Influence of dietary cod liver oil on fatty acid composition of plasma lipids in human male subjects after myocardial infarction.

A randomized crossover study was carried out to investigate the fatty acid profile and concentrations of plasma lipids in male patients with myocardial infarction (MI) who supplemented their diet with 20 ml cod liver oil daily for 6 weeks. Subjects were divided into two groups, A and B. Group A received cod liver oil daily for 6 weeks after hospital discharge, but none for the subsequent 6 weeks. Group B did not start taking cod liver oil until 6 weeks after hospital discharge, and they then took cod liver oil for 6 weeks. Diet, medication or smoking habits were kept as constant as possible during the study. During the period of cod liver oil intake, eicosapentaenoic acid (20:5 (n-3), EPA) and docosahexaenoic acid (22:6 (n-3), DHA) increased significantly in phospholipids (PL), triglycerides (TG) and cholesterol esters (CE), whereas linoleic acid (18:2 (n-6), LA), dihomo-gamma-linolenic acid (20:3 (n-6), DHGLA) and arachidonic acid (20:4 (n-6), AA) were significantly decreased in phospholipids. The plasma level of TG was significantly decreased during the cod liver oil intake. Total cholesterol, high density lipoprotein (HDL) cholesterol, and levels of apolipoproteins A1 and B were not affected by cod liver oil in these MI patients.

Cod liver oil does not reduce ventricular extrasystoles after myocardial infarction.

Previous work has shown that in experimental animal models a lower incidence of arrhythmias and sudden death was observed if the animals were fed cod liver oil or fish oil. After a 48-h control period starting, on average, 8 days after the onset of symptoms, 18 men who were recovering from acute myocardial infarction were given 20 ml d-1 cod liver oil for 6 weeks, either immediately after the control period, weeks 0-6 (n = 10), or during weeks 6-12 (n = 8). Forty-eight-hour Holter monitoring was carried out before cod liver oil administration and at the end of weeks 6 and 12. The eicosapentaenoic acid content of plasma phospholipids was increased by 230% during cod liver oil administration. However, no significant change was observed in the 24-h prevalence of ventricular extrasystoles or other arrhythmias during the study period. The mean ln number of ventricular extrasystoles was 2.95 +/- 0.51 (+/- SEM) during cod liver oil ingestion and 2.63 +/- 0.30 when not taking cod liver oil.

Additive effects of moderate dietary salt reduction and captopril in hypertension.

In a randomized, cross-over study 27 patients had diastolic blood pressure of greater than or equal to 96 mmHg during four visits without treatment. Following captopril 25 mg b.i.d. nine patients' blood pressure was less than or equal to 90 mmHg. The remaining 18 were randomized into two treatment modalities, captopril and moderate dietary salt reduction, and captopril and hydrochlorothiazide 25 mg daily. Following a wash-out period the groups crossed over to the alternative treatment. At the end of the control period the average blood pressure was 151/100 +/- 12/6 mmHg recumbent and 140/91 +/- 11/7 standing, following captopril 144/94 +/- 13/5 and 132/92 +/- 12/6, respectively, with low salt diet added to captopril 140/91 +/- 12/6 and 128/89 +/- 11/6 and with hydrochlorothiazide and captopril 133/86 +/- 12/7 and 120/84 +/- 11/7 mmHg supine and erect, respectively. It is concluded that moderate dietary salt reduction, which is easily advised, will significantly potentiate the blood pressure fall following captopril treatment in moderate arterial hypertension.

Ventricular dysrhythmias in middle-aged hypertensive men treated either with a diuretic agent or a beta-blocker.

The purpose of this study was to identify the frequency of cardiac dysrhythmias in two similar groups of hypertensive middle-aged males (age 45-66). They had previously been randomized either to a diuretic treatment (n = 42), or a beta-blocking agent (n = 41). A 24-hour ambulatory Holter monitoring, and serum potassium, was obtained in all patients, serum magnesium was measured in 35 patients. The mean number of ventricular premature beats (VPBs) and the frequency of complex arrhythmias (19 vs. 5) was significantly higher in the diuretic group (p less than 0.01). The serum potassium was significantly lower (p less than 0.001) in the diuretic group, and there was a significant (p less than 0.005) inverse correlation between the number of VPBs and the serum potassium in all treated patients. The patients with complex arrhythmias were older (p less than 0.01) than the remainder of the patients. No correlation between serum magnesium and VPBs or complex arrhythmias was found. This study demonstrates increased frequency of VPBs in older hypertensive males, treated with diuretics, and that hypokalaemia predisposes to increased cardiac arrhythmias. We conclude that in older mildly hypertensive men hypokalaemia should be avoided.

Hydrochlorothiazide and potassium chloride in comparison with hydrochlorothiazide and amiloride in the treatment of mild hypertension.

A randomized, double-blind, cross-over study comparing 50 mg hydrochlorothiazide plus 5 mg amiloride (HCTZ/A) with 50 mg hydrochlorothiazide plus 26 mmol potassium chloride (HCTZ/K) was conducted in 18 patients with mild essential hypertension (diastolic pressure 90-105 mmHg). The sequence of treatment was: placebo for 2 weeks, one active drug for 3 weeks, placebo for 2 weeks, the other active drug for 3 weeks. The two agents were significantly and equally efficacious in lowering the systolic and diastolic blood pressure. Baseline vs. treatment mean serum potassium levels were 3.82 vs. 3.78 mmol/l for HCTZ/A and 3.82 vs. 3.70 mmol/l for HCTZ/K. The decrease in serum potassium level from baseline was significant for both agents but not significantly different when the two treatment forms were compared. Both treatment forms elevated fasting serum cholesterol and glucose. Serum triglycerides and uric acid rose significantly with HCTZ/K. Amiloride may affect the tubular handling of uric acid causing increased uric acid excretion, thus counteracting thiazide-induced hyperuricemia. During 3 weeks' extension of the main study, 5 patients received HCTZ/A in double the original dose (100 mg/10 mg) and 6 patients received HCTZ/K in double the original dose (100 mg/52 mmol). No further blood pressure reduction was observed on treatment with these doses. The mean serum potassium levels did not decrease further on doubling the HCTZ/A dose, while a significant fall was observed for HCTZ/K (3.60 vs. 3.42 mmol/l) (p less than 0.05, single tailed t-test). Both drug combinations were well tolerated and side-effects were not significantly different from those during placebo administration. This study demonstrates that 50 mg hydrochlorothiazide plus 26 mmol potassium chloride are as effective as 50 mg hydrochlorothiazide plus 5 mg amiloride, both in reducing blood pressure and preventing hypokalaemia in the treatment of essential hypertension. A small extension study indicates that amiloride might be more effective than potassium chloride in preventing hypokalaemia when high doses (100 mg/day) of hydrochlorothiazide are administered.

Severe arterial hypertension (grade III and IV).

The aim of this study was to evaluate the number, outcome, survival time, and causes of death of patients with severe arterial hypertension who were admitted to the Department of Medicine at Landspitalinn (National Hospital) in Reykjavik during the years 1957 to 1971. During this period 117 patients were found to have severe arterial hypertension (12.6% of all cases of hypertension diagnosed) according to the grading of Keith and Wagener, 20 patients with grade IV retinopathy and 97 patients with grade III. The case histories were analysed according to age and sex distribution, blood urea, electrocardiographic changes, heart size by X-ray at the time of diagnosis and final outcome. The survival calculations were done by the decrement method (life tables) and aim taken from patient age 65 years and less. Relatively fewer patients with severe arterial hypertension were admitted during the last five year period (1967-1971) than during the two previous five year periods. The main causes of death were cerebrovascular accidents (26.6%), myocardial infarctions (22.8%), and renal failure (22.8%). Approximately 50% of the men and 60% of the women survived five years. Elevated blood urea values and signs of left ventricular hypertrophy on ECG at the time of diagnosis carried a more sinister prognosis.