Thallium 201 myocardial scintigraphy and exercise testing in patients prior to and following coronary artery revascularization.
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Biomedical subjects
Publications and source records attributed to L J Mills.
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Right-sided blunt diaphragmatic rupture is not uncommon. Its incidence has definitely increased. As expected, total or partial herniation of the liver commonly occurs with this entity. Diaphragmatic-pericardial rupture with visceral herniation into the pericardial cavity and other rare injuries have been diagnosed, but we found no report of extension of a diaphragmatic tear of a previously undiagnosed right-sided diaphragmatic rupture with total herniation of the liver. Such a case is reported here.
Prosthetic valvular dysfunction resulting in clinically significant complications occurred in six patients with Hancock porcine heterografts. In one patient with a prosthetic valve in the aortic position, massive prosthetic thrombosis resulted in sudden death. In two patients who had a mitral prosthesis, thrombosis resulted in congestive heart failure and systemic embolization; in one of the latter patients, the thrombi were infected with Candida sp. Calcification of organizing thrombi and cusp tissue resulted in valvular stenosis and congestive heart failure in one patient with an aortic prosthesis and in two patients with mitral prostheses. Four of the six patients died. The prosthetic valves had been in place for 6 months to 3 years before onset of complications. During the same 4-year interval, over 400 porcine prosthese were inserted. This report provides further clarification of the nature and frequency of clinical complications related to degeneration and thrombosis of Hancock porcine heterograft valves.
The high incidence of stricture following conventional therapy for caustic esophageal injuries prompted us to incorporate the esophageal stenting technique of Reyes and colleagues [3, 5, 6] into our protocol for management of such patients. Four adult patients were treated following severe esophageal burns caused by the ingestion of caustic drain cleaner. The severity of the burn was established by early esophagoscopy. Laparotomy and gastrotomy revealed severe but nontransmural gastric burns. The stent was left in place for 21 days. Antibiotics and corticosteroids were also employed. There have been no late strictures. One patient required laryngeal dilation for adhesions and another, tracheal dilation for subglottic stenosis. Contrast roentgenographic studies and esophageal manometry have revealed nearly normal esophageal function up to 20 months following the injury.
The prostaglandin synthetase inhibitor indomethacin was given orally or intravenously to pregnant ewes. This resulted in the fetal pulmonary to systemic arterial mean blood pressure difference across the ductus arteriosus rising significantly, presumably secondary to constriction of the ductus arteriosus. The pressure difference was due to pulmonary arterial hypertension, and not due to a fall in systemic arterial mean blood pressure. Fetal arterial blood gas tensions and pH values were normal throughout. In five experiments the pressure difference could be promptly but temporarily reversed by the administration of PGE1 into the fetal inferior vena cava. Indomethacin was present in fetal blood, and maternal plasma prostaglandin levels were suppressed. Indomethacin administration during pregnancy causes constriction of the fetal ductus arteriosus and fetal pulmonary arterial hypertension which, if severe, may cause rapid fetal death. It is possible that this mechanism may be one cause of persistent pulmonary hypertension or tricuspid insufficiency or both in the newborn infant.
Although electrocardiographic evidence of right ventricular hypertrophy is considered common in newborn infants with coarctation of the aorta, the reason for this finding is not well established. Investigations of the pulmonary vascular bed of these infants have resulted in variable findings, probably due to the differences in morphometric techniques, coexisting cardiac defects, and variable postnatal age at time of death. To study more carefully the pulmonary vascular bed, we produced coarctation of the aorta in fetal lambs at 103--126 days gestation. Twelve to 32 days later the fetuses were reoperated on and systemic and pulmonary arterial blood pressures, and arterial blood gas tensions were determined to be normal. At autopsy, juxtaductal coarctations extended a mean of 2.8 mm into the aortic lumen and occupied 9.5 mm of the aortic circumference. The fifth-generation pulmonary resistance vessels had increased medial width (p less than 0.01), decreased external diameter (p less than 0.001), and increased medial width/external diameter ratios (p less than 0.001) compared with vessels from control fetuses. The number of small muscular pulmonary vessels/cm2 lung tissue was significantly reduced (p less than 0.01) in the study animals compared with the control animals. These alterations of the pulmonary vascular bed were not due to fetal pulmonary arterial hypertension or fetal hypoxemia. These pulmonary vascular changes may explain the occurrence of pulmonary hypertension and right ventricular hypertrophy in newborn infants with coarctation of the aorta.
The prostaglandin synthetase inhibitor indomethacin was given orally or intravenously to pregnant ewes. This resulted in a significant rise in the fetal pulmonary-to-systemic arterial mean blood pressure difference across the ductus arteriosus, presumably secondary to constriction of the ductus arteriosus. In five experiments the pressure difference could be promptly but temporarily reversed by the administration of prostaglandin E1 (PGE1) into the fetal inferior vena cava. Fetal lungs from study and control animals were fixed by perfusion at measured pulmonary arterial mean blood pressure, and fifth-generation resistance vessels were studied. The medial width/external diameter ratio was significantly increased in the study vs the control lungs due to increased smooth muscle and decreased external diameter. In addition, study fetuses had acute degenerative myocardial changes in the tricuspid valve papillary muscles, the right ventricular free wall and the interventricular septum. Similar changes were not seen in control fetuses. Indomethacin administration during pregnancy causes constriction of the fetal ductus arteriosus, fetal pulmonary arterial hypertension, and right ventricular damage. If severe, this may cause rapid fetal death. If less severe, in the newborn infant, this mechanism may be one cause of persistent pulmonary hypertension due to vasoconstriction and increased pulmonary arterial smooth muscle and/or tricuspid insufficiency due to papillary muscle infarction.
Traumatic injury of the diaphragm is not an infrequent occurrence. With the rise in violence and increasing use of automobiles, more diaphragmetic injuries may be seen, especially in inner-city hospitals. Sixty-six cases from our institution within the last five years were reviewed. Of these there were 41 penetrating injuries and 23 secondary to blunt trauma. Two cases were surgically induced following a difficult decortication for pleuropulmonary tuberculosis. There were ten deaths (15 percent mortality). All deaths were related to the severity of associated injuries. In addition, we analyzed 307 patients with multiple injuries who were dead on arrival and were autopsied by the county medical examiners in a 24-month period. Of the 307 autopsied cases, 16 (5.2 percent) had ruptured diaphragms. Interestingly, all but one of these cases were associated with thoracic aortic injuries. Diagnoses of penetrating diaphragmatic injuries were made during exploration of other injuries. In blunt diaphragmatic rupture, a high index of suspicion in most important in the diagnosis. In 10 of 23 blunt injuries, visceral herniation was noted on initial x-ray films. In four, follow-up films several hours to a day later showed loops of bowel in the chest. In nine cases, there were no apparent visceral herniations on initial films, and in these, the diagnosis was made during surgery for other indications. The surgical approach to diaphragmatic injuries is individualized. Acute left-sided injuries are best approached through the abdomen. Acute right-sided injuries and all chronic injuries should be approached through the chest.
Tuberculous aortic aneurysm is a rare disease entity. The majority of affected patients succumb to perforation and exsanguination. The only chance for survival and cure is by resection and prolonged antituberculosis chemotherapy. Our case illustrates the high risk of rupture of tuberculous aortic aneurysms. Post-mortem examination revealed that the mechanism of aneurysm formation was by direct caseous involvement of the descending thoracic aorta from a juxtaposed left upper lobe parenchymal tuberculous process. Our findings also favor the concept that miliary dissemination (in the presence of tuberculous aortic aneurysm) is the result rather than the cause of the tuberculous aortic process.
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Fifty patients with the clinical syndrome of unstable angina pectoris were evaluated. Twenty-seven were randomized into medical or surgical treatment groups and subsequently followed up. The results of the study reveal that: (1) there is approximately a 16 percent incidence rate of significant left main coronary artery disease in patients with this entity at our institution; (2) 10 percent of patients do not have angiographically significant coronary artery disease; (3) pain relief is better in the surgically treated patients, but the 1 1/2 year survival rate is not significantly different between the groups; (4) 50 percent of the medically treated patients again had the syndrome of unstable angina pectoris in the initial few months of the follow-up period; (5) the operative and late postoperative mortality rate in patients presenting with unstable angina pectoris and left main coronary artery disease in this small group of patients was 43 percent; and (6) four of six patients with this syndrome whose condition was deemed inoperable and who were not randomized died within the subsequent few months.
Blunt injuries to the ascending aorta and branches of the aortic arch are unusual but must be considered in any victim of a high speed decelerating injury. Because there are no characteristic clinical or roentgenographic findings, aortography is the only definitive method of establishing the diagnosis. Aortography should therefore, be performed upon any patient who has had a high speed decelerating injury, regardless of the clinical or the roentgenographic findings. An early operation will prevent exsanguination.
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A patient with a dissecting aneurysm of the ascending aorta had fever of unknown origin. Although his clinical picture included a number of classical features of his disorder, these were initially misinterpreted, largely because fever was the patient's chief complaint. Polymorphonuclear leukocytes sequestered within the aortic hemagen as they disintegrated. This case emphasizes the protean nature of the dissecting aortic aneurysm, adding yet another distinct clinical manifestation, fever of unknown origin, with which it may be associated.
Forty-three patients with aortic rupture secondardy to blunt trauma have been treated at the University of Micigan within the past 10 years with an overall salvage rate of 70%. The diagnosis should be suspected in anyone who has sustained a high speed decelerating injury, if the chest roentgenogram shows media-stinal widening, whether or not there is hypertension of the upper extremities; systolic murmur, or external evidence of chest injury. Aortography should be employed to confirm the diagnosis and to determine the site or sites of rupture. Repair of the lesion should be undertaken as soon as possible and takes priority in most instances over associated injuries. Repair in almost all cases can be accomplished safely and quickly using a bypass shunt without the aid of extracorporeal circulation.