Showing papers in "The American journal of cardiovascular pathology in 1987"

Granulocytes as active participants in acute myocardial ischemia and infarction.

Abstract: The classical picture of the polymorphonuclear leukocyte--antimicrobal activities and participation in the inflammatory reaction--appears now to be expanded. It has been recognized that this cell may be highly injurious to other cells, has a propensity to be trapped in the capillary network, and may occlude microvascular pathways. The classical hypothesis that the granulocytes appear in the ischemic or postischemic myocardium as response to the associated inflammatory reaction may have to be revised. Instead, the granulocyte may actually be the key factor causing the inflammation. An array of future studies is needed to clarify the events step by step. Important aspects are the activation and degranulation sequence in the ischemic myocardium, the form and extent of injury caused by the oxygen free radicals and lysosomal enzymes, the source and nature of chemotactic substances, particularly in human forms of myocardial ischemia, and the degree to which granulocytes cause or magnify the injury.

Alterations of the myocardial skeletal framework in acute myocardial infarction with and without ventricular rupture. A preliminary report.

Abstract: Thinning and dilatation (expansion) of the infarct region and complete rupture of the ventricular wall are significant complications of acute transmural myocardial infarction associated with increased morbidity and mortality. The pathogenesis of these related events is unknown. Recent studies of myocardial connective tissue have delineated an extensive array of intercellular and pericellular structures which serve as a skeletal framework and which may modulate contractile activity. We have employed a modified silver impregnation method to visualize the connective tissue components by light microscopy. To explore whether the skeletal framework is altered in acute myocardial infarction with and without ventricular rupture, we studied 9 human hearts at autopsy, and 4 canine infarcts of known duration. The human infarctions included 4 nonruptured cases with infarcts 1-5 days old, and 5 ruptured cases with infarcts 3-10 days old. Sections from normal, lateral, and central infarct or ventricular rupture sites were stained with silver. The normal tissue from each heart served as a control. Silver staining was moderately decreased in the lateral infarct zones, and markedly decreased in the central non-ruptured infarct zones. In the 5 ventricular rupture cases, the rupture site had no silver staining. A similar pattern was observed in the 4 canine infarcts. Thus, we conclude that the skeletal framework is markedly altered in the central zone of acute myocardial infarction. The acute changes of silver stained connective tissue may contribute significantly to the development of infarct expansion or ventricular wall rupture.

Venous valves in subclavian and internal jugular veins. Frequency, position, and structure in 100 autopsy cases.

Abstract: Valves in the subclavian and internal jugular veins were studied in 100 autopsy cases (52 men and 48 women; range, 18 to 91 years old; mean, 67 years). In 87 cases, valves were present in all 4 veins, and in 13 cases, valves anatomically were absent from 16 veins, 9 of which were the left internal jugular vein. The average distance from the valve to the junction with the innominate vein was 1.7 cm for the subclavian vein and 0.3 cm for the internal jugular vein. Cuspid height averaged 0.9 cm. Valves were bicuspid in 347 (90%) and unicuspid in 39 (10%); unicuspid valves were more common in the internal jugular vein than in the subclavian vein. Catheter-induced trauma was observed in 4 cases and implied in 4 more. These findings may have important implications concerning the failure, in some cases, of closed-chest cardiac resuscitation to maintain forward blood flow at adequate pressure.

Ameroid constriction of the proximal left circumflex coronary artery in swine. A model of limited coronary collateral circulation.

Abstract: Gradual narrowing and occlusion of a coronary artery in patients with atherosclerotic heart disease frequently causes enlargement of the collateral circulation. Although these vessels may protect from development of myocardial infarction, they frequently do not supply sufficient blood flow to prevent ischemia during periods of augmented myocardial oxygen demand. The purpose of this study was to develop a model of the collateral circulation in pigs, a species that previously has been shown to develop sparse collateral vessels. Eighteen pigs were instrumented with an Ameroid constrictor around the proximal left circumflex artery and left atrial and aortic catheters. In four animals the constrictor was placed just distal to a large proximal obtuse marginal vessel. Seven of the pigs were treated daily with oral aspirin (325 mg) and disopyramide (200 mg) throughout the study; the other 11 served as controls. After an average of 24 days postoperatively, radioactive microspheres were injected at rest, during exercise (mean heart rate = 245 beats/min), and during intravenous infusion of dypridamole (700 micrograms/kg). At autopsy the extent of necrosis was assessed by a point counting technique in the bed at risk. We found that 75-83% of the bed at risk remained viable. Although aspirin and disopyramide did not significantly alter the extent of infarction (37 +/- 36% untreated vs 17 +/- 6% treated), there was less variability of infarction in the treated group, and subendocardial blood flow during exercise was higher in the treated group compared to controls. The majority of infarction occurred in the subendocardial region. Animals with a large obtuse marginal branch developed significantly smaller infarcts (8 +/- 3%).(ABSTRACT TRUNCATED AT 250 WORDS)

Pathological features of Kawasaki disease (mucocutaneous lymph node syndrome).

Abstract: Kawasaki disease (mucocutaneous lymph node syndrome) (MCLS) is an apparently infectious disease, an etiological agent of which has not been established, with peak age incidence at about 1 year, but with progressively fewer cases occurring into the fourth decade. Early clinical features include fever, rash, conjunctival injection, dry reddened lips, oropharyngeal reddening, enlarged cervical nodes, and swelling and redness of hands and feet. Peeling of skin of fingers and toes, arthralgia, and marked thrombocytosis are frequent 1-2 weeks after onset. Myocarditis, cardiac valvulitis, and lymphocytic or mixed interstitial infiltration of pancreas, renal, splenic, and hepatic hilar regions are seen in the early phase, but arteritis, typically of extraparenchymal arteries, is the most important aspect of MCLS, hence the term infantile periarteritis nodosa, formerly applied to fatal cases of MCLS. Thrombosis of coronary artery aneurysms is the most common cause of death (rate about 0.5%). The peak time of death is 3-4 weeks from onset, but death from coronary occlusion has been seen as late as 14 years after the acute phase. Aneurysmal rupture with hemopericardium or retroperitoneal hemorrhage is rare, as are late brachial, iliac, or other arterial aneurysms. Pathological features of MCLS in the early and later stages are described and illustrated, and the epidemiologic, etiologic, forensic, and other aspects of the disease are discussed.

Myocardial lymphocytes. Fact, fancy, or myocarditis?

Abstract: The diagnosis of active lymphocytic myocarditis by the use of the endomyocardial bioptome is at present a hotly debated topic. However, the question of whether lymphocytes reside in the myocardium of individuals without systemic or cardiac disease has rarely been addressed, but is obviously of critical importance in helping to resolve this issue. Therefore, we examined endomyocardial biopsies obtained from 86 young heart disease-free cardiac transplant donors at the time of transplantation. Foci of inflammatory cells were found in eight (9.3%) cases and by definition contained greater than five inflammatory cells per focus. The inflammatory infiltrates were predominantly lymphocytic. Based on these results and those of others, it is becoming evident that there is a normal myocardial lymphocyte population which must be reckoned with when considering the diagnosis of myocarditis, realizing the potential therapeutic implications of this diagnosis.

Ischemic myocardial necrosis and papillary muscle dysfunction in infants and children.

Abstract: Ischemic myocardial and papillary muscle dysfunction has considerable implication in newborn infants and children with normal or malformed hearts. Papillary muscle dysfunction in adults primarily involves coronary artery occlusion and ischemic necrosis in the left ventricle and papillary muscles. Infants and children rarely develop coronary artery occlusion. Their myocardial dysfunction and injury occurs with nearly equal frequency in both ventricles as a result of underperfusion from a wide range of causes, including severe birth asphyxia, congenital heart disease, and complications of premature delivery. A history of cardiogenic shock, acute congestive heart failure with cyanosis and atrioventricular murmur, or persistent fetal circulation in a newborn without congenital heart disease should alert the pathologist to the possibility of ischemic myocardial necrosis (IMN). Older infants with ventricular hypertrophy, persistent pulmonary hypertension (PPHN), bronchopulmonary dysplasia (BPD), and those with malformed hearts involving severe ventricular hypertension due to outflow obstruction or pulmonary hypertension may have IMN, fibrosis, or dystrophic calcification alone or in combination. Animal models of adult ischemic cardiac injury may not be suitable for study of the newborn.

Cardiovascular effects of congenital infections.

Abstract: In the course of gestation, many bacteria, parasites, and viruses may infect the pregnant woman, but few cross the placenta to affect the fetus and fewer still affect the fetal heart. Although the incidence of fetal cardiac infection is low, the effect on the fetus is major. In terms of frequency, rubella virus, Toxoplasma gondii, and Coxsackie virus B are the principal infectious agents affecting the fetal heart, but any number of organisms may cross the placenta to affect the fetus. The pathogenesis of infection of the fetal heart relates to the agent and to the time of gestation when the infection occurs. The agent affects the heart along one or more of three separate pathways: inhibition of cell growth, cytolysis, and interference with the blood supply. Most agents cause cytolysis, stimulating inflammation and scarring. Although several agents carry the suspicion of teratogenicity, only rubella virus has been incriminated with certainty as capable of functioning along each of the three pathways with the potential to serve as teratogen.

The effects of metabolic diseases on the cardiovascular system.

Abstract: Many metabolic diseases result in pathological changes within the cardiovascular system, often with the most severe effects on the function of the heart and great vessels. Metabolic disorders affecting the heart include disorders of amino acid metabolism, storage diseases, neuromuscular diseases, diseases of metal and pigment metabolism, carnitine deficiency, and connective tissue disorders. Several inborn errors of metabolism may involve the myocardium due to the accumulation of abnormal metabolites in the myocardial cells. In addition, the heart valves and coronary vessels may be involved. If the predominant effect is in the myocardial cell, it will be manifested clinically as a cardiomyopathy. Some disorders, in particular oxalosis, may involve the conduction system as a result of the deposition of oxalate crystals and result in conduction disturbances such as in alkaptonuria, primary oxalosis, and homocystinuria. Myocardial involvement may result in cardiomyopathy of the three functional types: (1) congestive, as in Fabry's disease, (2) hypertrophic, as in glycogen storage disease, type II, or (3) restrictive, as in Gaucher's disease. In the storage disease severe valvular as well as myocardial involvement occur predominantly in the glycogen storage diseases, types II-IV, mucolipidoses, sphingolipidoses, and neuronal ceroid lipofuscinosis. There are a variety of neuromuscular disorders that may be associated with cardiomyopathy, including the muscular dystrophies, Friedreich's ataxia, and Kugelberg-Welander syndrome. The pathological features of these conditions are not specific, but result usually in a congestive form of cardiomyopathy. Patients with metal and pigment metabolic disorders include iron storage disease, either hemochromatosis or transfusional hemosiderosis, Menkes' kinky hair syndrome, and Dubin-Johnson syndrome. Either a restrictive or a congestive form of cardiomyopathy may occur. The systemic form of carnitine deficiency is an autosomal recessive disorder and may present as a cardiomyopathy with congestive heart failure and lipid accumulation in the myocardial cells. Connective tissue disorders are generalized diseases that may involve the heart and valvular tissue, but also the blood vessels. These include Marfan's syndrome, Ehlers-Danlos syndrome, osteogenesis imperfecta, and pseudo-xanthoma elasticum.

Arterial involvement in genetic diseases.

Abstract: Whereas the information on the subject of arterial status is sketchy and haphazard with respect to any one genetic disorder, the number of these diseases would have precluded the provision of a critical review within the scope of this presentation. Thus, it was deemed more meaningful to approach the subject selectively. A brief summary was provided on the nature of the arterial wall and its involvement in genetic diseases either as a primary target or a secondarily affected organ, and on \"affinity\" of various genetic disorders for a type (elastic, muscular, or smallest), segment (proximal, distal), and layer (intimal, medial, adventitial) of the arterial tree or the arterial wall, respectively. Genetic diseases may affect arteries by \"causing\" (a) congenital malformations, (b) alteration of the arterial \"makeup\" without necessarily producing definable lesions, and (c) modification of a nongenetic arterial disease (e.g., atherosclerosis), or by \"producing\" (d) arterial lesions that are characteristic of (even specific for?) a given genetic disorder. A few examples were selected to illustrate (b) (tuberous sclerosis; infantile GM1-gangliosidosis), (c) Wolman's disease; familial hyperlipoproteinemias), and (d) [Hurler's disease, neurofibromatosis; Ehlers-Danlos syndrome (type IV)]. Whenever available, the results of electron microscopic studies carried out in our laboratories were included. Some of these have not been reported in the literature to date. The need for a coordinated multidisciplinary approach to the study of genetic diseases in general is stressed in closing.

Myocardial injury in patients with aortic stenosis.

Abstract: Clinical studies of patients with aortic stenosis suggest that left ventricular myocardial injury is frequent. To examine the morphologic basis of this observation, we studied 32 patients with isolated aortic stenosis, no cardiac surgery, and hearts studied at autopsy after postmortem arteriography and fixation in distension. The patients were 46-87 years old (average 69), and 21 (66%) were male. Calcific aortic stenosis was present in 19 hearts, 12 had congenital bicuspid aortic valve, and 1 had rheumatic aortic stenosis. In 19 hearts there was moderate or marked coronary atherosclerosis, and 12 hearts had 17 myocardial infarcts. However, among 13 hearts with no or mild coronary atherosclerosis, 9 had either subendocardial myocardial contraction band necrosis, a lesion occurring when periods of no perfusion are followed by reflow, or focal replacement fibrosis. In 13 hearts there was subendocardial vacuolization of myocytes, an alteration produced by ischemia, that was not accounted for by coronary artery disease. Our results are consistent with clinical observations and show that ischemic myocardial injury may be associated with isolated aortic stenosis in the absence of coronary artery obstruction. The contraction band necrosis and vacuolated myocytes suggest that both episodic and sustained reductions of subendocardial blood flow occur in the presence of aortic stenosis.

Hydrops due to myocarditis in a fetus.

Abstract: At 18 weeks of gestation a fetus was studied sonographically because of advanced maternal age and found to have hydrops of unknown etiology with ascites, pleural, and pericardial effusions. An abortion was performed and in the fetal/placental material myocarditis and thyroiditis were documented. Maternal antibodies to Coxsackie virus B5 showed a onefold rise. Tentatively, the hydrops is assigned to Coxsackie virus myocarditis, a lesion not previously identified in fetuses.

Arterial involvement in genetic diseases.

Abstract: Whereas the information on the subject of arterial status is sketchy and haphazard with respect to any one genetic disorder, the number of these diseases would have precluded the provision of a critical review within the scope of this presentation. Thus, it was deemed more meaningful to approach the subject selectively. A brief summary was provided on the nature of the arterial wall and its involvement in genetic diseases either as a primary target or a secondarily affected organ, and on "affinity" of various genetic disorders for a type (elastic, muscular, or smallest), segment (proximal, distal), and layer (intimal, medial, adventitial) of the arterial tree or the arterial wall, respectively. Genetic diseases may affect arteries by "causing" (a) congenital malformations, (b) alteration of the arterial "makeup" without necessarily producing definable lesions, and (c) modification of a nongenetic arterial disease (e.g., atherosclerosis), or by "producing" (d) arterial lesions that are characteristic of (even specific for?) a given genetic disorder. A few examples were selected to illustrate (b) (tuberous sclerosis; infantile GM1-gangliosidosis), (c) Wolman's disease; familial hyperlipoproteinemias), and (d) [Hurler's disease, neurofibromatosis; Ehlers-Danlos syndrome (type IV)]. Whenever available, the results of electron microscopic studies carried out in our laboratories were included. Some of these have not been reported in the literature to date. The need for a coordinated multidisciplinary approach to the study of genetic diseases in general is stressed in closing.

Autopsy-determined causes of death following heart valve replacement.

Abstract: Despite numerous attempts, the perfect artificial heart valve has not yet been designed1. While there is a plethora of clinical and haemodynamic reports on various valve prostheses, scanty data have been published on the pathology of patients who die with prosthetic valves. Although more than 30 000 patients in the United States alone undergo this procedure each year, few studies have analysed the autopsy-determined causes of death in a large population of such patients2. Newer and better prosthetic valves are being continuously introduced3. The ultimate evaluation of a prosthesis can only be obtained from patients with implants. Identification of fatal complications following heart valve replacement is of the greatest importance in evolving means of lowering the postoperative mortality rate. Autopsy evaluation of a patient’s cause of death is more accurate than a solely clinical assessment4,5 since it gives substantial evidence as to whether or not the death was valve-related6.

Familial aortic dissection in absence of ascending aortic aneurysms: a lethal syndrome associated with precocious systemic hypertension.

Abstract: The interaction of elevated blood pressure and aortic metabolism in the genesis of aortic dissection is uncharacterized. A kindred with fatal familial aortic dissection in association with precocious systemic hypertension and in absence of a definable connective tissue syndrome has undergone genealogical, clinical, pathological, and biochemical evaluation. Six family members spanning three generations have died of acute dissection. Five men died at a mean age of 28 years (range 22-34), while the proband's paternal grandmother died at 62 years of age. All were hypertensive. A constellation of subtle clinical features points toward deficient integrity of connective tissues; however, major hallmarks of known connective tissue syndromes including aortic root ectasia or aneurysms are absent. Studies of cultured dermal and aortae fibroblasts of two of the proband's brothers mitigate against Ehlers-Danlos IV syndrome. This family's susceptibility to aortic dissection reflects the synergistic liability of coexistent elevated blood pressure and metabolic abnormalities in the genesis of aortic degeneration.

The effect of hemodilution with fluorocarbon or dextran on regional myocardial flow and function during acute coronary stenosis in the pig.

Abstract: The effect of replacement of approximately 50% of the blood volume, in the presence of critical coronary stenosis, was investigated in anesthetized pigs. Two agents were used for replacement: 6% dextran 70 and Fluosol-DA, a fluorocarbon "blood substitute," capable of transporting oxygen by virtue of its high solubility. Critical coronary stenosis of 15-min duration was imposed on the circumflex coronary artery by means of a micrometer snare, before and after an exchange-transfusion with one of the above acellular agents, resulting in comparable reductions of myocardial blood flow (determined by microspheres) to the circumflex zone. In the ischemic zone, systolic wall-thickening (as determined by sonomicrometry) was reduced by 62 +/- 10% in the dextran-diluted pigs, but only by 33 +/- 7% in the Fluosol-diluted pigs (p less than .05). Estimated oxygen delivery-rate in this zone, during coronary constriction, was 6.2 and 7.5 ml min-1 100 g-1, respectively. Electron microscopic examination of the normally perfused zone of the heart showed no morphological change attributable to Fluosol. The findings suggest that, in the presence of critical coronary stenosis, hemodilution by Fluosol-DA can be tolerated, while similar hemodilution with dextran results in aggravation of myocardial hypoxia. In three instances, severe reactions were observed immediately following the administration of Fluosol. These were suggestive of complement-activation and were excluded from the analysis.

Ciliated smooth muscle cells in atherosclerotic lesions of human aorta.

Abstract: One or two rudimentary cilia were observed by electron microscopy in smooth muscle cells (SMCs) of fatty dots and streaks, but not in normal intima of human aorta Similar organelles are known to occur in many cell types and various species, but to the best of the author's knowledge, have never been found in the SMCs of arterial or other tissues of man in health and disease; recently, they were reported to be present in the SMCs of experimental atherosclerosis in rabbits The rudimentary cilia observed in this study had a "9 + 0" axoneme (microtubular complex) and differed also in other aspects from the classical cilia Semiserial sections of SMCs containing a diplosome disclosed that on several occasions both of its constituent centrioles gave rise to rudimentary cilia SMCs containing cilia or their basal bodies were observed more often in the human than in experimental atherosclerotic lesions Whereas the function and significance of the rudimentary cilia remain largely unknown, the current theory proposes that a sudden transformation from a mitotic replicative to a nonmitotic structured tissue "diverts" centrioles to the formation of these unusual organelles It is conceivable that rudimentary cilia could serve as morphological indicators of aborted mitosis in human atherosclerotic lesions

Evaluation of coronary native and coronary collateral pressure gradients in the conscious dog

Abstract: Sixteen dogs were instrumented chronically with a left circumflex (CIRC) Ameroid constrictor, and with CIRC, left anterior descending (LAD), aortic, left atrial and pulmonary artery (PA) catheters. Premature mortality was 12.5% prior to the last measurements of pressure at 50 +/- 3 days (mean +/- SE). Five animals developed closure of the Ameroid constrictor at 5 +/- 1 days with an LAD to CIRC pressure gradient of 57 +/- 8 mm Hg. Eleven animals developed closure of the Ameroid constrictor at 18 +/- 1 days with an LAD to CIRC pressure gradient of 29 +/- 3 mm Hg. Three animals in the former group had gross evidence of a myocardial infarction on postmortem examination. None of the animals in the latter group showed evidence of a myocardial infarction. Thus, closure of a CIRC Ameroid constrictor and subsequent collateral vessel development can be monitored chronically by the LAD to CIRC pressure gradient with a high survival, low infarction rate. This chronic model thus provides an accurate measure of coronary native and collateral pressures in unsedated dogs.

Ciliated smooth muscle cells in atherosclerotic lesions of human aorta.

Abstract: One or two rudimentary cilia were observed by electron microscopy in smooth muscle cells (SMCs) of fatty dots and streaks, but not in normal intima of human aorta. Similar organelles are known to occur in many cell types and various species, but to the best of the author's knowledge, have never been found in the SMCs of arterial or other tissues of man in health and disease; recently, they were reported to be present in the SMCs of experimental atherosclerosis in rabbits. The rudimentary cilia observed in this study had a \"9 + 0\" axoneme (microtubular complex) and differed also in other aspects from the classical cilia. Semiserial sections of SMCs containing a diplosome disclosed that on several occasions both of its constituent centrioles gave rise to rudimentary cilia. SMCs containing cilia or their basal bodies were observed more often in the human than in experimental atherosclerotic lesions. Whereas the function and significance of the rudimentary cilia remain largely unknown, the current theory proposes that a sudden transformation from a mitotic replicative to a nonmitotic structured tissue \"diverts\" centrioles to the formation of these unusual organelles. It is conceivable that rudimentary cilia could serve as morphological indicators of aborted mitosis in human atherosclerotic lesions.

The role of endomyocardial biopsy in the diagnosis of cardiac disorders in infants and children.

Abstract: Endomyocardial biopsies from 26 children were studied by light and electron microscopy. Follow-up biopsies were obtained in 2 patients. The biopsy showed evidence of myocarditis in 6 patients, including 1 with features of sarcoidosis. Twelve biopsies showed features consistent with dilated cardiomyopathy. Endocardial fibroelastosis was documented in two of these biopsies. In two biopsies striking myocardial hypertrophy with prominent myofibrillar disarray suggested hypertrophic cardiomyopathy. Two biopsies from patients with clinical hypertrophic cardiomyopathy showed ultrastructural evidence of a mitochondrial abnormality. No morphological changes were detected in five biopsies, of which two had carnitine deficiency. A biopsy sampled the overlying myocardium in 1 patient with a cardiac fibroma, and a biopsy of the right ventricle was normal in a patient with Noonan's syndrome and hypertrophic cardiomyopathy limited to the left ventricle. Thus, of 28 biopsies in this series, the morphological changes were diagnostic in 10 (35%) and an additional 13 (46%) biopsies documented an abnormality of the myocardium. Endomyocardial biopsies can be of significant use in the diagnosis of selected cardiac disorders in childhood.

Double valve disease in systemic lupus erythematosus. Case report and literature review.

Abstract: A young, nonhypertensive female with advanced systemic lupus erythematosus (SLE) presented in congestive cardiac failure due to aortic and mitral regurgitation. The valvular lesions resulted from organization of valvular pocket Libman-Sacks vegetations. Her clinical course mimicked infective endocarditis. She is only the third recorded patient with SLE valvular disease warranting double valve replacement. This patient, who had her valvular disease at presentation (prior to initiation of steroid therapy), illustrates that untreated SLE per se may produce severe organic valvular disease.

Constrictive and restrictive pulmonary hypertension in the newborn and infant.

Abstract: The normal pulmonary circulation is constricted at birth and, as judged by its low arterial density, is relatively more restricted than in the older infant and child. During adaptation to air breathing, pulmonary arterial dilatation occurs rapidly, but also the compliance of the resistance arterial segment increases. In the fetus and newborn, the resistance segment is proximal to the respiratory or alveolar surface. Further expansion of the pulmonary vascular bed occurs by growth in size of lumen diameter of existing arteries and growth of new ones. Multiplication of alveoli and arteries is relatively dissociated--alveolar density can increase normally without normal vascular multiplication. Persistent pulmonary hypertension of the newborn occurs because of (1) lung hypoplasia associated with hypoplasia of the vascular bed, usually affecting both size and number of units, (2) abnormal muscularization of intraacinar arteries before birth, causing restriction of vascular volume, (3) failure of the adaptation programs, and (4) hyperreactivity. Immaturity of the circulation is apparent as hyperreactivity or "twitchiness": this can be superimposed on each of the other types. A hyperirritable vascular bed can cause a labile and then a fixed pulmonary hypertension that does not respond to dilators.

Intracysternal crystalline cytoplasmic inclusions in a cardiac myxoma.

Abstract: Electron microscopy of an atrial myxoma removed at surgery from a 56-year-old woman revealed unusual intracysternal inclusions in the cytoplasm of tumor cells. These structures appeared in the rough endoplasmic reticulum and consisted of multilaminar arrays of crystalline plates of regular periodicity, about 10 nm apart. Although crystalline and other intracysternal inclusions may occur in different pathologic disorders, their occurrence in an atrial myxoma is a hitherto unreported observation.