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Biomedical subjects

M Kaltenbach

Publications and source records attributed to M Kaltenbach.

At least 37 records · Page 2Linked to original sources
PubMed1978

[Diagnosis, therapy and longterm results of atrial myxoma (author's transl)].

Refering to a case report of five patients with atrial myxoma the symptoms, diagnosis, and therapy of this disease were described. In one case a biatrial tumor was found. In four cases atrial myxoma imitated a mitral-valve disease. An elevated BSR was found in all patients. The non invasive diagnostic procedure of ultrasound-echocardiography led in the last two cases to the correct diagnosis before heart-catheterization. The diagnosis was ascertained in all cases by angiocardiography. If left atrial tumor is suspected transpulmonary laevocardiography can be considered as a save diagnostic procedure better than the direct injection into the left atrium after transseptal puncture. Even the left ventricular angiogram in right anterior oblique position led in four of the five cases to the diagnosis of left atrial tumor. Coronary-angiography was performed in three patients and revealed pathologic atrial vessels in all three cases. Immediate operation is the indicated therapy. Two of the five patients were reviewed over a eight year period after operation without any signs of recurrence of the tumor.

Adult↗
PubMed1978

[Echocardiography].

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Echocardiography↗
PubMed1978

[Regional ventricular function at rest during exercise before and after bypass surgery (author's transl)].

In 9 patients with coronary heart disease isovolumetric contractility indices and ejection phase parameters were measured simultaneously, using an angiographic catheter with a manometer at the tip (Millar). Regional wall motion at rest, after leg raising and during physical exercise (bicycle ergometer) was analyzed applying the hemiaxis method. Five weeks after aortocoronary bypass surgery the same examinations were repeated. Preoperatively left ventricular enddiastolic pressure (LVEDP) increased from 21 to 37 mm Hg following leg raising. The velocity mean of fiber shortening (Vcf) and of regional fiber shortening in the anterior wall decreased significantly.--All patients discontinued physical exercise due to angina pectoris. LVEDP increased from 21 to 39 mm Hg. Large hypokinetic and akinetic areas developed especially in the anterior wall. Velocity of fiber shortening of the anterior wall decreased from 1.43 to 0.76/s. Enddiastolic volume remained unchanged while endsystolic volume increased significantly. In six patients with patent grafts surgery had a beneficial effect. Comparing angiograms at rest no significant changes were found. After leg raising and physical exercise, however, marked improvement in ventricular function occurred, compared to the preoperative performance. All 6 patients were exercised without complaints at a load of 100 watts for 8 minutes. Velocity of fiber shortening in the anterior wall increased significantly from 0.76 to 2.56/s, mean Vcf from 1.11 to 2.12 circ/s, max dP/dt from 2302 to 4280 mm Hg/s and Vpm from 27.8 to 55.7/s. Functional improvement in individual wall segments amounted to 500% in the mean. Ejection fraction increased from 54 to 76%. Enddiastolic volume remained unchanged while endsystolic volume decreased from 67 to 33 ml/1.37 m2 (p less than 0.002). In three patients the bypass occluded or myocardial infarction occurred intraoperatively. Postoperative findings at rest and during exercise were unchanged as compared to preoperative values. Following successful bypass surgery ventricular function at rest did not change. During exercise, however, a marked improvement in overall and in regional ventricular function was found.

Angiocardiography↗
PubMed1978

[Contractile and relaxation reserve of the left ventricle. III. Patients with cardiomyopathy (author's transl)].

Seven of 22 patients with cardiomyopathy increased maximal rate of left ventricular pressure rise (max dP/dt) above 3200 mm Hg/s and dP/dt/P above 60/s. Relaxation reserve was normal with an increase of min dP/dt above 2400 mm Hg/s.--In 15 patients contractile and relaxation reserve was reduced. In congestive cardiomyopathy, contractility and relaxation reserve were equally reduced. Left ventricular enddiastolic pressure increased during exercise slightly or not (grade 1). Enddiastolic volume was elevated to 173 +/- 50 ml/1.73 m2 and endsystolic volume to 63 +/- 22 ml/1.73 m2; ejection fraction and mean circumferential fiber shortening were reduced (61 +/- 17%; 1.3 +/- 0.9 circ/s). In hypertrophic cardiomyopathy without obstruction, contractile and relaxation reserve and ejection phase parameters could be found to be normal. Enddiastolic pressure at rest was elevated. In severe cases, contractile and relaxation reserve were markedly reduced and enddiastolic pressure increased to a greater extent than in congestive cardiomyopathy. In addition, relaxation reserve was reduced, especially in patients with excessive hypertrophy of the myocardium. These had abnormal (grade 2) and pathological reaction to exercise: contractile and relaxation reserve were decreased and enddiastolic pressure (grade 3) increased. Left ventricular contractility was found to be almost normal in patients with hypertrophic obstructive cardiomyopathy. This was the case despite increases in enddiastolic pressure. Contractile reserve was reduced, however, in patients with excessive hypertrophy. Diastolic filling was impeded during exercise.--Measuring left ventricular function during exercise, different types of cardiomyopathy correlate with typical hemodynamic alterations.

Adult↗
PubMed1978

[Contractile and relaxation reserve of the left ventricle. IV. Patients with coronary heart disease (author's transl)].

51 patients with coronary heart disease had exercise tests on a bicycle ergometer (86 +/- 32 watts). Compared to a normal control group, only 13 patients had normal contractile reserve (group 4.1). In 32 patients the increase in contractility during exercise was reduced (max dP/dt below 3200 mm Hg/s, group 4.2). Patients with reduced contractile reserve were graded according to the height of left ventricular enddiastolic pressure during exercise: In patients with grade 1, enddiastolic pressure was normal. In patients with grade 2, enddiastolic pressure increased between + 4 and + 15 mm Hg and in the patients with grade 3a a above + 15 mm Hg. Contractile and relaxation reserve decreased along with a rise in enddiastolic pressure and an increase in the complaints of the patients. Severe chest pain led to termination of exercise in patients of grade 3b. Enddiastolic pressure increased above + 15 mm Hg. During ischemia, peak-measured velocity of contractile elements (dP/dt/P) and the maximal rate of left ventricular pressure fall (min dP/dt) decreased. In conclusion, with increasing chest pain a decrease of contractile reserve was observed. Left ventricular enddiastolic pressure rose excessively. This has to be taken as a sign of myocardial failure due to ischemic dyskinesia and impeded relaxation.

Adult↗
PubMed1978

[Hemodynamic effects of intracardiac diatritoic acid and their dependance on left ventricular function and severity of coronary sclerosis (author's transl)].

In 16 patients with coronary heart disease (n = 13) and cardiomyopathy (n = 3) heart rate, left ventricular pressure and contractility (max dp/dt, min dp/dt and Vpm) were measured prior during and after three consecutive left ventricular angiograms. Heart rate decreased during angiography and increased slightly but significantly after angiography. Systolic and diastolic left ventricular pressure, max dp/dt and min dp/dt increased after angiography, whereas Vpm remained unchanged. Any hemodynamic changes occuring were moderate and only of short duration. No significant differences were found a) between patients with angiographically proven normal and reduced left ventricular function, b) between patients with normal or increased left ventricular filling pressure or c) between those with slight or severe coronary heart disease. The investigations point to a good tolerance for the sodium methyl glucamine salt of diatrizoic acid (Urografin 76) even in patients with progressed coronary heart disease. Severe side-effects described in animal experiments indicate a poor comparibility between animal models and human studies. Moreover animal experiments are mostly done with high doses not used clinically.

Angiocardiography↗
PubMed1978

[New method of estimating x-ray magnification on angiographic volume determinations (author's transl)].

1. The necessity of a precise determination of the magnification factor for angiographic volume determinations is described. Each error of the linear magnification factor influences in its third power the volume calculation. 2. For the magnification of linear cineangiographic magnification a method is used in which the tip of the catheter is filmed in two positions. The distance approximately resembles a normal ventricular diameter. The relationship of virtuel shifting of the catheter tip versus real shifting of the patient is the magnification factor. 3. For the practicable handling of this method a new developed mechanical device is described which allows the performance of the calibration procedure with an adequate high precision. 4. The method is simple and can be done within a short period of time.

Angiography↗
PubMed1978

Effects of intravenous nitroglycerin on hemodynamics and ischemic injury in patients with acute myocardial infarction.

In 24 patients with acute myocardial infarction intravenous nitroglycerin in 2 different dosages was administered and the effect on hemodynamics and extent of myocardial ischemia was investigated. According to the initial left ventricular filling pressure (LVFP) the patients were divided in Group I: LVFP below 20 mm Hg (13 patients) and in Group II: LVFP above 20 mm Hg (11 patients). Following an infusion of 3 mg of nitroglycerin in the first and 6 mg in the second hour, a significant decrease (P less than 0.0001) in the filling pressure (in Group I from 15 +/- 4 to 9 +/- 3 (+/-1 SD) and in Group II from 28 +/- 11 to 16 +/- 7 mm Hg) was observed. The mean arterial pressure decreased in both groups by an average of 9 mm Hg. The changes in the heart rate were minimal. The cardiac output decreased in Group I from 4.4 +/- 1.0 to 3.9 +/- 0.8 1/min (P less than 0.005) whereas in the group with left ventricular failure it increased significantly from a lowered initial value (3.4 +/- 1.0 to 4.0 +/- 1.1 1/min) (P less than 0.001). By using precordial mapping for estimation of ischemic injury in 12 patient sigma ST elevation decreased from 14.6 +/- 11.9 to 12.2 +/- 9.8 mV at a dose of 3 mg/h (P less than 0.03). The dose of 6 mg/h, however, was less effective on the extent of myocardial ischemia than 3 mg/h. Thus, the dosage of nitroglycerin may be critical in respect to infarct size, despite the beneficial hemodynamic effects of the drug.

Adult↗
PubMed1977

[Serum and total body potassium during treatment with chlortalidone and hydrochlorothiazide. Influence of triamterene (author's transl)].

The serum and total body potassium was investigated in 25 patients with non-congestive cardaic failure before and during saluretic treatment. Treatment with triamterene (100 mg/d; n = 10) over a period of 3 weeks led to an increase of serum potassium (from 4.1 +/- 0.65 to 4.7 +/- 0.51 mmol/l) and of total body potassium (by 110 mmol). After treatment with chlortalidon for 7 days (100 mg/d; n = 6) serum potassium concentration decreased from 4.38 "/- 0.37 to 3.30 +/- 0.46 mmol/l (approximately 25%). The total body potassium decreased by 240 mmol (approximately 10%). Continuation of the treatment with a combination of chlortalidon (50 mg/d) and triamterene (150 mg/d) led to correction of the extra- and intracellular potassium loss after 1 to 2 weeks. No significant change of serum and total body potassium was found during and after 6 months of treatment with hydrochlorothiazide (50 mg/d) and triamterene (100 mg/d; n = 9). The results demonstrate the potassium loss which occurs in the early stage of saluretic treatment and show the antikaluretic potency of triamterene.

Adult↗
PubMed1977

Orally administered isosorbide dinitrate in patients with and without left ventricular failure due to acute myocardial infarction.

The oral effectiveness of 10 mg followed by 20 mg of isosorbide dinitrate in 21 patients with acute mycardial infarction was studied over a period of 13 hours. The patients were grouped according to initial left ventricular filling pressure: group I, pressure less than 20 mm Hg, and group II, pressure more than 20 mm Hg. Patients in group II had left ventricular failure. In both groups isosorbide dinitrate resulted in a significant decrease in pulmonary arterial pressure. The left ventricular filling pressure decreased in group I from 13.6 +/- 4.0 to 7.1 +/- 2.6 mm Hg (mean +/- 1 standard deviation) and in group II from 26.9 +/- 4.6 to 19.0 +/- 3.6 mm Hg (P less than 0.001). Cardiac output decreased in group I from 5.1 +/- 1.0 to 4.5 +/- 0.9 liters/min, whereas in group II it increased significantly from 3.5 +/- 0.8 to 4.1 to 0.9 liters/min (P less than 0.001). In both groups, peripheral arterial blood pressure decreased (P less than 0.60). Heart rate remained constant. Whether cardiac output increased or decreased was found to be dependent on the initial left ventricular filling pressure. In patients with an initially high value (above 20 mm Hg), the increase in cardiac output is probably due to the reduction of afterload. An additional factor may be the decrease in left ventricular filling pressure, which leads to an improved blood supply in the affected mural segments as a result of the decrease in the extravascular component of the coronary resistance. Significant changes in cardiac output and left ventricular filling pressure were achieved 3 to 5 hours after oral administration of isosorbide dinitrate. Clinical signs of failure were less pronounced. Isosorbide dinitrate is, therefore, a therapeutic agent in the treatment of left ventricular failure due to acute myocardial infarction.

Administration, Oral↗