Effect of apo E phenotype on plasma postprandial triglyceride levels in young male adults with and without a familial history of myocardial infarction: the EARS II study. European Atherosclerosis Research Study.

The goal of the present study was to assess whether the effect of the apolipoprotein E polymorphism on postprandial lipemia explained part of the risk attributable to familial history of coronary heart disease. Cases (n = 407) were students, aged between 18 and 28 years, whose fathers had a proven myocardial infarction before the age of 55 years. Age-matched controls (n = 415) were recruited from the corresponding student registers. Blood was obtained after an overnight fast and at 2, 3, 4 and 6 h after ingestion of a fatty meal for triglyceride measurements. Apolipoprotein E phenotype was associated with postprandial triglyceride variability in both cases and controls. However, the apolipoprotein E-dependent triglyceride response was not significantly heterogeneous between cases and controls. In the pooled data, postprandial triglyceride levels were higher in carriers of the E2 and, to a lesser extent, of the E4 isoform, than in E3/3 homozygotes, independently of fasting triglyceride levels. At 6 h, triglyceride levels were increased by 21.2% (P < 0.01) in E2 carriers and 11.5% (P = 0.053) in E4 carriers by comparison to E3/3 subjects. These effects were not significantly different between regions. In conclusion, the effects of the apolipoprotein E polymorphism on postprandial triglyceridemia are similar across regions of Europe, and homogeneous in healthy young subjects with and without a family history of early myocardial infarction. This suggests that the influence of apolipoprotein E on myocardial infarction risk may be acting through mechanisms other than through effects on postprandial triglyceridemia.

High incidence of dyslipidaemia in the offspring of Greek men with premature coronary artery disease.

AIM: The present study aimed to assess the incidence and type of lipid disorders in the offspring of young Greek coronary patients. METHODS: One hundred and ninety-three children and youngsters were divided into two groups. Group A consisted of 104 children whose fathers had sustained a myocardial infarction before the age of 55 years. Eighty-nine young subjects matched for age, gender, dietary and smoking habits without a familial history of coronary artery disease served as controls (group B). Total cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein cholesterol and lipoprotein(a) were measured in the children and the affected fathers. RESULTS: Fifty-three percent of the offspring of young coronary patients had elevated total cholesterol or elevated triglycerides or decreased high density lipoprotein cholesterol or a combination, while the 80.4% of the affected fathers had lipid disorders. The distribution of lipid disorders in the children bore a striking resemblance to those seen in their affected fathers and there was a significant correlation between offspring-father total cholesterol, low density lipoprotein cholesterol and lipoprotein(a). When excess lipoprotein(a) was added to the lipid disorders the incidence of dyslipidaemia in the offspring of the affected individuals was increased to 63.5%. CONCLUSIONS: Dyslipidaemia is very common in the offspring of Greek men with premature coronary artery disease; this occurrence emphasizes the need always to evaluate the lipid profile in these children. The detection of dyslipidaemia necessitates the early institution of preventive measures with the expectation that the incidence of cardiovascular disease will decrease later in life.

Plasminogen activator inhibitor 1 is elevated in the children of men with premature myocardial infarction.

To assess whether plasminogen activator inhibitor 1 (PAI-1) activity is elevated in the progeny of young coronary men, 193 young subjects were recruited and divided into two groups. Group A consisted of 104 children whose fathers had suffered a myocardial infarction before the age of 55 ("cases"). Eighty-nine young subjects matched for age, sex, body mass index (BMI) and smoking habits without familial history of coronary artery disease (CAD) served as controls (group B). Children with a family history of diabetes mellitus or hypertension were excluded from both groups. We measured PAI-1 activity, tissue-type plasminogen activator (t-PA) antigen, a2-antiplasmin, fibrinogen, lipids and apolipoproteins in both groups. PAI-1 activity levels were also determined in the men who suffered a premature myocardial infarction 4 months after their discharge. PAI-1 activity levels were higher in cases compared to controls (3.13 +/- 1.9 vs 2.17 +/- 1.9 U/ml, p = 0.0014). t-PA antigen and a2-antiplasmin did not differ significantly between the two groups, while fibrinogen, total cholesterol, low-density lipoprotein cholesterol, apolipoprotein B and lipoprotein(a) were significantly higher in group A. PAI-1 was positively correlated with triglycerides (r = 0.22, p = 0.024), apolipoprotein B (r = 0.21, p = 0.039) and fibrinogen (r = 0.22, p = 0.029) in cases and with BMI in both cases (r = 0.37, p = 0.0003) and controls (r = 0.23, p = 0.044). In stepwise multiple regression analysis, only apolipoprotein B (p = 0.008) and BMI (p = 0.0014) were significant determinants of PAI-1 activity in cases. There was also a positive correlation between PAI-1 activity levels of the affected fathers and their children (r = 0.30, p = 0.01). The present data support the hypothesis that elevated PAI-1 levels in the offspring of men with premature myocardial infarction impair their fibrinolytic capacity contributing to their familial predisposition to CAD.

Fibrinogen in the offspring of men with premature coronary artery disease.

We examined whether the levels of fibrinogen are elevated in the offspring of middle-aged coronary patients. One hundred and seventy-six young subjects were divided into two groups. Group A consisted of 100 children and youngsters (mean age 17 +/- 6 years) whose fathers had sustained a myocardial infarction under the age 55 years without associated history of diabetes mellitus or hypertension. Seventy-six healthy young subjects (mean age 18 +/- 5 years) matched for gender, dietary and smoking habits without familial history of coronary artery disease, diabetes mellitus or hypertension served as the control group (group B). Fibrinogen, total cholesterol, triglycerides, high and low density lipoprotein cholesterol, apolipoprotein A-1, apolipoprotein B and lipoprotein (a) were measured. Sons and daughters with a history of premature paternal myocardial infarction had higher levels of fibrinogen compared with control subjects (304.1 +/- 60 vs 274 +/- 53 mg. dl-1, P < 0.001). This difference was maintained when the above groups were divided into single sex groups. Total cholesterol, low density lipoprotein cholesterol, apolipoprotein B and lipoprotein (a) were also significantly higher in group A. Children of affected individuals who had a good lipid profile also had significantly higher fibrinogen levels compared to control group. The results support the hypothesis that the higher plasma levels of fibrinogen in the offspring of middle-aged coronary men could partially explain their predisposition for coronary artery disease. Since the levels of fibrinogen have a major genetic component, they could be a useful marker in identifying children at high risk for coronary artery disease, especially among those with no lipid abnormalities.

Recurrent atrial flutter in apical hypertrophic cardiomyopathy.

Palpitations are a symptom often reported by patients with apical hypertrophic cardiomyopathy (HCM), yet the arrhythmias associated with this type of HCM have not been studied adequately. Herein, a case of persistently recurrent atrial flutter in a 63-year-old Greek man with apical HCM is presented. Synchronized direct-current shocks were used twice during his hospitalization in order to convert atrial flutter to sinus rhythm. No definite precipitating factor for the induction of atrial flutter was identified.

Early detection of silent ischemia after bypass grafting.

Silent ischemia (SI) is one of the predictable factors for crises after coronary artery bypass grafting. During the last six months 31 consecutive patients (range of age fifty-one to seventy-one years) underwent twenty-four-hour electrocardiographic monitoring (Holter) in the second postoperative week under ambulatory hospital conditions (total time 750 hours). The patients were investigated by two-channel ST segment Holter (CM1CM5). The results of the analysis were controlled by two independent observers. Criteria for SI were horizontal or downslope ST depression greater than or equal to 1 mm greater than or equal to 1 minute. Five patients (16%) underwent two to eight SI crises/twenty-four hours (mean 4.3).

Q- versus non-Q-wave myocardial infarction: clinical characteristics and 6-month prognosis.

A prospective study of 208 consecutive survivors of acute myocardial infarction was undertaken to determine the differences between Q- and non-Q-wave infarction, concerning data from the history, clinical course, and 6-month follow-up. There were 177 patients with Q-wave infarction and 31 patients with non-Q-wave infarction. There were no significant differences for the following variables: age, sex, diabetes mellitus, smoking, positive family history, hypertension, obesity, previous infarction, history of unstable angina, heart failure or chronic obstructive pulmonary disease (COPD), Killip class in the Coronary Care Unit (CCU), arrhythmias and conduction defects in the CCU as well as drugs used. Patients with non-Q wave infarction had a higher incidence of stable angina before the myocardial infarction and a lower value of creatine kinase (CK) and serum glutamic oxalacetic transferase (SGOT). During the 6-month follow-up, 9 cardiac deaths and 17 reinfarctions occurred, while 74 patients presented angina. There were no differences between the two groups concerning the incidence of cardiac death or angina, but patients with non-Q-wave infarction had a higher incidence of reinfarction at 6 months (p less than 0.001). We conclude that although patients with non-Q-wave myocardial infarction have a lesser degree of myocardial damage, they have a high incidence of early reinfarction which puts them in a high-risk group.

Extent of the inferior myocardial infarction assessed by the frontal plane of the vectorcardiogram.

A correlation was made between the vectorcardiographic changes and the peak value of the L.D.H. in the serum of 21 patients with acute inferior (diafragmatic) M.I. The following vectorcardiographic variables showed changes proportional to the increase in serum L.D.H. The correlation was found to be statistically significant. The direction of the 0.025 sec vector (r = 0.63, P less than 0.005). The duration of the initial superior forces of the QRS loop (r = 0.87, P less than 0.001). The maximal leftward deviation of the initial superior QRS loop forces (r = 0.65, P less than 0.005). The maximal superior deviation of the initial QRS loop forces (r = 0.68, P less than 0.05). The ratio of the maximal superior deviation over the maximal inferior deviation of the QRS loop "QY/RY" (r = 0.76, P less than 0.001). The area under the initial superior forces of the QRS loop and over 0 degrees +/- 180 degrees axis in squared milimeters (r = 0.88, P less than 0.001). It is suggested that V.C.G. is a usefull means in assessing the extent of inferior M.I.