Use of fish oils appears to reduce infarct size as estimated from peak creatine kinase and lactate dehydrogenase activities.

In 753 patients with acute myocardial infarction, use of fish oils (FO, n = 242) before onset of infarction seemed to reduce infarct size as estimated from peak creatine kinase (CKmax) and lactate dehydrogenase (LDmax) activities. The study had an observational exposed/nonexposed design, and both crude and adjusted effects were looked for. CRUDE EFFECTS: In the restricted cohort of patients not receiving thrombolytic treatment (n = 411), FO reduced CKmax from 879 to 759 U/l (2 p = 0.030) and LDmax from 870 to 768 U/l (2 p = 0.011), respectively. More of these patients in the lowest enzyme quartiles used FO, p for linear trend was for CKmax 0.008 and for LDmax 0.06, respectively. ADJUSTED EFFECTS: In patients not receiving thrombolytic treatment, FO reduced CKmax (2 p = 0.007) and LDmax (2 p = 0.005), but in patients receiving such treatment, CKmax and LDmax values increased, 2 p being 0.036 and 0.097, respectively. In patients not receiving thrombolysis, FO increased the incidence of small infarcts (the 25% quartile), odds ratio for CKmax was 1.82 (2 p = 0.018) and for LDmax 1.66 (2 p = 0.048), respectively. The results indicate that FO may reduce infarct size and the incidence of large infarcts. In addition, FO seems to enhance the effect of thrombolysis.

Eating fish may reduce infarct size and the occurrence of Q wave infarcts.

OBJECTIVE: The present investigation was carried out to see whether intake of fish could influence infarct size as assessed by peak enzyme levels (CKmax and LDmax) as well as the occurrence of Q wave infarcts. DESIGN: The investigation was a prospectively planned cohort study. SETTING: The investigation was carried out at Ullevål University Hospital, Department of Cardiology and Department of Pharmacotherapeutics, University of Oslo, Oslo, and in four other Hospitals in Oslo and Lillehammer. SUBJECTS: Seven hundred and forty-five patients (median age 70 y, 64% males) admitted with proven acute myocardial infarction. RESULTS: Crude effects showed that the regression lines between the number of fish meals/week (FM/week) and CKmax in all patients and in the restricted cohorts of patients receiving/not receiving thrombolytic treatment were: y = 2086-157.x(2P = 0.004); y = 2807-156.x (2P = 0.110) and y = 1260-54.x (2P = 0.230); the corresponding results regarding LDmax were: y = 1329-76.x (2P = 0.009); y = 1556-73.x (2P = 0.120) and y = 1047-39 x (2P = 0.230). Odds ratio (OR) for developing Q wave infarcts in patients consuming > 1.0 FM/week was 0.52, 95% confidence interval (CI) 0.34-0.79; 2P = 0.001. For the adjusted effects, the coefficients of FM/week for log (peak enzyme levels) in all three groups of patients (all patients, and the restricted cohorts of patients receiving/not receiving thrombolytic treatment) were negative with 2P values of 0.014, 0.033 and 0.165 (CKmax), and 0.006, 0.033 and 0.158 (LDmax). OR for developing Q wave infarcts in patients consuming > 1.0 FM/week was 0.59, 95% CI 0.38-0.92; 2P = 0.022. CONCLUSIONS: The results indicate that consuming fish may reduce infarct size as assessed by CKmax and LDmax as well as the occurrence of Q wave infarcts.

Infarct size as estimated from peak creatine kinase and lactate dehydrogenase is probably reduced in patients using calcium antagonists at the onset of symptoms.

In animal models, calcium antagonists (Ca-A) administered before ischemia and reperfusion reduced myocardial necrosis, attenuated postischemic contractile dysfunction, and reduced tissue calcium. In 753 patients with acute myocardial infarction (AMI), we examined if use of Ca-A at the onset of symptoms (n = 127 patients) reduced infarct size as estimated from peak creatine kinase (CKmax) and lactate dehydrogenase (LDmax) activities. The study had an observational exposed/nonexposed design, and both crude and adjusted effects were investigated. Crude effects: In the restricted cohort of patients not receiving thrombolytic treatment (thr- pts; n = 411 patients), CKmax and LDmax were lower in Ca-A+ patients than in Ca-A- patients, being 643 versus 887 U/l (2 p = 0.004) and 708 versus 867 U/l (2 p = 0.005), respectively. When using log (CKmax) and log (LKmax) as outcomes, the same results were found (2 p = 0.002). More of the restricted cohort of the pts used Ca-A in the lower quartiles of CKmax and LDmax (p for linear trend = 0.005 and 0.004 for CKmax and LDmax, respectively). Adjusted effects: Thrombolysis was an effect modifier of the association between Ca-A and peak enzyme levels. In thr-pts, the coefficients of Ca-A were negative and borderline significant for log (CKmax; 2 p = 0.088) and negative and highly significant for log (LDmax; 2 p = 0.010) when adjusting for confounders. The present observational study indicates that the use of a Ca-A at the onset of AMI reduces infarct size, as estimated from CKmax and LDmax activities.

[Enzyme status in myocardial infarction]. / Enzymstatus ved hjerteinfarkt.

Less than 50% of the patients sent to hospital with suspected acute myocardial infarction do in fact suffer from myocardial necrosis. Changes in serum-enzyme levels are important findings when diagnosing acute myocardial infarction. Blood sampling frequency and which enzymes to measure are crucial for obtaining maximum information. We have studied different enzyme-regimes for the purpose of diagnosing acute myocardial infarction quickly and reliably. It is also necessary to consider consumption of resources. In our study, myoglobin was the best early parameter. The efficiency was only 66%, however, and the specificity was low. We therefore conclude that reliable early diagnosis of acute myocardial infarction based on serum-analyses is not yet possible. The best results were achieved using a strategy consisting of five blood samples (every eight hours during the first 24 hours and a final sample about 48 hours after hospitalisation). Changes in the activities of CK and LD in this period gave valuable information for the diagnosis, the size (measured as an increase in enzyme activity) of an eventual acute myocardial infarction, and the dynamic development of the disease. The sensitivity of the Nordic recommended regime, i.e. two samplings 10-20 hours after start of symptoms, was low (75%). The problem was estimating when the necrotic process had started.

Low and high risk coronary patients discriminated by blood platelet fatty acid composition.

The distribution of 11 long-chain fatty acids in platelet phospholipids were subjected to multivariate statistical analysis with groups of high and low risk coronary patients and controls. The alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) had significant explanatory power between the groups. As has been anticipated from studies in Eskimos, the EPA fraction was low in coronary patients. It was lower in high risk patients than in low risk patients, and lower in patients below rather than above, 60 years of age. Young high risk patients had 1.2 +/- 0.2% (Mean, SE) EPA against 1.8 +/- 0.2% in young controls, (p = 0.035). Old low risk patients had the highest EPA and also the highest DHA, 2.9 +/- 0.3% against 2.3 +/- 0.2% in controls. The ALA was low in low risk patients. Patients with low platelet EPA and high serum cholesterol should be included in trials with EPA rich diets.