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Objective - Heart rate variability (HRV) has been demonstrated to be a risk factor after acute myocardial infarction (AMI). In the present study serial measurement of SDNN (standard deviation of the mean of qualified NN-interval) in short intervals was used to assess HRV changes after AMI, and determine the role of these as independent risk factors compared to clinical, arrhythmic, ischemic and anamnestic variables. Measurements from a normal healthy middle-aged male population were used as reference (n = 63). Methods - SDNN from a five-minute period during day and night-time, respectively, was examined in 103 patients 1 week (n = 54), 1 month (n = 72) and 12-16 months (n = 54) after infarction. Results - Day SDNN did not change during one-and-a-half years after AMI, and was significantly reduced compared with healthy males. Night SDNN, low after 1 week, with recovery 1 month after AMI, was significantly reduced compared with healthy males early, but not late after AMI. Thus, the study indicated during day-time a continuous abnormal sympathetic preponderance in the course of 16 months after AMI, and during night-time a gradual recovery of parasympathetic preponderance beginning early after AMI. Conclusion - One week after AMI day-time SDNN of <30 ms, and night-time SDNN of <18 ms, age ≥60 years, and myocardial ischemia (Holter monitoring) were independent predictors of 9 years' mortality. One and 12-16 months after AMI reduced day and night-time SDNN had no prognostic implication. [ABSTRACT FROM AUTHOR]

An elevated urinary albumin excretion (UAE) in non-diabetic subjects without renal or cardiovascular disease has been shown to be predictive of ischaemic heart disease. An insertion (I)/deletion (D) polymorphism in the angiotensin I-converting enzyme (ACE) gene has been identified and the D allele may be associated with cardiovascular disease. The aim of this study was to find a potential linkage between this polymorphism and elevated UAE. For studies of UAE and cardiovascular pathophysiology, a highly selected population sample has been identified comprising all clinically healthy subjects aged 40-65 years with elevated UAE in a dipstick negative urinary sample (n = 27) from The Copenhagen City Heart Study. Neither the ACE genotype distribution (p = 0.12) nor the D and I allele frequencies (p = 0.69) differed significantly between subjects with elevated UAE and a matched normoalbuminuric control group (n = 46). Elevated UAE in clinically healthy subjects is not linked to the ACE gene polymorphism. [ABSTRACT FROM AUTHOR]

Microalbuminuria, a subclinical rise in the urinary albumin excretion, is a risk indicator of atherosclerotic cardiovascular disease. The aim of this study was to measure the urinary albumin excretion in patients with acute myocardial infarction, and to correlate this with known atherosclerotic risk factors. One-hundred-and-twenty-six patients and 56 healthy controls matched for age and sex were studied. The albumin/creatinine concentration ratio in morning urine specimens was calculated as an index of the albumin excretion. Microalbuminuria was defined as a urinary albumin/creatinine concentration ratio above 1 mg/mmol. Urinary albumin excretion (0.88 [95% confidence interval 0.69-1.11] versus 0.51 [0.40-0.63] mg/mmol; p = 0.001) and frequency of microalbuminuria (33 [95% confidence interval 25-41] versus 16 [9-23]%; p = 0.03) were higher in patients than controls. This difference was independent of blood pressure, body weight, smoking, diabetes mellitus, renal disease, and thrombolytic treatment. There was a positive correlation between urinary albumin excretion and thickness of the left ventricle wall (R = 0.28; p = 0.001) which was independent of blood pressure. Follow-up examination of the patients will reveal whether microalbuminuria increases the risk for recurrence of acute myocardial infarction. [ABSTRACT FROM AUTHOR]