Comparison of interventional cardiology in two European countries: a nationwide Internet based registry study.

BACKGROUND: The practice of interventional cardiology differs between countries and regions. In this study we report the results of the first nation-wide long-term comparison of interventional cardiology in two countries using a common web-based registry. METHODS: The Swedish Coronary Angiography and Angioplasty Registry (SCAAR) was used to prospectively and continuously collect background-, quality-, and outcome parameters for all coronary angiographies (CA) and percutaneous coronary interventions (PCI) performed in Iceland and Sweden during one year. RESULTS: The rate of CA per million inhabitants was higher in Iceland than in Sweden. A higher proportion of patients had CA for stable angina in Iceland than in Sweden, while the opposite was true for ST elevation myocardial infarction. Left main stem stenosis was more commonly found in Iceland than in Sweden. The PCI rate was similar in the two countries as was the general success rate of PCI, achievement of complete revascularisation and the overall stent use. Drug eluting stents were more commonly used in Iceland (23% vs. 19%). The use of fractional flow reserve (0.2% vs. 10%) and the radial approach (0.6% vs. 33%) was more frequent in Sweden than in Iceland. Serious complications and death were very rare in both countries. CONCLUSION: By prospectively comparing interventional cardiology in two countries, using a common web based registry online, we have discovered important differences in technique and indications. A discovery such as this can lead to a change in clinical practice and inspire prospective multinational randomised registry trials in unselected, real world populations.

C-reactive protein in migraine sufferers similar to that of non-migraineurs: the Reykjavik Study.

C-reactive protein (CRP), a marker of inflammation, has been associated with cardiovascular disease. Risk of cardiovascular disease is increased in migraineurs with aura. Results from a clinical report, case-control and a cohort study suggest that CRP is elevated in migraineurs compared with non-migraineurs. We examined the proposed association in a case-control study nested within two large population-based studies. The relationship between migraine and CRP (high-sensitivity CRP) was studied in 5906 men and women aged 55.0 +/- 8.5 years in the Reykjavik Study and 1345 men and women aged 27.7 +/- 5.5 years from the Reykjavik Study for the Young. A modified version of the International Headache Society's criteria was used to categorize people into migraineurs (two or more symptoms) or non-migraineurs. Migraineurs with visual or sensory symptoms were further defined as having migraine with aura (MA) or without aura (MO). Multivariable-adjusted CRP levels were similar in migraineurs and non-migraineurs for men (0.83 vs. 0.79 mg/l, P = 0.44) and for women (0.87 vs. 0.87 mg/l, P = 0.90). When further stratified by migraine aura and age, no differences were found between non-migraineurs, MO and MA among men. In women, CRP levels were borderline higher in those with MO compared with non-migraineurs and those with MA (1.01 mg/l vs. 0.81 and 0.75 mg/l, P = 0.08 and P = 0.08) in age group 19-34 years, but significantly lower in age group 60-81 years (0.52 mg/l vs. 1.07 and 1.01 mg/l, P = 0.007 and P = 0.03). CRP levels were not increased among migraine sufferers compared with non-migraineurs. Older women migraineurs without aura had lower CRP values than non-migraineurs and migraineurs with aura.

Increasing glucose levels and BMI predict future heart failure experience from the Reykjavík Study.

BACKGROUND: Heart failure is common in diabetes and ischaemic heart disease is the most likely link. Still, it has been suggested that the relation extends beyond such disease. METHODS: 7060 subjects with two or more visits in the Reykjavík Study were followed--during 30 years from 1967. All underwent oral glucose tolerance tests. Disease status was defined according to the glycaemic level and presence of heart failure. The incidence and predictive factors for these diseases were determined. FINDINGS: Age and sex standardized incidence of heart failure was 5.3/1000/year, of diabetes 4.6/1000/year and abnormal glucose regulation 12.6/1000/year. Body mass index (BMI) and fasting glucose predicted the development of these conditions (p<0.001). Increasing fasting glucose by 1 mmol/l increased the risk for heart failure by 14% (p=0.04) after adjusting for IHD, BMI and other risk factors for CVD. There was a strong association between diabetes and heart failure, OR 3.0 (2.3-4.0), and abnormal glucose regulation and heart failure, OR 1.8 (1.5-2.3). Diabetes and heart failure were, however, not independent predictors of each other. INTERPRETATION: There was an independent relationship between increases in fasting glucose and development of heart failure. BMI was a strong predictor of heart failure. Although fasting glucose and BMI were significant risk factors for glucose disturbances and heart failure the conditions themselves did not independently predict each other.

Smoking and a complement gene polymorphism interact in promoting cardiovascular disease morbidity and mortality.

We have demonstrated previously that carriers of a genotype called C4B*Q0 (silent allele of the C4B gene) have a substantially increased risk to suffer from myocardial infarction or stroke, and are selected out from the healthy elderly population. Because smoking carries a major risk for cardiovascular disease (CVD), it seemed worthwhile to study if these two factors interact. Study 1 involved 74 patients with angina pectoris (AP), 85 patients with recent acute myocardial infarction (AMI) and 112 survivors of a previous AMI and 382 controls from Iceland. Study 2 involved 233 patients with severe CVD and 274 controls from Hungary. Smoking habits were registered for each subject. The number of C4A and C4B genes was determined by phenotyping or genotyping. Compared to controls, C4B*Q0 carrier frequency was significantly higher at diagnosis in Icelandic smokers with AP (P = 0.005) and AMI (P = 0.0003) and Hungarian smokers with severe coronary artery disease (P = 0.023), while no such difference was observed in non-smoking subjects. Age-associated decrease in C4B*Q0 observed previously in two remote Caucasian populations was found, in the present study, to be associated strongly with smoking, and to already occur in smokers after age 50 years both in Iceland and Hungary. Our findings indicate that the C4B*Q0 genotype can be considered as a major covariate of smoking in precipitating the risk for AMI and associated deaths.

Migraine patients have lower systolic but higher diastolic blood pressure compared with controls in a population-based study of 21,537 subjects. The Reykjavik Study.

Several studies have explored a possible association between migraine and hypertension, with contradictory results. Because of this uncertainty the relation between blood pressure (BP) and migraine was studied in 10,366 men and 11,171 women in a population-based longitudinal study. A modified version of the 1988 International Headache Society criteria was used for diagnosis of migraine. Logistic regression analysis was used. The crude 1-year prevalence of migraine was 5.2% among men and 14.1% among women. No significant association was found between hypertension and migraine. For a one standard deviation (SD) increase in diastolic BP the probability of having migraine increased 14% (P = 0.11) for men and 30% (P < 0.0001) for women. For a 1-SD increase in systolic BP the probability of having migraine decreased 19% (P = 0.007) for men and 25% (P < 0.0001) for women. It was also found that for a 1-SD increase in pulse pressure the probability of having migraine decreased 13% (P = 0.005) for men and 14% (P < 0.0001) for women. In a population-based study of men and women it was found that subjects with migraine had lower pulse pressure, lower systolic BP and higher diastolic BP compared with controls.

Risk profiles and prognosis of treated and untreated hypertensive men and women in a population-based longitudinal study: the Reykjavik Study.

The aim was to examine the risk profiles and prognosis of treated and untreated hypertensive subjects and examine to what degree confounding by indication was present in a population-based cohort study with up to 30-year follow-up. The study population consisted of 9328 men and 10 062 women, aged 33-87 years at the time of attendance from 1967 to 1996. The main outcome measures were myocardial infarction (MI), cardiovascular disease (CVD) mortality and all-cause mortality. Comparing the risk profiles between treated and untreated subjects entering the study showed significantly higher values for some risk factors for treated subjects. During the first 10 years, hypertensive men without treatment, compared with those treated, had a significantly lower risk of suffering MI, CVD and all-cause mortality, hazard ratio (HR) 0.72 (95% CI; 0.57, 0.90), 0.75 (95% CI; 0.59, 0.95) and 0.81 (95% CI; 0.61, 0.98), respectively. No significant differences in outcome were seen during the following 20 years. In identically defined groups of women, no significant differences in mortality were seen between groups. Subgroup analysis, at two stages of the study 5 years apart, revealed that some cardiovascular risk factors had a higher prevalence in hypertensive men who were treated at the later stage, compared with those who remained untreated (P=0.004). In conclusion, hypertensive treated men had a worse prognosis during the first 10 years of follow-up than untreated ones, which is most likely due to worse baseline risk profile. Hypertensive men that were treated at a later stage had a worse risk profile than those not treated at a later stage.

Survival and trends of occurrence of left ventricular hypertrophy, gender differences, 1967-92: The Reykjavik Study.

OBJECTIVE: We estimated the prevalence, incidence and risk factors of left ventricular hypertrophy (LVH) in a prospective cohort study of 26 489 participants. MATERIAL AND METHODS: The LVH was defined as Minnesota Code 310 on electrocardiogram (ECG). Everyone with this code at first visit was defined as a prevalence case and those who developed it between subsequent visits were incidence cases. The comparison cohort were all other participants in the Reykjavik Study stages I-V. RESULTS: A total of 297 men and 49 women were found to have LVH of 3.2% and 0.5%, respectively. The incidence was 25 per 1000 per year amongst men and six per 1000 per year amongst women. Prevalence in both genders increased with increasing age. Risk factors at the time of diagnosis were systolic blood pressure [odds ratio (OR) per mmHg 1.02; 95% confidence interval (CI): 1.01-1.03], age (OR per year 1.04; 95% CI: 1.02-1.05), silent myocardial infarction (MI) (OR 3.18; 95% CI: 1.39-7.27) and ST-T changes (OR 3.06; 95% CI: 2.14-4.38) amongst men and systolic blood pressure and age for women with similar odds ratio. Predictive factors for acquiring LVH were systolic blood pressure [incidence ratio (IR) 1.01; 95% CI: 1.01-1.02] and angina with ECG changes (IR 2.33; 95% CI: 1.08-5.02) amongst men and systolic blood pressure amongst women (IR 1.03; 95% CI: 1.01-1.04). The risk for coronary mortality was significantly increased amongst women with hypertrophy [hazard ratio (HR) 3.07; 95% CI: 1.5-6.31] and their total survival was poorer with increasing time from diagnosis of LVH (HR 2.17; 95% CI: 1.36-3.48). CONCLUSIONS: We conclude that the presence of LVH and its appearance is associated with age and increased blood pressure amongst both genders. Women with LVH have poorer survival than other women and they are at threefold risk of dying of ischaemic heart disease.

The relationship between educational level and mortality. The Reykjavík Study.

OBJECTIVE: Epidemiological studies have indicated an association between socioeconomic factors and health. It has not been clearly established whether this association is wholly or partly independent of classical risk factors. Our objective was to estimate the relationship between educational level and coronary artery disease (CAD), mortality and all-cause mortality. The Reykjavík Study involving 18 912 participants followed-up 4-30 years provides an ideal opportunity to address this question. DESIGN AND SUBJECTS: The participants were aged 33-81 years and living in the Reykjavík area. They were divided into four groups according to education. The standard risk factors were assessed on entry and mortality, and cause of death registered during follow-up. Multiple Cox regression analysis was applied to assess the relationship between age at examination, year of examination, educational level and mortality. RESULTS: The all-cause mortality and CAD mortality was significantly related to education, even after adjustment for classical risk factors. For men, 14% (95% CI: 2-24) reduction was found in CAD mortality for those having high school education relative to elementary school. The figures for junior college and university education were 17% (95% CI: 1-31) and 38% (95% CI: 21-32), respectively. These figures were only slightly lower when major CAD risk factors were controlled for and still significant. Similar figures were found for all-cause mortality. For women 34% (95% CI: 18-48) reduction was found in CAD mortality for high school education and 55% (95% CI: 22-74) for junior college, but too few had university education for reliable results. The figures were lower for all-cause mortality, but significant. The figures were reduced when major CAD risk factors were controlled for, but still significant. CONCLUSION: Education is a strong protective factor both for all-cause and CAD mortality. Only a small part of this effect can be explained through conventional risk factors.

Involvement of MAP kinases in the control of cPLA(2) and arachidonic acid release in endothelial cells.

Cytosolic Phospholipase A(2) (cPLA(2)) has been implicated in receptor-mediated release of arachidonic acid from membrane phospholipids, the limiting step in prostacyclin and other eicosanoid production. Its activity is controlled by Ca(++) levels and enzymatically regulated phosphorylation. The purpose of this study was to assess the importance of phosphorylation of cPLA(2) in human umbilical vein endothelial cells and to identify the kinases involved. Inhibitors were used to study the pathways leading to phosphorylation and activation of mitogen activated protein kinases (MAP-kinases) and cPLA(2), as well as release of arachidonic acid and prostacyclin production after stimulation with different agonists. We have found that agonists that release arachidonic acid, including histamine, thrombin, AlF(4)(-), and pervanadate, all activate the MAP kinases ERK, p38 and JNK and cause phosphorylation of cPLA(2). Agonist specific differences in the signal transduction pathways included variable contribution of tyrosine phosphorylation, protein kinase C and ERK activity, and different effects of pertussis toxin. Treatment with PD98059 (inhibitor of ERK-activation) or SB203580 (inhibitor of p38) caused partial decrease in arachidonic acid release and cPLA(2) activity. In contrast the nonspecific protein kinase inhibitor staurosporin completely inhibited cPLA(2) activity. We conclude that in endothelial cells arachidonic acid release is largely mediated by cPLA(2) through agonist-specific pathways. The MAP kinases ERK and p38 both have demonstrable but not major effect on agonist stimulated arachidonic acid release and the data suggest that an additional unidentified kinase also has a role.

Follow-up study of patients randomized in the Scandinavian simvastatin survival study (4S) of cholesterol lowering.

The Scandinavian Simvastatin Survival Study (4S) and other randomized clinical trials have demonstrated that cholesterol-lowering treatment with statins improves prognosis in patients with coronary atherosclerosis compared with placebo. The effect of therapy with statins beyond the typical 5 to 6 years' duration of the trials, in particular regarding the risk of cancer, has not been investigated. This study examines the long-term effects of simvastatin for up to 8 years on cause-specific mortality in patients with coronary heart disease (CHD). We performed an observational, government registry-based study of mortality in the groups originally randomized to simvastatin or placebo in the 4S over an additional 2-year follow-up period, so that the median total follow-up period was 7.4 years (range 6.9 to 8.3 in surviving patients). Randomization took place at outpatient clinics at 94 clinical centers in Denmark, Finland, Iceland, Norway, and Sweden from 1988 to 1989. Of 4,444 patients with CHD, 2,223 and 2,221 were randomized to treatment with placebo or simvastatin therapy, respectively. Patients received treatment with simvastatin, starting at 20 mg/day, with titration to 40 mg/day at 12 or 24 weeks if total cholesterol was >5.2 mmol/L (200 mg/dl), or placebo. After the double-blind period, most patients in both treatment groups received simvastatin as open-label prescription. Of the 1,967 patients originally treated with placebo and surviving the double-blind period, 97 (4.9%) died during the following 2 years. In the group randomized to simvastatin the corresponding number was 74 of the 2, 039 survivors (3.6%). Adding these deaths to those occurring during the original trial, the total was 353 (15.9%) and 256 (11.5%) deaths in the groups originally randomized to placebo and simvastatin, respectively. The relative risk was 0.70 (95% confidence interval 0. 60 to 0.82, p = 0.00002). The total number of cancer deaths was 68 (3.1%) in the placebo group and 52 (2.3%) in the simvastatin group (relative risk 0.73, 95% confidence interval 0.51 to 0.05, p = 0. 087), and the numbers of noncardiovascular and other deaths were similar in both groups. We therefore conclude that treatment with simvastatin for up to 8 years in patients with CHD is safe and yields continued survival benefit.

Effects of controlled-release metoprolol on total mortality, hospitalizations, and well-being in patients with heart failure: the Metoprolol CR/XL Randomized Intervention Trial in congestive heart failure (MERIT-HF). MERIT-HF Study Group.

CONTEXT: Results from recent studies on the effects of beta1-blockade in patients with heart failure demonstrated a 34% reduction in total mortality. However, the effect of beta1-blockade on the frequency of hospitalizations, symptoms, and quality of life in patients with heart failure has not been fully explored. OBJECTIVE: To examine the effects of the beta1-blocker controlled-release/extended-release metoprolol succinate (metoprolol CR/XL) on mortality, hospitalization, symptoms, and quality of life in patients with heart failure. DESIGN: Randomized, double-blind controlled trial, preceded by a 2-week single-blind placebo run-in period, conducted from February 14, 1997, to October 31, 1998, with a mean follow-up of 1 year. SETTING: Three hundred thirteen sites in 14 countries. PARTICIPANTS: Patients (n = 3991) with chronic heart failure, New York Heart Association (NYHA) functional class II to IV, and ejection fraction of 0.40 or less who were stabilized with optimum standard therapy. INTERVENTIONS: Patients were randomized to metoprolol CR/XL, 25 mg once per day (NYHA class II), or 12.5 mg once per day (NYHA class III or IV), titrated for 6 to 8 weeks up to a target dosage of 200 mg once per day (n = 1990); or matching placebo (n = 2001). MAIN OUTCOME MEASURES: Total mortality or any hospitalization (time to first event), number of hospitalizations for worsening heart failure, and change in NYHA class, by intervention group; quality of life was assessed in a substudy of 741 patients. RESULTS: The incidence of all predefined end points was lower in the metoprolol CR/XL group than in the placebo group, including total mortality or all-cause hospitalizations (the prespecified second primary end point; 641 vs 767 events; risk reduction, 19%; 95% confidence interval [CI], 10%-27%; P<.001); total mortality or hospitalizations due to worsening heart failure (311 vs 439 events; risk reduction, 31%; 95% CI, 20%-40%; P<.001), number of hospitalizations due to worsening heart failure (317 vs 451; P<.001); and number of days in hospital due to worsening heart failure (3401 vs 5303 days; P<.001). NYHA functional class, assessed by physicians, and McMaster Overall Treatment Evaluation score, assessed by patients, both improved in the metoprolol CR/XL group compared with the placebo group (P = .003 and P = .009, respectively). CONCLUSIONS: In this study of patients with symptomatic heartfailure, metoprolol CR/XL improved survival, reduced the need for hospitalizations due to worsening heart failure, improved NYHA functional class, and had beneficial effects on patient well-being.

Resuscitation in Europe: a tale of five European regions.

AIM: To describe cardiac arrest data from five emergency medical services (EMS) systems in Europe with regard to survival from an out-of-hospital cardiac arrest. METHODS: Based on recommendations from various countries in Europe EMS systems were approached with regard to survival from out-of-hospital cardiac arrest. Five EMS systems were asked to report their cardiac arrest data according to the Utstein style. RESULTS: The five selected EMS systems were: Bonn (Germany), Göttingen (Germany), Helsinki (Finland), Reykjavik (Iceland) and Stavanger (Norway). For patients with a bystander witnessed arrest of cardiac aetiology the percentage of patients being discharged alive from hospital in these regions were: 21, 33, 23, 23 and 35. The corresponding percentages for patients fulfilling criteria as above and being found in ventricular fibrillation were: 32, 42, 32, 27 and 55. CONCLUSIONS: Many EMS systems in Europe show extremely good results in terms of survival after an out-of-hospital cardiac arrest. Some of the results should be interpreted with caution since they were based on relatively small sample sizes. Furthermore, the results from one of the regions (Stavanger) was unit based and not community based.

Effects of leisure-time physical activity and ventilatory function on risk for stroke in men: the Reykjavík Study.

BACKGROUND: Stroke is a major cause of illness, death, and health expenditures. Leisure-time physical activity may reduce the risk for stroke. OBJECTIVE: To examine the association of leisure-time physical activity and pulmonary function with risk for stroke. DESIGN: Prospective cohort study. SETTING: Reykjavík, Iceland. PARTICIPANTS: 4484 men 45 to 80 years of age followed for a mean (+/-SD) of 10.6 +/- 3.6 years. MEASUREMENTS: Patients underwent physical examination, blood sampling, and spirometry and completed a questionnaire about health and exercise. Computerized hospital records were used to identify strokes, and the Icelandic National Registry was used to identify deaths. RESULTS: New stroke developed in 249 men (5.6%) (hemorrhagic stroke in 44 [18%] and ischemic stroke in 205 [82%]). In a multivariable hazard analysis that controlled for known risk factors for cerebrovascular disease, leisure-time physical activity maintained after 40 years of age was associated with a reduced risk for stroke (relative risk, 0.69 [CI, 0.47 to 1.01] for total stroke and 0.62 [CI, 0.40 to 0.97] for ischemic stroke). Risk for stroke increased with diminished ventilatory function (FVC or FEV1) (relative risk, 1.9 [CI, 1.06 to 3.25] for the lowest compared with the highest quintile). CONCLUSION: Middle-aged men who participate in leisure-time physical activity and have good pulmonary function seem to have a lower risk for stroke than men who are not active or have diminished pulmonary function.

[Medical treatment of coronary heart disease in Iceland.].

OBJECTIVE: During the last decades the knowledge of prevention of coronary heart disease (CHD) has increased dramatically. RESULTS from large clinical trials on drug treatment of patients with CHD with various groups of drugs has given new possibilities to improve the prognosis of our patients. However, results from several studies have shown that this knowledge has not yet been put into practice. The main aim of our study, which is a part of a larger enquiry into the actual practice of secondary prevention of CHD in Iceland, was to evaluate the medical treatment of CHD, other than lipid lowering therapy. MATERIAL AND METHODS: All patients with residence in Hafnarfjörethur, Garethabaer and Bessastaethahreppur who have been diagnosed as having CHD were sent a letter with an invitation to participate in the study and a request for an informed consent. Those who choose to participate responded to a questionnaire and gave a permission for a review of their records with respect to a specific diagnosis and lipid values. The patients were divided into four groups on the basis of their history: I. myocardial infarction (MI), II. coronary artery bypass surgery (CABG), III. percutaneous transiluminal coronary angioplasty (PTCA) and IV. angina pectoris (AP). If a patient fulfilled the critera for more than one diagnostic group the CABG group had the highest priority followed by PTCA, MI and finally AP. RESULTS: A total of 533 patients with CHD were living in the study area and of those 402 (75%) participated in the study. Aspirin was used by 284 patients (71%), 75% among men and 65% among women (p=0.018). The highest proportion (91%) being among those who had undergone CABG, and the lowest among those with angina pectoris (56%). Half of the patients (52%) used beta blockers and 119 (30%) diuretics. A total of 172 patients received treatment with nitrates (43%), 57% of the women and 27% of the men (p=0.006). Calcium blockers were used by 145 patients (36%) and ACE inhibitors by 81 (20%). Among women in the age group 40 to 80 years, 16% were receiving hormone replacement therapy. CONCLUSIONS: These results indicate that in Iceland, as in many other countries, secondary prevention of CHD is not beeing fully implemented and the scientific evidence that has been obtained from large clinical trials, has not yet been put into practice. There is obviously a great potential to improve the medical treatment and prognosis of our patients with CHD.

[Medical surveilance and secondary prevention of coronary heart disease in general practice.].

OBJECTIVE: Prevention, both primary and secondary, is an important part in the daily work of most doc-tors. Family physicians (FP) carry the responsibility of implementing both stages of prevention. Coronary heart disease (CHD) is an example of chronic disease where FP have a responsibility both in treatment and prevention. Recent large double blind clinical trials have confirmed the efficacy of various methods of secondary prevention. However, it seems that these tools are used insufficiently, and there may be opportunities for improvement. The aim of this study, which is a part of a larger inquiry about CHD patients, was to evaluate what kind of surveillance these patients receive by their FP and how secondary prevention is organized and implemented in general. MATERIAL AND METHODS: All CHD patients with residence in Hafnarfjörethur, Garethabaer and Bessastaethahreppur (urban communities with 25,000 inhabitants), were invitated to participate in the study. They received an invitation letter and a request for an informed consent. If they chose to participate they answered a questionnaire about CHD risk factors and their medical treatment. Information about their CHD status was gathered by a review of their records at the respective health center. The patients were divided into four groups on the basis of their history: I. Myocardial infarction (MI), II. coronary artery bypass surgery (CABG), III. percutaneous transiluminal coronary angioplasty (PTCA), IV. angina pectoris (AP). If a patient fulfilled the critera for more than one diagnostic group the CABG group had the highest priority followed by PTCA, MI and finally AP. RESULTS: Of 533 patients with CHD 402 (75%) participated in the study. Electrocardiogram had been recorded for 225 (56%) of these patients. Information about blood pressure was found for 369 (92%) and the mean systolic blood pressure was 143 mraHg (SD 19.8) and diastolic 82 mmHg (SD 9.5). Of CHD patients 15% were followed solely by their FP, 31% were exclusively followed by other specialists (car-diologists), 23% were followed both by FP and other specialists and 11% were without any medical surveillance. About 15% of the participants smoked, 12% were daily smokers and 56% were ex-smokers. Consultation report from a cardiologist had been sent to the respective FP for 43% of the patients. CONCLUSIONS: These results indicate that there is a number of opportunities to improve medical treat-ment and secondary prevention of CHD in Iceland. Improved organization of medical surveillance with clear definiton of treatment goals and full utilisation of those possibilities that are in the Icelandic health care system for secondary prevention, including improvement in the exchange of informations between those involved in treating CHD.

[How is cholesterol lowering therapy implemented among patients with coronary heart disease in Iceland?].

OBJECTIVE: High serum cholesterol is one of the major risk factors for coronary heart disease (CHD). RESULTS from large clinical trials have convincingly shown the importance of cholesterol lowering therapy among patients with established CHD. Revised guidelines for cholesterol lowering therapy were published in Iceland in 1996 recommending reduction of total cholesterol below 5.0 mmol/L in the face of established coronary heart disease. We have today very limited knowledge about whether we are implementing these recommendations or not and the aim of this study was to evaluate this question. This study is a part of a larger enquiry into the actual practice of secondary prevention of CHD in Iceland. MATERIAL AND METHODS: All patients with residence in Hafnarfjörethur, Garethabaer and Bessastaethahreppur who have been diagnosed as having CHD were sent a letter with an invitation to participate in the study and a request for an informed consent. Those who chose to participate responded to a questionnaire and gave a permission for a review of their records with respect to a specific diagnosis and lipid values. The patients were divided into four groups on the basis of their history: I. myocardial infarction (MI), II. coro notnary artery bypass surgery (CABG), III. percuta notneous transiluminal coronary angioplasty (PTCA), IV. angina pectoris (AP). If a patient fulfilled a cri notterion for more than one diagnostic group the CABG group had the highest priority followed by PTCA, MI and finally AP. RESULTS: Of 533 patients with CHD 402 (75%) chose to participate. Average cholesterol in the total group was 6.2 mmol/L (95% C.I. 6.07-6.34). In the four subgroups the respective cholesterol values were: I 6.3, II 5.9, III 5.9, IV 6.5 mmol/L. Only 25% of the patients knew their cholesterol values, 20% in group I, 43% in group II, 30% and 15% in groups III and IV respectively. A total of 113 patients (28%) were receiving cholesterol lowering drug therapy at the time of the study. Respective treatment ratios in the four subgroups were 25% in group I, 47% in II, 42% in III and 13% in group IV. CONCLUSIONS: In spite of overwhelming evidence of the benefit associated with lipid lowering therapy for CHD patients this study has shown marked underuse of this therapeutic modality. Quality control study as this one is a valuable method to evaluate how practising physicians are implementing recommendations, based on scientific evidence, given by health authorities.

Differences in the treatment of coronary heart disease between countries as revealed in the Scandinavian Simvastatin Survival Study (4S)

AIM: To assess differences in treatment of ischaemic heart disease in the Scandinavian countries. METHODS AND RESULTS: The Scandinavian Simvastatin Survival Study (4S) lasted 5.4 years and showed that death rates in 4444 patients with coronary heart disease were 30% lower in those treated with simvastatin to lower serum cholesterol than in those given placebo. Apart from this main result, the 4S provided detailed information on rates of death and other manifestations of coronary heart disease, as well as on use of non-lipid forms of therapy. There were substantial differences in 4S placebo group rates of mortality, coronary deaths and major coronary events between countries. Surgical and medical therapy varied importantly between countries. CONCLUSIONS: Major inter-country differences in rates of death and myocardial infarction in patients with coronary heart disease were likely to be due to a composite of differences in baseline characteristics including smoking. They occurred in a setting of very uneven exploitation of the potential for improving survival of patients with ischaemic heart disease.

Potentiating effects of pertussis toxin on leukotriene C4 induced formation of inositol phosphate and prostacyclin in human umbilical vein endothelial cells.

Leukotriene C4 is an arachidonic acid metabolite and an important mediator of inflammation and anaphylaxis that is known to induce production of prostacyclin in endothelial cells. The goal of this study was to examine the signal transduction mechanisms activated by leukotriene C4 stimulation. Formation of inositol phosphates was measured to determine the activation of phospholipase C and pertussis toxin was used to explore the role of G-proteins. Additionally, we evaluated the role of protein kinase C in these events, especially whether there was an interaction between pertussis toxin mediated effects and the activity of protein kinase C. Leukotriene C4 induced a dose- and time-dependent formation of inositol phosphates and prostacyclin. The response to leukotriene C4 was greater than the response to leukotriene D4 even after treatment with L-serine borate complex, suggesting the presence of a specific leukotriene C4 receptor. Exposure to pertussis toxin potentiated, time-dependently, the leukotriene C4 induced formation of inositol phosphates and prostacyclin through a mechanism which was altered by manipulation of protein kinase C activity. The exact mechanism is not clear but our results are consistent with a postulated dual mechanism of phospholipase C control, in which leukotriene C4 induced stimulation is attenuated by a pertussis toxin sensitive G-protein.

Incidence and prevalence of recognised and unrecognised myocardial infarction in women. The Reykjavik Study.

AIMS: The incidence and prevalence of recognised and unrecognised myocardial infarction were determined in the Icelandic cohort study of 13,000 women (the Reykjavik Study), followed for up to 29 years (mean 15 years). METHODS AND RESULTS: Women attending the Reykjavik Study, born between 1908 and 1935, were examined in five stages from 1968 to 1991. A health survey included history and ECG manifestations of coronary heart disease. Data retrieved from hospitals, autopsy records and death certificates identified 596 fatal and non-fatal myocardial infarctions to the end of 1992 (61 prior to examination, 320 non-fatal and 215 fatal). The incidence of recognised myocardial infarction ranged from 22 cases/100,000/year at 35-39 years to 1800 cases/100,000/year at 75-79 years. The incidence of unrecognised myocardial infarction ranged from 18 cases/100,000/year at 35 years to 219 cases/100,000/year at 75 years. Thirty-three percent of non-fatal myocardial infarctions were unrecognised. More occurred in the younger age groups (40%) than in the older (27%). The prevalence of recognised myocardial infarction was influenced by age and calendar year. In 1990, it was 1.3/1,000 at 35 years and 60/1000 at 75 years. Prevalence showed a time trend, tripling in all age groups from 1968-1992. Fore unrecognised myocardial infarction, prevalence rose from 0.9/1000 at 35 years to 19.2/1000 at 75 years, although there was no evident time trend. CONCLUSION: Myocardial infarction in women is very age-dependent with both incidence and prevalence increasing continuously and steeply with age. There was a significant trend for an increase in prevalence of recognised myocardial infarction from 1968 to 1992. The proportion of unrecognised non-fatal infarctions ranged from 27% in the oldest age group to 40% in the youngest. On average, this form of coronary heart disease is as common as in men.