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Biomedical subjects

H A Heggtveit

Publications and source records attributed to H A Heggtveit.

At least 19 recordsLinked to original sources
PubMed1999

Pancreatic pseudocyst: heparin-induced haemorrhage through the ampulla of Vater.

Bleeding from a pancreatic pseudocyst through the ampulla of Vater is a rare cause of overt gastrointestinal haemorrhage. Previously described mechanisms of such haemorrhage are reviewed. We report a case of a 74-year-old female with a pancreatic pseudocyst that bled into the gastrointestinal tract following the administration of heparin. We believe that this is the first reported case of its kind.

Aged↗
PubMed1999

Left ventricular involvement in right ventricular dysplasia/cardiomyopathy.

OBJECTIVE: To characterize pathological features of left ventricular (LV) involvement in right ventricular dysplasia/cardiomyopathy (RVD/C). DESIGN: Retrospective morphological case study. SETTING: Two referral-based university medical centres. MATERIALS: Seventeen hearts were studied: 15 from sudden cardiac deaths outside hospital and two explanted hearts, one removed for intractable arrhythmias and the other for right-sided heart failure. The subjects (three female) were aged 16 to 60 years. MAIN RESULTS: All had typical right ventricular features of RVD/C and morphological evidence of LV wall involvement, seven with microscopic changes only. Of 10 hearts with gross and microscopic lesions, nine had large or laminar segments involved. The LV free wall was affected in all cases and the ventricular septum (VS) in 15. Sixteen hearts were hypertrophied. In involved areas, the LV or VS walls were of 'normal' thickness or slightly thinned. Five histological patterns of involvement were recognized, of which four were found in the LV. More severe LV involvement was seen in the hearts of older patients. Complete transmural fatty replacement of the myocardium was not observed, nor were the LVs aneurysmal. Minimal or mild focal aggregates of inflammatory cells were seen in nine hearts and moderate inflammatory changes in two. Inflammation was usually associated with myocyte atrophy and only rarely with myonecrosis. CONCLUSIONS: This study suggests that patients with RVD/C who live long enough will likely have LV free wall involvement with frequent VS involvement. Pathologists may miss LV involvement on gross examination. It should be sought diligently in patients dying of the condition or receiving transplants for heart failure. Appropriate histological sections from both free wall and septum must be examined.

Adolescent↗
PubMed1994

Sudden death due to coronary artery anomalies: a case report and clinical review.

Congenital anomalies of the coronary arteries are relatively uncommon conditions with an incidence of approximately 2% in the adult population. Although less common than acquired coronary artery disease, these anomalies may be associated with myocardial ischemia and its consequences; angina, arrhythmia, infarction, and sudden death. A 21-year-old female patient with no significant prior medical history was found dead at home. Postmortem examination revealed high take-off of the right coronary artery with acute down-ward angulation of the proximal right coronary artery and acute downward angulation of the left main coronary artery. Microscopic examination revealed global myocardial ischemia consistent with a terminal ventricular dysrhythmia. There was no evidence of any other disease processes. Detailed toxicological investigation was negative. The Regional Forensic Pathology Unit experience with sudden death due to congenital coronary artery anomalies is presented along with a review of the current literature.

Adult↗
PubMed1992

Right ventricular dysplasia: morphological findings in 13 cases.

OBJECTIVE: To characterize the pathological features of right ventricular dysplasia (RVD). DESIGN: Retrospective morphological case study. SETTING: Three referral-based university medical centres. PATIENTS: Thirteen subjects (one female) aged 16 to 55 years including 10 necropsy hearts from sudden deaths out of hospital, one explant heart and two partial right ventricular resections from patients with intractable ventricular tachycardia. MAIN RESULTS: Most hearts showed hypertrophy and localized or generalized dilatation of the right ventricle. Transillumination revealed myocardial thinning of variable configuration usually conforming to regions of dilatation. Common sites of involvement were apex, infundibular region and posterobasal wall. Histologically, focal or extensive segments of right ventricular myocardium were absent or replaced. Three patterns were found: right ventricle markedly thinned, epicardium and endocardium contiguous, virtually no intervening tissue; wall normal thickness or thinned, myocardium almost totally replaced by fat; and wall normal or thin, myocardium largely replaced by fat with scattered residual myocardial cells and fibrous tissue (the predominant pattern). Endocardial fibrosis was present in eight cases and focal mononuclear cell infiltrates in 10. Electron microscopy in two cases showed nonspecific findings. CONCLUSIONS: RVD has gross and microscopic features which permit its recognition. While a majority of cases are likely congenital (genetic or acquired in utero), the possibility of postnatally acquired conditions (inflammatory, toxic, ischemic) inducing RVD must be explored. The incidence and importance of RVD as a cause of sudden death can only be assessed by continued systematic and detailed studies of patients with recurrent ventricular tachycardia and of hearts, especially from sudden death victims. Although uncommon, RVD should be considered in the differential diagnosis of arrhythmia and sudden death by both clinicians and pathologists.

Adolescent↗
PubMed1990

Rupture of both left ventricular papillary muscles following acute myocardial infarction.

A 77-year-old woman collapsed shortly after arrival at the emergency department and attempts at resuscitation were unsuccessful. Autopsy revealed an evolving recent transmural myocardial infarct in the posterolateral free wall of the left ventricle with rupture of both papillary muscles. No well documented description of post infarction dual papillary muscle rupture was found in the literature.

Aged↗
PubMed1989

Food safety and health effects of canola oil.

Canola oil is a newly marketed vegetable oil for use in salads and for cooking that contains 55% of the monounsaturated fatty acid; oleic acid, 25% linoleic acid and 10% alpha-linolenate [polyunsaturated fatty acid (PUFA)], and only 4% of the saturated fatty acids (SFAs) that have been implicated as factors in hypercholesterolemia. It is expressed from a cultivar of rapeseed that was selectively bred from old varieties in Canada to be very low in erucic acid--a fatty acid suspected to have pathogenic potential in diets high in the original rapeseed oil in experimental animals. Canola oil is free of those problems. It is the most widely consumed food oil in Canada, and has been approved for Generally Recognized as Safe (GRAS) status by the Food and Drug Administration (FDA) of the United States Department of Health and Human Services. The fatty acid composition of canola oil is consistent with its use as a substitute for SFAs, in meeting the dietary goals recommended by many health associations: an average diet containing about 30% of calories as fat made up of less than 10% SFAs, 8-10% PUFAs in a ratio of linoleic to linolenic acids between 4:1 and 10:1, the remainder being monounsaturated fatty acids. No single oil meets these current recommendations for ratios of PUFA/monounsaturated/polyunsaturated fatty acid ratios as the sole source of cooking and salad oil.

Consumer Product Safety↗
PubMed1989

Death following coronary angiography in a young woman with isolated left coronary ostial stenosis.

A 35-year-old woman with angina of five years duration underwent elective cardiac catheterization and coronary angiography which revealed left main stenosis. Immediately afterwards, the patient became distressed, hypotensive and bradycardic. She died despite emergency percutaneous transluminal coronary angioplasty and resuscitative efforts. Autopsy confirmed isolated left coronary ostial stenosis due to the combination of a congenital abnormality of the ostium and initial segment of left main coronary artery, together with a superimposed myointimal flap bridging the ostium. A unique association was an abnormal configuration of the ostia of the branches of the aortic arch.

Adult↗
PubMed1985

Metal wear in Lillehei-Kaster heart valve prostheses.

Ten Lillehei-Kaster heart valve prostheses, in situ for up to 10 years and recovered at surgery or necropsy, were examined by light and scanning electron microscopy. All showed metal wear on the luminal aspect of their struts. The volume of wear related to the duration a prosthesis had been in situ. The worn metal showed distinct, transverse surface corrugations, which became more obvious with time. Aortic prostheses wore more and faster than mitral ones. One strut usually showed more wear than the other, a change likely due to specific manufacturing methods. It is believed that the pattern of wear is caused by a velocity-controlled stick-slip abrasive wear process, resulting from an interaction between the edge of the moving pyrolytic carbon disc, the struts' titanium surface, and the protein coat covering that surface. None of the patients had prosthesis dysfunction attributable to metal wear. Disc escape seems unlikely considering the degree of wear observed after 10 years. Furthermore, the surface corrugations did not appear to cause disc sticking or other problems. However, clinicians might consider monitoring patients who have borne these prostheses for greater than 10 years.

Aortic Valve↗
PubMed1982

Determinants of myocardial hemorrhage after coronary reperfusion in the anesthetized dog.

Intramyocardial hemorrhage often occurs with reperfusion in experimental acute myocardial infarction and is thought to be associated with extension of necrosis. To determine if hemorrhage was associated with extension of necrosis, 20 anesthetized dogs were reperfused after 6 hours of circumflex coronary artery occlusion and 10 others had control occlusion with no reperfusion. Fifteen of the 20 reperfused dogs had gross hemorrhage and none of the control dogs did. In 12 reperfused and 10 control dogs, radioactive microspheres were injected after coronary occlusion to quantitate collateral flow and in the reperfusion group microspheres were injected to quantitative reflow. Complete flow data were available in eight reperfused and 10 control dogs. Twenty-four hours after coronary occlusion, 1-g segments of infarct and control regions were analyzed for hemorrhage, collateral flow and creatine kinase activity. Serial microscopic examination was performed in eight additional dogs reperfused after 6 hours to determine if hemorrhage occurs into otherwise microscopically normal myocardium. Pathologic examination indicated that hemorrhage did not occur into otherwise microscopically normal myocardium. In dogs with hemorrhage, the extent of hemorrhage was inversely related to myocardial creatine kinase concentration and collateral flow. Mean collateral flow in 47 hemorrhagic segments was 4.5 ml/100 g (4.2% of control). Mean creatine kinase in 36 hemorrhagic segments was 233 mIU/g (21% of control). No hemorrhage was found in areas with collateral flow more than 21% of control or creatine kinase more than 37% of control. Mean reflow in hemorrhagic segments was 78.5% of control flow. These studies indicate that hemorrhage on reperfusion is associated with severe myocardial necrosis and markedly depressed flow before reperfusion and thus occurs only into myocardium already markedly compromised at the time of reperfusion. There is no evidence for hemorrhage into areas that had normal or even moderately depressed flows before reperfusion.

Animals↗
PubMed1982

Perioperative myocardial infarction caused by atheroembolism.

We have demonstrated a phenomenon occurring during coronary artery bypass grafting (CABG) which has not been previously described. Thirteen instances of fatal perioperative myocardial infarction following CABG were associated with intraoperative atheromatous embolization in the coronary microcirculation. In five cases the emboli originated from ulcerative atherosclerotic lesions in the aortic root at the site of the vein graft ostia; in two cases they likely emanated from coronary endarterectomy sites; and in two cases from mechanical disruption of plaques in the major epicardial coronary arteries during the operation. These nine cases occurred during initial revascularization procedures. We have performed 4,095 initial CABG procedures, and the nine cases represent a risk of 0.22%. A further four cases occurred during repeat CABG procedures and resulted from manipulative disruption of atheroma in old vein grafts. Our total number of repeat CABGs is 175, and the risk at reoperation is 2.29%; this represents a tenfold increase in risk for this complication at reoperation. Inadequate histologic sampling of the myocardium at autopsy will necessarily result in underestimation of the incidence of this phenomenon. Analysis of angiograms prior to repeat CABG can identify patients at increased risk who have severe graft atherosclerosis as opposed to myointimal hyperplasia. To reduce the incidence of atheroembolism at reoperation, we advocate ligation of the vein graft at the level of the distal anastomosis as early as possible during dissection on reopening the chest.

Adult↗