Complications of mechanical heart valve prostheses.
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Biomedical subjects
Publications and source records attributed to J Butany.
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Amiodarone, an antiarrhythmic drug, like chloroquine and chlorpromazine, is a tertiary amine with amphiphilic properties. Chloroquine and chlorpromazine are known inhibitors of phospholipases. All three drugs produce characteristic microcorneal deposits consistent with lysosomal accumulations of phospholipid. Similar lysosomal bodies were found in leukocytes of 15 patients on chronic amiodarone treatment as well as 3 patients each on chloroquine and chlorpromazine, suggestive of widespread systemic inhibition of lysosomal phospholipases. These lysosomal inclusions were similar in morphology, irrespective of the drug given, and were of four types: multilamellar, amorphous dense, amorphous light, or a combination of 2 or more of the preceding types. There was no simple relationship between the number of inclusion bodies per cell and the cumulative dose of amiodarone (r = 0.02) or amiodarone serum levels (r = 0.11). An in vitro assay was used to compare the effects of the three drugs on Ca2+-dependent phospholipase A2 and C activities. Phospholipase A2 activity was inhibited in a dose-dependent fashion (1-8 mg/assay) by all three drugs in the order: chlorpromazine greater than amiodarone greater than chloroquine. The inhibitory effect on phospholipase C was more pronounced with all three drugs, producing almost total inhibition at 8 mg/assay. In a Ca2+-independent lysosomal phospholipase A system, amiodarone had a greater effect, producing 85% inhibition at 1.2 mg/assay. These observations suggest that amiodarone, like other cationic amphiphiles, induces a generalized phospholipidosis by inhibiting phospholipid catabolism. Its therapeutic and toxic effects may be due to its ability to modulate both Ca2+-dependent membrane phospholipases and Ca2+-independent acid phospholipases.
A higher prevalence of Chlamydia trachomatis antibody occurred in 57.6% of women with recurrent abortion, but not in their male partners, compared to 33.7% of normal pregnant women (p less than 0.01) and 44.2% of infertile women (NS). The mean titer for the recurrent abortion group was not significantly elevated, compared to controls. Women with blocked fallopian tubes had the highest prevalence of elevated titers (p less than 0.01) and the highest mean titer (p less than 0.001). Despite multiple testing, no women or men were chlamydia culture-positive. The lack of isolation among patients with antibody could be due to cryptic infection at a site not amenable to culture or to inhibition by secretory IgA. There could also be nonspecific stimulation of chlamydial antibody caused by other infections such as mycoplasma. The presence, though at a low level, of antibody in culture-negative patients suggests chlamydia may not be directly associated with recurrent abortion but reflect previous exposure to chlamydia or an altered immune system.
In a study of 33 cases of perinatal death, chorioamnionitis was observed in 57.6% compared with 5% of 20 control cases (p less than 0.001) and in 70.8% of cases with no morphologic cause compared with 22.2% of cases with a defined cause of death (p less than 0.01). Chorioamnionitis was significantly associated with previous gestations (p less than 0.01), prolonged rupture of the membranes (p less than 0.001), prematurity (20 to 27 weeks' gestation) (p less than 0.001), and low birth weight (less than or equal to 1000 gm) (p less than 0.001) but not with elevated maternal white blood cell count or pyrexia. Overall, in patients with chorioamnionitis, the perinatal death rate was higher (p less than 0.01); more stillbirths occurred compared with early neonatal deaths (p less than 0.05), and there was a higher incidence of deaths with no defined cause (p less than 0.01) compared with cases without chorioamnionitis. Ureaplasma urealyticum or pathogenic bacteria were isolated more frequently from villous tissue of placentas from cases with chorioamnionitis (p less than 0.01) but not Mycoplasma hominis, Chlamydia trachomatis, or viruses. Furthermore, there was a higher prevalence of both elevated fetal antibody titer to U. urealyticum (p less than 0.025) and fetal titer fourfold above maternal titers (p less than 0.05) in cases with chorioamnionitis. The antibody responses and presence of microorganisms suggest that chorioamnionitis is associated with intrauterine infection and an associated increase in perinatal morbidity and mortality.
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Amiodarone, an antiarrhythmic agent, is known to cause photosensitivity and cutaneous hyperpigmentation. Five patients taking this drug for periods of 1 to 48 months were studied. Skin biopsy specimens taken from a sun-exposed site were assessed by light microscopy, electron microscopy, and direct immunofluorescence. Three patients allowed comparative studies to be done on a biopsy specimen from non-sun-exposed skin. Light microscopy findings, including special stains, were not diagnostic of amiodarone-associated cutaneous changes. Electron microscopy, however, displayed distinctive intracytoplasmic inclusions in many cell types, some of which have not been reported previously. These inclusions represent phospholipid membranes associated with amiodarone or its metabolites as the result of a drug-induced lipidosis. Previous reports had postulated the inclusions were lipofuscin. Sun exposure may accelerate the formation of these intracellular deposits because they are more prominent in sun-exposed skin. Four of the above five cases, plus two additional patients, had symptoms compatible with a photosensitivity. Porphyrin assays were normal. Of the six patients phototested, three showed acute reactions to ultraviolet A (UVA) and ultraviolet B (UVB) and significant delayed reactions to UVA and/or UVB. The patients who had normal phototesting were on the drug for shorter periods than those with positive tests.
A 61-year-old woman with symptoms of inferior vena caval obstruction was investigated with computed tomography and ultrasound imaging and found to have a tumor of the inferior vena cava. Transvenous biopsy revealed a leiomyosarcoma, which at surgical exploration was considered to be unresectable. Autopsy showed that the tumor extended form its origin in the inferior vena cava just above the left renal vein to the right atrium. Hepatic metastases were documented. This rare tumor has seldom been diagnosed prior to exploratory surgery or necropsy and should be included in the differential diagnosis of inferior vena caval obstruction. The case illustrates the relative ease and efficacy of transvenous biopsy in establishing this diagnosis antemortem.
We present a case of non-Hodgkin's lymphoma with massive cardiac involvement in a previously well 65-year-old man, presenting with pericardial tamponade and heart failure of recent onset. Results of echocardiography and of pericardial and pleural fluid cytology suggested the diagnosis. Within two weeks the patient's condition progressed to complete heart block and he died. Primary cardiac tumors are rare when compared with metastatic involvement of the heart. Their presentation includes congestive heart failure, cardiomegaly, pericardial effusion, and sudden death. The clinical diagnosis has seldom been made.
A xenon-chlorine excimer laser was used to irradiate normal endocardium of fresh sheep and pig hearts as well as unfixed human endocardial scar. Forty pulses of 370 J and 35 ns each resulted in penetration of up to 12 mm in normal tissue and only 3.5 mm in scarred endocardium. Dosimetry indicated that the volume of vaporized scarred tissue was 1/10th that of normal endocardium (0.19 to 0.40 versus 1.35 to 3.22 mm3/J). Ultrastructurally, there was a sharp demarcation of only 10 mu between the region of injury and normal myocardium, with little evidence of heat injury. The high power and short duration of these lasers coupled with the lack of a boundary zone of injury suggest that excimers may be an ideal tool for arrhythmia ablation.
The healing phase of acute myocardial infarction (AMI) is initiated by proteolysis of necrotic myocardium, followed by infiltration of fibroblasts and deposition of collagen. To assess whether ibuprofen, a potent antiinflammatory agent, preserves existing collagen and enhances deposition of new collagen during infarct healing, biochemical and morphologic studies were made of experimentally induced myocardial infarcts in untreated rats and in rats treated with ibuprofen. All treated rats received 12.5 mg/kg of ibuprofen at 1, 6 and 18 hours after AMI. Group 1 rats underwent measurement of myocardial hydroxyproline (HP) content at 24 hours after AMI. Group 2 rats received ibuprofen, 12.5 mg/kg, twice a day for 2 additional days, with measurement of myocardial HP at 3 days (group 2a) or 21 days (group 2b) after AMI. Group 3 rats received ibuprofen, 12.5 mg/kg, twice a day for 6 additional days with measurement of HP content, or infarct size and degree of thinning at 21 days after AMI. Compared with untreated rats, ibuprofen-treated rats had significantly greater amounts of HP in the infarct at 24 hours (group 1, 8.9 +/- 2.2 nmol/mg dry weight vs untreated, 7.1 +/- 2.8 nmol/mg dry weight, p less than 0.04) and at 21 days (group 2b, 112 +/- 37 nmol/mg dry weight vs untreated, 91 +/- 39 nmol/mg dry weight, p less than 0.05, and group 3, 125 +/- 51 nmol/mg dry weight vs untreated, 91 +/- 39 nmol/mg dry weight, p less than 0.003). Substantial scar thinning was noted in all rats; no difference in scar thinning was noted between treated and untreated rats at 21 days after AMI.(ABSTRACT TRUNCATED AT 250 WORDS)
No morphologic cause of death was found in 67.8% of 33 perinatal deaths. The mothers had experienced a previous loss in 48% of cases. Inflammation occurred in 65.6% of the cases of perinatal death compared to 4% of a control group (p less than 0.001) and in 73.1% of organism-positive cases of perinatal death compared to 7.1% of organism-positive cases of the control group (p less than 0.001). Incidence of maternal fever or prolonged membrane rupture was not statistically significant. Bacteria were present in 33.3% of the cases of perinatal death (not significant), with more pathogenic strains occurring in this group (p = 0.0028); 75.0% had inflammation compared to 0% of the control group (not significant). Genital mycoplasmas were detected in 78.8% of cases of perinatal death compared to 32.3% of control cases (p less than 0.001). Positive cultures (p = 0.0142) and elevated antibody titers in the fetus or neonate (p = 0.00052) or in the mother (p = 0.0122) occurred significantly more often than in control cases. Inflammation occurred in 78.9% of mycoplasma cases (p = 0.00032); incidences of maternal fever and prolonged membrane rupture were not significantly different. In perinatal death cases 20% had evidence of viruses, and 3.2% had evidence of chlamydia. Evidence of mixed microorganisms occurred in 46% of cases of perinatal death. However, 78.6% (11 of 14) with only one organism had Ureaplasma urealyticum (33.3% overall). Of the Ureaplasma-positive cases, 72.7% had inflammation, 45.5% had fever, and only 18.2% had prolonged membrane rupture compared to 28.6%, 0%, and 16.6%, respectively, in a negative-microorganism group with perinatal deaths. Our observations strongly support the concept that infection is a major cause of perinatal death and that genital mycoplasmas play a significant role.
Thrombosis of a prosthetic valve is one of the most serious cardiovascular events. Emergency replacement of the prosthetic valve has been the standard method of management but carries a high operative risk. This paper describes the successful use of streptokinase, given intravenously, to manage a patient with this complication in the acute phase. Eventually, operation was necessary because the presence of residual organized clot was suspected, but the procedure was performed electively 10 days later.
Aorta to right ventricular fistula is a rare complication of ascending aortic dissection that has previously been diagnosed ante mortem only by cardiac catheterization. This report describes a patient who had aorta to right ventricular fistula that caused a left-to-right shunt and marked hemodynamic instability. An anatomic diagnosis was made rapidly in this patient by use of echocardiographic techniques. Two-dimensional and Doppler echocardiography have an important role in defining the cause of cardiovascular collapse after aortic dissection.
Acute iron poisoning and chronic iron overload are well-known causes of myocardial failure. Although the exact mechanism is not known, excess iron-catalyzed free radical generation is conjectured to play a role in damaging the myocardium and altering cardiac function. We report here on the effects of acute and chronic iron-loading on the total iron concentration, glutathione peroxidase activity, and cytotoxic aldehyde production in the heart of a murine model (n = 35). Light microscopic examination for the presence of ferrous and ferric iron was undertaken following histochemical staining for these species. In addition, examination of representative samples by transmission electron microscopy was performed. Our findings show that iron-loading can result in significant increases in total iron concentrations, alterations to glutathione peroxidase activity, and increases in cytotoxic aldehyde concentrations in the hearts of mice. Furthermore, we observe that iron-loading can significantly alter and damage various cellular constituents (e.g., mitochondria, lysosomes, sarcoplasmic reticulum) and this may have bearing on the mechanism of iron-induced heart failure.
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Six (3 control and 3 explanted) bioprostheses were examined histologically after embedding the complete valve in "plastic" and sectioning across the valve at 90 degree to the horizontal plane, and then horizontally across a stent post, with a low speed saw. The prostheses, porcine or pericardial, had been in place 52 to 121 months. In addition to cusp changes of degeneration and calcification that have been previously reported, the authors found extensive pannus deposition on the cloth covering the inflow surface of the prostheses, with some extension onto the biologic components; evidence of insudation of tissue fluid and ingrowth of fibroblasts; deposition of collagen; and infiltration of mononuclear cells in the interstices and interfaces. Non-biologic components showed changes which may have affected prosthesis function. The synthetic material covering the metal/plastic frame showed interstitial mononuclear cells. Two of the three explanted valves showed changes in the polymeric plastic, and one in the metal components, including accentuated notching along the surfaces when compared to unimplanted prostheses. A larger number of prostheses must be examined before definite conclusions can be drawn.