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Biomedical subjects

K Landmark

Publications and source records attributed to K Landmark.

At least 37 records · Page 2Linked to original sources
PubMed1997

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.

Aged↗
PubMed1996

[Can vitamin E prevent development of coronary heart disease?].

Oxidation of low-density lipoprotein (LDL) probably plays an important part in atherosclerosis. Vitamin E (alpha-tocopherol) is a potent antioxidant carried in LDL. It increases the resistance of LDL to oxidation, thereby, among other things, inhibiting foam cell formation and proliferation of smooth muscle cells. Some animal experiments have indicated that vitamin E retards the development of atherosclerotic lesions. Observational studies (case-control and cohort) have shown that long-term treatment with vitamin E is associated with lower incidence of coronary heart disease in men and women alike. Randomisation to vitamin E in a large placebo controlled trial gave a nonsignificant reduction in mortality from ischemic heart disease. Although vitamin E seems to reduce the risk of coronary heart disease, randomised trials of adequate size are necessary in both secondary and primary prevention in order to test this. Such trials are in progress.

Antioxidants↗
PubMed1995

[Cocaine abuse and acute heart disease].

Cocaine abuse is an increasing problem in western societies, and health personnel should be aware of the cardiovascular effects of cocaine, of which myocardial infarction is the most frequent reported complication. Cardiac arrhythmia is another serious complication. We describe a young female who, after injecting cocaine intravenously, suffered from circulatory collapse, thought to represent an arrhythmia. The authors discuss the pharmacological and clinical aspects of cocaine-induced myocardial infarction and arrhythmias, and suggest guidelines for treatment.

Adult↗
PubMed1995

[Magnesium therapy in acute myocardial infarction. New points of view].

In some smaller placebo-controlled, randomized studies, and in one larger such study (LIMIT-2, 2,136 patients), intravenous infusion of magnesium was shown to reduce early and late mortality of ischaemic heart disease in patients admitted with suspected acute myocardial infarction. In contrast, the ISIS-4 trial, which included 58,050 patients, did not show any benefit from magnesium. These discrepancies may be explained as follows; In LIMIT-2, magnesium was given early and before spontaneous or therapeutic thrombolysis (36% of the patients), in ISIS-4, however, the patients were likely to have undergone myocardial reperfusion in response to thrombolysis (70% of the patients) before receiving magnesium. Myocardial stunning may develop in association with reperfusion. Magnesium given before and during ischaemia attenuates postischaemic myocardial dysfunction. The absence of effect of magnesium in ISIS-4 is also thought to be related to the higher dose administered during the first 24 hours in this study. Early infusion of magnesium in acute myocardial infarction is a useful addition to standard therapy, and is simple, cheap and safe to administer.

Humans↗
PubMed1995

[The migraine remedy sumatriptan (Imigran) and coronary heart disease].

The new drug, sumatriptan, used to treat migraine, causes substernal tightness and severe angina-like pain in 3-21% of patients. Several reports have described sumatriptan-induced death, ventricular fibrillation, myocardial infarction, ischaemia and coronary vasospasm. We describe the case of a woman aged 40 years who suffered from bronchial asthma but was without known coronary heart disease. She experienced chest pain after intake of 100 mg sumatriptan orally. ECG was normal and there was no increase in coronary enzymes. Sumatriptan has a weak coronary constrictor effect. Endothelial dysfunction, with reduced release of vasodilating nitric oxide, may potentiate vasoconstriction induced by sumatriptan in the presence of thromboxane A2.

Adult↗
PubMed1995

Glyceroltrioleate/glyceroltrierucate therapy in 16 patients with X-chromosomal adrenoleukodystrophy/adrenomyeloneuropathy: effect on clinical, biochemical and neurophysiological parameters.

UNLABELLED: We have investigated the effect of glyceroltrioleate/glyceroltrierucate (GTO/GTE) therapy on X-chromosomal adrenoleukodystrophy in 16 patients with adrenoleukodystrophy (n = 6), adrenomyeloneuropathy (n = 3), Addison disease without neurological involvement (n = 2), and neurologically and endocrinologically asymptomatic patients (n = 5). Therapy was carried out for 19.4 +/- 10 months. All patients showed a normalization of C 26:0 plasma fatty acid concentrations. None of the seven neurologically asymptomatic patients developed neurological symptoms. Somatosensory evoked potentials of the tibialis nerve was the most sensitive electrophysiological parameter, showing a slight improvement in neurologically asymptomatic patients during therapy. In none of the patients with normal cranial MRI at start of therapy (n = 6) has MRI deterioration been observed whilst on therapy. Follow up of the neurologically asymptomatic children supports the hypothesis that GTO/GTE therapy might prevent the development of neurological symptoms. Six of the nine neurologically symptomatic patients deteriorated to varying degrees whilst on therapy. MRI alterations have worsened in all patients with clinical deterioration. CONCLUSION: GTO/GTE treatment should be initiated in all neurological asymptomatic boys before first neurological symptoms develop. To discover these patients very long-chain fatty acid determination should be performed in all family members at risk when adrenoleukodystrophy or adrenomyeloneuropathy is diagnosed.

Adolescent↗
PubMed1995

Nitrendipine and mefruside in elderly hypertensives: effects on blood pressure, cardiac output, cerebral blood flow and metabolic parameters.

In this multicentre, randomised, double-blind, cross-over study, we evaluated and compared the effects of nitrendipine (a calcium entry blocker of the dihydropyridine group) and mefruside (a diuretic) on BP, cardiac output, cerebral blood flow and metabolic parameters in 22 elderly hypertensives. Eight weeks of treatment with nitrendipine (27.3 mg daily) and mefruside (30.7 mg daily) significantly reduced BP values to almost the same extent. Heart rate, cardiac output (n = 14), cerebral blood flow (n = 20), renin activity and aldosterone remained unchanged during nitrendipine and mefruside treatment. Nitrendipine did not alter any metabolic parameter (electrolytes, lipid values and blood glucose); in patients treated with mefruside serum potassium fell by 0.4 mmol/l (P < 0.001). Minor adverse events were reported in both treatment groups, mostly due to vasodilation. We conclude that both drugs possess potent and comparable haemodynamic and anti-hypertensive properties. They reduce BP by reducing total peripheral vascular resistance with maintained autoregulation of cerebral blood flow. The metabolic disturbances induced by mefruside seem to be less pronounced than that observed with other thiazide diuretics.

Aged↗
PubMed1993

Serum magnesium and potassium in acute myocardial infarction: relationship to existing beta-blockade and infarct size.

Patients (n = 314) with acute myocardial infarction (AMI) were divided into three groups according to the time elapsed from onset of chest pain to when the first sample for determination of magnesium (s-Mg1) and potassium (s-K1) was drawn (A: hours 0-6; B: hours 6-10, and C: hours 10-24). Potassium and Mg were also measured in a second sample drawn three to twelve days (mean 6.3 days) later (s-Mg2, s-K2). Whereas s-Mg1 was lower than s-Mg2 in all three groups, s-K1 was reduced only in group A. Ten patients in group A receiving nonselective beta-blockers had an attenuated drop in s-Mg1, whereas the drop in s-K1 was completely inhibited. The differences between s-Mg2 and s-Mg1 (delta s-Mg) in all groups, and between s-K2 and s-K1 (delta s-K) in group A, increased with increasing mean peak creatine kinase (CKmax) levels to approximately 1300-1800 U/L. In conclusion, these observations suggest that the initial drop in s-Mg and s-K in the early phase of AMI is due to increased stimulation of beta 2-adrenergic receptors; these changes can be prevented partly or completely by the use of nonselective beta-blockers.

Adrenergic beta-Antagonists↗
PubMed1993

Effects of fish oil, nifedipine and their combination on blood pressure and lipids in primary hypertension.

In a double-blind, crossover, placebo-controlled study the effects of four weeks' treatment with 4.55 g/day of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on BP and serum lipids were assessed in 18 males with hypertension (WHO stage I-II). At the end of the double-blind phase, eight patients on placebo (olive oil) and ten patients on fish oil treatment were given nifedipine 20 mg twice daily added to their regimens for four weeks. Four weeks' fish oil treatment slightly reduced BP values; however, compared with placebo no changes were found. VLDL-cholesterol and triglycerides were significantly reduced by 24%, whereas total and LDL-cholesterol remained unchanged. Placebo did not change BP and lipid values. When nifedipine was added to fish oil/placebo, BP in the two groups was reduced to almost the same extent. When nifedipine was added to fish oil, total cholesterol was significantly reduced by 12% in comparison with baseline value and LDL-cholesterol was reduced by 15%, albeit insignificantly. Placebo plus nifedipine was lipid neutral. A significant correlation was found between the nifedipine-induced changes in supine mean arterial pressure and total, LDL- and VLDL-cholesterol, respectively, in those patients with and without fish oil treatment. In conclusion, the combined administration of fish oil and nifedipine possesses favourable antihypertensive and metabolic properties in hypertensive males with elevated lipid levels.

Adult↗
PubMed1992

[Magnesium therapy in acute myocardial infarction].

Several small, double-blind, randomized studies have shown that infusion of magnesium in patients with acute myocardial infarction reduces incidence of arrhythmias and mortality quite considerably. These beneficial effects are found in elderly patients too. Compared with placebo, magnesium infusion seems to increase myocardial salvage and protect against evolution of infarct. The mode of action of magnesium in reducing arrhythmias and mortality in acute myocardial infarction has not been clarified. Several factors may be involved. It has been shown that the antiarrhythmic effect of magnesium is related to a rapid rise in serum concentration. Magnesium possesses calcium-antagonistic properties, and reduces tone in smooth muscle cells. The use of magnesium decreases coronary artery spasm and total peripheral resistance, and increases cardiac output. Beneficial effects on blood platelets have also been reported. Magnesium therapy is cheap and easy to administer; contradictions include reduced renal function, disturbances in atrioventricular conduction and hypotension.

Arrhythmias, Cardiac↗
PubMed1992

Mononuclear cell magnesium and retention of magnesium after intravenous loading in patients with acute myocardial infarction.

A magnesium (Mg++) retention test was performed in 19 patients with acute myocardial infarction (AMI) 4-11 days after admission to the coronary care unit. The retention of Mg++ was 45 +/- 23% of the 30 mmol given intravenously. It has been proposed that a retention of more than 20% represents Mg++ deficiency. The mononuclear cell Mg++ concentration before the retention test was on an average slightly higher in the AMI patients than in 25 healthy volunteers (72.5 +/- 24.2 vs. 62.9 +/- 9.2 mumol g-1 protein) indicating no Mg++ depletion in the first group. The reason why patients during the phase of AMI show an increased retention of Mg++ is unknown, but changes in concentrations of several hormones and a reduction in blood glucose could be of importance. Serum concentrations of Mg++ were lower on admission than after 4-11 days. These initial reductions are probably due to increased concentrations of circulating catecholamines during the early hours of AMI.

Adult↗
PubMed1991

[Treatment of hypertension with the ACE inhibitor lisinopril. A multicenter study of patients with mild to moderate hypertension in general practice].

367 patients with mild-moderate hypertension were included in a multicentre study for the purpose of examining the antihypertensive effect of six weeks of treatment with the ACE-inhibitor lisinopril 10 and 20 mg once daily. Both low-dose and high-dose lisinopril significantly reduced sitting and standing blood pressure values. The fall in blood pressure in the sitting position was slightly but significantly greater among the high-dose group compared with the low-dose group (a 3 mm Hg fall difference in systolic values and a 1 mm Hg fall in diastolic values). No such differences were found in the standing position. Heart rate remained unchanged during lisinopril treatment. Episodes of possible first dose hypotension were reported in six patients. Approximately 90% of the patients in both groups were classified as responders according to defined criteria. The frequency of side-effects was low, and was equal in both treatment groups. An evaluation of reduction in blood pressure, and of response rate and side-effects suggests that an initial dose of 10 mg lisinopril once daily is sufficient, and that this dosage will control blood pressure in the majority of patients.

Adult↗