In a controlled study comprising 176 patients, quinidine in the form of Kinidin Durules was found to reduced significantly the recurrence of the atrial fibrillation during a 1-year follow-up period after successful electric shock conversion. After one year, 51 per cent (52/101) of the patients in the quinidine group, and 28 per cent (21/75) in the control group remained in sinus rhythm (P smaller than 0.001). No less than 43 per cent of the patients converted to sinus rhythm during treatment with maintenance doses of quinidine sulphate before intended DC conversion. Gastrointestinal side-effects were not uncommon, and caused interruption of quinidine treatment in some cases.

The aim of this study was to test the question of hyperhomocyst(e)inaemia as a risk factor for intermittent claudication (IC) independent of other important risk factors for peripheral atherosclerotic disease, such as smoking, hypertension, diabetes mellitus, hypercholesterolaemia, hypertriglyceridaemia, low levels of high-density-lipoprotein (HLD) cholesterol and age. The study population was recruited from an epidemiological study in Linköping County, Sweden, where all middle-aged men (n = 15,253, 45-69 years of age) were screened for IC. Seventy-eight subjects with verified IC and 98 healthy sex- and age-matched controls were randomly selected. Plasma levels of homocyst(e)ine (including the sum of free and bound forms of homocysteine and their disulphide oxidation products, homocystine, and homocysteine-cysteine mixed disulphide) were significantly higher (16.74 +/- 5.45 mumol l-1, mean value +/- SD, P = 0.0002) in IC subjects than in controls (13.80 +/- 3.21 mumol l-1), with 23% of the claudicants above the 95th percentile for controls. Stepwise logistic regression analysis revealed that the difference in plasma homocyst(e)ine was independent of the other above-mentioned risk factors. Moreover, the elevation of plasma homocyst(e)ine in claudicants was mainly confined to subjects with serum folate levels of less than or equal to 11.0 nmol l-1. The results suggest that folic acid supplementation should be tried in IC subjects with hyperhomocyst(e)inaemia.

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Objectives. To examine the relation between left ventricular (LV) diastolic function and glucose metabolism in individuals without previously diagnosed diabetes mellitus. Design. A cross-sectional population-based study. Setting. A university hospital. Subjects. Thirty-five men and women 56-58 years of age without previously diagnosed diabetes or heart disease. Main outcome measures. Left ventricular diastolic function assessed by pulsed Doppler tissue imaging and its relation to fasting plasma glucose, glucose postload and glycated haemoglobin. LV diastolic function was determined by measuring early diastolic filling peak velocity (E m wave cm s )1 ), late diastolic filling peak velocity (A m wave cm s )1 ) and their ratio E m /A m . Results. Peak E m velocity, peak A m velocity and their ratio E m /A m correlated with fasting plasma glucose (r ¼ -0.42, P ¼ 0.01; r ¼ 0.47, P ¼ 0.04 and r ¼ )0.53, P ¼ 0.001, respectively). There was a correlation between peak E m velocity, the ratio of E m /A m and glycated haemoglobin. LV diastolic function was also related to glucose postload. Conclusions. Left ventricular diastolic function is related to concentrations of fasting plasma glucose, glucose postload and glycated haemoglobin even below the threshold of diabetes. This indicates that glucose concentrations already in the upper end of the normal range has negative impact on cardiac function.

The effect of 24 weeks of treatment with simvastatin, a new HMG coenzyme A reductase inhibitor (dosages of 20 and 40 mg day-1) on serum lipid, lipoprotein and apolipoprotein A-I and B concentrations as well as safety parameters and subjective side effects were studied in 11 patients with familial (FH) and 10 patients with polygenic hypercholesterolaemia (P-HC). The effects on plasma lipoprotein and apolipoprotein concentrations had already been achieved after four weeks in both groups and then remained during the study. In FH, mean fasting plasma total cholesterol concentration decreased from 10.51 to 6.71 mmol l-1 (36%), and in P-HC from 6.55 to 4.54 mmol l-1 (31%) at 24 weeks (P less than 0.001). Mean plasma low density lipoprotein (LDL) cholesterol concentrations also decreased, in FH from 8.87 to 5.05 mmol l-1 (43%) and in P-HC from 4.97 to 3.12 mmol l-1 (37%) at 24 weeks (P less than 0.001). Furthermore, apolipoprotein B concentrations decreased significantly from 2.21 to 1.57 g l-1 (29%) (less than 0.001) in FH and from 1.53 to 1.09 g l-1 (29%) (P less than 0.01) in P-HC. Plasma high density lipoprotein (HDL) cholesterol increased in both FH and P-HC during treatment. Increases were seen in both the subfractions HDL2 and HDL3. Simvastatin was well tolerated. No serious clinical or laboratory adverse effects were observed. It is concluded that 24 weeks of treatment with simvastatin in doses up to 40 mg day-1 effectively reduces plasma total and LDL cholesterol concentrations without causing subjective or significant objective side effects. Thus, simvastatin may be of great interest in future studies for prevention of coronary heart disease due to hypercholesterolaemia.