Cor pulmonale caused by recurrent pulmonary emboli

A 53-year-old black man developed femoral thrombophlebitis in 1983 following a Harrington nail implantation in his first lumbar vertebral region. There was evidence of pulmonary embolization at that time and recurrently until he developed ventricular fibrillation and died in 1987. The terminal event followed a hypotensive episode during the course of a right ventricular catheterization. Autopsy confirmed the clinical impression that he had multiple recurrent thromboemboli to his lungs. After several years of embolization, the pulmonary arterial circulation was sufficiently occluded to result in pulmonary hypertension. Cor pulmonale was produced, with congestive heart failure leading to a progressively downhill course in the 4 months before his death.     

The effects of l-norepinephrine on myocardial zonal lesions in dogs in hemorrhagic shock

Intravenous l-norepinephrine was given to dogs in hemorrhagic shock to determine the effect on myocardial zonal lesions which are characteristically seen in hypovolemic shock. Zonal lesions produced by hemorrhagic shock in drug-treated and nondrug-treated groups were quantitatively compared both at the light microscopic and ultrastructural levels. A significantly greater percentage of myocardium was found to be involved with zonal lesions in animals treated with l-norepinephrine following shock as compared to that found in nondrug-treated animals. The effect was greater for the right ventricle than for the left ventricle. The average size of zonal lesions was slightly smaller in the drug-treated group, indicating that there must have been a greater total number of zonal lesions produced in the treated group. Zonal lesions were not present in "sham shock" animals nor in animals given l-norepinephrine alone. The results indicate that the treatment of hemorrhagic shock with l-norepinephrine can be anatomically deleterious to the heart.     

Microproteins in amniotic fluid as an index of changes in fetal renal function during development

Protein content and protein composition were studied in amniotic fluid obtained from 171 healthy pregnant women between the 16th and 38th week of gestation, using microgradient gel electrophoresis to separate proteins according to their molecular size into albumin (68 KD), proteins of low molecular weight (LMW proteins, <68 KD), and proteins of high molecular weight (HMW proteins, >68 KD). Additionally -1-microglobulin (-1-MG, 33 KD) and -2-microglobulin (-2-MG, 11,8 KD) were analysed as micromolecular marker proteins. Concentrations of LMW proteins were 0.15–0.22 g/l, of -1-MG 28.4–34.5 mg/l, and of -2-MG 7.2–11.6 mg/l during the second trimester of gestation, and thereafter decreased progressively to 0.03 g/l, 14.1 mg/l and 2.4 mg/l respectively near term. The same developmental trends were confirmed by calculating the protein/creatinine ratios in amniotic fluid. The concentrations of LMW proteins found in the first postnatal urine of 73 healthy infants born prematurely or at term were similar to those in amniotic fluid of corresponding fetal age. Concentrations of albumin and HMW proteins in postnatal urine were about 5% and 15% respectively when compared with amniotic fluid concentrations. No strong correlation existed between gestational age and either of the analysed proteins which would allow accurate assessment of fetal maturation by protein analysis in amniotic fluid. It is concluded that fetal urinary excretion is the major determinant of the microprotein content of amniotic fluid. Microproteins seem to reflect an increasing tubular reabsorption capacity, which accelerates rapidly after the second trimester of gestation.     

The EGF receptor as central transducer of heterologous signalling systems

The cross-talk between heterologous signalling systems of the cell represents a new dimension of complexity in the molecular communication network that governs a great variety of physiological processes. In pathophysiologically transformed cells, key elements of this network could offer unique opportunities for pharmacological intervention. In this article, the current state of knowledge regarding the role of epidermal growth factor (EGF) in such a network is described and the recent advances made in the elucidation of the mechanism underlying EGF receptor transactivation are discussed.     

Evaluation of a QRS scoring system for estimating myocardial infarct size. II. Correlation with quantitative anatomic findings for anterior infarcts

The ability of an independently developed QRS point score to estimate the size of infarcts predominantly within the anterior third of the left ventricle was evaluated by quantitative pathologic-electrocardiographic correlation. The study was limited to 21 patients with a single infarct documented by postmortem examination, for whom an appropriately timed standard 12 lead electrocardiogram was available that did not exhibit signs of left or right ventricular hypertrophy, left or right bundle branch block or anterior or posterior fascicular block. At necropsy the heart was cut into five to seven slices. The location and size of the infarct was quantitated by computer-assisted planimetry of the slices.The electrocardiogram of 19 (90 percent) of the patients exhibited either a Q wave or an R wave of no more than 20 ms in lead V₂. The infarct in the two patients without this electrocardiographic finding was small, occupying 2 and 3 percent of the left ventricle, respectively. The percent infarction of the left ventricle correlated with the QRS point score (r = 0.80). Thus in patients without complicating factors in the electrocardiogram and with a single infarct, the electrocardiogram provides a marker for infarction in the anterior third of the left ventricle and permits estimation of infarct size.     

Acute myocardial infarction with papillary muscle rupture

The subject of this report is a 57-year-old obese, hypertensive woman who had been well until the onset of severe chest pain and hypotension. She had to be defibrillated four times on her way to the hospital. The diagnosis of acute inferior-posterior infarction was made by electrocardiogram (ECG) and there was a markedly elevated serum creatine kinase (CK) (including the MB fraction). The patient had a very low cardiac output and ejection fraction. A lung scan revealed possible pulmonary embolism for which she was anticoagulated. She remained hypotensive and hypoxemic and, on Day 17 of her hospital stay, she had a bout of severe dyspnea. A new systolic murmur was heard and the clinical diagnosis of ruptured papillary muscle was made and confirmed by echocardiography, and later at autopsy. All three coronary arteries were severely atherosclerotic and, in addition, the right coronary artery was completely closed by a thrombus. This case clearly illustrates the major pathological changes in the heart that correlate with the clinical findings in patients with a myocardial infarct that is complicated by left ventricular papillary muscle rupture. The pathophysiological effects of this condition, as illustrated in this case report, include the following: 1. The posterior papillary muscle was almost completely separated from its base, with only a thin strip of muscle intact. The mitral valve thus was insufficient (a “flail valve“); this markedly reduced the ejection fraction of the left ventricle, increased its end-diastolic volume and pressure, produced a damming of blood in the pulmonary circulation, and this resulted in the pulmonary edema seen on the chest x-ray. 2. Cardiac hypertrophy (weight = 561 g) was undoubtedly the result of the increased workload imposed on the left ventricle by the systemic arterial hypertension that this patient had for several years. A high blood pressure that persists after a myocardial infarct predisposes to myocardial rupture, but was probably not a risk factor in her case since it did not persist. 3. The cause of the myocardial infarct was the thrombotic occlusion of the right coronary artery (on top of severe three-vessel coronary atherosclerosis), which resulted in infarction of the right as well as the posterior left ventricle and can partly explain the mistaken clinical impression that she had pulmonary emboli.