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Biomedical subjects

M H Frick

Publications and source records attributed to M H Frick.

At least 19 recordsLinked to original sources
PubMed1992

Chronic Chlamydia pneumoniae infection as a risk factor for coronary heart disease in the Helsinki Heart Study.

OBJECTIVE: To investigate in the prospective Helsinki Heart Study, whether chronic Chlamydia pneumoniae infection, indicated by elevated antibody titers against the pathogen, chlamydial lipopolysaccharide-containing immune complexes, or both, is a risk factor for coronary heart disease. DESIGN AND SETTING: The Helsinki Heart Study was a randomized, double-blind, 5-year clinical trial to test the efficacy of gemfibrozil in reducing the risk for coronary heart disease. Participants were randomized to receive either gemfibrozil (2046 patients) or placebo (2035 patients). Fatal and nonfatal myocardial infarction and sudden cardiac death were the main study end points. Serum samples were collected at 3-month intervals from all patients. PATIENTS: One hundred forty cardiac events occurred during the follow-up period. Serum samples from 103 case patients obtained 3 to 6 months before a cardiac end point were matched with those from controls for time point, locality, and treatment. Samples were tested for markers of chronic chlamydial infection. MEASUREMENTS: Immunoglobulin A (IgA) and G (IgG) antibodies to C. pneumoniae were measured using the microimmunofluorescence method. Lipopolysaccharide-containing immune complexes were measured using two antigen-specific enzyme immunoassays, the lipopolysaccharide-capture and immunoglobulin M (IgM)-capture methods. MAIN RESULTS: Using a conditional logistic regression model, odds ratios for the development of coronary heart disease were 2.7 (95% CI, 1.1 to 6.5) for elevated IgA titers, 2.1 (CI, 1.1 to 3.9) for the presence of immune complexes, and 2.9 (CI, 1.5 to 5.4) for the presence of both factors. If we adjusted for other coronary heart disease risk factors such as age, hypertension, and smoking, the corresponding values would be 2.3 (CI, 0.9 to 6.2), 1.8 (CI, 0.9 to 3.6), and 2.6 (CI, 1.3 to 5.2), respectively. CONCLUSION: The results suggest that chronic C. pneumoniae infection may be a significant risk factor for the development of coronary heart disease.

Adult↗
PubMed1992

Leukocytes as a coronary risk factor in a dyslipidemic male population.

The role of an elevated serum leukocyte count (WBC) as a coronary risk factor was investigated using a nested case-control design in dyslipidemic middle-aged men (n = 420) participating in the Helsinki Heart Study, a coronary primary prevention trial. Baseline WBC was significantly higher, 6.93 (2.11) x 10(9)/L in subjects with cardiac events, than in controls, 6.26 (1.88) x 10(9)/L; p less than 0.002. This association was time-dependent, however, since the difference was not significant for events occurring during the second half of the 5-year study. Using nonsmokers in the lowest WBC tertile as the reference sample, the relative risks in the highest WBC tertile were 1.86 (95% confidence intervals [CI] 0.81 to 4.28) for nonsmokers and 3.07 (95% CI 2.23 to 8.19) for smokers. Logistic regression analysis including smoking in the model disclosed an independent contribution of elevated WBC to coronary heart disease. We conclude that elevated leukocyte count was a coronary risk factor even in this dyslipidemic population.

Case-Control Studies↗
PubMed1992

Effects of gemfibrozil treatment on serum levels of androstanediol glucuronide and adrenal androgens.

We have prospectively investigated the role of adrenal cortical androgens as a risk factor for coronary heart disease in the Helsinki Heart Study population. Simultaneously we studied the effects of gemfibrozil treatment on the serum levels of dehydroepiandrosterone (DHEA), its sulfate (DHEAS), and their metabolite androstanediol glucuronide (3 alpha AdiolG) with those of placebo. Gemfibrozil (n = 133) vs placebo (n = 159) treatment was associated with significant elevation of mean (SD) DHEAS (mumol/l) 8.35 (5.31) vs 6.98 (3.85); P less than 0.02, and of 3 alpha AdiolG (nmol/l) 17.45 (7.57) vs 8.62 (3.56); P less than 0.001), and of almost significant elevation of DHEA (nmol/l) 10.12 (6.64) vs 8.78 (5.86); P less than 0.07). These new observations suggest that gemfibrozil treatment increases the production and turnover of DHEA and DHEAS and may in addition stimulate the 5 alpha-reduction of androgens.

Androgens↗
PubMed1992

Joint effects of serum triglyceride and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Study. Implications for treatment.

BACKGROUND: We studied the joint effect of baseline triglyceride and lipoprotein cholesterol levels on the incidence of cardiac end points in the trial group (n = 4,081) of the Helsinki Heart Study, a 5-year randomized coronary primary prevention trial among dyslipidemic middle-aged men. The relative risks (RR) were calculated using Cox proportional hazards models with a dummy variable technique that allows simultaneous study of subgroup combinations from the placebo and treatment groups. METHODS AND RESULTS: In the placebo group (n = 2,045), the low density lipoprotein cholesterol (LDL-C)/high density lipoprotein cholesterol (HDL-C) ratio was the best single predictor of cardiac events. This ratio in combination with the serum triglyceride level revealed a high-risk subgroup: subjects with LDL-C/HDL-C ratio greater than 5 and triglycerides greater than 2.3 mmol/l had a RR of 3.8 (95% CI, 2.2-6.6) compared with those with LDL-C/HDL-C ratio less than or equal to 5 and triglyceride concentration less than or equal to 2.3 mmol/l. In subjects with triglyceride concentration greater than 2.3 mmol/l and LDL-C/HDL-C ratio less than or equal to 5, RR was close to unity (1.1), whereas in those with triglyceride level less than or equal to 2.3 mmol/l and LDL-C/HDL-C ratio greater than 5, RR was 1.2. The high-risk group with LDL-C/HDL-C ratio greater than 5 and triglyceride level greater than 2.3 mmol/l profited most from treatment with gemfibrozil, with a 71% lower incidence of coronary heart disease events than the corresponding placebo subgroup. In all other subgroups, the reduction in CHD incidence was substantially smaller. CONCLUSIONS: Serum triglyceride concentration has prognostic value, both for assessing coronary heart disease risk and in predicting the effect of gemfibrozil treatment, especially when used in combination with HDL-C and LDL-C.

Adult↗
PubMed1992

Coronary heart disease incidence in NIDDM patients in the Helsinki Heart Study.

OBJECTIVE: To determine coronary heart disease (CHD) incidence among dyslipidemic subjects with non-insulin-dependent diabetes mellitus (NIDDM) and to assess the effect of lipid-modifying treatment on serum and lipoprotein lipids and the CHD incidence in these patients. RESEARCH DESIGN AND METHODS: Of the 4081 men participating in the Helsinki Heart Study, a coronary primary prevention trial with gemfibrozil in middle-aged men with high non-high-density lipoprotein (HDL) cholesterol (greater than 5.2 mM; 200 mg/dL), 135 had NIDDM at entry. The incidence of definite myocardial infarction and cardiac death and changes in serum and lipoprotein lipids were determined during the 5-yr trial in the NIDDM patients and compared with those observed in nondiabetic trial participants. RESULTS: Compared with nondiabetic subjects, NIDDM patients had lower HDL cholesterol (P less than 0.001), higher triglyceride concentration (P less than 0.0001), and greater body mass index (P less than 0.001), there were more hypertensive patients (P less than 0.001) among them. The incidence of myocardial infarction and cardiac death was significantly higher among diabetic than nondiabetic participants (7.4 vs. 3.3%, respectively, P less than 0.02). CHD incidence in the gemfibrozil-treated diabetic men (n = 59) was 3.4% compared with 10.5% in the placebo group (NS). In multivariate analysis, diabetes (P less than 0.05), age (P less than 0.0001), smoking (P less than 0.0001), low HDL cholesterol (P less than 0.05), and high low-density lipoprotein cholesterol (P less than 0.005) were independently related to CHD incidence. Gemfibrozil-induced serum and lipoprotein lipid changes in diabetic patients were similar to those observed in nondiabetic subjects. CONCLUSIONS: Compared with similarly dyslipidemic nondiabetic subjects, patients with NIDDM are at markedly increased risk of CHD. This elevated risk can be somewhat reduced by gemfibrozil.

Blood Glucose↗
PubMed1992

Efficacy of conventional and sustained-release verapamil in stable angina pectoris.

The efficacy of sustained-release (s.r.) verapamil and conventional verapamil were compared in a double blind, crossover study in 20 patients (age 53 +/- SD6 years) who had stable effort angina and had used betablockers and long acting nitrates for at least two weeks. All patients received s.r. verapamil 200 mg b.i.d. and conventional verapamil 120 mg t.i.d. in a randomised order for two weeks. A symptom limited bicycle exercise test was performed at the end of the patients' previous medication period with betablocker plus long acting nitrate and at the end of both verapamil treatments in the morning before drug administration and three hours thereafter. All the patients improved subjectively during both verapamil regimens according to NYHA classification and they had fewer anginal attacks. The time to onset of ST-segment depression during exercise remained shorter during beta-blockade and long acting nitrates than during both verapamil regimens (P less than 0.05). During the peak action three hours after drug administration conventional verapamil was most effective at comparable workloads (P less than 0.05), whereas the exercise time was slightly prolonged with s.r. verapamil before drug administration.

Adrenergic beta-Antagonists↗
PubMed1991

Coronary collateral circulation.

The occurrence and influence of coronary collateral circulation and obstruction of the supplying coronary arteries on left ventricular contractility, prevalence of myocardial infarction, and bicycle exercise ergometer test were studied in a random sample of 286 patients with angiographically documented coronary artery disease. Collaterals appeared increasingly in all three main coronary arteries with grade of obstruction. The highest prevalence of collaterals occurred in stenosis of the right coronary artery (60%), followed by the left descending artery (45%); they occurred least in the left circumflex artery (21%) (p less than 0.001). The frequency of intra-arterial collateral circulation was 42%, 11%, and 12%, respectively (p less than 0.001). With total occlusion of the left anterior descending coronary artery, 22% of the patients had normokinetic anterior and apical left ventricular wall when collaterals were present. More often, the inferior wall showed normal contraction with total occlusion of the right coronary artery and collaterals [52%, p less than 0.001 compared with left anterior descending artery (LAD)]. The prevalence of inferior myocardial infarction was 39%, with collateral circulation to the totally occluded right coronary artery. The respective prevalence of anterior infarction and total occlusion in the left coronary artery was 58% (p less than 0.02). The presence or absence of collaterals had no obvious influence on ST-segment response during bicycle ergometer test. In triple-vessel disease, peak work capacity was better when collaterals to LAD were not jeopardized (427 kpm) than when jeopardized (321 kpm) (p less than 0.02).

Analysis of Variance↗
PubMed1991

Lipoprotein (a) and coronary heart disease risk: a nested case-control study of the Helsinki Heart Study participants.

To prospectively assess the role of lipoprotein(a) (Lp(a)) as a risk factor for coronary heart disease, the serum Lp(a) concentration was determined in 130 subjects without coronary events and in 138 patients in whom coronary events (i.e. fatal and non-fatal myocardial infarction and cardiac death) occurred during the 5-year Helsinki Heart Study. The participants of this study (n = 4081) were 40-55-year-old men who were devoid of coronary heart disease at the beginning of the trial; half were randomized to gemfibrozil and the other half to placebo treatment. In patients with coronary events blood pressure and total cholesterol were not significant predictors of the events but their LDL cholesterol was higher than compared to the control group in this cohort (P less than 0.05). The serum Lp(a) concentration was determined by immunoassay from samples obtained 3 months after the beginning of the trial and then stored at -20 degrees C until analysed. Studies on the effect of long term storage at -20 degrees C on serum Lp(a) levels did not reveal significant changes in Lp(a) concentration in sera stored for up to 8.5 years. The distribution of Lp(a) concentrations were similar in the men with coronary events and the controls. Nor did the mean or median levels of Lp(a) differ significantly between the two groups. Measurements of Lp(a) levels in fresh samples using 2 different immunoassays did not reveal any significant difference between the participants who had survived a myocardial infarction or participants without cardiac events. Thus, we conclude that in the Helsinki Heart Study cohort the serum Lp(a) level was not a predictor of future coronary events.

Adult↗
PubMed1991

Relationship of skeletal muscle fiber type to serum high density lipoprotein cholesterol and apolipoprotein A-I levels.

We measured the percentage of slow-twitch (ST) muscle fibers in the lateral portion of the quadriceps femoris muscle in 41 healthy sedentary male controls, 35 active male joggers, and 26 male coronary heart disease (CHD) patients. We then compared these percentages with serum levels of total cholesterol (TC), triglycerides (TG), high density lipoprotein cholesterol (HDL-C) and apolipoprotein A-I (apo A-I) found in these 102 middle-aged men. The percentage of ST muscle fibers in all men correlated positively with serum HDL-C (r = 0.57, P less than 0.001) and with apo A-I (r = 0.60, P less than 0.001) and negatively with triglycerides (r = -0.43, P less than 0.001). The proportion of ST fibers in joggers (65%; 61-69%, 95% confidence interval) was higher (P less than 0.001) than in sedentary controls (48%; 44-52%) or in CHD patients (44%; 39-49%). Moreover, 89% of the joggers had a proportion of ST fibers higher than 50%, whilst in sedentary controls and in CHD patients these values were 46% and 38%, respectively. Positive correlations were found between the percentage of ST fibers and both HDL-C and apo A-I in controls (r = 0.33, P less than 0.05 and r = 0.34, P less than 0.05) and in joggers (r = 0.46, P less than 0.01, and r = 0.40, P less than 0.05), respectively. Negative correlations in controls (r = -0.34, P less than 0.05) and in CHD patients (r = -0.43, P less than 0.05) were also found between the percentage of ST fibers and serum TG.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

The Helsinki Heart Study: central findings and clinical implications.

This paper describes the central findings and discusses the clinical implications of the Helsinki Heart Study. This was a controlled primary prevention trial to test the hypothesis that using gemfibrozil to lower the concentrations of serum low density lipoprotein (LDL) and very low density lipoprotein (VLDL) and to raise that of high density lipoprotein (HDL) protects subjects against coronary heart disease.

Adult↗
PubMed1990

Effect of gemfibrozil on the concentration and composition of serum lipoproteins. A controlled study with special reference to initial triglyceride levels.

We investigated the modulating effect of serum total triglycerides on the lipid composition of various lipoproteins, and on the response to gemfibrozil treatment. This placebo controlled study was conducted blind in 60 participants of the Helsinki Heart Study. An inverse relationship was observed between cholesterol content in all lipoprotein fractions and serum total triglyceride level. Gemfibrozil, in addition to changing the absolute amounts of lipoprotein lipids, also normalized the qualitative abnormalities associated with hypertriglyceridemia. Gemfibrozil increased the level of HDL-cholesterol with the main effect on HDL3-subfraction. The observed reduction in LDL-cholesterol was dependent on the initial triglyceride level.

Cholesterol, HDL↗
PubMed1990

Reduction in Q wave myocardial infarctions with gemfibrozil in the Helsinki Heart Study.

The Helsinki Heart Study demonstrated a 34% (p less than 0.02) reduction in the incidence of cardiac end points (myocardial infarction and cardiac death) with the use of gemfibrozil compared with the use of a placebo in dyslipidemic middle-aged men. The major effect was confined to nonfatal myocardial infarctions. In this study we analyzed the effect of gemfibrozil therapy on the incidences of Q wave and non-Q wave infarctions, since the long-term prognoses of these two types of myocardial infarction may be different. The analyses indicated a 45% reduction (P less than 0.02, log-rank test) in the cumulative incidence of Q wave infarctions in the gemfibrozil group without a statistically significant effect on either the rate of non-Q wave infarctions or of coronary deaths. The reduction in the incidence of Q wave infarctions became evident during the second half of the 5-year study period.

Creatine Kinase↗
PubMed1990

Lipoproteins and coronary heart disease in the Helsinki Heart Study.

The changes in serum lipids in men treated with gemfibrozil in the Helsinki Heart Study, a controlled primary prevention trial of coronary heart disease, varied according to baseline lipid levels, type of dyslipidaemia, and treatment compliance. In subjects with the best treatment compliance, gemfibrozil induced mean decreases of 14% in total cholesterol, 15% in low density lipoprotein (LDL)-cholesterol, and 45% in triglycerides, and a mean increase of 14% in high density lipoprotein (HDL)-cholesterol, compared with placebo. These changes were significantly greater than those observed in the entire cohort. There was a strong association between baseline levels and the response to treatment (expressed as the difference in mmol l-1 between the gemfibrozil- and placebo-treated groups) for LDL-cholesterol and triglycerides. In contrast, the corresponding change in HDL-cholesterol was not dependent on the baseline level. Ultracentrifuge analysis in a subsample of the cohort revealed that gemfibrozil raised the level of HDL3-cholesterol but had little effect on HDL2-cholesterol. The gemfibrozil-associated reduction in the incidence of definite coronary events varied according to lipid values at baseline and their changes during treatment. The greatest reductions were seen in subjects with low initial HDL-cholesterol and high initial triglycerides. In the gemfibrozil group, the increase in HDL-cholesterol and decrease in LDL-cholesterol were associated with significantly lower risk of coronary events.

Coronary Disease↗
PubMed1990

HDL-cholesterol as a risk factor in coronary heart disease. An update of the Helsinki Heart Study.

The aim of the Helsinki Heart Study, a 5-year primary prevention placebo-controlled study involving 4081 dyslipidaemic men (aged 40 to 55 years), was to investigate if increasing high density lipoprotein (HDL)-cholesterol plasma levels and decreasing low density lipoprotein (LDL)-cholesterol levels would reduce the incidence of coronary heart disease. Gemfibrozil 600mg twice daily was administered to induce these changes in lipoprotein levels. Baseline HDL-cholesterol levels in the study group were similar to those in the general population. Data from patients treated with placebo were analysed to investigate the influence of HDL-cholesterol levels on the incidence of coronary heart disease. Using the number of cardiac end-points per 1000 person-years to indicate the risk of coronary heart disease, it was clear that elevated HDL-cholesterol levels reduced the risk of coronary heart disease while the incidence increased at low HDL-cholesterol levels. This relationship was not altered when the effect of HDL-cholesterol levels was analysed jointly with other coronary risk factors (age, smoking or blood pressure). A weaker association was seen between LDL-cholesterol and risk of coronary heart disease, and triglycerides appeared to have no significant effect on the incidence of the disease. The data clearly suggest that HDL-cholesterol is a strong predictor of the incidence of coronary heart disease in the placebo group of the Helsinki Heart Study.

Cholesterol↗
PubMed1989

Relation between baseline lipid and lipoprotein values and the incidence of coronary heart disease in the Helsinki Heart Study.

A 34% reduction in the incidence of definite coronary heart disease events was observed in dyslipidemic men treated with gemfibrozil in the Helsinki Heart Study, a controlled 5-year, double-blind primary prevention trial for coronary heart disease. Over the entire study period, gemfibrozil therapy induced mean decreases of 10% in serum total cholesterol levels, 11% in low-density lipoprotein (LDL) cholesterol, 35% in triglyceride levels, and a mean increase of 11% in high-density lipoprotein (HDL) cholesterol level, compared with placebo. The differences in percentage changes in LDL cholesterol between gemfibrozil- and placebo-treated men varied among Fredrickson hyperlipoproteinemia types; after 1 year of treatment the difference was greatest for type IIA hyperlipoproteinemia (14 percentage units) and smallest for IIB hyperlipoproteinemia (3 percentage units). The treatment-associated changes in HDL cholesterol and triglycerides did not differ materially between the 3 hyperlipoproteinemia types, when calculated in the same way. The gemfibrozil-associated reduction in incidence of definite coronary events varied among Fredrickson types and among tertiles of baseline HDL cholesterol and triglycerides. The greatest rate reductions were seen in subjects with type IIB hyperlipoproteinemia, low initial HDL level or high initial triglycerides. These results suggest that subjects with low HDL cholesterol and type IIB hyperlipoproteinemia (and possibly type IV hyperlipoproteinemia) would benefit from treatment with gemfibrozil.

Adult↗
PubMed1989

Angiographic findings in patients exhibiting ischemia after oral dipyridamole.

We have assessed the angiographic features of a group of 37 patients given oral dipyridamole and 37 patients given matching placebo. Both groups represented severe coronary arterial disease and were studied prior to bypass surgery. Six patients (16%) had angina and 13 patients (35%) had electrocardiographic changes after dipyridamole. All the patients in the control group were nonresponders. In the group given dipyridamole the patients responding with angina had significantly more compromised collaterals than the patients without chest pain (P = 0.021). The same applied to the patients with electrocardiographic changes versus those with no electrocardiographic changes (P = 0.034). No differences between responders and nonresponders could be found in terms of the severity of coronary arterial disease, severity of anginal symptoms, exercise tolerance, antianginal medication, number of past myocardial infarctions, and left ventricular ejection fraction. In conclusion, the data strongly suggest that ischaemic responses to dipyridamole originate from myocardial steal accentuated by compromised flow in collateral vessels.

Administration, Oral↗