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Biomedical subjects

M Lesch

Publications and source records attributed to M Lesch.

At least 91 records · Page 5Linked to original sources
PubMed1981

Sudden death associated with thyroid hormone abuse.

Three patients with hyperthyroidism due to deliberate intake of excessive amounts of L-thyroxine are described wherein death was "instantaneous" and presumably due to ventricular fibrillation. Hyperthyroidism was not recognized on admission in two of these patients because of atypical presentations. Autopsy was performed in two patients. In one patient no coronary disease was present and focal myocarditis with leukocytic infiltration was noted. The second patient had an acute posterior myocardial infarction due to acute coronary thrombosis, but focal areas of leukocytic infiltration and fibrosis were also seen in the anterior wall not involved in the process of infarction. Factitious hyperthyroidism due to L-thyroxine abuse can be associated with sudden death in the absence of coronary artery disease and may be related to a drug induced myocarditis.

Adult↗
PubMed1981

A double antibody radioimmunoassay for canine cardiac cathepsin D.

We have developed a sensitive double antibody radioimmunoassay for measuring canine cardiac cathepsin D. Radioiodinated cathepsin D was prepared by chloramine T oxidation using a highly purified source of enzyme. High avidity antiserum to the canine cardiac enzyme was raised in rabbits. Antibody-bound cathepsin D was separated from free enzyme using goat anti-rabbit IgG second antibody. The least amount of immunoreactive enzyme measurable in the radioimmunoassay was 2.4 ng.cm-3 as determined by antibody titration. The assay was linear for concentrations of enzyme in the range of 10 to 120 ng.cm-3. Within-assay and between-assay variations were 12%. The radioimmunoassay described was used to measure the immunoreactive cathepsin D content of the 100 000 x g supernatant fraction of canine myocardial homogenates.

Animals↗
PubMed1981

Rabbit cardiac immunoreactive cathepsin D content during starvation-induced atrophy.

To determine whether the increased activity of cathepsin D observed during starvation-induced cardiac atrophy results from activation of preexisting enzyme or synthesis of new enzyme, a solid phase double-antibody radioimmunoassay was developed for measurement of immunoreactive cathepsin D in extracts of rabbit myocardium. Cathepsin D activity was significantly increased in the hearts of animals starved for 3, 7, and 14 days (82.6 +/- 0.8, 87.2 +/- 3.8, and 95.3 +/- 3.5 U/g wet wt, respectively) compared to controls (65.5 +/- 1.4 U/g wet wt; P less than 0.001). Immunoreactive cathepsin D was increased to a greater extent (168 +/- 7, 179 +/- 16, 200 +/- 17, and 104 +/- 5 micrograms/g wet wt for 3-, 7-, and 14-day starvation and controls, respectively; P less than 0.001) than that expected on the basis of the observed increase in enzyme activity. Sephadex G100 gel filtration of cardiac lysosomal extracts from starved and control animals revealed no evidence of high or low molecular weight forms of cathepsin D. The results suggest the observed increase in cathepsin D activity during starvation-induced cardiac atrophy is accompanied by an increased synthesis and/or decreased degradation of cathepsin D protein, rather than activation of preexisting enzyme. The lower activity levels observed during starvation possibly result from alterations in the concentrations of endogenous inhibitors or activators of cathepsin D.

Acid Phosphatase↗
PubMed1981

Systolic anterior motion in the absence of asymmetric septal hypertrophy. A buckling phenomenon of the chordae tendineae.

Systolic anterior motion (SAM) of the mitral valve in the absence of asymmetric septal hypertrophy or concentric left ventricular hypertrophy has been reported in several conditions. In this report we describe the clinical and echocardiographic findings in 15 patients who demonstrated SAM without associated organic heart disease (group 1, 10 patients) or in association with mitral valve prolapse (group 2, five patients). Cross-sectional echocardiography revealed the etiology of SAM in both groups to be early systolic anterior angular motion ("buckling") of mitral chordal structures, rather than movement of the body of the anterior mitral leaflet into the left ventricular outflow tract. In contrast to normal subjects and group 1, group 2 patients had auscultatory evidence of mitral prolapse, a slightly greater mean left ventricular ejection fraction (p < 0.05) (normals, 69 +/- 5.2%, group 1, 72 +/- 3.8%, group 2, 75+/- 5.6%), and a greater mean diastolic mitral valve (D-E) excursion (p < 0.05) (normals, 1.8 +/- 0.2 cm, group 1, 2.2 +/- 0.3 cm, and group 2, 2.6 +/- 0.4 cm). This spectrum of mitral excursion and left ventricular ejection fraction supports the concept that the mitral valve prolapse syndrome may have as its basis a mitral valve abnormality and/or a hyperdynamic state that predispose to both chordal buckling and mitral leaflet prolapse.

Adult↗
PubMed1979

Acquired cyanotic heart disease secondary to traumatic tricuspid regurgitation. Case report with a review of the literature.

A case of traumatic tricuspid insufficiency leading to right atrial enlargement and to a patent foramen ovale with right to left shunting is presented. Six similar cases previously reported are reviewed. The time course of clinical deterioration was related to the type of tricuspid valve damage incurred. Papillary muscle rupture led to surgery within a year, whereas less severe chordal damage allowed a more benign course that lasted from 10 to 25 years from the time of injury to the time of surgery. Surgical repair of the incompetent tricuspid valve and closure of the atrial septal defect led to significant improvement. The diagnostic usefulness of radionuclide imaging and echocardiography is demonstrated in this case. A mechanism of right to left interatrial shunting in the presence of normal pulmonary arterial pressures is proposed; this invokes phasic increases in right atrial pressure from tricuspid insufficiency and streaming of blood from the inferior vena cava into the left atrium across a patent foramen ovale in a manner that resembles conditions in the fetal circulation.

Adult↗
PubMed1979

Technetium-99m stannous pyrophosphate myocardial scintigraphy after cardiopulmonary resuscitation with cardioversion.

Thirty consecutive patients underwent technetium-99m stannous pyrophosphate myocardial scintigraphy 48--72 hours after successful cardiopulmonary resuscitation and direct current cardioversion. Five patients with transmural myocardial infarctions by ECG and enzyme determinations were correctly identified by scintigraphy. Myocardial scans were positive in five of nine patients with nontransmural infarction. Of 16 patients without evidence of myocardial infarction, only two (13%) had false-positive myocardial scans. The overall accuracy of imaging in this series was 80%. We conclude that false-positive scans after cardiopulmonary resuscitation with electrical cardioversion are infrequent, and do not significantly detract from the value of myocardial scintigraphy in the diagnosis of myocardial infarction.

Aged↗
PubMed1978

Myocardial scintigraphy with technetrium-99m pyrophosphate during the early phase of acute infarction.

To determine the sensitivity of myocardial scintigraphy with technetium-99m pyrophosphate during the early phase of acute myocardial infarction, 31 patients admitted to the coronary care unit with prolonged ischemic pain underwent imaging within 4 to 8 hours and again at 24 hours after the onset of symptoms. In 11 of 15 patients with documented acute myocardial infarction, increased focal myocardial uptake was demonstrated on early myocardial scintigraphy. Focal uptake was observed in only 2 of 16 patients with unstable angina pectoris. Three or four patients with normal early scintigrams had massive transmural myocardial infarction. Normal early scintigrams in these three patients may have reflected poor perfusion because the images were abnormal at 24 hours. In four patients the extent of technetium-99m pyrophosphate uptake increased more than 20 percent at 24 hours without other evidence of infarct extension. In the other seven patients, there was no significant change in the area of the abnormal radioactive uptake between early and delayed scintiscans. This study suggests that technetium-99m pyrophosphate scintigraphy can defect acute myocardial infarction as early as 4 hours after the onset of symptoms although the sensitivity rate (73 percent) is less than that at 24 hours.

Acute Disease↗
PubMed1978

Elevation of platelet factor four in acute myocardial infarction: measurement by radioimmunoassay.

A radioimmunoassay has been developed for the measurement of PF-4--a chemically well-defined heparin-neutralizing molecule. PF-4 was iodinated, repurified by affinity chromatography on heparin-Sepharose, and incubated with rabbit antiserum and a source of unlabeled antigen. Following incubation at 4 degrees C for 24 hr, bound PF-4 was precipitated with 2.2M ammonium sulfate. The assay, which could detect 25 pg of purified PF-4, was unaffected by the presence of plasma containing up to 50 U/ml heparin. The plasma concentration of PF-4 in 30 normal subjects was 16 +/- 4 ng/ml. This level was increased in patients with pulmonary emboli, prosthetic cardiac valves, and severe cardiorespiratory failure. In addition, 21 of 50 patients admitted to the hospital with acute chest pain who had sustained a myocardial infarct had a mean level of 95 ng/ml. In contrast, the mean level in 21 patients with chest pain but without evidence of infarction was 29 ng/ml. PF-4 remained elevated for at least 1 week after infarction in six of the eight patients studied and then returned to within the normal range. The data suggest that radioimmunoassay of PF-4 may be a useful test to measure activation of the coagulation system and an aid to the diagnosis and treatment of patients with thromboembolic disorders.

Acute Disease↗