[Full working capacity instead of threatened retirement. Thrombendarterectomy in chronic thromboembolic pulmonary hypertension]. / Volle Arbeitsfähigkeit statt drohender Berentung. Thrombendarterektomie bei chronischer thromboembolischer pulmonaler Hypertonie.

HISTORY AND CLINICAL FINDINGS: A 56-year-old man in marked right heart failure (stage III-IV of the New York Heart Association classification) and severe pulmonary hypertension was admitted to a rehabilitation clinic for therapeutic and social-medical assessment. On physical examination the important features were markedly distended neck veins, tachycardia at rest (90/min), a loud 2nd pulmonary sound and dyspnea. INVESTIGATIONS AND DIAGNOSIS: Non-invasive tests (ECG, echocardiography, abdominal ultrasound and lung functions) confirmed right heart failure; invasively obtained haemodynamic data indicated its severity. Selective pulmonary angiography defined the embolisation to be central and bilateral. TREATMENT AND COURSE: As intensive drug treatment and physiotherapy had failed to achieve significant improvement, operative removal of the bilateral central and some segmental pulmonary thrombi was performed and an inferior vena caval filter inserted. Immediately after operation the markedly elevated right-heart and pulmonary artery pressures fell markedly and there was dramatic improvement in the patient's general condition and in his physical capacity. Angiography demonstrated largely normal pulmonary perfusion. Instead of the anticipated retirement, the patient was discharged on anticoagulants, in the expectation of a return to full-time work. CONCLUSION: With pulmonary thrombendarterectomy severe chronic thromboembolic pulmonary hypertension may well be treated.

Increased number of high sensitive platelets in hypercholesterolemia, cardiovascular diseases, and after incubation with cholesterol.

The number of low density platelets was found to be increased in patients with hypercholesterolemia, as compared with the number in controls. The percentage increase of the low density platelet subpopulation was even more pronounced in patients with hypercholesterolemia when compared with that in patients suffering from myocardial infarction or angina. In vitro studies with control platelets incubated with cholesterol rich liposomes showed also an increase in the subpopulation of low density platelets. After incubation of control platelets with cholesterol rich liposomes, a higher membrane anisotropy and a higher cholesterol to phospholipid (C/P) molar ratio of the plasma membrane were found. Furthermore, cholesterol-enriched platelets were more sensitive upon thrombin stimulation. The results suggest that a shift of platelet subpopulations to a higher number of low density platelets could be caused by either the level of plasma cholesterol or an in-vitro incubation with cholesterol rich liposomes.

Atrial natriuretic peptide levels reflect hemodynamic changes under pacemaker stimulation.

Pacemaker stimulation influences plasma levels of atrial natriuretic peptide (ANP). This study evaluated in individuals without impaired myocardial function whether a consecutive increase of pacing rates results in reduced alteration of plasma ANP levels mirroring a putative decrease of atrial contribution to cardiac output. In nine resting patients with DDD pacemakers, absolute and relative ANP plasma levels were determined under DDD (175 msec AV delay) and VVI pacing at a pacing rate of 72, 82, 92, and 113 beats/min. When pacing rates were consecutively increased, higher plasma ANP concentrations were measured. However, the differences in relative ANP levels were nearly identical. Therefore, it seems likely that the atrial contribution to cardiac output at high pacing rates is less important than at lower frequencies, at least when the overall myocardial function is not impaired.

Influence of pacing mode and rate on peripheral levels of atrial natriuretic peptide (ANP).

The effect of acute modifications of pacing mode and rate on plasma ANP levels was evaluated. ANP was determined in ten resting patients with DDD pacemakers due to binodal disease or intermittent second-and third-degree AV block. At 82/minute pacing rate the ANP plasma levels (normal range 2 to 30 fmol/mL) corresponded to those under AAI (4.05 +/- 2.10 fmol/mL) and DDD (4.18 +/- 2.02 fmol/mL) pacing, but increased significantly (P 0.05) during VVI pacing (6.96 +/- 3.70 fmol/mL). Acceleration of DDD stimulation frequency from 82 to 113/minutes led to significant increase of ANP levels by the factor of three in all chosen AV delays. The lowest ANP plasma levels were measured at 175 msec AV delay under 82/minute pacing rate in DDD mode. Under 113/minutes the differences of ANP concentration after variations of AV delays were less pronounced. The influences of altered atrial pressure and tension on ANP release are discussed to account for changes in ANP plasma levels following different modes and rates of pacemaker stimulation.

[Modification of atrial natriuretic factor by the AV transmission time in pacemaker patients]. / Beeinflussung des atrialen natriuretischen Faktors durch die AV-Uberleitungszeit bei Schrittmacherträgern.

The possible relationship of variations in the programmed a-v interval on the peripheral-venous plasma level of the atrial natriuretic factor (ANF) was investigated in nine patients with dual-chamber pacemakers (DDD). During atrial and ventricular stimulation at 82 beats/min the pacemakers of the resting patients were programmed to give successive a-v intervals of 200, 175, 150, 125, 100, 50 and 15 ms. Blood samples were obtained from a peripheral arm vein ten minutes after each change of programme. ANF was extracted from each sample and determined by radioimmunoassay. Both the absolutely and relatively lowest plasma ANF level was obtained at an a-v interval of 175 ms. Lengthening the interval to 200 ms or shortening it to 150 ms or less increased the level. It is possible that both "too long" and "too short" a-v intervals produce an increase in atrial pressure and stretch, to which ANF reacts highly sensitively with an increase in peripheral-venous plasma levels of ANF.