1 year. The very low density lipoprotein (VLDL) level was unchanged. The high density lipoprotein (HDL) levels tended to rise after 1 year, when there was a significant increase of the HDL-2 subfraction. The lipid levels in the lipoprotein fractions showed a rise in mean HDL-2 cholesterol. Both the molar and fractional rates of LCAT were decreased. These results suggest that long-term calorific restriction reduces insulin resistance and production, and lowers VLDL levels and VLDL and cholesterol synthesis. However, the low density lipoprotein cholesterol levels are unchanged, probably because of a decrease in the previously elevated fractional cholesterol removal.
Ninety-seven men with unstable coronary artery disease (CAD), i.e. unstable angina or a non Q-wave myocardial infarction, entered a double-blind placebo-controlled study with heparin intravenously 30,000-40,000 U daily. Platelet function was evaluated as ex vivo aggregation toward collagen and ADP and as the platelet inhibitory effect of prostacyclin, before and after 5 days of treatment. Heparin increased aggregation induced by ADP 1 microM from 39.6 +/- 3.1% to 52.1 +/- 4.1% (p = 0.014) and reduced the inhibition of aggregation by prostacyclin 1.0 ng/ml from 59.6 +/- 3.7% to 39.3 +/- 5.6% (p less than 0.001). No changes occurred in the placebo group. Thus, treatment with heparin enhances the platelet sensitivity to ADP and decreases the platelet inhibitory effect of prostacyclin in men with unstable CAD. Concomitant treatment with acetylsalicylic acid abolishes the increased response to ADP, but does not seem to influence the interaction between heparin and prostacyclin.
The diagnostic and prognostic value of symptom limited exercise tests (ET) performed before discharge and after one month were compared in men admitted to hospital after an episode of unstable angina or a non-Q-wave myocardial infarction (MI). A 'Positive ET' was defined as either a maximal work load below 100 W or ST-depression greater than or equal to 0.1 mV in 1-2 leads below 130 W or ST-depression greater than or equal to 0.1 mV in more than 2 leads at any load at the ET. During follow-up, severe angina was the only indication for coronary angiography and revascularization. There were no significant differences in diagnostic findings between the tests--Positive ET in 47% and Negative ET in 25% at both ETs. The occurrence of MI or death and the need of revascularization were related to signs of ischemia at both ETs. There were no differences in prognostic value between the early and late tests regarding MI or death or future severe angina during the 11 months' follow-up after the one month ET. However, half (10%) of the overall event rate (20%) during the one year follow-up occurred during the first months. The risk of these events could be identified by the predischarge but, for obvious reasons, not by the one month ET. Therefore, the present study suggests that a symptom limited ET should be performed before discharge in men stabilized after an episode of unstable angina or non-Q-wave MI.
One-hundred-and-ninety-three men with unstable coronary artery disease (CAD) (i.e. unstable angina or a non-Q wave myocardial infarction) were randomized in a double-blind fashion to acetylsalicylic acid (ASA) 75 mg daily (n = 100) or placebo (n = 93) within 72 h of admission to the Coronary Care Unit. Platelet function was evaluated as ex vivo aggregation toward collagen and ADP before and after 5 days, 1, 12, 18 and 24 months of treatment. ASA decreased aggregation by collagen 1 mg l-1 from 81.3 +/- 1.7% before to 34.0 +/- 1.7% after 1 month (P less than 0.001), while no change was observed in the placebo group. Aggregation by ADP 1 microM after 1 month was 42.1 +/- 1.1% and 51.0 +/- 2.0% in the ASA and placebo groups respectively (P less than 0.001). The platelet inhibition by ASA was maintained during 24 months. All ASA patients had reduced aggregation during treatment. A cumulative dose of 300 mg (4 doses of 75 mg) was not enough for maximal inhibition at the second aggregation test. Thus, ASA 75 mg daily causes platelet inhibition in all patients without attenuation during long-term treatment. If low dose ASA is started in unstable coronary artery disease a loading dose exceeding 300 mg is suggested.
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Seventy-five menstruating women seeking contraceptive advice were randomly allocated to treatment with combined oral contraceptives containing either ethinyl estradiol 50 micrograms + levonorgestrel 250 micrograms (50/250), ethinyl estradiol 30 micrograms + levonorgestrel 150 micrograms (30/150) or ethinyl estradiol 50 micrograms + levonorgestrel 125 micrograms (50/125). The concentrations of cholesterol, triglycerides, phospholipids, high density lipoprotein (HDL)-cholesterol and HDL-phospholipids were determined after one, three and six months and compared to the mean of two determinations of the same parameters before medication. Triglycerides increased by 18--42 per cent after 1--6 months of treatment with 50/125. The HDL-cholesterol and HDL-phospholipids were reduced by 10 per cent during 50/250 treatment. No other parameters showed any consistent alteration in any of the treatment groups. Raised triglyceride concentration and/or decreased HDL concentration increases the risk for cardiovascular disease. It is therefore suggested that in order not to alter the HDL concentration a combined oral contraceptive agent should not contain more gestagen-androgen than corresponding to 125--150 micrograms of levonorgestrel. To avoid a rise of the triglyceride level the weight relation between levonorgestrel and ethinyl estradiol should be about 5:1.
Seventy-five menstruating women seeking contraceptive advice were randomly allocated to treatment with combined oral contraceptives containing either ethinyl estradiol 30 micrograms + levonorgestrel 150 micrograms (30/150), ethinyl estradiol 50 micrograms + levonorgestrel 125 micrograms (50/125) or ethinyl estradiol 50 micrograms + levonorgestrel 250 micrograms (50/250). The concentrations of cholesterol, phospholipids, high density lipoprotein (HDL)-cholesterol, HDL-phospholipids and triglycerides were determined prior to treatment and after one, three and six months of medication. Triglycerides increased by 18--42 per cent after one to six months of treatment with 50/125. The HDL-cholesterol and HDL-phospholipids were reduced by 10 per cent during 50/250 medication. No other parameters showed any consistent alteration in any of the treatment groups. Raised triglyceride concentration and/or decreased HDL concentration may increase the risk for cardiovascular disease. It is therefore suggested that in order not to alter the HDL concentration a combined oral contraceptive agent should probably not contain more 19-nortestosterone type of progestogen than corresponding to 125--150 micrograms of levonorgestrel. To avoid a rise of the triglyceride level the weight relation between levonorgestrel and ethinyl estradiol should be about 5:1.
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Serum FSH, LH and oestrone levels were determined in postmenopausal women before and at 1, 3 and 6 months after the onset of cyclical treatment with 0.05 mg of ethinyl oestradiol (n = 19) or 2 mg of oestradiol valerianate (n = 20). Most samples from the women taking oestradiol valerianate were also analyzed for oestradiol. Vaginal smears were obtained from all patients. Although all women were relieved of vasomotor symptoms, the FSH levels usually exceeded the fertile range. Ethinyl oestradiol reduced FSH by 70 to 75 per cent and LH by 30 to 40 per cent while oestrone was increased by 20 to 40 per cent. In the women taking oestradiol valerianate, FSH and LH levels were both reduced by 20 to 25 per cent wheras serum oestradiol increased by 200 to 300 per cent and oestrone increased by 600 to 700 per cent. The mean vaginal maturation value rose equally in the two groups but 40 per cent of the patients in both groups showed no change in the value. There was no correlation between the appearance of vaginal endocrine smears and hormone levels.