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O Hendriksen

Publications and source records attributed to O Hendriksen.

2 recordsLinked to original sources

Left atrial distension and antiorthostatic decrease in arterial pressure and heart rate in humans.

It was investigated to what degree left atrial distension augments the hypotensive effects of a 15-min moderate antiorthostatic maneuver in humans. Ten healthy males underwent a posture change from upright seated (Seat, legs horizontal) to supine (Sup) or to supine with simultaneous lower body negative pressure (Sup + LBNP) to keep left atrial diameter (LAD) unchanged. After 2.5 min of Sup, mean arterial pressure (MAP) decreased from 94 +/- 3 to 86 +/- 3 mmHg (P < 0.05), whereas a similar decrease was delayed 7.5 min into Sup + LBNP. Heart rate (HR) decreased within 2.5 min of Sup from 68 +/- 2 to 60 +/- 3 beats/min (P < 0.05) and remained significantly decreased for at least 2.5 min longer than during Sup + LBNP. Aortic systolic distension (ASD) increased by 59 +/- 17% during Sup (P < 0.05) but was unchanged during Sup + LBNP. The 29 +/- 4% decrease in plasma norepinephrine (NE) during Sup (P < 0.05) was abolished during Sup + LBNP. In conclusion, the increases in LAD and ASD seem important stimuli for the prompt decrease in MAP, the 2.5-min longer-lasting decrease in HR, and the sustained decrease in NE during a 15-min moderate antiorthostatic posture change in humans.

Adult

[Embolic episodes after treatment of atrial fibrillation in a patient with thyrotoxicosis].

Thyrotoxic artrial fibrillation is well known and occurs in 10-30% of all patients with thyrotoxicosis. The risk of systemic embolism has been found to be 10-40% in patients with thyrotoxic atrial fibrillation. We present a case of 53 year-old man, a healthy and active athlete, with atrial fibrillation and thyrotoxicosis. He was treated with a beta-blocking agent (sotalol) and sent home. Seven days later, he suffered systemic arterial emboli, one in the right arm and one in the left leg. After embolectomy the patient started anticoagulation and no further complications occurred. Previous studies are discussed, and the following conclusions made. When taken together the data suggest that the rate of embolism in patients with thyrotoxic atrial fibrillation exceeds that of non-thyrotoxic atrial fibrillation unassociated with rheumatic heart disease. The majority of clinically evident embolic events that occur in patients with thyrotoxic atrial fibrillation involve the central nervous system. The rate of embolic events appears to be greatest early in the course of thyrotoxic atrial fibrillation, but may persist for some weeks after conversion and may be particularly high in patients with associated heart failure. It is suggested that anticoagulation therapy should be considered in these patients.

Anticoagulants