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Biomedical subjects

K Landmark

Publications and source records attributed to K Landmark.

At least 55 records · Page 3Linked to original sources
PubMed1986

Hypertrophic cardiomyopathy.

Hypertrophic cardiomyopathy is characterized by a hypertrophic and non-dilated left ventricle with disproportionate involvement of the intraventricular septum compared to the free walls, and by varying degrees of outflow obstruction during systole. Its symptoms and clinical course, pathogenesis and treatment are briefly discussed. It is speculated whether hypertrophic cardiomyopathy and hypertension are both caused by systemic disorders of calcium channels and calcium uptake and binding by cardiac and smooth muscle membranes, respectively.

Animals↗
PubMed1985

Antihypertensive, haemodynamic and metabolic effects of nifedipine slow-release tablets in elderly patients.

In a double-blind, cross-over study for 8 weeks, including 10 non-hospitalized elderly hypertensives (average age 73.2 years), WHO stage I-II, the antihypertensive effect of nifedipine slow-release tablets, 20 mg twice daily, was compared with placebo. Nifedipine reduced supine and standing blood pressure values significantly, and no signs of orthostatic hypotension were noted. An initial increment in heart rate was found after 1 week with a subsequent fall towards control values after 8 weeks of nifedipine administration. Heart rate pressure product in the supine position was reduced, and this reduction became statistically significant at the 8th week. Cardiac output measured non-invasively in 8 patients after 6-8 weeks' nifedipine therapy, using an Irex echocardiograph, was on an average 34% higher than in the placebo period (p less than 0.05). Serum electrolytes, cholesterol, HDL cholesterol, blood glucose and renal function were not affected by the drug. Side-effects were few and mild. It is concluded that nifedipine is a potent antihypertensive agent which may represent an attractive first choice alternative in the treatment of elderly hypertensive patients.

Aged↗
PubMed1984

Evolution of infarct size during the early use of nifedipine in patients with acute myocardial infarction: the Norwegian Nifedipine Multicenter Trial.

In a multicenter double-blind study, 227 patients with suspected acute myocardial infarction (AMI) were randomized within 12 hr from onset of symptoms to treatment with nifedipine (112 patients) or placebo (115 patients). AMI was confirmed in 74 patients on nifedipine and in 83 on placebo. Patients with AMI received nifedipine 5.5 +/- 2.9 hr (mean +/- SD) after onset of symptoms. Infarct size was assessed by the release of creatine kinase isoenzyme MB (CK-MB). Infarct size index (CK-MB geq/m2) was 25 +/- 16 (n = 71) in the nifedipine group and 23 +/- 13 (n = 77) in the placebo group (NS). After the first 10 mg of nifedipine systolic blood pressure fell from 147 +/- 30 to 135 +/- 28 mm Hg (p less than .01) and heart rate rose from 75 +/- 18 to 79 +/- 19 beats/min (p less than .01). No change was observed after the first placebo dose. The treatment was continued for 6 weeks. Over this period there were 10 deaths in each group. Early treatment with nifedipine in patients with AMI does not seem to reduce infarct size as determined by enzyme level.

Adult↗
PubMed1983

The acute effects of nifedipine on calf and forefoot blood flow in patients with peripheral arterial insufficiency.

The calcium-blocking agent nifedipine, which possesses vasodilating potency, was tested in 8 patients with peripheral arterial insufficiency. 10 mg sublingually significantly decreased systolic arm and ankle blood pressure. Neither blood flow nor local peripheral resistance in the calf and the forefoot at rest and the calf during postischemic reactive hyperemia changed significantly. During postischemic hyperemia in the forefoot, the drug significantly reduced peak blood flow and increased local peripheral resistance. The drug-induced reduction in forefoot peak blood flow was correlated to the fall in systolic arm and ankle blood pressure. It is suggested that nifedipine may shorten the claudication distance in patients with peripheral arterial insufficiency.

Arterial Occlusive Diseases↗
PubMed1982

Plasma levels and cardiac electrophysiological effects of melperone in the dog.

The butyrophenone neuroleptic melperone has recently been shown to possess antiarrhythmic properties in man and animals. We studied the correlation between plasma concentration of melperone and the electrophysiological and blood pressure effects of the drug in 20 pentobarbital-anaesthetized dogs. Linear correlations were found between the log melperone plasma concentration and decreases in mean aortic blood pressure and heart rate, and increases in atrial and AV nodal refractoriness. The correlations were better after pretreatment with the beta 1-blocker atenolol. There was a linear correlation between log melperone plasma concentration and increases in ventricular refractoriness only after atenolol. No correlation was found between log melperone plasma concentration and decreases in AV nodal conduction time. Apart from the effect on AV nodal conduction time, the relationship between plasma concentration of melperone and the electrophysiological and blood pressure effects after beta 1-blockade fits well into an overall log concentration-effect relationship. The poorer correlation without beta 1-blockade was probably due to a combination of direct and indirect effects of the drug.

Animals↗
PubMed1982

The mode of antiarrhythmic action of melperone.

We studied the mode of antiarrhythmic action of melperone by His bundle electrography combined with programmed electrical stimulation in 21 pentobarbital anaesthetized dogs. Melperone alone (0.5 to 12.5 mg/kg) as well as melperone after sympathetic and parasympathetic blockade caused a dose-dependent increase in the ventricular and, even more, the atrial effective refractory period without affecting atrial and ventricular conduction times. Melperone shortened the atrioventricular nodal conduction time regardless of sympathetic and parasympathetic blockade. We conclude that the antiarrhythmic effect of melperone in most likely primarily due to a direct class III antiarrhythmic action.

Action Potentials↗
PubMed1982

Haemodynamic effects of nifedipine and propranolol in patients with hypertrophic obstructive cardiomyopathy.

The haemodynamic effects of nifedipine, propranolol, and the combined administration of the two drugs were studied in 12 patients with hypertrophic obstructive cardiomyopathy. The combined administration of nifedipine and propranolol appeared to be superior to that of nifedipine alone. The spontaneous heart rate was reduced in most cases after nifedipine plus propranolol, and at atrial pacing the following results were obtained: left ventricular peak systolic pressure was reduced from 200 +/- 39 to 157 +/- 30 mmHg; a positive correlation was found between the pre-drug left ventricular end-diastolic pressure and the magnitude of reduction in left ventricular end-diastolic pressure; systolic blood pressure was reduced from 125 +/- 31 to 111 +/- 27 mmHg, and total peripheral resistance was reduced from 1403 +/- 307 to 1160 +/- 209 dyne s-1 cm-5. The combined administration reduced the resting left ventricular outflow gradient from 76 +/- 19 to 45 +/- 26 mmHg, while cardiac index was left unchanged. The effects on mean pulmonary arteriolar resistance and mean pulmonary arteriolar resistance and mean pulmonary capillary venous pressure were in most cases slight and insignificant. The results indicate an improved haemodynamic condition in patients with hypertrophic obstructive cardiomyopathy after the combined administration of nifedipine and propranolol: a treatment that might provide a new and useful alternative to already existing medication.

Adult↗
PubMed1981

Pharmacokinetics of disopyramide in patients with imminent to moderate cardiac failure.

The parmacokinetics of disopyramide (DP) in 10 patients with imminent to moderate cardiac failure has been studied and compared with the results in normal volunteers. The biological half life of rapid distribution (T1/2 alpha) and of elimination (T1/2 beta) were increased (11.1 +/- 4.4 min and 9.7 +/- 4.2 h, respectively). Total body clearance (Clt) was decreased (0.467 +/- 0.215 ml . min-1 . kg-1), and the volume of distribution (Vd) was slightly reduced (0.610 +/- 0.1361 . kg-1), probably due to the lower cardiac index. After oral administration, the time of peak serum concentration was increased (139 +/- 89 min), and the mean peak serum concentration (2.4 +/- 0.8% dose . 1-1) was also higher than reported in normal subjects. Comparison of the areas under the concentration versus time curves after intravenous and oral administration (AUC i. v. and AUC oral) showed that DP was almost completely absorbed, its bioavailability being 97.5 +/- 15.0%.

Administration, Oral↗
PubMed1981

Electrophysiological effects of melperone in the dog heart in situ - a new antiarrhythmic drug.

In pentobarbital anaesthetised dogs, melperone (a neuroleptic butyrophenone) reduced mean aortic blood pressure and at lower doses (0.5 and 2.5 mg . kg-1) increased the heart rate. By means of His bundle electrography and programmed electrical stimulation, conduction velocity and refractoriness were measured at different frequencies of stimulation (170, 200, 230 and 260 beats.min-1). Melperone 0.5 and 2.5 mg.kg-1 decreased the atrioventricular nodal conduction time and refractoriness. Melperone (0.5 to 12.5 mg.kg-1) did not affect the intra-atrial or His-Purkinje conduction times or the QRS width. However, melperone increased the functional and effective refractory period of the right atrium and ventricle dose-dependently at all frequencies studied. This suggests that melperone may be a valuable drug in treating selected cardiac arrhythmias.

Animals↗
PubMed1981

Influence of beta-adrenergic and cholinergic blockade on the electrophysiological effects of melperone in the dog heart in situ.

Melperone (0.5 to 12.5 mg.kg-1) reduced mean aortic blood pressure in pentobarbital anaesthetised dogs to a greater extent after beta1-adrenergic receptor blockade with atenolol than after cholinergic blockade with atropine. Electrophysiological studies demonstrated that increased heart rate and decreased atrioventricular nodal refractoriness after lower doses of melperone (0.5 to 2.5 mg.kg-1), could be prevented by pretreatment with atenolol. The melperone-induced decrease in atrioventricular nodal conduction time was, however, not affected by pretreatment with atenolol or atropine. Intra-atrial and His-Purkinje conduction times and QRS width were not affected by atenolol or atropine plus melperone. Melperone caused a dose-dependent and very pronounced increase in ventricular and, even more, atrial refractoriness after atenolol. The ventricular and atrial refractoriness increased less after pretreatment with atropine. Some of the cardiac electrophysiological effects of melperone thus depend on the degree of beta-adrenergic stimulation. The overall cardiac electrophysiological effects of melperone results from a combination of direct and indirect actions of the drug.

Animals↗