Primary purulent pericarditis in an immunocompromized patient - an unusual cause of acute renal failure.
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Acute Kidney Injury↗
Biomedical subjects
K H Konz
Publications and source records attributed to K H Konz.
Hemofiltration in very severe hypothermia with favorable outcome.
Hypothermia is a dangerous situation. It is defined by a core temperature of less than 35 degrees C. Aggressive rewarming is used if it is lower than 30 degrees C, comprising extracorporeal therapies. A case of a 63 year old lady is reported whose temperature was 21.8 degrees C, circulation was unstable, respiratory insufficiency prevailed and severe neurological dysfunction. Serum potassium was 2.9 mmol/l and pH corrected for temperature 7.61. The patient was rewarmed by hemofiltration (HF) over 6 hours with substitution of 18 l of a solution containing a concentration of potassium of 5 mmol/l. Though potassium levels declined initially and than slowly normalized in 9 hours there were no arrhythmias documented. The ECG showed prolongation of the PQ-, QRS-, and especially the QT-times. All clinical and neurological sequelae had disappeared after four days. HF thus seems to be a safe method of rewarming in very severe hypothermia.
Electrocardiography↗
Diastolic dysfunction as a precursor of myocardial damage by reoxygenation.
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Animals↗
Selenium as a protector of diastolic function during oxidant stress.
Interventional studies yielded conflicting results on reperfusion injury. They are unable to discriminate between lesions due to ischemia or to additional damage during reoxygenation. Since reactive oxygen metabolites have been implicated as a major cause of reperfusion injury, 375 nmol/min of hydrogen peroxide was infused in a Langendorff rat heart preparation as a model of oxidant stress without previous ischemic contractile dysfunction. Impaired endogenous defense was remodeled, using selenium-deficient hearts with reduced glutathione peroxidase activity. Measurements of hemodynamic parameters demonstrate increased myocardial susceptibility to oxidant stress in hearts with decreased antioxidant defense. Defined concentrations of hydrogen peroxide produce isolated impairment of active and passive diastolic properties of the ventricle in this model.
Animals↗
Nitroglycerin and isosorbide dinitrate stimulation of glutathione disulfide efflux from perfused rat liver.
Nitroglycerin (GTN) and isosorbide dinitrate (ISD) are metabolized by glutathione S-transferase to nitrite with production of GSSG from GSH. Infusion of organic nitrates into perfused rat liver led to efflux of GSSG in the bile and nitrite in the perfusate. Biliary GSSG increased more rapidly than did nitrite release as GTN infusion rate was increased, indicating that GSSG reducing capacity was being exceeded. Rapid GTN-induced oxidation of GSH may be the mechanism of tissue GSH depletion by GTN and other alkylnitrates. Such depletion of glutathione may reduce nitrite production from organic nitrates and underlie tolerance to these drugs.
Animals↗
Diastolic dysfunction of perfused rat hearts induced by hydrogen peroxide. Protective effect of selenium.
Oxidant substances such as hydrogen peroxide are postulated to cause cardiac dysfunction and injury in a number of pathological conditions. Selenium is an essential nutrient which serves as an oxidant defense through the selenoenzyme glutathione peroxidase. This enzyme metabolizes hydrogen peroxide; its activity in rat heart is reduced to 5% of control by selenium deficiency. Left ventricular function of selenium-deficient and control rat hearts was studied in a Langendorff preparation under isovolumic conditions. A stabilization period of 20 min was followed by a 70 min infusion of hydrogen peroxide at 375 or 1500 nmol/min. When no hydrogen peroxide was infused, perfusion for 90 min had no effect on systolic or diastolic function and no effect of selenium deficiency was detected. Hydrogen peroxide infusion into selenium-deficient hearts at 375 nmol/min led to impaired isovolumic relaxation and a substantial increase in end-diastolic pressure after 45 min which worsened progressively until the experiment was terminated. By contrast no effect was observed on systolic contractile function as assessed by peak pressure or developed pressure. Infusion of this dose of hydrogen peroxide into control hearts had no significant effect on diastolic or systolic function. However, infusion of 1500 nmol hydrogen peroxide/min into control hearts caused diastolic dysfunction after 30 min without affecting systolic function. These results indicate that hydrogen peroxide injury to the perfused rat heart is manifested by diastolic dysfunction before systolic dysfunction occurs. Selenium deficiency lowers the dose of hydrogen peroxide needed to cause diastolic dysfunction. This suggests that the selenoenzyme glutathione peroxidase protects the heart against hydrogen peroxide injury.
Animals↗
[Digitalis therapy in medical practice. Research on indications and dosage criteria in general practice].
Two hundred digitalized patients under nine freely practising physicians were investigated. One hundred and ninety-six patients received digoxin or one of its derivatives. Of these, 50% did not have therapeutic serum glycoside concentrations, 48% were in the mostly subtherapeutic range and 2% were in the potentially toxic range. Signs of glycoside intoxication were not found. A substantiated indication for glycoside therapy was found in the final analysis in 55% of the patients. In 128 patients, the methyldigoxin dose calculated (0.16 +/- 0.030 mg/d) was markedly in excess of that actually prescribed (0.13 +/- 0.050 mg/d; p less than 0.001), so that there were indications of a general underdigitalization. In addition, it was not possible to anchor the restrictive kidney function as a reason for reduction of digoxin dosage in the prescription behavior. In the long run, only 36% of the patients with justified indication and therapeutic serum glycoside concentration as well as (with reservations) the 3% with potentially toxic serum glycoside concentration profited from the glycoside therapy.
Atrial Fibrillation↗
[Effect of tricuspid annuloplasty on the clinical course following mitral or aortic valve operation].
To assess the effect of additional tricuspid annuloplasty during mitral/aortic valve surgery on the clinical postoperative course in patients with severe preoperative tricuspid insufficiency, 64 patients were investigated pre- and 11 +/- 4 months postoperatively. Extent of left-side heart failure was graded as well as severity of right-side heart failure using a defined clinical score. Using preoperative biplane angiography of the right ventricle the patients were assigned to three different groups: group I (n = 30) with no preoperative tricuspid insufficiency (TI), group II (n = 19) with preoperative TI and without tricuspid annuloplasty, group III (n = 15) with preoperative TI and with annuloplasty of the tricuspid valve. The patients of all three groups postoperatively improved from an average of NYHA class III to class II. The clinical score of right-side heart failure in gr. III and gr. II was 1.4 +/- 1.0 and 1.5 +/- 1.0, respectively, and was significantly (p less than 0.05) higher than in gr. I (0.8 +/- 0.8). In all three groups there was a postoperatively significant decrease: gr. I: 0.3 +/- 0.5 (p less than 0.01); gr. II: 0.6 +/- 0.9 (p less than 0.02); gr. III: 0.7 +/- 0.8 (p less than 0.05). Mortality was 3% in gr. I; 5% in gr. II and 6% in gr. III. 3% of patients in gr. I, 30% in gr. II and 6% in gr. III had early postoperative hemodynamic complications.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Protection by ebselen against endotoxin shock in rats or mice sensitized by galactosamine.
Oral pretreatment with greater than 1 mg/kg ebselen protected Wistar rats from shock induced by 20 mg/kg endotoxin when heart stroke volume after 60 min. was taken as a measure. Similarly, the drug protected male NMRI mice sensitized by 700 mg/kg galactosamine and treated with 33 micrograms/kg endotoxin against fulminant hepatitis assessed by transaminases release after nine hours. The validity of the model was checked by administration of drugs interfering with arachidonate metabolism. Chemical depletion of hepatic glutathione resulted in an apparent protection from galactosamine/endotoxin shock in mice. It is concluded that peptido-leukotrienes are likely to be responsible for the manifestation of this pathophysiological condition.
Animals↗
[Biatrial myxomas--a diagnostic challenge].
Like isolated cardiac myxoma, biatrial myxoma may manifest itself only by extracardiac symptoms over a prolonged period. A 24-year-old patient presented over seven years a history of repeated arthalgia with concomitant anaemia, elevated blood sedimentation rate, positive antistreptolysin test and electrophoretic signs of inflammation. A discrete systolic sound on auscultation gave rise to an echocardiographic examination which revealed a biatrial myxoma.
Adult↗
Incidence, extent and localisation of left ventricular wall motion abnormalities in patients with mitral valve disease.
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Heart Ventricles↗
Right ventricular function in mitral/aortic valve disease with and without tricuspid incompetence.
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Aortic Valve Insufficiency↗
[Tricuspid valve insufficiency in patients with rheumatic mitral valve disease: angiographic diameter of the tricuspid ring and function of the right ventricle].
Dilatation of the right ventricle and a consecutive enlargement of the tricuspid valve ring are thought to be the main causes of functional tricuspid regurgitation in patients with rheumatic mitral valve disease. To study the effect of right ventricular dilatation as well as the dimension of the tricuspid valve ring, right ventricular volume indices, ejection fraction, regional shortening, pulmonary artery pressure, and the diameter and systolic shortening of the tricuspid valve were determined in 67 patients with rheumatic mitral valve disease (NYHA class II and III) from biplane ventriculographies. Patients with right ventricular enlargement (greater than 90 ml/m2) were divided into groups with (group IIA) and without (group IIB) tricuspid regurgitation and compared with patients with normal right ventricular size and function without tricuspid regurgitation (group I). There was no difference in the end-diastolic volume index, in the afterload or in the diameter of the tricuspid ring. Right ventricular ejection fraction was decreased in group IIA (51 +/- 9% vs. 59 +/- 10% (IIB) and 61 +/- 6% (control); (p less than 0.05). Regional function was also decreased in group IIA. 73% of the patients with tricuspid regurgitation had right ventricular enlargement, but only 44% of the patients with right ventricular enlargement had tricuspid regurgitation. Thus right ventricular dilatation promotes the development of a tricuspid insufficiency, but is not the only cause. Additional factors like decreased local wall motion, alterations of the valve or the valve apparatus may also account for functional tricuspid regurgitation.
Angiography↗
[Frequency, localization and extent of local wall function disorders of the left ventricle in patients with rheumatic mitral valve diseases].
In 59 patients with rheumatic mitral valve disease, local wall motion was assessed by analysing the diastolic and systolic left ventricular silhouette from biplane angiograms with a quantitative radial axes model using 90 radii in each projection. The left ventricle was dissected into 4 segments in the RAO and 2 segments in the LAO projection and a mean radii shortening for each segment was calculated. 27 patients had pure severe mitral stenosis (MS), 10 patients mitral insufficiency (MI) and 22 patients combined mitral valve disease (MSMI). A mean radii shortening less than 25% was diagnosed as wall motion abnormality. In 78% of all patients wall motion abnormalities could be detected in at least one segment. 32% of patients with MS, 27% of patients with MI and 33% of patients with MSMI had wall motion abnormality of the anteroapical wall. In only 8% of patients with MS and in no patients with MI and MSMI was the posterobasal segment disturbed. The anterobasal and diaphragmal wall motion showed wall motion abnormality in 16% and the septal and the posterolateral area in 17% of all patients. 78% of all patients had at least one diseased segment; motion abnormalities of the anteroapical wall (seg. 2) occurred most often whereas the posterobasal area (seg. 4) was diseased in only 4% of all patients. Ejection fraction was severely impaired (less than 55%) in 7 patients only (5 of these patients had MS) with wall motion abnormalities in more than 4 segments. There was no correlation between the extent of valve disease and occurrence and extent of wall motion abnormalities.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
[Unusual rhythm disorders with a DDD pacemaker].
A tachycardia caused by an inadvertent change of the lead connections in a patient with a DDD pacemaker is reported. This was demonstrated by operating in different modes (i.e. AOO, VOO) by displaying the marker channel graphically and by X-ray examination revealing unchanged lead positions.
Electrocardiography↗
[Cholestasis after antiarrhythmic therapy with propafenone].
Propafenone, three times 150 mg/d over 33 days and two years later at the same dosage over six days, was administered to an 84-year-old man with ventricular extrasystoles (Lown IVa). Both times intrahepatic biliary stasis occurred, presumably a sign of a drug-allergic hepatitis. All other possible causes in the differential diagnosis were excluded. The lymphocyte transformation test demonstrated in vitro propafenone-sensitive patient-lymphocytes.
Aged↗
[Spontaneous regression of residential stenosis of the infarct vessel following successful percutaneous transluminal coronary recanalization].
In 64 out of 90 patients with thrombolysis by intracoronary streptokinase (PTCR) in the acute stage of myocardial infarction coronary angiography was performed in the chronic stage after 28 +/- 20 days. 52 of 56 successfully treated patients had a patent infarct vessel in the chronic stage. 36 of these patients showed a spontaneous regression from the subacute to the chronic stage. In 49 of the 56 patients (age: 53.4 +/- 10.4 years) a residual stenosis of more than 75% after PTCR was found; in the chronic stage only 31 patients had a stenosis of more than 75%. Of 10 patients with a spontaneous regression of 25% or more (age: 48.0 +/- 14.9 years) 8 had a one-vessel disease. The infarct vessel was in 6 patients the left anterior descending, in 4 patients the right coronary artery and in no case the left circumflex branch. The results suggest that the indication for invasive interventions, such as acute coronary angioplasty or bypass surgery, does not only depend on the degree of the residual stenosis directly after reperfusion. If possible, the decision for further invasive treatment should depend on the clinical follow-up.
Adult↗
[Effect of chronic pressure and volume stress on the function of the right ventricle].
Biplane right ventricular angiography was performed in 36 patients with chronic pressure overload of the right ventricle; 12 patients additionally had tricuspid insufficiency (TI). There were 4 subgroups: patients with systolic pulmonary artery pressure less than or equal to 40 mm Hg without (group I, n = 10) and with TI (group II, n = 6), as well as patients with systolic pulmonary artery pressure greater than 40 mm Hg without (group III, n = 14) and with TI (group IV, n = 6). Compared with the normal volumes of groups I and III, a significant increase in end-diastolic right ventricular volumes (p less than 0.01) was found in groups II and IV with 112.2 +/- 22.3 ml/m2 and 116.3 +/- 27.4 ml/m2, respectively. In both groups II and IV end-systolic volumes were also significantly increased, with 51.0 +/- 10.3 ml/m2 in group II and 49.7 +/- 11.3 ml/m2 in group IV. Right ventricular ejection fraction was 53.8 +/- 11.9% in group II, 57.3 +/- 8.5% in group III and 57.8 +/- 7.3% in group IV. There was no significant difference between the ejection fraction of these groups in comparison to the normal ejection fraction of group I with 63.4 +/- 10.9%. The results suggest that the right ventricle can compensate for moderate chronic pressure and volume overload using the Frank-Starling mechanism. Overall right ventricular dysfunction is not determined primarily by the loading conditions alone. Local myocardial and septal involvement is suspected to be an important determinant of right ventricular function.
Aortic Valve Insufficiency↗