[Combined lytic and heart surgical therapy of in open foramen ovale incarcerated giant thrombus with pulmonary and cerebral embolization]. / Kombinierte lytische und herzchirurgische Therapie eines im offenen Foramen ovale inkarzerierten Riesenthrombus mit pulmonaler und zerebraler Embolisation.

A case of phlebothrombosis with recurrent pulmonary and cerebral embolism is presented which occurred in a 42 year old patient two weeks after treatment of a traumatic crural fracture despite of prophylaxis with low molecular heparin. By means of transthoracic echocardiography a large intracardiac thrombus was detected, entrapped in an patent foramen ovale (PFO) and prolapsing through both atrioventricular valves into both ventricles. This was found after systemic thrombolysis with rtPA had been performed because of fulminant pulmonary embolism. Subsequently the intracardiac thrombus was surgically removed and the PFO closed. The importance of an PFO for paradoxical embolism is discussed as well as the various therapeutical paths to treat an "embolus-in-transit" (cardiac surgery, thrombolytic therapy or anti-coagulation).

[Form fruste of long QT syndrome]. / Forme fruste eines langen QT-Syndroms.

The long QT syndrome (LQTS) is an inherited disorder associated with recurrent syncope and sudden death from ventricular arrhythmias. It is characterized by a prolonged QT interval on the ECG. A case is discussed in which a patient presented with recurrent syncopal episodes on exertion associated with a slightly prolonged QT interval. Family history revealed an increased incidence of sudden deaths in two generations. Some reports on similar patients suggest that there may be a forme fruste of the long QT syndrome. The additional diagnostic values of exercise stress test, Valsalva maneuver and genetic testing are evaluated. After analysis of the patient's and mother's ECGs the diagnosis of a forme fruste of LQTS is made. This case is presented to emphasize the importance of diagnosis of borderline cases of LQTS because of the high risk of sudden death for untreated patients.

Triamterene may preserve lymphocyte magnesium and potassium in patients with congestive heart failure.

Electrolyte abnormalities are a frequent and potentially hazardous complication in the treatment of patients with congestive heart failure. Medical treatment with diuretics and/or digitalis, as well as neurohumoral activation most likely initiated by the compromised cardiac function, contributes to this alteration. The addition of potassium- and magnesium-sparing diuretics (triamterence, amiloride) to therapy with frusemide or hydrochlorothiazide is of possible value in preventing intracellular electrolyte abnormalities.

[Magnesium and potassium content in patients with heart failure and in healthy persons. Determination in lymphocytes, erythrocytes and plasma]. / Der Magnesium- und Kaliumgehalt bei Herzinsuffizienten und Normalpersonen. Bestimmungen in Lymphozyten, Erythrozyten und im Plasma.

Therapy with diuretics and/or digitalis, as well as the compromised cardiac function, contributes to electrolyte alterations (magnesium, potassium) in patients with congestive heart failure. We determined in 29 patients with heart failure (NYHA classes II-IV) the magnesium and potassium content in lymphocytes and in erythrocytes, as well as in 25 healthy subjects. In patients with heart failure, lymphocyte magnesium (4.4 +/- 0.6 fmol/cell) and lymphocyte potassium (50.4 +/- 6.0 fmol/cell) were only slightly (n.s.) lower compared to controls (Mg++: 4.7 +/- 0.6 fmol/cell; K+: 54.6 +/- 6.8 fmol/cell). Only in healthy subjects did we find a positive correlation between magnesium and potassium in lymphocytes (r = 0.83). The electrolyte content in erythrocytes was also not different in patients with heart failure (Mg++: 2.2 +/- 0.1 mmol/l; K+: 96.6 +/- 6.1 mmol/l) and controls (Mg++: 2.2 +/- 0.1 mmol/l; K+: 97.8 +/- 4.0 mmol/l). There was no correlation between the intracellular electrolyte content and the electrolyte levels in plasma, either for lymphocytes, or for erythrocytes in both groups. It is concluded that 1) determinations of magnesium and potassium in plasma do not reflect intracellular electrolyte content; 2) the magnesium and potassium content of lymphocytes and erythrocytes were not different in patients suffering from heart failure compared to controls; and 3) in heart failure, the relationship of magnesium and potassium in lymphocytes may be altered.

Simultaneous determination of magnesium and potassium in lymphocytes, erythrocytes and thrombocytes.

A standardized method for the determination of magnesium and potassium in the lymphocytes, erythrocytes, and thrombocytes of normal subjects is described. The procedure consists of four steps: 1) the removal of platelets from the remaining cells and heparin plasma, 2) the isolation of platelet-poor lymphocytes by means of density-gradient centrifugation of the buffy-coat, 3) the purification of blood cells by repeated washings, and 4) the determination in cell lysates of magnesium by atomic absorption spectrometry and of potassium by flame photometry. In order to get reproducible lymphocyte magnesium values, it was necessary to obtain a mean lymphocyte recovery of 60% with a purity of 97% (nucleated cells), this yield containing less than 5 thrombocytes per lymphocyte and less than 4 erythrocytes per 100 lymphocytes. Under these conditions, the normal content of magnesium in lymphocytes was 3.5-5.7 fmoll/cell (n = 18), that of potassium was 38.8-63.5 fmol/cell. The precision (CV) of the whole procedure measured with 10 identical samples from each of 5 persons was 5.7% for lymphocyte magnesium and 7.8% for potassium, respectively. The concentration of magnesium in erythrocytes was 1.99-2.43 mmol/l and that of potassium was 85.8-102.5 mmol/l. The precision was 3.6% for magnesium and 2.2% for potassium. The content of magnesium in thrombocytes was found to be 0.07-0.12 fmol/cell.