PubMed Health⌕ Search

Biomedical subjects

M Jakob

Publications and source records attributed to M Jakob.

At least 19 recordsLinked to original sources
PubMed1995

Reduced epicardial coronary vasodilator capacity in patients with left ventricular hypertrophy.

BACKGROUND: Enlargement of the epicardial coronary arteries occurs in left ventricular (LV) hypertrophy as an adaptation to the increased coronary blood flow. METHODS AND RESULTS: Vasodilator capacity of the epicardial coronary arteries was determined in 44 patients. The dose-response relation of intracoronary nitroglycerin was assessed in 14 patients (7 control subjects and 7 patients with aortic stenosis [study A]) using quantitative coronary angiography. In a second study (B), vasodilator capacity of the epicardial coronary arteries was determined in 15 control subjects and 15 patients with valvular heart disease. In study A, a curvilinear dose-response relation with maximal vasodilation after 90 micrograms intracoronary nitroglycerin was found in both control subjects and patients with aortic stenosis. Vasodilator capacity was reduced in those with aortic stenosis, although sensitivity to nitroglycerin was similar in both groups. In study B, coronary circumferential length at baseline was larger in those with LV hypertrophy (12.2 +/- 2.2 mm) than in control subjects (8.6 +/- 1.5 mm; P < .001); after 100 micrograms intracoronary nitroglycerin, it increased to 12.9 +/- 2.2 mm (6 +/- 5%) in those with LV hypertrophy and to 10.3 +/- 1.5 mm (21 +/- 8%; P < .001) in control subjects. An inverse relation between baseline circumferential length and its percent increase after nitroglycerin was found (r = -.71, P < .001). CONCLUSIONS: Vasodilator capacity of the epicardial coronary arteries is reduced in patients with LV hypertrophy, although sensitivity to nitroglycerin is normal. This may be due to a flow-mediated decrease in coronary vasomotor tone and/or the occurrence of vascular remodeling with an enlargement of the coronary arteries.

Adult↗
PubMed1995

[Traumatic aortic rupture: diagnosis using biplanar transesophageal echocardiography].

Acute aortic rupture is a typical consequence of severe blunt chest trauma often associated with rapid deceleration in car accidents. Initial diagnostic findings are often misleading and multiorgan injuries add to the diagnostic complexity; therefore, the natural history of acute rupture is usually fatal during the first 24 h after injury if left untreated. Prompt and simple diagnosis is, hence, of paramount importance for successful treatment of acute aortic rupture. Transesophageal echocardiography, particularly with a biplane or multiplane probe, currently represents the diagnostic tool of choice to meet these criteria; because of its high sensitivity and specificity transesophageal echocardiography will replace aortography as "gold standard" for diagnosis of acute aortic rupture. We report on a 47-year-old woman with severe blunt thoraco-abdominal trauma resulting from a car accident; at hospital admission abdominal injuries were predominant and diagnosis of an acute rupture of the descending thoracic aorta was made only about 18 h after admission using biplane transesophageal echocardiography. Emergency surgical revision confirmed the diagnosis of complete transsection of the descending thoracic aorta immediately after the origin of the left subclavian artery; the site of transsection was surrounded by a large hematoma. Despite successful reconstruction of the descending thoracic aorta by means of graft interposition, a recurrent local bleeding event lead to complete circulatory destabilization and, finally, to the death of the patient.

Aortic Rupture↗
PubMed1994

Aortic dissection.

Explore the source record for details and available documents.

Aortic Dissection↗
PubMed1994

[Prinzmetal's variant angina: a case report].

Prinzmetal's angina is a variant of the classic exertion dependent angina pectoris. Typical is the appearance of the symptoms at rest during early morning hours. It is due to spasms in the coronary arteries. Various provocation tests may be used to trigger spasms, among others hyperventilation which leads to vasoconstriction of coronary arteries. The case of a 53-year-old patient with Prinzmetal's angina is described in whom spasms of the right coronary artery could be evoked by hyperventilation. The following pathogenetic mechanisms may be possible in Prinzmetal's angina: disturbed endothelial permeability, endothelial dysfunction, or secretion of vasoconstrictive substances as well as local hypersensitivity of segments disturbed by atherosclerotic lesions to circulating vasoconstrictors.

Angina Pectoris, Variant↗
PubMed1993

Left ventricular diastolic dysfunction late after coarctation repair in childhood: influence of left ventricular hypertrophy.

OBJECTIVES: Left ventricular systolic and diastolic function were evaluated late after successful operation for aortic coarctation in childhood. BACKGROUND: Persistent arterial hypertension and left ventricular hypertrophy after coarctation repair might impair left ventricular function. METHODS: Biplane angiography and simultaneous high fidelity pressure measurements were performed in 12 patients 3 to 12 years postoperatively (residual pressure gradient 4 mm Hg). Eight patients were normotensive and four had borderline hypertension. Data at rest and after nitroprusside infusion (1.7 micrograms/kg per min) were evaluated and compared with data from 12 control subjects. RESULTS: Systolic left ventricular function (ejection fraction-end-systolic wall stress relation) was normal in all patients. However, left ventricular muscle mass (113 vs. 86 g/m2), right atrial pressure (5.2 vs. 1.9 mm Hg) and left ventricular end-diastolic pressure (16 vs. 11 mm Hg) were significantly higher in patients than in control subjects. There was a linear relation between muscle mass and left ventricular end-diastolic (r = 0.66, p < 0.001) or right atrial (r = 0.60, p < 0.01) pressure. Left ventricular relaxation and myocardial stiffness were normal. However, there was an upward shift of the diastolic pressure-volume curve when compared with control values, but this shift was reversed by the administration of nitroprusside. CONCLUSIONS: Systolic function is normal late after coarctation repair. However, diastolic function can be abnormal with an upward shift of the diastolic pressure-volume curve that is reversed by nitroprusside administration and is probably due to residual left ventricular hypertrophy.

Adolescent↗
PubMed1992

Cloning and sequence analyses of cDNAs encoding aminoacylase I from porcine kidney.

cDNAs encoding L-aminoacylase (EC 3.5.1.14) were isolated from a lambda gt10 cDNA library derived from porcine kidney mRNA. The clones were identified by hybridization with a synthetic oligonucleotide probe based on partial peptide sequences, or with a DNA probe encoding human aminoacylase I. Several cDNA clones isolated from the library had a length of about 1.3 kbp. They contained an open reading frame of 1218 bp encoding a polypeptide of 406 amino acids. The deduced amino-acid sequence contains the known peptide sequences; in addition, M(r) (45.3 kDa) and amino-acid composition of the predicted polypeptide match those of purified aminoacylase I. Data base searches did not reveal significant sequence homologies of aminoacylase I with other well-known amidases.

Amidohydrolases↗
PubMed1992

[The anti-ischemic effect of gallopamil-retard in comparison with nifedipine-retard in stable angina pectoris].

To assess the antiischemic efficacy of slow-release (SR) gallopamil, 100 mg b.i.d., versus slow-release (SR) nifedipine, 20 mg b.i.d., 24 patients with chronic stable angina underwent symptom-limited bicycle ergometer exercise stress tests in a randomized, placebo-controlled, double-blind, cross-over protocol. Both medications caused a significant reduction in anginal attack frequency and nitroglycerin consumption as compared to placebo; similarly, exercise tolerance was augmented in association with a considerable reduction in ischemia-induced ST-segment depression. The antiischemic effect of gallopamil (SR) was marginally superior to that of nifedipine (SR). Since the incidence of adverse effects was also less with gallopamil (SR) this drug exhibited a more favorable risk-benefit ratio relative to nifedipine (SR).

Aged↗
PubMed1991

Right ventricular systolic function during exercise with and without significant coronary artery disease.

To evaluate the effects of exercise and coronary artery disease on right ventricular (RV) systolic function, rest and exercise biplane RV angiograms were recorded in 20 patients undergoing diagnostic cardiac catheterization. Thirteen patients had exercise angiograms of sufficient quality to undergo analysis and were classified into 2 groups. Group 1 had no or only mild coronary artery disease; group 2 had significant coronary artery disease as manifested by new, exercise-induced, left ventricular regional wall motion abnormalities. RV systolic pressure increased in both groups during exercise: 33 to 57 mm Hg in group 1 (p = 0.0002) and 33 to 55 mm Hg in group 2 (p = 0.0004). Pulmonary resistance did not change in group 1 during exercise but increased in group 2 (3.2 to 4.8 Wood units, p = 0.04). RV ejection fraction increased slightly, but not significantly, during exercise in group 1, but decreased in group 2 (73 vs 58% with exercise [p = 0.01]). The change in RV ejection fraction from rest to exercise correlated closely with the change in pulmonary resistance from rest to exercise (r = -0.89, p less than 0.0001). RV regional wall motion analysis demonstrated a generalized decline in regional ejection fraction in group 2 during exercise, even in patients without right coronary artery disease. In conclusion, there is a decline in RV ejection fraction during exercise in patients with significant coronary artery disease. The generalized reduction in regional RV ejection fraction coupled with the close correlation with the change in pulmonary resistance suggests that increased afterload, rather than RV ischemia, is the cause.

Angiography↗
PubMed1991

Left ventricular wall thickness measurements by magnetic resonance: a validation study.

Left ventricular (LV) wall thickness was determined by magnetic resonance (MR) in 15 patients (7 controls and 8 patients with coronary artery disease). End-diastolic (ed) and end-systolic (es) wall thickness were measured in a short axis view perpendicular to the LV long axis. Wall thickness measurements were compared to data obtained by digital subtraction angiography (DSA) and M-mode echocardiography (Echo). End-diastolic and end-systolic wall thickness were significantly overestimated by MR (34% and 37%, respectively) when compared to DSA. In contrast, LV end-diastolic and end-systolic chamber diameter were significantly underestimated by MR (25% and 30%, respectively) when compared to DSA. However, fractioned shortening was similar (all NS) for MR (48 +/- 22%), DSA (54 +/- 15%) and Echo (44 +/- 10%), respectively. The mean difference (= accuracy) and the standard deviation of difference (= precision) for LV wall thickness was 0.4 +/- 0.2 cm between MR and DSA, 0.4 +/- 0.3 cm between MR and ECHO and 0.03 +/- 0.1 cm between DSA and ECHO. The correlation of wall thickness between MR and DSA (correlation coefficient r = 0.74, p less than 0.001) and between MR and Echo (r = 0.70, p less than 0.001) was good although the standard error of estimate (SEE) was 17% for MR vs. DSA and 21% for MR vs. Echo. The corresponding SEE for chamber diameter was 16% between MR and DSA and 19% between MR and Echo, respectively. Intraobserver variability for wall thickness determination by MR was excellent (correlation coefficient r = 0.99, p less than 0.001) SEE of 4%. Interobserver variability was also good (correlation coefficient r = 0.90, p less than 0.001) with a SEE of 12%. It is concluded that LV wall thickness and chamber diameter (short axis plane) can be determined by MR with good precision but only satisfactory accuracy. LV wall thickness is significantly overestimated probably due to signals from static blood which might be indistinguishable from the subendocardium.

Angiography, Digital Subtraction↗
PubMed1991

Determination of left ventricular systolic wall thickness by digital subtraction angiography.

The accuracy of digital subtraction angiography (DSA) for determination of left ventricular (LV) systolic wall thickness and muscle mass was evaluated in 20 patients (mean age 50 +/- 11 years). Conventional LV angiograms were digitized and subtracted using a combined subtraction mode ('mask mode' and 'time interval difference' subtraction). Wall thickness and muscle mass were determined at end-diastole, after the first- and second-third of systole and at end-systole. M-mode echocardiography (Echo), which was obtained from beam selection of the two-dimensional echocardiogram and conventional angiography (LVA), served as reference techniques. Angiographic LV wall thickness and muscle mass were determined according to the technique of Rackley in both, right (RAO) and left (LAO) anterior oblique projections, whereas echocardiographic wall thickness was measured just below the mitral valve orthogonal to the posterior wall (= LAO equivalent). Percent wall thickening was calculated in all patients. LV end-diastolic wall thickness and muscle mass correlated well between DSA and LVA (LV end-diastolic wall thickness in LAO projection r = 0.72, biplane LV end-diastolic muscle mass r = 0.83), LV end-systolic wall thickness (1.44 vs 1.33 cm, P less than 0.05) and percent wall thickening (52 vs 42%, P less than 0.05) compared favourably between echocardiography and DSA but was significantly larger when echocardiographically measured than with DSA (LAO projection). DSA and echocardiography showed a good correlation in regard to LV end-diastolic and end-systolic wall thickness (correlation coefficient r = 0.89, standard error of estimate SEE = 0.15 cm or 13% of the mean value).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Comparison of dihydropyridine and phenylalkylamine calcium antagonists in patients with coronary heart disease.

To evaluate possible differences between dihydropyridine and phenylalkylamine calcium antagonists in the setting of chronic stable angina, 2 placebo-controlled, double-blind, crossover trials were conducted comparing the effects of gallopamil and nifedipine on exercise tolerance and ischaemic ST depression, using standard as well as slow release formulations. In the first study, 30 patients received standard formulations of gallopamil (50mg 3 times daily) and nifedipine (20mg 3 times daily). This trial was stopped after 9 patients had been enrolled, because of severe exacerbation of angina in 3 nifedipine recipients. 21 patients then entered a second protocol in which the nifedipine dose was reduced to 10mg 3 times daily. Compared with the preceding placebo periods, time to angina onset and total exercise time were statistically significantly (p less than 0.01) prolonged by gallopamil (by 30 and 18%, respectively), and nonsignificantly prolonged by nifedipine (by 20 and 13%, respectively), after 4 weeks' treatment. Increases in heart rate and rate-pressure product at maximal comparable workloads were less with gallopamil than with nifedipine (p less than 0.01). In contrast to nifedipine, gallopamil was associated with very few side effects. The second trial comprised 24 patients who received slow release formulations of gallopamil (100mg twice daily) and nifedipine (20mg twice daily) over 2 weeks. Again, both drugs exhibited significant anti-ischaemic efficacy, as evidenced by reductions in ST depression at maximal comparable workloads and increases in exercise time compared with placebo, but the differences between the treatments were not statistically significant. Side effects were more frequent with nifedipine, but less severe than with the standard formulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1990

Right ventricular diastolic function during exercise: effect of ischemia.

The effects of exercise on right ventricular diastolic function were evaluated in 14 patients who underwent supine rest and exercise right ventricular angiography. On the basis of coronary anatomy and exercise left ventricular regional wall motion analysis, these patients were classified into two groups: Group 1 (n = 7) had no or only mild coronary artery disease and Group 2 (n = 7) had significant coronary disease and exercise-induced left ventricular wall motion abnormalities suggesting ischemia. Chamber stiffness at rest was higher in Group 2 (48 x 10(-3) ml-1/m2) than in Group 1 (18 x 10(-3) ml-1/m2, p = 0.006). During exercise, right ventricular filling rate in the second half of diastole was significantly lower in Group 2 (126 versus 276 ml/m2 per s, p less than 0.03). The time constant of right ventricular pressure decay decreased significantly in both groups with exercise; however, both groups displayed a parallel upward shift of the pressure-volume curve with exercise. Because ischemia could not be demonstrated in Group 1, it is an unlikely explanation for this shift. Septal shifting was not a significant factor with exercise. Because of an increase in left ventricular end-diastolic volume with exercise and a close correlation between right and left ventricular end-diastolic pressures (r = 0.96 for Group 1 and r = 0.76 for Group 2), pericardial constraint is the most likely cause for this upward shift of the pressure-volume curve. Therefore, an increase in right ventricular end-diastolic pressure may not be a reliable indicator of ischemia during exercise because this pressure is coupled to changes in left ventricular volume and pericardial constraint.

Angiocardiography↗
PubMed1989

[Anemia in malignant tumor diseases. VI. Secondary siderosis caused by the shift of iron, unused for hemoglobin synthesis, into iron stores].

Impaired utilization of iron by the heme synthesizing red cell precursors was investigated in 258 patients with malignant tumors of different histological types and different tumor spread. There was evidence, that impaired iron uptake by the erythropoietic cells results in an increased flow of iron to the reticuloendothelial iron stores. Investigations on bone marrow smears showed that sideroblast counts were significant lower than in healthy controls reflecting a deficient iron supply to the erythropoietic cells. In contrast, reticuloendothelial storage iron was increased paralleled by an increased serum ferritin concentration. Both abnormalities correlated with the malignancy and the stage of the tumor. It could be demonstrated that the degree of the hyperferritinemia paralleled very closely the severity of the anemia becoming more pronounced with increasing tumor mass. This parallelism indicates that the siderosis is pathophysiologically related to the defect of erythropoiesis observed in malignant disease. Since the iron uptake by the erythropoietic cells is mediated by transferrin in a further series of experiments the serum transferrin concentration was investigated in malignant diseases. There was found a close inverse correlation between serum transferrin concentration and serum ferritin concentration. This correlation supports the concept of a defect in erythropoiesis due to an impaired transferrin mediated iron supply caused by tumor induced hypotransferrinemia. This defect is responsible for a shift of iron to the iron stores and a secondary siderosis.

Adolescent↗
PubMed1989

[Anemia in malignant tumor diseases. V. The relation of tumor-induced hypotransferrinemia and the degree of anemia].

Transferrin is a growth factor in malignancy. In this function, transferrin is taken up into the proliferating malignant cell. The tumor-induced loss of circulating transferrin results in a hypotransferrinemia which correlates with tumor mass and proliferation rate. The cellular uptake of iron into the erythropoietic precursors depends on the presence of iron-saturated transferrin. Thus, iron utilization for the hemoglobin synthesis correlates with the transferrin concentration in blood. In 256 patients with malignancies of different histological types and different tumor extension a strong correlation was found between the degree of tumor-induced hypotransferrinemia and anemia. This correlation between transferrin concentration and hemoglobin concentration could be demonstrated in the different histological tumor entities. Tumor progression was accompanied by a progressive fall in transferrin concentration and hemoglobin concentration. By contrast, tumor remission achieved by an effective antineoplastic therapy resulted in an improvement of hypotransferrinemia and anemia. These variations in the two parameters were found to be strongly correlated. We conclude from our data that tumor-induced loss of transferrin is one of the most important factors responsible for the development of anemia in malignancy.

Adult↗
PubMed1982

[Gel model for measuring crystallization inhibitor activity].

In an attempt to develop a method with the most favourable possible relationship of information gained to expenditure of material and time a simple way of measuring crystallisation inhibitor activity was developed. Calcium and oxalate ions are diffused against each other out of two opposite start holes in a layer of gel on a microscopic slide and form a strip of calcium oxalate crystals where they meet in the middle. The substances influencing crystallisation are allowed to diffuse into this central area. The density and extent of the calcium oxalate strips vary according to the inhibitory effect of the substances used. These differences were registered by means of photometric measurement for comparison against a control without any inhibitor added and an inhibition index was computed. Some of the best-known inhibitors were tested and also show a defined effect in this model. In physiological concentrations magnesium and citrate can be said to have particular importance. The range of inhibitory activities to be expected of human urine is covered by the present model.

Anthraquinones↗